Strength and Conditioning in Sports

A good sport scientist and coach must understand both the underlying
mechanisms and the practical application of training principles. Strength
and Conditioning in Sports: From Science to Practice is unique in that it
covers both of these areas in a comprehensive manner. This textbook
“connects” the mechanism with practical application.
Selecting the appropriate training process is paramount to success in
competitive sport. A major component of this textbook is the detailed
explanations of developing that process from creating an annual plan,
selection of the appropriate periodization model and how to program that
model.
In application, connecting physiology to performance can be enhanced
by using appropriate athlete monitoring techniques. Although there can be
overlap, monitoring can be divided into two components: fatigue
management and program efficacy. One of the features of this text is the in-
depth description of how the monitoring process should take place and how
monitoring data can be used in program application.
This exciting new text provides a comprehensive overview of the
application of science to sport and will be key reading for undergraduate
and postgraduate students of strength and conditioning, athletic training,
exercise physiology, human performance, personal training, and other
related disciplines of sport science and kinesiology.

Michael H. Stone, PhD, is the Exercise and Sports Science Laboratory

Director and the PhD Coordinator in the Department of Sport, Exercise,
Recreation and Kinesiology at East Tennessee State University, USA.
Timothy J. Suchomel, PhD, is an Associate Professor in the Department of
Human Movement Sciences at Carroll University, USA.
Strength and Conditioning in Sports
From Science to Practice

Michael H. Stone and Timothy J. Suchomel

with W. Guy Hornsby, John P. Wagle, and Aaron
J. Cunanan
Cover image: © South_agency / Getty Images
First published 2023
by Routledge
605 Third Avenue, New York, NY 10158
and by Routledge
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Routledge is an imprint of the Taylor & Francis Group, an informa business
© 2023 Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P.
Wagle, and Aaron J. Cunanan
The right of Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby,
John P. Wagle, and Aaron J. Cunanan to be identified as authors of this
work has been asserted in accordance with sections 77 and 78 of the
Copyright, Designs and Patents Act 1988.
All rights reserved. No part of this book may be reprinted or reproduced or
utilised in any form or by any electronic, mechanical, or other means, now
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Trademark notice: Product or corporate names may be trademarks or
registered trademarks, and are used only for identification and explanation
without intent to infringe.
Library of Congress Cataloging-in-Publication Data
Names: Stone, Michael H., 1948– author. | Suchomel, Timothy J., author.
Title: Strength and conditioning in sports : from science to practice /
Michael H. Stone and Timothy J. Suchomel ; with W. Guy Hornsby, John P.
Wagle, and Aaron J. Cunanan
Description: New York, NY : Routledge, 2022. | Includes bibliographical
references and index. |
Identifiers: LCCN 2021061822 (print) | LCCN 2021061823 (ebook) |
ISBN 9780367560249 (hardback) | ISBN 9780367560225 (library binding)
|
ISBN 9781003096139 (ebook)
Subjects: LCSH: Sports–Physiological aspects. | Exercise. | Physical
education and training.
Classification: LCC RC1235 .S747 2022 (print) | LCC RC1235 (ebook) |
DDC 613.7/1–dc23/eng/20211228
LC record available at https://lccn.loc.gov/2021061822
LC ebook record available at https://lccn.loc.gov/2021061823
ISBN: 978-0-367-56024-9 (hbk)
ISBN: 978-0-367-56022-5 (pbk)
ISBN: 978-1-003-09613-9 (ebk)
DOI: 10.4324/9781003096139
Typeset in Baskerville
by Newgen Publishing UK
Contents

List of Figures
List of Tables
About the Contributors
Preface

PART I

1 Neuromuscular Physiology

PART II

2 Bioenergetics

3 Neuroendocrine Factors

4 Nutrition and Metabolic Factors

5 Ergogenic Aids

PART III

6 Physical and Physiological Reponses and Adaptations

PART IV

7 General Concepts and Training Principles for Athlete

Development
 8 Exercise Selection

Part V

9 Athlete Monitoring

10 Developing the Training Process

Index
Figures

1.1 Typical muscle fiber arrangements and their variations

1.2 Organization and compartmentalization of skeletal muscle
1.3 Basic mitochondrial structure
1.4 Oxidative phosphorylation enzymes in the inner membrane
1.5 Mitochondrial replication
1.6 Basic structure of sarcolemma
1.7 The sarcolemma supporting cytoskeleton
1.8 (a) The sarcoplasmic reticulum. (b) The T-tubule networks
1.9 Myosin and myosin myofilament structure
1.10 Molecular structure of the myosin head
1.11 (a) Structure of the actin myofilament and regulatory proteins.
(b) The sarcomere and M-line. (c) The sarcomere and D- and
C-zones
1.12 Force as a function of sarcomere length
1.13 (a) Isolated muscle preparation for length–tension
investigations. (b) Stimulation for in vivo preparations
1.14 (a) Isometric twitch force production. (b) Force production
related to muscle length
1.15 Force production in relation to increased stimulation frequency
1.16 Force-velocity relation during concentric-isometric-eccentric
muscle actions in isolated muscle
1.17 Power as a product of concentric force and velocity
1.18 Force-velocity curve for intact muscle
1.19 Basic neuron anatomy
1.20 Example of an ionic dynamic equilibrium across cell
membranes
1.21 Action potential propagation
1.22 (a) Axonal branching at the neuromuscular junction. (b) Motor
end plate and neuromuscular junction
1.23 Somatic-somatosensory nervous system hierarchy
1.24 Effects of motor unit rate coding and recruitment on force
production
1.25 Order of recruitment of different motor units largely follows
the size of the neuron
1.26 (a) Simple myototic (stretch) reflex – group Ia afferent neurons.
(b) Static stretch – group II afferent neurons
2.1 Overview of metabolism: coupling of exergonic-catabolic
reactions with endergonic–anabolic reactions
2.2 Structures of adenosine triphosphate, adenosine diphosphate,
and adenosine monophosphate
2.3 (a) The glycolytic pathway (reaction numbers refer to panel
(b)). (b) Glycolytic enzymes
2.4 Lactate threshold and onset of blood lactate
2.5 (a) The Krebs cycle and hydrogen ion/electron transport
system. (b) The electron transport system
2.6 The energy substrate mobilizing cascade effect
2.7 Respiratory exchange ratio values for trained and untrained
subjects at rest and during increasing exercise intensity
2.8 Representation of low-intensity steady-state exercise
2.9 Representation of high-intensity non-steady-state exercise
metabolism
2.10 Approximate contributions of anaerobic and aerobic
metabolism to maximum sustained efforts (based on cycle
ergometry)
3.1 (a) Cyclic AMP second messenger system. (b) IP3/calcium
second messenger system. (c) Mechanism of action for steroid
hormone
3.2 (a) Feedback system for male reproductive hormones. (b)
Feedback for female reproductive hormones
3.3 The testosterone-to-cortisol ratio versus volume load over 12
weeks in four female and four male weightlifters
3.4 The “normal” menstrual cycle
3.5 Theoretical mechanisms of tension/stretch, metabolic,
endocrine, immune, and paracrine or autocrine response and
their effect on tissue remodeling and performance alterations
because of training
5.1 Running shoe and weightlifting shoe back squat comparison
5.2 Speedskating klapskate blade contact (a) without and (b) with
the hinge action of the skate
5.3 Swimmer wearing an Arena Powerskin Carbon-Air 2 Open
Back swimsuit for competition
5.4 Time-trial cyclist wearing an aero helmet during competition
6.1 Motor unit asynchronous activation
6.2 The mechanism for motor unit synchronization
6.3 Muscle tissue remodeling based on potential metabolic and
mechanical stimuli
7.1 Factors/stressors impacting sport development and adaptation
7.2 The stimulus–fatigue–adaptation paradigm
7.3 The fitness–fatigue relationship
7.4 Relative contributions of three energy systems
7.5 Example of block periodization over three microcycles for a
collegiate strength-power athlete (thrower) from December to
the outdoor conference meet in April
7.6 Characteristics of different prolonged average intensities
7.7 Relationship between effort and performance
7.8 Combining traditional and block periodization
8.1 Bilateral exercise example – back squat
8.2 Unilateral exercise example – rear foot elevated split squat
8.3 Partial squat performed from the safety bars
8.4 Load displacement comparison between (a) a shorter athlete
and (b) a taller athlete
9.1 Overview of the athlete monitoring process
 9.2 A team-based strength-power testing scenario
9.3 Athlete performing an isometric clean grip mid-thigh pull
9.4 Athlete performing a static (squat) jump
9.5 Athlete receiving verbal instruction prior to testing
10.1 Example of a stage of block periodization
10.2 Example portion of an annual plan for a single-factor sport
athlete (weightlifting)
10.3 Example portion of an annual plan for a multi-factor sport
athlete (soccer)
10.4 In-season weekly countermovement jump monitoring
illustrating changes in propulsion mean force and propulsion
time
Tables

1.1 Molecular characteristics of human muscle fibers

1.2 Elements of the sarcomere
1.3 Contractile and metabolic properties of skeletal muscle fibers
1.4 Muscle spindle characteristics
2.1 Theoretical complete degradation of glucose
2.2 Caloric equivalents
2.3 Caloric equivalents from the respiratory exchange ratio and
percentage kcal use from carbohydrates and fats during rest and
exercise
2.4 Energy sources: rates and capacities of anaerobic and aerobic
energy systems
2.5 Examples of bioenergetics and metabolic-limiting factors
2.6 Theoretical exercise-to-rest intervals
3.1 Distribution and action of catecholamine receptors in humans
3.2 Endocrine glands, hormones, target tissues, and primary
functions
3.3 Hormone metabolic effects
4.1 Caloric cost of various physical activities
4.2 Caloric cost and consumption of various sport activities
4.3 Essential and nonessential amino acids
4.4 Physiological functions and benefits of carbohydrates
4.5 Functions of different types of fat in the human body
6.1 Physical and physiological adaptations to endurance exercise
and training
7.1 Resistance training programming associated with Figure 7.5
7.2 Fatigue management
 7.3 Estimated training intensity
7.4 Residual effects: decay timelines with cessation of specific
training (adults)
8.1 Example exercise selections for specific sports within various
training phases
10.1 Summary of traditional periodization and its phases
About the Contributors

Aaron J. Cunanan, PhD, is the Director of Applied Sports Science for

the Cincinnati Reds.
W. Guy Hornsby, PhD, is an Assistant Professor in Coaching and
Performance Science at West Virginia University, USA, and Head
Coach of West Virginia Weightlifting.
Michael H. Stone, PhD, is a Professor, Exercise and Sports Science
Laboratory Director, PhD Coordinator in the Department of Sport,
Exercise, Recreation and Kinesiology, and Research Director for the
Center of Excellence for Sport Science and Coach Education at East
Tennessee State University, USA.
Timothy J. Suchomel, PhD, is an Associate Professor in the Department
of Human Movement Sciences, Director of the Master’s Program in
Sport Physiology and Performance Coaching, and Director of the
Sport Performance Institute at Carroll University, USA.
John P. Wagle, PhD, is Director of Performance Science and Player
Development with the Kansas City Royals.
Preface

Collectively, the authors of this textbook have a considerable background in

sport science and particularly strength and conditioning. Our background
includes coaching and teaching, as well as conducting substantial research.
From a coaching standpoint, the authors have coached from the local to
national and international levels, including Olympians. As coaches we have
attempted to use evidence-based methods and techniques. From a research
aspect, we have investigated strength and conditioning issues ranging from
their impact on health parameters to the design of training programs for
elite strength-power and endurance athletes. By the same token, as teachers
and researchers, our primary focus has been as sport scientists. As sport
scientists we have investigated physical, physiological, psychological, and
biomechanical parameters associated with improved sport performance.
Because of these endeavors, we believe that we have developed some
unique insights concerning adaptations to sport training, especially as it
concerns strength and conditioning, and particularly the development of
training and athlete monitoring programs. In Strength and Conditioning in
Sports: From Science to Practice we present information in a manner that
challenges the postgraduate but remains coach-friendly. The material
includes objective, research-based information, as well as empirical
observation when applicable. In cases in which key questions have not yet
been satisfactorily answered, we have offered speculative, but logical,
explanations based on the best available information and data. This process
is designed to stimulate additional observation and research that will
eventually offer a clearer understanding and resolution of the problems and
issues involved.
 Strength and Conditioning in Sports: From Science to Practice is
divided into five parts. Part I (Chapter 1) and Part II (Chapters 2–5) deal
with appropriate background material providing a strong scientific basis for
practical application. Part III (Chapter 6) focuses on physical and
physiological responses and adaptations to various types of training
programs. Part IV (Chapters 7 and 8) deals with training principles and
training theory, including the concepts of periodization and programming.
Finally, Part V (Chapters 9 and 10) discusses athlete monitoring and applied
development of the training process. Of note in Part V are observations of
the imperative nature of appropriate training program monitoring and how
monitoring can result in feedback allowing the coach and athlete to adjust
programs so that goals are more effectively and efficiently achieved. Each
chapter was written in a “stand-alone” manner so that readers can select
material as needed.
Although issues such as health-related adaptations to resistance training
are dealt with briefly, our primary reason for developing and writing this
book was to make contributions to coaching and sport science. In our
opinion, these are the most important contributions that a sport scientist can
make:

Provide coaches and athletes with logical, evidence-based theoretical

and practical information that can be used in creating and managing
the training process. A scientific background provides the sport
scientist, coach, and athlete with tools that can aid in making choices
concerning the monitoring and planning of training.
Assist coaches and athletes in developing a reasonable knowledge base
for interaction with sport scientists. This textbook can also provide
sport scientists with an understanding of various aspects of sport and
coaching that are not normally dealt with in academic programs.
Motivate and inspire sport scientists to greater creativity and
productivity.
Inspire potential sport scientists to consider pathways and experiences
not easily procured in the typical academic pathways.
It will be noticed by good students of history that most (perhaps all)
deviations in our evolution as a culture are typically pushed and even
“driven” by very few people. These very few, “the pushers,” often shared
psychological characteristics. Typically, they possessed great intellects,
most of them owned high standards, expected others to adhere to those high
standards, and were often surprised and frustrated when people could not
live up to them. A very important aspect to remember is that the Vulcan
approach to important scientific/cultural and historical alteration and
evolution of ideas does not always work for humans. Almost none of the
pushers were politically correct, and yet all of them possessed great passion
and emotion, including frustration and anger that drove their intellect. Most
of these people also had flaws and quirks. One need only investigate the
lives of Alexander II of Macedon, Timujin, Isaac Newton, Ludwig van
Beethoven, Alexander Graham Bell, or Albert Einstein to begin to
understand the passion and emotion which drove them, and consequently
the world, to a change in direction in thought and often to greater heights of
accomplishment.
Many readers of this text will probably be entering a new world, a world
the authors have only begun to contemplate. Artificial intelligence marches
on; the inevitable interface between man and machine will touch every
aspect of life, including sports. This new world will still need those
“pushers” to make a difference and drive sport science (and coaching)
forward. So, the authors ask this question: Do you have the passion, the
emotion, the intensity of intellect, the drive to push sport science forward?
Indeed, what will you be?
We sincerely hope that this book will provide an avenue, a spark, by
which readers (as well as the authors) can begin to fulfill potential
contributions to sport science.
\
Part I
1 Neuromuscular Physiology

DOI: 10.4324/9781003096139-2
Introduction
Most human activity requires muscle contraction and movement. Indeed,
very few activities engaged in by humans (e.g., thinking) do not require
muscle contraction. Even reading this book requires contraction of the eye
muscles, and hopefully you will turn the page. There are numerous reasons
for making a movement. Both humans and animals depend on movement
for survival. Humans and some animals often become engaged in
movement simply for enjoyment; and this movement often takes the form
of physical competition and sport among humans. The somatic
neuromuscular system is the fundamental organ system which “creates”
movements. The nervous system is integrated with skeletal muscle and
essentially acts as a contraction trigger and a control system for muscle
contraction. In a sense the nervous system acts as the steering wheel and
transmission and the skeletal muscle is the engine.
Skeletal muscle is made up of approximately 75% water, 20% protein,
and 5% non-protein substances such as minerals, carbohydrates, and fats.
There are approximately 650 muscles in humans, consisting of different
sizes and shapes. Skeletal muscles are typically attached to bones at two or
more places and create a lever system by crossing skeletal joints. The lever
ends move closer together as a result of muscle contraction, thus creating
movement and locomotion. Chapter 1 deals with the various macro and
micro components of skeletal muscle, its innervation, and function.
Defining Muscle and Its Function
Force generation is the primary task (function) of muscle, coupled with a
lever system (skeleton) movement is possible. Muscle also contributes a
morphological effect by providing substantial shape and form to the
organism. Based on its anatomy and function, muscle can be separated into
two types: striated and smooth. Striated (striped) muscle can be further
divided into skeletal muscle and heart (cardiac) muscle. All muscles,
regardless of the type, share the following basic properties (80, 125, 127,
153):

Conductivity: A muscle can conduct an action potential.

Irritability: A muscle will react when stimulated.
Contractility: A muscle can gain tension and shorten.
Relaxation: A muscle can return to its resting state after contraction.
Distensibility: A muscle can be stretched by an outside force. Provided
a muscle is not stretched past its physiological limits, no damage will
occur.
Elasticity: A muscle resists elongation and returns to its original
position after passive or active elongation. Elasticity is the opposite of
distensibility.
Adaptability: With consistent use (e.g., training) a muscle can alter its
physiology and/or size.
Depending upon the timeframe, volume, and intensity of the stimulus,
the alteration can be primarily sarcoplasmic or myofibrillar proteins.

Smooth versus Striated Muscle

Differentiation of smooth muscle and striated muscle can be accomplished
by a variety of methods, particularly microscopic appearance. For example,
smooth muscle fibers are mononucleated and their sarcomeres (the
functional units of muscle) are arranged at oblique angles. Resulting from
the orientation of its sarcomeres, smooth muscle appears to be relatively
indistinctive (smooth), as viewed through a light microscope. Striated
muscle fibers contain protein arrays (myofibrils) in parallel to each other
and thus form striations (stripes). Cardiac muscle fibers can be easily
identified from skeletal muscle by appearance. For example, unlike skeletal
muscle fibers, cardiac muscle fibers have a distinct end. The ends are
termed intercalated discs. So, one cardiac muscle fiber consists of the
substance between two intercalated discs. The intercalated discs are
somewhat thicker than the striations but are usually darker and distinctive.
Under a light microscope, intercalated disks appear as relatively dark lines
running from one side of the fiber to the other. Cardiac muscle fibers
contain only one or occasionally two nuclei and there are differences in
function, such as an intrinsic ability to contract. (A detailed discussion
dealing with smooth and cardiac muscle is not within the scope of this
book.)
Skeletal Muscle Structure and Function
Macroscopically, skeletal muscles appear in various shapes and sizes. In the
eye, only a few hundred muscle fibers (cells) are found, while the vastus
lateralis can contain several hundred thousand fibers. Muscle morphology
(shape) is largely dependent on its architecture. Importantly a muscle’s
architecture is a primary aspect for defining a muscle’s function (127).
Some muscles, such as the gluteus maximus, are relatively thick; some, for
example the sartorius, are long and relatively slender; and others, such as
the extensors of the fingers, have very long tendons. Differences in
morphology and architecture enable skeletal muscle, particularly those
crossing the same joint, to function effectively for wide range of tasks
requiring different forces, velocities, and power outputs.
For example, relatively short muscles with a large cross-sectional area
(CSA) can produce relatively large force magnitudes, whereas longer
muscles can contract with greater displacements and produce higher
shortening velocities. Muscles with long tendons (e.g., muscles of the
forearm controlling fingers flexion) can form pulley arrangements that
allow large external movement with relatively small movement of the
muscles and tendons. Anatomically, long slender muscles such as the
sartorius and biceps femoris are divided by transverse fibrous bands that
form distinct sections or compartments (127). Previously, muscle fibers
were thought to run the entire length of these muscles; however, as a result
of these compartments, the longest possible human muscle fiber is
approximately 12–20 cm (4.7–7.9 in.) in length (57, 127). Interestingly,
individual compartments, particularly in animals such as cats, can have
different fiber type distributions and CSAs (56), and these differences may
be present in human muscles (57). Each compartment has a separate
innervation; however, individual motor neurons often innervate muscle
fibers in adjacent compartments. The complete picture of functional
outcomes related to muscle compartmentalization is not completely
understood. As innervation is largely branched to a specific compartment, it
appears that it may be possible to recruit compartments separately, which
implies a different function (55, 57). From a functional standpoint, one
possibility is that compartmentalization could ensure that contraction occurs
relatively synchronously and rapidly along the muscle belly, particularly in
long muscles.
From a gross anatomical aspect, muscle fibers are arranged into two
basic structural patterns: fusiform or pennate (also spelled pinnate). The
fusiform arrangement makes up most human muscle, with the fibers largely
arranged in parallel arrays along the muscle’s longitudinal axis with tendons
at the proximal and distal ends. In many of the larger muscles the fibers
(and the fascicles) are inserted obliquely into the tendon, and this
arrangement resembles a feather (i.e., pennation). Pennate muscle fibers are
typically shorter than those of a fusiform muscle and insert on their tendons
in several different manners forming uni-, bi-, and multipennate muscles.
Fusiform fibers can largely run parallel, converge or form a circular
arrangement; the various arrangements of human fusiform and pennate
muscle fibers are shown in Figure 1.1.
Figure 1.1 Typical muscle fiber arrangements and their variations.

Pennate muscle fibers develop force and pull on the tendon at an angle.
The force magnitude actually exerted on the tendon can be calculated using
the cosine of the angle of insertion. However, it should be noted that as a
muscle contracts (eccentrically or concentrically) this angle is altered. At
rest, the angle of pennation in most untrained human muscles is about 10°
or less and this angle of insertion does not appear to have a marked effect
on most functional properties such as force production (157, 196, 197).
However, during muscle contraction, the angle of pennation can vary and
may change some functional parameters, at least in some muscles (72, 138).
It is possible that during muscle contraction the angle of pennation
increases enough to decrease speed of contraction and increase force
production. During dynamic high force production (maximum or near),
greater pennation angles can increase force and RFD, particularly late in the
force-time curve (7, 60). This may result through a gearing effect (fiber
rotation – velocity traded for RFD at high forces due to less rotation) (10,
24).
While fiber rotation decreases a muscle’s output force, it increases
contraction velocity by allowing the muscle to function at a higher gear
ratio (muscle velocity/fiber velocity). A greater degree of fiber rotation, and
therefore gear ratio, depends on how the muscle changes conformation
(shape) in dimensions that are orthogonal to the muscle’s line of pull on the
bone.
Muscle conformational changes during contraction promote fiber
rotation at low forces but resist fiber rotation at high forces. Because of the
alteration in muscle conformation, preprogrammed gearing varies with the
load, thus favoring velocity during low-load contractions and increased
force output for contractions during contractions with high loads. Muscle
conformational alterations allow pennate muscles to shift from a high gear
during rapid contractions to low gear during forceful contractions, much
like an automatic transmission. Thus, variable gearing in pennate muscles
provides a mechanism to modulate muscle performance during
mechanically diverse functions (10).
Sarcomeres are the functional unit of muscle. Conceptually, sarcomeres
in parallel are more related to force production. Sarcomeres in series are
more related to velocity of fiber shortening (196, 197). It is also possible
that muscle hypertrophy, which adds sarcomeres in parallel and can alter the
angle of pennation, and therefore functional properties (21, 110, 182).
Pennation offers a force advantage over fusiform fibers because with
pennation there is a greater fiber packing density (more fibers in a muscle
of a given volume), thus creating a larger effective CSA. Pennation also
permits more sarcomeres to be organized in parallel, again resulting in
enhanced force production (74, 157, 159). Additionally, this arrangement
causes the central tendon of the muscle to move a greater distance
compared to the shortening length of the muscle fibers, thus allowing
muscle fibers to operate closer to the optimum portion of their length–
tension curves (74, 127). It is also possible that muscle hypertrophy
contributing to an increased anatomical CSA could alter the angle of muscle
insertion on the bone, in effect altering the moment arm such that force,
particularly during slower movements could be enhanced (190).
A whole muscle consists of about 85% muscle fibers and approximately
15% connective tissue. The connective tissue organizes the muscle and
provides shaped. Connective tissue is composed of a ground substance,
collagen, reticular and elastin fibers in various proportions. The proportions
of these constituents depend upon a number of factors including the
muscle’s function, training, and nutritional factors. Importantly, the
connective tissue is largely responsible for force transmission (Ft). Indeed,
forces created at the sarcomere level are largely transmitted to the lever
system (bones) by a series of connective tissues terminating in the tendon-
bone interface. The degree of elasticity and distensibility of the connective
tissue (and the muscle) helps to ensure that the tension developed by the
muscle is efficiently transmitted and that the muscle will return to its
original shape after being shortened or stretched. So, it is the connective
tissue of muscle that provides a conceptual framework for the series and
parallel elastic components within a muscle. As a result of passive
stretching or active contraction the initial tension created is primarily a
result of the elastic properties of the connective tissue. During a shortening
or lengthening contraction, the muscle cannot develop force or perform
work against a resistance until the elastic components are stretched to the
point that muscle tension and the resistance (load) are in equilibrium.
 Muscle is compartmentalized on three levels as a result of layered
connective tissues of different size and orientation: epimysium,
endomysium, and perimysium (Figure 1.2). The muscle surface is covered
by the epimysium, which is relatively thick and very resilient connective
tissue and serves to separate a muscle from surrounding muscles. The
epimysium collagen fibers are woven into very tight packets that appear
wavy through a light microscope. These collagen packets are connected
with the perimysium. The perimysium divides muscle into bundles typically
containing about 100 to 150 muscle fibers, forming a fasciculus or fascicle.
Muscles producing small or very fine movements, such as in the eye, have
smaller fascicles containing relatively few fibers and a relatively larger
proportion of connective tissue (80). Because of the bundling (and the
endomysium), muscle fibers take on a polygonal cross-sectional shape
allowing a fascicle to contain a greater number of fibers (125, 127).
Interstitial spaces between fibers are usually about 1 µm. The perimysium
forms the intramuscular septa, which are connective tissue tunnels, running
through the muscle belly. These septa provide pathways for larger
arterioles, venules, and nerves. Around the outside of the fascicle, the
perimysium contains many large collagen bundles that encircle the outer
surface of the muscle fibers. Some of the collagen bundles circumscribe the
fascicles in a crisscross pattern, which adds stability to the fascicle
structure. Below the thicker perimysium connective tissue sheets is a looser
network of collagen fibers running in different directions and connecting
with the endomysium. The endomysium surrounds each muscle fiber and is
made up of collagen fibers approximately 60 to 120 nm in diameter, adding
additional stability. Arteries and veins run through the endomysium and
capillaries run between individual muscle fibers and are stabilized by the
connective tissue. Many of the endomysial fibers connect with the
perimysium and connect to the basement membrane (125, 127).
Figure 1.2 Organization and compartmentalization of skeletal
muscle.

Muscle Connective Tissue Interface

As muscle fibers approach the tendon they taper substantially, often into a
conical shape. The sarcolemma consists of extensive folds at the end of the
muscle fiber. These folds interlink with the folding of the connective tissue
surrounding the fibers. As a result of the extensive folding and interlinkage,
muscle force is dispersed over a relatively large area, which reduces stresses
at the surface (125, 127). Additionally, the fibers interact with the layers of
the basement membrane at an oblique angle, thus decreasing shearing stress
(180, 181). The myofibrils do not connect directly with the sarcolemma of
the muscle fiber; actin myofilaments filaments are attached to connecting
proteins, such as vinculin, talin, paxillin, and tensin, which are contained in
the basement membrane that is attached to the outer surface of the
sarcolemma (85, 125, 127). There are a remarkable number of inherited
muscle diseases that result from mutations in elements of the basement
membrane, the sarcolemmal cytoskeleton, or the sarcolemma protein
complexes that link the basement membrane to the cytoskeleton (32). Thus,
the biological importance of the basement membrane and associated
structures should not be underestimated.
The basement membrane is a non-lipid, carbohydrate-protein
extracellular matrix lying on the outside of the muscle cell sarcolemma and
is composed of two primary layers: an internal, basal lamina that is directly
connected to the sarcolemma, and an external, fibrillar reticular lamina
which contains numerous thin collagen fibrils and other specialized proteins
such as laminin that provide a scaffold to which the muscle fiber can adhere
(36, 131). The collagenous fibrils of the reticular lamina are embedded in
an amorphous proteoglycan-rich ground substance. The basal lamina
contains non-fibrillar collagen, non-collagenous glycoproteins, and
proteoglycans (36, 131). According to previous literature (39, 125), the
basic functions of the basement membrane include (160, 191):

Encapsulating satellite cells.

Providing a scaffold to orient and constrain cells during regeneration.
Attaching the neuromuscular junction (NMJ).
Guiding regenerating axons to the site of the original NMJ. Provides
signal for the development of specialized motor end plate structures.
Regulating the NMJ. This stimulates the development of synaptic folds
and the incorporation of acetylcholine receptors into the sarcolemma.
Playing a role in the termination of synaptic transmission. The
basement membrane contains acetylcholinesterase (AChE).
Attaching the muscle fiber to the endomysium (plays a role in force
transmission).

Muscle Fiber, Organelles, and Sarcoplasm

Muscle Fibers
While muscles have different shapes and sizes, they are made of individual
cells (fibers). Muscle fibers are elongated and taper into a conical ending.
Muscle fibers are typically about 50 µ in diameter (range: 10 to 150 µ), and,
within a muscle, fibers may run the entire length of the muscle or
compartment (64, 125, 127). Fibers can be quite long, up to 20 cm (7.9 in.)
(157). However, considering the presence of connective tissue intercepts
along the length of muscle fibers and using a variety of mammalian
muscles, Richmond and Armstrong (152) and Gordon and colleagues (79)
have found fibers typically to be about 2 cm (0.8 in.) in length. Early
studies (6, 159, 172), indicating that muscle fibers may be quite long, did
not use techniques that were adequate for identifying connective tissue
intercepts (157). Thus, typical mammalian including human muscle fibers
are likely to be in the range of 1 to 3 cm (0.4–1.2 in.) in length (120).
The muscle fiber is surrounded by the sarcolemma (see below) and
contains the sarcoplasm (cytoplasm) of muscle cells, a semifluid made up
of water, minerals, proteins, and several other substances. Suspended in the
sarcoplasm are various organelles, which are subcellular structures that can
have one or multiple specific functions. Organelles include nuclei,
mitochondria, cytoskeletal and cytotubular network systems, Golgi bodies,
glycogen granules, lipid vacuoles, etc. Generally, muscle cell proteins can
be grouped into four categories: (i) granules plus an organelle, (ii) stroma
and sarcolemmal, (iii) myofibrillar, and (iv) sarcoplasmic (80, 125, 127).
The spaces between myofibrils contain the sarcoplasmic proteins and
include myoglobin and glycolytic enzymes.
The organelles of muscle fibers have various specific functions,
including replication and energy production. Several of these organelles
have a nomenclature distinguishing them from similar organelles found in
other cells.

Nuclei
Human muscle fibers are multinucleated and contain 23 pairs of
chromosomes and many thousands of genes per chromosome. The nuclei
are contained within a double-layered membrane, and mature nuclei are
normally dispersed near the inner surface of the sarcolemma. Centrally
located nuclei may be indicative of nuclei damage, ongoing repair, or
neuromuscular disease (68). A particularly high density of nuclei is found
near the motor end plate. The muscle fiber nucleus contains chromosomes
that impart instructions for protein synthesis in the sarcoplasm.

Satellite Cells
Using a light microscope, muscle fiber nuclei and nuclei of satellite cells
are indiscernible. Satellite cells are quiescent mononucleated myogenic
cells that are located between the basement membrane and the sarcolemma
of muscle fibers and can lie either in parallel or transversely along the
longitudinal axis of the fiber (107, 125, 201). Satellite cells make up about
1% of the nuclei in adult human muscle and are particularly important in
regenerating muscle tissue subsequent to disease or injury (107, 127).
Satellite cells are important in the process of muscle hypertrophy and
hyperplasia, which has been speculated to occur resulting from high-
intensity training, particularly heavy weight training (9, 107).

Mitochondria
Resulting from densely packed myofibrils and other organelles, muscle
fiber mitochondria are typically shorter than those of other types of cells,
oblong in structure and approximately 1.5 µ in length. Mitochondria have a
major function of energy production and are primarily found in cellular
areas where energy supply is a primary requisite, for example, near the
myofibrils. Mitochondria have a double membrane structure with the inner
membrane folded into ridges termed “cristae.” This enfolding results in a
large inner membrane surface area (Figure 1.3). The matrix or matrix space
is contained within the cristae.
 Outer membrane. The outer membrane encompasses the mitochondria
and embedded proteins primarily function as transport molecules (125,
127). The transport proteins allow molecules of 10 kilodaltons (kD) or less
to pass freely into the intermembrane space but carefully regulate larger
molecules. The outer membrane also contains various enzymes that are
involved in diverse activities such as fatty acid synthesis (chain elongation),
oxidation of epinephrine, and the degradation of tryptophan (37). Outer
membrane disruption membrane permits proteins contained in the
intermembrane space to leak into the sarcoplasm, leading to cell death (37).
Inner membrane. The inner membrane is freely permeable only to
oxygen, carbon dioxide, and water (5). About 60–70 % of the proteins in
the mitochondria are found in the inner membrane, many of which are
transport proteins, largely controlling the movement of various substances
into and out of the matrix. The cristae extend into the matrix at different
depths are the main sites of mitochondrial energy conversion. A small
proton gradient between the intermembrane space (pH 7.2–7.4) and the
matrix (pH 7.9–8) drives ATP production catalyzed by the ATP synthase
enzymes in the membranes of the cristae.

Figure 1.3 Basic mitochondrial structure.

 The matrix space contains (inner membrane) enzymes for the Krebs
cycle, oxidation, and the formation of acetyl coenzyme A (CoA) from
pyruvate. The 15 molecules associated with cellular respiration are located
on the inner membrane (125, 127). The enzymes necessary for lipid
synthesis are found on the outer portion of the inner membrane. A unique
aspect of mitochondria is that they also contain a mitochondrial specific
DNA (deoxyribonucleic acid). Among humans, mitochondrial DNA
(mtDNA) spans about 16,500 DNA building blocks (base pairs) and
represents only a small fraction of the total DNA in cells. Apparently,
among primates, the DNA is derived directly from females (you can thank
your mother for your mtDNA). MtDNA consists of 37 genes, all of which
are essential for normal mitochondrial function. Thirteen of these genes
provide instructions for manufacturing enzymes involved in oxidative
phosphorylation (Figure 1.4). The remaining genes provide instructions for
making molecules called transfer RNA (tRNA) and ribosomal RNA
(rRNA), important in creating various mitochondrial proteins.
 Oxidative phosphorylation enzymes in the inner
Figure 1.4
membrane.

Interestingly, with assistance from the sarcoplasmic nuclei, mitochondria

can replicate (Figure 1.5). Indeed, mitochondrial biogenesis is a complex,
multifactorial cellular process requiring the coordination of several
mechanisms that involve nuclear-mitochondrial cooperation, enhanced
mitochondrial protein expression and import, mtDNA gene expression,
transcription factors activity, assembly of multi-subunit enzymatic
complexes, regulation of mitochondrial fission and fusion and
mitochondrial turnover (40). Physical training, including high-intensity
intervals, is a likely stimulus for mitochondrial replication (22).

Figure 1.5 Mitochondrial replication.

Sarcolemma
Muscle fibers, unlike other cells, often have specialized names for
structures. The sarcolemma (plasmalemma) surrounds the fiber and
 contains sarcoplasm (cytoplasm). The sarcolemma is an asymmetrical fluid
mosaic, approximately 7.5 nm thick, largely made of lipids and proteins. As
with other cell membranes, the sarcolemma has two major functions: (i)
enclosing the cell contents and (ii) regulation of entry and exit of various
substances into and out of the fiber. Analyses of the biochemistry and
ultrastructure of the sarcolemma indicate it is largely composed of a bilayer
of phospholipids arranged perpendicularly to the longitudinal axis of the
fiber (Figure 1.6). Hydrophilic lipid heads create most of the inner and
outer surface of membrane, with their hydrophobic tails forming the inside
of the membrane. The hydrophilic heads are primarily composed of choline,
phosphate, and glycerol; the tails consist of fatty acid chains (125, 127).
Structural stability and stiffness are added to the membrane as a result of
cholesterol bridges between the phospholipid molecules. Additionally,
periodic invaginations of the sarcolemma forming tunnels, gives rise to the
transverse tubules (TT). The TT is a network for sensing depolarization
through dihydropyridine receptors (DHP). The depolarization of this
sensing receptor results in a calcium flux caused by the subsequent
activation of ryanodine receptors (RYR).

Figure 1.6 Basic structure of sarcolemma.

As noted, the sarcolemma has an irregular surface due to several

convolutions and infolding of the membrane. One very specialized and
substantial group of folds occurs in the area of the synapse with the motor
end plate of an alpha motor neuron (α-MN). Along with the motor unit
(MU) membrane, this synapse is termed the NMJ. Typically, in comparison
with type I (slow) muscle fibers, type II (fast) muscle fibers have more
extensive junctional folding at the NMJ. Interestingly, many of the folds in
a resting muscle fiber are stretched smooth during eccentric or concentric
contractions (125, 127). There are also cavities, forming pockets or small
“caves”; the caveolae are connected to the outer surface by narrow necks. In
smooth muscle, the caveolae have a similar function to the TT in skeletal
muscle. Caveolae are unique membrane microdomains that appear to be
responsible for various functions including organizing signaling, lipid
metabolism, and homeostasis in relation to alterations in membrane tension.
Caveolae are frequently associated with muscle-specific stress fibers, which
are a major regulator of membrane tension and cell shape (122). Muscle-
specific stress fibers (non-muscle cells) are contractile areas that maintain
tension on the underlying substructure and form a primary element of the
mechanotransduction apparatus that link the cell interior and exterior (143).
Stress fibers are similar in structure to the alternating thick actin filaments
and Z bands in muscle myofibrils; however, the actin and myosin filaments
in stress fibers are less regular when compared to typical sarcomeres and
contraction occurs non-uniformly along their lengths (143). It appears that
stress fiber regulators (e.g., proteins such as zyxin and paxillin) play a
major role in control of caveolae activities providing a functional link
between caveolae and stress fibers (122). Additionally, the degree of tension
in the sarcolemma modulates the curvature of caveolae, as they flatten
during high tension and invaginate during low tensions, in essence
providing a tension-buffering system (122). Caveolae also appear to
regulate multi-cellular pathways, including RhoA-driven actomyosin
contractility and other mechanosensitive pathways, suggesting that caveolae
possibly couple mechanotransduction pathways to actin-controlled changes
in tension through their association with stress fibers. Therefore, the
association of caveolae with stress fibers could provide an important
strategy for cells to deal with mechanical stress (47, 50, 122). Additionally,
there are different types of proteins embedded in the lipid bilayer.
 Both extrinsic and intrinsic proteins are found in the sarcolemma lipid
bilayer (Figure 1.6). Extrinsic proteins are affixed only at the inner or outer
surface of the sarcolemma and are easily removed by chemical means,
intrinsic proteins completely penetrate the bilayer (125, 127). Many
proteins are glycosylated and have sugar residues extending up into the
basement membrane. The sugar residues appear to function as a “trap” for
various extracellular molecules, then direct them toward the protein in the
membrane. The basic functions of intrinsic and extrinsic proteins include
(125, 127):

Acting as receptors for various hormones.

Acting as second messenger system proteins such as adenyl cyclase,
which is responsible for catalyzing the reaction forming cyclic
adenosine monophosphate (cAMP).
Acting as regulatory proteins with various functions, such as G
proteins, which bind guanosine triphosphate (GTP) and are involved in
the activation of adenyl cyclase.
Transporting proteins, which include the proteins active in fat
transport, electrolyte movement, such as the sodium-potassium pump,
ion channels, and neurotransmitter receptors (acetylcholine).
Acting as kinases, which activate various proteins by phosphorylation
such as those responsible for, lipolysis, glycogenolysis and
carbohydrate use as an energy source.
Acting as integrins, which link the basement membrane and the
endomysium to the sarcolemma and cytoskeletal structures.

At body temperature, lipid portions of the sarcolemma are relatively fluid,

while the proteins are more stable and restricted in movement as a result of
being attached to intra- or extracellular structures through binding proteins.

Cytoskeletal System
The cytoskeletal system consists of a protein network that strengthens and
stabilizes various structures within the cell (125, 127). Proteins forming the
 cytoskeleton, such as dystrophin, actin, and spectrin, strengthen and support
the sarcolemma and prevent tearing during contraction. Near the Z-disc, the
proteins desmin, synemin, and vimentin encase the myofibrils and bind
them together. The cytoskeleton also supports and positions other organelles
such as nuclei and mitochondria (Figure 1.7).

Figure 1.7 The sarcolemma supporting cytoskeleton.

Cytotubular Systems
The tubular system of skeletal muscle fibers consists of two primary parts,
the sarcoplasmic reticulum (SR) and the TT system. The SR is analogous to
the smooth endoplasmic reticulum in non-muscle cells and as a network
that runs longitudinally down the fiber, parallel to the myofibrils and
surrounds them. The SR consists of a longitudinal portion (LTP) containing
a Ca++-ATPase (ATP using) pump and is connected to saclike terminal
cisterna (TC) at either end of the longitudinal portion (Figure 1.8a). During
a fiber contraction, the longitudinal portion becomes shorter and wider. The
pump in the LTP directs Ca++ into the TC where they are stored. Side
channels allow the SR to interconnect with rest of the SR throughout the
 cell; thus, forming a giant tubular network (125, 127). The SR acts as a
Ca++ reservoir (TC). Under normal resting conditions, compared to the
surrounding sarcoplasm the concentration of Ca++ in the TC is about 10,000
times higher (20). As a result of depolarization, Ca++are released through
RYR channels into the sarcoplasm, markedly increasing the sarcoplasmic
Ca++ concentration. The increased Ca++ concentration is necessary for
muscle contraction activation (192). With the removal of depolarization, re-
segregation of Ca++ into the SR results in muscle relaxation.

Figure 1.8 (a) The sarcoplasmic reticulum. (b) The T-tubule

networks.

The TT are located perpendicular to the longitudinal axis of the muscle

fiber. The TT are essentially extensions of the sarcolemma and invaginate
to the inside of the fiber and contain intercellular fluid. The invagination of
the TT occurs at regular intervals and create relatively narrow channels
which encircle the myofibrils near the junction of the A and I bands of the
sarcomere. The TT travel through the TC forming a cross-sectional triad
(Figure 1.8b). Using electron microscopy, the TT and the SR appear to be
connected by large protein complexes termed junctional feet (53, 70). The
junctional feet appear to be part of the proteins making up the RYR channel
in the SR and are likely connected to dihydropyridine (DHP) channels
embedded in the TT (70, 192). The TT functions to transfer an action
potential from the sarcolemma to the inside of the cell and to the SR (Figure
1.8b). It appears that an action potential arriving in the TT results in a
conformational change in the DHP channels. This conformational change in
turn causes the junctional feet to change conformation. The junctional feet
(RYR) are embedded in the membranes of the SR adjacent to Ca++ channel
proteins acting as a gate. Under resting conditions, Ca++ channel gates are
closed, and Ca++ remain segregated in the SR. Junctional feet
conformational change cause the Ca++ channel gates to open and Ca++
enters the sarcoplasm as a result of a concentration gradient. The
concentration of Ca++ in the sarcoplasm increases approximately 100-fold
(20). The increase in sarcoplasmic Ca++ concentration triggers events in
regulatory proteins leading to muscle contraction.
 The Sarcomere: Functional Unit of the Muscle
Fiber
Sarcomeres contain various elements and a variety of different proteins.
Within the sarcomere are myofibrils (protein arrays), which are largely
constructed from the contractile proteins (actin and myosin), along with
smaller amounts of regulatory and stabilizing/structural proteins.
Approximately 80% of the myofibrillar protein content consists of actin and
myosin (80). Myosin is the most prominent myofibrillar protein making up
about 60% to 70% of the protein content. Myosin is relatively large
weighing about 500 kD and has a relatively high viscosity. Actin makes up
approximately 20% to 25% of the myofibrils protein content and has a low
viscosity weighing about 75 kD. Myosin molecules, which are about 150
nm long, consist of two heavy chains with long tails wrapped in an alpha-
helix connected to two pear-shaped heads (Figure 1.9).

Figure 1.9 Myosin and myosin myofilament structure.

 The subunit nature of the myosin molecule can be examined using in-
vitro enzymatic treatments (165). For example, trypsin proteolysis cleaves
myosin molecules into two subunits, heavy meromyosin (HMM) and light
meromyosin (LMM). Papain treatment of HMM yields a linear fragment
(HMM-S2) and a globular fragment (HMM-S1) containing two myosin
heads. The HMM-S1 fragment contains myosin heavy chains (MHC),
which are largely responsible for ATPase activity; thus, the MHC “heads”
are the primary force-generating sites. As a result of the ATPase activity in
the MHC, they are also primarily responsible for the sarcomere and
ultimately muscle fiber shortening velocity (23, 58, 151). In the neck region
of the S1 fragment (Figure 1.9), each of the heads is bound to two
molecules of 20 kD light myosin (LMC) proteins that modulate the ATPase
activity of the globular heads. Modulation likely occurs as a result of LMC
regulation of the velocity of the power stroke during contraction (123).
Importantly, isoforms of MHC and MLC are the primary determinants of
human skeletal muscle fiber type classification (11, 19, 20, 75, 113, 130,
174). There are two basic isoforms of the MHC – fast and slow – and at
least four isoforms of LMC; different combinations of MHC and LMC
create fibers with different contractile characteristics (see Table 1.1).

Table 1.1 Molecular characteristics of human muscle fibers

Fiber type MHC MLC
IIx 2 FM (MHCIIx) 2 F2, 2 F3
IIa FM (MHCIIa, possibly IIa + IIx) 1 F1, 2 F2, 1 F3
IIc 1 FM (MHCIIa), 1 SM 2 F1, 2 F2
I 2 SM 2 S1, 2 S2
FM = fast heavy myosin chain (MHCIIx or IIa); SM = slow heavy myosin chain (MHCI); S1 =
slow light myosin chain type 1; S2 = slow light myosin chain type 2; F1 = fast light myosin chain
type 1; F2 = fast light myosin chain type 2; F3 = fast light myosin chain type 3.
* FM chains consist of two subtypes: HCIIx and HCIIa.
Myosin ATPase activity: IIB > IIX > IIA > IIC > I.
Among mammals, the relative shortening velocity (unloaded) appears to be I < IIa < IIax < IIx <
IIab < IIb. Data indicate that human and primate muscle contain only IIx MHCs, types IIb and IIab
are found in small mammals.
 Fiber type MHC MLC
Sources: Based on references 11, 19, 23, 143, 144, 160, 163, 172, 175, 176.

Figure 1.10 illustrates myosin heads consisting of three globular subunit

proteins of approximately 20 kD, 25 kD, and 50 kD. The LMCs attach to
the 20 kD subunit protein. A cross-bridge is formed by the 50 kD protein
myosin head subunit that binds actin. The pocket (cleft) in the 50 kD
subunit appears to have a variable size. The size of the pocket and the
strength of the attachment to actin is controlled by ATP (150, 194).

Figure 1.10 Molecular structure of the myosin head.

The myosin myofilaments consist of an overlapping array of 200 to 400

myosin molecules, with the heads projecting outward and the LMM
subfraction overlapping in parallel to form the spine of the filament. The
heads of the project away from the spine and when bound to actin form the
cross-bridges of the sarcomere. The molecules of myosin are oriented in
opposition along each half of the myosin filament with the LMM tails
directed toward the center. The HMM-S1 and the HMM-S2 are attached by
flexible joints (hinge) to the LMM. These joints increase the range of
movement during a power stroke (101, 148).
Actin molecules exists in a globular form (G-actin), which is made of a
single peptide chain and a filamentous form (F-actin) (Figure 1.11a). Actin
filaments (F-actin) result from the polymerization of G-actin monomers. F-
actin myofilaments consist of two G-actin polymers wrapped around each
other, creating a double helix with a 360 Α period, and form the thin
filaments of the sarcomere. Each actin myofilament contains about 350 G-
actin molecules. In solution, actin and myosin bind, forming actinomyosin,
strands of which will contract in the presence of ATP (127).
Globular actin (G-actin) is polymerized and forms F-actin. Two F-actins
wrap around each other in an alpha-helix to form an actin myofilament. The
regulatory proteins troponin and tropomyosin (forming regulatory units) are
embedded in regular intervals in the actin myofilament.
Tropomyosin and troponin are the proteins most responsible for the
regulation of cross-bridge formation and muscle contraction regulation. The
tropomyosin molecule (≈ 70 kD) is rod-shaped and bound to the actin
filaments, and consists of α and β polymers wrapped around each other
forming an alpha-helix. Tropomyosin consists of multiple isoforms
resulting from different encoding genes and alternative splicing, along with
post-translational modifications (105). The ratio of α and β chains are
specific to type I and type II skeletal muscle fibers and play a role in the
speed of contraction (144). In human muscle, tropomyosin spans seven G-
actin residues of the actin myofilament and is attached to troponin complex,
the second major regulatory protein(s). The troponin complex consists of
three globular-shaped proteins, each having a specific function (troponin C,
troponin I, and troponin T) that are necessary for muscle contraction in
striated muscle, but not smooth muscle (20, 77). The troponin complex is
bound to tropomyosin by troponin T; troponin C binds Ca++; and troponin I
spatially blocks actin and myosin interaction. A tropomyosin molecule plus
the attached troponin complex is termed a regulatory unit (127). In humans,
actin filaments (thin filament) contain 52 regulatory units and consists of
about 350 G-actin molecules and there is one regulatory unit for every
seven G-actin molecules (20, 77, 140). When troponin C binds to Ca++ a
change in conformation of the regulatory unit occurs, the tropomyosin
strands to which troponin C is attached move across the face of the actin
filament, this conformational change allows actin to activate and bind
myosin heads (myosin ATPase) resulting in contraction (48, 189).
The sarcomere is the smallest functional unit of muscle. Using light
microscopy, the myofibrils of a sarcomere can be observed to lie in a
parallel orientation. A Z-disc establishes the boundaries of a muscle
sarcomere. The Z-discs are the bonding sites for actin filaments. From each
Z-disc, actin filaments extend into the two adjacent sarcomeres. The interior
of a Z-disc containing actin filaments from adjacent sarcomeres are
crosslinked by the protein α-actinin. At rest, myosin filaments extend the
length of the A band and the actin filaments pass from each I band into the
A band as far as the H zone. Because the H zone contains only the myosin
myofilament, it is less dense than other areas of the A band. The least dense
portion of the sarcomere is the I zone as it contains no myosin filaments.
However, the H zone is not uniform as the density varies considerably. In
the skeletal muscle sarcomere, the M-line provides an attachment site for
the myosin myofilaments as is the structure that cross-links myosin
myofilaments into a hexagonal lattice and defines their relative rotations
around their longitudinal axes (116). The M-line also binds creatine kinase,
an enzyme associated with ATP synthesis. The M-line lies in the center of
the A band and is denser than the surrounding H zone. The M-line is made
up of thin filaments (M-filaments) approximately 5 nm in diameter that are
connected to the myosin filaments and to each other. The proteins making
up the M-line are primarily myomesins (186). These proteins form a
complex elastic latticework providing structural stability to the three-
dimensional aspects of the sarcomere (Figure 1.11b).
Figure 1.11 (a) Structure of the actin myofilament and regulatory
proteins. (b) The sarcomere and M-line. (c) The sarcomere
and D- and C-zones.

Using electron micrographs of sarcomere cross-sections, the relationship

of the actin and myosin filaments to fiber banding can be clearly observed
in various portions of the sarcomere (80, 127). For example, cross-section
near the M-line shows that each myosin filament is surrounded by a
hexagonal array of actin myofilaments. The actin myofilaments are attached
to regulatory units, the structural protein nebulin and actinin at the Z-disc.
Additional protein filaments primarily composed of titin (connectin)
stabilize myosin myofilaments along the longitudinal axis. Titin is a large
protein (3000 kD) that runs half the length of a sarcomere, essentially the
length of the myosin myofilaments, and also attaches them to the Z-discs
(91, 185). Titin also appears to stabilize and maintain myosin positioning
within the middle of the sarcomere as well as stabilizing the entire
sarcomere during both contraction and relaxation. Nebulin likely stabilizes
actin in a similar manner. Titin is a molecular equivalent of a steel spring;
both titin and nebulin likely contribute to the elastic properties of muscle
(91, 127, 185). Differences in protein isoforms, particularly titin, may
contribute to differences in strength, power (71, 126), and running economy
(115) and may be related to training status. Skeletal muscle myosin-binding
protein C (MyBP-C) is a myosin myofilament-associated protein (Figure
1.11c). It is localized in distinct regions (C-zones) of the sarcomere. MyBP-
C activated by Ca++-sensitizes the actin myofilament and modulates actin
myofilament velocity. At least two isoforms of MyBP-C (fast- and slow-
type) are expressed in a fiber type specific manner (118).
Several proteins make up the Z-disc including spectrin, vimentin,
synemin, desmin, and α-actinin. Actin myofilaments are attached to both
sides of the Z-discs by α-actinin (127). Desmin, vimentin, and synemin
form a structural scaffolding that wraps around the actin myofibrils and the
Z-disc. The central part of α-actinin consists of four tandem spectrin-like
repeats each of which comprises a triple α-helix anti-parallel bundle. The
specialized ends of the dimer allow α-actinin to crosslink with actin
myofilaments. Together these proteins serve to hold the actin myofibrils in
position at rest and during stretch or contraction. Additionally, Z-disc
proteins are connected to the cytoskeletal proteins in the sarcolemma and
basement membrane and ultimately to the endomysium connective tissue
surrounding the muscle fiber (see Table 1.2).

Table 1.2 Elements of the sarcomere

Element Associated Function
protein
Thick Myosin 1. Interacts with actin
myofilament 2. Myosin ATPase activity
Titin 1. Associated with parallel elastic properties
2. Stabilizes the thick filaments longitudinally
3. May offer some control of myosin molecule number per
filament
Thin Actin 1. Interacts with myosin
myofilament
Nebulin 1. Longitudinal stabilization of thin filaments
2. May control the number of G-actin monomers linked
together in a thin filament
Tropomyosin 1. Transfers the conformational change of the troponin-
tropomyosin complex to actin

Sources: Based on references 20, 118, 127, 143, 175.

Element Associated Function
protein
Troponin – 3 1. Tc: Binds calcium
globular 2. TI: Inhibits actin and myosin interaction
subunits 3. TT: Binds Tropomyosin
Z-disc α-actinin 1. Holds the thin filaments in place and in spatial alignment;
type I fibers contain more α-actinin
Desmin 1. Forms Z-disc scaffolding – attaches Z-disc to sarcolemma
Vimentin and basement membrane
Synemin
Dystrophin
Spectrin
M-line M-protein 1. Holds the thick filaments in a proper alinement
Myomesin 1. Attaches and anchors titin
Creatine kinase 1. Contains creatine kinase: catalyzes production of ATP
from creatine phosphate
C-zone (C- C-, X-, H-protein 1. Probably help hold actin myofilaments in proper array
stripes) 2. May control the number of myosin molecules in the thick
filaments at a relatively constant value
3. Modulates the velocity of the actin myofilament
Sources: Based on references 20, 118, 127, 143, 175.
Muscle Contraction
Obviously, muscle contraction is necessary for human movement, thus an
understanding of how a muscle contracts is necessary to understand human
movement, adaptations to training, and certain disease states that limit
movement. At the most fundamental level, contraction involves an
interaction of myosin and actin myofilaments and the sliding of the thin
myofilaments past the thick ones (99, 100, 102). However, understanding
exactly how muscle contraction takes place requires a knowledge of the
molecular mechanistic basis of contraction. Although muscle contraction
has been studied for more than 70 years, the details of the molecular basis
are still not entirely clear.
Voluntary muscle contraction (and movement) is initiated in the central
nervous system. Simplistically, this occurs when a series of depolarizations
(action potentials [AP] travel down a chain of neurons (usually beginning in
the motor cortex) and arrives at the motor end plate. The AP is transferred
to the sarcolemma by the release of the neurotransmitter acetylcholine
(ACh) into a synaptic cleft, the NMJ. The ACh then binds to sarcolemmal
receptors initiating Na+ influx into the fiber. This influx transfers the AP to
the sarcolemma and the AP moves along the sarcolemma, down the TT into
the interior of the fiber (73, 125). At the terminal cisternae the AP is
transferred to the SR, likely by way of voltage activated DHP Ca++
channels (125, 135). Upon depolarization, the junctional feet of the SR
change conformation, releasing Ca++ into the sarcoplasm through the action
of RYR Ca++ channels. The probability of Ca++ binding with troponin C is
enhanced by the volume of Ca++ released which is on the order of 100-fold
(20).
The attachment of the myosin head to actin and subsequent contraction
is quite complex and may occur as follows (125, 127, 150, 173, 177).

Muscle Contraction Sequence

 1. At rest there is no interaction between actin and myosin, as this
interaction is blocked or inhibited by the regulatory unit that covers
binding sites on the actin (steric block model).
2. An AP arrives at the NMJ resulting in sarcolemmal depolarization.
3. The AP travels across the sarcolemma and down the TT.
4. Depolarization is transferred to the SR and Ca++ is released into the
sarcoplasm.
5. Four Ca++ bind to Tc resulting in a conformational change in the
regulatory unit and activation of the myosin heads. This allows a
strong bond (cross-bridge) to form between actin and myosin in the
absence of ATP.
6. After the strong bond is formed, ATP enters the cleft of the 50 kD
portion of the head. The adenine ring is left protruding out of the cleft.
The entry of ATP opens the cleft, creating a weak bond.
7. As the weak bond is established, the cleft widens and ATP completely
enters the cleft, causing the head to detach from actin and a
conformational change in the myosin causes the head to move 5 to 11
nm farther down the actin filament and reattach. ATP is hydrolyzed
with the end products remaining in the cleft, forming a transient
intermediate complex.
8. The lower part of the 50 kD portion re-forms a weak bond with actin.
The reattachment closes the cleft, expelling inorganic phosphate (Pi)
and adenosine diphosphate (ADP).
9. The removal of Pi and ADP opens the cleft and simultaneously causes
the lower part of the S1 fragment to swivel, resulting in the power
stroke, producing approximately 3 to 4 pN of force and between 5 and
11 nm displacement (66, 150).
10. The process starts over.

Each cross-bridge cycle requires the hydrolysis of one ATP molecule. In

order for the cross-bridge cycling and a specific level of force-power
generation to continue, ATP must be replenished. Maintaining a specific
force or power output requires that ATP regeneration must match the rate of
use (see Chapter 2). Force-power generation and ATP hydrolysis creates
metabolic breakdown products, including ADP, Pi, and H+, which, if
enough is accumulated, can interfere with cross-bridge formation and
performance. The heat liberated and work accomplished is proportional to
the amount of ATP hydrolyzed during dynamic conditions (Fenn effect)
(65).
When the CNS stops generating α-MN AP, and the AP is no longer
arriving at the NMJ, AChE, which is present in the synaptic cleft, reduces
the NMJ concentration of ACh. As the ACh concentration decreases, the
number of activated ACh receptors in the sarcolemma are also reduced,
terminating the AP stimulated Ca++ release by the SR. As the muscle fiber
returns to a resting state, the SR pump in the longitudinal portion
resegregates Ca++ reducing the sarcoplasmic concentration and Ca++
availability for binding with troponin C is reduced. As a result,
conformational alterations in the regulatory units result in a return to their
resting shape, thus reducing the probability of strong actin-myosin binding
interactions. The muscle returns to resting conditions:

Muscle Relaxation: Event Sequence for a Voluntary Contraction

1. AP from CNS is removed (no stimulus from motor cortex).

2. ACh is no longer being released into NMJ.
3. AChE in NMJ begins breaking ACh down into choline and acetic acid.
4. Choline and acetic acid are taken up by the α-MN transported to the
soma – repackaged in vesicles and transported back down to the
neuron terminal.
5. Without sufficient ACh attached to sarcolemma receptors,
depolarization of the muscle fiber ceases.
6. Ca++ is then re-segregated by the SR – this occurs by way of the Ca++
pump in the longitudinal portion of the SR.
7. As Ca++ is removed from the sarcoplasm into the SR, troponin C gives
up its Ca++ – returns to its resting conformation and the regulatory unit
covers up the binding site on the actin filament.
Length–Tension Relationships
The number of cross-bridges formed depends upon the degree of myosin
Ca++ activation and the degree of overlap of actin and myosin filaments.
Using length-clamp/isometric techniques, sarcomeres (and whole muscle)
has been shown to have optimum lengths at which maximum force can be
produced (29, 51, 78, 183). The change in isometric force with a change in
sarcomere length appears to be related to the number of cross-bridges
formed (Figure 1.12). The optimum sarcomere length appears to be
approximately 2.3–2.8 μm (29, 51, 119, 121, 124). However, some evidence
indicates that the sarcomere length at which peak force occurs may be
longer than the length providing optimal overlap of myofilaments. The shift
of optimal length appears to be due to increased Ca++ sensitivity, resulting
from the myofilaments lying closer together allowing greater force than
expected at slightly longer lengths (124). At very long lengths (>2.8 μm),
few cross-bridges can be formed because the filaments are too far apart and
the myosin cannot reach the actin binding sites. However, at short lengths
(<2.0 μm), fewer cross-bridges can be formed because the actin filaments
(I-filaments) slide into the opposite half of the sarcomere, causing actin and
myosin myofilament to have considerable overlap; and it is possible that
cross-bridges interact with the opposite actin filament; essentially, one part
of the sarcomere pulls against the other, reducing the force generated.
Isolated whole muscle shows similar length–tension relationships.
Figure 1.12 Force as a function of sarcomere length.
Source: Based on Edman and Reggiani (51) and Moo et al. (132).

Using an isolated muscle preparation (Figure 1.13a) in which both ends

are fixed, electrical stimulation results in contraction in which muscle gains
tension but does not change length (isometric contraction). For “in vivo”
preparations, the innervating nerve can be stimulated directly. For example,
the sciatic nerve which innervated the triceps surae can be attached to
suture (attached to an electrode) and pulled inside of a syringed containing
Ringer’s solution. This type of preparation increases the likelihood of
stimulating all the MU in the muscles (Figure 1.13b). A stimulation within
the physiological time frame (0.2 ms) results in an isometric twitch (Figure
1.14a, b) and a force-time curve can be recorded. Different characteristics
(variables) of the isometric force-time curve can be used for physiological
or biomechanical comparison. These variables include total tension,
developed force, time to peak tension, time to relaxation, and rate of force
 development. Using these variables, muscles with different myosin ATPase
capabilities or the same muscle from animals that have been treated or
trained differently can be compared (176).

Figure 1.13 (a) Isolated muscle preparation for length–tension

investigations. (b) Stimulation for in vivo preparations.
FT = force transducer; Stim = stimulator; REC = recorder.

When stimulated, total muscle tension is a function of the resting tension

and the developed force. Resting tension is strongly associated with the
muscle elastic properties, and the developed force is a function of the
contractile apparatus (sarcomere). Alterations in muscle resting length
results in different magnitudes of developed force and total tension during
isometric contractions (Figure 1.14b).
Figure 1.14 (a) Isometric twitch force production. (b) Force
production related to muscle length.

Increasing the stimulation frequency results in tetany (Figure 1.15).

Tetany likely results from the inability of the Ca++ pump of the SR to keep
up with the increasing Ca++ concentration in the sarcoplasm resulting from
inadequate relaxation as the frequency of contractions increase.

Figure 1.15 Force production in relation to increased stimulation

frequency.
Force-Velocity Relationships
Isotonic contraction refers to having the same tone or force during the
contraction. Because of the skeletal lever system, as a muscle action occurs,
force changes as the lever arm angle is altered, thus isotonic contractions
can occur only in isolated muscle preparations. Two types of dynamic
contractions can occur. When a stimulated muscle contracts (shortens) and
lifts a load producing external work (W = f × d), the contraction is termed a
concentric contraction. If the load is greater than the maximum isometric
capabilities of a muscle, the muscle will lengthen, even though it is
attempting to contract. The lengthening contraction results in a negative
displacement and velocity. A lengthening contraction is termed an eccentric
or negative contraction. It has been argued that the terms isometric and
eccentric contraction are inappropriate since substantial contraction (i.e.,
shortening) does not occur. Thus, the term “muscle action” has been
suggested as a more appropriate term instead of “contraction” (112). In
actuality there is a very slight initial muscle shortening during isometric and
eccentric contractions in removing the slack from the tissue system and
during whole-muscle eccentric contractions fibers shorten as the tendon
lengthens until the lengthening is so great that fiber lengthening is required
(103). As the load increases, the velocity of shortening decreases during
concentric contractions. During eccentric muscle actions, as the load
increases, so does velocity to a point. These relationships are illustrated in
Figure 1.16. In terms of maximum force production during isolated muscle
actions (contractions), note that Concentric < Isometric < Eccentric.
Figure 1.16 Force-velocity relation during concentric-isometric-
eccentric muscle actions in isolated muscle.

Differences in concentric and isometric contraction force are related to

the number of cross-bridges formed at any moment in time (69, 98, 156).
There appear to be several basic causes for variation between contraction
types: as the muscle (sarcomere) begins to move, it is difficult for the cross-
bridges to attach to a moving filament/target, the faster the movement, the
fewer cross-bridges formed (96, 98) and there is a higher rate of cross-
bridge detachment (156). Thus, the greater the velocity of contraction, the
shorter the time period in which myosin can bind actin. Additionally, during
fast contractions, the flexible S2 complex of the myosin molecule, close to
the globular head, cannot not fully extend, resulting in compression of the
S2 complex and a lower pulling force applied by the myosin myofilament
on actin (69).
The higher maximum forces produced by eccentric muscle actions,
compared to concentric and isometric, can be explained by the additional
force generated by stretching the elastic elements of muscle (92, 96). There
are two types of elastic elements which contribute to the elastic properties
of whole muscle: the parallel and series elastic components. The parallel
elastic component consists muscle fiber factors the proteins of the
sarcomere (particularly titin), sarcolemma, sarcoplasmic reticulum, the
perimysium, and the epimysium, whereas the series elastic components
reside in the muscle aponeuroses and tendons.
The fastest possible cross-bridge cycling rate of a muscle (Vmax: Figure
1.17) represents an estimate of the fastest possible cross-bridge cycling rate
of a muscle and correlates strongly with the maximum rate of ATP
hydrolysis (12, 52, 144). As a result, force and velocity of shortening
appear to be strongly related to myosin ATPase activity (12); however,
other contractile force-time characteristics, such as time to peak tension, are
not as strongly related (144). Power (force × velocity) reaches its maximum
in isolated muscle at about 30% of maximum velocity or maximum
isometric force (157). Figure 1.17 shows this relationship for isolated
muscle. Note the marked differences between muscles consisting largely of
type II fibers (cat medial gastrocnemius) versus a muscle containing almost
wholly type I fibers (cat soleus). Also note that the unloaded maximum
velocity cannot be measured (the muscle itself weighs something). It can
however be mathematically interpolated (estimated).
Figure 1.17 Power as a product of concentric force and velocity.
MG = cat medial gastrocnemius; SO = cat soleus.

Source: Modified from Roy and Edgerton (157).

For intact whole muscles, internal tension and the resulting external
force produced is a function of the interaction of a number of sarcomere
lengths and the mechanical characteristics of the skeletal lever system.
Although, the force-velocity characteristics of intact muscle are largely like
those of isolated muscle, there can be differences during high force
productions in which (particularly for single-joint exercises) force is
approaching the isometric maximum, input from various mechanoreceptors
(including joint receptors and golgi tendon organs) inhibit the agonist
muscle force output in order to reduce tissue strain (4, 195). Thus, dynamic
force can be higher near the isometric value (Figure 1.18). Resistance
training can increase neural activation of the muscle and reduce the force
deficit at high force outputs, thus the force-velocity relationship of isolated
and intact muscle become more similar at the high force end.
Figure 1.18 Force-velocity curve for intact muscle.
Somatic Nervous System Structure and Function
Fundamentally, the nervous system is a network of nerve cells and its
supporting connective tissue. The nervous system can be evaluated in two
basic ways: based on its anatomical characteristics or based on functional
characteristics. Anatomically, there are two parts: the central nervous
system (CNS), consisting of the brain and spinal cord, and the peripheral
nervous system (PNS) consisting of 43 pairs of peripheral nerves (12
cranial and 31 spinal). The function of the CNS is either autonomic or
somatic. The autonomic nervous system is responsible for involuntary
actions involved in “housekeeping” and homeostasis maintenance, such as
peristalsis and regulation of heart rate and blood pressure. The somatic
system innervates skin, muscles, joints and provides the CNS with
environmental information. The primary function of the somatic nervous
system is working in an integrative fashion with the muscular system, thus
forming the neuromuscular system. The neuromuscular nervous system’s
primary function is in producing voluntary movement and reflex arcs.
Two types of nerve cells make up the CNS: neurons and glial cells. Glial
cells (neuroglia) are specialized, and do not conduct AP and do not have a
direct role in impulse transmission. However, they may respond to neuron
activity and modulate communication between neurons (104). Glial cells
provide a structural/support matrix, a guide for developing neurons to the
appropriate destination, play a role in synapse formation, function in the
formation of myelin and myelin sheaths around neurons, and provide
metabolic support for neurons in controlling the passage of substances from
capillaries into and out of the neuron (61, 109). Three types of glial cells are
found in the adult central nervous system: astrocytes, oligodendrocytes, and
microglia. Astrocytes have local projections that give these cells a starlike
(thus the name astro-) appearance and are found only in the CNS (brain and
spinal cord. The primary function of astrocytes deals with maintaining an
appropriate environment for neuronal signaling. Oligodendrocytes, also
confined to the CNS, produce the myelin found around some neuronal
axons. Myelin, which is laminated and lipid rich, helps to modify AP
conduction velocity. Schwann cells are responsible for the myelin sheath in
the PNS. Microglial cells are smaller and are derived can be derived from
hematopoietic stem cells unlike most nerve cells which are derived directly
from neural stem cells. Microglia are primarily scavenger cells, similar to
macrophages, and remove cellular damage and debris as a result of injury or
from normal cell turnover. Indeed, as a result of brain damage, microglia at
the site of injury substantially increase in number. Some of these scavenger
cells proliferate from microglia in the brain, while apparently come from
macrophages that migrate to the injured area from the circulation (61, 109).
The smallest functional unit (transmission unit) of the nervous system is
the neuron. In terms of information transmission, neurons are either motor
(efferent) or sensory (afferent). Motor neurons transmit information from
the CNS to effector cells. Sensory neurons transmit information from
various sensory receptors to the CNS. Basic neuron anatomy is shown in
Figure 1.19. Anatomically, the human nervous system consists of billions of
neurons, having different shapes and sizes. Information transmission results
from changes in the electrical potential of the cell.
Figure 1.19 Basic neuron anatomy.

Under resting conditions, cells (including neurons and muscle fibers) are
electronegative on the inside of their cell membrane compared to the
outside; this resting membrane charge is referred to as the resting
membrane potential (RMP) and results from an excess of negative ions
(anions) trapped inside the cell and a relative excess of positive ions
(cations) on the outside of the cell. The RMP is created by selective
permeability of the plasmalemma (neurolemma in neurons). The cations
and anions ions accumulate along a relatively narrow band on either side of
the neurolemma, resulting in a RMP that essentially straddles the plasma
membrane. The RMP can be altered as a result of changes in the number of
anions or cations on the outside or inside of the neurolemma.
The RMP is a function of two basic processes: active transport of ions
through the neurolemma and a concentration gradient related diffusion of
ions across the membrane. At rest and undisturbed, the RMP is primarily a
function of [Na+] and [K+]. The [Na+] is relatively high outside the cell
(≈142 mEq/L), and the [K+] relatively high inside the cell (≈140 mEq/L).
An ATP-dependent Na+/K+ electrogenic pump largely maintains these
concentrations (41, 125) (Figure 1.20). In neurons, the RMP is typically –70
to –85 mV, inside relative to the outside. The RMP exists because the
neurolemma is 50 to 100 times more permeable to K+ compared to Na+.
This difference in permeability allows K+ to “leak” out of the intracellular
fluid into the extracellular fluid, resulting in more cations on the outside of
the cell and an electronegative intracellular environment (31).
Figure 1.20 Example of an ionic dynamic equilibrium across cell
membranes.
Source: Based on Guyton (86, 87).

Some anions such as chloride (Cl–) diffuse through the neurolemma

relatively easily and are not dependent on a pump. This results in [Cl–]
being largely determined by electrical potential, as Cl– is repelled by the
negative anions inside of the cell. The result is a high concentration (≈103
mEq/L) on the outside of the cell. Because of this mechanism, the role of
Cl– in the maintenance of the RMP is passive. However, the duration and
magnitude of an action potential can be affected by the movement of Cl–
anions. Typically, other ions are affected in the same way as Na+, K+, and
Cl–. However, the concentrations and the permeability of the neurolemma
to these ions is small, thus the RMP is little affected. The most important
role for these additional ions, particularly Ca++ and Mg++, is in their effect
on the membrane permeability of other ions. For example, Ca++ may affect
the distribution of electrons on proteins and alter the atomic/intra-molecular
bond angles potentially modifying the structural conformation of the
pore/channel proteins, creating differences in membrane permeability to
specific ions (86). Permeability is also affected by membrane composition.
For example, alterations in the cholesterol content of the neurolemma can
alter its permeability to most ions (15).
The Action Potential
Several stimuli, including extreme temperature changes and chemical,
mechanical, and electrical stimuli, can cause an excitable membrane to
depolarize. A wave of depolarization that occurs along the surface of
excitable tissue such as muscle and nerve is termed an AP. The AP is a
result of sequential alterations in the membrane potential lasting a fraction
of a second. Depolarization of an excitable membrane, such as the
neurolemma or sarcolemma, is followed by a rapid return to RMP values.
Rapid alterations in membrane permeability for Na+ and K+ are associated
with the AP. Alterations in membrane permeability for various ions can be
quite rapid and these rapid movements are associated with the opening and
closing of ionic gates (channels). These gates, along with electrogenic
pumps such as the Na+ / K+ pump, largely control the movement of
specific ions across the plasmalemma (13, 33, 108, 125, 127).
Two stages control the AP: depolarization and repolarization (87, 125).
These two stages are largely influenced by a sequential alteration in
membrane permeability to Na+ and K+ (Figure 1.21):

1. Resulting from a stimulus, Na+ membrane permeability suddenly

increases (Na+ channels open) and substantial Na+ rapidly move to the
inside of the fiber as a result of the initial Na+ concentration gradient.
The net effect is a reversal potential and cell depolarization caused by
cations entering the fiber making the inside positive compared to the
outside.
2. The permeability of the membrane for Na+ returns to the resting state
immediately after the reversal potential takes place; concurrently there
is an increase in the plasmalemma’s permeability to K+ as K+ channels
open. The change in permeability allows substantial amounts of K+ to
diffuse out of the cell down a concentration and ionic gradient,
returning the membrane potential back to its negative resting state. The
 AP repolarization phase (lasting a few milliseconds) initially results in
hyperpolarization. During this period (hyperpolarization), the cell
reaches a more negative potential than at rest (about −80 mV). This
negative potential is due to the slow inactivation of voltage-gated K+
delayed rectifier channels, which are the primary K+ channels
associated with repolarization.
3. Once the resting highest electrical potential is reached, the membrane
permeability for K+ is reestablished at the resting state. As resting
permeabilities for ions are reached, the electrogenic Na+/ K+ pump
reestablishes the resting concentrations of the cell.

An AP takes place at one spot on an excitable membrane. In due course,

adjacent portions of the membrane become excited causing AP propagation.
AP propagation occurs resulting from the completion of a local circuit of
current flow (87, 125). The AP can travel in all directions away from the
initial site of the AP; however, in neurons the physiological direction of AP
propagation is largely determined by anatomy: soma to axon to synapse to
effector cell. Once the AP is initiated, the wave of depolarization travels
over the entire surface of the membrane and propagation occurs in an all-or-
none fashion. Additionally, alterations occur in the extra- and intracellular
physiological environment (e.g., ionic concentrations, pH) can affect the
strength of the AP. The AP lasts for about the same length of time at each
point on the plasmalemma. Repolarization begins at the point that was
initially depolarized and then is propagated progressively behind the AP in
the same direction and about 0.002 s behind depolarization.
Figure 1.21 Action potential propagation.
TA = threshold activation.

Source: Based on Guyton (87).

Action potential propagation requires that a RMP threshold must be

reached; typically this requires a positive increase of 10 to 15 mV in the
RMP. In neurons, alterations in the RMP are initiated by increased Na+
permeability; however, if the influx of Na+ is small and the threshold value
is not reached, no AP will occur. Physiologically, the threshold value can be
reached by several mechanisms. For example, through temporal summation
in which an increased frequency of impulses arrives from the same neuron
(or a few), by spatial summation when a large number of separate neurons
excite the effector cell simultaneously or both temporal and spatial
summation.
Neurons often transmit a series of AP in very short periods of time.
However, once an AP occurs the membrane becomes refractory a second
AP will not occur if the membrane is depolarized from the preceding AP.
Independent of the stimulus strength, an AP cannot be propagated during
the absolute refractory period (about 0.0025 s) in a myelinated fiber. Thus,
the maximum number of impulses possible (non-physiological) is about
2500 s–1. Physiologically, in human α-MNs, the maximum rate of firing
appears to be approximately 250 Hz (59).
Neuron Structure and Function
In the intact human, voluntary muscle contraction is initiated in the motor
cortex in the cerebrum. Information is sent to the directly to the muscle as a
series of AP initiated from large MNs present in the ventral gray matter of
the spinal cord or a similar area of the brainstem (125, 127). The basic
structure of a typical α-MN (Figure 1.19) consists of a soma (cell body),
relatively short projections from the soma known as dendrites, and a long
projection (the axon) with terminal endings that release neurotransmitters.
The soma of MNs makes up longitudinal columns within the spinal cord.
The neurons within a column normally innervate the same muscle (125,
127, 154, 155). Two primary types of MNs function in the periphery: α-
MNs, which innervate extrafusal muscle fibers, and γ-MNs (gamma motor
neurons), which innervate intrafusal muscle fibers (muscle spindle).
Under normal intact conditions, the physiological direction of AP
transmission is dendrites and soma receive information from other neurons,
and this information is transmitted down the axon to the terminal endings.
At the terminal endings, the release of a neurotransmitter transfers
information across a synapse to an effector cell. In the neuromuscular
system, an effector cell will be another neuron or a muscle fiber. The type
of transmitter released depends upon the neuron’s location and function. For
example, in different parts of the brain, the neurotransmitter may be ACh,
norepinephrine, serotonin, or γ-aminobutyric acid. Peripheral α- and γ-MNs
that innervate muscle fibers release ACh.
The soma of an α-MN is much larger than the soma of a γ-MN and has a
diameter of about 70 μm. The neuron soma contains one large nucleus with
a prominent nucleolus. The soma also contains several different organelles
including mitochondria, a tightly packed endoplasmic reticulum (Nissl
bodies), and a complex cytoskeleton system. Typically, a soma has several
dendrites radiating in various directions, often causing the soma to take on a
star shape. The dendrites often show substantial branching and can extend
relatively long distances into the gray matter of the spinal cord. This
arborization allows the neuron to receive information from a variety of
other neurons (125, 127).
Arising from the axon hillock, a cone-like projection of the soma, the
axon may extend only a few centimeters or more than a meter. The length
of the axon depends on the location of the neuron and tissue innervated. In
the neuromuscular nervous system, the axon forms a cylinder extending
into the muscle. The plasma membrane surrounding the axon has properties
like those of the sarcolemma of muscle. A long axon of a large α-MN may
have as much as 100 times more cytoplasm than its soma and in some
neurons represents as much as 99% of the total neuroplasm (127, 158). For
structural support and axonal transport, the axonal cylinder contains arrays
of cytotubules and neurofilaments that run its entire length.
As the result of a myelin sheath formed by Schwann cells, all neurons
have an intermittent lipid covering around the axonal cylinder (76). Myelin
is an excellent insulation material that increases the capacitance of the
sheathed portion of axon and prevents the flow of ions. However, neurons
can be classified as myelinated or unmyelinated depending on the thickness
of the sheath, which in turn is related to the number of layers of
sphingomyelin. Unmyelinated fibers have a single wrapping of myelin;
somatic motor neurons have multiple layers of myelin and are classed as
myelinated. In myelinated neurons, the sheath is about as thick as the axon
cylinder (87). In adults, the node of Ranvier is created by interruptions in
the myelin sheath approximately once every 1000 μm. The node is a small
area of non-insulation where ion flow is largely unimpeded between the
extracellular fluid and the inner surface of the plasma membrane of the
axon (Figure 1.19). As a result of the relative ease of ion flow at the node,
saltatory conduction takes place in which the AP can actually jump from
node to node. Advantages of saltatory conduction over typical local circuit
conduction include increased velocity of propagation; in typical α-MNs,
propagation velocity is about 40 to 120 m s–1 (87, 127). Also, because only
the nodes depolarize, fewer ions are transported and thus, less energy is
used in reestablishing the RMP.
 Neural transmission is also influenced by neuron diameter. Generally,
larger axon diameters produce a faster conductance velocity. In neurons,
such as those associated with many sensory functions that are largely
unmyelinated, the velocity of conduction increases with the square root of
the diameter of the axon. However, in myelinated axons, the velocity
increases in an approximate linear fashion with the change in axon diameter
(87). As the axon approaches the muscle, it branches and may innervate as
many as several hundred muscle fibers, creating a MU. The NMJ is a
specialized synapse between the terminal ending of an axonal branch and a
muscle fiber.
Structure and Function: Neuromuscular Junction
The NMJ represents the interface between a MN and the muscle fiber. Upon
entering a muscle, the MN loses its myelin sheath and divides into axonal
branches (87, 95, 125, 127). The branches lie in grooves within the
sarcolemma and form a somewhat circular area on the surface of a muscle
fiber (Figure 1.22a). A Schwann cell covers this circular area, forming a cap
such that it is electrically isolated. Terminal boutons are small irregular
expansions at the end of an axonal branch that correspond to the area of
neurotransmitter release. The axon terminals contain numerous small
spheres (vesicles), with membranous linings. These vesicles are
approximately 55 nm across. The vesicles contain ACh. Vesicles are
assembled in the soma and then transported to the terminal boutons, or they
can be formed by invagination and pinching of the axonal plasma
membrane of the terminal ending (93).
Evidence indicates that ACh is synthesized in the cytoplasm of nerve
terminals by the enzyme choline acetyltransferase and then transported into
synaptic vesicles. ACh enters the vesicle as a result of an H+ gradient that
attracts the ACh into the vesicles (8, 109). Vesicles contain about 10,000
molecules of ACh (114). There is also a large concentration of
mitochondria in the terminal ends that provide energy for the synthesis of
new neurotransmitters.
Figure 1.22 (a) Axonal branching at the neuromuscular junction. (b)
Motor end plate and neuromuscular junction.

Under the Schwann cell cap is an area of muscle termed the motor end
plate (Figure 1.22b). The motor end plate includes the sarcolemma and a
mound of sarcoplasm known as the sole plate. Contained within the sole
plate is a substantial concentration of various organelles including nuclei,
mitochondria, ribosomes, and pinocytic vesicles (125, 127). A synaptic cleft
of approximately 70 nm separates the terminal ends of the axon from the
sarcolemma. Secondary synaptic clefts are created by enfolding and
invaginations of the sarcolemma into the sole plate and can be as deep as 1
μm. These secondary clefts markedly increase the surface that can combine
with ACh. The sarcolemma which lines the motor end plate is thicker than
other parts of the muscle fiber. This thickening is largely a result of an
increased number of ACh receptors (AChR) in the outer membrane. The
AChRs are continually renewed and replaced and are not permanent
fixtures within the sarcolemma; this synthesis, degradation, and
replacement of the AChR is a process controlled by the myonuclei within
the sole plate (62, 125, 127, 187). Importantly, the secondary clefts
(invaginations) allow an increased in the number of AChRs as well as the
amount of AChE available for interaction with ACh.
When an AP arrives at the terminal endings of the MN, depolarization
results from the opening of Na+ gates, which in turn triggers Ca++ channel
activation. A substantial concentration gradient causes Ca++ to enter the
terminal endings. The activation of the Ca++ channels result in ACh-
containing vesicles attachment to the sarcolemma near the Ca++ channels.
The vesicles fuse with the sarcolemma and release ACh into the NMJ by
exocytosis, the ACh then diffuse into the cleft and bind with AChRs (17,
109). The nicotinic AChR is a ligand-gated ion channel. AChRs are
composed of five protein subunits arranged symmetrically around a central
conducting gate. Attachment of two molecules of ACh to an AChR on the
sarcolemma causes the Na+ gate in the center of the receptor to open.
Opening this channel allows Na+ and K+ to move in or out of the muscle
fiber according to concentration and electrical gradients and produces an
end plate potential (EPP). A single AP causes the release of 25 to 45 quanta
(vesicles) in human muscle (54, 170). If a sufficient quanta of ACh are
released (and bound to the AChRs) the EPP will be large enough and
depolarization is transferred to the muscle fiber and an AP will be
propagated.
To stop the depolarization and muscle fiber contraction, a first step is the
degradation of ACh. The enzyme AChE is located in the basement
membrane near the sarcolemma and is positioned between the site of ACh
release and the AChRs (109, 125, 127). Although AChE is continuously
activated, ACh cannot alter the ACh–AChR interface because during
depolarization there are more molecules of transmitter released than there
are molecules of enzyme present in the basement membrane. After the
opening of AChR channels, ACh molecules detach and diffuse toward the
basement membrane. The transmitter is then deactivated by hydrolysis and
transmission is eventually finished within a few milliseconds. ACh
hydrolysis products, choline and acetic acid, are taken up by the axon
terminals, converted into ACh, and repackaged into vesicles. Acetylcholine
is re-synthesized from choline and acetyl coenzyme A catalyzed by choline
acetyltransferase. The rate-limiting step in the synthesis of ACh is transport
of choline into the nerve terminal via a high-affinity choline transporter
(30).
The Motor Unit
A MU consists of a MN and all the muscle fibers it innervates (168). When
a MN AP is propagated and transferred to the sarcolemma, all of the muscle
fibers innervated by that MN are caused to contract; thus, the muscle and
MN fibers function as a unit (the all-or-none principle). For voluntary
muscle contraction, the CNS “plans” and initiates movement in terms of
MUs, rather than by individual muscle fibers. So, the functional unit of the
neuromuscular system is the MU.

Extrafusal Fiber Motor Units: The Alpha Motor Neuron

The distribution, within a muscle, of fibers from a single MN generally
covers a relatively broad area. Adjacent fibers are typically from different
MUs. The innervation ratio is the relation of a single α-MN to the number
of muscle fibers innervated by that α-MN. The innervation ratio is altered in
concert with the functional characteristics of the muscle. Fine motor control
requires a small innervation ratio. For example, in the intraocular muscles
of the eye, the innervation ratio ranges from approximately 1:5 to 1:100,
and in the small muscles of the fingers the range is 1:3–1:150. However, in
muscles that can produce large amounts of force and fine movements are
not an issue, the innervation ratio may be as low as 1:2000 (80, 127). Type
II fibers (particularly IIx) tend to have very low innervation ratios (more
muscle fibers per MN). Although there can be considerable inter-subject
variation, MU number per muscle can vary from about 100, in the first
dorsal interosseous, to about 3000 in the intraocular muscle. There can also
be considerable variation of MU size within the same muscle (109, 125,
127).
MU classification is an important tool for sport scientists because these
classification schemes allow for the delineation of specific muscle fiber
populations with similar functional properties. However, it is quite
important to note that MUs display considerable plasticity of phenotypic
expression and are not static structures (144). Resulting from functional
demands and neuromuscular activity patterns, MUs can adapt to a variety of
neural, hormonal, and metabolic stimuli. Because of their dynamic nature,
classification as distinct and separate entities is difficult at best.
Classification difficulty is compounded by the possibility of local factors
modulating gene expression in different fibers within MUs and along the
length of single fibers (144). MUs have been separated and identified
according to their contractile characteristics (27, 28). Based on contractile
properties, three basic types of MUs have been characterized:

1. Fast-twitch fatigue sensitive (FF). These are large MUs found

primarily in “white” muscle associated with high power outputs and
explosiveness; FF produce the fastest time to peak force, highest peak
force, greatest rate of force development (RFD) and greatest speed and
power of contraction. However, FF also fatigue at the fastest rate
during sustained tetanic contractions and during prolonged repetitive
isometric twitches.
2. Fast-twitch fatigue resistant (FR). These are large MUs found in
“mixed” muscle; they produce intermediate time to peak force, force,
RFD, speed, power, and endurance capabilities.
3. Slow-twitch (S). These are relatively small MUs found in “red” muscle
associated with maintaining posture and low force output over
sustained periods; they produce the slowest time to peak force and
lowest force, RFD, speed, and power; however, they have the greatest
endurance capabilities.

While this system (27) works well in small animals, due to differences in
muscle size and the invasive nature of the methods necessary for
classification (137) classifying human MUs in this manner is difficult.
The biochemical consistency from fiber to fiber within an α-MN is
relatively constant (144, 145). This finding allowed for the development of
MU classification schemes based on histochemical and
immunohistochemical identification.
Three basic histochemical schemes are currently used:

1. Myosin ATPase and metabolic (enzymatic) properties (14, 142). This

classification system is based on myosin ATPase activity and the
activities of specific metabolic enzymes. Using this system, three types
of MUs can be identified. Importantly, the ATPase properties have
been associated with the contractile characteristics exhibited by the FF,
FR, and S MUs (27, 28):
a. Fast-twitch glycolytic (FG) MU has contractile properties similar
to those of the FF and displays a strong glycogenolytic enzymatic
activity profile but relatively low oxidative characteristics.
b. Fast-twitch oxidative glycolytic (FOG) MU has contractile
properties similar to those of the FR and displays both a high
oxidative and a high glycolytic enzyme activity characteristics.
c. Slow-twitch oxidative (SO) MU has contractile properties similar
to those of the S and has a high oxidative enzyme activity profile
but a relatively weak glycogenolytic activity.
2. Myofibrillar ATPase. Slow and fast myosin have different alkaline and
acidic stability (166). Based on this observation, the development of
delineated methods for myosin ATPase histochemical determination
have been developed (25, 75, 144, 175).
3. Immumohistochemistry (identification of MHC and MLC),
conceptualized by Albert Coons, was used in the late 1940s and has
continued to be further developed (38, 178). Immunohistochemistry
(IHC) is a process of using antibodies-antigens interaction in
biological tissues. IHC detects specific antigens (proteins) in a tissue
cell section by antibodies binding specifically to antigens in biological
tissues. Thus, heavy and light myosin isoforms can be detected in this
manner.

Visualizing the antibody–antigen interaction can be accomplished by

several methods. The simplest method uses an antibody conjugated to an
enzyme, such as peroxidase, that can catalyze a color-producing reaction.
The different colors or shades of reaction correspond to different proteins.
Alternatively, the most commonly used methods are to tag the antibody to a
“fluorophore” (florescent molecule). The florescence can then be viewed,
depending upon the specific antibody different proteins can be identified
within the tissue.
Based on these methods, a continuum of MU types based on myosin
ATPase has been identified relating to the content of MHC (Table 1.1).
While some overlap exists, evidence relating the myosin ATPase system to
the metabolic-based system indicates that the two systems are not
completely compatible (145, 161). There is general agreement, in normal
large-animal limb muscles, that IIB, IIA, and I MUs correlate to the FF, FR,
and S MUs described by Burke and colleagues (28). However, in some of
the smaller muscles, such as those in the hand and foot, MU types do not
seem to correlate well (26, 125, 127). Metabolic attributes do correspond
with the general classification of type II and type I. Type II fibers are
metabolically and enzymatically suited for anaerobic strength-power-type
activities and type I MUs are better suited for aerobic endurance activities.
Additionally, MU contractile properties, such as specific force and
particularly velocity of shortening and power outputs, also correlate well
with myosin ATPase activities. Because of this correspondence, a
continuum of maximum contractile speed and power output has been shown
to exist: IIB > IIX > IIA > IIC > I (23, 127, 130, 141, 144, 175). Although
some early studies suggested that humans contained similar muscle fiber
types to that of small mammals, it was realized that this was not the case.
Indeed, evidence indicates that while the IIB fiber type exists in small
animals (e.g., rats), it is not identifiable in humans, where the fastest fiber
type (MU) is the IIX (75, 141). Characteristic contractile and metabolic
properties of MUs are shown in Table 1.3.

Table 1.3 Contractile and metabolic properties of skeletal muscle fibers

Parameter Type I Type IIa Type IIx Type IIb

Sources: Based on references 11, 19, 75, 143, 144, 160, 163.
Parameter Type I Type IIa Type IIx Type IIb
Relative contraction time Slow Moderately Fast Very fast
fast
Relative size of alpha motor Small Medium Large Very large
neuron
Relative resistance to fatigue High Fairly high Intermediate Low
Activity used for Aerobic Long-term Short-term Short-term
anaerobic anaerobic anaerobic
Maximum duration of use Hours < 30 minutes < 5 minutes < 1 minute
(when isolated)
Relative power produced Low Medium High Very high
Relative mitochondrial density High High Medium Low
Relative capillary density High Intermediate Low Low
Relative oxidative capacity High High Intermediate Low
Relative glycogenolytic activity Low High High High
Major storage fuel Triglycerides Creatine Creatine Creatine
Glycogen phosphate phosphate phosphate
Glycogen Glycogen Glycogen
Myosin heavy chain, human MYH7 MYH2 MYH1 MYH4
genes
Sources: Based on references 11, 19, 75, 143, 144, 160, 163.

A muscle biopsy technique (18) has been typically used to provide a

sample of muscle tissue for muscle fiber typing in humans. When used in
appropriate muscles, this tissue sampling technique has allowed for intra-
and intermuscular comparison of human muscle and has allowed insights
into the functional capabilities of human muscle. This technique, along with
the advent of immunohistochemistry, has allowed better identification of
muscle fiber biochemistry. It is now quite clear that fiber type hybrids
(combinations of MHC) exist. Hybrid fibers apparently have two primary
roles (128): first, functioning as intermediates during fiber-type transitions
associated with skeletal muscle development, adaptation to training and
aging; second, providing a functional continuum of fiber phenotypes, as
they possess physiological properties that are in between those of pure fiber
types. One property of hybrid fibers that is not widely recognized deals with
fiber-type asymmetries including differences in the MHC composition
along the length of single fibers (128).
 Evidence indicates that fiber (MU) type generally associates quite well
with athletic and sport performance. As might be expected, high-level
endurance athletes have a predominance of type I fibers while strength-
power athletes have a predominance of type II fibers which are reflected in
terms of genotype (67, 139, 198, 202). Unclear, and a subject of
controversy, is the degree to which physical activity affects changes in MU
type. However, evidence does indicate that as a result of specific conditions,
changes in muscle fiber type and MHC can take place. Fast-to-slow
transitions can occur as a result of increased neuromuscular activity,
mechanical loading, and hypothyroidism. Slow-to-fast transitions can occur
with reduced neuromuscular activity, mechanical unloading, and
hyperthyroidism (145, 146). With increased volumes of training, hybrids
tend to disappear and move toward pure fiber types. While these transitions
have clearly been shown to occur within the type II fibers, for example
increased activity tends to promote IIX to IIA transitions, it is largely
unknown to what extent complete fiber transformation can take place.
 Voluntary Movement
Voluntary muscle contraction, and therefore purposeful, directed
movements, are planned and organized in the CNS (109, 136). These
intentional movements have a hierarchical nature. Therefore, to gain a
better understanding of how these movements are organized and the
patterning of MU activation in carrying out coordinated movement, an
understanding of the hierarchy of the somatic-somatosensory system is
crucial (Figure 1.23).

Figure 1.23 Somatic-somatosensory nervous system hierarchy.

PMC = premotor cortex; SMA = secondary motor area; MS = muscle spindle; GTO = Golgi
tendon organ.
Source: Based on Kandell et al. (109) and Noth (136).

Simplistically, voluntary movement is initiated by the primary motor

cortex (MC) with input from the premotor cortex (PMC) and the
supplementary motor area (SMA) (109). Information from cortical and
subcortical nuclei is relayed by the PMC to the primary MC. For
coordinated movement to occur sensory information transfer from
subcortical areas to the MC is necessary. The PMC functions in the
preparation for voluntary movements and also in postural control, visual
guidance of movement, and rapid corrections during movement in response
to sensory cues (109, 136). The function of the SMA include postural
stabilization, bilateral coordination, control of movements that are
internally generated rather than triggered by sensory events, and the control
of movement sequencing (109, 117, 169, 199).
Anatomically, the PMC lies within the central gyrus and extends into the
central sulcus of the cerebrum (109, 136). The PMC is the terminal focal
point of subcortical sensory input. Originating in large Betz cells of the
PMC, the primary outflow is along the corticospinal tract. The primary
function of the PMC is voluntary movement. During the initiation of
voluntary moment, MUs within a specific set of muscles are activated or
inhibited such that a specific movement pattern is produced. This, “task
specificity” occurs because there are multiple discrete and separate nuclei
within the MI that are task related. Thus, the MC is able to organize MUs
according to muscle synergies rather than as isolated muscles contractions
(109, 136, 162).
Approximately 50% of the neurons in the brain are found in the
cerebellum (136). Unlike most areas of the brain, the relative uniformity of
the cerebellar neuronal matrix suggests that the cerebellar internal
functioning in all areas is similar. Interestingly, the cerebellum is involved
in coordinating movement, balance, and motor learning, which is its
primary function (109, 136). Both voluntary actions and reflexes require
information input from the cerebellum in the learning process. Information
arrives at the cerebellum from a variety of sensory pathways and this
information is used for the refinement of the motor learning process. The
cerebellum is in part associated with highly precise movement adaptation
associated with changes in internal or external restraint (109, 136). Unlike
the cerebellum, the basal ganglia do not appear to receive direct sensory
input. The basal ganglia provide a major output system from the neocortex,
which connects to neural systems involved in generating behavior. The
main input structure of the basal ganglia is the striatum and the primary
outputs are GABAergic neurons in the medial globus pallidus and
substantia nigra pars reticulata. The basal ganglia appear to be involved in
mediating reward, cognition as well as motor control. Its motor control
function is associated with its connection with aspects of the frontal cortex
that mediate many motor control tasks. Its primary functions involve the
release of motor programs and also in the preparation of axial and proximal
limb muscles initiating goal-oriented movements. Additionally, the basal
ganglia appear to be important in choosing relevant internal and external
behavioral cues (43, 109, 111, 129, 136).
Motor neurons are located in the spinal cord (SC), as well as in the
brainstem. The SC is the lowest portion of the CNS hierarchy and is the
location of MNs innervating most skeletal muscles. The integration of
descending motor commands with peripheral sensory input is the primary
function of the SC. Sensory information is processed and transmitted to
supraspinal areas by way of the SC. Another important function of the SC
affecting both daily and athletic movement deals with the initiation and
generation of spinal reflexes. Evidence suggests that coordinated voluntary
movement depends on a series of spinal reflexes and feedback loops
including “dynamic movement primitives” (94, 171). Dynamic movement
primitives (DMP) are a “formula” of movement primitives with
autonomous nonlinear differential equations, whose time evolution creates
smooth kinematic movement plans. DMPs form complete kinematic control
programs, not just a particular desired trajectory. DMPs form complete
kinematic control policies, not just a particular desired trajectory (163).
 Motor Unit Recruitment
Muscle contraction force can be altered through two basic mechanisms:
recruitment (changing the number of MUs activated) and rate coding
(changing the frequency of MU activation). Recruitment increases muscular
force in an additive manner and is to an extent fiber type dependent (Figure
1.24). Type II fibers add more to force production partly due to intrinsic
properties and partly because they are recruited at higher frequencies of
activation.

Figure 1.24 Effects of motor unit rate coding and recruitment on force
production.
MUs provide force as IIx >> IIa > I. Alterations in rate coding (frequency of activation) can
alter the force production with greater rate coding increasing force.

Source: Based on Raikova et al. (149).

The pattern of recruitment appears to be largely based on the size

principle (88–90). The MU threshold of activation appears to depend
primarily upon the size of the neuron’s soma, the larger the soma the higher
the threshold. So, as the intensity of contraction (force or power output)
increases, MUs are recruited in a relatively orderly fashion from smaller to
larger (26, 88–90, 109). Smaller MUs tend to be type I and larger MUs tend
to be type II; thus, as contraction intensity increases, more type II fibers are
recruited. The recruitment order in this model (based on the size) can be
approximated by exponential equations (149). This relationship is
illustrated in Figure 1.25. Generally, the order of recruitment is I > IIa > IIx.
It also suggests that the IIx and IIa MUs will be likely be recruited less
frequently in daily and sport tasks that do not require high contraction
forces or power outputs. Recruitment of larger MUs as contraction intensity
is increased is in concert with the contractile and metabolic characteristics
of the larger fibers (i.e., type II). However, this model does not consider
task specificity which could modify the recruitment order and it may be
possible to preferentially activate type II fibers during specific high-
intensity tasks (35, 45, 106, 133, 179, 193). The degree to which the size
principle can be bypassed is the subject of considerable debate (63).
Figure 1.25 Order of recruitment of different motor units largely
follows the size of the neuron.
Source: Based on Henneman et al. (89).

Rate coding deals with the frequency of activation of MUs; thus, as the
frequency of activation increases, so does force. This holds true for single
fibers, MUs, and whole muscles. While the discharge rate (rate coding)
during gradual increases in muscle force increases progressively, ballistic
contractions are characterized by a high frequency of MU discharge at the
initiation of activation followed by subsequent decline during successive
discharges. As a result of an electromechanical delay between the discharge
time of the AP and onset of force exerted by the MU, recruitment
thresholds occur at lower forces during rapid contractions likely as a result
of the relatively synchronized arrival of excitatory postsynaptic potentials at
the MNs. For example, the upper limit of MU recruitment in most large
muscles declines from ∼80–90% of maximal force during slow
contractions to ∼40% of maximum during high velocity contractions (44,
46, 59, 188). As a result, in the muscle force output during fast contractions,
rate coding assumes a much more important role. Furthermore, the rate
coding capacity of MNs on the plateau of the force–frequency relation
during rapid contractions indicates that rate coding is restricted during slow
changes in force during isometric contractions (59). However, the degree of
dependence on recruitment or rate coding varies from muscle to muscle (46,
127).
Proprioception, Kinesthesis, and Neuromotor
Control
Often used interchangeably, proprioception, kinesthesis, and neuromuscular
control are terms having somewhat different definitions. Proprioception is
the awareness of joint position. Kinesthesis deals with the ability to
navigate space and the awareness of movement; thus, kinesthesis is the
cognizance of joint movement (16, 147). Neuromotor control deals with
how the CNS selects or inhibits MUs and whole muscle through the
integration of sensory and motor aspects of the nervous systems.
Mechanistically, neuromotor control can be defined as voluntary efferent
(motor) initiation or motor response to an afferent (sensory) input. Exercise
acutely disrupts proprioception, and therefore can associate with
musculoskeletal injuries. On the other hand, training can enhance
proprioception and therefore, kinesthesis (147). Proprioceptive senses,
particularly of limb position and movement, deteriorate with age and are
associated with alterations in balance and increased risk of falls in the
elderly (147). Proprioception, kinesthesis and neuromotor control depend
upon specialized sensory receptor providing constant feedback to the
peripheral and CNS concerning aspects of joint position and movement.
These are referred to as proprioceptors.
In 1906, Sherrington (167) noted that proprioceptors consisted of end
organs that are “stimulated by the body itself.” Proprioceptors are
somatosensory organs found in locations such that information concerning
various aspects of position and movement such as joint angle, muscle
length–tension–speed characteristics, and contact with surfaces can be
accumulated and “interpreted” by the nervous system. These types of
proprioceptors are in essence mechanoreceptors. The nervous system can
use this information to adjust the following muscle actions by way of
feedback loops. Much of this sensory “guidance” can operate in negative
feedback loops forming reflexes, allowing motor activity to become self-
regulating.
Three proprioceptors (mechanoreceptors) that have a major impact on
aspects of muscle function are the muscle spindle, Golgi tendon organ, and
joint receptors. Muscle spindles (MS) are in parallel with muscle extrafusal
fibers and are fluid-filled fusiform-shaped capsules approximately 2 to 20
nm long enclosing 5 to 12 specialized intrafusal muscle fibers (80, 109,
125). The MS capsule contains two types of intrafusal fibers based on the
number and distribution of their nuclei. There are 8 to 12 nuclear chain
fibers, which have nuclei distributed fairly evenly (chain-like) along their
length. Typically, there are two to four nuclear bag fibers; in this type of
fiber, most of the nuclei are located in the middle forming a bulge in the
intrafusal fiber. The bag fibers are thicker and longer than the nuclear chain
fibers. The bag fibers are innervated by γ-1-motor neurons, and the nuclear
chain fibers by γ–2-motor neurons (109, 127). Group Ia sensory neurons
innervate the central portions of both the bag and chain fibers, while group
II sensory neurons innervate one end, typically opposite the MNs, of both
fibers. The characteristics of the intrafusal fibers are shown in Table 1.4.

Table 1.4 Muscle spindle characteristics

Trait Nuclear bag Nuclear chain
Fibers per capsule 2–4 8–12
Diameter (µm) 20–25 10–12
Motor unit type γ1 γ2
Afferent neuron type x x
1a myelinated (13–20 µm) x x
II myelinated (6–12 µm)
Type of response to stimuli Dynamic Static
Sources: Based on MacIntosh et al. (125) and Kandell et al. (109).

The primary functions of MS are associated with muscle contraction

length–velocity characteristics (84, 109, 127, 137). These characteristics
can be summarized as follows:
 The MS allows the extrafusal fibers to contract at appropriate force
levels when the resistance encountered is altered either during a
contraction or between successive contractions.
Fatigue induced drops in muscle contraction force (and velocity) can
be partially compensated for by a stretch reflex.
The MS function has servo-assist characteristics which allow the brain
to create voluntary muscle contraction with less energy expenditure.
Appropriate use of the stretch-shortening cycle can create a stretch
reflex that can augment concentric muscle force.

Rapid or forceful contractions that activate the group Ia fibers, by stretching

the extrafusal fibers, can result in a myotatic or stretch reflex, thus
generating a more forceful concentric contraction following the stretch
compared to no strength. The stretch reflex results in muscle prime mover
and synergist muscle facilitation and simultaneous inhibition of the
antagonistic muscles. Activation of the group II fibers resulting from a very
slow or static stretch can result in facilitation of the antagonistic muscles
and inhibition of the prime mover and synergists (Figure 1.26). The static
reflex can be used to enhance stretching programs (97). As extrafusal fibers
contract, it is necessary for the intrafusal fibers to maintain an appropriate
length, otherwise the MS’s ability to sense changes in length–velocity
parameters will be compromised. Simultaneous co-contraction of intrafusal
and extrafusal fibers is accomplished by concurrent activation of both α-
and γ- MNs (109, 136).
Figure 1.26 (a) Simple myototic (stretch) reflex – group Ia afferent
neurons. (b) Static stretch – group II afferent neurons.

Golgi tendon organs (GTO) are oblong capsules located primarily within
the musculotendinous junction in series with the extrafusal fibers. The GTO
responds to changes in tension and contain a single Ib sensory fiber with
connections to the SC. Using both dynamic and isometric contractions, and
largely based on animal studies (49, 81, 82), the GTO appears to have a
protective function for the muscle and tendon. When muscle contraction
produces excessive forces that could result in tissue damage, the GTO
generates a reflex similar to that of the MS group II fibers, resulting in
prime mover and synergist muscle inhibition and antagonist facilitation.
Some evidence suggests that disinhibition of the GTO can result as an
adaption to strength training (1–4). However, recent re-examination of data
concerning the potential functions of the GTO suggests that activation may
have variable effects depending on multiple factors, such as the type of task,
the forces encountered, the type of contraction, the muscles contracting or
being inhibited, and input from higher centers (2, 3, 34). Thus, training-
induced alterations, including specific strength training, in GTO function
probably do occur; however, they likely depend upon task specificity.
Joint receptors are located in the synovial capsules and ligaments
between bones (42, 83, 109, 134, 200). Joint receptor sensory afferents are
not particularly sensitive to cutaneous or muscle stimulation but respond
primarily to moderate pressure applied directly over the joint, to joint
movements, and to contraction of muscles inserting into the joint capsule
(83). They detect mechanical deformation within the capsule and ligaments.
They function in two primary ways: (i) to protect the joint from potentially
injurious flexion and extension; and (ii) proprioception. There are four
types of sensory endings that make up joint receptors: free nerve endings,
Golgi-type endings, Ruffini endings, and paciniform endings.
 Free nerve endings (FNE) are innervated by Group III, unmyelinated
fibers and are found in the joint capsule and connective tissue surrounding a
synovial joint. FNE are the most numerous types of receptor innervating the
joint capsule and are also the smallest in size. FNE are activated only by
extreme mechanical stimuli, have a high threshold for activation, and they
are slow to adapt.
Golgi-type endings (GTE) are only found in the ligaments of a joint.
Neuron axon endings are tightly intertwined with the collagen fibers of the
ligament. These collagen strands straighten when the ligament is stretched
causing a physically deformation in the axon endings. The deformation
causes the Golgi-type endings to become activated, primarily occurring at
the end of joint range. GTE have a high threshold of activation and are slow
adapting. Evidence indicates that GTEs likely play a primary role in the
protection of the joint.
Ruffini endings (RE) are innervated by Group II fibers (medium
myelinated fibers) and found mainly in the joint capsule. They are activated
both at rest and during movement. RE are slow to adapt and have a low
threshold of activation. They are primarily stimulated by stretching the
surrounding tissue. RE can detect the joint position as a result of movement
and are capable of signaling static joint position, joint movements, and
direction and speed of movements.
Paciniform endings (PE) are large receptors located in the periosteum
near the articular attachments and the fibrous part of the joint capsule. PE
are activated at movement onset and termination. They have a low
threshold of activation and adapt rapidly. PE detect rapid mechanical
induced deformations and vibrations. RE do not detect static position but
inform the CNS of joint movements. They appear to be particularly suited
to detect movement velocity and are known as “acceleration receptors.”
It has only been recently that joint mechanoreceptors have been shown
to be active at the extreme ends of movement (109). Thus, there is always
some “amount” of joint receptor activation at any point in the range of
motion of that joint. Therefore, joint receptors as a group signal
considerable information concerning static and dynamic joint position,
velocity of movement, vibration and joint strain, to the CNS.
Chapter Summary
This chapter dealt with basic muscle and nerve physiology and the function
of the neuromuscular system. The neuromuscular system, which governs
physical and influences psychological aspects of behavior, depends upon its
functional/physiological abilities as well as its capacity. The mechanism of
information transfer among neurons and between neurons and muscles
depends upon the AP. Initiation and propagation of APs are dependent upon
cell structure, its electrical properties, and the interaction and exchange of
electrolytes, particularly Na+ and K+. A neuron is the functional unit of the
nervous system. The neuromuscular system is created by the interaction of
the nervous system and muscle fibers.
The smallest unit containing the necessary contractile and regulatory
components is the sarcomere; thus, the sarcomere serves as the functional
unit of the muscular system. Muscle fibers contain thousands of
sarcomeres, and whole muscles contain many muscle fibers. Motor units
are made up of a MN and all the muscle fibers it innervates and represent
the functional unit of the neuromuscular system. Motor units can have
different sizes, contractile, and metabolic characteristics, and their
activation patterns are compatible with these profiles. Motor units and
whole muscles activated by groups of task-specific nuclei in the cortex
result in task-specific voluntary movements. Information on how these
systems operate is fundamental to the development of the understanding
necessary to plan and design logical and efficient training processes and
programs.
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Part II
2 Bioenergetics

DOI: 10.4324/9781003096139-4
Introduction
From a biological standpoint, energy is the ability or capacity to perform
work. Energy can be conceptualized as either potential (stored) or kinetic
(performing work). Various forms of energy exist; for example, elastic,
nuclear, electromagnetic, mechanical, and chemical. Biochemical processes
form the basis of metabolism and metabolic energy transformations are
necessary for all activities accomplished by living systems. Indeed, the
concepts of specificity of exercise and training depend to a great extent
upon understanding underlying aspects of metabolism, energy use, and
generation. Background knowledge of how energy is created for different
types of exercises, and how specific types of training can modify energy
production, can lead to more efficient and efficacious designs for training
programs. Thus, a thorough understanding of bioenergetics and metabolism
is necessary for sport scientists and coaches alike.
Bioenergetics is concerned with the flow of energy in living systems and
how food (carbohydrates, fats, and protein) is converted into chemical
energy that can be stored or used for work. The energy stored in the
chemical bonds of various molecules (i.e., fats, carbohydrates, proteins)
represents metabolic potential energy. It is the transformation of chemical
energy into mechanical energy that allows for the attainment of kinetic
energy that actually performs work. This transformation process requires
the destruction of chemical bonds subsequently releasing energy for muscle
contraction.
Catabolism is the breakdown or destruction of large molecules (food and
energy substrates) into smaller molecules which is associated with the
release of energy. Anabolism is a synthetic process that occurs when larger
molecules are fabricated from smaller molecules using energy released
from catabolic processes. An example of catabolism would be the
breakdown of fats into fatty acids and glycerol for use in energy production;
the synthesis of triglycerides from fatty acids and glycerol is an anabolic
function. Typical catabolic reactions are exergonic (exothermic) in nature
and release heat and energy. In living systems, anabolic reactions and
muscle contraction are energy-requiring reactions and are endergonic
(endothermic) in nature. Metabolism delineates the summation of all
exergonic-catabolic and endergonic–anabolic reactions occurring
simultaneously in biological systems. Figure 2.1 depicts a basic concept of
metabolism; energy derived from exergonic-catabolic reactions cannot be
used directly by endergonic-catabolic reactions. In a sense, metabolism is
like a seesaw, if it tips one way, the cellular environment is more catabolic;
the other direction the environment is more anabolic. Some of the energy
released from endergonic-catabolic reactions is used to create an
intermediate molecule that serves as an “energy conveyor,” adenosine
triphosphate (ATP). ATP allows the “coupling” between energy transfer
from exergonic-catabolic to endergonic–anabolic reactions to take place.
Because it is a primary energy conveyor, ATP is of critical importance for
muscle contraction, sustaining contractions and therefore human movement.
Figure 2.1 Overview of metabolism: coupling of exergonic-catabolic
reactions with endergonic–anabolic reactions.
Adenosine Triphosphate
ATP is critical for life; indeed, the inability to create ATP is a reasonable
definition of death. ATP has numerous functions, including energy supply
for muscular contraction, DNA and RNA synthesis, extracellular signals,
intracellular signals, neurotransmission, amino acid activation for protein
synthesis, and ATP binding cassette transporters (30, 68, 171, 200). ATP is
fabricated from the nitrogen-containing base adenine, ribose (five carbon
sugar), and three phosphate groups (Figure 2.2). The removal of phosphate
groups releases energy and is accomplished through the addition of water in
a hydrolysis reaction. The hydrolysis of one phosphate group produces
adenosine diphosphate (ADP); removal of the second phosphate yields
adenosine monophosphate (AMP). When a phosphate group is removed,
some energy, usable to accomplish work, as well as heat is released (35, 45,
171, 187). Typically, during normal cellular environmental conditions, the
terminal phosphate group is removed (hydrolyzed) enzymatically to drive
various endergonic reactions. Potentially, this hydrolytic process could
substantially diminish ATP concentrations resulting in limited muscular
activity. As sustained muscular contraction(s) requires a constant ATP
supply and the [ATP] in muscle is small, it is imperative that ATP is
constantly reconstituted. Depending on the intensity of muscular
contraction, energy (ATP) use can occur at a variety of rates dependent;
therefore, replenishment of ATP must be available at a rate which matches
the rate at which ATP is being used if the intensity of the muscular
contraction is to be maintained. The ability to match ATP requirements with
supply is accomplished through bioenergy systems that have different rates
and capacities of ATP production.
Figure 2.2 Structures of adenosine triphosphate (ATP), adenosine
diphosphate (ADP), and adenosine monophosphate
(AMP).
The Bioenergetic Systems
The rate of ATP use during different activities spans from very low (resting
levels) to very high during maximum efforts. To replenish energy at
different rates there are three basic energy systems that can be used.
Although these energy systems operate simultaneously to replenish ATP,
they have different maximum rates and capacities of ATP production.
Energy is ultimately derived from food; however, only carbohydrates can
produce energy without the direct use of oxygen. Therefore, during high-
intensity exercise in which energy demand depends upon anaerobic
mechanisms, the importance of carbohydrate metabolism should not be
underestimated. It should be noted that while these systems are
simultaneously and continually active, the degree to which any one of these
systems is used depends primarily on the intensity of physical activity and
secondarily on the duration (77). The three bioenergetics systems are:

1. Phosphagen system (ATP-PCr system and the myokinase reaction).

2. Glycolytic system (anaerobic/fast and aerobic/slow).
3. Oxidative (aerobic) system.

The Phosphagen System

The phosphagen system attains increased activation at the initiation of all
exercise regardless of intensity but is primarily engaged in providing energy
for short-term high-intensity activities such as weight-training exercise and
sprinting. (14, 35, 50). The phosphagen system involves ATP and creatine
phosphate (PCr), and three enzymes: myosin ATPase, creatine kinase (CK)
and myokinase. Energy is supplied for muscle contraction by the hydrolysis
of ATP, catalyzed by myosin ATPase, producing ADP and inorganic
phosphate (Pi). During high-intensity work, CK catalyzes the reaction in
which PCr donates its phosphate group to ADP, re-forming ATP and
producing creatine (Cr). These reactions provide energy rapidly and at a
high rate:
Myosin ATPase
ATP ————————> ADP + Pi + energy + heat
CK
ADP + PCr ———> ATP + Cr

The phosphagens, ATP, and PCr, are stored within muscle in very small
amounts and concentrations. In humans, approximately 5–6 mmol of ATP
and 16–18 mmol of PCr are stored per kilogram of wet muscle (45, 129,
171). The total amount of ATP in a human adult is approximately 0.10 mol
L–1. Approximately 100 to 150 mol L–1 of ATP are required daily
independent of exercise. Therefore, ATP molecules recycle approximately
1000 to 1500 times a day. The relatively small intramuscular stores of
phosphagen limit exercise duration during high-intensity exercise, and this
system cannot meet the energy requirements for long-duration continuous
events (49). While phosphagens alone cannot support exercise for long
periods (≈ 8–12 s), ATP can be delivered to the working muscle quite
rapidly and is well suited for high-intensity exercise requiring rapid energy
supply. Although type II muscle fibers can use phosphagens at a higher rate,
they typically contain higher concentrations of phosphagens than type I
fibers (83, 148).
While its importance is often overlooked, the myokinase (or adenylate
kinase) catalyzed reaction is associated with the phosphagen system and is
important in high-intensity work (35, 171):
myokinase
2 ADP ————> ATP + AMP

The activation of myokinase is stimulated by an increase in the ADP:ATP

ratio because of the rapid use of ATP during high-intensity exercise. This
reaction is important not only because of its rapid ATP production but also
because AMP is a potent stimulant of phosphofructokinase (PFK), the rate-
limiting enzyme for glycolysis (35, 171). Thus, within a few seconds, the
production of AMP and an increase in the ADP:ATP ratio begin to
stimulate glycolysis, enhancing the energy supply to the working muscle.
Phosphagens along with the myokinase reaction are especially important in
high-intensity exercise such as jumping, strength training, or sprinting (29,
197, 280).
Crucial to performance, particularly high-intensity work, is the
regulation of ATP concentrations in the muscle. Maintenance of ATP
depends upon negative feedback. The activity of the enzyme CK is the
primary regulator of the breakdown of PCr. An increase in the cellular ADP
and an increase in the ADP:ATP ratio stimulates CK activity, while
increases in ATP or a decrease in the ADP:ATP ratio inhibit its activity
(171, 229). Initiation of exercise increases the ADP:ATP ratio as a result of
ATP hydrolysis. The change in ADP stimulates CK to catalyze ATP
formation from the breakdown of PCr. If exercise is continued at high
intensities, then CK activity remains elevated. When exercise is terminated
or the intensity decreases to values low enough that glycolysis or the
aerobic system can match energy consumption rates, then the cellular ATP
will begin to increase. As a result, the increasing ATP and the decreasing
ADP:ATP ratio will reduce the activity of CK, allowing the concentrations
of PCr to increase. Recovery of PCr is primarily dependent on aerobic
metabolism.

The Glycolytic System

The process by which glucose can be catabolized to produce energy is
termed glycolysis. Two sources of glucose are available: blood glucose and
glucose derived from the breakdown of stored glycogen. The glycolytic
process is catalyzed by a series of nine cytoplasmic enzymes (Figure 2.3).
As a result of exercise intensity, glycolysis can proceed at either a faster
(anaerobic) or a slower (aerobic) rate. In the past, the terms anaerobic and
aerobic glycolysis have been used based on the final fate of pyruvate, either
being converted to lactate (anaerobic) or decarboxylated and entering the
Krebs cycle. However, the terms fast and slow better describe these
processes because the glycolytic pathway itself does not depend directly on
oxygen and because energy production occurs at a more rapid rate during
fast compared to slow glycolysis (35).
Figure 2.3 (a) The glycolytic pathway (reaction numbers refer to
panel (b)). (b) Glycolytic enzymes.
MG = muscle glycogen; G-1-P = glucose-1-phosphate; BG = blood glucose; G-6-P = glucose-6-
phosphate; F-6-P = fructose-6-phosphate; F-1,6-DIP = fructose-1,6-diphosphate (glucose splits);
G-3-P = glyceraldehyde-3-phosphate (2); 1,3-DPG = 1,3-diphosphoglycerate; 3-PG = 3-
phosphoglycerate; 2-PG = 2-phosphoglycerate; PEP = phosphoenolpyruvate.

Fast Glycolysis
When the intensity of exercise is such that the aerobic mitochondrial
enzymes become saturated with hydrogen ions, fast or anaerobic glycolysis
can continue the production of ATP at a faster rate. Thus, fast glycolysis is
particularly important for moderately high- to high-intensity exercise (35,
229). As a result of fast glycolysis, a relatively rapid production of ATP
occurs as a result lactate production that is a consequence of the rapid
donation of hydrogen ions to pyruvate from NADH+. In contrast, during
slow glycolysis, pyruvate is transported into the mitochondria,
decarboxylated to acetyl, and used in the Krebs cycle. Although muscle
glycogen is the preferred source for glucose, the fast glycolytic process can
use either blood glucose or muscle glycogen (35).
Lactic acid is the final product of fast glycolysis. Lactic acid is often
associated with fatigue, the production of NADH + H+ increased [H+] and
decreased pH. Intracellular muscle pH may fall below 6.5 as a result of
high-intensity exercise and the rise in [H+] can decrease the rate of
glycolysis and glycogenolysis through enzymatic inhibition (35, 42, 224).
Increased [H+] increases muscle fatigue by directly inhibiting muscle
contraction, possibly by displacing Ca++ at the troponin-tropomyosin
complex or interfering with cross-bridge formation (84, 89, 94, 119, 276).
The increase in [H+] stimulates pain receptors which can also be associated
with the expression of fatigue (224, 276).
However, exactly how and the degree to which lactic acid and muscle
pH alterations affect exercise fatigue is not clear. In fact, some evidence
indicates that increased [H+] may offset fatigue to a point, perhaps by
stimulating PFK or by off-setting the force inhibiting effects of K+ efflux
(72, 218). Some evidence indicates that [H+] and other metabolites such as
K+ and phosphate ions must reach a threshold value before there is muscle
contraction interference (27, 227). Indeed, alterations in these other ions
(e.g., Ca++, K+, PO3+++) may be more important contributors to muscle
fatigue than [H+] (15, 17, 210, 296). Investigations using isolated muscle
indicate that an increase [H+] has little negative effect or may even improve
muscle performance during high-intensity exercise (46). However, induced
acidosis can exacerbate fatigue during whole-body dynamic exercise and
alkalosis can improve exercise performance in events lasting 1–10 minutes
(46, 189). The differences in results from isolated muscle fibers versus
whole-body exercise may be a function of the drop in pH that accompanies
very intense exercise causing a reduced CNS drive to muscle (46).
It appears that lactic acid may play a role in muscle and whole-body
fatigue as a result of several possible mechanisms (278) and is likely the
primary means of acidification during intense exercise. Thus, it is
imperative to ameliorate lactic acid production or at least the potential
negative effects produced by its production. One mechanism is to convert
lactic acid to lactate.
Importantly, lactate, the salt of lactic acid, can act as an energy substrate
and is an important gluconeogenic precursor during long-term exercise and
recovery, and has not been directly associated with fatigue manifestations
(33, 182, 198, 224). Buffering systems in the muscle and blood can rapidly
convert lactic acid into lactate (33, 35). These buffering systems are
basically involved in acid-base regulation; there are three primary buffering
systems:

PRIMARILY MUSCLE

The protein buffer system (cellular) accounts for about three-quarters of all
chemical buffering in the body fluids:

The buffering ability of proteins is due to certain side groups of their

amino acid residues.
Some proteins contain carboxyl (–COOH) side groups that release H+
when pH begins to rise.
 Other proteins amino (–NH2) side groups that bind H+ when pH falls
too low.

The phosphate buffer system is a solution of the cations HPO4– and

H2PO4–:

It works like the bicarbonate system, with the reaction shifting to the
right to liberate H+ or to the left to bind H+.

H2PO4– ↔ HPO4– + H+

The optimal pH for this system is 6.8, so that it has a stronger

buffering effect than an equal amount of bicarbonate buffer.
Phosphates are much less concentrated in the extracellular fluid (ECF)
than bicarbonate; as a result, they are less important in ECF buffering.
Phosphate buffers are more important in the kidneys (renal tubules)
and the intracellular fluid (ICF), where they have a relatively high
concentration and the pH is lower.

PRIMARILY BLOOD

The bicarbonate buffer system is a solution of carbonic acid and

bicarbonate ions in the blood and is the primary buffering system.

Carbonic acid (H2CO3) forms by the hydration of carbon dioxide and

then dissociates into bicarbonate (HCO3–) and H+.

CO2 + H2O ↔ H2CO3 ↔ HCO3– + H+

In mammals, the bicarbonate system is found primarily within red

blood cells and works quite well in maintaining pH because the lungs
and kidneys constantly remove CO2, preventing equilibrium from
being reached.
If environmental alterations occur increasing pH, the kidneys can
excrete HCO3–.
 Physiologically acids or bases can be neutralized by a chemical buffer
system that depends on the concentration of the buffers and the pH of their
environment. Each buffer system has an optimum pH at which it functions
best.

Lactate Accumulation
Lactate accumulation in the blood is a function of production, clearance,
and exercise intensity. Blood lactate concentration post-exercise is a
function of the degree of disturbance of resting homeostasis resulting from
exercise. Lactate removal from the blood is associated with a return toward
resting homeostasis and reflects recoverability. Typically, post-exercise
lactate concentrations return to baseline within an hour; some evidence
indicates that light aerobic exercise (<70% VO2max) may facilitate removal
(100, 195).
Because of the high energy demands of type II muscle fibers, it is not
surprising that these fibers contain higher concentrations and activities of
glycogenolytic and glycolytic enzymes, as well as enzymes of the
phosphagen system (18, 39, 74, 213). Different isozyme patterns are found
in type II fibers (fast-twitch) compared to type I (slow-twitch). For
example, LDHM (muscle type) is found in higher concentrations in type II
fibers, whereas LDHH (heart type) is found in higher concentrations in the
heart muscle and slow-twitch fibers (5, 18, 39, 74, 182, 303). Based on
these differences, type II fibers have a greater rate and capacity for lactic
acid production compared to type I fibers. For example, Meyer and Terjung
(196) found the maximum rate of lactic acid production to be about twice as
great in type II (0.5 mmol g–1 of wet muscle) compared to type I (0.25
mmol g–1). Differences in enzyme activity and other differences (e.g.,
capillarization, sarcolemma lactate/H+ cotransport mechanism, etc.) also
allow type I fibers and heart muscle to take up lactate and convert it to
pyruvate, which can then be oxidized in the Krebs cycle (33, 224, 245).
The production of lactic acid can accelerate for several reasons apart
from insufficient oxygen. For example, during aerobic exercise, if the
intensity is suddenly increased, as often occurs in long-distance races, then
glycolysis will be accelerated because the aerobic system can be
momentarily unable to keep up with the sarcoplasmic production of
NADH+. As a result, during the initiation of exercise and during periods of
increasing intensity, some lactic acid may be produced until the aerobic
system “gears up” and accommodates the increased NADH+ production.
Furthermore, a finding of a constant blood lactate concentration does not
necessarily mean that no lactic acid is being produced; it may mean that a
dynamic equilibrium has been established and production and removal are
equal (33, 35). Blood lactate accumulation can be influenced by several
factors. Basically, this means that production has to increase faster than
clearance or clearance is reduced or both. For example, glycogenolysis
acceleration can result from increased catecholamine concentrations and
increases in type II muscle fibers recruitment (35, 224). These factors tend
to increase with increasing intensity of exercise with clearance being
reduced above approximately 65% of VO2max (117, 118).
The state of training also effects blood lactate accumulation (74, 100). At
absolute submaximal power outputs, aerobically trained subjects can
maintain lower blood lactate concentrations compared to untrained subjects
(133, 163, 224). This reason(s) for lower lactates includes enhanced
mitochondrial activity (97, 98), increased muscle capillary density (254),
lower catecholamine concentrations, and a shift in isozyme patterns, for
example, LDHM to LDHH as a result of aerobic training (74, 253). Weight-
trained athletes have also been shown to produce lower lactate
concentrations at submaximal power outputs during weight training
exercises compared to untrained subjects (221, 222, 265) – an observation
consistent with post-training lactate responses in anaerobically trained men
(240) and after short-term anaerobic interval training (233). Mechanisms
underlying anaerobic training (including weight training) producing lower
lactate concentrations at submaximal exercise intensities are unclear but
may in part relate to changes in the lactate threshold (180).
As a result of maximum effort exercise (with enough volume),
anaerobically trained athletes typically accumulate higher [lactate] than
untrained or aerobically trained athletes (139, 208, 265). As a result of
anaerobic training, the ability to accumulate high concentrations of lactate
at maximum exercise intensities could be related to training-induced
increases in anaerobic enzyme activities, alterations in isozyme patterns,
and increased lactic acid-buffering capabilities, allowing more work to be
accomplished or attainment of a higher maximum exercise intensity (22,
208, 265). Very intense exercise of sufficient duration can elicit blood
lactate concentrations of over 20 mmol L–1 (118, 139). The highest blood
lactate concentrations are typically observed as a result of repeated high-
intensity exercises with short rest periods (118, 158).
Lactate production is also affected by low glycogen concentrations (99).
Low-carbohydrate diets and/or previous exercise can decrease glycogen
stores, resulting in lower blood lactate concentrations during exercise (6).
Increased training strain leading to an overtrained state may also produce
low exercise lactate concentrations as a result of chronic glycogen depletion
(261).

POST-EXERCISE LACTIC ACID AND LACTATE CLEARANCE AND REMOVAL

Continuous short-term high-intensity exercises of less than 8 min produce

relatively high blood lactate concentrations that are similar to each other
(99). Multiple bouts of high-intensity intermittent exercise typically
produce the highest blood lactates (118). There is a lag-time of
approximately 5–7 min post-exercise until peak blood lactates occur (99).
However, peak blood lactate concentrations during intermittent high-
intensity exercise can occur before the last bout, and peak muscle lactate
concentrations can occur within 2 min of the initiation of intense exercise
(119, 140, 149, 238, 239). It is the muscle lactic acid concentrations that
appear to be the limiting factor during exercise and not the blood lactate
concentration. The post-exercise lag time in peak blood lactate
concentration results from a cellular transport mechanism for lactate (146),
the monocarboxylate transporters. Although diffusion contributes to lactate
initial removal (and uptake), movement into and out of the cell is facilitated
by monocarboxylate transport proteins (MCT) (25). The MCTs are a family
of proton-linked plasma membrane transporters that can transport
molecules having one carboxylate group (monocarboxylates), such as
lactate and pyruvate, across the cell membrane (107). MCTs are expressed
in cells of nearly every type of tissue (216). In muscle, MCT1 is responsible
for enhanced uptake, while MCT4 is responsible for facilitated removal of
cellular lactate against a concentration gradient. Although various types of
training can increase MCTs, it is believed that endurance training primarily
enhances the expression of MCT1 and that anaerobic training, including
strength training, enhances the expression of MCT4 (25, 279) and these
alterations may be fiber-type specific (279).
While blood lactate has not been directly associated with fatigue (16),
very high concentrations of lactate have been associated with reduced
muscle force production (126), and its clearance/removal, to an extent,
reflects recovery capability (224). Lactate clearance post-exercise can be
represented as a first-order exponential function operating independently of
the initial concentration (90, 92). Post-exercise blood lactate concentrations
typically return to baseline within an hour (99, 142, 307). Clearance rate
can be affected by the type of recovery (active versus passive) and the
trained state; training appears to accelerate lactate removal. Active post-
exercise recovery schemes enhance lactate recovery. Relative aerobic
exercise intensities of 50% to 70% of VO2max appear to be optimal for
increasing lactate removal rate among endurance-trained subjects (92, 99,
124, 224). Importantly, evidence also indicates that both aerobically trained
(99, 224) and anaerobically trained athletes (188, 221, 222, 289) display
enhanced lactate recovery rates. Although faster lactate post-exercise
clearance is associated with recovery, this does not necessarily produce
enhanced performance for all types of subsequent exercise. For example,
enhanced lactate clearance resulting from active recovery had no effect on
isokinetic measures of maximum strength or fatigue profiles (28);
observations such as this agrees with the authors’ observations of sprint
cyclists, advanced and elite weightlifters and powerlifters compared to
aerobically trained athletes. These types of observations indicate that from a
metabolic standpoint, other factors such as increases in intracellular PO4+4,
Ca++, or K+ efflux may be more important associates of fatigue than lactate
(209, 296).

LACTATE THRESHOLD AND ONSET OF BLOOD LACTATE

Evidence (70, 153, 156) indicates that, as exercise intensity increases,

specific breakpoints in the blood lactate accumulation curve can occur
(Figure 2.4). The lactate threshold or LT occurs at an exercise intensity or
relative intensity at which blood lactate begins an abrupt increase above a
lower intensity exercise baseline near steady state (304). The LT is
associated with increasing reliance on anaerobic mechanisms as the
exercise intensity increases. In untrained subjects, typically the LT begins at
approximately 50% to 60% of VO2max; however, among well-trained
subjects and athletes, the LT increases to about 70% to 80% of VO2max
(48, 86). Some evidence has indicated that a second increase in the rate of
lactate accumulation occurs at higher relative intensities of exercise. This
second inflection point, termed the onset of blood lactate (OBLA),
generally occurs when the concentration of blood lactate is approximately 4
mM (123, 252, 274). It has been suggested that the breaks in the lactate
accumulation curve are somewhat similar to the points at which type II
MUs are recruited (size principle) as exercise intensity increases (85, 144).
Typically type II fibers are less aerobically efficient and are metabolically
suited for anaerobic metabolism and lactic acid production.
Evidence indicates that training at intensities at or above the LT, or some
combination of high-volume training (lower intensity at the maximal lactate
steady state plus intensities above the LT), likely have the greatest effect on
moving the LT to the right on the lactate accumulation curve (114, 294).
This shift in the LT occurs as the result of several mechanisms: (1) changes
in hormone release, particularly reduced catecholamine concentrations, (2)
reduction in the recruitment of type II fibers at a given relative intensity, (3)
MHC chain shifts with training, and (4) decreased production/increased
clearance capabilities (including isozyme alterations, increase
mitochondrial activity, and increased pillarization). Regardless of the
mechanism, the shift in LT allows training or competition to be perform at
 higher percentages of VO2max without as much lactate accumulation in the
blood (35, 70). From a practical standpoint, the LT often occurs at RPE
(Borg scale) values of approximately 11 to 13 for running (244).

Figure 2.4 Lactate threshold (LT) and onset of blood lactate (OBLA).

Importantly, while VO2max is a primary determinant of endurance

performance, particularly for events such as 1500 m, which are performed
at VO2max or above throughout, most of the event almost all well-trained
and elite athletes have high aerobic powers. Furthermore, endurance
performance can vary substantially among athletes even when VO2max
values are equal. Among well-trained individuals, endurance performance,
especially at high percentages of VO2max, may be more closely related to
lactate production and removal, glycogen utilization, and running economy
than to VO2max. High-volume weight training has been shown to increase
high-intensity work time without substantial alterations in VO2max (120,
121, 268) and can affect positive changes in intermittent high-intensity–
endurance activities such as football (soccer) (88). Additionally, Marcinik et
al. (180) provide evidence indicating that resistance training can
beneficially alter the LT and increase endurance on a cycle ergometer, a
finding suggesting that there can be a transfer of metabolic training effect
from one mode to another.
Stone et al. (268) suggested that some types of weight training,
particularly high-volume and high-volume resistance training with
relatively high repetitions preset, may in some manner modify the
underlying mechanisms leading to enhance endurance – particularly high-
intensity exercise endurance. More recently, many of these underlying
mechanisms have been shown to be altered in order to support increase
metabolism and provide greater endurance including alterations in
“aerobic” enzymes and mitochondria (105, 165, 194, 228). Both cross-
sectional (188, 265) and longitudinal training investigations (221, 222)
indicate that resistance training can reduce serum lactate at submaximal
loading and submaximal cycling intensities (137).

Slow (Aerobic) Glycolysis

Although blood glucose is preferentially used, slow glycolysis can use
either blood glucose or muscle glycogen as an energy source. Aerobic or
slow glycolysis is a result of mitochondria activity being sufficient to accept
the two NADH produced during glycolysis (Pasteur effect (161, 187)
(Figure 2.5). An additional six ATP can be created resulting from the
entrance of the two NADH into the electron transport system. During slow
(aerobic) glycolysis, pyruvate can enter the mitochondrial matrix via a
localized carrier mechanism in the outer and inner membranes (35, 51,
186). Two proteins are believed to be involved in pyruvate mitochondrial
transport, mitochondrial pyruvate carriers MPC1 and MPC2 form a hetero-
oligomeric complex in the inner mitochondrial membrane to facilitate
pyruvate transport (186). In this manner, pyruvate can lose a carboxyl group
(as CO2) and be made available for oxidation.
Glycolytic Energy Yield
Beginning with glucose, the glycolytic yield can be calculated using the
following equations.
Fast (anaerobic) glycolysis:

glucose + 2 Pi + 2 ADP ——> 2 lactate + 2 ATP + H2O

Slow (aerobic) glycolysis:

glucose + 2 Pi + 2 ADP + 2 NAD+ ——> 2 pyruvate + 2 ATP + 2

NADH + 2 H2O

Beginning with one molecule of glucose, the net production of glycolysis is

two molecules of ATP. However, starting with glycogen, which is broken
down into Glucose-6-phospohate (G-3-P) via the enzyme phosphorylase,
then three ATP are produced (Figure 2.3a). The additional ATP is produced
as a result of the phosphorylation step that uses an ATP (via hexokinase) is
bypassed and one ATP is spared. In comparing fast versus slow glycolysis
and the fate of the two sarcoplasmically produced NADH2, it can be argued
that the net ATP production for slow glycolysis can be as much as eight
ATP when the process starts with glucose. This occurs as a result of the
NADH2 entering the mitochondria and producing an additional 6 ATP
through oxidative phosphorylation. It should be noted that there can be
differences in ATP production between cardiac and skeletal muscle.
Evidence indicates that two different shuttle systems operate to transfer
electrons into the mitochondria, one in heart muscle (malate-aspartate) and
the other in skeletal muscle (glycerol-phosphate) (226). In the glycerol-
phosphate system, FAD picks up the NADH+ and carries it to the electron
transport system, thus reducing the number of ATP being produced. Some
evidence indicates that the glycerol-phosphate system predominates in type
II muscle fibers, while type I fibers can also use the malate-aspartate system
(128, 226).
Control of Glycolysis
Glycolysis can be stimulated by ammonia, Pi, ADP, and pH and is very
strongly stimulated by AMP and an increase in the AMP:ATP ratio, which
is associated with fall in energy charge (35, 237, 270). Glycolysis is
inhibited by markedly lowered pH, ATP, and a decreased AMP:ATP ratio,
PCr, citrate, and free fatty acids (FFA) (35, 116, 171, 237). Primary control
of glycolysis is a result of the glucose phosphorylation (G–6-P) by
hexokinase (35, 161, 171). The rate of glycogen breakdown catalyzed by
phosphorylase also must be considered (35, 223, 231) as this provides a
readily available supply of glucose. The primary rate-limiting step for
glycolysis is control by PFK:

F-6-P —— [PFK] ——> F-1-6DiP

Therefore, the relative activity of PFK is especially important for the

regulation of glycolytic rate. AMP and Ca++ are strong stimulators of PFK
and glycolysis (56, 65). Phosphagen system activation and AMP production
resulting from the myokinase reaction can strongly stimulate PFK,
glycolysis, and energy production during high-intensity exercise (35, 56,
277). However, AMP and other metabolites such as ADP do not completely
account for the acceleration of glycolysis during intense exercise;
considerable evidence indicates that muscle activation and Ca++ release are
potent glycolytic stimulators. Furthermore, ammonia (NH+++) produced
during high-intensity exercise, resulting from AMP deamination or amino
acid deamination, can also stimulate PFK (270). Some evidence indicates
that stimulation of PFK by ammonia may partially offset the exercise
intensity related fatigue effects of decreasing pH, as a result of an increase
in [H+], otherwise this increased proton content would inhibit several
glycolytic and glycogenolytic enzymes including PFK and phosphorylase.
However, both phosphorylase and PFK are almost completely inhibited at
pH values below 6.88–6.3 (118, 145).

The Oxidative (Aerobic) System

Proteins, fats, and carbohydrates can all be used as a substrate in the
oxidative (aerobic) system. At rest, about 70% of the ATP produced is
derived from fats and about 30% is derived from carbohydrates. Almost all
of the resting energy production occurs aerobically. The relative
contribution of energy substrate contributing to ATP production is altered
during exercise. During low-intensity exercise, such as walking, the
contribution of fats (and protein) typically increases with exercise duration.
However, as exercise intensity increases, relative substrate preference shifts
toward carbohydrates, as carbohydrates are a more fuel-efficient substrate
(35, 108, 229).
Protein oxidation: Proteins are constructed from nitrogen-containing
molecules, amino acids (AAs). Proteins are constructed from AAs and can
be broken down by several catabolic processes. It is important to realize
that skeletal muscle constitutes the primary reserve pool of AAs. Proteins
contain nitrogen, which cannot be used in energy production. The nitrogen
can be removed as a result of transamination and deamination reactions,
thus AAs can be converted to their carbon skeletons, which in turn can be
converted into glucose (via gluconeogenesis) or directly enter the Krebs
cycle (35, 171). Therefore, most AA carbon skeletons and AA residues are
converted to pyruvate or Krebs cycle intermediates (35, 129). Elimination
of the nitrogenous waste resulting from AA catabolism occurs primarily as
a result of urea formation and excretion, along with the release of small
amounts of ammonia (35, 196, 284, 299). The removal of most nitrogenous
waste products, particularly ammonia, is important because they can be
toxic and also likely act as fatigue products, particularly as it affects the
CNS (35, 284, 299, 306). During short-term exercise, very little protein is
used for energy. However, evidence indicates that during long-term exercise
(>90 min), and perhaps long-term repeated high-intensity exercise, if no
additional substrate such as carbohydrate is ingested, there can be a
substantial increased use of protein (gluconeogenesis); perhaps as much as
15% to 20% of the energy consumed may be derived from protein (103,
170, 305).
 Fat oxidation: The most common form of fat storage in mammals are
triglycerides. Triglycerides are primarily stored in fat cells (adipocytes)
with small storage amounts in muscle. Triglycerides are degraded by
hormone-sensitive lipase into energy substrates, three free fatty acid (FFA)
chains and glycerol. FFA and glycerol released from triglyceride catabolism
in adipocytes can be released into the circulation, taken up by muscle and
used for energy (116, 138, 167).
In adipocytes, there are two enzymes that are involved in degrading
triglycerides: hormone-sensitive lipase and adipose triglyceride lipase.
Adipose triglyceride lipase has a greater affinity for triglycerides compared
to hormone sensitive lipase, and acts as the primary enzyme for triglyceride
hydrolysis in adipocytes. Hormone sensitive lipase is found in small
concentrations in muscle and can provide an intramuscular source of FFA
and glycerol. In the sarcoplasm of muscle fibers, FFA are bound to CoA.
Using a carnitine carrier, the FFA -acyl CoA molecule enters the
mitochondria (35, 51, 129, 143). The triglyceride “backbone” glycerol can
be converted to glycerol 3 phosphate and enter glycolysis for energy
production.
Beta-oxidation is a process of extracting energy from FFA. Beta-
oxidation is primarily a function of the mitochondrial trifunctional protein.
The MTFP is an enzyme complex associated with the inner mitochondrial
membrane, although especially long-chain FA are oxidized in oxidative
organelles, the peroxisomes. The peroxisomes use a similar oxidative
enzyme group as found in the inner mitochondrial membrane. Free fatty
acids undergoing β-oxidation result in the accumulation of acetyl-CoA, and
H+. The acetyl-CoA can enter the Krebs cycle and the protons, which are
carried to the ETS by nicotinic adenine dinucleotide (NAD) and flavin
adenine dinucleotide (FAD), can enter the electron transport system (ETS)
(see Figure 2.5). Type I muscle fibers generally contain high concentrations
of oxidative enzymes compared to type II, thus the process of FFA
oxidation is quite important for these fibers (35, 79). Fat use during exercise
becomes increasingly important with duration (108).
 Carbohydrate oxidation: Oxidation of carbohydrate depends upon the
rate of glucose degradation of glucose during glycolysis. If the activity of
the mitochondria is high and the ETS is not saturated, pyruvate can lose a
CO2 (decarboxylation), form acetyl, which then combines with coenzyme A
(CoA) and enters the Krebs cycle (Figure 2.5a). Substantial H+ are
produced during glycolysis, and during other degradative processes such as
the oxidation of fats. As a result, considerable amounts of NADH2 are
created by combining with the H+. NADH2 can enter the mitochondria via
specific shuttle systems and used to produce ATP (35, 51, 155). NADH2 is
processed through the ETS and is used for ADP rephosphorylation
(oxidative phosphorylation) (Figure 2.5b). Theoretically, complete
oxidation of glucose yields 38 ATP. This value (38 ATP) is an
approximation as one of the shuttle systems necessary to move NADH+
across the mitochondrial membrane and other factors require energy. It is
also an approximation because the reactions themselves do not always
proceed with the same efficiency depending on cellular metabolic
conditions such as changes in pH (171, 207) (see Chapter 4).
Figure 2.5 (a) The Krebs cycle and hydrogen ion/electron transport
system. (b) The electron transport system.
(a) FAD = flavin adenine dinucleotide; NAD = nicotinic adenine dinucleotide; GTP = guanine
triphosphate; GDP = guanosine diphosphate. (b) Pi = inorganic phosphate; CoQ = coenzyme Q;
CYT = cytochrome.

ATP Production of the Oxidative Systems

Beginning with glucose and under aerobic conditions, two cytoplasmic ATP
are produced (three ATP when starting with glycogen) for each glucose
molecule. Additionally, the two cytoplasmic NADH+ from glycolysis can
be shuttled into the mitochondria. Hydrogen ions, and therefore electrons,
are introduced to the ETS by NADH2 and FADH2. Starting with NADH2
the oxidative phosphorylation potential (P:0) is three ATP and two ATP for
FADH2 (171, 187). Slow glycolysis and subsequent oxidation through the
oxidative system can produce as many as 38 ATP, depending on the cellular
environment. The complete theoretical oxidation of glucose and the
associated energy conversions are shown in Table 2.1.

Table 2.1 Theoretical complete degradation of glucose

Reaction Coenzyme ATP yield Location
GLU → PYR – 2 Cytoplasm
GLU → PYR 2 NAD+ 6 Mitochondria
PYR → A-CoA 2 NAD+ 6 Mitochondria
ISOCIT → α-KGLUT 2 NAD+ 6 Mitochondria
α-KGLUT → SUC-CoA 2 NAD+ 6 Mitochondria
SUC-CoA → SUC† 2 GTP 2 Mitochondria
SUC → FUM 2 FAD 4 Mitochondria
MAL → OXAL 2 NAD+ 6 Mitochondria
Net ATP – 38* or 39** –
† Substrate level transformation.
* Yield starting with glucose.
** Yield starting with glycogen.

Control of the Oxidative System

Regulation of the Krebs cycle is partially controlled by the need for energy
(ATP) and therefore by reactions producing NADH2+ or FADH2+ and the
ratio of oxidized to reduced coenzymes (O:Rc). The O:Rc is controlled by
ADP and Pi availability for oxidative phosphorylation in the ETS. The rate
at which the Krebs cycle proceeds becomes limited if the coenzymes FAD+
and NAD+ are not available to accept electrons (along with H+ in biological
systems). Additionally, accumulation of guanine triphosphate (GTP) can
result in an increase in succinyl-CoA which inhibits the initial Krebs cycle
reaction: oxaloacetate + acetyl-CoA → citrate + CoA. Isocitrate → α-
ketoglutarate is the rate-limiting step for the Krebs cycle, which is catalyzed
by isocitrate dehydrogenase. Isocitrate dehydrogenase is generally inhibited
by ATP and strongly allosterically stimulated by the accumulation of ADP.
Secondarily, the Krebs cycle is controlled by α-ketoglutarate dehydrogenase
which catalyzes the conversion of α-ketoglutarate to succinyl-CoA and
produces NADH, thus, providing electrons for the ETS. α-ketoglutarate
dehydrogenase is inhibited by increased concentrations of succinyl-CoA
and NADH, which are produced by the reaction that it catalyzes. α-
ketoglutarate dehydrogenase and the Krebs cycle rate are inhibited by a
high energy charge (high concentration of ATP). General control of the ETS
is relatively simple: stimulated by ADP and inhibited by ATP (35, 171,
283).

Hormonal Regulation of Energy Metabolism

Hormonal actions play a substantial role in the mobilization and release of
substrates required for the energy systems. Detailed characteristics of the
actions hormones exert on physiological and metabolic functions related to
aerobic or anaerobic exercise are covered in Chapter 3.
Substrate mobilization initiation and sustainability for use in energy
production is a function of several hormones such as glucagon, growth
hormone, and epinephrine. For example, epinephrine receptors on muscle
cell membranes initiate a series of intracellular signals known as a cascade
effect. Figure 2.6 illustrates this effect (4, 35, 171). These intracellular
signals are responsible for the release of glucose by the liver, the
intramuscular breakdown of triglycerides and glycogen, the mobilization
and release of FFA by fat cells for use in energy production.
Figure 2.6 The energy substrate mobilizing cascade effect. A
hormone such as epinephrine attaches to a protein receptor
(R) in the plasmalemma. The hormone–receptor
interaction changes the conformation of a regulatory
protein (G), which in turn activates an enzyme (such as
adenyl cyclase), usually by phosphorylation, or a calcium
channel. The activated enzyme then initiates a cascade of
intracellular events. This example illustrates a second
messenger system, the hormone (epinephrine) is the first
messenger, cyclic adenosine monophosphate (cAMP),
which affects alterations in energy substrate mobilization
is the second messenger.
Fuel Efficiency
It is commonly believed that anaerobic mechanisms supply energy in an
inefficient manner; however, this is not always the case. Glycolytic and
oxidative system efficiency can be considered in different ways. One very
simple method of estimating energy production efficiency is to consider
calories extracted relative to calories stored in a molecule, as in the
following example (35, 171).
Calories contained per mole (Avogadro’s number of molecules) with
complete combustion:

ATP = 7.3 kcal mol–1; glucose = 686 kcal mol–1; palmitate = 2340
kcal mol–1

Physiological caloric yield:

1. Fast glycolysis = 2 ATP (14.6 kcal)

2. Slow glycolysis = 38 ATP (277 kcal)
3. Oxidation of palmitate = 129 ATP (941 kcal)

Using this information, we can calculate a ratio of calories extracted to

calories stored as follows:

Physiological energy yield/total energy available × 100 = % released

1. Fast glycolysis = 14.6/686 = 2%

2. Oxidation of carbohydrates = 277 /686 = 40%
3. Oxidation of palmitate = 941/2340= 40%1

Using this method, anaerobic metabolism is apparently quite inefficient

compared to aerobic metabolism and FFA metabolism is equal to or greater
than carbohydrate. However, the total rate of ATP production or free energy
production in biological systems is not considered using this method.
However, we should consider what actually occurs in biological systems.
Free energy refers to energy free to perform work (35, 171). In biological
systems, the energy change (∆ H) during fast glycolysis from starting with
glucose and ending with lactate is approximately –47 kcal mol–1. The
potential energy available (∆ G) for ATP is approximately –7.3 kcal mol–1.
A negative sign indicates that the energy given up during exergonic
reactions is available to perform work. However, note that in living
systems, the ∆ H for physiological release of ATP is approximately –11 kcal
mol–1. Thus, more accurate methods of calculating efficiency for fast
glycolysis and the total oxidation of glucose would be as follows:

1. Fast glycolysis: efficiency = 2 (–11)/47 = 47%

2. Oxidation of glucose: efficiency = 38 (–11)/686 = 61%

Using this reasoning, fast glycolysis is only somewhat less efficient than the
oxidative system.
Another method of assessing energy production efficiency is an
examination of the relation of lactate accumulation to constant decreases in
VO2 during increasing work rates. Using this relationship, evidence
indicates that ATP synthesized by anaerobic pathways is not much less
efficient than aerobically synthesized ATP (96); this agrees with ∆ H
changes in biological systems. However, when work produced was
compared with the amount of energy expended, anaerobic efficiency (high-
intensity exercise) was less than aerobic efficiency (steady-state light work)
(35, 96). This result may have been obtained because metabolism is not
directly related to an increase in external work, or because high-intensity
exercise does result in decreasing muscle work efficiency or both (96). It
should be noted, however, that the actual energy expenditure during
anaerobic work is difficult to ascertain and has often been underestimated;
thus, the efficiency of anaerobic work may be higher than has been believed
(248). Regardless of the mechanisms, exercise becomes less efficient as
maximum intensity is approached. Several variables can affect alterations in
energy production efficiency including changes in the cellular environment.
For example, decreased pH and increased [H+], and alterations in inter-
intracellular K+, PO3+4, and Ca++ can interfere with excitation–contraction
coupling and enzyme activity, all of which can change system efficiency.
Although type II muscle fibers reach their greatest efficiency at higher
velocities and power outputs, type I motor units (MUs) appear to be more
fuel-efficient because of tighter coupling in the ETS (112, 248).
Respiratory Exchange Ratio
The respiratory quotient (RQ) is the ratio between CO2 produced and the O2
used during the oxidation of energy substrates (i.e., protein, carbohydrate
and fat) and is another important consideration in determining bioenergetic
efficiency. Respiratory quotient and kilocalories per mole of a substrate can
be accurately measured using a bomb calorimeter in which a substance is
completely oxidized by combustion (154). It should be noted that bomb
calorimetry is not feasible when examining what energy substrates are
being used during exercise. However, the use of respiratory gases may be
used to create a respiratory exchange ratio (RER). The RER can be
calculated through the measurement of expired CO2 and oxygen uptake (35,
229). The term RQ is not completely accurate for this measurement, so the
term RER is used. This is because a small amount of additional energy can
be expended in the digestion of protein that is not accounted for completely
by the RQ value, and additionally, because of the effect of hyper- or
hypoventilation and buffering systems, which can cause a disproportionate
change in gaseous exchange, particularly for CO2. Buffering systems can be
overwhelmed as a result of high-intensity exercise in which excess CO2 can
be exhaled through the lungs. This can result in an inflated exchange ratio
(above 1.0) that is not completely indicative of the oxidation of food.
Therefore, the RQ is actually a better measure of cellular respiration,
whereas the RER is a measure of exchange at the lungs and can be used as a
criterion for making near or maximum aerobic efforts. By using both
calorimetry and the RER, caloric equivalents have been established (Table
2.2 and 2.3).

Table 2.2 Caloric equivalents

Protein Carbohydrates Fats
Calorimetry 4.1 5.6 9.3

RER = respiratory exchange ratio.

 Protein Carbohydrates Fats
Physiological RER Kcal L O2–1
Protein 0.8 4.5
Carbohydrate 1.0 5.0
Fat 0.7 4.7
RER = respiratory exchange ratio.

Table 2.3 Caloric equivalents from the respiratory exchange ratio (RER) and percentage kcal use
from carbohydrates and fats during rest and exercise
RER Kcal L O2–1 Carbohydrates (%) Fats (%)
0.71 4.69 <1 > 99
0.75 4.74 15.6 84.4
0.80 4.80 33.4 66.6
0.85 4.86 50.7 49.3
0.90 4.92 67.5 32.5
0.95 4.99 84.0 16.0
1.00 5.05 > 99 <1
Sources: Modified from Cumminns et al. (66) and Kenny et al. (152).

This method (Table 2.3) assumes that protein is not a major energy
source – however, this assumption may not be correct in the case of
continuous long-term exercise or long-term repeated bouts of exercise (35)
(see also Chapter 4).
Considering RER values, carbohydrates are the most efficient fuel,
producing about 6% more energy per liter of O2 used compared to fats and
about 10% more compared to proteins. Considering this information it
becomes clear that carbohydrates would be the preferred fuel (35). Thus,
carbohydrate has two major advantages over fat, as an energy substrate and
metabolic fuel; carbohydrates can produce ATP in the relative absence of
oxygen, and greater amounts of ATP are produced per unit of O2 used when
glucose is oxidized, compared with when fat is oxidized. Therefore, as a
result of increasing exercise intensity, there is an increase in the use of fast
glycolysis. During exercise, the RER value can be used to qualitatively
determine the primary energy source (food) being used for energy and for
an estimation of the relative intensity of exercise. During light exercise,
such as walking or a slow jog, the RER value can decrease, but will rapidly
rise as the intensity increases (Figure 2.7). The shift from resting values
toward a relatively low RER during low-intensity exercise indicates a
greater reliance on fats (and perhaps proteins during exercise lasting longer
than about 90 min). Total fat oxidation reaches its peak at exercise
intensities of approximately 65% of VO2max supplying about 50% of the
total energy requirements; the remainder is supplied primarily by
carbohydrates (236). The enhanced use of fats during long-term low-
intensity exercise is due to three factors: (1) the mobilization of FFA caused
by release of specific hormones, especially growth hormone (35, 229, 275),
(2) a short-term acceleration of the ETS compared to glycolysis during
which the capacity for oxidation exceeds the supply of pyruvate, and 3)
FFA mobilization and subsequent use for energy inhibits PFK, the rate-
limiting enzyme for glycolysis.
The need for rapid energy supply rises and ADP concentrations increase
with an increase in exercise intensity. As exercise intensity increases, so do
ADP concentrations; processes that rephosphorylate ADP at the greatest
rate with the least O2 use will be favored (14, 35). Evidence indicates that
increasing blood lactate concentrations as a result of intense exercise may
inhibit FFA mobilization (101, 134, 143, 235, 285), furthering decreasing
oxidative processes. However, these studies do not take into account the
complete physiological environment created by exercising muscle.
Evidence also suggests that increasing lactate concentrations in exercising
humans does not completely inhibit FFA mobilization or totally block their
use as an energy substrate (188, 263). The reduced FFA mobilization is also
associated with hormonal influences (188, 263). Interestingly, FFA
mobilization and oxidation appears to be elevated post-exercise, particularly
high-intensity exercise including strength training (188, 263).
Although a value of 1.0 is the maximum obtainable value in non-
biological bomb calorimetry reactions, the RER can exceed this value
during near-maximum and maximum efforts. The RER exceeding 1.0
occurs because of the rapid proton production during fast glycolysis which
 increases blood and tissue [H+], lowering pH. This occurrence overcomes
the blood buffering systems (35). For example:

Buffering reaction: CO2 + H2O ↔ H2CO–3 ↔ H+

↑Increasing exercise intensity = H+ (causes reaction shift to the left)

Figure 2.7 Respiratory exchange ratio (RER) values for trained and
untrained subjects at rest and during increasing exercise
intensity.

The increased blood [H+] pushes this reaction to the left, causing
additional CO2 to be released; the excess CO2 is removed through the lungs
during exhalation. The excess CO2 raises the RER values above 1.0 (35).
The importance of RER values above 1.0 (as high as 1.45) is in estimations
of heavy and maximal efforts (35, 230).
Subjects and athletes that are aerobically trained typically display lower
RER values during exercise than untrained subjects, except at maximum or
near-maximum efforts. Lower submaximal RER values transpire as a result
of aerobic training, partially as a result of metabolic adaptations that allow
trained people to use FFA more efficiently. These adaptions can include
alterations of oxidative enzymes creating a predominance of specific
isozymes (35, 303). For example, LDHH (catalyzes lactate to pyruvate)
concentration can be enhanced in aerobically trained subjects and LDHm in
anaerobically trained. The importance of increased FFA use in trained
people is that it can spare glycogen, a mechanism that could enhance long-
term endurance activities. Of special note, a reduction in glycogen use can
be especially important for the central nervous system, which relies
primarily on carbohydrates for energy (35).
Lower RER are commonly observed post anaerobic exercise. After a
training session, lower recovery RERs have been noted among weight
trainers (192), and weightlifters (188). This effect can persist for several
hours after a weight training session. Mobilization and oxidation of FFA for
recovery energy post-exercise are probably associated with hormonal
effects and exercise-induced glycogen depletion. This observation indicates
that fats are being used during recovery processes resulting from anaerobic
exercise and may have implications for body composition alterations.
Energy Production Power (Rate) and Capacity
How energy systems are used in a practical setting is quite important for
sport scientists, coaches, and athletes. Bioenergetic systems supply energy
at different rates for various intensities and durations of exercise (Table
2.4). Conley et al. (57) using cycle ergometry, and Harman (personal
communication) using a treadmill, have shown that power (intensity) at
VO2max is approximately 25% to 35% of peak power capabilities.
Therefore, aerobic exercise even at 100% of VO2max should not be
classified as high-intensity exercise. It should be noted that a maximum-
intensity of exercise requires a maximum rate of energy production in order
to reach and sustain the intensity. High-intensity exercise can be supported
by fast (anaerobic) glycolysis; however, long-term aerobic exercise must be
supported by the oxidative system because of its high capacity for ATP
production. Because of the time required to fully activate other energy
systems, the ATP-PCr system is also used to a small extent at the initiation
of most exercises (35).
It should be clear that the prominent bioenergy system used during
exercise is primarily a function of exercise intensity. Thus, typical sprints or
weight training will be supported primarily by anaerobic mechanisms,
while typical endurance training is supported largely by oxidative systems.
Depending upon the intensity and duration of the exercise, the primary
energy system(s) will shift. However, it is important to realize that in no
case does any exercise or even the resting condition rely completely on one
system. During physical activity, anaerobic and aerobic systems continually
contribute to energy needs to a greater or lesser extent, primarily depending
on intensity and secondarily on duration (35, 65). These observations are
the primary basis for interval training (see “The Metabolic Cost of
Exercise” section below).

Table 2.4 Energy sources: Rates and capacities of anaerobic (in italics) and aerobic energy systems
Fuel source Approximate time at peak Maximum rate of ATP Total P–
rate (event duration) production (mmol min–1) available
(mmols)
Muscle ATP <6s 200+ 223
Creatine phosphate 6–30 s* 73.3 446
Conversion of muscle 30 s to 2 min 39.1 6700
glycogen into lactate
Conversion of muscle 2–3 min 16.7 84,000
glycogen into CO2
Conversion of liver 2–3 min** 6.2 19,000
glycogen into CO2
Conversion of adipose- > 3 min 6.7 4,000,000
tissue fatty acids into
CO2
ATP = adenosine triphosphate.
P- = inorganic phosphate.
* Includes some fast glycolysis.
** Augments slow glycolysis.
Sources: Based on Hultman et al. (130) and Hultman and Sjoholm (131).

Time is also an important factor when considering the use of

bioenergetic systems. Athletic movements range from a vertical jump or
shot put (1–2 s) to marathons (more than 2 h). While a sustained maximum
effort is possible for very short periods (<10 s), longer events require
pacing, resulting in a relative “best-effort” performance. The approximate
relationships between exercise time, relative intensity, and bioenergy
systems are illustrated in Table 2.4 (35, 80, 116, 130, 131, 232, 276, 280).
Substrate Depletion and Repletion: Recovery
As a result of exercise of varying intensities and durations, energy
substrates can be selectively depleted. Typically, exercise-induced fatigue is
at least partially due to substrate depletion, particularly in terms of
phosphagens and glycogen (99, 116, 131, 140, 166). Depletion of substrates
such as AAs and FAs typically do not occur to the extent that performance
is limited. Because of this observation, the depletion and repletion of
phosphagens and glycogen have received substantial examination by
exercise and sport scientists.
Exercise Depletion and Post-exercise Recovery of
ATP-PCr and Glycogen
Phosphagens
Although the exact mechanism(s) is unclear (32), acute fatigue resulting
from exercise is at least partially related to the fall in phosphagen
concentration (99, 131). Phosphagen muscle concentrations are intensity
dependent and more rapidly depleted as a result of high-intensity anaerobic
exercise than by aerobic exercise. However, muscle ATP concentrations
will not typically decrease markedly, even as the result of very intense
exercise (115, 150), typically to no more than about 40% or 60% of initial
values (139). PCr concentration can decrease to a greater degree (50–70%)
during the first few seconds (5–30 s) of high-intensity exercise and close to
zero as a result of maximum effort or very intense exercise to exhaustion
(124, 141, 149, 185). It should also be noted that compared to isometric
actions, muscle contractions producing external work (dynamic) typically
use a greater amount of metabolic energy and typically deplete phosphagens
to a greater extent (32).
Intramuscular ATP concentration is largely maintained during exercise.
This maintenance occurs as a result donation of a Pi to ADP from PCr (as it
is depleted) and due to the contribution of additional ATP from the
myokinase reaction and from other energy sources such as glycogen or
FFA. Phosphagen repletion post-exercise occurs in a relatively short time.
Complete resynthesis of ATP can occur within 3 to 5 min (110, 131) and
complete PCr resynthesis can occur within 8 min (110), although relatively
sustained very high-intensity exercise results in a slower PCr repletion rate
(up to 15 min), which is likely related to an increased [H+] (183).
Replenishment of phosphagens is accomplished primarily as a result of
aerobic metabolism during recovery (110), although for a brief period (≈30–
45 s) fast glycolysis can contribute to recovery following high-intensity
exercise (48, 75).
The effects of training on phosphagen muscle concentrations have not
been well studied or understood, particularly in terms of high-intensity
training. A small amount of ATP may be lost during and after high-intensity
exercise as a result of the nucleotide cycle and the conversion of AMP to
inosine monophosphate (IMP). Although most of the IMP is reaminated to
AMP, a small amount is subsequently dephosphorylated, producing
hypoxanthine and uric acid, thus indirectly, some ATP is lost in this manner
(286). However, high-intensity training results in adaptations that minimize
this loss (286). Some evidence indicates that aerobic training may increase
resting concentrations of phosphagens (82, 150) and decrease their rate of
depletion at a given submaximal power output (58, 150), but apparently not
at a relative submaximal power output (58).
As a result of sprint interval training, indications of increased resting
concentrations of phosphagens have been noted (233). However, this
finding has not been consistent; short-term (8 weeks) studies of sprint
training have not shown marked alterations in resting concentrations of
phosphagens (29, 281). It should be noted that total phosphagen content can
be substantially greater after sprint training due to increases in muscle mass
(281). Based on muscle biopsy techniques, weight training has been shown
to increase the resting concentrations of phosphagens in the triceps brachii
after 5 weeks of training (176). It is possible that selective hypertrophy of
type II fibers, which contain substantially higher concentrations of
phosphagens compared to type I fibers, account for most of the increases in
total muscle phosphagen concentration (177).

Glycogen
Liver and muscle glycogen stores are quite limited, especially in terms of
exercise and training. Glycogen is stored in small amounts in the CNS,
heart, smooth muscle cells, kidney, red and white blood cells, and even
adipose cells. However, most stored glycogen is found in skeletal muscle
(≈300–400 g) and the liver (≈70–120 g) (205, 250). Resting concentrations
of both liver and muscle glycogen can be substantially influenced by
training and dietary manipulations (93, 250). During strength training, in
addition to being used as an energy source, glycogen is necessary to
resynthesize the phosphate pool, providing energy during high-intensity
muscle contractions (179). Thus, adequate glycogen storage is quite
important for performance. Considerable information indicates that
anaerobic training, including sprinting and weight training (29, 176, 179),
as well as aerobic training (97, 98), can increase resting muscle glycogen
concentrations.
As with phosphates, the rate of glycogen use and depletion is related to
exercise intensity (250). During very high-intensity short-term exercise,
phosphagens clearly are the predominate energy source; however, muscle
glycogen becomes a primary energy source during moderate- and high-
intensity exercise. Liver glycogen appears to be more important during
prolonged low-intensity exercise and its contribution to metabolic processes
increases with duration of exercise. Increases in relative exercise intensity
to 50%, 75%, and 100% of VO2max result in steady increases in the rate of
muscle glycogenolysis of 0.7, 1.4, and 3.4 mmol kg–1 min–1, respectively
(242). At relative intensities of exercise above 60% of VO2max, as muscle
glycogen becomes an increasingly important energy substrate, and the
entire glycogen content of some muscle cells can become depleted during
exercise, particularly in type II fibers (241).
Blood glucose concentrations can be maintained at very low exercise
intensities (<50% VO2max) as a result of relatively low muscle glucose
uptake (2); however, as exercise duration increases, glucose concentrations
can drop after 90 min but rarely fall below 2.8 mmol L–1 as a result of
gluconeogenic mechanisms. As a consequence of liver glycogen depletion,
long-term exercise (>90 min) at higher intensities (>50% VO2max) may
result in substantially decreased blood glucose concentrations (3). During
exercise-induced blood glucose values below 2.5 mmol L–1, it is possible
that hypoglycemic reactions may occur in some individuals (3, 61). A
decline in blood glucose to 2.5 to 3.0 mmol L–1 can be a consequence of
liver carbohydrate decline, which results in decreased carbohydrate
oxidation and eventual exhaustion (55, 61, 250). Hypoglycemia during
exercise is not uncommon as a result of several factors such as an
imbalance between training volume, nutrition, and external influences such
as chronobiology, temperature, humidity or altitude, particularly in
individuals characterized by an acute and chronic increase in glucose
effectiveness and insulin sensitivity (38, 91). Although it is usually
preventable by adequate pre-exercise feeding with carbohydrates, it can
also be induced by a prior carbohydrate meal with high glycemic load.
Appropriate training can result in adaptations which induce resistance to
hypoglycemia via a shift in the balance of oxidized substrates and marked
hormonal adaptations. However, non-functional overreaching and
overtraining can interfere with the positive adaptations of training, and
favor hypoglycemic episodes (38, 91). It should be noted that exercise
hypoglycemia can be a cause of fatigue and often precipitates exercise
cessation. Hypoglycemic events can also impair thermoregulatory
adaptation and is assumed to “fragilize” muscles and tendons predisposing
them for traumatic events (38).
Very high-intensity intermittent exercise such as weight training can
result in substantial muscle glycogen depletion (20–50%) with relatively
few sets (low total workloads), which can exacerbate fatigue (167, 217,
232, 276). While from an energy source standpoint, phosphagens are the
primary limiting factor during resistance exercise performed with a few
repetitions or few sets (179), muscle glycogen can become a limiting factor
if many total sets and larger total amounts of work are performed (167).
This observation is especially important when resistance training is
combined with additional non-resistance exercise requiring glycogen use as
is typical in many sport scenarios (172). It is also important to note that
higher intensities of exercise can demonstrate some muscle fiber type
selectivity (greater depletion in type II fibers), which could also have
negative impacts on performance (167). Typical of dynamic exercise, the
rate of muscle glycogenolysis during resistance exercise is driven by
exercise intensity. The rate of muscle glycogenolysis during six sets of six
repetitions of leg extensions at 70% 1RM was double that of six sets at 35%
of 1RM (0.46 ± 0.05 mmol kg–1 s–1 vs. 0.21 ± 0.03 mmol kg–1 s–1);
however, equal volumes of work resulted in equal amounts of glycogen
depletion regardless of relative exercise intensity (167). Indeed,
observations of the rate of muscle glycogenolysis during resistance training
exercise are similar to those observed during electrical stimulation of the
vastus lateralis (258) and maximal intermittent isokinetic cycling (185,
258).
Restoration of muscle glycogen, occurring during post-exercise recovery
periods, can be related to post-exercise carbohydrate ingestion. Reviews of
the literature suggest that repletion appears to be optimal if 0.7 to 3.0 g of
carbohydrate kg–1 is ingested every 0.5 to 2 h post-exercise (93, 136, 205,
250). This level of carbohydrate consumption can maximize muscle
glycogen repletion at 5 to 6 grams per gram of wet muscle mass during the
first 4 to 6 h post-exercise. Muscle glycogen can be completely replenished
within 24 h provided sufficient carbohydrate is ingested (93, 250). Some
evidence indicates that glycogen restoration may be enhanced by
simultaneous protein ingestions (136). However, some evidence suggests
that the rate of muscle glycogen replenishment can be reduced as a result of
exercise having a large eccentric component (4, 8, 60, 76, 298). Some
evidence suggests that the rate of restoration resulting from eccentric
exercise is linear for the first 6 to 48 h post-exercise and not different from
replenishment post concentric exercise (76, 298). After the first 6 to 48 h,
the rate of resynthesis can be reduced up to 10 days depending on the
trained state and carbohydrate intake (76). The reduced glycogen
resynthesis may be related to impaired glycogen synthetase activity,
impaired insulin action, or glucose uptake as a result of effects on GLUT 4
concentrations (4, 7, 8, 162), possibly as a result of muscle damage (76).
The reduced glycogen restoration rate may be partially offset by a large
intake of carbohydrates (at least 1.5 g kg body mass–1 h–1) with feedings
beginning immediately after exercise and occurring every 2 h. This type of
carbohydrate feeding raises insulin and glucose to higher and more
consistent blood concentrations, enhancing glycogen resynthesis (76).
Bioenergetic and Metabolic-Limiting Factors
Maximum effort performance can be limited by several bioenergetic factors
(35, 37, 82, 116, 138, 229). These factors must be considered as
mechanisms relating to the accumulation of fatigue from exercise and
training. Examples of the various possible limiting factors based on
depletion of energy source or substrate and increases in muscle [H+] are
shown in Table 2.5.
For both long-term low-intensity exercise supported primarily by aerobic
metabolism and repeated very high-intensity exercise primarily supported
by anaerobic mechanisms, glycogen can be a limiting factor. Of importance
for higher volumes of weight training, sprinting, and other primarily
anaerobic activities is the possible effect of lactic acid production and
increased tissue [H+] in both indirectly and directly limiting contractile
force (116).

Table 2.5 Examples of bioenergetics and metabolic-limiting factors

Exercise intensity Phosphagens Muscle glycogen Liver glycogen Fat [H+]
Low 1 5 4–5 2–3 1
Moderate 1–2 3 1 1 2–3
Moderately high 3–4 2–3 1 1 4–5
Maximum 2–3 1 1 1 1
Repeated maximum 4–5 1–4 1 1–2 4–5
Low = long-term (marathon, 100-mile cycling ride).
Moderate = relatively short-term (1500 m, 400 m freestyle).
Moderately High = short-term (400 m, 100 m freestyle).
Maximum = very short-term (shotput, VJ).
Repeated maximum = very short repeated (5 × 10 power snatches, Wingate test).
The Metabolic Cost of Exercise
Oxygen consumption (uptake) is a measure of an organism’s ability to
function aerobically. The volume of oxygen uptake per minute (VO2)
depends on a central (cardiac output) and a peripheral (a-v O2 diff) factor. A
rearrangement of the Fick equation describes this relationship:

VO2 = CO × a-vO2 diff

VO2 = oxygen uptake (L × min–1)

CO = cardiac output (L × min–1)

a-v O2 diff = arterial – venous oxygen concentration difference

Therefore, maximum oxygen consumption (VO2max) depends on reaching

the maximum attainable values for the central and peripheral factors.
During constant submaximal power output, VO2 increases for the first
few minutes until a steady state of VO2 can be reached (9, 123). During
steady-state exercise, oxygen demand is equal to oxygen consumption
(Figure 2.8). However, during the initial phase (3–5 min) of reaching an
aerobic steady-state exercise, some of the energy cost must be supported
anaerobically (9, 35). This anaerobic bioenergetic contribution to the total
energy cost of exercise has been termed the oxygen deficit (35, 123). When
exercise ends, VO2 remains elevated for a period of time depending on the
exercise intensity and duration. Post-exercise VO2 (above resting) has been
termed the O2 debt (123), or more accurately, the excess post-exercise
oxygen consumption (EPOC), or simply, recovery oxygen (35, 40).
Figure 2.8 Representation of low-intensity steady-state exercise. In
this example, VO2max is 5.5 L min–1 and the exercise
being performed is at 4.2 L min–1.
ROC = recovery oxygen (energy) consumption.
Figure 2.9 Representation of high-intensity non-steady-state exercise
metabolism. In this example the exercise is being
performed at 80% of maximum power output,
approximately 2.5 times the power developed at VO2max.
In this case the required VO2 is considerably above the
maximum possible VO2. Thus, the oxygen deficit is
sustained throughout the exercise and becomes quite large,
thus markedly influencing the ROC and the amount of
energy necessary for recovery.

When the intensity of work is above VO2max, then much of the work
must be supported by anaerobic mechanisms. This occurrence is described
in Figure 2.9. Typically, as the contribution of anaerobic mechanisms
supporting an exercise increases, exercise time decreases (35, 113, 229,
293, 297). Measurement and evaluation of the oxygen deficit can provide
good estimates of the contribution of anaerobic metabolism for both steady-
state and high-intensity exercise (191, 212, 271).
 The relative contributions of anaerobic and aerobic mechanisms to
maximal sustained efforts can be examined using a cycle ergometer
(modified Wingate test); values are shown in Figure 2.10 (255, 287, 301).
During maximum sustained efforts on a cycle ergometer, contributions from
anaerobic mechanisms are the primary energy-supplying systems for about
0 to approximately 60 s; thereafter, aerobic metabolism becomes the
primary. Thus, maximal sustained efforts to complete exhaustion may
depend greatly on aerobic metabolism. The total contribution of anaerobic
metabolism to this type of exercise represents the anaerobic capacity (190,
287).

Figure 2.10 Approximate contributions of anaerobic and aerobic

metabolism to maximum sustained efforts (based on cycle
ergometry).
 Note from Figure 2.10 that as the contribution of energy from aerobic
mechanisms increases power output decreases. The power output that can
be briefly sustained at VO2max is typically 35% or less of the peak power
output achieved using the same exercise mode (262). Thus, as aerobic
mechanisms create energy relatively slowly, exercise primarily supported
by aerobic metabolism must proceed at low mechanical intensities relative
to maximum power output capabilities. While enhancement anaerobic or
aerobic capacity can increase endurance and the total amount of work
accomplished during sustained maximal efforts to exhaustion, training
aerobically has little effect on peak power (262, 287). Different types of
specific training can enhance either anaerobic or aerobic capacity (190).
Simultaneous enhancement of aerobic and anaerobic power, and anaerobic
capacity is possible through appropriate manipulation of exercise-to-rest
intervals (190, 271, 272).
Few sports or other physical activities necessitate maximum sustained
efforts to exhaustion or near exhaustion. Most sport and training activities
(such as football, interval jumping and sprinting, weight training) produce
metabolic profiles that are very similar to those of a series of high-intensity
constant- or near-constant-effort exercise bouts interspersed with rest
periods. For exercise of this type, the intensity (force or power output) that
must be met during each exercise bout is much greater than the maximal
force or power output that can be sustained using aerobic energy sources.
Enhancing aerobic power through aerobic training while simultaneously
compromising (or neglecting) anaerobic power and capacity training will be
of little benefit to strength-power athletes (157, 264).
Interval training is a method of training that allows the appropriate
metabolic systems to be targeted and stressed. Conceptually, interval
training, compared to continuous exercise, is based on the premise that
more work can be performed at higher exercise intensities with the same or
less fatigue (35, 69). The theoretical metabolic profile for exercise-to-rest
intervals targeting the phosphagen system, fast glycolysis, and the aerobic
system is based on the knowledge of which energy system predominates
during exercise and time of substrate recovery. Examples in Table 2.6
represent logical exercise-to-rest intervals based on exercise relative to
maximum attainable power, and substrate (phosphagen) recovery times
(262).

Table 2.6 Theoretical exercise-to-rest intervals

Maximum power (%) Primary energy systems Typical duration (s) E:R
90–100 Phosphagen 5–10 1:12–1:20
75–90 Fast glycolysis 10–30 1:3–1:5
30–75 Fast glycolysis + aerobic systems 60–180 1:3–1:4
30–35 Aerobic systems >180 1:1–1:3
E:R = exercise–rest ratio.
Source: Based on Stone and Conley (262).

However, it should be noted that the dynamics of many sports do not

lend themselves to a strict application of exercise-to-rest intervals. From a
practical point of view, perhaps a more “usable” method would be training
using intensity–time profiles. Using this method, the intensities and
durations of athletic events are replicated during training (225). This
method allows for an interval type of training that essentially simulates the
intensities and exercise–rest intervals that are likely to occur in an actual
contest situation. For example, football (soccer), the number of plays,
distance covered, and relative intensity of play can be approximated for
each position and then duplicated in training programs, thus readily
ensuring that the athlete will possess sufficient conditioning to play the
game.
Targeting appropriate exercise intensities, exercise durations, and rest
intervals enables the training of appropriate energy systems. Note that
physiological adaptations can be made across a training program or as a
result of changes in long-range programming (i.e., periodization), so
optimum exercise–rest intervals may change as well.
Recovery Oxygen Consumption: Recovery Energy
Coaches and athletes have often underestimated the energy cost of
resistance training. Many also believe that resistance training has little or no
metabolic impact or effects on body fat. These misconceptions may arise
from the commonly held beliefs that energy cost of typical aerobic exercise
is substantially higher and that only aerobic exercise can burn fat. However,
these beliefs are likely incorrect.
Post-exercise recovery energy consumption is an important
consideration for several reasons, including its possible effect on body mass
and body composition and its effect on subsequent exercise. Exercise
energy cost is not simply confined to exercise time but can persist for a
substantial period post-exercise. The effects of typical aerobic steady-state
exercise on recovery energy consumption and total energy expended have
been well studied (11, 12, 31, 44, 81, 164, 246, 249). Although both
exercise intensity and duration affect recovery energy, these studies indicate
that intensity has a somewhat greater effect on recovery energy
consumption than does the duration of exercise (164, 192). While
increasing the duration of low-intensity exercise (<60% VO2max) results in
linear increases in total recovery energy (11, 12, 192), increasing the
intensity of exercise can produce an exponential effect (12, 164, 192).
Indeed, higher exercise intensities appear to disturb homeostasis to a greater
degree than low-intensity exercise, resulting in greater post-exercise energy
consumption. This observation suggests that non-steady-state intermittent
high-intensity exercise, such as weight training or sprinting, could require
more energy and longer durations for recovery.
During recovery from high-intensity exercise, most of the recovery
process from all types of exercise is accomplished through aerobic
metabolism, although fast glycolysis can contribute during the early phases.
Measurement of the recovery oxygen consumption (ROC) and converting it
to a caloric value is an important method of describing recovery energy
consumption. The ROC is the amount of O2 uptake above baseline used to
restore the pre-exercise homeostatic condition (259). Initially, experiments
suggested that the ROC was moderately or strongly related to the O2 deficit
and was largely due to the resynthesis of glycogen from lactate (80%) or the
further oxidation of lactate (20%) via pyruvate and the Krebs-ETS pathway
(123). However, Margaria and colleagues (181) noted that the initial portion
of the ROC occurred without any decrease in blood lactate and that a small
ROC could be incurred (2–3 L) without any significant change in blood
lactate. They speculated that the ROC is made up of two phases: the alactic
phase and the lactic acid phase. The alactic phase was believed to represent
O2 consumption used for the restoration of ATP-PCr stores and for
reloading myoglobin and hemoglobin. The lactic acid ROC was believed to
be the O2 used in reconverting lactate to glycogen. Presently, it becomes
clear that these observations were not completely accurate.
Depending upon the anaerobic metabolic contribution to exercise, only
small to moderate relationships have been established between the O2
deficit and the ROC (24). While the O2 deficit can influence the total ROC
consumed, the two are not equal. Furthermore, infusion of radioactive
labeled lactate into rat muscle immediately post-exercise showed that 75%
of the labeled carbon appeared as CO2 (34). This finding indicates that the
major portion of lactate accumulated could be used to produce energy
aerobically during recovery. Furthermore, blood lactate can be substantially
reduced at 10 min post-exercise with essentially no glycogen resynthesis
occurring (295). Thus, only a small amount of lactate is re-synthesized to
glycogen post-exercise.
Increases in physiologic functioning during exercise that persist into
recovery may account for substantial and perhaps major portions of the
ROC. For example, increased body temperature elevates metabolism and
O2 consumption (36). Increased respiratory muscle and heart function
resulting from exercise requires an elevated rate of energy consumption
(149). Interestingly, only using these criteria (increased temperature and
cardiorespiratory function) to account for ROC, apparently the theoretical
maximum O2 debt should not exceed 3 to 5 L (34, 36, 292). However, after
steady-state exercise of greater than one hour, total recovery oxygen values
as high as 18 L have been reported (181). Higher values (over 19 L) have
been reported for weight training sessions lasting 30 to 90 min (40, 192).
These large total post-exercise oxygen consumptions values may be wholly
or partially accounted for by a variety of factors including resynthesis of
phosphagens, resynthesis of glycogen from lactate (<20%), increased
temperature, additional cardiorespiratory work, resaturation of tissue water,
oxygen resaturation of venous and skeletal muscle blood, oxygen
resaturation of myoglobin, redistribution of ions within various
compartments, the effects of Ca++ on mitochondrial respiration, residual
effects of hormone release and accumulation, and tissue repair and
remodeling (34–36, 291). Furthermore, the CNS may play a prominent role
in recovery (199).

Recovery: Submaximal Exercise

The ROC resulting from 2 to 3 min of submaximal steady-state work can be
larger than the ROC of longer exercise periods at equal intensities (297).
This suggests the ROC may be partially accounted for during steady-state
aerobic work. Support for this idea is provided by the observation that
lactate removal (a measure of recovery) can be increased by light to
moderate aerobic exercise at 50–70% of VO2max during recovery (201,
224).

Recovery: Intermittent Anaerobic Training

Intermittent non-steady-state work, such as repeated sprints, allows for the
completion of a larger total workload or a higher work rate; this is a basis
for the concept of interval training (169, 224). The intermittent rest periods
of interval training sessions can result in an increased total ROC and an
increased total caloric consumption as compared to continuous exercise of
the same approximate length or caloric expenditure (67, 104). This
increased caloric cost occurs because several bouts can be performed at the
same or a higher relative intensity compared to continuous exercise,
creating more total work.
Resistance training exercise has been shown to disturb homeostasis
sufficiently to produce moderate to large ROCs, depending on the volume
of exercise (40, 81, 104, 192, 193, 204). Furthermore, resistance training
can produce larger ROCs than typical aerobic exercise (40, 81, 104, 246), a
factor that may be important in a variety of health, fitness and performance
parameters.
The use of resistance training in body mass and body composition
management is somewhat controversial (192, 260, 290). Weight training
exercise can elevate recovery energy consumption beyond that with typical
aerobic exercises; however, the levels may not be high enough to
substantially alter body mass or composition. For example, Burleson et al.
(40), found that approximately 95 kcal (19 L of O2) was used in 30 min of
recovery from circuit weight training exercise. This value is unlikely to
make a marked impact on body mass or composition even if training takes
place several times per week. However, the training protocol used did not
result in a high relative weight training intensity (60% of 1RM) or a large
volume of work (volume load <6000 kg [13,200 lb]). Weight training more
typical of protocols used by strength-power athletes, lasting 60 to 90 min
and producing volume loads of 15,000 to 40,000 kg (33,000–88,200 lb) per
session, resulted in much greater total energy consumptions such that
complete recovery might not be achieved even at 15 h post-exercise (192).
Thus, the volume of weight training exercise (and other concurrent training
modes) may be a critical factor substantially influencing recovery.
Additionally, the accumulative effect of high-volume weight training
among athletes training multiple times per week can be sufficient to
maintain body composition among those athletes with relatively low body
fat content and higher levels of lean body mass (64, 174). Furthermore,
resistance training is likely to affect alterations in body mass and
composition, especially among athletes having a relatively poor body
composition profile (i.e., novices or athletes returning from active rest
periods or holidays), particularly if training consists of multiple sessions per
day (174, 268).
Indeed, literature reviews indicate that resistance training can increase
lean body mass as well as affect positive alterations in percentage fat and
losses in total fat (73, 260). While substantial fat use as an energy source is
unlikely during resistance exercise, the use of FFA can be enhanced post-
exercise (26, 188, 192, 214, 246). The increased mobilization and use of
FFA after resistance training exercise may be related to decreased muscle
glycogen concentrations and residual effects of hormones, particularly
human growth hormone (158, 159, 188, 192). Therefore, body mass and
body composition can be affected by both energy consumption and the
enhanced use of FFA during recovery. Furthermore, resistance training
which precedes aerobic work can enhance FFA mobilization and use (147).
The training and competition frequency of most high-level athletes
exceeds three sessions per week during large parts of a season or
macrocycle, and many athletes use multiple training sessions per day.
Among strength-power athletes, the number of weight training sessions per
week may exceed eight, particularly during a preparation phase. Recovery
becomes an extremely important issue when training at this level (261,
264).
Using competitive weightlifting as an example, training twice per day,
four to six days per week, and lifting 30,000 to 70,000 kg per week is not
uncommon among advanced weightlifters (263). During a preparation
phase or planned overreaching, volume loads over 90,000 kg per week can
be associated with energy expenditures as high as 600 to 1000 kcal per hour
and ≥ 3000 kcal per week (168, 243, 263). As competition approaches,
energy costs typically decrease concurrently during a taper in which the
volume of work declines. Much of the energy expenditure resulting from
weight training and weightlifting takes place during rest periods between
sets and during recovery between train sessions (40, 43, 192, 243, 247).
Furthermore, the magnitude of energy expenditure during recovery appears
to be dependent on the volume of training (192), and complete recovery, in
terms of measurable energy expenditure, may take as long as 38 h (247).
Therefore, in a high-volume weight training session, with multi-joint, large
muscle-mass exercises, it appears that a sizable portion of the energy cost, if
not most, occurs during recovery.
Adequate energy intake is necessary to maintain body mass and support
the extra energy requirements associated with training and to promote
positive adaptation. Considering the relatively large total energy
expenditure that can occur during weightlifting training, particularly during
accumulation (preparation) phases, caloric intake can be rather large,
especially among the heavier weight classes. An increased mobilization and
use of fats during recovery coupled with the relatively high total energy cost
of weight training (132, 188, 263), helps to explain the relatively low
percentage body fats observed among elite weightlifters and other strength-
power athletes.
The acute effects of recovery from previous exercise can persist for
hours and in some cases, days. This prolonged recovery, often accompanied
by substantial fatigue, could alter subsequent exercise performance
resulting in reduced training adaptations. Although it is known that fatigue
can alter various aspects of muscular force production (267), few studies
have specifically addressed the physiologic or metabolic effects of a
training session on subsequent weight training or other anaerobic exercise
sessions (52, 269, 273). Weight training may alter metabolism and
performance during subsequent training sessions (52, 269). However,
exercise volume likely plays a role in recovery and therefore subsequent
exercise (20, 192). Additionally, a weight training session may affect
various strength-related components differently. For example, unpublished
data from our laboratory indicate that a 1RM squat and vertical jump were
less affected than strength-endurance when preceded by a high-volume
training session performed 4 h earlier (267).
Investigators have addressed the effects of weight training on subsequent
aerobic exercise. Crawford et al. (63) suggest that resistance training has
minor effects on subsequent aerobic (treadmill) exercise. However, in that
study, only a few sets of one isokinetic leg extension were used, resulting in
a very low training volume. Using a routine consisting of nine upper and
lower-body exercises with a much larger training volume, Baily et al. (13)
found that weight training exercise can alter the typical rate-pressure
product response and the heart rate–VO2 relationship. Running economy
has been shown to be negatively altered by weight training consisting of a
moderate-high volume (215). Interestingly, some evidence suggests that
knee extension resistance exercise at 40, 60, and 80% 1RM induces an
increased VO2 in non-exercised muscle (forearm flexors) that can persist
several minutes after aerobic exercise (206). While not definitive, these
studies suggest that the volume of weight training may influence
physiological and performance sequelae related to recovery. For various
reasons during a daily training routine, many athletes complete a strength-
training session first and then move to a different type of conditioning
exercise such as a running session, or vice versa. Often, only a few minutes
separate these training sessions. Unfortunately, information is lacking with
regard to the metabolic efficacy of this type of training routine.
It is logical to believe that insufficient recovery time between training
sessions could alter physiological responses and performance responses
during a subsequent exercise session. The reduction in subsequent exercise
performance could reduce the expected training adaptations to a given
exercise session. Furthermore, insufficient recovery time could expose an
athlete to excessive fatigue; constant exposure to this scenario could result
in non-functional overreaching or overtraining (261). Although evidence
indicates that prior exercise can have a negative effect on subsequent
exercise, guidelines and timelines for recovery are not known. Thus,
coaches and athletes should be circumspect in allowing sufficient time for
adequate recovery from an exercise session prior to subsequent training
sessions, especially from higher volumes of resistance training or resistance
training to failure (202, 267).
Metabolic Specificity of Training
Appropriate exercise intensities, durations, and rest intervals are necessary
for the appropriate selection of energy systems during exercise. With
appropriate selections, specific adaptations for different athletic events can
result (35, 157). Interval training is the basis for weight training and
typically forms the foundation for the training programs of most anaerobic
and aerobic sports. Although weight training and other forms of anaerobic
interval training can increase aerobic power among aerobically untrained
subjects to a small extent (4–10%) over a short term (184, 257, 265), major
effects concern anaerobic factors. Weight training, sprint training, and other
forms of anaerobic training have been shown to increase stores of
phosphagens and glycogen, enhance the myokinase reaction (36, 176),
result in preferential hypertrophy of type II fibers (102, 127), and generally
enhance anaerobic metabolism (1, 35, 47), leading to improved
performance.
Oxidative metabolism is important in recovery from heavy anaerobic
exercise (e.g., weight training, sprint training) (35); however, care must be
taken in prescribing aerobic training for anaerobic sports. Although not all
studies agree, there is substantial evidence that aerobic training, even at low
volumes, may reduce anaerobic performance capabilities, particularly high-
power and speed performance (106, 111, 220, 300).
Interestingly, anaerobic energy production capabilities in rats have been
shown to be reduced by aerobic training (288). Additionally, several studies
suggest that combined resistance and aerobic training can reduce the gain in
muscle girth compared to resistance training alone (21, 62, 95). This
observation has also been noted for maximum strength (21, 41, 62, 122) and
especially speed- and power-related performance (78, 106, 160, 220, 300).
The inhibition of alterations in strength and related factors is more apparent
in well-trained athletes compared to recreationally trained or untrained
subjects (53, 95, 220). While the mechanisms are unclear, reductions in
performance gains resulting from combined training may be partially
related to alterations in the nervous system, molecular regulation, muscle
fiber types (myosin heavy chains), and testosterone and cortisol
concentrations (111, 160, 175, 256). One possible explanation for the
difference between trained and untrained subjects is that the potential for
adaptation is lower in trained athletes requiring more specific and more
intense training in order to produce additional performance improvements
(219, 220). This observation is supported by evidence indicating that block
periodization results in superior adaptations compared to a traditional
training approach for strength-power development in athletes (135, 220,
264). Although the underlying molecular/metabolic alterations supporting
this observation are not clear, examinations of the acute responses post-
resistance exercise indicate that trained athletes have a blunted expression
of several genes and proteins associated with the anabolic adaptation
process as compared with untrained subjects (54, 87, 95, 111, 220).
Furthermore, evidence also indicates that mTORC1, a key protein kinase
regulator of muscle hypertrophy, can be negatively affected by concurrent
training in trained but not in untrained subjects (95).
Interestingly the results of some studies have shown an enhanced
molecular response and increased hypertrophy in untrained and moderately
trained participants after concurrent training (87, 151, 220), although the
type of hypertrophy (sarcoplasmic versus myofibrillar) is unknown. On the
other hand, interference has been demonstrated in untrained and moderately
trained subjects (106, 122). Therefore, the degree of interference is likely
dependent upon many factors in addition to the trained state, such as the
volume of work, length of the concurrent training period, use of single
versus multi-joint exercises, resistance training to failure (or not), and the
state of accumulated fatigue (264). While the addition of endurance training
to a strength-power training protocol can, under some circumstances, make
little difference or even result in beneficial adaptations for a less trained
population, there are a variety of factors to consider (220, 264).
Although, aerobic training can compromise alterations in strength, RFD,
and power as a result of resistance training, it does not appear that strength
training interferes with endurance. Furthermore, several studies and reviews
indicate that high-intensity training, including strength training, can
improve low-intensity exercise endurance (19, 120, 122, 266, 302).
Suggestions that some aerobic training should be added to the training of
primarily anaerobic athletes to enhance recovery (224) is not uncommon as
post-exercise recovery relies largely on aerobic mechanisms. However,
whether or to what extent this is actually necessary is unclear, as the extent
to which increased aerobic power can influence recovery is not clear. While
several investigations indicate an association between VO2max and
metabolic recovery parameters including lactate removal, replenishment of
PCr, and post-exercise oxygen consumption (125, 251, 282), other
investigations have not (10, 23, 59). However, Hoffman (125) indicated that
post-exercise recovery rate increases with increased aerobic power only to a
point, after which there is no additional benefit. Thus, there may be an
upper limit of VO2max above which there is no additional effect on
recovery parameters. Hoffman (125) suggested this upper limit is
approximately 45 ml kg–1 min–1 for men, which is not much above average.
Interestingly, training at high intensities with a primary anaerobic metabolic
component can have substantial effects on both anaerobic and aerobic
metabolism (173, 203, 211), and can result in increases in VO2max, stores
of CrP and glycogen, and both anaerobic and aerobic enzyme activity (71,
109, 178, 234). As a consequence of these observations, the amount of
aerobic training necessary for recovery from primarily anaerobic sports is
likely small to negligible.
In this context, although increases in aerobic power are small to
moderate and largely confined to relatively aerobically untrained individual,
we note that specific anaerobic training programs can increase and maintain
aerobic power. Furthermore, anaerobic training has been shown to enhance
several markers of recovery (188, 203, 261, 263, 265, 271, 272). Indeed, the
results of both cross-sectional (188) and longitudinal (221, 222, 263)
studies suggest that weight training, particularly high-volume weight
training, can enhance markers of recovery including a faster return to
baseline values for heart rate, lactate, ammonia, and various hormones.
Thus, extensive aerobic training to enhance recovery from anaerobic events
is not necessary and may be counterproductive for most strength-power
sports (157).
Chapter Summary
The underlying biochemical/metabolic basis for the concept of specificity
of exercise and training has been presented in this chapter. Staying alive and
physical activity require a continuous energy supply. Physical activity is not
possible without the contraction of muscle, which depending upon the
intensity of the exercise, can require varying rates and amounts of energy.
Energy in biological systems can be derived from the hydrolysis of the
energy conveyor ATP. Therefore, ATP must be continuously created.
Essentially, the higher the intensity of muscular contraction, the faster
energy (ATP) is consumed. Three bioenergetic systems are available ATP
replenishment. These energy systems operate with different rates and
capacities for ATP production, matching energy production to energy
consumption. Fatigue is partially related to depletion of energy sources;
recovery enables replenishment of energy stores and aids in restoration of
normal muscle function. Training-induced adaptations can be enhanced by
understanding how energy production can be modified by specific training
programs. Basically, exercise selection and energy system selection are
dependent upon exercise intensity, duration, and rest/recovery intervals.
These fundamental aspects are important considerations in the development
of productive training programs.

1 Most unsaturated FFAs have a greater relative yield an apparent efficiency – for example,
stearate is about 51% efficient using this method, as consumed fat is a mixture of FFA the
average ratio is approximately 48%.
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3 Neuroendocrine Factors

DOI: 10.4324/9781003096139-5
Introduction
The neuroendocrine system (NES) works with the nervous system to
regulate homeostasis. Additionally, to having normal homeostatic effects,
the NES is involved in morphogenesis and exercise-induced homeostatic
responses as well as chronic training alterations. Homeostasis is associated
with the equilibrium and constancy of the internal environment. Providing
mechanisms for regulation of functions involved in the internal
environment (e.g., cardiovascular, renal, and metabolic systems) and
homeostatic control requires systems that can sense information, organize a
response, and deliver the response to the appropriate tissues. Both the
nervous system and the endocrine system are structured in order to provide
a mechanistic homeostatic control. These two systems are tightly integrated
and operate together; the term “neuroendocrine system” reflects this
interdependence (163). Thus, the primary function of the neuroendocrine
system is homeostatic regulation. Importantly, the neuroendocrine system
functions in promoting adaptations in various tissues and systems in concert
with a changing external environment (e.g., training, nutrition, etc.).
Homeostasis is accomplished through the initiation of tissue responses
and adaptations as a consequence of endocrine gland release of a hormone
directly into the circulation, or by neural function and neurotransmitter
release. A secretory cell is the functional unit of an endocrine gland.
Endocrine glands are ductless and manufacture, store, and secrete
hormones. Hormones are chemical messengers that are released in very
small amounts and have specific effects on specific target tissues. Some
hormone and hormone-like substances are produced and act within a cell
(autocrine function), or a hormone can be released from one cell but act in
another cell without entering the circulation (paracrine function). Neurons
synthesize, store, and release neurotransmitters, which act to relay
information (action potentials) from neuron to neuron or from a neuron to
an effector tissue such as a muscle fiber. Some neurotransmitters act as
hormones such as epinephrine. Therefore, hormones and neurotransmitters
released by the endocrine and nervous systems have “neurohormonal”
properties and integrative functions and effects.
Neurotransmitter Release
A brief description of how the autonomic nervous system functions to
provide a relatively fast-acting feedback loop in the control of homeostasis
is discussed in this section. The sympathetic nervous system, in particular,
is an important system regulator, including organ systems such as the lungs
and heart, various tissues such as the peripheral vasculature, and various
metabolic processes. Catecholamines are examples of a major group of
neurotransmitters having hormone regulatory activity. Primary
catecholamines are epinephrine (EPI) and norepinephrine (NEPI), which
are secreted by the majority of postganglionic sympathetic fibers and have
profound effects on a number of tissues. Dopamine is an important third
naturally occurring catecholamine found predominately in the basal ganglia
of the brain.
Norepinephrine is the primary catecholamine released by the
sympathetic neuron (80% NEPI and 20% EPI), while EPI is the primary
catecholamine released by the adrenal medulla (80% EPI, 20% NEPI) (139,
181). In the process of neural catecholamine synthesis, phenylalanine, an
amino acid, is converted to NEPI in 4 enzymatic steps. A small amount of
NEPI is converted to EPI by an additional step. Upon release,
catecholamines can bind to different types of receptors, causing various
effects in different tissues (153) (Table 3.1). The release of catecholamines
by the sympathetic nervous system and subsequent physiologic actions
occurs rapidly compared to effects of the endocrine system.

Table 3.1 Distribution and action of catecholamine receptors in humans

Membrane Tissue Response Enzyme Mediator
receptor
type
Alpha1 Most vascular Contraction Phospholipase Ca++/IP3
smooth muscle
Membrane Tissue Response Enzyme Mediator
receptor
type
Radial muscle, iris, Contraction/hair erection
pilomotor smooth
muscle
Cardiac Positive inotropic effect
Alpha2 Post synaptic CNS Multiple Adenyl cAMP
receptors cyclase
Adrenergic and Post synaptic inhibition of NT
cholenergic release; generally blocks
terminals response of β1 and β2
Platelets Aggregation
Some smooth muscle Contraction
Adipocytes Lipolysis inhibition
Beta1 Heart Positive inotropic and Adenyl cAMP
chronotropic effect cyclase
Beta2 Respiratory, Relaxation Adenyl cAMP
uterus,vascular cyclase
smooth muscle
Skeletal muscle Increased K+ uptake
Liver, skeletal muscle Activates glycogenolysis
Adipocytes, skeletal Activates lipolysis
muscle
Skeletal muscle Increased contraction force
Pancreas Enhanced insulin secretion

Catecholamines are stored in terminal boutons within synaptic vesicles;

release occurs by exocytosis (120, 139). Synaptic transmission is terminated
by a number of factors including:

Synaptic concentration dilution by diffusion out of the synapse.

Synaptic enzyme catechol-O-methyltransferase (COMT).
Reuptake, which is the primary terminator of transmission.

Additionally, intra- and intercellular (among various tissues) turnover and

metabolic transformation of catecholamines result from catalysis by both
COMT and mitochondrial monamine oxidase (MAO) (139).
Hormone Release
Endocrine glands are stimulated by chemical substances (e.g., releasing
factors or neurotransmitters). Stimulation subsequently leads to the
secretion of a hormone, a process that has several characteristics including:

Secretion occurs in very small amounts; many, if not all, endocrine

glands release their hormones in a pulsatile fashion.
The hormone has no effect on its secretory gland; only the target tissue
is affected.
The target tissues may be discrete or ubiquitous.
Hormones may trigger alterations in the rate of biochemical reactions,
which can persist even after the hormone has returned to baseline
concentrations.

The target tissues’ response to the hormone depends on factors that

influence receptor–hormone interaction and the blood concentration of the
hormone. These factors are as follows:

Blood concentration. Concentration is related to the amount of

hormone released, clearance rate, and plasma volume changes.
Clearance is a function of metabolic inactivation and excretion.
Hormone inactivation can take place at or near the receptor, or more
typically, in the liver or kidneys. Excretion of degraded products is
usually through the kidneys. Plasma volume shifts can alter the
hormone concentration independent of secretion or clearance rates.
Plasma volume alterations and loss or gain of water from the blood
compartment resulting from can cause substantial changes in hormone
concentration. Exercise can result in substantial water loss and
increased hormone concentrations. Regardless of the mechanism
(secretion, clearance, plasma volume), changes in the concentration of
a hormone will influence receptor–hormone interaction. The following
three factors are important aspects of hormone release.
Free versus bound transport proteins. Several hormones, including
steroid hormones, insulin, growth hormone, and thyroxin, are
transported bound to proteins in the blood. Binding transport proteins
protect the hormone from being attacked by hydrolytic enzymes and
can act as a storage depot. However, for a hormone to interact with its
receptor and exert its biological activity, it must be in the free form.
The amount of free hormone depends on the binding affinity of the
protein for the hormone, the quantity of the protein present, and the
binding capacity (104, 108). Changes in the binding affinity, capacity,
or binding protein concentration can change the ratio of free to bound
hormone. Additionally, some binding proteins may have biological
functions beyond transport of hormones (81, 108, 115).
The health of the target tissue. Unhealthy target tissue can alter the
production and excretion of a hormone. For example, the response of
the testes to luteinizing hormone can be exaggerated as a result of a
testicular tumor, producing testosterone concentrations several times
higher than normal.
The number and activity of hormone receptors. Hormone–receptor
interaction must occur in order to stimulate its target tissue. Although
some cross-reactivity occurs within a family of hormones, hormone–
receptor interaction is specific and behaves in a lock-and-key fashion.
Receptors are typically large proteins embedded in the cell membrane
or bound to the nuclear membrane of a cell. Some receptors contain
allosteric binding sites, which interact with hormone cofactors, altering
the receptor affinity and therefore the cellular response (108, 115).
Receptors may transmit a signal directly to the nucleus or stimulate a
membrane-bound regulatory protein, resulting in an enzyme-activated
cascade effect. Receptor affinity for a hormone can change with
chronic hormone concentration alterations. Desensitization of a
receptor (decreased receptor and tissue response) can occur as a result
of exposure of the receptor to the hormone. For example, on an acute
level, after a peak level is reached (e.g., increased cellular cyclic
adenosine monophosphate [cAMP] concentrations, Na+ flux), there is
a gradually diminished response over seconds or minutes (23).
Desensitization is reversible upon removal of the hormone for a few
minutes. Chronic saturation of the receptors will result in
downregulation, in which the number of receptors decreases. However,
chronic exposure to a low concentration of hormone can result in
upregulation, or an increased number of receptors. Up- or
downregulation can markedly alter a tissue’s responsiveness to
hormonal stimulation.
Hormone Mechanisms of Action
Hormones can stimulate target tissues and modify cellular activity by at
least three different mechanisms (23, 108). Our current understandings of
these mechanisms encompass alteration of membrane transport and second
messenger formation.
Membrane transport can be altered because some hormones, such as
insulin can affect target tissues by activating carrier molecules in or near the
cell membrane (10, 163). Activation of these carrier molecules can increase
the movement of various substances into and out of the cell.
Second messenger formation is a mechanism that transmits the hormonal
signal (hormone–receptor interaction) into the cell. Peptide and polypeptide
hormones do not easily cross cell membranes because of their lipid
insolubility. These hormones bind to the intrinsic and extrinsic protein
receptors embedded in the cell membrane and eventually result in the
formation of a second messenger. Formation of second messengers occurs
as a result of the hormone signal, causing conformational changes in a
series of membrane-bound proteins (23, 54, 150).

hormone ⇒ receptor ⇒ regulatory protein (G-protein) ⇒ effector

element

Activation of the effector element (enzyme or a calcium channel) creates a

second messenger and results in a cascade effect. Guanine nucleotide-
binding proteins (G proteins), are embedded in the cell membrane and
contain alpha, beta, and gamma subunits. These regulate the activity of
enzymes or calcium channels important for second messenger production.
Based on current knowledge, two primary second messenger systems can
be activated: cAMP and Ca++/IP3 (Figure 3.1a, b). G-protein activation of
the enzyme adenyl cyclase results in cAMP formation; in the Ca++/IP3
system, the G protein simultaneously activates inositol triphosphate (IP3)
formation and opens Ca++ channels. The cAMP and Ca++/IP3 systems are
complementary in some cells but can have opposite effects in other tissues
(23, 108). For example, for liver glycogenolysis the effect is
complementary, but contraction and relaxation of smooth muscle can
require different second messengers. A third type of second messenger,
cyclic guanosine monophosphate (cGMP), has been established in a few
tissues (23, 108).
Figure 3.1 (a) Cyclic AMP second messenger system. (b)
IP3/calcium second messenger system. (c) Mechanism of
action for steroid hormone (gene derepression and
activation).
DAG = diacylglycerol; PIP2 = phosphatidylinositol 4,5 bisphosphate; IP3 = phosphatidylinositol
3.

Formation of the second messenger and the resulting cascade of events

involve a series of reversible phosphorylation steps (23, 108).
Phosphorylation is an important regulatory event starting with the receptors,
then moving to the subsequent activation of protein kinases and eventually
to the substrates that the kinases act on in the cascade effect.
Phosphorylation results in the formation of a covalent bond and produces
two important functions: amplification and flexible regulation.
Amplification requires a phosphate group attachment to a specific amino
acid residue; this attachment creates a molecular memory that the pathway
has been activated. While the memory is erased by detachment of the
phosphate group, the molecular memory can persist even after complete
removal of the hormone and allosteric ligand. This persisting effect occurs
as a result of dissociation of the covalent bonds and removal of the
phosphate group requiring more time. Flexible regulation provides a
mechanism whereby a second messenger system can produce different
effects in different cells. This occurs as a result of the presence or absence
of specific kinases or substrates in a particular type of cell.
Lipid solubility allows several hormones to move through the cell
membrane and interact with a cytosolic or nuclear receptor (Figure 3.1c).
These “gene-activating” (gene derepression) hormones include steroids,
vitamin D, and thyroxin. Receptors for these hormones in the cytosolic,
upon binding the hormone–receptor complex, move into the nucleus;
exceptions are estrogens and thyroxin, which have receptors already located
inside the nucleus (24, 108). Hormone–receptor interaction produces a
protein-hormone complex (activated receptor) that is able to bind to specific
DNA sequences called enhancers. DNA binding and activation of the
enhancer result in transcription of specific genes (gene derepression), and
eventually the synthesis of a specific enzyme. The enzyme then initiates the
characteristic cellular response to the hormonal signal.
Unlike the second messenger systems with their relatively rapid
response, gene-activating hormones, which result in protein synthesis,
require 0.5 h or more to produce their effects (23, 108, 163). Furthermore,
the effects of hormones can persist for several hours or even days after the
hormone has returned to baseline blood concentrations. There are likely two
reasons for the long-lasting effects: the receptors have a very high affinity
for the hormone, producing a slow dissociation, and turnover of the
synthesized enzymes is relatively slow.
Interestingly, some perhaps all steroid hormones may also activate
protein receptors in the cell membrane (47, 178). Thus, steroid hormones
may activate both short-lived and long-term pathways.
Hormone Action and Regulation
Hormones are secreted from several different glands and have many
different biological actions (Table 3.2). This section deals with the
endocrine glands and hormones that have marked effects on muscle
physiology, function, performance and are of particular interest to sport
scientists.

Table 3.2 Endocrine glands, hormones, target tissues, and primary functions
Endocrine Hormone Target tissue Primary effects
gland
Anterior Growth hormone Ubiquitous Growth and development of all tissues.
pituitary Promotes protein synthesis and a positive
nitrogen balance. Promotes FFA
mobilization and indirectly reduces
carbohydrate use.
Luteinizing hormone Gonads Promotes estradiol secretion from ovaries
(LH) and testosterone from testes. Promotes
ovum release.
Follicle-stimulating Gonads Promotes follicle development and secretion
hormone (FSH) of estradiol. Promotes growth and
development of the germinal epithelium
of the testes. Promotes sperm production.
Prolactin Breast Breast development and milk secretion.
Adrenocorticotropic Adrenal Modulates secretion of cortisol.
hormone (ACTH) cortex
Thyroid-stimulating Thyroid Modulates secretion of T3 and T4.
hormone
Posterior Antidiuretic hormone Kidneys, Vasoconstriction and modulation of body
pituitary (ADH) vasculature water (decreases water loss through the
kidneys).
Kidneys Renin Adrenal Modulates control of blood pressure.
cortex
Erythropoietin Bone marrow RBC production.
Endocrine Hormone Target tissue Primary effects
gland
Adrenal Epinephrine (80%) Ubiquitous Mobilize glycogen and FFA release.
gland Increase skeletal muscle blood flow.
medulla Positive inotropic and chronotropic
cardiac effects. Increased VO2.
Norepinephrine (20%) Ubiquitous Similar to EPI, promotes vasoconstriction.
Adrenal Mineralocorticoids Kidneys Increased Na+ retention and K+ excretion,
gland (aldosterone) body water regulation.
cortex Glucocorticoids Ubiquitous Modulates energy substrate use. Has anti-
(cortisol) inflammatory properties.
Sex steroids: Primary and Development of sex secondary and primary
estrogens and secondary sex characteristics. Increased skeletal
androgens sex tissues, muscle.
muscle
Pancreas Insulin (Islet β cells) Ubiquitous Increased substrate cell entry, storage
hormone. Promotes protein synthesis.
Glucagon (Islet α Ubiquitous Increased blood glucose and fat
cells) mobilization. Protein catabolism and
gluconeogenesis.
Somatostatin (Islet D Depression of insulin and glucagon
cells) secretion. Inhibits the activity of the
gastrointestinal tract and the rapid
reproduction of normal and tumor cells.
Parathyroid Parathormone Bone, blood Increases plasma calcium.
Thyroid Triiothyronine (T3) Ubiquitous Increased metabolism. Mobilization of
energy substrates. Inotropic and
chronotropic effects. Modulates free
testosterone concentrations.
Gonads Testosterone Protein synthesis, primary and secondary sex
(testes) (interstitial cells of characteristics, promotes sperm
Leydig) production. Anabolic effects: promotes
muscle and connective tissue growth.
Gonads Estrogens Sex organs Primary and secondary sex characteristics.
(ovaries) and Increase fat storage, menstrual cycle
adipose regulation. Aids in the development of the
tissue thyroid.
Catecholamines (Sympathomimetic Amines)
Catecholamines secreted by the adrenal medulla are fast-response hormones
involved in the homeostatic regulation of various central and peripheral
functions, including carbohydrate and fatty acid metabolism, appetite,
cardiovascular response, bronchial airway tone, and psychomotor activity
(215, 219). Sympathetic nervous system stimulation is mediated primarily
by the neurotransmitter NEPI; the stress response can simultaneously
activate the adrenal medulla, resulting in increases in both NEPI and EPI in
the circulation (108, 219). The hormonal output of the adrenal medulla is
approximately 20% NEPI and 80% EPI. Although there are some
similarities between the actions of NEPI and EPI at some sites, there can be
both quantitative and qualitative differences depending on the type of
adrenergic receptor activated (Table 3.1) or the ratio of alpha to beta
activation (107, 163, 219). For example, compared to NEPI, EPI has
equivalent or greater effects α receptors, equal effects on β1 receptors, and
much greater effects on β2 receptors (163, 219).
Catecholamines are potent cardiac stimulants, with both inotropic and
chronotropic effects mediated by β1 receptors on the sinoatrial (SA) node
and conducting tissues (108, 219). Heart rate can be accelerated through an
increase in the slow depolarization of the SA nodes during diastole (219). It
is generally believed that increased heart rate after β-adrenergic stimulation
is caused by modulation of ionic channels, particularly Ca++ channels,
located in the surface membrane of conduction fibers (39). Ventricular
arrhythmias, including premature ventricular contractions (PVCs),
tachycardia, and fibrillation, can be caused by endogenous release of
catecholamines, particularly EPI, in a sensitized heart (43, 132, 219).
Increased blood pressure (BP) can be a myocardial sensitizing factor for
catecholamine-induced arrhythmias; thus, factors such as exercise that
simultaneously increase catecholamines and BP may induce arrhythmias
among susceptible individuals (11, 219). Epinephrine can also cause a
decreased T wave amplitude, and large doses can cause S-T segment
depression (EKG) (204, 219).
The vasopressor response is in part mediated by catecholamines; the
exact result depends on the ratio of α to β receptors stimulated in various
vascular beds (180, 219). As a consequence of these observations,
catecholamine response to stress, including exercise, is quite important
(along with other integrative systems) in elevating BP and heart rate as well
as in regulating appropriate blood flow and blood redistribution responses
(108, 170, 216). Changes in blood catecholamine concentrations or receptor
sensitivity as a result of training or overtraining could produce abnormal BP
responses or problems in blood distribution.
Catecholamines have profound effects on metabolism, especially in
influencing the rate of carbohydrate and fatty acid metabolism. Insulin
secretion is inhibited by α receptor stimulation (89, 162, 219).
Glycogenolysis and gluconeogenesis are stimulated via β2 receptors and
mediated by cAMP (162, 180, 219). However, evidence suggests that
hepatic glycogenolysis is mediated by α1 receptors causing an increase in
the cytosolic [K+] and [Ca++] which activates phosphorylase kinase (which
activates phosphorylase) (33, 93, 158). Furthermore, catecholamines may
activate phosphofructokinase (PFK) by both α and β receptor stimulation
(33, 34), particularly in cardiac tissue (34).
Catecholamines stimulate free fatty acid mobilization and blood
concentration by β2-stimulated activation of cAMP and the subsequent
activation of hormone-sensitive lipase. This is an important mechanism for
supplying fatty acid substrate to the working muscle during aerobic
exercise, and during recovery from resistance exercise, (along with growth
hormone).
Catecholamine infusion also increases plasma cholesterol and low-
density lipoprotein cholesterol (LDL-C) (219), suggesting that chronically
raised catecholamine concentrations could influence atherosclerotic events.
Indeed, chronically elevated cortisol has been shown to produce elevated
blood pressure, truncal obesity, hyperinsulinemia, hyperglycemia, insulin
resistance, and dyslipidemia (223). Training can alter both the responses
and chronic elevations of hormones, including catecholamines, reducing the
potential negative effects.
Catecholamines are a primary regulator of CNS energy metabolism
through β2-adrenergic mechanisms, and NEPI is responsible for the
stimulation of accelerated energy requirements in specific areas of the CNS
such as the motor cortex activated during exercise (27, 172).
The effects of exercise on catecholamines are quite apparent. Increases
in NEPI can occur even at relative intensities below 50% VO2max (15, 83).
Serum EPI does not increase appreciably during light exercise unless it is
accompanied by emotional stress (180). However, during more intense
exercise (>60% VO2max), EPI can increase markedly (15, 83). Both NEPI
and EPI have been shown to increase up to 15-fold during anaerobic
exercise (106, 141). Some studies have indicated that NEPI and EPI can
show differential responses to stress, including exercise, suggesting a partial
separation of the sympathetic nervous system and the adrenal medulla (141,
240). Catecholamine responses to exercise appear to be more associated
with absolute intensity than to relative intensity. Appropriate training can
reduce exercise serum catecholamine concentrations at a given exercise
intensity, thus potentially reducing any physiological consequences
resulting from higher catecholamine concentrations (141, 163, 208).
During exercise, the rise in catecholamines supports cardiovascular
adjustments and is partly responsible for the increase glycogenolysis
associated with supplying glucose to fuel the increased metabolic rate (48,
159). As a result, glycogen concentrations would diminish. However, the
effect of catecholamines (and perhaps other hormones) is not limited to the
working muscles. Decreased glycogen concentrations also occur in
nonexercised muscles due to a non-specific catecholamine-mediated effect
(16, 17). Chronically depleted glycogen stores may be related to aspects of
fatigue, overreaching and overtraining.
Generally, training does not markedly affect resting catecholamine
concentrations (244). However, it should be noted that the body position
and time of day may influence catecholamine concentration. Lying and
sitting have often produced concentrations that are markedly lower than
standing. So, it is important in comparisons of athletes or training that blood
is collected at the same time of day and in the same position (64, 244).
Endurance training generally lowers catecholamine concentrations at
absolute loads but produces similar values at submaximal relative
intensities (% VO2max) (95, 244). Cross-sectional studies of weight-trained
athletes such as weightlifters indicate a similar effect (141). Interestingly, at
relative maximal efforts, such as at or near VO2max, high-intensity repeated
sprints or repetitions to failure, athletes, both endurance and anaerobically
trained, tend to produce higher catecholamine responses. Zouhal et al. (244)
suggest this represents a “sports adrenal medulla’ and a more sensitive
autonomic nervous system. In part, this may be explained as the trained
athletes are working at higher intensities at a given percentage of relative
maximum effort. It may also be partially explained by the idea that trained
athletes simply have a greater capacity to produce catecholamines (244),
which could be an advantage during higher intensities of exercise in terms
of energy and cardiorespiratory support.
Cortisol
Cortisol (C) is a steroid hormone secreted by the zona reticularis and zona
fasciculata of the adrenal cortex. Production and secretion are stimulated by
adrenocorticotropic hormone (ACTH), which is released by the anterior
pituitary and regulated by hypothalamic-pituitary feedback mechanisms
(100, 108). Cortisol is the primary stress hormone and is involved in a
number of physiological actions including fuel substrate mobilization,
gluconeogenesis, and immune system suppression. Cortisol generally has
anti-anabolic and catabolic effects (108, 147). These effects are mediated by
gene derepression and RNA synthesis (176). The primary functions of
cortisol are described in the following paragraphs.
Cortisol suppresses the primary immune responses, including inhibition
of the synthesis of interferon, lymphokine, and interleukins 1 and 2, and
depresses the activity of natural killer cells (145, 147). The immune system
is affected by preventing the production of inflammatory mediators,
including suppression of histamine production. Immune system suppression
prevents an “overshoot phenomenon” and the resulting damage in response
to stress (147). Chronic elevations can result in immune system “resistance”
prompting an accumulation of stress hormones and increased production of
inflammatory cytokines that further compromise the immune response
(145). It is possible that long-term strain-stress, which chronically elevates
plasma cortisol, could be related to the appearance of immune diseases,
cancers, or both (183).
Cortisol stimulates gluconeogenesis by mobilizing both fat and protein
(180). Additionally, the rate of muscle glucose uptake can be reduced and
adipocyte lipolysis increased along with the synthesis of adipolytic lipase
(108, 180).
Cortisol is a catabolic hormone, and its administration (or derivatives)
can cause substantial muscle wasting as well as a reduction of bone matrix
and increased calcium loss (114, 115, 180). Cortisol also has anti-anabolic
effects and antagonizes testosterone production (41, 114, 115, 227).
Cortisol may also facilitate release and activity of EPI (an activator of
cAMP) as well as enhance the activity of glucagon, and other
catecholamines. Additionally, cortisol can affect fluid balance by increasing
sodium retention and concomitant potassium excretion (180).
Alterations in cortisol concentration can result in behavioral effects. For
example, Cushing’s disease (increased cortisol) produces euphoria,
insomnia, and restlessness; on the other hand Addison’s disease (decreased
cortisol) produces apathy, depression, and irritability (84). These behavioral
effects could be due to a receptor-mediated response or to changes in the
brain’s electrolyte balance (84, 94). The importance of cortisol can easily be
ascertained by observing adrenalectomized animals. These animals do not
respond well to any form of stress, especially exercise and work capacity is
substantially diminished. They become diseased more rapidly and usually
cannot complete a normal life span without exogenous cortisol
supplementation (84, 180).
Generally, short-term lower intensity aerobic exercise (<60% VO2max)
produces no change or a slight decrease in serum cortisol concentrations
(15, 65, 203) unless the exercise is of long duration (>45 min) (25). The
increase in cortisol with long-term low-intensity exercise is partially in
response to decreased blood glucose concentrations (203). Higher intensity
aerobic exercise (>60% VO2max) and anaerobic exercise can produce
substantial increases in cortisol concentrations (106). High-volume
resistance training sessions result in marked increases in cortisol (114, 115),
especially with large multi-joint exercises (141, 161). Cortisol
concentrations can be elevated for more than an hour post-exercise (141,
202), and the responses are sometimes greater in the afternoon (73). As
with catecholamines, emotional state can modify the cortisol response (137,
234). Severe anxiety before physical exercise (201) or psychological stress
(90) can increase plasma concentrations of ACTH or cortisol, or both, to
concentration as high as those in Cushing’s disease, suggesting that
maximum stimulation of the adrenocortical system can be attained during
extreme emotional states.
In animals, physical training can produce increased serum cortisol and
adrenal enlargement during the first few weeks of adaptation (180). Unless
the animal is otherwise stressed, as training continues, concentrations can
return to normal or slightly below baseline, indicating an adaptation to the
stress (180, 208). This same adaptive response appears to function in
humans as a result of both aerobic (101, 180, 208) and resistance training
(141, 194). Both endurance and resistance training generally reduce cortisol
concentrations at submaximal exercise values (141, 169). However, as with
many hormonal alterations occurring with training, resting concentrations
and response to exercise appear to be related to changes in training volume
and intensity (58, 156, 191). Indeed, severe (very high-volume or intensity)
training can result in adrenal exhaustion in animals (213) and is likely
related to some aspects of non-functional overreaching and overtraining in
humans. Reduced training volume has been reported to produce reductions
in resting cortisol concentrations, sometimes substantial, in a variety of
athletes (18, 92, 156), indicating reduced training strain (155).
Another important factor when considering training-induced alterations
in cortisol is potential season variations. Indeed, substantial seasonal
alterations in overnight glucocorticoids (and catecholamine) concentrations,
as well as saliva cortisol, have been shown to occur in response to
awakening. When not accounted for, these alterations could induce errors in
the interpretation of hormonal variations with training (67).
Testosterone
Testosterone is the primary androgenic-anabolic hormone. It is a member of
the steroid family termed androgens. Androgens are primarily produced and
secreted by the Leydig (interstitial) cells in the testes, although small
amounts are produced by the adrenal cortex and ovaries (108, 189). The
primary mechanism of action of testosterone is through gene derepression
(52, 134). In males, testosterone production is regulated primarily by
gonadotropin, luteinizing hormone (LH), secreted from the anterior
pituitary. Luteinizing hormone stimulates testosterone production via cAMP
(44). Some of the testosterone produced is converted, within the testes and
peripherally, to dihydrotestosterone (DHT), estrone, and estradiol (E2).
These testicular metabolites are also active in the hypothalamic-
hypophyseal negative feedback regulating LH and follicle-stimulating
hormone (FSH) release (Figure 3.2a). The negative feedback system in the
female human is similar to that of the male (Figure 3.2b). Neural
stimulation of the testes also contributes to androgen release (168). In sex-
related tissues, DHT is biologically more active than testosterone (26, 189).
The primary functions of testosterone through gene derepression are as
follows:

Testosterone is largely responsible for the development of male

primary and secondary sex characteristics (androgenic) and has
profound protein anabolic properties affecting nearly every tissue and
organ system, including the central and peripheral nervous systems (8,
116, 171, 189). Testosterone has been shown to activate myogenic
satellite cells (stem cells). Activated satellite cells can cause
myonuclear accretion or fusion with existing muscle fibers to form or
renew myotubes supporting increased muscle CSA (hypertrophy)
(242). Androgens, particularly testosterone, may act by binding with or
inducing changes in glucocorticoid cytoplasmic receptors, inhibiting
the catabolic effects of cortisol and enhancing anabolic effects (138,
214).
Testosterone has been associated with muscle CSA, the magnitude and
rate of force production, and power production (22, 74, 198). The
decline in testosterone with aging appears to be associated with the
decline in neuromuscular performance capacity, including the decline
among women (74).
Testosterone likely promotes a greater glycogenolytic profile in type II
compared to type I muscle fibers and promotes the production of
glycogen synthetase and thus, plays a role in glycogen synthesis (2, 7,
116).
Testosterone and its derivatives have also been related to various
behavioral phenomena, including aggression (189).
Figure 3.2 (a) Feedback system for male reproductive hormones. (b)
Feedback system for female reproductive hormones.
GRF = gonadotropin releasing factor; FSH = follicle-stimulating hormone; LH = luteinizing
hormone; ST = seminiferous tubules; IC = interstitial cells; CL = corpus luteum; F = follicle; G
= granulosa before conversion to CL.
 Low-intensity aerobic exercise (<60% VO2max) has little effect on
serum testosterone concentrations (226), although long-term light (> 45
min) exercise can produce reductions (38) or an increase due to reduced
clearance (31, 65). Decreased serum testosterone concentration as a result
of prolonged low-intensity exercise could be due to a reduced production,
cortisol antagonism or a decrease in sex steroid hormone-binding globulin
(SHBG), or a decreased testosterone-to-SHBG ratio, which would expose
more free testosterone to hydrolytic enzymes (122).
In males, both aerobic exercise (98, 226) and anaerobic exercise (96,
106, 117, 118, 142, 177, 220) result in testosterone increases approximately
proportional to the exercise relative intensity, volume, and the size of the
muscle mass exercised. Women typically show little or no exercise response
(119). The primary mechanism of exercise-induced increases in testosterone
is unclear, but they probably result from catecholamine stimulation of β2
receptors in the testes (45, 97, 98) and not via enhanced LH secretion by the
pituitary (65, 97), or a reduced clearance rate due to decreased splanchnic
blood flow (37, 206). The degree of alterations in response to exercise are
in part dependent on several variables including the type of exercise, sex,
trained state, age, and the volume and intensity of the exercise (167).
However, as the duration of endurance exercise increases (> 45 min),
testosterone concentrations tend to decrease (65), sometimes to levels
below baseline resting concentrations (106).
Conflicting results have appeared from training studies dealing with
resting serum or plasma testosterone concentrations. In animals, long-term
endurance training has produced serum testosterone decreases (42, 70).
Aerobic training in humans has produced no change (49), as well as both
lowered (55, 241) and increased (241), resting testosterone concentrations.
Resistance training has also produced a variety of effects, including no
change or a decrease in sedentary and moderately trained young men (154,
200) and middle-aged men (151) and increased resting testosterone
concentrations in boys (209), young men (185), middle-aged sedentary men
(99), and young women (136). Combined endurance plus strength training
and the effect of diurnal variation (morning versus evening) indicated no
difference in the physiological and performance adaptations (123).
However, among well-trained weightlifters, short-term (1–4 weeks) very
high-volume (increased volume load) resistance training programs can
decrease resting testosterone concentrations (30, 75, 76). Although
perturbations due to changes in volume have been observed, relatively long-
term training in weightlifters and other strength-power athletes appears to
have little substantial effect on resting testosterone (75, 156). Although
findings are somewhat inconsistent, lowering the volume of training among
weightlifters and other strength-power athletes (e.g., tapering) has resulted
in increased resting testosterone concentrations (30). Among younger
weightlifters (14–20 years), both short-term and long-term weightlifting
training can result in increased resting testosterone concentrations and
increased testosterone response to exercise (60, 117, 194).
The changes in hormonal concentrations during long-term training can
be quite subtle (156). While small alterations in resting total testosterone
occur, marked alterations in associated parameters can include increased
free testosterone, free testosterone-to-cortisol ratio (T:C), and total T:C (60,
75–78, 156, 194). Increased total hormone turnover and altered receptor
activity has also been observed (6). The difference in adaptation among
training programs may result from differences in trained state, sex, age, and
general health (117, 241). It likely also results from the type and intensity of
exercise (e.g., weight training [anaerobic] versus jogging [aerobic]) (14, 99,
192) or the size of the muscle mass engaged (114, 117). However, it does
appear that there is a negative relationship between large increases in
training volume or abrupt increases in training volume and resting
testosterone concentrations and other related parameters.
It should also be noted that testosterone has been shown to have marked
short-term effects through activation of cell membrane receptors and
intracellular signals (9, 149, 225). The long-term effects (gene derepression)
tend to target protein metabolism, skeletal muscle growth, and neural
development. The short-term effects (intracellular signals) tend to deal with
activation of lipid and protein synthetic pathways, energy metabolism,
neuron activation, muscle electrophysiological properties, motor system
activation and function, and particularly, behavioral aspects such as
aggression and arousal (9, 36, 119, 149).
In many sports, gaining muscle mass, strength, and power are important
factors that can impact performance. The potential to gain muscle mass, and
perhaps strength, as a result of resistance training has been associated with
testosterone and both short- and long-term mechanisms (9, 214).
Additionally, along with testosterone-related factors such as T:C appear to
be related to alterations in body composition and performance in both men
and women (72, 79, 80, 156, 185).
The T:C ratio has been associated with the general anabolic or catabolic
state (1) and LBM, as well as to measures of strength-power performance
(78, 112, 156). These relationships may partially explain and characterize
the importance of the balance between androgenic-anabolic activity
(testosterone) and catabolic activity (cortisol) during prolonged strength-
power training (5, 187).
Exercise appears to have little effect on the T:C, with resting values
being similar to the post-exercise response (60, 194). However, stressful
(high-volume) weight training has been associated with reductions in
testosterone and the T:C and T:SHBG ratios with a simultaneous increase in
LH (78). During periods of “normal” or reduced training, cortisol and LH
concentrations decrease (78). The stressful training resulted in a fall in
strength performance.
Long-term strength training may or may not increase the resting and
exercise response values for the T:C (58, 60, 194). However, alterations
(sometimes subtle) in the T:C accompanying strength training programs
have resulted in moderate to strong correlations with strength performance
(6, 30, 59, 73, 75, 112, 156). As with other endocrine parameters, training
intensity and particularly volume appear to have a strong influence in
changes in these ratios and their relation to performance (92, 156). For
example, Figures 3.3a and 3.3b (unpublished data) shows the T:C ratio
among national-level American weightlifters over a 12-week period; note
that the changes in T:C tend to be inversely related to the alterations in
training volume (volume load). As a result, T:C (and T:SHBG) may be
relatively sensitive indices reflecting the stress response to training strain
and perhaps overall stress manifestations. Thus, changes among individual
T:C or T:SHBG may be an index for poor fatigue management, non-
functional overreaching or the overtrained state (5, 75, 156). Additionally,
the T:C may be an indicator of “preparedness” in relation to physical
performance (92). For example, if the T:C is high, then an athlete has a
greater potential to perform well than if the T:C is low (156). A training
taper may increase the T:C sometimes beyond baseline (i.e.,
supercompensation effect), thus potentially augmenting preparedness (92)
(Figure 3.3).
Figure 3.3 The testosterone-to-cortisol ratio (T:C) versus volume
load over 12 weeks in four female (a) and four male (b)
weightlifters. Generally, volume and the T:C are inversely
related. The T:C was higher than baseline values after a
taper, possibly indicating a supercompensation effect.
Alterations in women are more a function of C alterations,
in males both alterations in T and C.
Estrogens
Estrogens are a family of steroid hormones that are primarily produced and
secreted in the ovaries; however, other tissues including the placenta,
adrenal cortex, liver, skeletal muscle, and particularly fat can also form
estrogens. Small amounts of estrogens are also produced in the testes (29,
148). The primary mechanism of action of estrogens is through gene
derepression. Estrogens are formed as a result of the aromatization of the A
ring of either androstenedione or testosterone, a reaction catalyzed by the
enzyme aromatase. The primary estrogens are estrone, estriol, and estradiol
(E2), which has the greatest estrogenic activity.
During the menstrual cycle, production and secretion of estrogens by the
ovaries is regulated by cyclical LH and FSH production of the pituitary. LH
stimulates androgen production by the follicle during the follicular phase
(days 1–13); during the ovulatory phase (day 14), there is a large surge in
FSH that subsequently influences the conversion of androgens to estrogens
by the corpus luteum in the luteal phase (days 15–28). Thus, the menstrual
cycle consists of two phases and double peaks in estrogen concentrations
over an average of 28 days (Figure 3.4). Because of the cyclical fluctuation
in estrogens and other hormones, as well as normal individual variation, it
is difficult to ascertain the exact estrogen status of a woman at any one
point in time (29). Estrogens stimulate primary and secondary female
characteristics and fat accretion and have marked metabolic effects (46).
Figure 3.4 The “normal” menstrual cycle. Note that testosterone is
essentially at a constant concentration except near
ovulation.
Source: Modified from Wilmore and Costill (230).

The primary effects of the estrogens include (29, 108, 148, 163):

Feminization patterns in girls at puberty, which includes directly

stimulating the growth and development of the primary and secondary
sex tissues.
Retention of salts, water, and nitrogen and have weak protein anabolic
properties. Estrogens also promote bone mineral incorporation and
increased bone strength.
Modification of blood lipid profiles, resulting in lower total cholesterol
and higher HDL2 cholesterol and triglyceride concentrations.
Additionally, normal physiological concentrations of estrogens appear
to produce beneficial effects for glucose tolerance.
Metabolic effects include increased lipolysis in muscle and fat tissue
and decreased rates of gluconeogenesis and glycogenolysis. Estrogen
 effects on gluconeogenesis are partially related to its stimulation of an
increased insulin-to-glucagon ratio (I:G).

Assessing the effects of exercise or training on estrogen concentrations can

be quite difficult. However, the general pattern of response of estradiol (also
progesterone and gonadotropins) appears to be small increases in
concentration as the intensity of exercise rises, which can occur
independently of menstrual cycle phase (102, 163). The increased estradiol
may be partly a result of plasma volume shifts and changes in clearance
rather than increased production (28, 206).
Findings on short-term aerobic training effects have been equivocal at
best (29, 163). Long-term resistance training does not seem to markedly
affect resting E2 concentrations in women (186); however, other studies of
women involved in high-volume training programs such as distance running
and gymnastics have noted lower E2 concentrations, which have been
associated with athletic amenorrhea (88, 104). Athletic amenorrhea (absent
menses) can be associated with aberrant blood lipid profiles and bone
mineral loss (88, 104, 125, 163). It should be noted that some evidence
indicates that postmenopausal women using estrogen replacement tend to
carry less abdominal fat, have a more favorable lipid profile, and may be
less likely to develop metabolic syndrome compared to those receiving not
estrogen replacement (69).
As a result of aerobic training, increased E2 production has been noted
among males; concomitant to testosterone reductions (55) and decreases in
E2 concentrations were observed among middle-aged sedentary males after
a short-term weight training program (14). Interestingly, some evidence
indicates that increased E2, or an increased E2-to-testosterone ratio,
increases the risk for cardiovascular disease in males (160).
As a fuel substrate, women have been shown to use less carbohydrate
and more fat during aerobic exercise compared to men (205), an effect
consistent with the properties of E2. Estrogen supplementation has been
shown to augment this effect (29, 46) and can also increase endurance as
measured by treadmill time in both male and female animals (105).
Estrogen supplementation has been used in postmenopausal women to
reduce bone mineral loss, with varying degrees of success (29);
additionally, supplementation of both E2 and progesterone may be related to
strength increases in women (85). These effects suggest that estrogens may
be a potential ergogenic aid.
Growth Hormone (Somatotropin)
Growth hormone (GH) is a polypeptide released in a pulsatile fashion by
the anterior pituitary. The release can be modified in response to a variety of
stimuli including emotional stress, fasting, sleeping, certain amino acids,
certain drugs, and exercise (190). Its release is activated by growth
hormone-releasing factor (GH-RF), which is secreted by the hypothalamus.
Growth hormone interacts with insulin-like growth factors (IGF), which are
primary effector hormones for protein synthesis. These two hormones (GH
and IGF) regulate each other’s secretion in a feedback system, possibly
including GH-RF and the stimulation of somatotropin releasing inhibitory
factor (SRIF or somatostatin) in the hypothalamus (115, 127). There are
several isoforms of GH, and it appears that their effects are mediated
through a single receptor, although more research is necessary to fully
evaluate this phenomenon (119).
Growth hormone(s) functions to stimulate anabolism in nearly all tissues
(115, 119, 127). This is primarily accomplished through IGF1 or
somatomedin C (20, 53, 127). Long-term exposure to relatively high
concentrations of GH can result in acromegaly, a condition in which all
tissues show substantial enlargement and deformity and sometimes
gigantism. The primary effects of GH include:

Promoting a positive nitrogen balance and growth in all tissues (53).

Testosterone may enhance the pulsatile release of GH (129), and these
two hormones appear to work synergistically in promoting muscle
growth and development (179). Additionally, there is evidence that
IGF1 may be active in promoting skeletal muscle satellite cell
proliferation (40, 119).
Stimulating lipolysis through hormone-sensitive lipase via cAMP.
Growth hormone is antagonistic to insulin.
Growth hormone increases (often after several minutes) as much as 20- to
40-fold in response to both aerobic and anaerobic exercise. The final serum
concentration appears to be related to both duration and intensity of the
exercise, sex, age, and the size of the muscle mass involved (106, 114, 119,
180, 211). The concentrations may increase to a greater extent as a result of
intermittent anaerobic exercise compared to other exercise forms (58, 211).
Multiple training sessions per day do not appear to alter the GH response to
exercise (76). Growth hormone can remain elevated for 30 min or longer
post-exercise (118, 119, 141). However, the trained state can substantially
influence the exercise and post-exercise responses of GH. Well-trained
aerobic and anaerobic (weightlifters) subjects have demonstrated muted GH
responses to standardized exercise and a faster recovery to baseline (141,
180, 206).
Insulin
Insulin is a peptide hormone synthesized and released by the beta cells in
the islets of Langerhans of the pancreas. Insulin production and release are
controlled by a complex interplay of nutrients, gastrointestinal hormones,
and various other hormonal and neural stimulus-inhibitory factors (115,
126, 165). Glucose appears to be the only physiological stimulus for both
synthesis and secretion (126). However, this effect is mediated by
gastrointestinal hormones, especially gastric inhibitory peptide, which is
similar in structure to glucagon (165). Both EPI and NEPI can inhibit
insulin secretion by α-adrenergic mediation, although selective β2 receptor
activation can stimulate secretion (126). The primary functions and
properties of insulin include (108, 115, 126, 135, 224):

Increasing cell membrane permeability to glucose, amino acids, and

free fatty acids, and promoting the storage of energy substrates.
Promoting cell division and growth through its mitogenic effects.
Having anticatabolic properties (as an anabolic hormone), and
generally promoting growth.
Underlying mechanisms of insulin action may include insulin–cell
membrane receptor-mediated increases in cGMP, activation of IGF
receptors, a decreased activity of adenylate cyclase, activation of
phosphodiesterase, a decreased activation of cAMP, an increased
activity of glycogen synthetase, increased polyribosome formation,
and activation of membrane-bound lipoprotein lipase (86, 115, 126,
135).
It is antagonistic to glucagon and GH (126).

Aerobic exercise lasting less than 5 min has little effect on resting serum
insulin concentrations (124). Long-term aerobic exercise can result in
decreased serum insulin, as much as 50% (232). This exercise-induced fall
in insulin concentration is believed to be due to a decreased secretion by the
pancreas as a result of α-adrenergic stimulation (95) as well as increased
working muscle uptake. Short-term (<2 min) anaerobic exercise has
produced substantial increases in serum insulin concentrations; the
mechanisms are unclear, but may be related to the short-term high-intensity
exercise-induced increase in glucose (106). However, intermittent anaerobic
exercise (30 min of weight training) has been shown to produce decreases
in insulin like those observed with aerobic exercise. This decrease occurred
even though glucose was elevated (141). The post-exercise decrease in
insulin may persist for several hours or until a meal is eaten (141).
Well aerobically trained (124, 232) and weight-trained (141) subjects
had lower insulin concentrations at rest and during exercise. Although
short-term training studies using animals agree with the observation of
reduced insulin concentrations in trained humans (233), short-term training
in sedentary human subjects does not always produce similar responses
(71), suggesting that the trained response may require a substantial time to
develop. Insulin concentrations differences resulting from exercise may be
partially related to lower catecholamine responses noted among trained
versus untrained subjects (83).
Both aerobic (13, 124) and anaerobic training (141, 144, 224, 238, 239)
appear to enhance insulin sensitivity and glucose tolerance. Several factors
may be responsible for these observations, including an increased number
of insulin receptors, an increased muscle mass, and a decrease in the ratio of
body fat to LBM (144, 238). Some evidence indicates that resistance
training may have some advantages in that it increases the number of
insulin receptors (increased muscle mass), reduces inflammation, may
positively alter lipid profiles, increases insulin signaling, and alters body
composition (157, 199, 237).
Glucagon
Glucagon is a peptide hormone secreted from the alpha cells in the islets of
Langerhans of the pancreas. Glucagon functions in energy substrate control,
particularly for glucose. The primary regulation of glucagon appears to
occur through stimulation or inhibition by nutrients (108). A rise in serum
glucose results in a reduction in serum glucagon, and vice versa (107, 126).
In animals, fatty acids and ketones inhibit glucagon secretion and glucose
metabolism (126). Gastric inhibitory peptide (GIP) and secretin are released
as a result of gastrointestinal and hormonal signals; GIP may stimulate
glucagon secretion, while secretin may decrease glucagon secretion (126,
210). Glucagon is also stimulated by the sympathetic nervous system and
sympathomimetic amines (126). Glucagon has several primary effects
including (109, 126, 202, 210):

Antagonism of the actions of insulin.

Serving to mobilize energy substrates (i.e., glucose and fatty acids).
Having thermogenic and anorectic effects.
Being mediated by cAMP, and its metabolic effects in the liver and
adipose tissue are essentially similar to those of EPI.

Both animal studies and human studies (107, 131) show that serum
glucagon concentration increases with prolonged (>1 h) aerobic work.
Animal and human studies suggest that a catecholamine response causes the
rise in glucagon during prolonged exercise (63, 206); however, in humans,
decreased blood glucose concentrations appear to be the more important
factor (124, 206). Short-term anaerobic work produces little change (218)
or a delayed post-exercise increase (62). Weight training exercise also
produces a delayed post-exercise increase in glucagon concentration (141,
212).
Both aerobically trained and resistance-trained subjects display muted
glucagon responses to exercise at both absolute and relative intensities (71,
141, 231). The training adaptations may occur in response to training-
induced reductions in serum catecholamines. However, adrenergic receptor
blockade does not markedly alter the typical glucagon response to exercise
(206). Training does not appear to cause major alterations in the serum
glucose response to exercise (124). Therefore, the muted exercise response
post-training may be unrelated to either serum catecholamine or glucose
concentrations, and the exact mechanism remains unclear (141).
Hormone Function During Resistance Exercise
and Training
The basic response of a hormone to exercise, including resistance exercise,
is an increased concentration, which is dependent on intensity, duration, and
size of muscle mass. Indeed, many hormones, such as catecholamines,
clearly display an exercise intensity threshold after which hormonal
concentrations exhibit a sharp increase. The only major exception is insulin,
which typically shows a decline in concentration with exercise. Training
generally results in a muted response to an absolute submaximal intensity of
exercise and a shorter time to return to baseline values suggesting greater
sensitivity (107, 141, 161). With the exception of GH, compared with lesser
trained, well-trained subjects produce similar or higher hormonal responses
at relative intensities (107). Furthermore, responses to near-maximum and
maximum efforts are typically higher in trained subjects (107, 141). These
training adaptations appear to alter the acute physiological response to a
given submaximal level of exercise in a manner indicating reduced
physiological and perhaps psychological stress.
Although there is considerable overlap at times, hormone function can
be divided into (i) substrate control and mobilization, and (ii) anabolic and
catabolic actions.
Table 3.3 shows the primary hormones affecting substrate control and
mobilization during resistance exercise, which includes catecholamines,
cortisol, insulin, glucagon, GH, and thyroxin. Ratios of hormones having
antagonistic effects are often better indicators of the control of metabolic
actions than individual hormones. For example, the insulin-to-glucagon
ratio (I:G) may be a better indicator of blood glucose control than either
hormone alone (103, 141, 229). During resistance training exercise,
substantial increases in serum concentrations of lactate and glucose can
occur (141, 211). These metabolic exercise responses result from energy
production (fast glycolysis) and the mobilization of glucose through
glycogenolysis. There is little doubt that the neuroendocrine system is
activated to aid in driving these responses (107). Hormonal responses
involved in supporting the short-term metabolic alterations resulting from
resistance exercise would include catecholamines, glucagon, thyroxin, and
perhaps cortisol as it potentiates the release of EPI (Table 3.3).

Table 3.3 Hormone metabolic effects

Process Positive effect Negative effect
Blood glucose Glucagon Insulin
Catecholamines
Cortisol
Blood glucose uptake Insulin Glucagon
Glycolysis Catecholamines Glucagon
Growth hormone
Muscle glycogenolysis Catecholamines Insulin
Growth hormone
Liver glycogenolosis Glucagon Insulin
Catecholamines
Glycogen synthesis Insulin Catecholamines
Testosterone Glucagon
Lipolysis Thyroxin Insulin
Catecholamines
Growth hormone
Glucagon
Triglyceride synthesis Insulin Catecholamines
Sources: Based on Hoffman (91); Kleine and Rossmanith (108); Lefkowitz and Caron (128);
Powers and Howley (163).

Post-exercise, responses include free fatty acids (FFA) mobilization and

the initiation of glycogen replenishment. Growth hormone, catecholamines,
and cortisol all likely have an effect on mobilizing FFA, partially supporting
recovery needs (141, 143). Blood glucose homeostasis maintenance post-
exercise requires reductions in the I:G (56, 235). Glycogen recovery post-
exercise is partially a function of insulin. Insulin (and exercise) increases
the uptake of glucose and stimulates glycogen, protein, and fat storage. The
concentration of insulin during and after exercise can be enhanced by
carbohydrate, protein, and particularly carbohydrate-protein
supplementation; higher concentrations of insulin stimulate a faster rate of
glycogen repletion (12, 110, 243). Furthermore, testosterone can affect
glycogen synthesis and restoration post-exercise in that it increases the
production of glycogen synthetase.
Anabolic hormones that act in restructuring and remodeling muscle and
connective tissue include testosterone, GH, IGF1, and insulin, and perhaps
to a small extent, estrogens in women and the catabolic hormone cortisol. A
very complex interplay of nutrients, the immune system, and the
neuroendocrine system is required to remodel connective and muscle tissue,
including exercise induce repair of damage and for the hypertrophy process.
As muscle CSA is related to performance (i.e., strength, power) (32,
195), an important question regarding hormonal exercise responses and
training adaptations concerns the extent to which these hormones affect
tissue remodeling and hypertrophy. It is commonly believed that higher
repetitions per set (8–15), short rest periods (≤1 min) between sets, and
multiple sets per exercise stimulate muscle hypertrophy to a greater extent
than other methods of training. Short-term studies have shown that
resistance training using high repetitions and short rest periods produced
greater increases in several anabolic hormones, especially GH and
testosterone (66, 113, 118, 182). Higher repetitions engage fast glycolysis to
a greater extent than do lower repetitions, and the resulting lactate
production may influence hormonal (particularly human GH) responses
(130, 212). Evidence suggests that among untrained and moderately trained
men, over a short term, multiple-set training with higher repetitions per set
(8–12) may stimulate hypertrophy to a greater extent than lower repetitions
with higher intensities or very high–low-intensity repetitions per set (196).
Data also indicate that increased volume created by multiple sets can
produce greater hormonal responses and greater hypertrophy than a lower
number of sets at least to a point (35, 146, 174). Indeed, evidence indicates
that resistance training volume is a primary factor in producing
hypertrophy, although strength and power are more function of intensity
(50, 57, 174). Furthermore, Kraemer (114) presented a reasonable argument
that the interaction of resistance training exercise variables and changes in
hormone concentrations may stimulate protein synthesis and tissue
remodeling.
However, several observations suggest that the link between hormone
responses to exercise and tissue remodeling is a best unclear:

Most (and perhaps all) hormonal responses observed as a result of

resistance exercise also occur as a result of aerobic exercise,
particularly aerobic exercise near VO2max; however, aerobic exercise
is not known to be a particularly potent stimulus for tissue hypertrophy
(188). It should be pointed out, however, that the adaptive interactions
between the hormonal responses and the stimuli offered by different
types of exercise may differ and therefore, the hypertrophy response or
adaptation will differ.
Small muscle mass exercises such as biceps curls do not result in
marked hormonal responses compared to large muscle mass exercises
(117); indeed, hormonal responses may be quite small. However,
training with these small muscle mass exercises still produces
substantial hypertrophy in the trained muscles.
Bodybuilders tend to train with short rest periods “to get a better
pump,” and use higher repetitions per set in the belief that this may
augment the hypertrophy response (207). Part of the reason for the use
of short rest periods must do with the potential to augment hormonal
responses to resistance exercise (114); this in turn is believed to
augment hypertrophy. However, there is no convincing evidence that,
within a commonly trained muscle, the average cell size in advanced
bodybuilders is significantly larger than that of advanced powerlifters
or weightlifters who do not consistently train with short rest periods or
high repetitions per set (61, 193, 207). Nor is there convincing
evidence that short rest periods increase the hypertrophic response
(175). For example, using moderately trained young males, Nimmons
(152) compared the gain in CSA of quadriceps muscles over 9 weeks
of training using short (30 s) and long (3 min) rest periods; no
difference was noted in the average gain in thigh circumference or the
 CSA (magnetic resonance imaging, MRI) of the quadriceps or of any
individual muscle. If the short rest period hormonal responses were
greater than the long rest group, these results suggest that the
hypertrophic adaptations were not augmented by hormonal responses.
Since there is substantial evidence that hormonal responses may be
involved with metabolic responses to exercise (107, 108), it is possible
that there will be little or no effect on the hypertrophic mechanisms
resulting from hormone responses to exercise. Basically, this means
that if a molecule of a specific hormone interacts with a receptor that
functions in a metabolic activity, it cannot simultaneously activate
receptors involved in tissue remodeling. Thus, some of the hormone
molecules released as a result of exercise will be “tied up” modulating
metabolic reactions. However, it is possible that there are different
isoforms of hormones, some having greater or smaller anabolic
properties and responding to different stimuli (i.e., high vs. low
intensity) (119).
Studies of exercise-induced hormonal responses and hypertrophy are
at best equivocal. Considerable evidence does not indicate a strong
relationship between hormonal responses performance and
hypertrophic adaptation (87, 140, 173, 221). On the other hand, several
investigators indicate that both resting and exercise responses strongly
correlate with both strength and hypertrophy gains (3, 82, 119, 164,
184).

In the authors’ opinions, it is illogical to believe that hormonal responses

have no effect; however, until more data are available, we must conclude
that hormonal responses to exercise likely have relatively minor influences
on muscle or connective tissue hypertrophy. This suggests that the critical
factor in gaining a marked hypertrophy adaptation may not be the hormonal
response to exercise but rather other factors such as the immune system
response, metabolic, hormonal adaptation, paracrine and autocrine
responses (222, 236), and particularly tension and stretch (19, 111, 121,
217). Although hormonal responses to exercise may not be the critical
factor related to alterations in size and function, it must be pointed out that
these responses may not be inconsequential. Thus, training routines that
maximize the hormonal responses may play a positive role in tissue
remodeling. Maximization of the training session could include several
elements:

Volume. Although some short-term studies have not substantiated a

volume effect (154), most studies indicate that greater volumes of
work – which typically result in larger hormonal responses (66) –
generally augmenting the hypertrophy gains afforded by resistance
training (51, 133, 166, 196, 228). These larger volumes of work are
generally accomplished using relatively high repetitions per set (6–12)
and multiple sets (193, 197).
Size of the muscle mass exercise. Multi-joint large muscle mass
exercises stimulate greater hormonal responses than using single-joint
and smaller muscle-mass exercises (114, 117).
Power output. Maintaining higher power outputs during the exercise,
independent of repetitions per set, may enhance the production of
testosterone; higher repetitions per set may enhance the accumulation
of GH (21), perhaps because of a greater lactate accumulation (68).

Chronic hormonal alterations likely play an important role in tissue

hypertrophy development, as well as in gains in strength and power (119).
Chronic hormonal adaptations may have a greater effect on tissue
hypertrophy. A chronic elevation of the resting concentrations of an
anabolic hormone, or the decrease of a catabolic hormone, would allow a
greater opportunity for chronic exposure of the receptors involved in
protein synthesis and muscle remodeling to occur. This chronic hormonal
alteration, coupled with periodic muscle damage stimuli resulting from
resistance training exercise, could enhance the possibility of a hypertrophic
adaptation. Support for this contention comes from two areas. First, studies
indicate that chronically increased androgen concentrations can alter muscle
size and function (198). Second, as previously noted, studies using both
 men and women have related subtle chronic alterations in resting hormone
concentrations to changes in muscle size and strength (4), particularly for
testosterone and the T:C (59, 72, 185). Figure 3.5 offers a sequential model
of events for the interaction of major factors involved in tissue hypertrophy
because of resistance exercise.

Figure 3.5 Theoretical mechanisms of tension/stretch, metabolic,

endocrine, immune, and paracrine or autocrine response
and their effect on tissue remodeling and performance
alterations because of training.
Source: Based on Stone et al. (195).
Chapter Summary
The neuroendocrine system is primarily responsible for regulating
homeostasis. The neuroendocrine system acts by releasing
neurotransmitters and hormones that can interact with a specific set of
receptors. Activation of these receptors results in a specific response,
altering metabolism.
Endocrine glands release hormones that have multiple effects ranging
from substrate mobilization or storage of fuel sources to anabolic and
catabolic actions. Exercise typically causes concentrations of hormones
(except insulin) to increase. These increases are generally dependent on
exercise intensity. Training typically produces muted absolute submaximal
exercise intensities. At maximum efforts, the response is typically higher in
trained subjects as a result of their ability to exercise at higher absolute
intensities.
Training can result in substantial adaptations in physiology and
performance characteristics. These chronic effects may reflect the manner
in which the neuroendocrine system functions (i.e., muted hormonal
responses and greater hormone sensitivity), or they may reflect adaptations
partially mediated by the neuroendocrine system (i.e., muscle CSA). The
physiological responses and adaptations resulting from altered
neuroendocrine function during exercise or from training should be viewed
as a complex interaction of a variety of neural and hormonal factors, and
not simply the effects of isolated hormones or neurotransmitters.
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4 Nutrition and Metabolic Factors

DOI: 10.4324/9781003096139-6
Introduction
Since the late 1970s, studies of vitamin, mineral, fat, carbohydrate, and
particularly protein needs for exercise and training have brought about a
reevaluation of nutritional needs and a restructuring of diets for athletes. As
a result, sport nutrition has become one of the most thoroughly investigated
areas of sport science. The diet of athletes – specifically, what they eat, how
they eat, and when they eat – can have significant effects on both their
health and performance. Poor nutrition may lead to non-beneficial
adaptations to training (and health), such as poor recovery and potentially
overtraining. Therefore, it is important that sport scientists work with sport
nutritionists and registered dieticians to design and implement a dietary
strategy that will help supply an athlete with the necessary amounts of
energy to train, compete, and recover while achieving training goals that
may contribute to their performance (e.g., increased muscle mass, fat loss,
etc.). In this light, knowledge relating to the consumption of both
macronutrients (protein, carbohydrates, and fats) and micronutrients
(vitamins and minerals) is warranted. The goal of this chapter is to provide
an overview of various nutritional and dietary aspects, particularly those
that may impact an athlete’s performance.
Energy Expenditure and Energy Intake
Energy, typically measured in kilocalories (kcal), may be defined as the
ability or capacity to perform work (205). A kcal is the energy required to
increase the temperature of one kilogram of water by one degree Celsius.
The total cost of energy and the rate of energy expenditure are related to
several physical, physiological, and performance factors such as the
intensity and duration of exercise. Simply, as exercise intensity increases,
the rate of energy expenditure also increases. In addition, as more total
work is completed, more kcal are used. It should be noted, however, that
energy expenditure from exercise is directly or indirectly influenced by
body mass and composition and the efficiency of substrate mobilization.
Researchers have indicated that energy expenditure from exercise also
has effects on post-exercise energy consumption and recovery parameters
(38). In addition, the summative effects of energy expenditure as a result of
training appear to be related to several training adaptations that include
altered body mass and composition, serum lipids, cardiovascular function,
and sport performance (202). Based on these relationships and training
effects, reasonable rates of energy consumption and energy cost may be
estimated for various activities (Table 4.1). This information may be
valuable to sport scientists and coaches when designing training programs
for their athletes. It should be noted that some of the values listed within the
table may provide wide ranges of energy expenditures. These results are
due, in part, to differences in body mass, exercise intensity, training
intensity, intermittent activity, and practical aspects of sports (e.g., linemen
vs. backs).

Table 4.1 Caloric (kcal) cost of various physical activities

Activity Caloric cost (kcal
min–1)
 Activity Caloric cost (kcal
min–1)
Daily living Lying supine 1
Sitting 1–1.5
Standing still 1–1.5
Sport-based Basketball (mean values for a game) 3–15
activities Cycling (4 km h–1) 7–8
Football (during activity) 6–15
Jogging (160 m min–1) 7–9
Sprinting (maximum running) 18–22
Volleyball (mean values for a game) 3–7
Resistance Circuit priority training 5–10
training Large muscle mass exercises 6–18
Small muscle mass exercises 3–7
Combined large and small muscle mass exercises (large 9–10
muscle mass emphasis)
Source: Based on American Alliance for Health, Physical Education, Recreation and Dance (4);
Hunter et al. (108); Nicolette (156); Scala et al. (179); Stone et al. (205); Wilmore and Costill
(234).

There may be a reduction in health risk based on exercise volume and

intensity thresholds (151); however, individual responses to exercise may
modify these results. While the suggested intensity threshold is
approximately 7.5 kcal min–1, and the volume threshold ranges from 500–
2000 kcal week–1, it should be noted that training programs costing more
than about 2000 extra kcal week–1 may provide performance benefits but
are unlikely to further affect health parameters. Based on the energy
expenditures associated with different activities and sport training (Tables
4.1 and 4.2), it is obvious that several different activities, including weight
training, can meet the intensity and volume threshold requirements as long
as the activity is performed in a vigorous manner and the volume of training
is high.

Table 4.2 Caloric (kcal) cost and consumption of various sport activities
Activity Caloric cost (kcal kg–1 day–1) Caloric consumption (kcal day–1)
Activity Caloric cost (kcal kg–1 day–1) Caloric consumption (kcal day–1)
Untrained <40 2000–3000
Basketball 55–70 5000–6000
Judo 55–65 3000–6200
Marathon 50–80 2500–6000
Sprinting 55–65 4300–6000
Throwing (field events) 60–65 6000–8500
Weightlifting 55–75 3000–10,000
Values based on men; women’s values are typically 10–25% less.
Source: Based on McMillan et al. (147); Scala et al. (179); Stone et al. (205); Wilmore and Costill
(234).

Due to the frequency and intensity of training sessions, the energy cost
of training for sport is typically much greater than that necessary (or
practiced) to provide for good health. For example, athletes such as elite
weightlifters and throwers may train 2–3 times per day and 4–6 times per
week during a preparatory phase. Due to the accumulative amount of work
performed during these sessions, this type of training requires a large
amount of energy to complete. Thus, it important that sufficient kcal are
consumed to balance out the energy expenditure cost to reduce the potential
for detrimental training effects such as overstress or overwork (204) and a
loss of body mass or lean body mass (LBM). While Table 4.2 displays
typical caloric expenditures and consumptions, it should again be noted that
some sports may have a wide range of values due to differences in body
mass, training intensities, and volumes of exercise and training. For
example, a football lineman will likely expend more energy performing the
same training routine at the same relative intensities as a wide receiver and
would thus, require greater energy consumption at the conclusion of the
workout. Additional factors such as the size of the muscle mass, length of
inter-set rest, and post-exercise energy expenditure should also be
considered when it comes to the rate of energy expenditure and total energy
cost. Simply, large muscle exercises and/or short rest periods may increase
the energy expenditure of a training session.
 Energy expenditure is typically influenced by four primary factors that
include basal metabolic rate (BMR), the thermic effect of food (TEF), the
thermic effect of physical activity (TEA; i.e., the energy used during
exercise), and adaptive thermogenesis (AT). Briefly, BMR may be defined
as the necessary energy required to maintain homeostasis at rest. BMR is
typically measured within a laboratory setting in a fasted state where the
participant is isolated, recumbent, and free from medications and stress
(140). However, due to the inconvenience of an overnight stay in the
laboratory to measure BMR, and its within 10% agreement, resting
metabolic state (RMR) is often used as an alternative. In contrast to BMR, a
RMR measurement requires a participant to rest in a usually fasted state for
a specified period of time before metabolism is measured. It should be
noted that RMR accounts for a smaller percentage of daily energy
expenditure among athletes (20–45%) compared to sedentary participants
(174, 218). This may partially be due to several modifying factors that
include age, sex, body mass, LBM, trained state, and heredity.
The TEF, typically measured in a metabolic chamber, may be classified
as the extra energy expended above the RMR that results from food
consumption during the day, including digestion, absorption, transport,
metabolism, and storage (6–10% of total energy expenditure per day).
Women typically fall on the lower end of the TEF range with expenditures
of about 6–7% above RMR (140). Although the TEF concerns the
cumulative effect of eating throughout the day, it may be difficult and time-
consuming to assess with many athletes. As a result, most researchers have
decided on measuring the thermic effect of a meal (TEM), which can last
several hours after a meal and is influenced by meal composition. For
example, the TEM of carbohydrate, fat, and protein is approximately 5–
10%, 3–5%, and 20–30%, respectively (69).
The TEA represents the energy expenditure above RMR that is required
by physical activity and may include activities of daily living, planned
exercise, and involuntary muscle actions such as shivering. The TEA is
quite variable and may represent as little as 10% of total energy expenditure
in sedentary individuals and as much as 50–60% in athletes (140).
 The AT is the result of several factors that modify the three primary
thermic effects (RMR, TEF, TEA). These factors may include growth,
pregnancy, environmental temperature, altitude, medication, drug use (e.g.,
alcohol, methylated xanthines, smoking), and physical and emotional stress
(140).
Caloric Density and Nutrient Density
The amount of energy metabolically liberated from food is based on its
molecular structure. Protein and carbohydrate yield approximately 4 kcal g–
1, and fat about 9 kcal g–1. These values are typically termed as

physiological fuel values (PFV) and represent averages of different

molecules of each food type. Using these values, it is possible to calculate
the energy intake within a specific diet by adding up the grams of protein,
carbohydrates, or fat ingested and multiplying them by the PFV associated
with the food type. From here, the percentages of total kcal eaten can be
calculated for each food type if the total caloric value is known. For
example, if a 100 kg athlete consumes 100 g of protein, 600 g of
carbohydrate, and 130 g of fat, then the total calories taken in are as
follows:

protein = 100 g × 4 kcal g–1 = 400 kcal

carbohydrate = 600 g × 4 kcal g–1 = 2400 kcal

fat = 130 g × 9 kcal g–1 = 1170 kcal

total kcal = 3970 kcal

These are the percentages of each food type (as calories):

protein = 400 ÷ 3970 = 10.0%

carbohydrate = 2400 ÷ 3970 = 60.5%

fat = 1170 ÷ 3970 = 29.5%

It should be noted that adjustments may be made to ensure that each food
type reflects a specific percentage of the total diet. In addition, adjustments
may be needed to allow an athlete to gain or lose mass based on their
training goals. For example, if an athlete seeks to lose fat mass, a smaller
percentage of fat and/or carbohydrates within the diet may be recommended
and the total kcal calculated to determine specific food options.
Another aspect of nutrition that is important to mention due to its impact
on food choices is nutrient density. Nutrient density refers to the amount of
macro- and micronutrient(s) present in a food per calorie. For example,
meat and many vegetables are dense as they contain high concentrations of
energy as well as vitamins and minerals. In contrast, many packaged and
processed foods containing mostly sugar, salt, and preservatives lack a
similar nutrient density. While larger athletes that consume more food
typically do not have an issue with nutrient density, smaller athletes that
consume fewer kcals may have to pay more attention to micronutrient
(vitamin and mineral) content.
Recovery Energy Expenditure
A common factor of exercise energy expenditure that is often overlooked is
what occurs post-exercise, also known as recovery energy expenditure (see
Chapter 2). Researchers have indicated that the intensity of steady-state
aerobic exercise may have a greater effect on recovery energy expenditure
than duration (13, 14, 30, 186). Furthermore, higher intensities resulted in a
greater magnitude of recovery energy expenditure compared to lower
intensities (38, 121), likely due to a greater disruption of homeostasis. The
previous findings support the notion that anaerobic exercise such as weight
training may require greater recovery energy expenditure and possibly a
longer duration of recovery compared to aerobic exercise. Several studies
that investigated recovery energy expenditure following weight training
support this conclusion (34, 38, 63).
Although low-volume, recreational weight training may not require a
large magnitude of recovery energy expenditure due to its low intensity, this
may not be the case during weight training sessions of athletes. For
example, Melby et al. (148) indicated that considerable amounts of
recovery energy expenditure are required following high volumes of weight
training. This may be especially true among strength-power athletes who
train at high levels during phases of training that require large volumes.
Furthermore, the accumulative effect of an entire high-volume training
phase may require a substantial recovery energy requirement and
expenditure. Thus, it is important to consider the energy expenditure
requirements and consumption (intake) of these athletes to ensure that they
are properly fueled for each training session and that the necessary nutrients
are being consumed to facilitate recovery and prepare them for subsequent
training sessions.
Types of Weight Training and Energy
Expenditure
As noted above, weight training sessions may place a significant energy
strain on an athlete due to the combination of volume and intensity during
the session and the post-exercise energy requirement that follows. This
becomes an important issue when it comes to designing weight training
sessions. A method that places the most important exercises (relative to the
goals of each training phase and the sport) first is termed priority weight
training. Using this method, less important exercises are programmed later
in a training session. Typically, this means that larger muscle mass exercises
(e.g., back squats) are programmed prior to smaller muscle mass exercises
(e.g., biceps curls). Furthermore, priority training has individuals perform
all of the sets and repetitions of an exercise prior to moving to the next
exercise while including sufficient rest periods between sets to ensure that
the appropriate number of repetitions per set is completed. It should be
noted that the energy expenditure of a priority training session may be
manipulated if eccentric exercise(s) are included. For example, Isner-
Horobeti indicated that despite the potential to use substantially heavier
loads with eccentric exercise, the energy cost may be 4–5 times lower than
that of concentric work (110). Thus, it is important for the sport scientist
and practitioner to be wary of the energy cost of specific exercises during
various training phases.
In contrast to priority training, exercises may be completed in a “circuit”
fashion in which a series of exercises that may include large and small
muscle mass exercises and both upper and lower-body exercises are all
completed before circling back to complete another set. This type of
training is termed circuit weight training and it is typically characterized by
short rest periods (< 1 min) between exercises and/or sets and exercise
alterations between upper and lower body each set (141). In theory, the
shorter rest periods are meant to stimulate metabolism and increase energy
expenditure. In other words, one could argue that the goal of circuit training
programs is to simply burn kcal. Compared to priority training programs,
circuit training programs typically place a greater emphasis on smaller
muscle mass, often single-joint exercises. However, despite the shorter rest
periods, the average training intensity is considerably lower in circuit
training programs compared to priority training programs due to lower
masses being lifted. If large muscle mass exercises are included, circuit
training programs can produce fairly high energy expenditures. However,
priority training (Table 4.1) that emphasizes large muscle mass exercises
can produce similar kcal expenditures, despite the use of longer inter-set
rest periods, since heavier loads are used (179).
Like aerobic (endurance) training, the energy cost of weight training is
related to energy (food) intake (41). Thus, when the volume load of training
is increased, the amount of kcal consumed should also increase. This
becomes a crucial point of understanding between the strength and
conditioning coach and athlete when it comes to exercise selection, the
length of training phases, the volume and intensity of exercise, and the
number and type of training sessions per day. Moreover, because the energy
expenditures may be quite large with heavy training, in addition to the
potential of prolonged recovery, the goals of the athlete should be clearly
identified and a plan for energy consumption should be discussed and
developed with qualified personnel.
Recommended Dietary Intakes (Dietary Reference
Intakes)
Before considering intakes of macro- and micronutrients, it is important to
discuss the current recommendations for these nutrients. In 2009, a joint
Canada–U.S. expert report was released that provided a comprehensive set
of reference values for nutrient intakes for healthy U.S. and Canadian
individuals and populations (171). Within this report, the authors
established a set of reference values to expand and replace previously
published U.S. recommended dietary allowances (RDAs) and Canadian
recommended nutrient intakes (RNIs). In an additional article published in
2006, scientists considered the values recommended within the previous
report and applied its conclusions to physical activity and athletes (241).
The report states that the dietary reference intake (DRI) encompasses the
following concepts:

Acceptable macronutrient distribution range (AMDR): a range of

dietary intakes (as a percentage of energy intake) for a particular
energy source that is associated with decreased risk of chronic disease
while providing adequate intakes of essential nutrients.
Recommended dietary allowance (RDA): the average daily dietary
nutrient intake level that sufficiently meets the nutrient requirement of
nearly all (97–98%) healthy individuals in a specific life stage and
biological sex group.
Adequate intake (AI): the recommended average daily intake level
based on observed or experimentally determined approximations of
nutrient intake by a group (or groups) of apparently healthy people that
are assumed to be adequate, used when an RDA cannot be determined.
Tolerable upper intake level (UL): the highest average daily nutrient
intake level that is likely to constitute no risk of adverse health effects
to almost all individuals in the general population. As intake increases
above the UL, the potential risk of adverse effects may increase.
Estimated average requirement (EAR): the average daily nutrient
intake estimated to meet the requirement of half the healthy
individuals in a particular life stage and gender group.
Estimated energy requirement (EER): the average dietary energy
intake among healthy adults of a defined age, gender, weight, height,
and level of physical activity, consistent with good health, that can be
predicted to maintain energy balance.
Protein
Athletes, coaches, sport scientists, and strength and conditioning coaches
have a general interest in the role of protein in the diet and the effectiveness
of protein supplementation. Some of this may be based on the belief that
protein intake is necessary for optimal performance, gains in LBM, and
recovery. It should be noted that scientists may disagree on the exact protein
requirements for athletes, especially for those who participate in very high-
intensity or high-volume training. However, this lack of agreement may
stem from the design of many scientific studies, many of which have
included poorly designed training programs, various training statuses
among the participants, or short training durations. It could also be argued
that a lack of understanding regarding protein metabolism may also
contribute to the confusion. The purpose of this section is to briefly review
current knowledge regarding the major features of protein metabolism, the
effects of training on protein requirements, and current protein
supplementation recommendations.

Protein Metabolism and Function

A typical American diet consists of approximately 9–16% of the total
caloric intake being made up of protein (96, 163). However, many athletes,
particularly strength-power athletes, may increase these values to
approximately 15–25% of their total caloric intake (112, 214, 215). Proteins
are relatively complex molecules that have a variety of enzymatic and
structural functions related to body growth, maintenance and repair, and
energy production. Under normal resting conditions, only about 1–2% of
the total energy required is supplied by protein; however, it should be noted
that greater quantities of protein may be used as an energy source if dietary
carbohydrate and fat become inadequate fuel sources (105). In this light,
skeletal muscle serves as a reservoir for protein and can be catabolized for
energy in situations such as starvation (198) or long-distance endurance
events, such as a marathon (199).
Because muscle protein is in a constant state of turnover, the amount of
protein contained within the muscle at any given time is largely determined
by the balance between protein anabolism and catabolism (26). Thus, if
excess dietary protein is ingested, it may be oxidized for energy or
converted to fat dependent on the muscle’s physiological state (96, 215,
217). On the other hand, if excess protein is consumed in a low exertional
state, it can be converted to fat, as is the case with excess carbohydrate that
has not been stored or metabolized for energy.

Composition of Protein
The biological value (BV) of a protein is a measure of the absorption and
utilization of a protein. If the BV of a protein is higher, more nitrogen is
absorbed, used, and retained, making proteins with higher BV those that
can better promote greater levels of tissue remodeling and muscle gains.
Protein synthesis (anabolism) in humans requires approximately 22 distinct
amino acids, nine of which are classified as essential amino acids (EAA) in
adults. Essential amino acids are defined as those that cannot be synthesized
within the human body and must instead be consumed within an
individual’s diet (Table 4.3). In contrast, nonessential amino acids can be
synthesized from other substances, such as carbohydrate, assuming an
adequate nitrogen source (such as other amino acids) has been made
available. Regarding various food sources that supply EAA, some dietary
proteins have been classified as either complete or incomplete proteins.
Complete proteins are those that contain all the EAA needed for the
synthesis of human tissue and have a high BV. Many of these proteins are
typically found in animal sources and products such as red meat, dairy
products, eggs, fish, and fowl. In contrast, incomplete proteins are those
that contain very low amounts of one or more EAA. These proteins
generally originate from plant sources and include nuts, grains, legumes,
and seeds. However, it should be noted that the quantity of protein available
in some plant sources (e.g., beans) is relatively high and may partially offset
the lower BV that is typical of incomplete proteins.

Table 4.3 Essential and nonessential amino acids

Essential Nonessential
Histidine* Alanine
Isoleucine Arginine
Leucine Asparagine
Lysine Aspartic acid
Methionine Cystine, cysteine
Phenyalanine Glutamic acid
Threonine Glutamine
Tryptophan Glycine
Valine Hydroxyproline
Proline
Serine
Tyrosine
* Some adults have the ability to synthesize histidine. Histidine is an essential amino acid for most
adults and for infants.
Source: Modified from Stone et al. (205).

As mentioned above, stored protein is remodeled by a continuous

process of anabolism and catabolism. For example, daily remodeling
amounts to about 3–4% of whole-body protein in adults (52) and potentially
there could be a greater percentage among athletes during intense training.
However, compared to carbohydrate or fat turnover, the breakdown and
replacement of protein is less efficient, accounting for 10–25% of the RMR
(52, 168). A common method of measuring protein turnover includes the
examination of nitrogen balance, which provides an estimate of nitrogen
intake versus loss and a reasonable estimate of protein balance. Simply, a
negative nitrogen balance occurs when nitrogen loss is larger than intake
(state of catabolism) and a positive nitrogen balance occurs when intake is
greater than loss (state of anabolism). The formula for nitrogen balance is as
follows:
 Bn = I – (U + F + S + SW)

where Bn = nitrogen balance, I = nitrogen intake, and U, F, S, and SW =

nitrogen loss in urine, feces, skin, and sweat, respectively.
Nitrogen balance can be modified several factors including the
physiological state and health of the individual, energy intake, and essential
and nonessential amino acid intake. Regarding the latter, very low dietary
intake of an EAA may reduce the rate of protein synthesis and impair the
use of other amino acids for protein synthesis. As a result, if protein
synthesis is reduced sufficiently, a catabolic environment may predominate,
ultimately producing an increased excretion of nitrogen. This negative
nitrogen balance may occur if the proportions of EAA in the diet are
unbalanced or if protein intake is insufficient. Furthermore, the catabolic
environment and negative nitrogen balance can occur even if only one EAA
is limited as a result of inadequate diet (163).
Because not all athletes eat animal-based protein sources, the authors
acknowledge that it is important to provide insight for athletes who are
vegetarians. As mentioned above, individual plant-based sources of protein
may not provide all of the necessary EAA. Thus, in order for vegetarians to
obtain sufficient complete protein for good health, it is essential for them to
consume foods that contain complementary proteins, which when combined
together, supply all of the necessary EAA, a practice referred to as mutual
supplementation. The following are examples of food combinations that can
provide complementary proteins:

Soybeans and rice.

Peas and wheat.
Beans and corn.
Lentils and rice.
Cereals and legumes.
Whole grains and sunflower seeds.
Peanuts and wheat (bread).
Another important aspect to consider is the timing of meals to allow for
optimal protein synthesis. Some researchers suggest that mutual
supplementation may be less effective if all EAA are not ingested within
two hours (3). Although not all researchers agree with this idea, it is
possible that eating two meals containing incomplete proteins widely
separated in time may not result in the most efficient mutual
supplementation. Additionally, it should be noted that exercise immediately
after meals tends to reduce absorption of amino acids and other nutrients.
Thus, the timing of protein intake should be considered, especially during
heavy training.

Protein Metabolism and Control

Currently, the U.S. RDA for protein is 0.8 g kg–1 day–1 (0.83 g kg–1 day–1
in Canada), a value established in 1989 (183). The RDA is supposed to
include a margin of safety to account for individual differences in protein
metabolism, normal nitrogen loss, and levels of physical activity. According
to RDA standards, due to the safety margin, there is no need for additional
protein in the diet for any reason among healthy humans. While some
literature supports this notion for active and athletic populations (161, 241),
further literature suggests that additional protein is needed for endurance
(171, 213) and particularly strength athletes (162, 171). Indeed, several
factors may reduce the effectiveness of and call into question the standards
for the RDA and therefore the DRI among very physically active groups
such as elite athletes.
While it has been assumed that the RDA may not be affected by caloric
consumption, caloric intake must be adequate, or total protein requirements
may increase (214). Simply, as energy demands of physical activity and
training increase, so too must food consumption and caloric intake to meet
the demands. Furthermore, protein intake would have to increase in
proportion to the greater caloric consumption to maintain a normal nitrogen
balance. However, when an athlete changes from one training phase to
another, an increased protein intake may not always occur. For example, 2
to 4 weeks may be necessary to readjust energy and protein intake and
output as training phases change, while even longer adjustment periods may
be required if body mass is gained or lost (11, 163). It is important to note
within this situation that if changes in volume and intensity are not
accompanied by the necessary changes in kcal and protein, detrimental
effects in body mass, body composition, and protein status (body protein
content) may result, at least during the adjustment period.
The effect of various hormones on protein metabolism should not be
overlooked (52, 86, 219). For example, testosterone, insulin, insulin-like
growth factors, and growth hormone are anabolic hormones that can
directly enhance protein synthesis or inhibit catabolism. Additionally,
epinephrine may also promote an anabolic environment by decreasing the
rate of protein degradation (52). In contrast, cortisol has catabolic properties
that antagonize the effects of testosterone to promote protein catabolism.
Furthermore, glucagon and thyroid hormones also have net catabolic effects
due to their metabolic actions. Each of the previous hormones have wide-
ranging metabolic and physiological effects as they not only impact protein
metabolism but also carbohydrate and lipid metabolism, water and
electrolyte balance, behavior, growth, and numerous other physiologic
functions related to protein status. Thus, changes in resting and post-
exercise hormone concentrations resulting from exercise and training can
affect protein metabolism from both a synthesis and degradation standpoint.
Further detail on the effects of these hormones is provided in Chapter 3.

Effects of Exercise and Training on Protein Synthesis

Protein synthesis is depressed, and degradation of noncontractile muscle
proteins and degradation in the liver are unchanged or increased depending
on exercise intensity and duration (55, 89, 149). In addition, the degradation
of contractile proteins is generally reduced during exercise (89).
Collectively, amino acids are made available for catabolic processes,
especially as a result of aerobic exercise. In contrast, protein catabolism
returns toward baseline and protein synthesis can increase during recovery
(55).
The notion that protein degradation resulting from exercise is
accelerated is based on previous observations of the amino acid, 3-
methylhistidine. This amino acid is formed primarily as a product of
contractile protein (actin and myosin) degradation and does not contribute
to the synthesis of new protein (26, 89). Thus, it can be concluded that
changes in 3-methylhistidine excretion may be associated with the degree
of contractile protein degradation occurring during and after exercise.
Research involving both animal (40, 57, 58) and human (169) participants
suggests that 3-methylhistidine released from muscle may decrease during
aerobic and anaerobic exercise, including weight training (58, 65, 164);
however, its release is greatly increased post-exercise, suggesting that
contractile protein catabolism does take place. While further research is
needed, the exact nature of protein catabolism resulting from exercise is not
clear and likely depends on several factors, including exercise type, volume,
and intensity. Furthermore, caution must be used when interpreting existing
information, as a few extramuscular sites contain contractile protein (gut
and skin) that could contribute substantially (up to 25%) to the 3-
methylhistidine excretion in humans (2).
While training (both aerobic and anaerobic) increases the need for
dietary protein intake (130, 133, 176), the primary use of the additional
protein may vary depending on the type of exercise and training regimen.
For example, aerobic training results primarily in an increased oxidation of
amino acids (protein) for energy while anaerobic training, particularly
weight training, primarily results in an increase in amino acid use in tissue
repair and hypertrophy (131, 149, 214, 216). Research based on both
nitrogen balance and isotope dilution have shown that aerobic (78, 87, 88)
and anaerobic training (134, 149, 217), including weightlifting (42, 127),
can result in an increased requirement for protein. Thus, a negative nitrogen
balance, depending upon its degree and duration, could result in LMB
losses that may include hormones, structural and enzymatic proteins,
antibodies, and other necessary proteins. Furthermore, these maladaptive
effects could result in an increased potential for injury, disease, reduced
performance capabilities, non-functional overreaching, and overtraining
(149, 204).
An important factor that may influence the rate of protein oxidation is
the initial muscle glycogen concentration (132), since a greater reliance on
protein and protein degradation is higher if skeletal muscle glycogen
concentrations are low. Lemon and Mullin (132) indicated that ≥ 10% or
more of total energy demands can be derived from protein during aerobic
exercise if muscle glycogen is inadequate. Furthermore, the probability of
LBM loss is increased when high training loads are coupled with
inadequate diets, which may increase the likelihood of overtraining (204).
As a result, dietary protein should represent approximately 15% of the
calories consumed by both endurance and strength-power athletes in hard
training, especially during high-volume phases, or among physical laborers
performing very hard work (214, 215). Carbohydrate in turn, should
represent about 55–60% of the dietary kcal to ensure adequate glycogen
concentrations in muscle and liver, thus reducing potential protein catabolic
effects (176, 204).

Protein Intake
Although precise protein recommendations are still somewhat
controversial, an abundance of evidence supports the notion that athletes
require protein intakes beyond the RDA, especially during periods of high-
volume training (39, 56, 129, 131, 135, 136, 162, 171, 176, 235, 237). As
previously mentioned, protein requirement may be dependent on several
factors such as exercise type, volume and intensity of training, length of
training period, carbohydrate intake, environmental factors, the timing of
intake, quality of protein ingested, and perhaps sex (129, 136). Although the
exact mechanisms and reasons for increased protein may be different (131,
135, 149), both aerobic and anaerobic training require additional protein
intake (129, 214, 215). Specific to endurance athletes, an increased protein
requirement may be partially associated with tissue repair but is more
associated with the increased potential use of amino acids, particularly
branch chained amino acids (BCAA), as energy substrates. In contrast, an
increased protein requirement for strength-power athletes may be more
focused on underlying mechanisms that promote hypertrophic adaptations
such as tissue repair, tissue remodeling, and maintenance of a positive
nitrogen balance (129, 214).
Previous recommendations of protein for endurance athletes suggest
intakes between 1.2 and 1.4 g kg–1 day–1 (68, 131, 135). While much of the
protein requirement beyond the RDA is likely due to the increased
oxidation of amino acids, particularly BCAAs (78, 129, 131, 135),
Blomstrand et al. (22) indicated that BCAA supplementation could
theoretically prolong endurance performance. The rationale for this may be
due to two reasons. First, BCAAs may influence metabolic changes, which
could prolong endurance. For example, the exogenous source of BCAAs
promotes the use of free fatty acids as an energy substrate, which may
reduce protein catabolism and spare glycogen (54). The second reason
BCAAs may influence metabolic changes has to do with the relationship
between BCAAs and the brain’s uptake of tryptophan. Tryptophan has been
associated with feelings of sleepiness, lethargy, and fatigue due to its
conversion to the neurotransmitter serotonin. Additional research has also
suggested that tryptophan is related to fatigue caused by exercise and in the
etiology of the overtrained state (1, 137, 155). This may be due to the
competition between tryptophan and the BCAAs to enter through the
blood–brain barrier (239). Research focused on the relationship between
tryptophan, its conversion to serotonin, and fatigue has been inconclusive.
Some evidence suggests that alterations in serotonin can affect aerobic
endurance performance in both rats and humans (51); however, further
research indicated a lack of association between alterations in training
volume that increased feelings of fatigue and changes in tryptophan-to-
BCCA ratios among humans (128, 212). Furthermore, there is little
convincing evidence to suggest that alterations in serotonin would result in
the same type of fatigue as is associated with anaerobic activities or with
overwork (81).
 In humans, supplementation with BCAAs has produced increases (23) or
no effect (21, 222) on endurance performance. Decreased endurance
performances may be associated with increased ammonia concentrations
that may occur with BCAA supplementation (54, 139) or due to a decrease
in Krebs cycle intermediates as a result of BCAA increases in the BCAA
amino transferase reaction, which requires additional Krebs cycle
intermediates (226). It should be noted, however, that carbohydrate
ingestion may attenuate or markedly reduce the reliance on BCAA
oxidation during exercise (50, 226), which may have a positive effect on
endurance performance. Further research is needed to examine the role of
BCAA supplementation as it relates to fatigue and overwork.
Researchers have suggested that the protein requirement for strength-
power athletes is approximately 1.4 to 2.0 g kg–1 day–1 (68, 114, 131, 135,
215). Indeed, some researchers showed that increases in dietary protein may
enhance strength and muscle mass among strength athletes, despite the
initial values for dietary protein intake being above the RDA. For example,
Dragon et al. (60) showed that an increase in protein intake from 225% to
438% of the RDA (approximately 3.5 to 4.0 g kg–1 day–1) was associated
with gains in both strength (5%) and muscle mass (6%) among elite
Romanian weightlifters; however, the potential influence of androgen use
among these athletes is an unknown factor. Additional researchers
displayed gains in body mass and LBM when participants ingested 3.3
versus 1.3 g kg–1 day–1 of protein combined with weight training over 4
weeks (67). A more recent series of studies indicated that protein intakes of
> 3.0 g kg–1 day–1 may have positive effects on body composition in
resistance-trained individuals (5–8). The authors of these studies also noted
no harmful effects on blood lipids or markers of kidney and liver function.
The findings of the previous studies demonstrate a clear potential for
protein supplementation combined with resistance training to enhance
muscle and performance gains.
The training status of athletes may impact the amount of dietary protein
intake and their training responses. Weideman et al. (231) showed that
increasing dietary protein to 3.67 times the RDA showed no unique changes
in body composition compared to control participants. Moderately trained
subjects that increased both protein and caloric intake while performing a
weight training program showed greater increases in body mass, LBM, and
strength compared to controls (157). However, during periods of very heavy
training, advanced athletes may require greater protein intake (2.0–2.2 g kg–
1 day–1) to gain strength or LBM (112). Because some athletes that compete
in weight class sports may routinely lose weight by using hypocaloric or
calorie restricted diets, an increased protein intake may be necessary in
order to partially offset the accompanying negative nitrogen balance and
loss of lean tissue (228). Additional research suggests that ingesting 2.3–3.1
g kg–1 of fat-free mass may yield improvements in strength, hypertrophy, or
maintain fat free mass during calorie-restricted diets.
Even when adequate energy is being supplied through the diet, the
impact of training should not be overlooked. Previous research has
indicated that the initiation of training or increasing the training volume or
intensity may lead to a decreased or negative nitrogen balance (87, 88,
129); however, as training proceeds, nitrogen balance returns toward
positive values due in part to changes in exercise intensity. While protein
use during exercise is associated to the intensity and relative intensity
(percentage of maximum) of exercise and training (39, 129), the relative
intensity may decrease and reduce the dependence on protein as an athlete
adapts to the training stimuli (129). It should be noted that increases in
training volume or intensity may be accompanied by a reduction in
testosterone or an increase in cortisol concentrations, resulting in a reduced
“anabolic state” of the organism (95). In fact, Butterfield (39) indicated that
increased training volume or intensity of training in which short-term
negative nitrogen balances are likely to occur, protein intakes as high as 2 g
kg–1 day–1 may not be sufficient to maintain a positive nitrogen balance.
Furthermore, the ingestion of too little protein, especially when associated
with a hypocaloric diet, may promote or worsen overreaching and
overtraining symptoms.
The timing of protein ingestion is another factor that should be
considered within an athlete’s dietary plan. While some literature supports
the notion that ingesting protein during and immediately after exercise
(particularly strength exercise) may produce greater tissue repair and
protein accretion (68, 119, 153, 224), more recent analyses suggest that the
amount of ingested protein may be more important that than the timing of
ingestion (152, 181). Regardless of the timing, it is apparent that protein
intake for athletes should be higher than the RDA, especially during high-
volume training. This realization was evidenced in the joint position stand
published by the American Dietetic Association, Dieticians of Canada, and
American College of Sports Medicine (171). The authors of this statement
on protein consumption recommend 1.2 to 1.4 g kg–1 day–1 for endurance
athletes and 1.2 to 1.7 g kg–1 day–1 for strength athletes. Further analyses
also support protein intake of 1.6 g kg–1 day–1 to aid in increases in LBM
and maximal strength (152). Assuming caloric intake increases in
proportion to the energy requirement of training, protein intake should
represent approximately 15% of the caloric intake. However, if there is a
marked decrease in caloric intake, the percentage of protein should be
raised above 15% (228).
Carbohydrate
Carbohydrates are chemical compounds that consist of carbon, hydrogen,
and oxygen in the ratio of approximately 1:2:1, with at least three carbon
atoms. There are three primary groups of carbohydrates that include:

1. Monosaccharides. Consist of simple sugars generally composed of

three to seven carbon atoms (e.g., glucose and fructose).
2. Oligosaccharides. Carbohydrates that consist of 2–10
monosaccharides chemically bonded together (e.g., raffinose is a
trisaccharide composed of galactose, glucose, and fructose).
3. Polysaccharides. Carbohydrates that consist of >10 monosaccharide
units chemically bonded together in linear or complex branching
chains (e.g., glycogen and starch).

Carbohydrates make up approximately 45–52% of the total caloric intake

within the typical American diet. While excess dietary carbohydrate may be
converted to body fat and promote obesity without adequate exercise, the
majority serves as the preferred metabolic fuel for energy production (106).
This may be due to the ability to metabolize carbohydrates without the
direct involvement of oxygen (anaerobic) and/or oxidize it for use during
long duration exercise (aerobic). Haff et al. (94) indicated that carbohydrate
is especially important during long-duration aerobic activities, as well as
high volumes of repeated anaerobic exercise. Thus, the regular consumption
of carbohydrate physical activity is crucial. In fact, low-carbohydrate diets
(less than 30% of total kcal) have been associated with symptoms of fatigue
and are difficult to adapt to (31, 163, 204). Table 4.4 lists the physiological
functions associated with carbohydrate consumption.

Table 4.4 Physiological functions and benefits of carbohydrates

Function Benefit(s)
Function
Energy supply
Avoid ketone formation
Reduce the loss of cations
Cell coat
Ground substance of cartilage
and bone formation
Helps for heparin
Source: Based on Brooks et al. (31); Pike and Brown (163).
Benefit(s)
Spares fat (metabolized at higher intensity activity)
Prevents the formation of ketones that contribute to the
development of ketoacidosis (metabolic acidosis)
Maintenance of normal ionic balance (e.g., resting membrane
potential)
Adds structure to cells
Structure
Increases the formation of anticoagulant

Carbohydrate Metabolism and Control

The uptake of glucose by muscle cells is regulated by a family of proteins
termed glucose transporters or GLUTs (16, 17, 79, 107, 193). While
transport is regulated by glucose transporter-1 (GLUT-1) during normal
basal conditions, glucose transporter-4 (GLUT-4), normally stored in an
intracellular pool, may be more important within skeletal muscle due to its
transport efficiency. Exercise or an increase in insulin stimulates the
translocation of GLUT-4 from the intracellular pool to the plasma
membrane and the T-tubules of the cell. This process may accelerate the
uptake of glucose into the muscle cell, where it may then be used for energy
production or storage, based on the needs of the cell. Thus, it is important to
consider the storage and breakdown of carbohydrate to understand for an
understanding of how muscles maintain and supply adequate energy
substrate for muscle activity. It should be noted that GLUT-4 concentrations
are unique across different muscles (27) and may also be greater in type I
muscle fibers (80). Furthermore, researchers have also noted that GLUT-4
concentration and activity may be greatly influenced by the level of
physical activity (49).
As discussed in Chapter 2, glycogen is stored in both the muscle and the
liver bound to two enzymes, glycogen synthetase and phosphorylase (79).
These enzymes are assisted by two additional enzymes (isozymes):
hexokinase (in muscle, liver, and other cells) and glucokinase (only in the
liver). Collectively, these enzymes and isozymes are used to help regulate
glucose and glycogen by facilitating their synthesis or breakdown based on
energy production needs.
The regulation of carbohydrate as an energy substrate, similar to protein
and fat, is dependent on both neural and endocrine mechanisms that can be
modified by factors such as nutritional status, physical exercise, and
training (31). Hormones can have a significant impact on carbohydrate
storage and catabolism (see Chapter 3). While some hormones may increase
blood glucose concentrations (e.g., catecholamines, cortisol, glucagon, and
indirectly by growth hormone), others, such as insulin, may decrease
concentrations. In contrast, glycogen synthesis and storage in liver and
muscle are enhanced by insulin and testosterone while glycogen stores are
mobilized by catecholamines and glucagon. Of these hormones that directly
alter metabolism, insulin and cortisol may have the greatest influence on the
responses and adaptations to resistance training.
Insulin serves as an anabolic hormone in that it acts to enhance glycogen
storage and promote energy substrate uptake. In addition to increasing the
uptake of carbohydrate, insulin also increases the uptake of amino acids,
thereby promoting protein synthesis. Thus, an increase in insulin
concentration during or after exercise may enhance the recovery of
glycogen and create a more anabolic environment to increase muscle mass
(i.e., hypertrophy). Therefore, ingesting carbohydrate during and
immediately after exercise may provide a stimulus for enhanced glycogen
recovery and protein anabolism. Furthermore, the intake of carbohydrate
and small amounts of protein appears to enhance the anabolic effects of
insulin, as well as stimulating increases in growth hormone (43, 66). It
should be noted, however, that both aerobic (210) and resistance exercise
(147) may decrease post-exercise insulin concentrations. This in turn may
enhance free fatty acid mobilization and promote glycogen catabolism and
release glucose into the blood, facilitating substrate availability (210).
While a reduction in insulin concentration would normally decrease cellular
glucose uptake, exercise itself enhances glucose uptake. In fact, research
indicates that both aerobic- and resistance-trained athletes may have an
increased insulin sensitivity at rest and during exercise and thus, less
hormone is required to control substrate availability (147, 210).
In contrast to insulin, cortisol is a stress hormone and is catabolic in
nature. Its basic functions include (47, 52):

Maintaining blood glucose concentrations.

Reducing inflammation by inhibiting the shift of water away from the
blood into the tissues.
Converting amino acids to carbohydrate.
Induction of proteolytic enzymes.
Inhibiting protein synthesis and increasing general protein degradation.
Antagonizing testosterone.

Despite its ability to aid in the resistance to stressors, cortisol may also
elicit physiological responses that are counterproductive to the normal
training adaptations, particularly resistance training. For example, the
primary metabolic effect of cortisol appears to be gluconeogenesis, which
requires protein degradation. Research has shown that muscle atrophy and
loss of strength may be associated with chronically elevated cortisol
concentrations (70). From a practical standpoint, elevated cortisol
concentrations resulting from heavy exercise or overtraining may suppress
immune system function, increasing tissue repair time and perhaps interfere
with tissue hypertrophy. Since an efficient immune function appears to be
critical to tissue repair post-exercise and likely influences the hypertrophy
effect of resistance training (177, 194, 232, 238), a diet that supplements
these effects would be beneficial. Evidence suggests that carbohydrate
ingestion may inhibit the secretion of cortisol (150), which may promote a
more anabolic environment for muscle growth. In time, this anabolic
environment may produce enhanced adaptations to resistance training (47).

Carbohydrate Intake
Carbohydrates were recognized as a valuable aspect of an athlete’s diet as
early as 1901 (233). In 1939, Christensen and Hansen (44) indicated that
diets high in carbohydrate content enhanced the ability to perform
prolonged heavy work. Further researchers have displayed strong
relationships between a high-carbohydrate diet, pre-exercise muscle
glycogen concentrations, and work performance or endurance (19, 47, 116)
as well as relationships between muscle glycogen concentrations and
muscle strength, short-term high-intensity (anaerobic) exercise, and the
ability to repeat or sustain high-intensity exercise (47, 76, 92, 94, 113, 125).
Due to the relationships shown in previous research, the effect of dietary
carbohydrate on muscle and liver glycogen stores (47, 191), and the
protein-sparing effect of high concentrations of muscle glycogen (129), it is
clear that the consumption carbohydrate is an important factor to consider
in physical training.
Stone et al. (204) suggested that diets with low carbohydrate content or
training programs that chronically deplete glycogen stores may be a strong
contributor to overtraining and reduced performance. Regarding the type of
carbohydrates within diets, it has been suggested that complex
carbohydrates should predominate over simple sugars (163). An exception
to this may be during and immediately after exercise since simple sugars
tend to be absorbed faster than more complex carbohydrates and can have a
greater effect on insulin release. Daily intake of carbohydrate should range
from 6 to 11 g kg body mass–1; however, it should be noted that
carbohydrate intake beyond this range may not provide additional benefits.
Previous recommendations suggest that calories derived from carbohydrate
should consist of approximately 55–60% of an athlete’s dietary intake for
athletes in hard training, especially during high-volume periods, who are
eating sufficient calories (47, 208).
Aerobic work can be prolonged, and the amount of work during a given
period of time increased, through carbohydrate intake and supplementation
(47, 200, 223). Some evidence (115, 144), but not all (124), suggests that
carbohydrate intake may benefit intermittent anaerobic exercise (e.g.,
resistance training). However, the quantity, timing, and form of
carbohydrate ingestion and its impact on resistance training have not been
well studied. The earliest investigation concerning carbohydrate ingestion
and resistance exercise examined the effects of a carbohydrate beverage on
multiple bouts of leg extensions and found that a glucose polymer (1 g kg–
1) ingested immediately before exercise and 0.17 g kg–1 after every five sets

produced more total sets and repetitions than a placebo drink (125).
Similarly, Haff et al. (93) found that carbohydrate supplementation
increased the total amount of work performed during 16 sets of 10
repetitions on a semi-isokinetic device at 120° s–1. However, other
researchers have not shown an ergogenic effect of carbohydrate
supplementation during resistance exercise. Conley and colleagues (46)
indicated that consuming 0.3 g kg–1 of carbohydrate immediately prior to
exercise and 0.15 g kg–1 after each completed set of squats did not enhance
the work completed during squat sets of 10 repetitions at 65% 1RM.
Similarly, Kulik et al. (122) indicated that consuming 0.3 g kg–1 before
exercise and after every other successful set did not enhance the squat
performance to volitional failure with 85% 1RM. The previous results
suggest that carbohydrate supplementation during resistance exercise that
occurs over relatively long periods of time or requiring greater total
workloads may not be effective (92). It should be noted, however, that it is
not uncommon for advanced and elite athletes to train multiple times per
day. Therefore, it is possible that carbohydrate supplementation may benefit
second or third training sessions provided that enough is ingested (94).
As mentioned above, combined protein and carbohydrate
supplementation, especially when ingested pre- and post-exercise, may
promote a more anabolic environment and aid glycogen resynthesis and
tissue remodeling to a greater extent than supplementing either protein or
carbohydrate alone (224).
Fat
Fat is present in all human cells and the physiological functions are quite
diverse, ranging from their use as energy substrates, physiological
structures (e.g., cell membranes and myelin sheath of nerve cells), vitamin
transporters, and their role in the production of cholesterol and associated
steroids. Fat (lipid) serves as the largest energy store that is readily
available for biological work and may consist of approximately 35–45% of
the total daily caloric intake within the Western diet (101). While fat is
involved in a variety of metabolic processes within the human body, it has
been associated with disease states including cardiovascular disease and
some types of cancer.
Fats can be classified into three groups: simple fats, compound fats, and
derived fats (Table 4.5).

Table 4.5 Functions of different types of fat in the human body

Type of fat Function(s)
Simple Monounsaturated Reduces LDL concentrations and inflammation
Polyunsaturated Build cell membranes and insulate nerves
Saturated Make up at least 50% of cell membranes
Triglycerides Primary storage form of fat and 95% of the fat found in food
Compound Lipoproteins Antioxidant, anti-inflammatory, and cardioprotective effects
(HDL); transports cholesterol and reduces plaque on artery
walls (LDL); delivers triglycerides to cells in the body (VLDL)
Glycolipids Make up various structures in the cell membrane and myelin
sheath
Phospholipids Components of cell and subcellular membranes and liaisons
between fat- and water-soluble materials that pass through a
membrane
Derived Cholesterol Cell membrane integrity, synthesis of vitamin D, synthesis of
cholesterol, and precursor to steroid hormones
HDL = high-density lipoprotein; LDL = low-density lipoprotein; VLDL = very low-density
lipoprotein.
Source: Based on Hawley (101).
Fat Metabolism
The use of fat as an energy source is important during aerobic exercise
(101) and can be a post-exercise consequence of anaerobic exercise,
including resistance exercise (147, 160). As discussed in Chapter 2, fatty
acids are oxidized within the mitochondria by the process of β-oxidation
where acetyl-CoA is produced before entering the Krebs cycle. Like
proteins and carbohydrate substrates, less complex fatty acids are oxidized
faster than long-chain fatty acids (101, 167). It should be noted, however,
that fat metabolism is significantly impacted by the endocrine system.
Researchers have indicated that fat synthesis may be enhanced by insulin,
whereas lipolysis may be enhanced by growth hormone, thyroxin,
catecholamines, and cortisol (101, 147). Taking this into account, a variety
of nutritional strategies have been proposed to enhance the mobilization and
oxidation of fat during and after exercise.
Strategies to enhance the mobilization and oxidation of fat have different
goals including raising the rate of fat oxidation to spare glycogen during
long-term exercise and to promote fat loss. As discussed in Chapter 5, it
may be possible that to spare the use of glycogen as an energy substrate
through the use of ergogenic aids (101); however, the efficacy of this
practice may be questioned. Another way to spare the use of glycogen may
be through fat supplementation. This practice, which has included pre-
exercise feedings and the ingestion of long- and medium-chain triglycerides
during exercise, may enhance the rate of fat oxidation; however, it has been
noted that these interventions may fail to enhance an athlete’s performance
(101).
A second strategy to enhance fat oxidation involves the long-term
adaptation to a high-fat, low-carbohydrate diet. While this type of diet may
increase the relative contribution of fatty acids as an energy substrate for the
total energy required for an exercise by about 40% (101), the rate of muscle
glycogen use and moderate-intensity endurance exercise performance may
not be impacted (120). Thus, while the long-term implementation of a high-
fat, low-carbohydrate diet could theoretically enhance ultra-endurance
performance, limited evidence supports this practice. Furthermore, the
potential health risks associated with this diet (e.g., increased LDL, obesity,
metabolic disfunction, etc.) do not support its long-term use (32). When a
high-fat, low-carbohydrate diet is combined with high-protein intake, it may
be possible to promote body fat loss among individuals such as
bodybuilders. In theory, this type of diet may enhance fat oxidation (101),
while the combination of additional protein and training will help maintain
LBM (228). Similar to the above, this strategy may work acutely for
bodybuilders; however, its long-term use may be questioned due to
potential prolonged fatigue, ketosis, decreased calcium concentrations, and
adverse blood lipid profiles (29, 118).
While the long-term benefits of a high-fat, low-carbohydrate diet may
not benefit performance, it may be possible to use this strategy over a
shorter duration. For example, “carbohydrate loading,” which implements a
high-fat, low-carbohydrate diet for about five days, may be used to deplete
muscle glycogen and increase the oxidation rate of fat. Using this strategy, a
high-carbohydrate diet is implemented on the sixth day or over several days
to restore and supercompensate muscle glycogen. This may allow muscle
glycogen to remain elevated over several days (9, 84, 85). From an efficacy
standpoint, researchers have shown that this strategy may decrease muscle
glycogen use during two hours of moderate-intensity cycling (70% of
VO2max); however, it may not impact performance times to a greater extent
than high-carbohydrate diets (36, 37). Additional researchers have shown
that despite an increase in fat utilization with carbohydrate loading, high-
intensity sprint performance was negatively impacted (100). While a
number of carbohydrate loading strategies may be used to supercompensate
carbohydrate, a complete discussion on this topic is beyond the scope of
this chapter. Readers are directed to Sedlock (185) for a practical discussion
on carbohydrate loading implementation.
Both endurance and resistance training can significantly reduce body fat
and percentage fat losses in relatively short-term periods (months) given
that a sufficient training stimulus (volume and intensity) is provided (82,
104, 109). An abundance of fat loss or fat-reducing products exist and may
be purchased at local drug or grocery stores. While increasing the rate of
FFA mobilization (e.g., with methylated xanthines and ephedra) or
increasing the rate of FFA entry into the mitochondria (with L-carnitine)
could theoretically increase the loss of fat the efficacy of these ergogenic
aids is questionable at best. Moreover, it is important that athletes exercise
caution and consult sport nutritionists and dieticians to confirm the efficacy
of such products and avoid substances that are banned in competitive sports
(18).
Vitamins and Minerals
Vitamins are organic compounds that are essential in small quantities for
normal metabolic functioning. Except for vitamin D, it is important to note
that humans cannot naturally synthesize most vitamins and thus, they must
be ingested as part of an individual’s diet. For this reason, it should be noted
that vitamin D levels among athletes living in higher altitudes or that are
often inside may have low vitamin D concentrations and supplementation
may be needed.
Vitamins can be classified as either fat-soluble or water-soluble. Fat-
soluble vitamins (e.g., vitamins A, D, E, and K) typically have antioxidant
properties or possess hormone-like properties. In contrast, water-soluble
vitamins (e.g., B complex vitamins and vitamin C) may act as coenzymes,
which are organic molecules loosely bound to enzymes that are necessary
for full activation of the enzyme. Vitamins are largely active in muscle
contraction and energy expenditure reactions in both a direct or indirect
fashion, but also serve a role in hemoglobin synthesis, immune function,
and bone metabolism.
Minerals are inorganic salt ions that may act as cofactors (similar
functions as coenzymes) or as part of mineralized various structures such as
teeth or bone. There are two primary classifications of minerals.
Specifically, minerals may be classified as either macrominerals (e.g.,
sodium, potassium, calcium, phosphorus, and magnesium) or trace elements
(iron, zinc, copper, chromium, and selenium) based on dietary
requirements. The daily allowance for macrominerals is greater than 100
mg day–1 and is less than 20 mg day–1 for trace elements (73).
Vitamins and minerals are essential micronutrients that are also
important for optimal and maximal performance. While it is commonly
believed that all the essential micronutrients can be obtained in a “well-
balanced” diet, many coaches recommend additional vitamin and mineral
supplements. This is based on the belief that vitamins and minerals are
beneficial for recovery, adaptation, and better performances (173). It should
be noted that a lack of consistent evidence exists to indicate that a large
intake of micronutrients largely impacts performance (33, 73). Additional
evidence suggests that large amounts of some micronutrients, such as fat-
soluble vitamins, may be detrimental (146). While some studies have
suggested that micronutrient supplementation can benefit performance
(208), most have not (73).
Vitamin and mineral supplementation may be useful if the RDA or the
athlete’s personal requirements are not being met with their diet (190).
While vitamin and mineral deficiencies may negatively impact performance
(208), athletes who ingest enough calories and eat a nutritionally sound diet
will likely ingest adequate amounts of vitamins and minerals without
supplementation. However, because athletes do not always eat a “balanced”
diet, and many athletes may need to “make weight,” it is reasonable to
assume that dietary intake of vitamins and minerals may not be sufficient.
For example, Guillard and colleagues (91) showed that fifty-five 20-year-
old male athletes from various sports displayed lower than normal
concentrations of vitamins B1, B6, and E. Furthermore, the frequency, and
in many cases the severity, of the deficiency was greater in the athletes
compared to the control participants. After one month of vitamin
supplementation to combat specific vitamin deficiencies, the micronutrient
status of the controls markedly improved, but did not completely restore the
deficiency status among the athletes. Furthermore, it is possible that caloric
restriction and making weight can negatively alter the micronutrient status
(71, 73).
For athletes, one possible exception to simply meeting the micronutrient
RDA (and DRI) is the potential of antioxidants and their influence on
performance outcomes. Because exercise may increase the production of
free radicals and other forms of reactive oxygen species (ROS) that may
impact a muscle’s redox status (166, 211), it is important to combat free
radicals and ROS to reduce their potential impact on fatigue and cellular
injury. This may be possible through the ingestion of both enzymatic (e.g.,
superoxide dismutase, glutathione peroxidase, and catalase) and
nonenzymatic (e.g., vitamins C and E) antioxidants that work to reduce the
harmful effects of ROS at the cellular level. It should be noted, however,
that while animal studies have demonstrated improved endurance
performance with antioxidant supplementation (10, 97, 99, 184), limited
evidence directly or indirectly supports these findings in humans (12, 90,
166, 172).
The requirements for some vitamins such as vitamin B1, B2, and niacin
are approximately proportionate to the metabolic demand. As a result,
requirements may increase with physical activity and training demands (24,
221). However, the assumption that extra food intake with adequate
micronutrients will be sufficient to compensate for the increased metabolic
demand with increased physical activity may not be valid. It is possible that
environmental factors and hard training (either high-volume or high-
intensity) may alter micronutrient status to such an extent that performance
is impaired. Furthermore, the accumulation of training and external stress
could contribute to overtraining and an altered micronutrient status.
Although a paucity of literature indicates that alterations in single nutrients
lead to a decrement in performance, at least over the short term, marginal
deficiencies of multiple micronutrients can (at times) negatively impact
performance (73). To compensate for any deficiencies, some research
suggested that multivitamin supplementation may enhance the performance
and “general well-being” of athletes with a low work tolerance (240).
However, individual needs should be considered before implementing new
dietary strategies.
Subnormal resting serum concentrations of minerals have also been
noted among athletes. For example, some researchers indicated that female
athletes who participated in a variety of sports displayed potassium and
magnesium deficiencies (208) while other researchers reported anemia and
low iron and ferritin (protein that binds iron) concentrations among male
and particularly female endurance athletes (45, 53). Regarding the latter,
some researchers reported that relatively mild iron deficiencies may
negatively impact endurance performance (53). While iron uptake may
increase during periods of deficiency, low iron values may not be very
responsive to diet and may require supplementation in some athletes (170).
Further research suggests that compared to anemic, sedentary participants,
athletes may absorb less than half the iron within their diets (62). Poor iron
absorption and the potential for increased hemolysis due to vigorous
physical activity could contribute to anemia. This in turn may further the
case for iron supplementation. It should be noted that a vegetarian diet can
produce alterations in ferritin status, especially when combined with
physical training. Snyder et al. (196) indicated that female distance runners
that consumed less than 100 g (3.5 oz) of red meat per week had
significantly lower resting serum ferritin concentrations and iron-binding
capacity than a control group who consumed substantial amounts of red
meat. Despite the substantial amounts of iron within the vegetables in this
study, the researchers concluded that the form of dietary iron intake can
affect iron status.
Two other minerals crucial to the skeletal structure are calcium and
phosphorus. Bone acts as a reservoir for both minerals and can store or
release minerals (particularly calcium) in response to changes in blood
concentrations and endocrine influence. However, calcium and phosphorus
both have high turnover rates and must be continuously replaced within an
athlete’s diet or potentially, supplementation. Failure to do so may lead to
maladaptation to training stimuli or a chronic condition such as
osteoporosis (loss of bone mass). Although osteoporosis is less of a concern
in younger athletes, it is important to develop a well-balanced diet high in
calcium and physical training plan at a young age to prevent such a
condition from occurring. This notion is supported by several studies (48,
126, 189) and reviews (187, 201, 203) that indicate that physical training,
especially weight-bearing and weight training exercises, can increase the
density and tensile strength bone and other connective tissue. However, it
should be noted that long-term, high volumes of some training, such as
distance running, may reduce bone density. For example, researchers have
shown that both male (103) and female distance runners (209) may possess
lower bone mineral density and content compared to sedentary controls or
lower-mileage athletes. Furthermore, female athletes who become
amenorrheic are especially susceptible to training-induced reductions in
bone density and bone mineral content (61, 138, 209). Regarding older
female athletes, menopause and the associated reduction in estrogen may
also explain the greater prevalence of osteoporosis in women. It should be
noted that while postmenopausal estrogen replacement therapy may slow
the rate of bone loss, it will not replace bone (138). Thus, the importance of
dietary calcium in preventing osteoporosis, especially in aging women,
cannot be overlooked (154).
Practical Nutritional Considerations for Athletes
While it is important for athletes to consume a balanced diet, several
additional aspects of nutrition are commonly encountered by athletes. For
example, when food is ingested may be just as important as what is
ingested. Pre- and post-event meals can provide considerable benefits if the
appropriate amount, type, and timing of ingestion are taken into account. In
addition, athletes, particularly those competing in sports with weight
classes, are constantly faced with “making weight,” while all athletes must
consider fluid balance in order to avoid dehydration and its consequences.

Pre- and Post-Event Meals

Pre-competition meals may provide both physiological and psychological
benefits to athletes. For example, protein intake shortly before training may
enhance tissue remodeling and hypertrophy (224) whereas protein
consumed within a larger meal several hours before competition may be
psychologically satisfying despite a lack of physiological benefits. In
contrast, a pre-training or pre-competition meal with higher fat content may
negatively impact performance by slowing gastric emptying despite
providing a satiating feeling.
As outlined above, pre-event carbohydrate intake is an important
consideration given the relationship between carbohydrate and
performance. However, consuming relatively large amounts of glucose or
sucrose 30–60 min pre-exercise may lead to a rebound depression of blood
glucose due to an insulin spike in susceptible individuals (77). Other studies
show contrasting results and suggest that a rebound effect will not occur
with the ingestion of simple sugars and that glucose ingestion 30–60 min
pre-event may increase glucose availability within the muscle during
exercise (83, 98). It is suggested that larger amounts of carbohydrate (and
protein) ingested as pre-event meals should be in liquid form, especially
immediately before or during exercise, due to the potential of digestion
discomfort from the ingestion of a large amount of carbohydrate in the form
of food.
Drinks containing glucose or glucose polymers may reduce
cardiovascular and thermoregulatory disturbances better than water alone
during prolonged aerobic exercise (123) and repeated bouts of anaerobic
exercise (125), especially in hot environments. It is recommended that the
“strength” of the solutions should comprise of 4–20% carbohydrate and that
the drink should be consumed every 15–20 min, especially during the final
stages of long-term endurance events when blood glucose may be
decreasing. It should be noted that solutions above 6% may be unsuitable
for some types of endurance events due to digestion discomfort or delayed
gastric emptying. In addition, carbohydrate solutions that contain greater
than 20% carbohydrate should not be used because of their potential to slow
gastric emptying to the point that increased absorption will not compensate
for the higher concentrations.
In order to create an anabolic environment to aid in glycogen restoration,
post-event meals should consist of high carbohydrate content. It has
previously been recommended that consuming 1–3 g kg–1 of carbohydrate
within 2 h and continuing every 2 h following exercise may maximize
glycogen recovery (79, 188). Additional evidence suggests that simple
carbohydrates ingested within the first 6 h following exercise promote
greater glycogen repletion than do complex carbohydrates (117). In this
light, glucose may more readily promote muscle glycogen storage
compared while fructose may more adequately restore liver glycogen (79).
Finally, although not all studies agree, the addition of protein may enhance
glycogen repletion likely facilitates an anabolic cellular environment,
muscle tissue repair, and remodeling, particularly when ingested as an
immediate pre-training or recovery drink (111, 224).

Water and Electrolytes

Water is the most plentiful component in the human body (102) and its
importance to the variety of functions it has cannot be overlooked. It should
be noted that small changes in either intra- or extracellular water content
can impact a number of biological reactions, thermoregulation, and
electrolyte balance. Because of this, dehydration and preventing
dehydration are a common concern among coaches, sport scientists, and
athletes.
Hydration of athletes is of utmost importance, especially at altitude and
in hot environments (159). Dehydration can cause a variety of performance
and health problems, and in severe cases, even death. In fact, the loss of as
little as 1–2% of body mass in water, even for short periods of time (i.e.,
hours), can negatively impact a variety of physiological processes and
mental function. For example, researchers have shown that mild
dehydration (1–2%) can result in loss of performance, including
cardiovascular function and performance (143, 178), intermittent cycling
performance (229), muscle strength (182), and memory processing and
cognitive function (236). Furthermore, prolonged mild dehydration has
been associated with central nervous system damage (236).
The relationship between hydration state and thermoregulation is an
important consideration considering that dehydration can promote feelings
of fatigue, heat exhaustion, and heatstroke. During exercise, factors such as
temperature, humidity, and type of clothing may all impact sweating rates.
In fact, it is not uncommon to lose 2–3% of body mass, mostly water,
during a typical exercise session, especially in hot environments.
Researchers have reported losses of up to 8% of body mass during very
long-term exercise, such as marathon running, or repeated high-intensity
exercise such as fall football training when fluid replacement is inadequate
(28, 175). In light of these findings, it is important to note that thirst may
often lag behind the actual need for water (64). Therefore, it is important
that athletes ingest fluid regularly even if they had not yet recognized their
thirst as a symptom. Typically, consuming 450–600 ml (15–20 fl oz) every
30 min should provide adequate fluid replacement for both long-term
exercise and prolonged intermittent high-intensity exercise such as football
training. Sport scientists should note the importance of monitoring
hydration to ensure proper practices. While blood measures of hydration
may provide the most accurate information, they are invasive and quite
expensive. Thus, additional practices such as urinary specific gravity
measured by refractometry or something as simple as weighing the athlete
before and after practice may provide valuable information regarding the
hydration status of athletes.
Electrolytes are soluble minerals that have a positive or negative charge
and play a role with membrane potentials (102). It should be noted that a
substantial loss of electrolytes may interfere with various physiological
functions (e.g., active and passive transport systems and fluid balance) but
may also indirectly affect thermoregulation and other metabolic functions.
Of the electrolytes potentially lost during exercise, sodium, potassium, and
chloride are the most important (142). While sodium and potassium are
positively charged (cations), chloride has a negative charge (anion). Most
electrolytes, including sodium, potassium, and chloride, are easily obtained
in the diet but may also be obtained by consuming most sport drinks. While
electrolytes and some vitamins may be lost in sweat during exercise, losses
are not typically large or significant, and thus, the replacement of
electrolytes may be unnecessary, especially among acclimatized athletes
(102). However, sport drinks may offer additional benefits to athletes, at
least under certain conditions. For example, non-acclimatized or partially
acclimatized athletes training in hot environments may also produce low
sodium concentrations, usually over the course of 3–5 days (145, 197).
Thus, chronic ingestion of a sport drink could offset the low sodium
concentrations.
Rehydration may take more than five hours. While dehydration–
rehydration practices are common within weight class sport athletes, the
potential positive effects of these practices may be negated during
subsequent competition. It has been suggested that while the effect of
dehydration is often quite negative (225), these effects may be exacerbated
with losses of more than 2% body mass. Furthermore, repeated bouts of
rapid dehydration may also be negative due to accumulative effects of such
practices (225). It should be noted that rehydration by artificial means (e.g.,
intravenous infusion of fluid), can be dangerous and should be avoided if
possible. It is recommended that weight class athletes should avoid foods
that cause water retention (salty foods) and high-fiber foods in order to
make weight.

Weight Gain
Because some athletes in sports such as American football, rugby, and
throwing events, and in the heavier classes for boxing, judo, and
weightlifting, may range from 100–160 kg (220–353 lb), much thought
must go into achieving these large body masses to ensure that LBM gains
are optimized, and fat gains minimized. It should be noted that the planning
should include not only physical training, but nutritional strategies as well.
While increases in LBM may be the goal of a number of athletes, several
considerations should be taken into account. First, it should be noted that
well-trained athletes will almost always gain some fat while increasing
LBM (74–76). Moreover, researchers have shown substantial gains in body
mass are almost always accompanied by an increased body fat percentage
(75). This may be further exacerbated if diets containing more fat calories
are used for a longer period (25, 59, 220) even if the number of kcal stays
consist. Thus, it would be prudent when one is gaining body mass to keep
the fat content of food eaten to under 30% of total calories and ingest a
relatively greater amount of unsaturated fats (70–80% of total fat intake).
The combination of a well-planned diet and specific physical training,
particularly weight training, can lead to the greatest improvements in body
composition and LBM. Previous recommendations suggest that gains in
body mass should be relatively slow (0.5–1.0 kg week–1 (1–2 lb), as this
lower rate may reduce gains in body fat (20). It should be noted that when
larger amounts of weight are gained over a prolonged period, gains in body
mass should occur at an even slower rate (0.25 to 0.5 kg week–1 (0.5–1.0 lb)
to minimize fat gain.

Weight and Fat Loss

Whether athletes are competing in sports that include weight classes or not,
maintaining low body weight and body fat are necessary to be competitive.
However, in some instances, athletes, especially those in weight class-based
sports (e.g., weightlifting, judo, wrestling, etc.), athletes may have to lose
body mass and fat mass. However, it is important take care take care in both
maintaining and losing body mass to prevent performance decrements from
occurring. If reductions in body mass are being considered, the following
issues should be addressed.
Untrained individuals and novice athletes can lose body fat (and
sometimes body mass) while increasing LBM by reducing caloric intake
and consistent training (206). However, it may be difficult for already
relatively lean athletes to lose substantial body mass without losing some
LBM as well, especially if caloric restriction is used to enhance body mass
loss (15, 228). While the potential loss of LBM due to caloric restriction
may be reduced with structured resistance training (15) and the
incorporation of a high-protein diet (228), the needs of the athlete should
always be considered. For example, since the influence of hormones during
puberty can impact an athlete’s body mass and relative body fat percentage
to a large extent, it is important that the long-term dietary needs of a young
athlete adjusted as necessary.
While the ideal weight for performance may not necessarily coincide
with the lowest body mass an athlete can maintain, semi-starved or
dehydrated athletes do not perform well. Previous literature has indicated
that caloric restriction can potentiate depleted energy stores, fatigue, and
overtraining (204). With novice individuals, such as children and
adolescents, some evidence suggests that chronic caloric restriction can
reduce adult stature (195).
The recommended maximum rate of body mass loss is approximately
1% or about 0.5–1.0 kg week–1 (1–2 lb) per week (71). Slower rates of
body mass loss are typically more desirable as faster rates can result in
LBM, glycogen stores, dehydration, and vitamin and mineral intake losses,
and increased potential of overtraining (71, 227). Caloric restriction and
loss of body mass for 4 weeks, or a total body mass loss of more than 5%,
may also alter an athlete’s micronutrient status and negatively impact
performance (71). It should be noted that evidence is lacking on the weight
loss needs of very small or very large athletes.
Another factor that should be considered with body mass and fat loss is
the fact that an athlete’s body fat can be too low. Some evidence has
indicated that low body fat content in males may be associated with
lowered testosterone concentrations and increased incidence of injury (207,
225). Additional literature has suggested that the incidence of impact and
perhaps overuse injuries may be increased due to low percentages of body
fat (158, 230). The lower limits of body fat in athletes should be no lower
than 5 and 12% for male and female athletes, respectively (72).
While rapid reductions in body mass may be accomplished with fluid
restriction (short-term), some practitioners believe that these rapid
reductions could enhance performance since LBM acquired at heavier body
masses may be retained. However, practitioners should note that this
method of rapid weight loss may be accompanied by several non-beneficial
effects including (227):

Reduced strength (probably least affected unless weight loss is very

rapid) and power.
Decreased low- and high-intensity endurance.
Lowered plasma volumes.
Reduced cardiac function.
Impaired thermal regulation.
Decreased renal function.
Decreased glycogen concentrations.
Loss of electrolytes.

Monitoring Nutrition
It is important to monitor the dietary of intake of athletes to ensure that
athletes are consuming the appropriate macro- and micronutrients to meet
their dietary needs to address their goals. The dietary information of
athletes can be tracked using a variety of resources. Beyond paper and
pencil, a number of nutritional apps may be used; however, athletes and
practitioners should be aware of their benefits and limitations (180).
Obvious benefits of such apps are their convenience and the creation of
awareness regarding food and kcal intake in relation to their training (35).
Creating awareness among athletes can help them take ownership of their
dietary intake, but also educate them about improved dietary practices.
However, a limitation of such apps is that they may cause some athletes to
develop obsessive kcal counting if their body composition goals are not
achieved within an athlete’s ideal timeframe. For example, some research
has indicated that nutrition apps may increase the risk for developing
disorders such as anorexia nervosa, body dysmorphic disorder, and
obsessive–compulsive disorders (165, 192). This limitation stresses the
importance of educating the athlete on best nutritional practices and the
negative health and performance effects of eating (and associated)
disorders.
Chapter Summary
Great strides have taken place in nutrition, and especially sport nutrition, in
the past three decades. Several factors have brought nutrition, sport
nutritionists, and dieticians to the forefront of sport management and have
made nutrition an integral part of planning programs for sports. These
factors include the realization that the RDA values for nutrients such as
protein, can be inadequate for the demands of many sports, the
understanding that pre- and post-training or event drinks can enhance
recovery, and the improved practices of gaining and losing weight. As more
universities offer specialty degrees and certifications in sport nutrition, it is
likely that future research will benefit the nutritional practices of athletes.
Furthermore, it is our hope that this research will benefit an athlete’s sport
performance.
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5 Ergogenic Aids

DOI: 10.4324/9781003096139-7
Introduction
Ergogenic aids play a key role in high-level performance of athletes and can
include devices, substances, or certain practice constraints. More explicitly,
ergogenic aids may be physiological (e.g., creatine), pharmacological (e.g.,
caffeine), environmental (e.g., hypoxia), mechanical (e.g., footwear), or
psychological (e.g., imagery). Physiological ergogenic aids are substances
that occur naturally in the body, and the ergogenic effects are experienced
when supramaximal levels are achieved. Alternatively, pharmacological
ergogenic aids are substances or drugs that do not occur naturally in the
body and therefore are dosed according to the observed effects.
Environmental ergogenic aids are deliberate changes in environment that
inherently alters the body’s internal milieu in a manner that would lead to
supramaximal acute performance or chronic adaptation relative to the
expected training response in a more typical setting. Physiological and
pharmacological are more difficult to distinguish, as both involve
substances that improve the body’s response to training or readiness to
compete when consumed. Mechanical ergogenic aids are used with the
intention of improving the body’s acute performance in training or
competition.
Most ergogenic aids can be thought of as an augmentation aimed at
boosting a particular aspect of training or competitive performance.
However, it is often the case that an ergogenic aid is creating an unfair
advantage for the athletes that use them or is exposing the athlete to side
effects that are a threat to the athlete’s health or well-being. The various
governing bodies overseeing each sport and its levels work tirelessly to
carefully police ergogenic aids to uphold the integrity of competition and
preserve the health status of the athletes. Therefore, the authors will forgo
any discussion of banned substances (e.g., anabolic steroids) or processes
(e.g., blood doping), as these would not be useful for practitioners aligned
with the ethical standards universally agreed upon in sport. Because sport
science, as we have defined it in previous chapters, includes both the
improvement of sport performance and its equipment, we will move
forward with a rather inclusive discussion. However, only a brief discussion
of psychological ergogenic aids will be provided, as it falls outside the
authors’ collective scopes of practice. Readers interested in the various
psychological ergogenic aids and their efficacy are directed towards the
work of Baltzell (8).
Physiological and Pharmacological Ergogenic
Aids
Vitamin D
Vitamin D is a fat-soluble vitamin produced in the skin. Although vitamin
D is considered a vitamin, it has distinct characteristics relative to others.
First, it is not obtained in the typical human diet in large quantities (though
foods like fatty fish have vitamin D, inordinate amounts would need to be
consumed to meet RDA requirements) and therefore the principal source of
circulating vitamin D is from endogenous production stimulated by
cutaneous ultraviolet B radiation in sunlight (23, 89). Secondly, activated
vitamin D is a secosteroid hormone, not a cofactor in an enzymatic reaction
like many other vitamins (23, 89). For the reader’s information, a
secosteroid hormone can be thought of as a hormone with a broken “ring”
in its molecular structure. Thirdly, vitamin D is unique from other vitamins
because its steroid system begins in the skin and not the mouth (23, 89).
Vitamin D deficiency is extremely prevalent in athletes (76, 79, 82, 115)
and therefore sport scientists must be concerned with the vitamin D status
of the athletes under their watch. Furthermore, deficiency is associated
increased incidence of serious illnesses (54) and a risk factor for all-cause
early morbidity (88). Therefore, withholding vitamin D would violate
modern medical ethics. The definition of vitamin D deficiency changes
regularly, and is generally agreed to be greater than 50 ng mL–1 (49, 55).
This is supported physiologically, as cholecalciferol (vitamin D’s parent
compound) is not stored in the fat or muscle tissue for future use until
25(OH)D levels exceed 40–50 ng mL–1 (49, 55). Furthermore, the body will
divert all available vitamin D to immediate metabolic demands when below
that threshold, which suggests that such a status is a state of substrate
starvation (49, 55). Therefore, most evidence regarding the ergogenic
effects of vitamin D are aimed at achieving levels of 50 ng mL–1.
 Supramaximal dosages of vitamin D – technically required per our
definition of a physiological ergogenic aid – have yet to be explored
extensively. Nonetheless, the robustly demonstrated favorable effects of
increasing vitamin D levels warrant its discussion as an ergogenic aid. As
far back as the 1930s, sport scientists began exploring the effects of
ultraviolet irradiation on athletic performance. In 1938, a group of Russian
scientists demonstrated improvement in sprint performance following
irradiation (44). From there, evidence of irradiation improving
cardiovascular fitness (75), muscular endurance (2), and even pain
sensitivity followed (103). In the 1950s, the irradiation approach was
refined to elucidate that the vitamin D-producing ultraviolet B range was
the most effective wavelength for improvements in performance (e.g.,
forearm strength, work output) and health markers (e.g., resting heart rate,
basal metabolic rate) (51, 74). Since then, vitamin D has demonstrated the
ability to increase both the percentage and area of type II (fast) muscle
fibers (98, 101), which may be particularly advantageous for strength-
power athletes or athletes aiming to retain sufficient muscle mass. Adequate
vitamin D levels have also been associated with better reaction times and
balance (23), potentially providing important impact for skill-intensive
sports such as baseball, gymnastics, or tennis. However, these associations
do not behave linearly, disappearing at vitamin D level in excess of 50 ng
mL–1 (23). It is worth mentioning that virtually every recent study beyond
the original investigations by the Russian sport scientists has been done on
non-athletic – and even pathologic – subjects. That need not raise any
skepticism in the reader regarding the results discussed, but such drastic
effects may not be observed in athletes. Nonetheless, the aforementioned
prevalence of deficiency in athletic populations makes it a logical best
practice recommendation to have athletes at levels of at least 50 ng mL–1 to
avoid any performance impediments.

Antioxidants
The maintenance of redox balance and mitigating damage caused by free
radicals are essential functions that exogenous and endogenous antioxidants
must work cooperatively to achieve (50). However, it is also clear that the
production of reactive oxygen species (ROS) as a result of skeletal muscle
work, play a key regulatory role in adaptation to endurance training (91).
Antioxidants possess different solubility, which in turn impact its
localization in biological tissue and ultimately its effects (83). For example,
lipid-soluble antioxidants protect against oxidative damage of membranes
due to their localization in that tissue type (83). Alternatively, water-soluble
antioxidants may not have access to ROS located within lipid membranes,
but would be able to function in the cytosol, mitochondrial matrix, or
extracellular fluids (83). Vitamin E and vitamin C are the most extensively
studied lipid-soluble and water-soluble antioxidants, respectively, within the
context of athletic performance. Therefore, attention will be paid to these
two, especially considering their interaction in scavenging radicals (3).
Vitamin E – a group of antioxidants that includes tocopherols and
tocotrienols – are only synthesized by plants and are therefore necessary
components of a normal diet, regardless of desired performance outcome
(64). It scavenges peroxyl radicals and inhibits oxidative damage in lipid
cell membranes (52). There is a fair amount of evidence that vitamin E
reduces muscle damage via mechanical stress in addition to its oxidative
damage capabilities (20, 62, 94). However, this is far from definitive, as
vitamin E has shown little effectiveness in attenuating muscle damage or
soreness in other investigations (5, 11). Furthermore, there is a paucity of
research to the authors’ knowledge that vitamin E has a favorable impact on
physical performance of any kind – inclusive to both endurance (20, 62, 94)
and strength-power (5). Therefore, though vitamin E may protect from
mechanical and oxidative stress, it cannot be recommended at this time as
an efficacious ergogenic aid.
Vitamin C (or ascorbic acid) is essential for many physiologic functions
and must be obtained exogenously since it cannot be synthesized by
humans (3). It plays an important role in the athlete’s defense mechanisms
against ROS, which are elevated during training and performance (50).
More specifically, vitamin C has demonstrated the ability to reduce delayed
onset muscle soreness and creatine kinase concentrations following
eccentric exercise (29). It possesses strong reducing properties and
contributes to redox cycling through generating transition metal ions (e.g.,
Fe3+ to Fe2+; Cu2+ to Cu+) that stimulate free radical chemistry (83). In
addition to the direct free radical scavenging activity, vitamin C supports
collagen synthesis as a positive regulator and is therefore beneficial for
athletes with respect to tendon, ligament, bone, and blood vessel health and
function (36, 100). Lastly, vitamin C plays an important role in enhancing
the antioxidant action of vitamin E (3, 83). Because the phenol group of
tocopherol is located at the water-membrane interface of biological
membranes, interaction between vitamin C and vitamin E occurs and
facilitates antioxidant action (83). Therefore, vitamin C plays a fundamental
role in the antioxidant network. However, if taken in excess, there is also
evidence that vitamin C may induce damage and it is therefore not
recommended to dose in excess of the upper limit of the recommended
daily allowance (3).
Though neither vitamin E nor vitamin C is ergogenic when taken in
isolation, it is logical that the two taken together may elicit a different
effect, especially considering the facilitated antioxidant action as a result of
their interaction. However, Bryant and colleagues (20) tested the effects of
vitamin E and vitamin C both in isolation and in combination. Though
differential anti- and pro-oxidant outcomes occurred, no supplemental
regime improved performance. Therefore, despite a decrease in oxidative
damage, vitamin E and vitamin C – whether taken exclusively or
collectively – do not have sufficient evidence to expect performance
improvements.

Creatine
Creatine (Cr) is one of the most popular and evidenced ergogenic
nutritional aids used by athletes. Cr is a member of the guanidine
phosphagen family and is a naturally occurring amino acid compound that
can be found in commonly consumed foods such as red meat and seafood
(69). Most endogenous Cr (approximately 95%) is found in the skeletal
muscle, though small amounts can be found in both the brain and the testes
(69). Narrowing to the skeletal muscle, the Cr pool (which includes both
phosphocreatine and Cr) averages around 120 mmol kg–1 of dry muscle
mass for a 70 kg individual (61). However, the upper limit is substantially
above this value at around 160 mmol kg–1 of dry muscle, which provides
the foundational rationale for Cr supplementation. Furthermore, about 1–
2% of the intramuscular Cr present is degraded into creatinine (the
metabolic byproduct) in daily living, which means that the body must
replenish 1–3 g of Cr per day in order to maintain normal stores. About half
of the daily need for replenishment will be consumed in a regular diet (7),
though this number can be influenced adversely by vegetarian diets (21).
The remaining amount of Cr that requires resynthesis that is expended in
daily living (independent of athletics) occurs in the liver and the kidneys
from arginine and glycine and a cascade of enzymes.
As previously mentioned, the normal diet will contain in the realm of 1–
2 g day–1 of Cr, which would saturate muscle created stores to about 60–
80% (depending on the athlete’s body mass). Therefore, Cr supplementation
would aim to close the gap on the remaining 20–40% and achieve full
muscle saturation (61). Studies have consistently demonstrated that
supplementing Cr will increase intramuscular Cr concentrations under a
variety of dosing protocols (69). Though a variety of supplementation
protocols have been proposed and subsequently studied, the most effective
appears to begin with a “loading” phase. “Loading” involves ingesting
about 5 g of Cr per day (or 0.3 g kg–1 of body mass) four times daily for 5–
7 days (68). There may be deviations from this protocol however, such as if
an athlete were starting from an even greater deficiency due to diet,
pathology, or extremely high physical workloads. Furthermore, it should be
clarified that the aforementioned loading protocol is aiming to fully saturate
the muscle and even higher dosages may be required if increasing brain
concentrations were desired (15, 17). Nonetheless, once the muscle is fully
saturated, a retaining dosage of 3–5 g day–1 appears to suffice (61), but
larger athletes may need to ingest even higher amounts (upwards of 10 g
day–1) (69). For larger athletes or those with high levels of exertion, it may
be advised to ingest Cr concurrently with carbohydrates, as this
combination has demonstrated efficacy in improving retention (47, 104).
Another approach to muscle saturation is to ingest approximately 3 g d-1 of
Cr for around one month and avoid any “loading” altogether. Though it may
eventually lead to muscle saturation, it is generally agreed to be less
effective than loading due to the prolonged period before any performance
or training enhancement would be realized. Therefore, Cr “loading” is the
most frequently recommended dosing protocol. It should also be noted that
it generally takes approximately 4–6 weeks following Cr supplementation
cessation for Cr levels to return to baseline values. Acknowledging such a
time course may be critical for weight class sports like wrestling, as Cr will
reasonably add body mass. Following cessation, no evidence suggests any
suppression of endogenous Cr production is experienced and therefore the
detrimental long-term effects of Cr supplementation are reasonably
negligible if not non-existent (70).
Generally, Cr is ingested in an attempt to support phosphagen
metabolism and has demonstrated the ability to improve high-intensity
exercise performance acutely and lead to greater strength-power adaptations
(31). However, Cr has demonstrated much more versatility as an ergogenic
aid beyond phosphagen metabolism. Cr supplementation has been shown to
increase glycogen replenishment rate, which would drive higher
performances both in athletes that have to sustain submaximal efforts (e.g.,
65–75% VO2max) or engage in repeated or intermittent high-intensity
efforts (e.g., most team sports). Considered collectively, it may be inferred
that Cr supplementation could favorably impact the phosphagen system,
oxidative metabolism, and even reduce muscle acidosis. Furthermore, Cr
supplementation has demonstrated efficacy in improving cognition and
neuroprotection (15), which may have implications for skill development,
decision making within sport, concussion injury risk reduction, and even
indirectly support sport tactics. Lastly, Cr supplementation may be used as a
recovery aid in a variety of athletic populations (32, 92).
Bicarbonate Loading
Bicarbonate loading refers to the ingestion of bicarbonate – an extracellular
buffer with an integral role in maintaining electrolyte homeostasis (i.e.,
stable electrolyte gradient) between intra- and extracellular environments
(63) – in the hours prior to competition. Doing so elevates the pH and
bicarbonate levels of the blood both before and during exertion, which is
theoretically beneficial to sports that involve explosive efforts, multiple
bouts, and large muscle mass recruitment (48). The rationale being that
acute bicarbonate loading would improve muscle buffering capacity of
hydrogen ions produced through anaerobic glycolysis. The increase in the
rate of removal of hydrogen ions from working muscle delays the metabolic
acidosis induced from the sport action, which would also stave off the onset
of impaired force production. Though acute doses of 0.3–0.4 g kg–1 are
generally recommended, oftentimes these higher-end, short-term doses lead
to gastrointestinal discomfort or diarrhea. Therefore, delayed-release
capsules for bicarbonate loading have been explored and appear to alleviate
some of the gastrointestinal distress while still eliciting favorable
performance changes (53).
Despite sound theoretical underpinnings and a relatively robust body of
literature, the ergogenic effects on endurance performance remain
equivocal. Generally, bicarbonate loading is considered ergogenic when the
duration of high-intensity effort is between 30 s and 10 min (84). Though
this sentiment considers the research to date at an aggregate level,
McNaughton (86) provides direct support of this conclusion. They
examined the effects of bicarbonate loading on anaerobic power
performance on a cycle ergometer at work intervals of 10 s, 30 s, 120 s, and
240 s. No meaningful effect was observed on the 10 s and 30 s trials, but
performance was substantially improved for work periods of 120 s and 240
s (86). Because most studies that have explored the ergogenic effects of
bicarbonate loading have used exertion periods greater than 30 s, it is
generally agreed that bicarbonate loading is efficacious for high-intensity
muscular endurance. Furthermore, efforts less than 30 s could reasonably be
classified as efforts of muscular strength, not muscular endurance – where
bicarbonate loading effects are practically negligible (48). Though this is a
reasonable interpretation of the literature, it does appear that there are some
other factors at play outside of the work duration as several studies have
observed null effects using intervals greater than 30 s (48). This may be in
part because the exact mechanisms by which bicarbonate loading enhances
muscular endurance may not be fully understood. More specifically, it may
not exclusively pertain to the buffering of hydrogen ions. Instead,
bicarbonate loading may play a role in the overall management of
membrane excitability during exercise, including the regulation of
potassium ions (102). Future research should aim to elucidate the various
mechanisms by which bicarbonate loading may enhance high-intensity
endurance performance, as this may have important implications for the
practical usage of this physiological ergogenic aid.

Caffeine
Caffeine is yet another ergogenic aid that is among the most widely used in
the sport community. Though it appears in many beverages (e.g., coffee,
tea), it is not essential for health. Furthermore, it is probably the most
complementary ingredient in supplements and other nutritional products, so
understanding its mechanisms and efficacy is extremely valuable for the
sportsperson and supporting practitioners. Several mechanisms for the
action of caffeine have been identified, but the most important
physiologically is the inhibition of adenosine receptors. Caffeine is able to
elicit this inhibition by holding a very similar structure to that of adenosine
and can therefore bind to the receptors (adenosine A2A receptors) and block
its action. Adenosine receptors are ubiquitous, appearing on tissues of the
brain, heart, smooth muscle, adipocytes, and even skeletal muscle (45).
Furthermore, caffeine may have intracellular actions. These are not well
understood, but likely include direct effects on enzymes or influence post-
receptor events (45). Collectively, this implies that caffeine can have a
relatively pervasive effect and therefore have a variety of cooperating
responses that are both primary and secondary actions.
A plethora of studies have demonstrated enhanced aerobic endurance
performance following caffeine ingestion (26, 27), which have often been
complemented by lower ratings of perceived exertion (RPE) during
submaximal aerobic training and activity (6). These outcome-related
findings in aerobic performance are mostly attributed to increased lipolysis
or the sparing of muscle glycogen following caffeine ingestion, partly as a
result of inhibiting phosphodiesterase. To observe such effects, it is mostly
recommended that a dosage of 3–9 mg kg–1 of body mass be ingested
within 60 minutes of exertional activity (i.e., training, competition). It
should be noted that the timing of caffeine ingestion is the subject of much
debate. The 60-minute window alluded to manifests from the rapid
absorption of caffeine – whereby plasma concentrations reach maximum
levels at approximately 60 minutes. However, caffeine is slowly
metabolized, and some individuals can maintain these concentrations for
upwards of three to four hours – though this does appear to be dependent on
genetics (16, 65, 95). The three- to four-hour mark also appears to be where
free fatty acid levels are at their highest due to caffeine-induced lipolysis.
Therefore, though 60 minutes is generally recommended, the optimal
window for endurance performance enhancement may be much wider.
Additionally, the dosage is likely dependent upon lean mass (due to its
water-solubility) and fat mass (due to its fat-solubility). Similar to the lack
of conclusiveness that exists with the timing of caffeine, such is the case for
the dosage as well as indicated by the rather wide recommended range
provided.
Despite relatively robust study of caffeine’s efficacy in endurance
performance, the support pertaining to strength-power performance has
much greater paucity. On one hand, caffeine ingestion has been shown to
acutely improve maximal strength in the bench press (4, 43) and peak
torque in leg extension and flexion (60) – all with dosages of 6 mg kg–1
body mass. Studies have also shown improvement in strength-endurance,
measured by repetitions to failure, when supplementing with similar
dosages of caffeine (46). Though the existence and reproducibility of this
literature gives reason for optimism, there is just as much evidence to the
contrary. Beck and colleagues (13) provided a fixed dosage of 201 mg of
caffeine to 31 males from diverse training backgrounds in hopes to enhance
maximal strength and were unable to demonstrate any ergogenic effect. The
lack of favorable effects may be due to the absolute nature of the dosage
rather than prescribing relative to body mass. This appears to be an
important factor, as Williams and associates (114) even increased their
absolute dosage to 300 mg and saw no meaningful improvements in
maximal strength or anaerobic power performance. Furthermore, training
background appears to be an important consideration, as many of the
aforementioned studies that were able to demonstrate ergogenic effects of
caffeine used at least moderately trained subjects, while those that were not
tended to have at best a blend of trained and untrained within their subject
pools. Consequently, more work must be done in this area, with special
attention paid to different relative dosages, training statuses, and
performance tasks.
Environmental Ergogenic Aids
Intermittent Hypoxic Training
Training at altitude has been a common practice for endurance athletes for
decades, but not all athletes have the geographic convenience to “train
high” with the consistency needed to experience ergogenic changes. As a
result, many athletes have acquired technology such as nitrogen houses,
hypoxia tents, and specialized breathing devices to induce inspired hypoxia
to simulate being at higher altitudes. Intermittent hypoxic training (IHT)
refers to the discontinuous use of normobaric or hypobaric hypoxia in an
attempt to reproduce the ergogenic effects of training at altitude and permit
supramaximal sea-level performance (77). Though “training” is used in the
naming, IHT is inclusive of hypoxia in both exertion and resting states –
each with a myriad of strategies and programming variables (e.g., duration,
frequency) to consider. Unfortunately, a paucity of literature exists directly
comparing the effects of rest and exertion-related hypoxia, so findings must
be generalized inclusively with consideration to the “dose.” Furthermore,
whether the hypobaric hypoxia is real or simulated does not appear to alter
the effectiveness or the corresponding adaptive mechanisms, and so the
discussion will move forward absent of delineation between the two types.
Exposure and acclimatization to hypobaric hypoxia has demonstrated
favorable physiological changes that would be beneficial to both training at
altitude and subsequent performance when returning to sea level. Increases
in alveolar ventilation and reductions in mixed venous oxygen content have
been observed – leading to enhanced performance at altitude (107). These
changes may be paired with favorable angiogenic changes as well, with
increased capillary density observed in animal studies (9, 108).
Furthermore, both fat and carbohydrate metabolism may be favorably
altered, leading to decreased metabolite accumulation (e.g., lactate,
ammonia) (18, 117). Exposure to hypoxia at rest may also have
implications for eventual glycogen sparing.
 Though the mechanistic underpinnings discussed to this point are sound
and have demonstrated efficacy in improving endurance performance
following hypoxic acclimatization, improved sea-level performance is most
clearly associated with increases in hemoglobin and hematocrit – allowing
for greater oxygen-carrying capacity of the blood. Although some studies
using athletes have failed to demonstrate such an effect, it is appropriate to
be inclusive of cross-sectional studies of populations that are indigenous to
high-altitudes – where increased red cell mass has been unequivocally
observed (96). Though natives of high-altitude environments clearly have
chronic exposures, shorter bouts of exposure (84–114 min) have also shown
to be a sufficient stimulus to induce erythropoietin increases (1, 40).
Because of this dose-response relationship, many athletes have explored the
“living high–training low” model for improving sea-level endurance
performance, originally introduced by Levine and Stray-Gundersen (78).
This combinatory lifestyle and training approach has demonstrated the
ability to improve time-trial performance (24), erythropoietin concentration
within 48 hours of returning to sea level, and improved oxygen uptake (84).
Though some of this evidence is quite compelling, the IHT literature is
far from conclusive and some even question whether it enhances the
training stimulus. Specifically, when studying competitive athletes, a
meaningful body of literature suggests no effect from IHT. Vallier and
colleagues (110) found no statistically significant differences in VO2max
between groups of triathletes following IHT. This agrees with the findings
of Meeuwsen and associates (87), who also studied triathletes and found no
differences in VO2max. Interestingly, Meeuwsen’s group did observe
improvements in peak power output during a Wingate test 9 d after
returning to sea level. This is an interesting performance implication, but
even more intriguing is that it included the potential delayed effects of IHT.
Few studies include an appreciation for delayed training effects, which may
explain some of the negligible effects observed by many. However, there
are concerns that the hypoxic environment is detrimental to training and
subsequent performance regardless of lag effects. For example, the
environment permits only submaximal training (e.g., lower power outputs,
reduced oxygen uptake, metabolic compensation) which may ultimately
lead to a lesser performance, especially under the maximal demands of
time-trials or bouts of exhaustion. The collective uncertainty warrants
further investigation on the efficacy of IHT on endurance performance,
especially in trained populations.
Mechanical Ergogenic Aids
Footwear
Perhaps one of the most researched topics is the effect of footwear
construction or type on injury and running performance (28, 41, 106). In
2020, Sun et al. (106) indicated that running shoe constructions that
increased forefoot bending stiffness at the optimal range may benefit
performance-related variables such as reducing energetic cost, maximum
volume of oxygen consumption (VO2), energy lost at the
metatarsophalangeal joint, and sprint time. Furthermore, the authors
concluded that softer and thicker midsoles may reduce impact forces and
attenuate shock during impacts and that minimalist shoes may improve
running economy and increase the cross-sectional area of the Achilles
tendon, but increase metatarsophalangeal and ankle loading compared to
conventional shoes. From a performance standpoint, much of this research
has led to the development of running shoes designed to break the men’s
two-hour marathon (56, 93). In 2018, world records were broken over the
15 km, half-marathon, marathon, and 100 km distances (22), with each of
the runners wearing the Nike Vaporfly 4% running shoe (herein known as
the Vaporfly), which differed from a conventional running shoe with the
inclusion of an embedded carbon-fiber plate, Pebax foam, and a thicker
midsole. The carbon-fiber plate within the shoe works to stiffen the
metatarsophalangeal joint by acting as a lever to reduce the ankle work rate
(57). The Pebax is a lighter and more resilient midsole material compared to
ethylene vinyl acetate (EVA) and thermoplastic polyurethane (TPU) (22). In
fact, Hoogkamer et al. (56) showed that the Pebax material “returns” 87%
of the compressed energy during foot fall compared to 66% and 76%
energy return of EVA and TPU materials. Finally, the thicker midsole of the
Vaporfly effectively increases the leg length of a runner (greater flight time)
and provides increased cushioning without the typical loss of energy as a
result of added weight (109). Overall, a previous analysis of the Vaporfly
shoe displayed a 4% improvement in running economy and 3.4% increase
in running speed (56). It should be noted that the Vaporfly served as the
predecessor to the Nike Air Zoom Alphafly Next%, which included
additional air-filled sacs, termed by Nike as “Zoom Air Pods,” meant to add
cushioning and increase energy return (93). Senefeld et al. (99) examined
the times and footwear of the Top 50 male and 50 female finishers of the
World Marathon Major series in the 2010s before and after the
aforementioned Nike shoes were introduced. The authors concluded that
marathon finishing times were considerably faster for both male (2.0% or
2.8 min) and female (2.6% or 4.3 min) who wore technologically advanced
Nike shoes compared to others. Furthermore, marathon times substantially
improved 0.8% or 1.2 min and 1.6% or 3.7 min in male and female runners,
respectively, who changed from a previous shoe to a new Nike shoe (99).
Advances in running shoe technology cannot be ignored given the nearly
one hour decrease in marathon time from the first Olympic marathon (2 h
58 min 50 s in 1896) to Eliud Kipchoge’s 1 h 59 min 40 s marathon
performed in a controlled setting on October 12, 2019.
Another example of footwear that may contribute to positive
performance adaptations comes in the form of weightlifting shoes.
Researchers have shown that weightlifting shoes (Figure 5.1b) that have a
raised heel may reduce trunk lean and increase foot segment angle
compared to running shoes (Figure 5.1a), which may reduce shear stress in
the lower back and increase knee extensor muscle activation during the
back squat, respectively (97). Additional research has also shown that
weightlifting shoes may increase squat depth while maintaining upright
posture via reduced ankle flexion, increased knee flexion, and a more
upright trunk (73). The results of the previous studies support the notion
that weightlifting shoes may contribute to an athlete’s ability to produce
force and potentially increase strength. Legg et al. (73) suggest that this
may be partially explained by the non-compressible nature of weightlifting
shoes. Combined with a solid, flat sole, the non-compressible nature of
weightlifting shoes increases the stability of an athlete. Previous research
has shown that greater stability may contribute to greater force and rate of
force development (85), which in turn, may contribute to greater strength
adaptations.
Figure 5.1 (a) Running shoe and (b) weightlifting shoe back squat
comparison.

While the two previous examples have discussed the use of various shoe
types, perhaps one of the most impactful and innovative advances in sport
science history came with the introduction of the klapskate at the 1998
Winter Olympics in Nagano, Japan. Klapskates (Figure 5.2) were first
described within the literature by van Ingen Schenau and colleagues in 1987
(111). Prior to klapskates, speed skaters were forced to take shorter strokes
(strides) to prevent themselves from stubbing the blade of the skate into the
ice (105). However, researchers concluded that the klapskate allowed speed
skaters to lengthen their stroke, which in turn allows them to utilize the
extensor muscles of the leg to apply more force and power to the ice (35,
112). Houdijk et al. (58) indicated that skating velocity and mean power
increased in elite speed skaters when using klapskates compared to
traditional skates. The authors noted that the increase in velocity and power
output was due to an increase in 11 J increase per stroke and an increase in
stroke frequency. The findings of the previous study were attributed to the
hinge mechanism which allows the blade to remain in contact with the ice
throughout the skater’s stroke, allowing plantar flexion of the ankle to
contribute to generation of power (113). In a later study, Houdijk and
colleagues (59) supported this notion and concluded that the increased
power output from using klapskates may be explained by an increase in
gross efficiency. With improved equipment and greater skating efficiency,
world records in speed skating have shown a steady downward trend in
both male and female skaters (71). However, Kuper and Sterken (71)
specifically mentioned that the klapskate was a major contributor to
enhanced performances.
Figure 5.2 Speedskating klapskate blade contact (a) without and (b)
with the hinge action of the skate.

Attire
An abundance of studies have examined the effect of compression garments
and their impact on performance. These garments apply mechanical
pressure to the body’s surface and compress and/or stabilize an athlete’s
underlying tissue (81). However, the studies have displayed mixed findings
with improvements in vertical jump (37, 66), 5 min repeat cycling bouts
(25), and 40 km cycling performance (34), but no improvement in 20 m and
60 m sprint (37), intermittent sprint activity (38, 39), or endurance running
performance (33). Because compression garments may not display
consistent improvements in performance, some research supports their use
as a method of recovery (19, 39, 42, 67). This may be due to the potential of
increased venous blood flow within the previously active musculature.
Additional attire that has led to numerous Olympic medal winners and
world record performances was the use of swimwear that allowed for less
drag in the water. For example, swimwear such as the Speedo S2000,
Aquablade, Fastskin, Fastskin FSII, LZR Racer, TYR Aqua Shift, Arena
Powerskin Carbon-Air 2, and Arena Powerskin Carbon-Air Limited Edition
are technologically advanced suits developed by the manufacturers to
reduce drag. Previous literature has examined the drag characteristics of
different swimwear fabric and determined that the surface structure (e.g.,
roughness, seam, and its orientation) have a statistically significant effect on
hydrodynamic drag (90). However, it should be noted that much of the
swimwear research has been performed internally by the manufacturers
with limited data in the scientific literature. It should be noted that due to
the incredible number of world records broken at the 2008 Beijing
Olympics, certain suits, including the LZR Racer swimsuit, have been
banned from Olympic competition.
Figure 5.3 Swimmer wearing an Arena Powerskin Carbon-Air 2
Open Back swimsuit for competition.

Equipment
Sport-specific equipment that may contribute to enhanced performances is
traditionally sought by both athletes and coaches. One example of this type
of equipment that has been thoroughly studied is the time-trial helmet used
within cycling competitions, also known as the aerodynamic helmet (herein
known as the aero helmet). While there are several factors that contribute to
success in the sport of cycling, a common factor that has been investigated
has been aerodynamics and the influence of drag. Whether time-trials are
being performed on the road or an indoor track, an aero helmet may reduce
wind drag and improve the finishing time of the cyclist (80). In fact, Kyle
and Burke (72) indicated that there may be a 7% reduction in drag when
cyclists wear an aero helmet. Using computational fluid dynamics, another
study showed that a combination of an aero helmet’s shape and the cyclist’s
head position may significantly impact drag forces, pressure, and wall shear
stress distributions on the cyclist’s entire body (12). It is important to note
that the construction of the helmet may impact drag as well. For example,
Chowdhury and Alam (30) indicated that there may be substantially less
drag using aero helmets that are longer and include smooth vents that have
a minimum area. As evidenced above, the science behind testing and re-
testing different aspects of equipment in combination with cyclists may help
provide the cyclists with the best equipment and racing strategies when it
comes to improving their time-trial performance.
Figure 5.4 Time-trial cyclist wearing an aero helmet during
competition.
Source: Image modified from “At the Front” by chuckwaters83 licensed under CC BY-SA 2.0.
Psychological Ergogenic Aids
Psychological state can have profound impacts on motor performance. Of
particular importance for the strength and conditioning professional are
athlete motivation, arousal, and effort. Indeed, sport psychology provides
several theories on the effect of psychological arousal on sport
performance. Additionally, the effect of effort on performance (10) and
training adaptations are well documented (14).
Athlete monitoring programs typically include performance tests that
attempt to capture various characteristics of physical ability (e.g., maximum
strength, rate of force development, maximum sprint speed) and rely on an
athlete’s ability to provide maximum effort. The effects of athlete effort
during training exercises may also compound over the long term to
influence the type and magnitude of training effects. Therefore, strength and
conditioning practitioners must be concerned with their athletes’ ability to
exhibit appropriate levels of arousal and effort during training and testing.
The Optimizing Performance through Intrinsic Motivation and Attention
for Learning (OPTIMAL) theory of motor learning focuses on the primary
components of enhanced expectancies, autonomy, and an external focus of
attention as a framework for influencing an athlete’s psychological state to
maximize motor performance (116). Strength and conditioning coaches
may find the OPTIMAL theory useful to devise strategies intended to
modify arousal and level of effort during exercise and training for both
acute and long-term performance adaptations. These strategies may include
activities such as breathing techniques, verbal cuing and encouragement,
and biofeedback.
Chapter Summary
Ergogenic aids come in many forms, including physiological,
pharmacological, environmental, mechanical, or psychological.
Physiological and pharmacological aids such as Cr and caffeine, as well as
the others discussed above, may have positive effects on an athlete’s
performance during training and/or competition. However, it should be
noted that the dosage, timing, and combined effects of other supplements
should be considered when incorporating these aids within the athlete’s
training regime. In addition, the athlete’s tolerance to specific physiological
or pharmacological aids and the goals of their training should be considered
due to the efficacy that some of these aids may have. Environmental
ergogenic aids such as IHT may have the potential to produce favorable
physiological adaptations for aerobic athletes; however, additional research
is needed before concrete conclusions can be drawn regarding its
effectiveness at enhancing training stimuli. Mechanical ergogenic aids,
namely running shoes, klapskates, and competitive swimsuits, have
contributed to many notable achievements and improvements in sport
performance. As a result, sport scientists will likely continue to investigate
modifications to existing mechanical ergogenic aids to further improvement
in sport.
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Part III
6 Physical and Physiological Reponses
and Adaptations

DOI: 10.4324/9781003096139-9
Introduction
There are a wide variety of physical and physiological adaptations that may
occur as a result of exercise and training. These adaptations may range from
an increase in an individual’s work capacity and sprint speed to increased
cardiac output and motor unit recruitment. While individual characteristics
and training intensity are just two factors that may impact these adaptations,
it should be noted that the adaptations are also specific to the type(s) of
training that an individual has or is currently undertaking. This chapter
outlines specific physical and physiological adaptations that may occur as a
result of resistance, sprint, endurance, and concurrent exercise and training.
Resistance Exercise and Training
The underlying factors associated with strength (ability to produce force)
are as follows:

Motor unit recruitment.

Motor unit activation frequency (rate coding).
Synchronization (ballistic movements).
Motor unit activation pattern (intramuscular activation).
Muscle action pattern (intermuscular activation).
Use of elastic energy and reflexes (stretch-shortening cycle).
Neural inhibition.
Motor unit type (muscle fiber type).
Biomechanical and anthropometric factors.
Muscle cross-sectional area.

These factors can be roughly divided into three areas: (i) neural, (ii)
hypertrophic, and (iii) anthropometric. Neural factors predominate during
the early phases of initial training, while hypertrophic alterations
predominate in the later phases of training.

Neural Factors
Motor control involves a basic pattern of nervous system activity and at the
same time improving motor control is a complex process and a critical
factor in sport performance. The intent to perform a movement is developed
in the higher brain centers and transferred to the motor cortex. The motor
cortex transmits signals by way of the brainstem and spinal cord to the
appropriate motor neurons.
In the initial stages of training, strength, power, and other performance
variables such as rate of force development, increase at a much faster rate
than muscle girth or measures of lean body mass (32, 67); therefore, the
strength gains are assumed to be the result of one or more neural
components. At the other end of the spectrum, advanced and elite strength-
power athletes have difficulty increasing lean body mass and muscle mass,
particularly athletes in body weight classes such as weightlifters and
powerlifters. However, these advanced athletes do still make strength gains
(although relatively small) with little or no alteration in body composition
or muscle size, again suggesting that neural component adaptation is taking
place (79, 80).

Recruitment and Rate Coding

The force of muscle contraction is primarily altered as a result of the
number and type of recruited motor units (MU) and the frequency of
stimulation (rate coding). The exact degree to which one mechanism is
emphasized over the other during muscle activation depends on the amount
of force required and the size and type of muscle being activated (25).
However, there is some doubt that an untrained muscle can be fully
activated under normal voluntary conditions (1, 75). Furthermore, strength
training can result in a greater activation of muscle, thus influencing
strength production.
Recruitment and rate coding of whole-muscle tension (force) is directly
related to the number of MUs activated and their frequency of activation.
Larger MUs tend to be activated at a higher frequency.

Motor Unit Recruitment

Motor unit recruitment within a muscle normally takes place in a
reasonably orderly fashion according to size (34, 35). To an extent, the size
of the MU dictates the activation threshold; larger MUs have higher
thresholds. Motor unit size covaries with MU type (25); thus, larger, more
powerful MUs would be recruited last in a mixed muscle. However, even
within muscles containing only or primarily one fiber type, the size
principle is still evident (12).

Rate Coding
Rate coding deals with the frequency at which recruited MUs are activated.
Typically, faster MUs are activated at higher frequencies. Rate coding
strongly influences the rate of MU and whole-muscle activation and is a
primary factor influencing the rate of force development (42). A study by
Viitasalo and Komi (85) clearly pointed out that the rise in MU activation as
measured by electromyography is associated with a rise in muscle force.
Typically, high rates of force development are necessary for success in
explosive and high-power activities such as sprinting, throwing, and
weightlifting. An important consideration for developing explosive
performance deals with improving an athlete’s maximum strength.
Maximum strength has strong relationships with rate of force development;
thus, building maximum strength may be a prime ingredient in producing
high rates of force development and explosive strength for many sport
activities (5). This is an important concept, and it may not be intuitive for
coaches, when designing their training prescriptions.

Activation Frequency and Synchronization

Another mechanism that can affect the ability of a muscle to produce force
is the synchronization of MUs. Motor units typically are activated as brief
“dynamic” twitches. Figure 6.1 depicts the asynchronous activation patterns
of several MUs. Note that during asynchronous activation, when one MU
deactivates, another is being activated; this pattern creates a relatively
smooth muscle tension production, which allows a relatively smooth
movement to occur. Increased muscle activation through recruitment or rate
coding can increase muscle force.
Under normal low-intensity muscle activation, MUs fire asynchronously.
However, as the maximum level of strength is approached, some MUs are
activated at exactly the same time as other MUs. As force output is
increased, greater levels of synchronization can occur (Figure 6.2). The
maximum frequency of activation can range from 30 to 50 Hz for low-
threshold MUs and up to 100 Hz for high-threshold MUs, depending upon
the type and the intensity of the muscle action. Furthermore, strength
training can enhance the number of MUs synchronizing and can result in
 synchronization at lower force outputs (76). The degree to which
synchronization affects maximum strength, especially when measured
isometrically, appears to be minimal (90). However, synchronization does
appear to play an important role in ballistic movements.

Figure 6.1 Motor unit asynchronous activation.

Source: Based on Semmler (74).

Task Specificity
There is a great deal of evidence for the concepts of intra- and
intermuscular task specificity. Intramuscular task specificity has to do with
specific patterns of activation for MUs, while intermuscular task specificity
relates to the interplay and pattern of activation among muscles during a
specific task. Some muscles are compartmentalized anatomically, and these
compartments may be more or less active during different tasks (88).
Furthermore, neurons are compartmentalized functionally into task groups,
such that specific groups of neurons are activated as a result of specific
tasks being performed (49). The concept of intramuscular task specificity
may help explain the phenomenon of regional hypertrophy (3, 6, 22, 82), in
which a specific exercise causes hypertrophy in one region of a muscle but
not in others. Bodybuilders have intuitively recognized this aspect of
training, arguing that to more completely develop a muscle, it is necessary
to perform many different exercises for that muscle.
Both intra- and intermuscular activation patterns can change with very
slight alterations in movement pattern, eccentric versus concentric actions,
or changes in velocity (75, 91). Because of these alterations in activation
patterns, selection of exercises for strength-power training should be
viewed as movement specific rather than simply a matter of training one or
more muscles. Improvement in the efficiency of intra- and especially
intermuscular activation implies an enhanced coordinative ability and is an
important mechanism contributing to improved strength expression (75).

Neural Inhibition
Somatic-reflexive neural inhibition includes feedback from various muscle
and joint receptors and has been suggested to be part of a protective
mechanism. This protective mechanism can reduce muscle tension during
maximum and near-maximum efforts. Strength training appears to reduce
receptor sensitivity and diminish inhibition, and this diminished inhibition
is partially responsible for the greater forces achieved (1).

Stretch-Shortening Cycles
The use of reflexes and stretch-shortening cycles (SSC) can also alter the
production of force (13, 20). In essence, a SSC consists of a plyometric
muscle action in which an eccentric action immediately precedes a
concentric action. The mechanisms involved in concentric enhancement
may include use of elastic energy, a stretch reflex, optimization of muscle
length, and optimization of muscle activation and muscle activation patterns
(13, 14). Learning to use the SSC more efficiently can markedly increase
force production. Evidence indicates that improving maximum strength can
augment both the eccentric and the concentric portion of the SSC (1, 20).

Motor Unit Types

Motor unit and fiber type also influence strength and particularly power.
Studies and reviews of the literature have indicated that a greater percentage
and a large cross-sectional area of type II muscle fibers may be
advantageous in terms of dynamic force production (31), even when muscle
architecture and other mechanical factors are taken into consideration.
Strength-power athletes typically have both a somewhat higher percentage
of type II fibers and a large total type IIx cross-sectional area compared to
untrained subjects. Strength training, particularly explosive strength
training, appears to increase the ratio of type II to type I muscle fiber cross-
sectional area in a manner favoring strength and particularly power
production (31). However, myosin heavy chain adaptation appears to be
such that a reduction in the percentage of type IIx fibers and an increase in
IIa fibers occur as the volume of resistance training increases (4, 41).
Although this alteration (IIx to IIa) would slightly reduce the myosin
ATPase activity of the fiber and therefore the potential power output, other
adaptive mechanisms more than compensate. Indeed, changes in the
nervous system and fiber or muscle hypertrophy could offset the potential
reduction in power. As the nervous system effect and perhaps hypertrophy
are longer lasting than the MU transformation effect, short-term reduction
in training volume, as with a taper, appears to allow a transformation back
toward the IIx MU type and slightly higher power outputs (69).
Biomechanical and Anthropometric Factors
Factors such as gross muscle architecture, angle of pennation, muscle
insertion point, height, limb length, and moment arm may alter the
mechanical advantage of the intact muscle lever system. For example,
weightlifters possess a high ratio of body mass to height (BM h-1) compared
to untrained subjects and other athletic groups. This BM h-1 is advantageous
because it can provide an increased force production. This advantage is
associated with the strong positive relationship between a muscle’s
physiological cross-sectional area and maximum muscle force-generating
capabilities (75). If two athletes of different heights and different limb
lengths have the same muscle mass and volume, the shorter athlete will
have the greatest muscle cross-section and therefore, greater force
production.
Muscle responds to resistance training by enlarging its cross-sectional
area (i.e., hypertrophy). In this manner, additional contractile elements
(myofibrils) are added to the muscle fiber. The underlying mechanisms are
complex and still not completely understood. The primary stimulus for
skeletal muscle hypertrophy appears to be a gain in tension and mechanical
strain (26, 62). Secondarily, there may be metabolic factors as a result of
repeated contractions that also stimulate the hypertrophic adaptations (7,
62). The stimulus causes a cascade of multi-level effects as illustrated in
Figure 6.3. The degree to which muscle damage stimulates hypertrophy is
unclear and is not likely a major factor (62).
Figure 6.2 The mechanism for motor unit synchronization.
Source: Based on Farina and Negro (23).
Figure 6.3 Muscle tissue remodeling based on potential metabolic
and mechanical stimuli. Activation of focal adhesive
kinase (FAK) by tension (through the costamere) is the
primary stimulus for myofibrillar hypertrophy.
Source: Adapted from Nosaka et al. (62); Stone et al. (77); West et al. (87); Zanchi and Lancha
(92).
Importance of Loading
Hypertrophy appears to be somewhat load-independent (50, 86). However,
the type of hypertrophy produced early in the training program (first few
weeks) may not be primarily myofibrillar but rather sarcoplasmic in nature
(21). However, evidence indicates that over long periods, myofibrillar
hypertrophy predominates and that this hypertrophy is related to strength
alterations (52). Indeed, the effect of loading on the degree of and type of
hypertrophy is unclear. The type of hypertrophy produced resulting from
high load/low repetitions versus low load/high repetitions and ballistic
movements appears to be different. Type II fibers produce somewhat
greater specific tension, substantially higher rates of force development,
velocities, and power outputs, and may respond to stimuli differently.
Training to failure can result in substantial hypertrophy. Although, as a
result of fatigue, training to failure can recruit high threshold MUs; the
recruitment appears to be incomplete and selective (55). Training to failure,
particularly with higher repetitions, tends to select type I MU and heavier
loading and ballistic movements target type II MU (61). However, strength
alterations appear to be strongly related to the load with heavier loads
producing superior effects (50).

Specificity of Training
As discussed previously, specificity of training refers to the degree of
similarity between regularly used training exercises and those making up
performance. Transfer-of-training effect refers to the degree of performance
adaptation that can result from a training exercise and is strongly related to
the concept of training specificity. Mechanical specificity concerns the
kinetic and kinematic associations between a training exercise and a
physical performance. Thus, mechanical specificity includes movement
patterns, peak force, rate of force development, acceleration, and velocity
parameters. The more similar a training exercise is to the actual physical
performance, the greater the possibility of transfer (9, 72, 77).
Sprint Exercise and Training
The mechanical demands of sprinting alone make it one of the most potent
of all training stimuli. Sprinting – at its simplest – is the net horizontal
displacement of the athlete’s center of mass in a maximal run that lasts less
than 15 seconds from start to finish (71). However, sprinting is generally
divided into phases (i.e., acceleration, transition, top speed) and the
mechanistic differences between them make sprinting more or less
compatible with other training contents (60). Furthermore, it should be
noted that sprinting is itself a skill that should be progressively matured
under the tenets of motor learning (e.g., constraints-led approach) (56).
Nonetheless, sprinting will be considered as a training stimulus and not a
training outcome for the sake of this discussion.

Neural Factors
The high rates of force development required during sprinting are going to
be mediated in large part by a muscle’s contraction abilities, which are
determined by the neuron innervating the activated fibers. Sprinting elicits
both central and peripheral changes to the nervous system – collectively
increasing neural drive (71). There is considerable overlap in the neural
adaptations to sprint and resistance training, with the nature of sprinting
permitting potentially greater efficacy with a select few targeted
adaptations. First, because of the very rapid storage and return of energy
required in sprinting relative to what can be experienced in resistance
training, muscle spindle excitation, voluntary activation, and firing
frequency adaptations may all logically be greater in sprinting (47, 71). H-
reflex at rest is also considerably lower in sprinters relative to other athletes,
likely due to the high activation threshold of the fast fiber MUs
preferentially recruited during sprinting (46). Therefore, a program
containing both resistance training and sprinting is thought to be best
practice in most (if not all) power sports (individual or team) due to the
unique overload placed on the nervous system during training by each
respective training modality. Sprinting, however, may be the most powerful
and workloads should be managed accordingly.

Muscular
Because of the unique neural demands of sprinting, it is also logical that
this training tactic will target the type II muscle fibers. This may be
advantageous in facilitating shifts to faster myosin heavy chain isoforms,
increasing the existing type II fiber size, or improving the type II to type I
cross-sectional area ratio (thus improving rate of force development
potential) (5, 84). Furthermore, changes in muscle architecture are likely
present, as sprinters tend to possess longer muscle fascicles – potentially
giving them an advantage in shortening velocity due to the addition of
sarcomeres in series (2). This shortening velocity advantage (and possibly
even the architecture changes themselves) may be in part due to an increase
in sarcoplasmic reticulum volume, which drives more calcium ion release
and creates a more favorable environment for rapid contraction (64, 70).
There may also be adjustments to muscle tissue and muscle–tendon
complex stiffness because of sprinting in training (44, 45). This can be
advantageous for running itself, but may also transfer well to other tasks
(e.g., changing direction, jumping) in team sports athletes.

Metabolic
Though not often considered, sprinting may be leveraged as a metabolic
stimulus as well. The rapid breakdown of phosphocreatine and the stress on
the glycolytic system during sprinting make it a favorable stimulus to
increase the enzyme content and kinetics. For example, myokinase and
creatine phosphokinase have been shown to increase following sprint
training (39, 65). Similarly, a host of glycolytic enzymes (e.g., LDH) have
been shown to increase following continued exposure to both long and short
sprint efforts (70). Obviously, changes may extend to aerobic metabolism
through the manipulation of sprint duration and rest intervals, but those
adaptations are more appropriately discussed within the context of
endurance training (65).
Endurance Exercise and Training
Adaptations to endurance exercise and training range from
cardiorespiratory (i.e., those related to delivery of oxygen to the working
musculature) to those related to metabolic processes (i.e., those related to
the production and utilization of energy) and musculoskeletal adaptations
(i.e., those related to joint structure and the production of force during
endurance training). These adaptations and their physical or physiological
effects are discussed in the sections below and a summary of the
adaptations are shown in Table 6.1.

Cardiorespiratory Adaptations
There are several cardiorespiratory adaptations that occur due to chronic
aerobic (endurance) training that include increased maximal cardiac output,
stroke volume, capillary density, and tidal volume. In addition, there may be
a decrease in resting heart rate and heart rate during submaximal exercise,
as well as a decreased breathing frequency during submaximal activities.
Cardiac output (i.e., the amount of blood pumped by the heart in liters per
minute) is the product of stroke volume (i.e., the amount of blood ejected
from the heart per beat) and heart rate (i.e., beats per minute) (33). Because
well-trained endurance athletes can have a resting heart rate of 40–60 beats
per minute (33, 53), an increased stroke volume can increase an athlete’s
cardiac output. Changes in stroke volume are the result of an increased end
diastolic volume and the influence of catecholamines such as epinephrine
and norepinephrine. Chronic aerobic training may increase venous return
due to an increase in sympathetic nervous system activity causing
vasoconstriction (8), the skeletal muscle pump pushing blood towards the
heart during exercise (30), and the respiratory pump caused by an increase
in breathing frequency and tidal volume (57). Collectively, these factors
contribute to a greater volume of blood returning to the heart and more
blood available for ejection out of the left ventricle. With more blood within
the left ventricle, the myocardial fibers may be stretched, which may then
recoil with a greater amount of ejection force causing a greater degree of
cardiac emptying, termed the Frank-Starling mechanism (33). Due to an
increased cardiac output, more oxygenated blood may be delivered to active
tissues. Furthermore, increased capillary density allows for a greater
diffusion of oxygen and metabolic substrates by decreasing the diffusion
distance (43).

Metabolic Adaptations
An increase in aerobic capacity is an obvious adaptation to endurance
training due to the frequent stimulation of type I muscle fibers. Not only
does this adaptation allow athletes to perform exercise at a given absolute
intensity with greater ease, but it also allows them to exercise at a higher
relative intensity of an enhanced aerobic power (81). These adaptations are
the result of a decreased utilization of glycogen and increased utilization of
fat as energy sources, resulting in the ability to prolong exercise at a given
intensity (37). Further adaptations may include an increased percentage at
which the onset of blood lactate occurs due to a reduced production of lactic
acid, changes in hormone release (e.g., catecholamines at high intensity),
and an increased rate of lactate buffering (53).
Additional adaptations at the cellular level include an increase in the
number and size of mitochondria (15), as well as an increase in myoglobin
content (19, 36) within the muscle cell. Combined with the greater diffusion
of oxygen from the bloodstream described above, the increased myoglobin
content helps increase the availability and utilization of oxygen, which in
turn may be used to break down glycogen and free fatty acids to produce
greater quantities of adenosine triphosphate (ATP) by the increased number
of mitochondria via the Krebs cycle and electron transport system. Due to
the increased availability of oxygen within the cell, aerobic metabolism
enzyme activity is also increased resulting in an enhanced breakdown of
glucose (17), which may then increase both glycogen (27, 28) and
triglyceride (58) stores. Metabolic adaptations within the muscle due to
chronic endurance training result in several adaptations that ultimately
increase muscle ATP, as well as stored creatine phosphate, glycogen, and
triglycerides. Simply, there is an increased oxidation of glucose for energy
purposes which spares other energy substrates allowing them to be stored
for tasks that demand greater volumes of ATP.

Musculoskeletal Adaptations
As discussed in Chapter 1, type I muscle fibers are more aerobic in nature.
Because endurance exercise requires repeated, submaximal efforts, type I
MUs are consistently recruited, whereas the threshold to recruit some
higher threshold type II MUs may never be reached (35). As a result, the
type I muscle fibers are prone to adapt more to an endurance training
stimulus to exceed their baseline aerobic potential (28). It should be noted,
however, that if the relative training intensity is high enough or if there is
substantial fatigue, type II MUs may be recruited. In this case, type II
muscle fibers may contribute to the aerobic effort through an increase in
aerobic capacity (81); however, long-term endurance training may reduce
the glycolytic enzyme concentration and potentially reduce the mass of
these fibers (48). This in turn may reduce the force production capacity of
the musculature. To counteract this effect, researchers have suggested the
inclusion of a resistance training program for endurance athletes (10). Due
to the consistent recruitment of Type I fibers, chronic endurance training
can elicit selective hypertrophy of these fibers (18). Further adaptations
within the muscle may include the conversion of fiber types based on the
recruitment pattern. For example, Luden et al. (51) showed that 13 weeks of
marathon training, followed by a 3-week taper, may increase vastus lateralis
type I and type I/IIa composition, but decrease type IIa and IIa/IIx
composition. Further research supports these findings that show a shift
towards a type I or more oxidative phenotype (38, 40, 83).
Other musculoskeletal adaptations to endurance training may include
stimulating bone growth and strengthening tendons and ligaments.
Endurance training activities exist on a spectrum with low-intensity, long-
duration activities on one end and high-intensity, shorter duration on the
other end. While the relative intensity of the endurance activity must reach
a threshold above an individual’s daily activity strain to stimulate
osteogenesis (15), it has been suggested that higher intensity activities such
as running and high-intensity aerobics may stimulate bone growth to a
greater extent (15, 17). Based on this rationale, higher intensity activities
would benefit bone growth to a greater extent. For example, researchers
have shown interval training (16) and weight training (24) to stimulate bone
growth to a greater extent than lower intensity activities. The relative
intensity of the training stimulus also appears to influence the ability of
tendons, ligaments, and cartilage to grow and become stronger (63).

Table 6.1 Physical and physiological adaptations to endurance exercise and training
Variable Adaptation
Cardiorespiratory
Cardiac output Increased
Capillary density Increased
Heart rate (resting) Decreased
Heart rate (submaximal exercise) Decreased
Oxygen diffusion Increased
Stroke volume Increased
Tidal volume Increased
Metabolic
Aerobic enzyme activity Increased
Glycolytic enzyme activity Variable*
Lactate buffering Variable*
Mitochondrial size Increased
Mitochondrial density Increased
Myoglobin content Increased
Onset of blood lactate VO2 max % Increased
Stored ATP Increased*
Stored creatine phosphate Increased*
Stored glycogen Increased
Stored triglyceride Increased
Musculoskeletal

* Highly dependent on relative training intensity.

Variable Adaptation
Bone density No change, decreased, or potentially increased*
Ligament strength Increased
Tendon strength Increased
Type I muscle fiber cross-sectional area No change or potentially increased
Type I muscle fiber content No change or potentially increased
Type II muscle fiber cross-sectional area No change or potentially decreased
* Highly dependent on relative training intensity.
Concurrent Training Adaptations
Many sports require athletes to perform skills that are dependent on
different physical characteristics. For example, in top-flight soccer, players
may cover distances exceeding 10 km, of which around only 800 m might
involve high-speed running and sprinting (68). These high-intensity efforts
often play a key role in goal scoring, and hence match outcomes (29), but
players must also possess the work capacity to tolerate the potential large
total distances covered during match play. It is clear from this example that
athletes may need to possess a combination of strength-power dependent
qualities in addition to aerobic or endurance-based characteristics.
Practitioners must be able to effectively manage these different
components of training. It seems reasonable to attempt to include aerobic
and resistance training concurrently. However, there are very real practical
constraints and potential dire consequences to simply trying to address all
training objectives simultaneously. Strength and conditioning practitioners
must fit training units within the available time while also being mindful of
total training load to manage the risk of non-functional overreaching,
maladaptation, or overtraining. Furthermore, the interference effect of
aerobic training on important adaptations that are typically targeted through
resistance training.
It is important for practitioners to understand the physical characteristics
necessary for competitive success. Selecting an appropriate periodization
model can further guide the strength and conditioning professional on how
to most effectively distribute different training units to minimize any
interference effect and maximize training adaptations. Periodization models
and constructing the training process are presented in Chapters 7 and 10.
Practitioners should be mindful of several variables that influence the
interference effect, as well as the practical implications of concurrent
training for both strength-power and endurance athletes.
 Several reviews and meta-analyses have documented the interference
effect of aerobic training on resistance training-induced adaptations,
primarily hypertrophy, strength, and power adaptations (54, 73, 89). Some
studies have suggested that the aerobic exercise mode (e.g., cycling,
running) may influence the magnitude of interference for all three
adaptations (54, 89). However, more recent evidence suggests that aerobic
exercise mode does not negatively impact hypertrophy and strength
adaptations from resistance training among untrained or moderately trained
subjects unless the volume is quite high (59, 66, 73). It should be noted that
among well-trained strength-power athletes, substantial interference with
strength gains can occur, particularly if the endurance and strength training
occur on the same day (66). Power, RFD, and velocity adaptations appear to
be subject to an interference effect regardless of the aerobic exercise modes
studied in various concurrent training paradigms (73, 89).
Practitioners may consider reducing the frequency of aerobic training to
less than three times per week and less than 30 minutes per session to
reduce the interference effect (89). Additionally, it appears that separating
resistance and aerobic training sessions by as much time as possible also
helps to reduce the interference effect (73, 89). On days when both aerobic
and resistance training sessions are included, the first session should be
whichever type is the higher priority in terms of training adaptations (5, 7,
8). If hypertrophy, strength, or power are the primary training objectives,
the resistance training should occur before aerobic training. Conversely, if
aerobic or endurance adaptations are the first priority, then the aerobic
training session should occur before resistance training.
It is also worth noting that endurance athletes experience both training
and performance benefits from concurrent training. Several studies have
documented increases in strength and power with the inclusion of resistance
training for a variety of endurance performances in running, cycling, skiing,
and swimming (10). Concurrent training has also been observed to reduce
the energy cost of locomotion in upright and swimming performance (10).
While specific paradigms must ultimately be determined based on
contextual factors, it seems apparent from available evidence that
minimizing the volume of aerobic training is beneficial to minimize the
interference effect (11, 54, 73, 89). Furthermore, higher intensity activities,
such as provided through high-intensity interval training, can help reduce
the interference effect on strength and power adaptations (11, 73). Higher
intensities of resistance training appear favorable to maximizing adaptations
during concurrent training in endurance athletes (10).
Chapter Summary
There are unique training adaptations that may occur because of resistance,
sprint, endurance, or concurrent training. While these adaptations may
improve various physical and physiological characteristics of the athlete,
the magnitude of the adaptations may be specific to each individual and
dependent on their dietary intake (Chapter 4), training intensity, and
training volume. Thus, it is important for athletes, coaches, and sport
scientists to understand the specific adaptations of different types of training
in order to train the characteristics that may contribute to performance.
Moreover, it is important to organize a training plan (Chapter 7) to allow an
athlete to peak the necessary adaptations during their most important
competitions of the year.
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Part IV
7 General Concepts and Training
Principles for Athlete Development

DOI: 10.4324/9781003096139-11
Introduction
It is quite clear that performance outcomes are a function of how the
training process influences underlying mechanisms (28, 44, 146, 157, 160).
For example, high-volume resistance training programs generally have a
greater influence on body composition, enhancement of muscle cross-
sectional area (CSA), metabolic factors, and work capacity factors than do
lower-volume, higher intensity programs (50, 148, 153, 166). In contrast,
high-intensity (e.g., heavy loading, ballistic movements) programs have
been shown to have a greater influence on high threshold motor unit
recruitment, maximum strength, rate of force development, peak power, and
velocity of movement compared to low-intensity programs (25, 56, 94, 99,
139, 140, 148, 173). Several additional factors also impact the efficacy of a
training process. For example, the developmental level and training
background of the athlete can result in somewhat different training
adaptations both quantitatively and qualitatively (71, 82, 98, 174). Evidence
also indicates that among poorly trained and weak athletes, strength training
alone can provide as great or greater increases in power as compared to
power training alone. Furthermore, prior strength training or having higher
maximum strength levels can potentiate further training for explosiveness
and power output (33–35, 70, 88, 89, 173, 174). Therefore, it becomes
vitally important to examine coaching practices, experiential data, and
scientific literature carefully and critically in order to create and develop
programs and processes leading to desired training goal(s).
Logically, for athletes to attain the highest possible levels of
performance, training should be viewed as a multifactorial process. The
training process should prepare them technically, tactically, psychologically,
physiologically, and physically (155). As noted, training is a process that
requires considerable forethought and planning. Because training is
multifactorial in nature, known principles of physics, physiology, and
psychology must be exploited to maximize the effects of the training
stimulus. Positive enhancement of performance is clearly the primary
concern of training – therefore the training process must provide (41, 149,
155):

An appropriate stimulus (overload) to “drive” adaptation.

A reasonable degree of task specificity to properly direct the
adaptation.
A reasonable (and logically sequenced) degree of variation (including
down sets, heavy and light days, unload weeks and rest–recovery
phases) in the training stimulus such that goals can be appropriately
directed and fatigue appropriately managed.
Recovery-adaptation enhancement beyond the stimulus (i.e., sets, reps,
exercise selection) such as psychological reinforcement, daily
nutrition, supplements, sleep, etc., such that recovery-adaptation is
optimized.
An appropriate means for assessing progress (i.e., athlete monitoring),
including methods of data return to coaches and athletes.

Progressing the athlete as close as possible to their genetic limitations is

the ultimate goal of the sport training process, so training is not simply
recreational exercise or recreational sport. This concept should not be
taken lightly and places a great deal of responsibility on the coach and sport
scientists. It is not unrealistic to expect a good coach to be viewed in the
same context as a good physician (76); therefore, the training process can
be regarded as a prescription that effects the well-being and development of
the athlete and aids them in achieving the best possible performance.
There are several major factors that become apparent in the development
of a successful training process (Figure 7.1). Two major factors that should
be carefully considered are genetics (nature) and training (nurture) These
factors should not be underestimated as to their importance in athlete
development.

First Major Factor: Genetics

 Every athlete does not and likely cannot progress to the elite level (48, 67).
Although there are many reasons for athletic success, there is no substitute
for innate talent (genetics). Epigenetic influences also contribute, and some
are likely inherited to an extent (47). Epigenetic mechanisms (e.g.,
methylation, acetylation, etc., of DNA resulting in a histone modification of
the genome, miRNA, etc.) are susceptible to external/environmental factors
such as nutrition and likely training itself. Environmentally induced or
inherited epigenetic patterns are highly specific to the individual and may
represent crucial control centers directing/predisposing an athlete towards
higher or lower physical performance abilities. However, ultimately the
degree of epigenetic influence upon performance may also be under
considerable genetic control (16, 47, 63). Georgiades et al. (63) state this
concisely:

Despite this complexity, the overwhelming and accumulating

evidence, amounted through experimental research spanning almost
two centuries, tips the balance in favour of nature in the “nature” and
“nurture” debate. In other words, truly elite-level athletes are built –
but only from those born with innate ability.

Figure 7.1 Factors/stressors impacting sport development and

adaptation. While a number of factors are important, two
 factors have a major impact on the athlete’s ability to
recover and adapt to the training stimuli: heredity and the
training process. Training and additional factors may
impact epigenetic caused gene expression; however,
heredity (the genome) appears to have the greatest
influence.
Source: Georgiades et al. (63).

This inheritance factor has three aspects that relate to superior performance:

1. Genetically linked characteristics: These heritable characteristics

include psychological aspects (79, 129), somatotype and height (125,
143), higher testosterone concentrations in both men and women, and
differences in metabolic enzymes and muscle fiber types (49, 92, 120).
As a result of these heritable physiological links, athletes with specific
psychological and physiological traits are simply able to perform at a
higher level in specific sports (170). For example, athletes with more
type I fibers tend to have higher VO2max values and greater endurance
(110, 117). In contrast, athletes with more type II motor units typically
have an advantage in strength-power sports, show greater maximum
strength, higher rates of force production, and power outputs (57, 108,
109).
2. The relationship between genetic inheritance and the training-related
“Window of Adaptation” (36, 49, 73, 137): All athletes eventually
respond to a well-planned training process to a greater or lesser extent.
However, as a result of heredity, some athletes respond to the same
program with substantially greater adaptation and are able to progress
further than typical athletes.
3. Athletes having both genetic traits are the ones most likely to progress
to the elite level. Large multi-nation genomic projects are currently
underway to better characterize the influence of hereditary on sport
(127).
Second Major Factor: Training
In order to develop toward one’s genetic limitations or develop beneficial
epigenetic factors, training must take place. Training in a sport context
deals with developing knowledge, fitness, and the skills that relate to
specific performance outcomes. Therefore, training has the specific goals of
improving an athlete’s capabilities, capacities, and training productivity
leading to improved performance. The training stimulus can be
conceptualized as psychological and physiological strain, as a result of
accumulative loading factors over time, that produce stress (psychological
and physiological responses to the level of strain) (32, 54). Greater loading
factors (e.g., greater intensity, greater volume, etc.) produce greater
resultant stress responses. There are two primary conceptual paradigms that
represent the basic underlying mechanisms associated with training
outcomes (38): the stimulus–fatigue–adaptation paradigm and the fitness–
fatigue paradigm.

Stimulus–Fatigue–Adaptation Paradigm
Yakovlev’s concept of “supercompensation” (178, 179) describes the
adaptation process as the interaction of a stimulus – followed by fatigue and
a subsequent adaptation (Figure 7.2) and serves as a basis for emphasizing
non-linearity and rhythmicity during training. Yakovlev’s concept is
supported by Selye’s general adaptation syndrome (38). This mode of
adaptation depends upon homeostatic mechanisms and the homeostatic set
point. Homeostasis refers to the ability to maintain a stable internal
environment (regulating hormones, body temperature, water balance, etc.).
Continuous monitoring of the internal environment is required to maintain
homeostasis. Each physiological variable (e.g., body temperature, blood
pressure, hormone concentrations, specific nutrient concentrations, etc.) has
a specific set point, the physiological value around which the normal range
fluctuates. A normal range is a restricted set of values that are relatively
stable at rest and that optimally maintain health. For example, the set point
for normal resting human core temperature is approximately 36–37°C. At
rest, physiological parameters, such as heart rate and blood pressure, tend to
fluctuate within a normal above and below the set point. A number of
controlling mechanisms including the endocrine system and central nervous
system control centers play roles in regulation and stabilizing values within
the normal range (66). Any significant deviation from the normal range, as
occurs during exercise, will be resisted through positive or negative
feedback loops (see Chapter 2). Importantly, the set point can be altered
through training (39, 40, 144). This conceptual model is characteristic of
both acute response to an exercise bout and adaptation to chronic training.
 (a) The stimulus–fatigue–adaptation paradigm: note that
Figure 7.2 training results in homeostatic disturbances that “provoke”
adaptation. Fatigue accumulates as a result of training and
reduces performance (P). Additionally, as a result of
accumulative fatigue the adaptations that can enhance
performance are masked (see fitness–fatigue paradigm)
until fatigue is reduced. (b) Depending upon the strength
of the training stimulus (and outside stressors) the training
strain can result in a level of training stress producing
different performance results. (c) Effects of positive
accumulative adaptation. Note that as fitness (underlying
mechanisms) improves, potential performance also
improves, and a new homeostatic set point is established.
Also note that it becomes increasingly difficult to establish
higher and higher fitness levels (and set points).

Fitness–Fatigue Paradigm
The interaction between underlying mechanisms (fitness) and accumulated
fatigue as a result of training can be represented by the fitness–fatigue
paradigm (Figure 7.3). Fitness and fatigue can be conceptualized as factors
which contain the primary residual effects of training. Fitness includes the
physiological/physical and performance mechanisms underlying the display
of fitness and therefore preparedness. This display includes psychological
aspects (e.g., training drive and the emotional effects of accumulative
fatigue), performance aspects (e.g., measures of strength, power, RFD, and
endurance), and physiological aspects (e.g., fatigue, CSA, II:I CSA ratio,
body composition, nervous system activation of muscle, VO2max, lactate
threshold, etc.) (41, 42, 84, 106, 115, 116, 149, 168). Training factors such
as volume, intensity, and exercise selection can contribute to the after-
effects and residual effects. As a result, there are multiple fitness
mechanistic after-effects and residual effects, each one associated with
different performance characteristics (e.g., strength, RFD, power, etc.).
Although specific fitness and fatigue residual effects are somewhat
independent of each other, they have an aggregate effect. Because
accumulative fatigue masks the expression of fitness and impedes recovery,
fatigue becomes a primary concern for both adaptation and competitive
performance. Therefore, as training progresses, particularly as training
volume is elevated, fitness can improve but fatigue can accumulate
simultaneously, and preparedness and performance are muted.
Preparedness is the difference between fitness expression and fatigue.
Preparedness represents the potential to perform well. Accumulated fatigue
tends to increase with training volume; conversely, fatigue declines with a
decrease in training volume. Importantly, fatigue decreases at a faster rate
than fitness; as a result, fitness is “unmasked” and the expression of
preparedness can increase to a peak or a plateau depending upon how
volume and intensity are manipulated (6–8). A peak can be maintained until
fitness deteriorates to a point affecting performance. This performance
decline occurs as a result of a prolonged decrease in training volume.
Therefore, preparedness reaches its peak at some point, usually within
about 4 weeks, after the training stimulus has been reduced. A reduction in
training volume and concomitant increase in preparedness is the basis of a
taper and, in part, the driving mechanism of a planned overreaching-taper
phase and a fundamental characteristic of block periodization (5, 10, 19, 61,
70, 86, 97, 122, 134–136, 149).
Figure 7.3 The fitness–fatigue relationship.
Preparedness: the potential to perform – the difference between fitness and fatigue. Fitness: the
underlying mechanisms driving performance capability. Fatigue: negative alterations in force
production capability – masks the ability to express fitness.

Sources: Based on Plisk and Stone (128); Chiu and Barnes (26); Stone et al. (149).
Training Principles: Factors to Consider for the
Development of the Training Process
The four basic training principles are overload, variation, specificity, and
reversibility. A sound knowledge of these basic training principles and their
application can make a substantial difference in training process outcomes
(18, 56, 70, 131, 146, 153, 155). Appropriately developing and properly
integrating these principles into the training process can optimize
adaptation, enhance fatigue management, reduce non-functional
overreaching/overtraining potential, and augment the potential for attaining
a superior performance.

Overload
Overload represents a training stimulus that forces the athlete beyond
normal levels of physical performance and creates a “disturbance in
homeostasis” such that chronic alterations (adaptation) occur. Furthermore,
overload is concerned with providing an appropriate stimulus for reaching
(and maintaining) a desired level of physical, physiological, psychological,
and performance adaptations. Therefore, overload represents the application
of an appropriate stimulus including exercise range of motion, work
performed, absolute and relative intensity (RI) levels, frequency, and time
factors. All overload stimuli will have some level of intensity, relative
intensity (RI = percentage of maximum), and volume. The determination of
appropriate overload stimuli for different modes (running, swimming,
cycling, weights, variable resistance devices, semi-isokinetic devices, etc.)
of training can be challenging. Quantification of some forms of overload,
including some forms of resistance exercise, is at best difficult. For
example, the work quantification or estimation of variable resistance
devices including the use of chains and elastic bands requires considerable
effort (142, 146). For this discussion, the quantification of overload stimuli
will primarily deal with weight training and other conditioning factors (e.g.,
sprints, cycling, flexibility, etc.).
An important aspect of a training stimulus and the ability to sustain an
overload for long periods deals with the development of adequate levels of
strength. While resistance exercise commonly aims to increase maximum
strength, strength entails substantially more than how much force you can
produce or how much you can lift. Conceptually, strength should be viewed
as a “vehicle” that transports a substantial number of characteristics that can
positively impact sport performance. Thus, the principle of overload applied
to improve strength and its dependent qualities encompasses more than
traditional, heavy resistance training. As a result, increasing maximum
strength can make a marked difference in performance outcomes (2, 3, 12,
20, 33–35, 43, 52, 64, 96, 141, 147, 150, 155, 161). Maximum strength is
related to:

Alterations in tissue CSA, architecture, stiffness, and tensile strength,

which can enhance force transmission and may reduce injury potential.
The magnitude of force production with greater peak and average
forces that can allow for higher velocities and power outputs to be
achieved when using submaximal loads.
The RFD, which is associated with faster muscle activation with
resultant greater force production during critical time periods (e.g.,
foot contact time) – may be a product of training and partially be
independent from maximum strength.
Greater absolute and perhaps relative endurance, especially high-
intensity exercise endurance (HIEE), resulting from both metabolic
alterations and reduced “central” (nervous system) fatigue (i.e., more
total work can be accomplished).
Greater peak and average power; work (F × d) is accomplished at a
higher rate.
Greater ability to develop and respond to stretch-shortening cycles
(SSC).
 Greater postural strength, enhancing the ability to hold static and
dynamic positions better during performance, resulting in enhanced
technical skill capability.
Some evidence indicates that force modulation, sensitivity, and
sensation are enhanced (may be a result of strength training and
partially independent of maximum strength development).
An enhanced ability to gain RFD, power, and speed of movement.

Considerable evidence exists that among weaker athletes (including most

high school and collegiate athletes), superior improvements can occur for
“explosive strength” (RFD), power, etc., through an emphasis on strength
training alone compared to power or speed training (33–36, 82, 150, 174).
There is also evidence that increasing strength initially then moving to a
power/speed emphasis provides an advantage in gaining explosiveness,
speed, and power (88, 89, 174). The transfer effects of increased strength
may be enhanced when strength training is performed in an integrated
fashion with sport training components such as sprints and jumps and with
sports training programs (55, 91, 113, 133, 161, 180).
Although it is quite arguable that one should always strive to become
stronger, once an adequate strength base is established the emphasis of
training can shift toward aspects of performance such as power and speed.
A primary factor then becomes, how strong is strong enough (150)? To an
extent this question is exercise dependent in that the level of “required”
strength in both absolute and relative values will be different from exercise
to exercise. For example, there is evidence that a parallel back squat of
approximately 2 times body mass represents a threshold value that provides
considerable positive characteristics, including the ability to better adapt to
power and speed training (160, 161). Alternatively, if full-body isometric
strength assessments (e.g., isometric mid-thigh pull) on force platforms are
being used, then an approximate threshold of 300 N kg–0.67 may be used
(M. H. Stone, unpublished data).
Obviously, to maximize adaptations in power or velocity of movement
(i.e., jumping, sprinting, etc.) and endurance activities, overload must be
applied to these fitness/performance characteristics as well. Therefore, as
with strength-power training, factors dealing with the enhancement of
power, speed, and endurance require appropriate training manipulations
(see Chapter 10).

Variation
Variation is a primary component of the periodization paradigm and
concerns the removal of linearity from the training process by manipulating
overload characteristics and the degree of specificity. Conceptually,
variation assists in obviating training monotony/strain and staleness, can
reduce fatigue, and offer force, velocity, and power spectrums across macro
to micro time-frames (11, 24, 25, 38, 41, 42, 122, 123, 149). First, using
resistance training as an example, consider a simple observation: neither
untrained subjects nor athletes can typically tolerate constant multi-joint
exercise loading for extended periods, especially high volume or heavy
loading, without experiencing non-functional overreaching or perhaps
overtraining and certainly increased injury potential. Indeed, in pilot studies
in our lab (East Tennessee State University), we consistently observed that
subjects/athletes with various training backgrounds performing multi-joint
heavy loading (95–100% of 1 RM) or high-volume training can improve or
maintain performance for approximately 3–5 weeks. However, with
continued training they could only, at best, maintain performance (sprints,
jumps, 1 RMs) for an additional 1–2 weeks – longer periods resulted in
performance, particularly velocity-related, declines. This agrees with the
resistance training-induced non-functional overreaching/overtraining
observations of Fry et al. (58, 59) and with a systematic review which
indicated that providing essentially the same training stimulus for longer
than approximately 6 weeks can result in a plateau in maximal strength
development, necessitating training variation to elicit further improvement
(162). Furthermore, if periodization and programming variation was
ineffective, then changing the sequences of the periodization fitness phases
should not alter adaptation. However, several studies in which the order of
fitness phases (and therefore programming) was reversed from the typical
strength-power paradigm produced different outcomes, sometimes subtle,
nevertheless different. This observation has occurred in various sports such
as swimming (28–31), as well as resistance training studies (130, 132).
Importantly, most of the early resistance training
periodization/programming studies were examinations of variation in
programming versus various constant repetition programming with both
high and low volumes, to failure and not to failure (104, 118, 156, 176,
177). In each case, the programmed variation group produced superior
results. Additionally, there is evidence indicating that how the variation
occurs in a periodization/programming context can also make a difference
(149); for example, with resistance training: block versus daily undulating
(122, 123) or failure versus non-failure (24, 25), and block versus
traditional within an endurance training paradigm (111). Indeed, the
majority (decidedly) of reviews and meta-analyses have concluded that
periodization offers advantages over other methodologies (149).
From a programming standpoint, resistance training, and likely most
other forms of training (53), combination training (heavy plus light loading)
can be used to create a wavelike variation throughout a microcycle and can
result in a positive difference in performance adaptation, particularly for
RFD and power output. This training method can be combined into the
same training session (163–165) or take the form of unload weeks and
heavy and light days (22, 23, 25, 53, 122, 145). Furthermore, this variation
method can also be summated in that combination training can take place
both within a training session and across the microcycle (heavy and light
days) and is commonly used in resistance training (25, 70, 122). It should
be noted that this method is unlikely to work efficiently if training is taken
to failure. Training to failure represents a constant relative maximum and
heavy and light days cannot be accomplished (25, 149).
Additionally, a considerable degree of flexibility can be assembled in the
periodization paradigm. Typically, for most sports, the periodization
paradigm proceeds from higher to lower volume. However, as noted above,
these phases can be reversed for some sports to produce somewhat different
effects, often enhancing specific endurance factors (149). Furthermore, the
fitness-phase time-frames can be manipulated based on multiple factors,
including the competition calendar, the trained state, or the level of
accumulated fatigue carried over from the previous stage (149). Using
block periodization as an example, if the time from the last active rest stage
until the next major competition is 10 weeks, then several variations of the
block time periods could occur:

In underdeveloped athlete (based on monitoring): accumulation (6

weeks), transmutation (3 weeks), realization (1 week).
In an elite athlete in good condition (based on monitoring):
accumulation (2 weeks), transmutation (5 weeks), realization (3
weeks).

Thus, there can be considerable individualization and flexibility within both

the paradigm of periodization and the programming constructs (38, 149).
Appropriate periodization and programming variation are important for
the development of strength-power characteristics and producing a power
spectrum during training (24, 25, 76, 78, 122, 123, 158). Furthermore,
appropriate variation of loading factors across training may be the most
important factor in regulating fatigue and guiding training toward a specific
goal. Appropriate variation is an essential consideration for continued
adaptation over a long-term training program for all levels of athletes (72,
122, 123, 128, 155, 157). Variation involves manipulation of the training
variables including intensity factors, velocity, volume factors, rest and
recovery periods, and exercise selection. Emphasis and proper sequencing
of these variables can result in the enhancement of a number of abilities and
skills (25, 70, 122). Most importantly, appropriate sequencing and timely
emphasis of fitness characteristics are part of the foundation of “block
periodization.” Careful observation (74, 101, 102, 128, 149) indicates that
the degree of necessary variation in the training program is related to the
level of the athlete and relative level of the “window of adaptation.”
Therefore, it appears that advanced athletes require a greater degree of
variation as compared to novices and beginners. Thus, prudent
consideration of multiple levels of variation is necessary in a well-planned
training program (i.e., quadrennial, annual, intermediate, weekly, day-to-
day, etc.).

Specificity
Specificity is the degree of bioenergetic/metabolic and mechanical
similarity between a performance task and training exercises. The aim of
increased specificity throughout the training process is enhancement of the
transfer of training effect, a measure of the degree of training transfer to
actual sport performance. If sport performance enhancement is the primary
goal, then specificity of exercise and training become the most important
considerations for selecting methods and modes for resistance training.
There are two fundamental aspects to specificity: mechanical and
metabolic. Mechanical specificity refers to the kinetic (force) and kinematic
(displacement, velocity, power, RFD) relationships between a training
exercise and a physical performance. Therefore, mechanical specificity
includes characteristics such as movement patterns (e.g., direction, range of
movement, open versus closed kinetic chain exercise, etc.), peak force,
RFD, acceleration patterns, and velocity parameters. Based on observations
of inter- and intramuscular task specific activities (146, 155, 159),
mechanical specificity has a strong conceptual underpinning. Task
specificity is associated with the means by which the motor cortex is able to
organize both motor unit activation (intra-muscular tasks) and whole-
muscle activation patterns (inter-muscular tasks). There is substantial
evidence that both intra- and inter-muscular task specificity aspects play a
major role in strength-power training and likely endurance training (81, 90).
Fundamentally, greater training exercise similarity results in a greater
probability of transfer to the actual performance (15, 138, 146, 153). From a
motor control aspect, intra-muscular task specificity indicates that, for a
defined activity, only a specific motor unit task group will be activated (93,
138). Evidence of this can be found from practical observations and
experimental research aspects. For example, bodybuilders (and strength
coaches) have observed that, to achieve complete development of a specific
muscle or group of muscles, a variety of different exercises are required, an
observation that is supported by considerable research. Although not all
researchers agree (95), several studies and reviews (1, 100, 166, 169, 170,
172) have indicated that resistance training-induced CSA alterations and
changes in muscle thickness occur non-homogeneously throughout a
muscle, nor does training increased CSA homogeneity occur uniformly in
different regions (e.g., upper versus lower body). The observation of
inhomogeneous hypertrophy resulting from resistance training could result
in indiscriminate hypertrophy, which could potentially interfere with
performance. For example, most of the hypertrophy among track and field
sprinters, because of training (and possibly genetics), was relatively
localized in the proximal (upper) portion of the thigh (1), which tends to
reduce the moment of inertia at the hip joint, providing an advantage for run
sprinting. However, among cyclists, hypertrophy was more evenly
distributed from proximal to distal (80). Therefore, training which
emphasizes increased CSA of the distal portion (lower) of the quadriceps,
such as front squats, may not always be advantageous for all athletes (e.g.,
runners).
As noted in Chapter 2, sport activities rely on different combinations of
bioenergetics systems (Figure 7.4) and thus produce different metabolic
profiles. Indeed, as the mechanical intensity increases so does the rate of
ATP use.
Thus, training the most appropriate energy system(s) is primarily a
function of exercise intensity. From a bioenergetics/metabolic standpoint,
training the relevant energy systems can be largely met by an understanding
of the time-motion requirements of the sport performance. It is obvious that
a shot-putter does not perform the same movements or the same work, at
the same intensity, as a 10k runner. Thus, most of the training efforts for the
shot-putter would be aimed toward training anaerobic mechanisms that can
provide rapid energy (phosphagens, fast glycolysis) while the 10k runner
 spends most of their time training the aerobic system which can deliver a
relatively large quantity of energy over time.

Figure 7.4 Relative contributions of three energy systems.

Sources: Based on Stone et al. (155); Gastin and Lawson (62).

Reversibility
Reversibility describes the loss of originally accumulated training-induced
fitness characteristics that will eventually result in a loss of performance.
This reversal typically results as an occurrence of two factors. First, the
removal or reduction of the stimuli causing adaptation. This alteration in the
stimuli results in a “de-training” effect, essentially a “negative”
physiological adaptation and may be somewhat factor specific. For
example, muscle atrophy can occur as the result of resistance training
volume being reduced, even though the stimulus reduction may be planned
as an in-season maintenance program or taper (13, 14, 167). Although
volume reductions can decrease muscle CSA, aspects of performance can
increase because of the removal of fatigue precipitating an increase in the
expression of fitness and a concomitant increase in preparedness (as noted
in the fitness–fatigue paradigm). It is also possible that improvement in
some aspects of performance, such as RFD and power can occur at least for
short periods, provided intensity is maintained or increased (13, 14, 155).
Second, involution can take place, a reversal of performance capability that
occurs even though the stimulus is still being applied. Typically, there are
two types of involution:

1. Monotonous training. A plateau or decreased performance often arises

in response to a monotonous, relatively unchanging program that is
likely a result of too little mechanical variation in the training program
(54). Through discussion with athletes and coaches worldwide and
considerable observation, involution appears to be not uncommon
among advanced athletes after approximately 12–16 weeks of training
the same basic fitness characteristic (i.e., basic strength, power). This
type of involution appears to occur although some variation in the
exercise type, sets and repetitions, etc., and a reasonable fatigue
management process has been implemented. In the final analysis, this
type of involution occurs because of simply doing about the same
thing for relatively long periods of time.
2. Poor fatigue management. A type of involution can also occur as a
result of maladaptation resulting from poor fatigue management (i.e.,
non-functional overreaching) (59, 60).

Because fitness characteristics can deteriorate, a periodic brief return to an

accumulation phase can be beneficial. This programming characteristic is
shown in Figure 7.5. Note that in this example the accumulation block is
prolonged, although it contains more than one stage. Also note that the
realization blocks increase over time. This is accomplished in several ways
such as manipulation of the volume, intensity, and length of time the three
each of the three concentrated loads last. The programming of the
concentrated loads (summated microcycles) can also affect the overall
volume and intensity of periodization blocks (149) (Table 7.1).
Table 7.1 Resistance training programming associated with Figure 7.5
Mesocycle 1 Mesocycle 2 Periodization Mesocyle 3 Accumulation,
Periodization accumulation block transmutation, realization
accumulation block
Strength – 3 × 10 repetitions, Planned overreaching: 5 × Planned over-reaching: 5 × 5
endurance primarily multi- 5 repetitions, primarily repetitions, primarily multi-
joint exercises multi-joint exercises joint exercises (i.e., squats,
(i.e., squats, (i.e., squats, pulls, pulls, presses, pull-up, etc.) –
pulls, presses, presses, bench press, 1 week – heavy and light
pull-up, etc.) – 4 pull-up etc.) – 3 weeks – days
weeks heavy and light days
Basic 3 × 5 repetitions, 3 × 5 repetitions first week 3 × 5 repetitions first week
strength primarily multi- descending to 2 descending to 2 repetitions
joint exercises repetitions 4th week, 4th week, primarily multi-
(i.e., squats, primarily multi-joint joint exercises (i.e., squats,
pulls, presses, exercises (i.e., squats, pulls (cluster sets), presses,
pull-up etc.) – 4 pulls, push press, bench pull-up, etc.) – 3 weeks –
weeks press using dumbbells, heavy and light days
pull-up, etc.) – 4 weeks
– heavy and light days
Strength – Multiple sets of 3, 3 × 3 repetitions, primarily 3 × 3 repetitions, primarily
power primarily multi- multi-joint exercises multi-joint exercises (i.e.,
joint exercises (i.e., squat complex squat complex (heavy 1/3
(i.e., squat (heavy 1/3 squat squat followed by lightly
complex (heavy followed by weighted weighted jumps first week
squat followed jumps), pulls, presses, followed by ball throws
by weight pull-up, etc.) – 2 weeks weeks 2–3), pulls, presses,
jumps), pulls, – heavy and light days pull-up, etc.) – 3 weeks –
presses, pull-up, Weight-training – M, T, Th, heavy and light days
etc.) – 1 week S (or competition) Weight-training – M, Th, S (or
Weight-training – Sprints, mid-section work: competition)
M, W, F, S (or T, Th, S Very short sprints, mid-section
competition) Throw practice T, W, T, S work: T, Th, S
Sprints, mid- (or competition) Throw practice T, W, Th, S (or
section work and competition)
throw practice: All major (large multi-joint)
T, Th, F, S exercises during the basic
strength and strength-power
blocks: target sets are
followed by a down set 1 × 5
repetitions.
Figure 7.5 Example of block periodization over three microcycles for
a collegiate strength-power athlete (thrower) from
December to the outdoor conference meet in April. Note
that from macrocycle 1 to macrocycle 3 the volume of
strength-endurance and basic strength blocks are reduced
and intensity increases from initial levels, and the
emphasis on RFD, speed, and power is increased.
Additional Programming Factors and
Considerations
The development of a training process depends upon the four basic training
principles previously discussed. These principles guide the formulation of
programming factors such as intensity, volume, training sessions per week,
and training density and assist in fulfilling the tenants of periodization,
which will now be discussed at length.

Intensity of the Overload

Intensity as part of the programming prescription is often misinterpreted.
From a biochemical/metabolic standpoint, intensity of exercise deals with
the rate of ATP use; the higher the intensity of activity, the greater the rate
of ATP used (17). Thus, an increase in force or power production will
increase ATP use rate (119). Therefore, there are several important aspects
to the intensity component to consider. This means that alterations in
intensity factors (and energy use) can be accomplished through
manipulating loading, velocity of movement, and rate of performing work
(119, 148). It must be realized that the form alterations in intensity can take
depends upon the goal of the phase (summated microcycle). For example,
during resistance training, if the goal is to increase maximum strength
(accumulation), then intensity (load lifted) would be increased. On the other
hand, if an increase in power is the goal (realization), then the load would
be decreased and the velocity of movement increased (increased power).
Intensity factors can also be separated into two related aspects: exercise
intensity (EI) and training intensity (TI) (154, 155):

EI is the actual power (F × V) output of a movement and is related to

the load lifted (force exerted) and velocity of movement. Therefore,
provided a maximum effort is made for a given exercise as the load or
 power output of movement increases, so does the intensity (rate of
ATP use).
TI is related to the rate at which a training exercise or training session
proceeds. TI can be estimated by calculating the average load lifted per
exercise, per day, per week, etc. For example, during a training
session, the time taken for completing an exercise is directly related to
the load lifted; generally, the heavier the load, the more time taken for
completion. Thus, for completion of a stipulated number of repetitions,
a greater load requires more time and increasing the repetitions
requires a longer time to complete a set. Considering these factors,
when typical self-selected rest periods (≈2–5 min between sets) and
maximum efforts are used, the work rate will be controlled by loading
and repetition number.

The relative intensity (RI) is a percentage of the 1 RM or a percentage of a

given set and repetition scheme (RISR) (25). However, the 1 RM value is
relatively unstable among untrained and minimally trained weight trainers
across time; indeed, the 1RM and related characteristics may improve daily.
Furthermore, due to accumulated fatigue, the 1 RM can change across as
little as one of week of training; this is illustrated in Table 7.2.

Table 7.2 Fatigue management

Athlete Monday Thursday
Weightlifter 120 117.5
Weightlifter 250 245
Thrower 270 255
Weightlifter 200 185
Mean 210 201
Note: 1RM can change across a week (1978) – twice/day resistance training M–T–Th–F. Example
– advanced strength-power athletes: 1 RM Squat (n = 4). 4.3% loss in 1RM strength over one week
(4 days).

Therefore, using RI to plan resistance training programs must be carried

out with these aspects in mind. Alternatively, using percentages of the 1
RM is best suited for more advanced trainees and based on the literature,
provides advantages compared to other methods particularly using RM
zones and training to failure (161). However, use of RISR (25, 150, 154)
obviates the basic problems with using the 1RM for planning a loading
scheme. Using the RISR, various set and repetition combinations (e.g., 3 ×
10 versus 3 × 5 versus 3 × 3, etc.) have a specific 100% value, as opposed
to constantly being related back to a 1RM. This can allow the athlete to
work at a set-repetition scheme that has a greater suitability for their current
abilities.

Training Volume
Training volume is a measure of the total work accomplished during a
specified exercise or time frame (e.g., per exercise, training session, weekly,
monthly, etc.). For resistance training, volume is a function of the load,
number of repetitions and sets performed, the number and types of
exercises performed (e.g., large versus small muscle mass), and the
frequency (e.g., number of times per day, week, month, etc.) with which
these exercises are performed. Resistance training volume is also impacted
by factors affecting the loading or number of repetitions performed; for
example, rest periods that are too short will necessarily decrease loading
and therefore the work accomplished. Volume load (VL) is a reasonable
estimate of the amount of work accomplished during training and is
commonly used in both research and practical settings, particularly if the
same exercises are repeated. VL can be calculated as the product of the load
(kg) and the number of repetitions for each set (68, 75, 152). This
calculation can be performed for each exercise within a specified time
period (e.g., weekly, monthly, etc.) and the total sum of the combined
exercises represents an estimate of the total work accomplished. However,
this approach may not work well if changes in the types of exercises take
place, and particularly if the displacement of the mass lifted is altered
substantially. For example, partial movements could be used to temporarily
replace full movements (i.e., 1/3 squats versus full squats) during the
competition or realization phase. In order make better comparisons, the VL
for each exercise should be multiplied by the vertical displacement of the
load (75). Vertical displacement can be measured using movement analysis
instruments (e.g., videography), infra-red systems (e.g., V-scope) or easily
estimated using a steel tape measure (75). Resistance training work
accomplished is strongly associated with total energy expenditure and
subsequent metabolic alterations (21, 103, 107, 126, 175).
Additionally, the amount of work for additional conditioning activities
(e.g., running, agility, swimming, etc.) can be estimated by time, TRIMPS,
GPS load, or more subjectively by session RPE (37, 51, 105). As constant
high work volumes, sharp increases in volume can precipitate loss of
performance and increase injury potential (45). The provision of valid
estimates of the total work accomplished in training is necessary to
adequately estimate all forms of training. Thus, creating a valid work
estimate and tracking it throughout training can be an important factor in
managing fatigue (69).

Repetitions × sets × load × displacement = VLd

Often the range of movement of exercises is altered across time; in this

case, VLd is necessary to provide a more complete picture of work estimate
alterations and thus fatigue. For example, for a person 184 cm (6 ft 1 in) in
height, a typical squat displacement would be approximately 59 cm.
However, in a quarter-squat in the rack, the displacement is reduced to
approximately 26 cm. So, squatting (to parallel) 210 kg for 5 repetitions
(day 1) would represent at VL of 1050 kg. When performing a quarter-squat
(day 2), the same athlete may use 320 kg for a VL of 1600 kg. However,
when considering the actual work accomplished and a better estimate of the
work, and consequently the metabolic cost, the VLd should be used: VL
(squat) = 1050 kg × 0.59 m = 620 kg-m while the quarter-squat would be
1600 kg × 0.26 m = 416 kg-m. Thus, the heavier day would actually be Day
1 with a lighter load but greater displacement. For obvious reasons, this
method should be used in research settings, but in practical applied settings
the strength coach should also consider this method as fatigue management
can be enhanced substantially by better estimating work and thus metabolic
costs and injury potential.

Training Session
An understanding of the training stimulus (overload factors) is necessary
for the creation of appropriate programming for training. The application of
TI and training volume can be considered in terms of the training session
and encompass all of the exercises performed during a specific period or in
terms of single exercises. This includes programming methods including
sets and repetitions, rest periods, loading, velocity of movement, power
output, and exercise selection. By calculating these two factors for two
different training sessions, the interaction and association between VL and
TI can be demonstrated. Table 7.3 displays data for training day 1 (early
accumulation phase) and day 2 (late accumulation phase). In this example,
the VL for day 1 was larger than that for day 2 (7800 versus 4400 kg);
however, the average TI was larger for day 2 than for day 1 (146.7 versus
130). So, VL and TI are inversely related. Importantly, provided that
reasonable loads and maximum efforts are maintained, it should be noted
that TI is directly related to the rate at which the load is lifted (kg s–1) and
can be used as an indication of the rate of training. However, from a
practical aspect, calculation of the TI is less time-consuming than
measuring and calculating kilograms per second. The average VL and TI
can be easily calculated per week, month, or phase of training. Considering
the practical aspects of using these variables, a reasonable record of training
progress can be made.

Table 7.3 Estimated training intensity (based on squats)

Load (TI) Sets Reps VL Time/set kg s–1 RI
 Load (TI) Sets Reps VL Time/set kg s–1 RI
Day 1 60 1 10 600 26 23.1 27.3
100 1 10 1000 32 31.3 45.5
140 1 10 1400 40 35.0 63.6
160 1 10 1600 48 33.3 72.7
160 1 10 1600 48 33.3 72.7
160 1 10 1600 53 33.3 72.7
Total 780 6 60 7800 242 189.3 354.5
Mean 130 1 10 1300 40.3 31.5 59.1
Day 2 60 1 5 300 15 20.0 27.3
100 1 5 500 15 33.3 45.5
150 1 5 750 19 39.5 68.2
190 1 5 950 23 41.3 86.4
190 1 5 950 23 41.3 86.4
190 1 5 950 25 38.0 86.4
Total 880 6 30 4400 120 213.4 400.2
Mean 146.7 1 5 733 20 35.6 66.7
1 RM = 220 kg. Abbreviations: VL = volume load, sum of load lifted (repetitions × mass); TI =
VL/repetitions (or mean load per set); load = kg; RI = relative intensity (% initial 1 RM); time is
measure in seconds – note the mean TI is proportional to kg lifted per second. Day 1 (D1):
representative of a typical squat session during the first summated micro-cycle of the accumulation
block. Day 2 (D2): representative of a typical squat session during the second summated micro-
cycle of the accumulation block. Down sets are also performed after last target set (not shown).
Sources: Based on DeWeese et al. (41, 42); Hornsby et al. (75); Stone et al. (153, 155).

Training Density
Training density (TD) is associated is concerned with the frequency of
training per unit of time (e.g., session, per day, per week, etc.) and therefore
influences the training variables volume and intensity. Alterations in TD are
important and necessary as this type of alteration can aid in managing
fatigue but still allow for higher intensities (or volumes) to be briefly
introduced at specific times (e.g., planned overreaching). TD can be
intensity oriented (TDi) or volume oriented (TDv); for example, TD can be
manipulated allowing higher training intensities to be maintained during a
training session (TDi). For example, training day 1 could contain three
relatively short, very intense training sessions, each session of
approximately equal volume, while training day 2 could contain one
training session of similar total volume to day 1. Day 1 would have a higher
TDi considering the average intensities of each smaller volume session
could be maintained at higher intensities compared to day 2. Typically,
training is distributed across several weeks with each week representing a
different TDv. One week could consist of four training sessions, while the
second week could contain ten sessions and the third, three sessions. The
TDv in week 2 would be higher compared to weeks 1 and 3. Additionally,
TD can be manipulated to alter planned, functional overreaching and
tapering protocols (4). For example, TDv could be higher in the potentiating
aspects of planned overreaching (high-volume phase).

Rate of Progression
First is the realization that rapid gains in performance are rarely in the best
interest of the athlete. Figure 7.6 represents the general relationship
between performance gains and the average intensity of training. Usually,
accelerated gains in performance occur coinciding with greater absolute or
relative intensities. However, as these rapid gains occur, the final
performance level, and the length of time a high level of performance can
be sustained, will likely be substantially reduced. Furthermore, over a long-
term, initiation of programs with a high average intensity will likely retard
the development of the athlete. Additionally, athletes, particularly in USA
collegiate settings, often take time off (e.g., summer, Christmas break, etc.),
and thus, very rapid increases in training intensity of volume designed to
get the athlete back into shape rapidly may ultimately decrease the level of
attainable performance and markedly increase injury potential. Examples of
programs likely to produce rapid gains in performance, early performance
plateaus, and diminished returns include (4, 46, 59, 60, 112, 114, 124, 156):

Constant high absolute or RI (e.g., Bulgarian system in weight

training), consistent high-intensity running or team practices.
 Weight training use of RM zones and subsequent training to failure on
a regular basis.
Linear programs using consistent increases in intensity.

Figure 7.6 Characteristics of different prolonged average intensities.

A: The rate of gain is directly related to the average
intensity of training. B: the final level of performance is
inversely related to the average rate of gain. C: the rate of
gain is inversely related to the length of time (time period)
that peak performance can be sustained. Thus for initial
rate of gain A > B > C; for final level of performance C >
B > A; and for time period of maximum of maintaining
performance C > B > A.
Sources: Based on Edington and Edgerton (46); DeWeese et al. (41).

Intent of Movement
 Second is the realization that maximum efforts should be produced when
necessary. A superior training stimulus and adaptation can result from
making greater efforts. Figure 7.7 represents the association between
performance and effort (6–9). Both objective evidence and careful
observation indicates that athletes making maximum or near-maximum
efforts during training and competition can expect substantial performance
benefits. Making a greater effort entails pertinent and focused emotional
intent (6, 27, 87). This idea is of considerable importance during resistance
training as producing and maintaining higher RFD, velocity, and power
outputs for a given load results in greater adaptations for maximum strength
and related characteristics (e.g., RFD, velocity. etc.) even among well-
trained, stronger athletes compared to self-selected velocities (65, 83, 121).
So, it becomes quite important that the coaches commit to the use of
teaching and coaching methods that promote and implant a proficiency for
producing maximum efforts for each movement when necessary (41, 42).

Figure 7.7 Relationship between effort and performance.

Sources: Based on Banister (6, 7).
Delayed Training Effects
Third, it must also be understood that training has consequences that can
extend far into recovery (26, 84, 128, 149). After- effects deal with effects
that persist only a short time period post training, such as elevated
respiration, HR, or blood pressure. However, once the training stimulus is
reduced or removed, psychological and physiological residual effects
persist. Residual effects are those that accumulate as a result of training and
persist for relatively long time periods (weeks, months, years). Residual
effects can be summated and expressed as fatigue or fitness factors
(mechanisms) that impact preparedness and performance (Figure 7.3).
Training-induced accumulative fatigue is the primary cause for the inability
to completely express fitness characteristics. Thus, accumulative fatigue
represents the underlying factor that inhibits fitness expression and
preparedness. Table 7.4 shows the relative timeline for after and residual
effects that can occur (149).

Table 7.4 Residual effects: Decay timelines with cessation of specific training (adults)
Type Physiological adaptations Rate of
loss**
Long-term* Musculoskeletal: increased CSA and architectural alterations No large
(muscle, skeleton, joints), until mid-old age; increased BdM alteration
Neural: enhanced coordination, general movement skills and Years
general event specific skills
Intermediate- Cardiovascular/respiratory: resting bradycardia, enhanced Months
term capillary density, mitochondrial density, resting and exercise SV,
CO, myocardial hypertrophy and volume alterations
Neuromuscular: enhanced effort discrimination and force Months
modulation, sport-specific balance and movement abilities
Short-term Cardiovascular/bioenergetic: Enhanced VO2peak, enhanced Weeks
lactate threshold
Type Performance alterations Rate of loss

* Assumes no substantial alteration in training status.

** Decay by 5%.

Sources: Based on Issurin (84); Mujika and Padilla (115, 116); McMaster et al. (106); Viru and
Viru (168); Stone et al. (149).
Type Physiological adaptations Rate of
loss**
Short-term Strength-related: maximum strength > strength – endurance Weeks to
(high-intensity exercise endurance) > Power days
* Assumes no substantial alteration in training status.
** Decay by 5%.

Sources: Based on Issurin (84); Mujika and Padilla (115, 116); McMaster et al. (106); Viru and
Viru (168); Stone et al. (149).
The Training Process Overview
The training process is multifactorial. The process consists of a mixture,
synthesis, and manipulation of components designed to result in athlete
enhancement. The process and components should be distinct within the
annual plan. The annual plan is a blueprint used to guide training through
the coming competitive season. This list of components within the annual
plan can be quite extensive and should include the competition calendar, the
periodization model, and the programming. The periodization model
provides the basic framework for the training process in terms of fitness
phases and timelines. Programming involves decisions related to how the
fitness phases will be brought to fruition through manipulations of the
exercise type and form, exercise intensity and volume, rate of progression,
etc. Additionally, the annual plan can contain timelines for sport medicine
evaluations, sport science evaluations, types of recovery aids (i.e., nutrition,
sleep, physiotherapy, and modes of travel). The sport science aspect
includes periodic meetings with coaches and other sport enhancement
personnel (planned and unplanned), an evidence-based approach to training,
and the athlete monitoring program. Athlete monitoring includes objective
and subjective fatigue management evaluations and objective program
efficacy testing to ensure appropriate athlete development occurs at the
right times.
As noted in the periodization model selection, block periodization has
some advantages not found with traditional periodization (149). Block
periodization has been demonstrated to produce superior outcomes
associated with training and competition for most of sports. For example,
block periodization, with appropriate programming, can foster a more
efficient prioritization of training components, thus maximizing the
development and maintenance of performance characteristics, leading to
performance realization at a major competition.
Periodization: Summary
Periodization is an integral part of annual planning and represents the
framework for developing a training process. Based on the definition,
historical development and appropriate use in the training process – a basic
tenet of periodization is training non-linearity (149). Primary goals of
periodization include (a) fatigue management and the curtailment of non-
functional overreaching and overtraining potential, (b) an optimized
manipulation of training loads leading to competitive preparedness during
the season or climax (peak) of the annual plan, and (c) optimally staging
and timing peak performance (41, 42, 128). Non-linearity (variation), which
largely results from appropriate manipulation of programming factors,
allows these goals to be met. Sport enhancement personnel, including
coaches, should realize the importance of appropriate variation and that
variation should occur at multiple levels (e.g., quadrennial plan, seasonal,
etc.) down to the daily training sessions.
Substantial literature and observational evidence indicates that most
advanced and elite athletes, worldwide, use some form of periodization
(149). A predominate feature of sound periodization and appropriate
programming is variation (non-linearity). Variation is a necessity resulting
from several factors, including: first, variation assists in obviating training
monotony/strain and staleness, reduces accumulative fatigue, and offers
force, velocity, and power spectrums across macro to micro time-frames;
second, among advanced athletes, training with greater volumes and
intensities than beginners and novices may be closer to a non-functional
overreaching or overtraining threshold, and thus, they require greater
fatigue management; third, as genetic limitations are approached, greater
variation along with unique and creative approaches to training may be
necessary to sufficiently perturb homeostasis and induce additional
adaptation. Thus, to further stimulate and promote sport performance
adaptations, innovative training approaches are often required.
 Substantial evidence indicates that block periodization has advantages in
promoting athlete development (149). Conceptually, block periodization
uses a design in which a specific sequence of concentrated loads is linked
together. Concentrated loads are unidirectional, such that one fitness
characteristic is being emphasized. However, training is not completely
exclusive but rather that training emphasizes a particular performance
characteristic, or a group of related underlying mechanisms, and other
aspects of training are de-emphasized for the duration of the concentrated
load. Using this unidirectional training approach can allow specific
characteristics to develop beyond that of typical simultaneous training.
These enhanced characteristics will regress (reverse) if not periodically
trained. Regression can occur as a result of a decline in specific training
volume such as during active rest or during long-term competitive seasons.
Through the periodic re-introduction of retaining loads (minimal doses to
maintain specific fitness characteristics), long-term maintenance of these
characteristics can be accomplished. When programmed correctly,
concentrated loads can produce residual effects that persist into the next
phase. These residual effects can potentiate adaptation during the next
concentrated load. Phase (block) sequencing offers advantages not inherent
in other methods of training. For example, in terms of speed and power
adaptations, previous exposure to a strength training concentrated load
(block) resulting in increased maximum strength can potentiate speed and
power gains during a subsequent concentrated load of power training (88,
89, 174). Indeed, substantial evidence indicates that heavy weight training
over a few weeks followed by speed-strength training, or combination
training (heavy training plus high-power or high-speed training) can
produce superior results in explosive strength (RFD), speed, and power
gains compared to heavy weight training or speed-strength (high power,
high velocity) training alone (70, 122). More importantly, evidence
indicates that this type of sequenced training can alter a wide variety of
athletic performance variables to a substantially greater extent than either
heavy weight training or speed-strength training (41, 42, 70, 122, 149).
A Final Thought
For many sports, the traditional periodization paradigm has been shown to
produce superior results. One important criticism of block periodization is
that by breaking up the training process over a macrocycle into many small
blocks, attaining high levels of fitness and development of the athlete may
not be possible (41, 42, 85, 149). Often, appropriate sequencing and
programming block periodization stages over a macrocycle basically follow
a more traditional pattern of periodization (149). For example, Figure 7.8,
represents a training process for an advanced athlete, not that there are three
stages (3 mesocycles) making up a 34-week macrocycle. In accordance
with traditional concepts, the greatest emphasis on developing “general”
fitness (general preparation) occurs in the first stage. Thus, the first stage
accumulation and transmutation blocks contain the greatest volume of
training relative to the same blocks later in the macrocycle, and the
emphasis during this first mesocycle is developing sport specific fitness.
There is a return to the accumulation block, after each active rest phase, and
high levels of general fitness are re-established. Note that after the initial
block, each accumulation block is smaller in extent as are the transmutation
blocks. This reduction in accumulation and transmutation is consistent with
the traditional periodization paradigm of general and special preparation
reduction over a macrocycle. This reduction is based on (i) sufficient
loading during the active rest phase such that “fitness” is not reduced to
baseline levels, and (ii) residual effects and retaining a reasonable level of
“general” and “specialized” fitness; thus, extensive retraining during the
accumulation and transmutation phases are not needed and more time can
be spent on realization. Programming additional “waves and oscillations”
such as heavy and light days, unload weeks, etc., are necessary and would
be included. From this perspective, block periodization can be considered to
be an integral part of traditional periodization. Importantly, both single-
factor and multiple-factor block periodization would be congruent with this
 concept (Figure 7.8) as the programming for each phase could be
appropriately adjusted to serve team or individual sports (149).

Figure 7.8 Combining traditional and block periodization.

Source: Modified from Stone et al. (149).
Chapter Summary
This discussion has provided the reader with an overview of the concepts
underlying periodization, and in particular block periodization. Evidence
indicates that block periodization and appropriate programming can provide
a superior training stimulus. Chapter 6 provides details on nuances dealing
with the underlying mechanisms associated with block periodization.
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8 Exercise Selection

DOI: 10.4324/9781003096139-12
Introduction
There is a plethora of factors that may affect the rationale of why a strength
and conditioning (S&C) practitioner chooses a specific exercise for their
athletes. In this light, it is important that S&C practitioners understand the
biomechanics and physiology behind why certain training stimuli may
produce superior adaptations or motor transference compared to other
stimuli. Beyond theory, practitioners should also be able to consider the
plethora of factors that may impact exercise selection. The following
chapter will first discuss biomechanical and physiological principles that
affect exercise selection before providing readers with practical examples of
these principles as they relate to exercise selection within an athlete’s
training program.
Biomechanical and Physiological Principles
Affecting Exercise Selection
Lever Systems
The muscles within the human body work as lever systems in which there
are fulcrums (joints), pulleys (tendons), and levers (perpendicular distance
between point of the muscular force or resistance to the fulcrum) (36).
However, it should be noted that both the force and resistance lever arms
within each lever system may impact the amount of force necessary to
complete a giving task. That is, the human body consists of three different
types of lever systems that offer athletes a mechanical advantage (i.e.,
require less force to be produced to complete a movement) or disadvantage
(i.e., require greater force to be produced to complete a movement). These
lever systems have been identified as either 1st, 2nd, or 3rd class levers
(36).

1st Class Levers

1st class lever systems have force and resistance arms whose distances are
both similar from the fulcrum, like a seesaw. An example of a 1st class
lever within the human body is the C1 joint within the cervical spine.
Within this lever system, the weight of the head is held upright by the
shortening of the erector spinae musculature, which is positioned a similar
distance from the fulcrum (i.e., atlanto-occipital joint). Within this joint,
each weight of the head and erector spinae musculature act as opposing
forces (resistances) to each other. Thus, due to the balance of forces on
opposing sides of the joint, it is possible that an athlete’s head may remain
upright. Because musculature can hypertrophy or atrophy to the point where
its potential to produce force is enhanced or weakened, respectively, head
posture may be impacted. This may be the result of an athlete’s age,
posture, or even activities of daily living, which is why it is important to
maintain proper posture within training and activities of daily living.
Furthermore, it is important to continue lifelong training, but not to the
point of excessive hypertrophy where posture may be negatively impacted.

2nd Class Levers

The structure of 2nd class lever systems is largely different from 1st class
levers. While both consist of the same components, 2nd class levers have
the advantage of a longer force lever arm, which requires less force to be
produced to complete a task relative to the resistance arm. An everyday
example of this type of lever is a wheelbarrow. Previous literature has
indicated that 2nd class lever systems are the least common within the
human body (36). One of the most well-known examples is the ankle joint
within the foot. Within this joint, the gastrocnemius muscle shortens to lift
the resistance of the athlete’s body to perform plantar flexion and raise the
heel off the ground. While the relative joint contribution of the ankle joint
was only approximately 23% during maximal vertical jumps (knee: 49%;
hip: 28%) (46), it is important to note that this joint still plays an important
role in lower limb force production, especially when it comes to ballistic
tasks (e.g., jumping, sprinting, change of direction, etc.).

3rd Class Levers

Opposite to 2nd class levers, 3rd class levers are at a natural mechanical
disadvantage due to shorter force arms compared to resistance arms; 3rd
class levers are the most common within the human body (36), with the
knee joint serving as an example. In this joint, the resistance is located at
the distal end of the shank or foot while the force arm is located near the
knee joint where either the quadriceps or hamstrings musculature attach.
Interestingly, the required amount of force required to rotate this joint
increases until the knee is fully extended in a seated position or until the
toes of the foot are perpendicular to the ground in standing position. This is
due to the resistance arm being at its longest length due to the influence of
gravity, while the force arm length remains the same. Although 3rd class
levers possess a natural mechanical disadvantage, these levers allow
athletes to naturally move with greater velocities, which benefits common
sport tasks such as running, jumping, and throwing.

Internal and External Force Production

While it is important to understand the relationship between force and
resistance arms within human movement, it is arguably more important to
understand that the amount of force created within the muscle (i.e.,
intramuscular force) does not produce the same external force needed to
complete a movement or overcome the inertia of an external load (e.g.,
barbell, dumbbell, etc.). While intramuscular force is created due to the
interaction between actin and myosin myofilaments as discussed in Chapter
1, the magnitude of force is dissipated as it passes through the layers of the
muscle belly and the tendon before reaching the bone(s) the muscle attaches
to in order to create movement. Previous researchers have examined this
concept with simple tasks (e.g., finger flexion) (47) and more complex tasks
(e.g., power clean) (51).

Mechanical Advantage and Disadvantage

From a practical standpoint, lever systems primarily affect the mechanical
advantage/disadvantage that an athlete may experience. Simply, a shorter
resistance arm requires less force to be produced, while a longer resistance
arm requires larger magnitudes of force to be produced (36). For example,
athletes are at a greater mechanical advantage when the external load used
during training is kept close to them. This is based on the notion that a load
that is farther away from the axis of rotation requires more effort on the
athlete’s part to maintain its position against the force of gravity. Swinton et
al. (98) indicated that a hexagonal barbell deadlift may serve as a more
effective training exercise compared to the straight barbell deadlift since the
former reduces the resistance arms based on the placement of the load
around the athlete compared to in front of the athlete. Thus, from a
technique standpoint, the ability to perform exercises without shifting the
load farther away from the axis of rotation or athlete center of mass would
be advantageous. Another instance of mechanical advantage/disadvantage
may be based on an athlete’s anthropometrics. Assuming two athletes of
different heights start a hexagonal barbell deadlift using the same handle
height, it is possible that the taller athlete may have to start the movement
with a greater degree of hip and knee flexion compared to the shorter
athlete. As a result, the hip and knee extensors may be starting a greater
length and may thus be at a mechanical disadvantage due to decreased
potential of actin-myosin cross-bridge formation as discussed in Chapter 1.

Physiological Adaptations
Exercises may be chosen based on their ability to provide a sufficient
training stimulus for muscular hypertrophy, strength, rapid force
production, and/or power output. Much of this may be due to the nature of
the exercise, the musculature involved, an athlete’s technical competency,
and the goals of the current and future training phases. For example, the
back squat may serve as an effective exercise to promote muscle
hypertrophy and strength because it requires an athlete to recruit a large
number of motor units in the form of large, multi-joint muscle groups to
serve as the prime movers (e.g., quadriceps, hamstrings, and gluteal
muscles), synergists that may assist with the movement (e.g., hip abductors
and adductors), and stabilizing musculature (e.g., erector spinae, quadratus
lumborum, and psoas major and minor) (36). While it may be possible to
elicit increases in muscle hypertrophy and strength from single-joint
exercises such as a leg extension (1) or leg curl (59), it should be noted that
these exercises may be limited in their capacity to transfer to sport tasks that
involve multi-joint coordination (e.g., sprinting, jumping, and change of
direction). Furthermore, single-joint exercises may be limited by the ability
of an athlete to provide a proper loading stimulus due to the inclusion of
only a single muscle group. Therefore, it is important that S&C
practitioners select exercises that provide an opportunity to elicit an
effective training stimulus for the goals of the individual within each
training phase. This can be accomplished using a combination of both
multi-joint and single-joint exercises; however, given their ability to
transfer to sport tasks, S&C practitioners should place a larger emphasis on
multi-joint exercises within their training programs.
In addition to muscle size adaptations, exercise selection can also induce
specific changes to a muscle’s architecture that may be advantageous for
performance as well as have implications for injury risk. For example,
Nordic leg curls – though not without their own limitations regarding
transferability – can induce fascicle lengthening due to the magnitude and
direction of the eccentric stress on the hamstrings (37, 72). On the
performance side, increasing a muscle’s pennation angle may improve its
force producing abilities either through additional sarcomeres in parallel
(100) or creating a more favorable fiber orientation overall (3).
Exercise Selection Based on Biomechanical and
Physiological Principles
As mentioned within the introduction to this chapter, the remainder of will
focus on applying the biomechanical and physiological principles that affect
exercise selection. There are numerous factors that may affect exercise
selection such as an athlete’s anthropometrics, sport/event(s), training age,
relative strength, training phase goals, and many others.

Machine-Based and Multi-Joint Free-Weight Exercises

Exercise machines are common within commercial gyms and may allow the
general population to receive an adequate training stimulus to benefit their
health if performed regularly. However, it should be noted that machine-
based exercises, particularly those that use single-joint muscle actions, may
not provide an optimal strength-power training stimulus since the muscle
groups involved in athletic movements are not typically used in an isolated
manner (5, 81). This in turn may reduce the task specificity of isolation
exercises and reduce the transfer of training to athletic performance (2, 7,
70, 81). While single-joint isolation exercises may improve an athlete’s
strength, this alteration may not transfer to athletic performance due to a
lack of coordinative patterns between muscle groups (81). For example,
Nordic hamstring curls provide a great eccentric strength training stimulus
(22); however, the stiff-legged deadlift may serve as a more advantageous
exercise due to the incorporation of both the knee and hip joints as well as
the stabilization of the shoulder joints and back. Furthermore, the stiff-
legged deadlift serves as an assistance exercise to other movements such as
weightlifting derivatives (i.e., variations of a traditional snatch or clean and
jerk movement altered by modifying the starting position, the depth of the
catch position, or the omission of the catch phase).
 Researchers have shown that throwing velocity in softball improved
after 12 weeks of training with closed kinetic chain exercises (3.4%, p <
0.05), but not after training with open-kinetic chain exercises (0.5%, p-
value not specified) (73). Additional researchers indicated that muscle
stabilizers may be recruited to a greater extent during free-weight exercises
compared to machine-based exercises (39, 81). Thus, evidence supports the
notion that free-weight, multi-joint exercises may require greater muscle
coordination and recruitment that may produce favorable strength-power
adaptations that benefit athletic performance. Because machine-based
exercises and free-weight exercises exist on a continuum, S&C practitioners
should consider selecting exercises based on the individual needs of each
athlete. For example, enhanced tissue capacity may be achieved using
machine-based isolation exercises while free-weight multi-joint exercises
may be used to provide a greater neuromuscular training stimulus due to the
required coordinated muscle recruitment patterns. S&C practitioners should
note that, regardless of the athlete, free-weight isolation and multi-joint
machine-based exercise may serve as exercise progressions or regressions
within the aforementioned exercise continuum (91).

Task Specificity
As noted within Chapter 6, the exercises within an athlete’s resistance
training program should benefit their ability to produce force during
movements that are commonly performed within their sport and/or event(s).
This concept is commonly known as task specificity. Simply, task
specificity refers to the degree in which either bioenergetic or mechanical
training variables are associated with one another (82, 83). It should be
noted that the one task that is truly sport specific in nature is the sport itself.
While practitioners should aim to train the movements that athletes perform
within their sport/event(s), becoming overly specific may be detrimental to
the athlete’s motor patterns. For example, baseball and softball players
perform a combination of both hip, knee, and ankle extension (i.e., triple
extension) and rotation within the transverse plane when they swing a bat or
throw a ball. An obvious solution to training these movements would be to
swing and throw progressively heavier bats and balls, respectively. While
some research supports the use of weighted bats and balls for hitting and
throwing velocity (25, 26), it is important to note that only small increments
in load may be used before the mechanics of the athlete may be disrupted.
Thus, it is important to consider the overall training stimulus provided
compared to how much an exercise “looks like” a movement performed by
the athlete.

Task-Specific Hypertrophy Example

Sprinters and track cyclists are some of the most powerful athletes on Earth;
however, the biomechanical requirements of each sport/event are unique.
For example, a sprinter performs greater hip flexion to elevate their thigh to
a greater degree relative to their torso to increase the amount of force they
can attack the track with during ground contact (60). In contrast, track
cyclists are constrained by the amount of hip flexion that is performed
based on the seat height and leg length. Squat variations are common
exercises that both sprinters and track cyclists may perform; however, based
on the biomechanical demands of their events, it may be counterproductive
to perform squatting variations that may target specific regions of the
quadriceps musculature since muscle hypertrophy may not always uniform
across the muscle (34, 69, 105). Thus, it may be disadvantageous for
sprinters to gain additional mass at the distal portion of their thigh as this
would create a greater resistance arm and require greater force production
to maintain optimal running mechanics. In fact, Hoshikawa et al. (45)
indicated that junior sprinters with a high psoas major to quadriceps femoris
ratio have an advantage when it comes to accelerating the displacement of
the thigh when running. In addition, Ema et al. (33) showed that sprinters
possessed greater hip flexor and extensor, adductor, gracilis, and psoas
major muscle volume compared to untrained men, whereas there was no
difference in monoarticular knee extensor and flexor volumes. In contrast,
cyclists possess greater muscle volumes within the monoarticular knee
extensors, semitendinosus, and psoas major compared to untrained men
before and after both groups completed 6 months of cycling training, but no
differences existed at either time point when comparing biarticular thigh
muscles (35). Collectively, the development of proximal and distal thigh
hypertrophy and strength may be beneficial for sprinters and track cyclists,
respectively. From an exercise selection standpoint, Yavuz et al. (104)
showed greater vastus medialis activation during the front squat, but greater
semitendinosus activation during the back squat. Additional research
showed greater rectus femoris activation during the front squat compared to
the back squat (19). The authors suggested that their results may indicate
that the front squat may be more effective for knee extensor development.
Therefore, it is suggested that the back squat may benefit sprinters to a
greater extent than track cyclists, while the latter may benefit more from
performing front squats.

Phasic Training Goals

Each phase of training has specific goals that should be addressed by
implementing specific exercise and load combinations. This section
discusses exercise selection considerations for specific training phases (e.g.,
strength-endurance, general and absolute strength, and strength-power).
Examples of exercises that may be implemented for various sports in
different training phases can be found in Table 8.1.

Table 8.1 Example exercise selections for specific sports within various training phases
Sport Strength-endurance General/absolute strength Strength-power
Baseball Back squat Clean pull for floor Mid-thigh pull
Shoulder press Push press Power jerk
RDL + bent over row Back squat ½ back squat
Lateral lunge Walking lunge
Basketball Push press Push press Push press
Hex bar deadlift Clean pull from floor ¼ back squat from pins
RDL ½ back squat from pins RDL
Bench press Lateral lunge
Sport Strength-endurance General/absolute strength Strength-power
Soccer Back squat Clean pull from knee Mid-thigh pull + mid-thigh clean
Single leg RDL Back squat ½ back squat from pins
Lateral lunge RDL + bent over row Nordic leg curl
DB row
Sprinter Clean pull from floor Clean pull + power clean Power clean
Back squat ½ back squat from pins ¼ back squat from pins
DB step up Bent over row DB step up jump
DB row
Thrower Clean pull from floor Clean pull + power clean Power clean + clean
Back squat Push press ½ back squat from pins
Bench press Back squat Board bench press
Board row Bent over row Bent over row

Strength-Endurance
The two primary goals of a strength-endurance phase are to increase an
individual’s force production capacity (i.e., work capacity) and task-specific
hypertrophy (91). As discussed within Section 8.3 above, multi-joint
exercises may have an advantage over single-joint exercises when it comes
to motor unit recruitment. Thus, because multi-joint exercises include a
greater magnitude of muscle fibers that contribute to the completion of a
movement, more muscle fibers will receive a training stimulus for
adaptation. Furthermore, these exercises should be performed through a full
range of motion to ensure that the necessary musculature is trained to its
fullest extent (9, 18, 38, 55). It should be noted that although multi-joint
movements will comprise of most exercises programmed within a strength-
endurance phase, single-joint exercises may serve as effective supplemental
exercises to help further develop musculature that may contribute to an
athlete’s performance, posture, or joint stability. This in turn will allow
single-joint exercises to isolate specific muscle groups that are less
emphasized during multi-joint movements (e.g., dumbbell lateral raise vs.
military press).
An additional consideration within the strength-endurance phase is the
use of both bilateral and unilateral exercises. It is possible that this
combination may allow individuals to develop force production capacity
(i.e., work capacity) and improve task-specific hypertrophy with bilateral
and unilateral exercises, respectively. For example, a back squat and split
squat may be paired within a strength-endurance phase to recruit additional
stabilization musculature that may be recruited to a lesser extent during a
bilateral exercise. Unilateral exercises may place a greater stress on
stabilization musculature as shown within previous research (27, 62). As
some may classify unilateral exercises as more sport specific than bilateral
exercises, the inclusion of unilateral exercises may help athletes further
develop contributory musculature.
In summary, to enhance the work capacity and task-specific hypertrophy
of contributory musculature, athletes may benefit most from a training
program that includes a foundation of bilateral, multi-joint full range of
motion exercises (Figure 8.1) that are supplemented by unilateral (Figure
8.2) and single-joint exercises.
Figure 8.1 Bilateral exercise example – back squat.
Figure 8.2 Unilateral exercise example – rear foot elevated split
squat.

General and Absolute Strength

Following the strength-endurance phase, strength development phases focus
on the development of the magnitude and rate of force production (91). It
should come as no surprise that lifting heavy loads will benefit an athlete’s
muscular strength characteristics. While the use of heavy loads may benefit
both strength and rapid force production (12), some researchers have
suggested using partial range of motion movements to improve
performance (74). An obvious advantage to using partial range of motion
movements within a strength phase may be the ability to use heavier loads
than what are possible with full range of motion movements. However,
while the relative effort of movements increases with a larger range of
motion with heavier loads (8), additional researchers have shown that full
range of motion squats may increase an individual’s strength throughout the
full range of motion as well as their functional performance to a greater
extent than half-squats and partial squats (71). When it comes to increasing
the magnitude of peak force production, it appears that full range of motion
movements (e.g., squats, presses, and pulls) may serve as the foundation of
the training program; however, in order to provide a unique force stimulus,
practitioners may consider supplementing the full range of motion
movements with partial movements (4).
The second goal of a strength phase is to increase rapid force production.
Since many of the exercises within these phases will be loaded with heavier
loads, this presents a unique challenge to the practitioner. Rather than
simply moving heavy loads with maximal intent, practitioners may consider
implementing exercises that train rapid force production with maximal or
even supramaximal loads. Weightlifting pulling derivatives are exercises
that are modified from traditional weightlifting movements (e.g., snatch and
clean and jerk) by omitting the catch phase and potentially altering the
starting position (e.g., mid-thigh, knee, floor, etc.) (87). While these
exercises may be classified as either force- or velocity-dominant exercises
(86), the force-dominant pulling derivatives such as the countermovement
shrug (65), mid-thigh pull (13, 17, 65, 88, 89), hang pull/pull from the knee
(64), and pull from the floor (41) may use loads in excess of an athlete’s
1RM power clean. Due to their semi-ballistic nature and small load
displacement, athletes may train with loads upwards to 140% 1RM (13, 17,
64, 65) with maximal intent. This in turn may allow athletes to develop
rapid force production characteristics and lay the foundation for future
training phases focused on moving lighter loads quickly.

Strength-Power
Strength-power training phases, which are characterized by strength-speed
(e.g., moving heavy loads quickly) and speed-strength (e.g., moving light
loads quickly) exercises, are focused on the further development of rapid
force production and improving power output (91). While there are a
number of considerations when it comes to power development (20), an
important consideration is the selection of exercises that will address the
goals of a strength-power phase. Because muscular strength may serve as
the foundation upon which rapid force production and power output are
built (92), S&C practitioners must consider the maintenance of this
characteristic during a strength-power phase. For example, while more
exercises will focus on rapid force production and power output via
strength-speed and speed-strength exercises, foundational exercises such as
squat, press, and pull variations may allow athletes to maintain their
maximal strength qualities.
Previous literature has discussed the importance of using a wide
spectrum of loads using a combination of both heavy (i.e., strength-speed)
and light (i.e., speed-strength) exercises to develop rapid force production
and power output in athletes (40, 101). An effective way to maximize
power output is to train using specific load ranges for each exercise.
Soriano et al. (79, 80) discussed the different loading ranges that may be
used to optimize power output in both lower and upper-body exercises. In
addition to load ranges, it important to also consider the loading potential
and effort put forth with specific loads. For example, while it is common to
implement snatch and clean catching derivatives within resistance training
programs (30, 31, 78), athletes may be limited by the range of loads that
may be implemented effectively with these exercises. Athletes cannot train
with more than their one repetition maximum (1RM) of the snatch or clean,
thus limiting the amount of force that may be produced during the rapid
extension of the hip, knee, and ankle (plantar flexion) joints (i.e., triple
extension) (86, 87). Moreover, athletes may not use maximal effort when
using loads less than approximately 50% of their 1RM and will instead use
the minimal effort necessary to elevate the barbell to the necessary height to
complete the lift. This in turn may negatively impact the training stimulus
that they may receive (23). In contrast to catching derivatives, weightlifting
pulling derivatives may expand the loading spectrum for athletes and allow
them to use maximal effort with loads more than their 1RM clean or snatch
since they will not have to catch the barbell (86, 87). Furthermore, athletes
may use maximal effort with lighter loads (<50% 1RM) with weightlifting
pulling derivatives that are more ballistic in nature (e.g., jump shrug and
hang high pull) (86, 87). Although they are not as common within
resistance training programs, several training studies have shown that
weightlifting pulling derivatives may provide a similar (11) or greater (88,
89) strength-power training stimulus compared to catching derivatives. It
should be noted that the latter studies investigated the loading potential of
weightlifting pulling derivatives within a training group to provide either a
force (i.e., heavier loads) or velocity (i.e., lighter loads with more ballistic
pulling derivatives) overload stimulus compared to submaximal loading
with weightlifting catching or pulling derivatives and showed greater
overall improvements in isometric and dynamic strength, sprint speed,
change of direction speed, and jumping performance. Thus, while a gray
area exists when choosing weightlifting exercise and load combinations
(84), S&C practitioners should consider the ability of each exercise to
develop the desired fitness characteristics.
Another example within a strength-power phase may be the use of
loaded jumps. Researchers have investigated the differences in power
output between the jump squat and hexagonal barbell jump at 20, 40, and
60% of the participants’ 1RM squat (99). Their results indicated that the
hexagonal barbell jump may provide a superior power output training
stimulus compared to the jump squat, which may in part, be due to the
placement of the load around the participant (hexagonal barbell jump)
compared to the upper back (jump squat). Similar findings were displayed
in another study that compared the jump squat, hexagonal barbell jump, and
jump shrug (90). Suchomel et al. (90) showed that resistance-trained men
produced greater power output during the hexagonal barbell jump and jump
shrug compared to the jump squat exercise across a spectrum of loads (i.e.,
0–100% body mass), while no meaningful differences existed between
hexagonal barbell jump and jump shrug. It should be noted that the authors
also showed that each exercise possessed a unique force-velocity profile
when compared across the loading spectrum. For example, the authors
showed that the jump shrug force at peak power dropped off considerably at
heavier loads, while it was maintained to a greater extent during the
hexagonal barbell jump. This may be due to the hip hinge
countermovement of the jump shrug, where the center of mass of the
system (athlete plus load) is shifted forward before returning to a more
mechanically advantageous position. As noted above, a shift in the system
center of mass may create a mechanical advantage/disadvantage, which
may ultimately impact the athlete’s ability to produce force effectively. The
same research group also displayed similar characteristics in resistance-
trained women, although the only meaningful differences between exercises
were the force at peak power produced during the jump shrug compared to
the other two exercises (63). Based on the characteristics of the examined
exercises, it appears that the hexagonal barbell jump and jump shrug may
serve as better alternatives to the jump squat for power output purposes;
however, S&C practitioners may note that the force-velocity characteristics
of each exercise may dictate when to implement these exercises. For
example, the hexagonal barbell jump may be classified as a strength-speed
exercise (i.e., moving heavy loads quickly) based on the ability of athletes
to maintain their power output at heavier loads (63, 90). In contrast, the
jump shrug may be more effectively implemented with lighter loads and
classified as a speed-strength exercise (i.e., moving light loads quickly)
based on the potential fall off in power production at heavier loads (52, 63,
85, 90, 96, 97).
Progressions/Regressions
Full and Partial Squats
Squatting movements and their variations are common exercises within the
resistance training programs of a variety of sports (29–32, 78). This is likely
due to the incorporation of large, multi-joint muscle groups that work as the
prime movers in tasks such as running, jumping, and changing direction.
While previous literature has provided a detailed description of proper squat
technique (14), it is important to note that the range of motion of squatting
movements may produce slightly different adaptations. Hartmann et al. (43)
showed that full squat training resulted in greater strength improvements
that transferred to countermovement and squat jump performance and rate
of force development characteristics compared to quarter-squats. In
contrast, Rhea et al. (74) showed that training with quarter-squats may be
effective at improving both jump and sprint performance to a greater extent
than full squats. However, these authors also noted that the strength
adaptations of the participants were angle specific for the quarter-squat
(Figure 8.3), half-squat, and full-squat groups. While full range of motion
squats may require greater relative muscular effort (8) and stimulate greater
increases in muscle volume (55) compared to partial range of motion squats
(e.g., half-squats and quarter-squats), the latter may still provide a unique
training stimulus for athletes. Moreover, there may be specific training
phases in which different squatting depths may be more appropriate.
Additional research suggested that the combination of both full squats and
partial squats may provide superior adaptations compared to full squats
alone (4). It is also important to take an athlete’s training season into
account. For example, as mentioned above, full squat training results in
greater relative muscular effort (8). As a result, it could be hypothesized
that full range of motion squats produce greater levels of fatigue. Thus,
while the bulk of the training year may be spent performing full range of
motion squats, athletes may benefit from performing partial squats during
the in-season training phase. This in turn may allow the athletes to
potentially decrease their relative levels of fatigue and still receive a
sufficient training stimulus for both force and power output (28), especially
when performed with ballistic intent (95). Therefore, it is important that the
S&C practitioner understand the benefits and limitations of both full and
partial range of motion squats to effectively develop their athletes.
Figure 8.3 Partial squat performed from the safety bars.

Weightlifting Exercises and Derivatives

Weightlifting derivatives may be defined as variations of the traditional
competition weightlifting movements (i.e., snatch and clean and jerk) that
modify the starting position and/or catch depth (i.e., weightlifting catching
derivatives) or omit the catch phase and potentially modify the starting
position (i.e., weightlifting pulling derivatives) (86, 87). While it is
important to progress athletes through a learning progression with squat
variations to ensure proper movement mechanics, this concept may be
magnified due to the technical nature of weightlifting derivatives. Previous
literature has provided teaching progressions that may be used to effectively
teach athletes to perform less complex weightlifting derivatives before
progressing to those that are more complex (68, 84). While each of these
models may allow athletes to progress to the traditional snatch and clean
and jerk exercises, it is important to note the models also allow athletes to
regress the exercise complexity based on competency or the training
goal(s).

Exercise Selection Based on Testing

Dynamic Strength Index
A long-term athlete monitoring program is of utmost importance when it
comes to the continued development of an athlete. While athlete monitoring
will be covered in more detail within Chapter 10, it should be noted that
consistent monitoring of an athlete may help guide a S&C practitioner in
terms of what an athlete may need to improve their overall performance.
For example, the dynamic strength index (DSI) (also known as dynamic
strength deficit) is calculated by comparing the magnitude of the same
variable (e.g., peak force) achieved in both a dynamic (e.g.,
countermovement jump) and isometric (e.g., isometric mid-thigh pull) test
(15). In theory, the DSI may be used to determine if an athlete needs to
emphasize ballistic training or improving maximal strength. Sheppard and
colleagues (77) indicated that if athletes achieve a DSI of <0.60, their
training emphasis should be focused on improving ballistic strength.
Furthermore, the authors indicated that if athletes achieve a DSI of >0.80,
their training emphasis should focus on improving maximal strength. While
additional research has shown that the DSI of individuals may change based
on the prescribed training (16), it is important to understand that additional
context may be needed to understand the athlete’s strengths and
weaknesses. Suchomel et al. (94) indicated that despite an athlete’s DSI
value, additional testing variables may suggest that an athlete could be at
their “optimal” profile and that it may be detrimental to select exercises and
training methods solely on a DSI value.

Force-Velocity Profiles
A series of studies have suggested that an athlete’s force-velocity profile
may provide S&C practitioners with an indication of what an athlete needs
to improve to enhance their vertical jump (49, 67) or sprint performance
(21, 75). For example, an athlete’s force-velocity profile may be determined
using a series of several jumping and strength-based tests, which are then
used to determine an athlete’s “optimal” profile for enhanced jumping
performance. In theory, an athlete’s profile may be used to prescribe
specific exercises and/or training methods to improve their jump or sprint
performance. In other words, it is possible that S&C practitioners may
structure their resistance training program based on the vertical jump or
sprint force-velocity profile with the intent of improving both vertical and
sprint performance. Researchers have shown that training based on the
force-velocity imbalance may improve the desired performance (49, 106).
While the force and velocity imbalance for an individual may be calculated
mathematically based on testing data, it should be noted that vertical jump
and sprint force-velocity profiles may not be related (50, 61). For example,
several studies showed questionable inter-session reliability of the force-
velocity profile (53, 56, 102). Furthermore, another study indicated that
training based on the individualized force-velocity imbalance did not
improve performance to a greater extent compared to training focused on
training away from a force-velocity imbalance or irrespective of the force-
velocity profile (57).
Relative Strength
Previous literature has suggested that athletes who are relatively stronger
may outperform relatively weaker athletes, as well as those who possess
greater absolute strength within their respective sports (92). While Behm et
al. (6) showed that youth athletes may benefit more from focusing on
gaining strength prior to shifting their focus to power-type training, athletes
with greater relative strength may require a novel training stimulus due to a
smaller window of adaptation from only gaining strength (54). Thus, while
the exercise selection may be similar to a weaker athlete, S&C practitioners
may consider implementing advanced training methods such as potentiation
complexes, variable resistance training, and accentuated eccentric loading
as a way to shift the training emphasis from focusing solely on relative
strength gain to more ballistic, power-type training methods. Potentiation
complexes, variable resistance training, and accentuated eccentric loading
may be considered advanced training methods based on the need to develop
fatigue resistance using heavy training loads, technique competency, and
the ability to accept external forces, respectively.
Researchers have shown that stronger individuals potentiate faster to a
greater extent compared to their weaker counterparts (76, 93). Much of this
may be attributed to greater fatigue resistance to heavy loads within
stronger athletes based on their previous training. Variable resistance
training requires exercise technique competence due to a unique change in
force production throughout the movement. For example, an athlete
experiences greater forces (i.e., load) during the initial eccentric and later
concentric phases, but a decrease in force during the late eccentric phase
during a traditional exercise (e.g., squat) (48). Thus, if an athlete cannot
demonstrate technique competence without changes in the external force
throughout the movement, this may inhibit their ability to learn and perform
the motor task (i.e., exercise) correctly. Finally, accentuated eccentric
loaded exercises require an athlete to perform the eccentric phase of a
movement with a greater external load before a portion of the load is
immediately removed and the concentric phase is performed (103).
Previous literature has noted that a baseline level of strength is needed to
perform this method of training (66). Simply, before implementing
accentuated eccentric loading in an athlete’s program, the S&C practitioner
should ensure that they are able to accept high eccentric forces and then
develop their ability to transition to a concentric phase with minimal
disruption. The advanced methods of training discussed above may provide
a novel training stimulus to relative strong athletes and thus, they should not
be incorporated too early in a developing athlete’s training program (91). If
they are incorporated too early, they may not be able to be used as a novel
training stimulus later, which may lessen their impact. Finally, it should be
noted that programming these advanced methods of training requires the
S&C practitioner to understand their benefits and limitations, as well as
how they may address the goals of each athlete within each training phase.
For example, programming potentiation complexes throughout the training
year may not be the most appropriate or effective training method for
athletes given that time may be better spent developing the underpinning
characteristics that impact power output (e.g., strength and rate of force
development). For future detail on using training principles to develop
athletes using a variety of training methods, readers are referred to Chapter
7 within this text.

Anthropometrics
The body dimensions of athletes within different sports or events, or those
that have different positions within the same sport, are often unique
regarding their anthropometric characteristics. In fact, athletes within the
same sport may exist on a wide spectrum (e.g., Major League Baseball’s
2017 Most Valuable Player José Altuve: 1.67 m or 5 feet and 6 inches tall;
Hall of Fame pitcher Randy Johnson: 2.08 m or 6 feet and 10 inches tall).
While it may be advantageous in some sports to have longer limbs (e.g.,
basketball, volleyball, etc.), this may create a challenge when selecting
exercises for these athletes. This is an important consideration because not
all resistance training equipment is adjustable for athletes of different sizes.
Researchers have shown that height and limb length may alter the starting
position and mechanics of both lower- (10, 24, 58) and upper-body (42)
resistance training exercises. Thus, athletes with longer limbs must perform
more overall work compared to an athlete with shorter limbs due to
different starting joint angles (Figure 8.4). This is supported by evidence
that has shown that the inclusion of displacement with volume load may
provide a better quantification of mechanical work compared to volume
load alone (44). Although it would require more work, it would appear
advantageous to measure the displacement of each exercise and/or modify
the starting position of certain exercises (e.g., deadlift) in order to
compensate for the additional work performed by athletes with longer
limbs. This in turn may allow the S&C practitioner to monitor their
athletes’ overall workload more accurately and potentially modify their
exercise selection when necessary.
Figure 8.4 Load displacement comparison between (a) a shorter
athlete and (b) a taller athlete.
Chapter Summary
Several biomechanical and physiological principles may impact a S&C
practitioner’s decision to choose a specific exercise or training method over
another. Biomechanical principles that should be considered may include
types of levers involved with specific muscle groups, internal and external
force production differences, and the mechanical advantage/disadvantage of
certain body positions during various exercises. Practitioners should also
understand the physiological impact that specific exercise and load
combinations have on the body and how they may help athletes train
various fitness characteristics. From a practical standpoint, it is important to
note that while bilateral exercises may serve as the foundation of athlete
training programs, there may be an appropriate time to incorporate
unilateral exercises to address specific fitness characteristics and needs. The
S&C practitioner should ensure that the chosen exercises and loads provide
a sufficient training stimulus to increase an athlete’s work capacity, task-
specific hypertrophy, muscular strength, rapid force production, and power
output characteristics as they relate to the athlete’s sport/event.
Furthermore, practitioners should consider the monitoring results of the
athlete (see Chapter 9), as well as their relative strength and
anthropometrics when choosing specific exercises and/or training methods
to provide an optimal training stimulus.
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Part V
9 Athlete Monitoring

DOI: 10.4324/9781003096139-14
Acknowledgment
The authors would like to thank Dr. Ben Gleason for his help in completing
this chapter.
Introduction
While many of the various scientific sub-disciplines that support and shape
sport science are certainly not new (e.g., biology, chemistry, physics), sport
science as its own interdisciplinary scientific discipline is a relatively young
and rapidly developing science. Admittedly too simplistic, sport science in
many ways began to branch off from exercise science during the 1950s to
the 1970s. While overlap exists between the two fields, the fundamental
goals differ (sport = performance, exercise = health and well-being) as does
much of each field’s respective research process (e.g., sport science =
research on competitive athletes). A major aspect of sport science deals
with how research informs decision making and actions of coaches. This
process can be driven by both using existing peer-reviewed research as well
as data collected by various sport performance enhancement group (SPEG)
members (sport scientists, coaches, medical staff, etc.) within a given sport
organization. In this context, existing literature provides a framework (a
map) for much of the planning (e.g., training plan, athlete monitoring
strategies) while “in house” data provides more detailed steering (e.g.,
GPS). Over the long-term, “in house” data can be impactful not just for
more immediate decision making, but can inform larger, bigger picture
assessments and decisions (e.g., did the training plan work?). In this way,
sport science shares some important similarities with the study and practice
of medicine (21). Firstly, and most generally, is the appreciation that sport
science involves those two major components, study and practice, and
often, these two aspects may be intertwined.
To compare to the field of medicine, medical research is carried out to
address specific questions and solve problems allowing physicians (and
other medical professionals) to be better armed to face and address various
medical issues and best care for their patients. Medical research can inform
a physician’s diagnostic decisions (what tests should be run), the patient
evaluation (interpretation), and the resultant prescription(s) (e.g., drugs,
procedures, therapies, etc.). Medical research can also be undertaken in a
more exploratory nature, in which a physician providing care for a patient is
also collecting data “along the way” to ensure evidence led and data
informed practice. Eventually, retrospective analysis of the data occurs in a
more formal manner to publish for the greater medical community. To
compare to sport science, we can replace patient with athlete and to a large
degree, sport science can be conceptually explained and described. Perhaps
the biggest difference is that a coach may not also be a scientist and thus,
sport scientists work alongside coaches to help deliver scientific aspects of
their program and assist with athlete monitoring endeavors. Lastly, similar
to the medical profession, while some “in house” data may end up in a
research journal, the vast majority of “in house” data will likely go
unpublished. Describing the use of athlete monitoring data while being
imbedded as a sport scientist within a U.S. intercollegiate team while at the
same time maintaining a productive research agenda as a professor in
higher education, Dr. Guy Hornsby explains:

Real-world athlete monitoring research is perhaps the most inefficient

way (to collect data and) publish sport science research, the profound
time commitment is met with a very low yield of publications,
however for certain topics, such as periodization, this type of research
is unbelievably impactful and allows us to capture athletes in real
world settings that we would otherwise not be able to … best of all,
this work can positively impact the athletes and coaches involved in
these projects.

Figure 9.1 provides a graphical overview of how sport science research,

often from athlete monitoring, can inform coaches and provide insight into
the overall training process of an athlete. These three general areas include
(i) a better understanding of training, (ii) a better understanding of how to
efficiently and effectively monitor athletes, and (iii) a better understanding
of the various components and aspects of high-level performance.
Figure 9.1 Overview of the athlete monitoring process.
Introduction to Athlete Monitoring
Assessment, both for individuals and organizations, is a key ingredient
within many professional endeavors. In coaching/strength and conditioning,
a suggested practice is to annually present (i) the previous year’s training
plan, (ii) various monitoring data (workloads, adaptations), and (iii) provide
a reflective narrative along with thoughts moving forward to members of
the SPEG (22). With this in mind, it is important to define and contrast the
terms subjective and objective, as evaluation with purpose requires a largely
objective focus. The following definitions come from dictionary.com.

Subjective:

Existing in the mind; belonging to the thinking subject rather than to

the object of thought.
Placing excessive emphasis on one’s own moods, attitudes, opinions,
etc.; unduly egocentric.
Philosophy; relating to or of the nature of an object as it is known in
the mind as distinct from a thing in itself.
Relating to properties or specific conditions of the mind as
distinguished from general or universal experience.
Pertaining to the subject or substance in which attributes inhere;
essential.

Objective:

Being the object or goal of one’s efforts or actions.

Not influenced by personal feelings, interpretations, or prejudice;
based on facts; unbiased: an objective opinion.
Intent upon or dealing with things external to the mind rather than with
thoughts or feelings, as a person or a book.
 Being the object of perception or thought; belonging to the object of
thought rather than to the thinking subject (opposed to subjective).

Ideally, a tremendous amount of care is placed into the creation of the

training prescription for a given athlete. The training prescription should be
built with specific goals in mind, mapping out timelines and fitness phases
allowing for optimal “directing” of adaptations over time (7, 19). The
training prescription should inform the athlete monitoring plan (19),
specifically: what to monitor, when to monitor, and the lens from which the
coach and sport scientist contextualize the monitoring data. Generally,
athlete monitoring involves measuring an athlete’s training dose (external
load) and subsequent response (internal load) (34). While the planned
training for a given session (e.g., practice, weight room) may often match
(or nearly match) the actual session that was carried out, it is important to
monitor workloads in real time as sometimes sessions can go off script for
various reasons (e.g., coach decides to change practice structure, athletes
show up to the weight room much more fatigued than expected, etc.). This
ensures that the training program being evaluated is what the athletes
performed vs. simply what was written ahead of time. Frequent to periodic
measurements related to preparedness throughout an athletes training
provide cyclical feedback to which the coach can better understand the
athletes training-related responses, and gauge if (i) the athlete is developing
as anticipated and (ii) any training (or recovery, nutrition, rehab, etc.)
related adjustments are needed (8, 9, 34).
Sands and McNeal (31) have referred the process of athlete monitoring
as “post-dicting” training and performance. The idea that while we might
not be able to, with precise accuracy, predict the adaptation(s) and
performance outcomes ahead of time, that through a sound and structured
monitoring program we can post-dict with 100% accuracy. In a simplistic
sense, it involves telling a scientific story of the past that can hopefully help
better guide the future. Sands and McNeal (31) go on to explain that the
better coaches understand the past (what did they do, and what were the
results?), the better they can direct future training. For example, Mujika and
Padilla (28) have described how tapering strategies for advanced swimmers
may differ based on previous macrocycle monitoring data. Not only can
previous monitoring data help guide future training, but it may impact the
approach of a coach when new athletes join their care. For example, a better
understanding of strength levels and various strength-related adaptations of
collegiate freshmen and sophomore athletes may influence the subsequent
training plans for incoming freshmen (12). Conceptually, it may be helpful
for coaches to view their individual athletes as single-subject case studies
and collectively, as their own subject population. The authors of this text
believe that sport science is currently in an exciting period due to the
greater number of highly ecologically valid, observational studies on
trained athletes recently published in peer-review literature.
Sound training and monitoring can be thought of as managing an
athlete’s preparedness and is a two-part process: first, develop the
physiological tools that improve an athlete’s performance capabilities, and
second, manage fatigue and training in a manner that best allows them to
express their adaptations when it matters most (raising preparedness and
their performance potential) (7, 8, 19). Raising an athlete’s preparedness
does not guarantee a great performance but it does increase the chances of it
occurring. Indeed, athletes, particularly genetically gifted athletes, may still
be able to have a successful performance if training didn’t lead to increase
preparedness (31). However, coaches should view this example of a great
performance in spite of the training as “chaotic” (less predictable and more
unstable) and less ideal (31).
For example, a recent investigation assessed seven championship finals
and semifinals from 42 Diamond League (track and field) competitions; in
total, 7,087 individual results were observed (25). The athletes largely
performed their best (or very close to it) in the championship finals (success
rates were more than 70% higher at championships compared to “basic”
events, p < 0.001). Additionally, for racing events, success rates (larger
performance improvements) were greater (over 60% higher) for the top
three versus those placing fourth and below (p < 0.001). The authors noted
the importance of appreciating that when competing in a finals event, a
peak performance is likely necessary to achieve a medal (25). While
performance is certainly multifaceted, it is very likely many of these
athletes achieved a season best or a personal best (or very close to their
bests) in large part due to their training bringing them to a physical peak,
elevating preparedness.
Not only can a well-thought-out athlete monitoring program help inform
a coach during an athlete’s training cycle; the construction of the
monitoring plan can inform, to some degree, the construction of the training
prescription. Periodization can be viewed as a process of creating a
blueprint for when specific responses and performance alterations are
desired. Thus, contextualizing the monitoring plan beforehand can aid in
developing the prescription; for example: “What do we want to make
happen? Why? And how?” (31, 34). For a trained athlete, preparedness will
fluctuate based on the training phase and monitoring must be viewed by
comparing expectations and outcomes vs. simple “did the athlete improve
this block?” First and foremost, the training block, the emphasis/de-
emphasis, and the programming contents within the block (e.g., exercises,
loading progressions, etc.) drive this evaluation; however, many other
aspects should be considered, such as the athlete’s sport, training history,
genetics, competition calendar, long-term goals, etc. (12). Indeed, it is a
process of comparing the qualitative forecasted response (e.g., the general
expected response, such as “the primary adaptation from this block of
training will be maximal strength”) and the quantified outcome (e.g., the
specific value for a given measured adaptation, such as peak force from an
isometric mid-thigh clean pull or a 1 repetition maximum back squat).
Conceptualizing Athlete Monitoring
Athlete monitoring is driven by two primary aims:

Aim 1 = fatigue management – aids in avoiding non-functional

overreaching and overtraining by using fatigue related metrics in an
effort to assess whether the athlete is well suited to recover and adapt
(or has recovered/adapted) appropriately to the given training stimuli.
Aim 2 = program efficacy – encompasses an athlete’s training,
adaptation, and performance data/history allowing for the assessment
of the athlete’s training process allowing for coaches to assess the
efficacy and efficiency of their training program.

Similar to how periodization uses concepts and terms to describe the

purposeful development of an athlete’s training prescription (35),
conceptually scaling athlete monitoring can be helpful for handling athlete
monitoring data (26). Below is a general conceptual approach for scaling
athlete monitoring allowing for helpful contextualization (the specifics of
the plan and the athlete) while keeping these two important aims at the
forefront of the monitoring program. This scaling simply involves viewing
monitoring data through three distinct “levels.”

Micro-level monitoring: week-to-week, day-to-day monitoring (e.g.

volume, intensity, sleep, nutrition, mood state). Micro-level monitoring
is primarily aimed at fatigue management.
– Duration = a few weeks, a week, intra-week, intra-day
Meso-level monitoring: phased-based monitoring in which both
fatigue management and program efficacy are assessed. Focus is
placed on adaptations related to preparedness and performance.
Examples: force characteristics, field tests, endurance, etc.
– Duration = a block or several blocks of training (4 weeks to 16
weeks)
 Macro-level monitoring: “big picture” view (e.g., program efficacy).
– Duration = a macrocycle or beyond (e.g., an annual plan, multiple
annual plans, etc.)

Conceptually, micro- and meso-level monitoring “feed into the macro.” For
example, a well-executed micro- and meso-level training and monitoring
system allows for increased chance of success at the macro-level. From a
reflective standpoint, micro-level and meso-level monitoring allows for
coaches and sport scientists to better “connect the dots’ between the training
performed and the programs results. Sound training and monitoring steering
through the micro and meso-level can help coaches stay on their pre-
determined course as best they can; and if and when they need to make a
programming-related adjustment (e.g., injury, a practice being moved, a
game being rained out), they can do so in a meaningful way. As previously
noted, an athlete monitoring program should start with a scientifically
supported training prescription and coaches should avoid simply using
monitoring solely as a fatigue management tool. Thus, for micro- and meso-
level monitoring, the lens through which the coach/sport scientist
contextualizes the data may shift depending on where the athlete might be
within in their annual training plan. When connecting monitoring to the
periodized plan, meso-level monitoring can be viewed as a specific block of
training (e.g., did the block of training bring about the desired effects?),
while micro-level monitoring deals with directing training within the block.
Relating to training management, macro- and meso-level monitoring should
be viewed through the lens of periodization (timelines and phases) while
micro-level monitoring should be viewed as programming (8, 9, 35).
Figure 9.2 A team-based strength-power testing scenario.

While macro-level monitoring remains rather constant (e.g., “did the

athlete(s) develop/improve from previous the macrocycle(s)?”) (12, 39),
various aspects of the athlete should be used to think through the evaluation
(e.g., training age, training history, talent level, etc.). Perhaps the most
obvious factor for evaluating at the macro-level is how long has the athlete
been training the relevant performance-related adaptations and how long
(how developed are they?) within the sport? Scientists have noted that as
athletes get closer to their genetic ceiling, the magnitude of potential
adaptation is minimized (1). For very advanced athletes, smaller gains in
performance can be incredibly important and very much a challenge (1).
Indeed, advanced athletes have been shown to require a greater stimulus
(i.e., they possess a higher intensity threshold necessary to facilitate
adaptation) to achieve a positive adaptation(s) (supercompensation) (10).
Thus, when evaluating a very advanced athlete, the goal of given block(s)
of training may be more to revisit and re-establish a given adaptation(s)
versus establishing a much higher homeostatic level.
What if Things Go Wrong?
To state the obvious, athletes can respond to training by getting better,
getting worse, or staying the same; but coaches and sport scientists are
interested in understanding not just how, but why an athlete developed or
failed to develop or performed well or perform poorly. Various aspects
related to this process can include (i) the expectations of the coach (e.g., are
the expectations reasonable?), (ii) the adaptations to training over time, (iii)
how the accrued adaptations relate to sport performance enhancement, and
(iv) psychological factors during the competition (e.g., athlete may have
been prepared but still performed poorly) (12). An important aspect of the
appreciation of macro-level monitoring is that it extends well beyond
simply tracking performance in competitions. Certainly, at the end of a
competition phase/competitive season, critically reflecting specifically on
an athlete’s (and the team’s) in-competition performances is worthwhile.
However, how their training was managed and alterations in adaptations
critical to their performance should also be closely reviewed: “How did the
changes in various adaptations, preparedness, and performance capabilities
potentially affect changes in in-competition performance?” This process is
complicated; there are numerous examples of athletes having a “bad day”
without a specific measure to explain “why? (31). In-competition
performance is multifaceted and for team sport can be incredibly
challenging to quantify due to the nature of competing against different
levels of opponents, different positions, athletes having different playing
times (starter, bench, sub), etc., and just generally the nature of open skill
games-based sports. Individual sports tend to more closely link with
preparedness; however, it is still not a black box situation involving training
input = performance output. Indeed sport performance involves a white box
scenario in which the more we know, the better, but outcomes are not
definite (I Mujika, personal communication).
 There are numerous examples of high-level athlete monitoring programs
not only in the form of peer-reviewed studies but also in reviews and
coach/sport science-focused chapters and summaries. Several of these
reviews/summaries describe not only important reasons for monitoring but
also reasons for why an athlete’s training may fail due to non-functional
overreaching and either negligible gains in relevant adaptations and
performance, or even a decrease in performance (12). These reasons can
include:

1. The overall program was not well constructed.

a. Programming does not support adaptation objectives.
b. Lack of adaptation objectives/specific phases focused on a
specific adaptation objective(s).
c. Sequencing issues.
d. Fatigue mismanagement; this can be due to a poor overall
program or specific aspects of the program either not being well
constructed/implemented or a lack of training integration.
2. Outside stressors related to aspects such as social life, diet, sleep,
work, etc., do not support the athlete’s training and at times, can be
detrimental.
a. This is a major reason for a sound micro-level monitoring plan.
b. A big reason why training responses are idiosyncratic in nature.
3. Genetics is the largest factor influencing recovery/adaptation and
performance.
a. Not all athletes possess physiology that promotes long-term
development (a smaller window of adaptation).
4. The athlete must make a long-term commitment and consistently be
driven in training.
a. Not every athlete is willing to make this commitment; coaches
play an incredibly important role fostering this commitment.
b. Aspects related to “outside stressors” can play an important role.
In the case of a team sport athlete (or an individual sport athlete that trains
with a team) not developing to near the magnitude expected (or worse,
performance declined), a helpful exercise can be to compare them to other
athletes on the team. This coupled with micro- and meso-level monitoring
data can hopefully help the coach better understand what went wrong.
Ideally, monitoring can “turn around” a potentially catastrophic situation.
There are several good examples for evaluating monitoring based on the
training prescription. What to do when things go wrong is less clear and
often there likely is not a perfect answer. Generally, three options exist: (i) a
substantial deload for a given period of time, (ii) continue as best you can,
or (iii) start the macrocycle or mesocycle over. How to handle this
unfortunate situation begins by identifying the issue and then attempting to
troubleshoot the reason(s) for the problem (12). Of particular importance is
whether the athlete is at risk for health, well-being, and/or safety issues due
to overreaching complications. In this case, rest (and potentially other
recovery related or medical related modalities) is needed. The next
determining factor likely deals with the calendar. For example, “starting
over” may be ideal; however, this is often difficult to impossible (e.g., if the
athlete is in the middle of a competitive season).
Monitoring Training Dosage
The athlete’s overall stress involves a combination of training and non-
training stress (life stressors) and an athlete’s response to stress is the output
of the dose-response relationship. Athletes do not have an infinite capacity
to respond to stress; appropriate loading depends on the athlete and requires
the proper interplay between work and recovery. It is indeed a balance that
Stone et al. (37) have referred to as a “Goldilocks complex”: too little
training load = no adaptation, too much training load =
overtraining/burnout, optimal training load = increased adaptation,
enhanced performance. Even for activities such as weight training and
conditioning that are highly reliant on numbers (e.g., sets, reps, percentage
intensity), it is important for coaches to monitor training dosage as the
training is carried out and not assume that the plan (what was written ahead
of time) is what was implemented by the coach/athlete (27). For various
reasons a coach may modify the plan ahead of time or even in the moment.
If a change in training occurs between what was prescribed and what was
implemented, this should be properly reflected in the training dosage data.
Training dosage is perhaps the easiest and most logical area of
monitoring (27, 33, 37). Indeed, a training diary is not a new practice used
by diligent coaches and athletes. Various software and technologies can aid
in athletes inputting and coaches storing, viewing, and handling the data
(excel, tableau, etc.) (15). Training dosage can be divided into volume,
intensity, density, and frequency (13). Volume is the quantity of training
demands and is proportional to the amount of work performed (13). Most
sports usually measure volume as sets × repetitions × an intensity factor
such as time or load. Intensity can be measured as the force, rate of work
(power), or how a subjective rating of how hard the athlete performs
training. Density refers to the amount of training that is packed into a given
time period. “Two-a-days” is a denser training dosage than “one-a-days.”
Frequency simply refers to the number of training sessions (13).
 Resistance training provides many relatively easily measured dosage
variables. The type of exercise, number of repetitions, resistance used,
percentage of 1RM, speed of the movement, range of motion of the
movement, number of sets, rest period between sets, body positions, order
of exercise, time of day, preceding exercise characteristics, activities during
rest, and many other variables can be assessed and recorded (13, 39). All of
these variables have some impact on the character of the athlete’s training
and ultimately on the character of the athlete’s response to training.
Resistance training has traditionally monitored the number of sets,
repetitions, weight lifted, percentage of 1RM, and duration of rest periods
between sets. However, we now know that these variables, while important,
are often not sufficient to fully characterize athlete training (17). Power
monitoring, rate of force development, speed of movement, and even the
shape of the force-time curve of an explosive effort can be used to
characterize and monitor resistance training.
Volume and Intensity as a Monitoring Tool:
Micro, Meso, and Macro Lens
Daily recording of volume and intensity is an essential micro-level
monitoring tool that should not be ignored even though it is likely less
immediately actionable compared to other micro-level measures. Not only
is training volume and intensity a helpful micro-level monitoring tool
allowing for comparisons from one training session(s) to the next, ensuring
that unintended, inappropriate spikes in workloads are avoided, but over the
long term is an incredibly valuable and perhaps too often underappreciated
meso- and macro-level monitoring tool.
Absolute training volume and absolute training intensity (along with
sport performance outcomes) are perhaps the best examples of macro-level
monitoring when viewing training and development across many
macrocycles (e.g., several years). As athletes develop, their absolute
volume and intensities rise for their given phases of training. Most
commonly when volume and intensity is discussed, it is in relative terms.
For day-to-day planning purposes, relative workloads are much more useful
for coaches. Highly trained athletes perform more work and at higher
intensities compared to lesser developed at the same relative volume. For
example, if a college senior that developed well across 4 years did the same
annual plan as their freshmen year, the absolute volume load is ideally
substantially higher while the relative volume remains relatively unchanged
(12, 21). Similarly, for training intensity, coaches can use intensity to gauge
adaptation for a given training block or blocks (e.g., if a well-trained
strength athlete sets a PR on their VH squat day for their 3 × 10 or 3 × 5
block the coach can be confident that the athlete adapted well across the
training block(s)). This example involves both a mixture of both meso-level
and macro-level monitoring of intensity (39) in that at the meso-level the
athlete experienced a success and at the macro-level the coach can adjust
(raise) future weight room goals. Specifically, for macro-level monitoring a
coach can view training intensities across several macrocycles; and if the
intensities are slowly rising from one macrocycle to the next with a similar
mix of heavy, moderate and light days throughout the coach can be
confident a more resilient, stronger athlete is developing. Certainly, for
more advanced athletes, there is a point at which volume and intensity will
begin to stagnate.
Monitoring Response
In my opinion, you are not really monitoring if you are not
monitoring dose and response.
– Dr. Bill Sands (personal communication)

Response variables are generally used to determine two things – changes in

fitness and changes in fatigue or recovery, and summarily, alterations in
preparedness. Fitness variables, when they decline, may be attributed to
fatigue. However, recent investigators have begun to address recovery as a
separate aspect of response to training.
Testing, in the sport or sport science context, deals with detailed
examination of the characteristics and properties of an athlete or of
equipment related to sport. Testing can be biomechanical, physiological,
psychological, or performance oriented. Measurement deals with
quantifying (assigning numbers) to the properties and characteristics being
tested. Evaluation is the decision made about the significance or quality of
the sport or the sport-related characteristic or property based on the
measurements made. Evaluation must be based on a careful consideration
of the significance of the measurement. Often in sport, the evaluation has to
do with the degree of change in a specific measure, which can reflect either
a positive or negative adaptation to training. Adequate evaluation is
possible only if the testing and measurements have been appropriately
carried out.
One of the most important aspects of sport science and coaching is the
ability to make accurate measurements (18), for two primary reasons. The
first is the need to accurately assess the characteristics or value of
something, leading to answers to certain kinds of questions: How much did
it weigh? How large is an object? How much time elapsed? How long is it?
The second reason is the need to differentiate and objectively evaluate
potential differences. This evaluation process can allow determination of
the winner in a race or throwing contest, or it can allow a coach to
determine if a training program is accomplishing the desired goals.

Measure what is measurable and make measurable what is not so.

– Galileo Galilei

The frequency of measurements depends on factors such as the

availability of the athletes, the sophistication and intricacy of
measurements, and the amount of time taken for return (4, 40). Athletes in
residence, as at colleges or at Olympic training centers, can typically be
tested more often and on a more regular basis; but for many sports, the
athletes may be spread out over a large geographical area, and in such cases
regular camps, must be organized so that testing can be carried out. If
testing results cannot be returned rapidly (usually within zero to three days),
then the coach cannot make potential alterations in training load in time to
make a difference in the outcome of the training program. However, certain
tests, such as technique analysis using videography, are time-consuming
and may take weeks for return, especially if large numbers of athletes are
involved. Certain types of invasive tests, such as blood draws and hormone
analyses, can take several days to weeks to analyze. The potential time lag
between testing and data return should be communicated to the coach and
athlete before the testing session. Less involved, easily administered, rapid-
return tests can be administered more often.
Without a doubt, making good measurements in an effort to assess
athlete response is at the core of good sport science and athlete monitoring.
Below are a number of important considerations related to making good
measurements in an effort inform coaches and sport scientists on various
facets of the athlete’s training process.
It is well established that idiosyncratic responses occur between athletes
when carrying out a given training plan (31). Simply put, if a team of
athletes (even a rather homogeneous group of athletes) undergoes the same
training prescription (sets, reps, relative intensity), the adaptation response
will be somewhat different for each athlete. This is not to say that training,
especially when employing a block periodization approach, results in
random outcomes (35, 38); quite the contrary, but the exact magnitude of
adaptation is impossible to predict beforehand (31). Thus, through block
periodization coaches can qualitatively predict the adaptation outcome;
however, measuring the adaptation response is necessary in an effort to
precise quantify individual changes (31, 35). Several factors influence the
resultant adaptation: (i) genetics, (ii) training background, (iii) commitment
of the athlete, etc. (12). A major factor, for a specific athlete’s given
adaptive response is outside stressors.
Monitoring Outside Stressors
The influence of outside stressors on an athlete’s recovery-adaptation
process can be illustrated by the following hypothetical, and admittedly,
fantastical situation. An athlete carries out a prescribed 8-month macrocycle
of training and is closely monitored along the way. The athlete then boards
a time machine and travels back to the start of that 8-month macrocycle and
before beginning the training for a second time, their previous 8 months of
training and adaptation have been removed before the athletes then
complete the macrocycle for the second time. It is likely that when
comparing the same 8-month macrocycle, for the same athlete, with the
same training background, that even then, the response will (however
similar) not be exactly the same. Indeed, even if the training is the same, the
athlete’s life surrounding training will be different. Categories related to
outside stressors include (i) sleep, (ii) diet, (iii) psych-soc aspects, (iv)
recovery strategies, etc. (16). Obvious aspects, such as work, school, and
friends affect an athlete’s stress both directly and indirectly; e.g., negative
stress from an interpersonal relationship can result in both direct
psychological stress as well as affect other life-related habits, e.g., sleep,
diet, alcohol consumption, etc. (12, 16). Selye often referred to stress in two
distinct categories: eustress (good stress) and distress (bad stress) (7). While
perhaps stress isn’t always so clearly good or bad (e.g., a typical relatively
inconsequential day) certain examples can be given of an athlete lifestyle
and the world around them either promoting or sabotaging their recovery-
adaptation process and their overall development. These life factors can
include:

An educated, highly skilled coach to plan and direct their training

process.
Provided resources that aid their training (e.g., a monitoring program,
support in the areas of psychology, nutrition, sport medicine, recovery,
 etc.).
A social network (friends, family, etc.) that is supportive of the athletes
training and performance goals.
Is the athlete responsibilities outside of the sport (e.g., work, school)
reasonable to not interfere (too much) with their training process?
Has the athlete experienced proper age and stage development?

Daily monitoring in an effort to get a handle on an athlete’s outside

stressors is not new. Banister (3), Kellman (24), Sands (30, 31), etc., have
been involved in daily, non-training- related athlete monitoring (in addition
to training-related monitoring) several decades prior. Many daily or
periodic survey options exist to coaches for tackling this area of monitoring
(24); RESTQ, POMS, ARSS, SRSS. Additionally, advances in technology
allow for both the delivery and storing/displaying/communicating of data
from these surveys to be easier and more user friendly (15). For example,
smart phone applications allowing athletes to easily enter data replaces the
need for using a specific computer, or even less convenient, paper and pen.
While smart phone applications certainly help with user ability, it is
important that:

1. Coaches frequently educate and communicate the purpose of outside

stressor monitoring.
2. Outside stressor monitoring should not be used to punish damaging
lifestyle habits.
3. If, based on the data, an athlete’s health/safety is of concern
appropriate, help is provided.
4. Coaches/sport scientists frequently check the data to make sure
athletes are entering the data daily (or almost daily) and checking to
make sure the information is reliable (athletes are putting thought into
their answers).
Considerations for Measurement
Regardless of whether a project is research, service, or a combination of the
two, the tools used to measure the variables of interest must be valid and
reliable. Validity refers to whether or not the instrument is actually
measuring what it is supposed to be measuring. There are basically four
different types of measurement validity:

Internal validity refers to how well the tool measures the variable in
question (e.g., strength, power, speed, endurance).
External validity concerns the ability of the tool to predict changes in a
population other than the one being studied (e.g., when investigators
measure strength in one group and then generalize to another group).
Prediction validity refers to the ability to predict one variable from
another (e.g., when investigators measure strength to predict the
vertical jump).
Ecological validity deals with how the parameters of the
intervention/test approximate real-world setting. This is particularly
important in sport science application and research.

For performance testing, a maximal effort is necessary on the part of the

athlete. Similar to coaches employing various coaching/teaching strategies
to promote maximal effort in the weight room and on the field, performance
testing requires similar strategies. Certainly, the athlete’s understanding the
purpose of the given test and how it relates to their training can promote
maximal effort as well as creating a competitive environment. Figure 9.3
shows the display of a live results video board to an athlete while
performing an isometric mid-thigh clean pull. This helps motivate the
athlete to perform the test with maximum effort and allows the athlete to
know how they compare to previous tests and how they compare within
their team. The results of this display is similar to a record board for various
strength, speed, and power tests commonly found in weight rooms. An
important consideration may deal with how often an athlete should perform
a given test to avoid a situation in which the athlete grows “numb to the
test.”
Figure 9.3 Athlete performing an isometric clean grip mid-thigh pull.
Immediate data feedback is being provided on the video
board.
Figure 9.4 Athlete performing a static (squat) jump.

Measurements must also be reliable. Reliability refers to the degree of

consistency of measurement, that is, how much error is in the measurement.
Sport scientists and coaches must be concerned with test-retest reliability.
Test-retest reliability has to do with the degree to which an instrument can
produce the same measurements at different times under the same
conditions. Methods of establishing reliability include intraclass correlation
(ICC), coefficient of variation (CV), and the standard error of the mean
(SEM) (see (18) for more detail on these methods).
Calculating reliability is a must, otherwise comparison between groups
or longitudinal alterations in performance cannot be established. If the
measurement instrument is not reliable, then any data gathered with that
instrument cannot be trusted, as it will not be possible to know with any
degree of certainty whether potential differences in performance or
physiology, for example, are real or are a result of measurement error.
A common issue in sport science deals with measurement due to
measurement error being larger than the actual differences. Often, changes
in physiology (and performance) are smaller than can be detected by
laboratory measures. At the elite performance level (world championships
and Olympics), the difference between first and fourth place is often less
than 1%, and underlying physiological mechanisms explaining those
differences may not be detected with current instrumentation.
Those involved in testing must ask a number of questions to ensure
adequate validity and reliability:

1. Is the measurement device appropriate for the population? Are age,

sex, skill level, and so on taken into consideration? If the test is too
difficult or otherwise not suitable for a particular group, then its
validity and reliability will be questionable.
2. Is the measurement relevant to sport or activity requirements? If a test
does not reflect specificity and cannot be shown to be associated with
sport performance, then other more specific tests should be found. The
 most efficient test or tests for some sports may not be known; in this
case, studies should be undertaken to establish what tests are relevant
for a particular sport before long-term testing or monitoring of athletes
takes place.
3. Has prior experience of the athletes (familiarization) been considered?
As with most activities, some period of practice time before testing
may be necessary so that the subjects can become familiar with the
tests. Otherwise, early testing results may be simply reflecting a
learning process.
4. How aware is the investigator of the testing environment? The testing
environment should be controlled as closely as possible so that the
athletes will have the best possible chance of performing well, and if
tests are repeated later on, the environment should be the same as in
the first testing period. The environment includes not only temperature
and humidity but also factors such as measurement precision of
investigators, time of day, day of the week (similar short-term training
status, degree of fatigue), extraneous noise, appropriate lighting, and
clothing.
5. Are the instruments properly calibrated? Instrument calibration is a
must in providing reasonable reliability and validity. Lack of
appropriate instrument calibration can be a major source of error. The
investigator must know how to calibrate all instruments and have them
calibrated well in advance of the testing.
6. Have biases been removed (subjectivity vs. objectivity)? In order to
remove as much subjectivity as possible, the testing instrument must
allow all of the subjects to have an equal chance of performing well.
Furthermore, investigators must be objective in their selection of an
appropriate measurement instrument and in their interpretation of the
data.
7. Has a “floor or ceiling effect” been inadvertently set up? If the test is
too easy and all subjects perform well (ceiling), or if the test is too
difficult and all subjects perform poorly (floor), then differentiation
among subjects (or groups) will not be possible.
8. What is the optimal order of testing? When several tests are
administered in the same testing period, it is important that a given test
not be fatiguing to the extent that it greatly alters the results on
subsequent tests. For example, if a 1RM squat, a countermovement
vertical jump (CMJ), and a static vertical jump (SJ) are to be
administered on the same day, an appropriate order might be VJ, SJ,
1RM squat; because the 1RM squat is the most fatiguing, performing it
first may affect performance on the other two tests. Also, with the
order VJ, SJ, 1RM squat, the jumps may serve as additional warm-up
for the squat. Consistency of testing order is also quite important; as a
result of fatigue or potentiation, both validity and reliability can be
greatly affected if the order of testing changes from one testing period
to another.
Handling Data
A detailed overview of the statistical handling of athlete monitoring data is
beyond the scope of this chapter. We thus refer the reader to Sands et al.’s
open access article “Recommendations for Measurement and Management
of an Elite Athlete” (30). In this article, several strategies for single athlete
assessment are discussed, including statistical process control, split middle
analysis, and various trend analyses (e.g., training data, outside stressors).
These strategies are particularly useful for longitudinal data that is collected
relatively frequently. Indeed, a core concept in applied sport science is the
importance of monitoring individual athletes versus using group means and
appreciating single-subject research that is aimed at best directing the
training of that specific individual athlete is not aimed at generalizing to a
population. For example, a coach is likely not as concerned with how the
group changed from one test point to the next but rather how each
individual athlete changed. Similarly, some commonly used, traditional
statistics such as p-value assessments are likely less helpful in applied sport
and in many instances, due to the relative homogeneity of highly trained
athletes and the degree to which they are close to their genetic ceiling, small
gains are very unlikely to be statistically significant but can very practically
important (i.e., impact where an athlete places in competition). With this in
mind, magnitude-based assessments (e.g., effect size, smallest worthwhile
change, etc.) can be helpful when assessing changes in an individual athlete
for data involving periodic performance assessments (e.g., isometric mid-
thigh pull, sprint tests, agility tests).
Creating a System
Recently, several authors have demonstrated that maximal strength is a
more stable adaptation throughout the course of training (20, 38) and that
adaptations more dependent upon the nervous system (e.g., RFD) are better
for assessing an athlete’s fatigue status. While maximal strength does not
fluctuate much over short periods, and in well-trained athletes does not
change much even across several mesocycles, for strength-power athletes it
is certainly a variable to be mindful at the macro-level. Are athletes
increasing their peak force capacity over a year to several years? Similarly,
for highly trained endurance-based athletes, VO2 max has been shown to be
a stable adaptation (28), and thus, is not a good fatigue indicator, but
certainly over the long term, a variable that a coach will want to nudge
higher. Joffe and Tallent (23) demonstrated that even among very highly
trained weightlifters (all international level) over the span of several years,
maximal strength can indeed slowly increase over time.
Variables that are more sensitive to fatigue (e.g., RFD) and training
nuances, and therefore fluctuate more often, can be incredibly helpful for
micro-level monitoring, but also, if important for sport performance, should
be viewed through a meso and a macro lens (20, 38). For example, day-to-
day and week-to-week RFD or power output may be used more as fatigue
monitoring tool; however, with a macro view, coaches should be aiming to
increase RFD and power output over the long term as explosive strength
and power capabilities are incredibly important in anaerobic-based sports.
Creating an athlete monitoring system can involve creating “buckets” in
which various data streams are measured and managed. For example,
internal load, external load, adaptation, and key performance indicators
(KPIs) allow for the assessment of training, training response, and how
these factors potentially influence changes in sport performance. When
communicating data to coaches, connecting how the data impacts
competition performance is imperative, and as much as possible these
conversations should be framed with the end goal of performance in mind.
If one is in charge of working with various teams (as typical within U.S.
collegiate sport), it is likely most efficient to create a large-scale monitoring
of the “basics” (e.g., volume load in the weight room, general fatigue, and
performance tests) while adding specific measurements for specific sports
(sport-specific sprint and agility tests, etc.). Often connecting general
performance data to sport-specific tests can help the coach appreciate the
importance of the “basics.” For example, correlating general strength data
to a batted-ball test for a baseball team or a no-arm swing static jump test to
an approach with arm-swing jump for a volleyball team. Certainly, more
detailed analysis of sport specific performance may be helpful (e.g.,
biomechanical analysis of on field performance).
Indeed, communicating information to the coaching staff and other
SPEG members is a key responsibility of a sport scientist. Below is a
discussion related to communicating with coaches and a philosophical
narrative on the current state of sport science.
The Role of the Sport Scientist
Certainly, coaches with a sport science (SS) background can collect and
assess/interpret their own data. However, often coaches (particularly within
higher level sport settings) rely on sport scientists who are trusted to collect
analyze, interpret, and communicate data to invested parties (coaches, sport
medicine, sport pysch, etc.) (4, 21, 40). When in a SS role, important
considerations exist when communicating data to coaches and various
SPEG members. Various structures and ideas have been presented in the
literature regarding the concept of a high-performance model (32): a
process-based organization system in which a framework for what (and
why) data is collected, delegating various responsibilities, and feedback
loops (21, 32). Hierarchal models for roles, flowcharts for targeting various
data systems are helpful examples for thinking through one’s specific SS
situation. Ideally, roles are clear, “boxes” targeting specific questions are
checked, and plans are set in place, timing the delivery of information and
whom it is communicated to. Athlete management systems (AMS) allowing
for data to be steered to one place can allow coaches to receive data more
quickly and be provided helpful visuals to explain the data and how to think
through it (15). However, important aspects of AMS use exist:

1. For data in which an application programming interface is utilized, the

data in the AMS is consistently and constantly checked by the sport
scientist.
2. The sport scientist knows if the invested parties actually check/read the
data reports.
3. Simply providing leaderboards and “top 5s” likely do not address
specific problems and questions.
4. Data is interpreted through a lens of (i) the individual athlete’s
background/situation, and (ii) what is the training plan and sport
scenario?
 5. The AMS is not a substitute for real life, in-person communication!

Point 5 is a critical point that sometimes may be lost in high-speed world of

high-level sport. Additionally, it is important to appreciate that a good sport
scientist should know the underpinning science for a given topic,
understand the scientific process for evaluating/addressing the given topic,
and possess a skillset that involves a trained lens for which SS information
is processed.
Figure 9.5 Athlete receiving verbal instruction prior to testing.
Errors in Training and Education
A lens is a device that facilitates and influences perception, comprehension,
or evaluation. The sport scientist’s lens, which governs their personal
overarching SS perspective, is a critical aspect that makes the sport scientist
valuable to the sport team and coaches alike. As a law school trains a
lawyer to view the world through a particular lens, a sport scientist should
be prepared (i) from an appropriate sport and exercise science curriculum,
(ii) by relevant mentors, and (iii) through performing meaningful practical
work (14). The combination of these three factors in training helps shape
the sport scientist’s lens. This training should be viewed as a journey in
which the scientist learns over time to formalize their lens with experience
conceptualize how to best go about problem-solving in their setting, but
also help bridge the gap between theory and application.
When discussing the process of SS, Dr. John Ivy explained, “If you’re
not truly a scientist, you can’t do science” (personal communication, 2018).
Training to become a sport scientist requires conducting applied sport
research – with athletes – that helps the developing professional understand
training methodology and concepts, potential training outcomes, and the
underlying psychological and physiological mechanistic factors associated
with those outcomes (14). Studying subject matter outside of SS (or even
relevant SS aspects in isolation) does not provide the necessary tools for
developing the sport scientist’s lens (36). What, why, and how a sport
scientist performs their professional duties is governed by their lens’
perspective; thus, poorly trained individuals placed in SS roles may cause
problems and damage the reputation of the field. While the number of SS
jobs has rapidly increased in U.S. intercollegiate sport, challenges still exist
in the education and training of sport scientists, the structure and framework
sport scientists are sometimes asked to work within, and lastly those
making hiring decisions (e.g., athletic directors, coaches) who may be ill-
informed to do so (5, 22).
 An appreciation of three important aspects of the role and the functional
breadth of a sport scientist can help resolve the issues mentioned above.

1. The sport scientist fills a problem-solver role (14). The sport scientist
should help coaches identify problems and answer coach-driven
questions. These “coach-driven” questions can often be inspired
through educational or self-reflection processes. The sports scientist is
trained to know where to go to find good applied and evidence-based
research to these questions (14).
2. The sport scientist is an educator. This involves making sure the sport
performance enhancement team is aware of cutting-edge developments
that can affect training outcomes. This involves sharing results and
best practices with coaches and coaching communities (14). This
formal and informal education can be specific to data collected, but
can also be more general in nature. As noted sport scientist Mike Stone
explained, “ideally the head coach drives the sport performance
enhancement group; sometimes they might need help driving.”
3. The sport scientist plays a supporting synergistic role in the
organization. The sport scientist should be viewed as a key cog within
the SPEG (e.g., SS, sport medicine, sport psychology, nutrition, sport
coach, strength and conditioning coach) and expertise of all the
individuals this group should be integrated in sport processes (4, 40).
While the benefits of this interdisciplinary team-based approach are
well known, it is more difficult to achieve a true team approach in real-
world practice, particularly within U.S. intercollegiate sport
organizations due to their breadth of sport sponsorship and cultural
norms. It is encouraging that many universities are hiring full-time
sport-enhancement team members (e.g., sport scientist, sport
psychologist, nutritionist); however, it is our observation that often the
present framework of a given SPEG within an athletic department
limits an integrative, highly communicative approach. For example,
the nutritionist is tasked with nutrition counseling, providing “training
table” meals, and post-workout nutrition; the sport psychologist is
charged with counseling and mental skills training; and the “sport
scientist” (usually a sport physiologist or data analytical specialist) is
charged with using certain sport monitoring technologies. In this
example, there is no specific “cross-over” and integration between
these professionals (e.g., workload monitoring, subjective
psychological-sociological monitoring, body composition planning
and assessment) leading to professional silos.
Process Problems in Sport Organizations
Typically, a structured system begins with a deliberately designed
hierarchical model in which organizational structures are constructed,
responsibilities are identified, and communication streams are planned.
While high-performance models have been discussed in the literature and
there are many great examples for professional and Olympic sport (see
www.ownthepodium.org/en-CA/Initiatives/Sport-Science-Innovation).
Within in the United States (the home country of the authors), one of the
largest outlets for higher-level sport (and in some cases, very high-level
sport) is within NCAA intercollegiate sport. While there has been some
growth in recent years, the NCAA still has a long way to go for SS to be
supported similar to the example above (21, 22, 36). Interestingly, (sadly)
NCAA sport is housed within the American Higher Education system; thus,
a connection between the athletic department and an academic unit
allowing for better SS support (research, expertise, student help, etc.) would
seem like a natural fit; however, several hurdles exist impeding this process
(21, 22, 36).
At the 2015 NSCA National Conference Dr. Andy Fry questioned: “Is
technology driving sport science or is sport science driving technology?”
(NSCA National Conference, Orlando Florida, 2015). Well before
technology is purchased and data are collected, relevant coaching and
training questions should be asked and problems identified that drive the
various financial commitments to technology. It is our observation that too
often data are collected without a well-crafted “why,” or simply in an
attempt to “keep up” with other peer programs. In a research project, this is
the research design phase. The right design will answer the questions in a
focused effort using appropriate scientific methodology and equipment to
derive possible, expected, or unexpected outcomes. Data should be
collected and used for decision making and practical use (4, 40). This is not
meant to suggest that data should constantly and immediately direct
decisions, but that the various data streams should fill clear voids in the
overall SS/coaching puzzle. It is likely that some athletic departments
purchase technology with the hope that it boosts recruiting (or at least puts
them on equal footing with other programs), thinking: “if successful team X
has this device then we need to have it.” Particularly concerning is how
often commercially available devices are purchased by athletic departments
and internal evaluations of reliability are not established and error rates not
well understood (2, 11).
Sport science should not be viewed as a luxury item (“We have an extra
$50,000 left in the annual budget, lets buy some technology!”). It is a
deliberate process involving evaluation, validation, and optimization of
internal organizational processes – an essential theme for any high-
performing organization and requires personnel to implement. Indeed, SS is
analogous to the white-box research approach popularized among other
multi-layered, multi-dimensional organizations. In U.S. intercollegiate
sport, it is disheartening to so often observe that large amounts of money
have been spent on SS technology, while in comparison much less of a
commitment was made to personnel and process. A device or strategy that
is much cheaper may provide the same (related or similar) information as a
more expensive device, but the coach and/or AD is only interested in the
more expensive option (e.g., it is what professional team X uses). Cost-
effective solutions can not only be helpful for budgetary reasons, but
cheaper options can sometimes be helpful for coach education. For
example, a logical progression may involve first collecting session RPE (6)
for a year or so and then adding collection of TRIMP scores (3) using heart-
rate monitors. Through this progression, the coaching staff and sport
support personnel may iron out processes and explore value before
venturing into purchase of GPS devices. Indeed, it has been our observation
that typically the evolution of monitoring methods progress such that
multiple methods can be eventually integrated in a generative manner
producing a superior product. The idea of starting small and diligently
planning out the various lines of questions and resultant approaches to
address said questions is a process that could potentially prevent frivolous
spending and poor practices.
Non-deliberate or unframed technology integration is certainly an all-
too-common issue. Instead of choosing technology deliberately and with
purpose, if athletic departments simply purchase the “newest gadget” that
may well be lacking in validation, programs could begin to operate on some
level that ranges from misapplication to charlatanism. This may happen if:

1. SS is abused as an empty recruiting tool, providing “flash” during the

recruiting trip and social media campaign, but misrepresented in terms
of actual service provided to the athletes. In this case, value of
operations is falsified. A message is broadcast that is well beyond what
is actually taking place and the decision making processes at the
university are projected to be much more informed than they really
are.
2. Sport science is used incorrectly, such as when an individual applies a
technology tool without accounting for error. Even worse, devices may
be used abusively. In one recent event, for example, a coach was
literally running off players using unreasonable heart rate targets in
practice using heart-rate monitors. In another, student-athletes were
punished with running for not achieving eight hours of sleep per night,
as reported by sleep-tracking devices. Beyond the problems caused in-
house, these events can damage the reputation of the career field and
sets us all (strength and conditioning and SS) back when media
representations occur.
Importance of Sport Science Support within the
Sport Organization
A well-planned, inclusive, integrative SS structure and system utilized to
successfully carry out SS is imperative. Carving out this framework is
where an organization (team(s)) should begin. At the center of this
systematic process should be constant communication with and
involvement of the sport coaches and sport support specialists. Ideally,
coaches would be involved in the early planning stages and truly have
interest in data collection and SS; this may require substantial education
before investing in SS. Indeed, coaches should want the data as part of the
established, socialized process, as this helps sport coaches and strength
coaches develop a better understanding of what they are observing.
Parallels can be drawn from the area of reflective coaching in which
detailed planning, diligent observation, and reflection constantly take place
in a cyclical fashion (29). It has been noted that a difference in languages
often exist, particularly in the U.S., between the coach and scientist, making
communication difficult (36). A solid communication structure is not a
long-term professional fix for this issue as formal SS education is needed
for coaches (and sport scientists) but it can help the coach learn along the
way.
Lastly, resources are an incredibly important component for carrying out
SS. Adequate numbers of personnel (including a mix of full-time staff,
interns, and grad students) must do the work, and should not be
overwhelmed. Excessive duties reduce the quality and consistency of data.
Sufficient personnel allocation enables proper communication and a
consistent SS presence for a given sport team. Certainly, athletic department
budgets are often stretched, and there is usually much more wanted than can
be paid for. It is worth considering first investing in personnel over
technology (particularly incredibly expensive technology) and appreciating
that the most expensive technology available is not always the best – even if
it is, does it come at the cost of number of personnel and other devices?
Indeed, we have observed a few situations in which an entire athletic
department has employed one sport scientist (with no funding for assistants)
with an expectation of carrying out SS duties for 20+ sports. This prevents a
meaningful impact on operations because the responsibilities are too broad.
Impact of False Processes and Erroneous
Application
For many college athletes, their first exposure to athlete monitoring
technologies occurs during on-campus recruiting visits. Coupled with
locker room perks and scholarship offers, the possibility of training using
sport monitoring technology can heighten an athlete’s sense of going from
high school sport to “the big time.” The opportunity to train and develop in
high-tech environments can be a powerful incentive for signing top recruits.
Unfortunately, poorly designed protocols have the potential to do
considerable programmatic damage as well.
The use of monitoring technology can align well with the trend towards
athlete-centered coaching, an approach geared towards understanding the
needs of the individual to support autonomy, holistic growth, and sport-
specific development of the individual. Keeping track of individual training
response variations can be challenging particularly in large team settings
and when training may occur at different times under the supervision of a
variety of staff members. Individual monitoring can provide coaches with a
starting point for follow-up observations and questions, particularly when
results vary from the team norm or expectations. Additionally, when the
usage of technology is well thought out and integrated into a program that
includes regular performance meetings to support development, it can
provide athletes with individualized attention and support important for
program investment. Ultimately, a well-designed monitoring program that
is coupled with routine and clear process goal-related feedback can help
develop and support an athlete’s ability to self-monitor their own
engagement and process in the training model.
Conversely, the misuse or misguided use of monitoring technology can
damage the coach–athlete relationship, undermine team trust and have an
overall negative impact on athlete performance. Wearing monitoring
technology can feel invasive and intrusive, particularly when required in
out-of-training contexts. While capturing out-of-training data like sleep can
provide valuable information, it can also foster a “big brother is watching”
mentality without clarity of purpose and expectations. Clear communication
and expectations are essential within the coach-athlete relationship. How
performance data will be used to inform individual and team training should
be both transparent and applied unilaterally. Monitoring data that appears to
only be used as the grounds for punitive consequences or as evidence of a
perceived lack of effort or compliance (e.g., with sleep expectations)
undermine a positive training culture, athlete compliance, and will
overshadow the positive potential of monitoring data.
Within high-level sport teams, athletes compete not only against other
teams but also for starting positions and for coach attention within the team.
In addition to protecting individual data in compliance with regulations
such as HIPAA, and because monitoring technology allows for both
aggregate and individual data analysis with regards to training progress,
coaching staffs should carefully consider how data will be used when doing
within-team comparisons. Perceptions of unequal or preferential treatment
can contribute to within-squad jealousy and an unhealthy culture of
comparison that is counter to a constructive performance culture. Unequal
application of training metrics for either promotion or demotion within the
team setting will foster unrest as well as uncertainty.
Ideally, the investment in the time and manpower necessary to
effectively use athlete monitoring technology is made as a cohesive staff
with full buy-in. Presenting a united professional front to athletes about the
value of collecting training data is essential for compliance and the capture
of quality data to inform coaching decisions. Individuals within a program
who don’t value monitoring or understand the proper application of the data
will undermine program effectiveness. There are numerous examples of
evidence-based athlete monitoring protocols that have been carefully
designed and integrated into coaching systems with notable success.
Successful adoption and application requires both an administrative and
programmatic understanding of what monitoring technology can and cannot
do, the best practice principles for data collection and usage, and
understanding of the core science principles behind the information being
captured. Engaging in ongoing professional development is also essential to
stay current within the profession of SS.
There can be considerable psychological implications for athletes going
through testing and monitoring processes without purpose. This can be
damaging to morale and the team culture and foster distrust within the
organization. Athletes will likely appreciate specialist support as it provides
a sense that they are being looked after and cared for. Indeed, a good
monitoring program also helps to educate the athlete, providing the athlete
with information related to their current level of fatigue, degree of
adaptation, and more broadly clues them into their training. These types of
programs have been successfully implemented in other countries with
considerable success. Without open and committed support and education
among administration, coaching staffs, and sport scientists, SS can lose
credibility within the organization. This attitude could follow athletes into
their careers as coaches, perpetuating issues that currently exist.
Chapter Summary
Athlete monitoring is a staple of SS, coach education and high-level
coaching. Depending on how SS is used, it can inform practitioners, the
field, or in some cases, both. High-level athlete monitoring should prioritize
people and process with a supportive structure that holds education and
communication to a premium. A scientifically supported training process
should always underpin the athlete monitoring strategy driven by
appropriate age and stage athletic development.
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39. Suchomel TJ, Nimphius S, Bellon CR, Hornsby WG, and Stone MH.
Training for muscular strength: Methods for monitoring and adjusting
training intensity. Sports Med 51(10): 2051–2066, 2021.
40. Torres-Ronda L and Schelling X. Critical process for the
implementation of technology in sport organizations. Strength Cond J
39: 54–59, 2017.
10 Developing the Training Process

DOI: 10.4324/9781003096139-15
Introduction
This chapter is an extension of the material in Chapter 7. The complexities
of modern sport demand a holistic approach to preparation and
performance. The training process must be viewed as a long-term process
that encompasses the skill, technical-tactical, psychological, emotional,
physical, and personal development of the athlete. A robust training process
must also address the demands of competitive sport in a modern, globalized
world.
For example, athletes may enter athlete development or high-
performance programs, common in professional and Olympic sport, during
youth or early adolescence. Athletes may progress along this developmental
pipeline over several years, potentially into adulthood, to higher levels of
competition. Incidentally, athletes are likely to progress through several
developmental stages of biological, psychological, intellectual, and personal
maturation during their participation in these high-performance pathways.
Advances in scientific understanding and technology have better enabled
coaches and practitioners to integrate several areas such as sport medicine,
strength and conditioning, sport psychology, performance nutrition, skill
acquisition, etc. The development of an effective training process requires
the coordination of these domains into a cohesive long-term plan.
Periodization has proven to be a useful framework for developing the
training process in such a manner. In its most basic form, periodization is
the division of time into smaller distinct units. The earliest form of
periodization in sport occurred in Ancient Greece and was largely borne
from the influence of seasonal variations and crop cycles on training and
competition. Training periodization eventually grew to consider the type,
quantity, and distribution of training interventions to direct skill, technical-
tactical, psychological, and physical development aligned with the
competition/performance schedule. This evolution of the periodization
concept applied to training also coincided with the emerging view of the
training process as a year-round and multi-year affair.
This maturation of the concept of the training process has opened the
door for creativity in how coaches and practitioners decide the phases and
subphases of the periodized plan, their duration and distribution, the
preparatory elements they wish to include, and the specific objectives
within these areas.
Some debate exists regarding the specific form a periodized training plan
should take, primarily concerning aspects related to strength and
conditioning. However, a scientific approach enabled by research and
technology does permit flexibility in how practitioners may choose to
execute the periodized plan and respond to inevitable perturbations and
disruptions that may arise. For example, competitions may take place in a
different time zone or climate than an athlete is used to. Other unforeseen
circumstances may necessitate minor adjustments to the training content or
schedule, such as facility or equipment access when traveling. Other
scenarios may cause more drastic effects, such as experienced during the
COVID-19 global pandemic.
A comprehensive athlete monitoring program is indispensable for
identifying the occurrence of mitigating factors that coaches may wish to
adjust for. Thus, different practitioners may craft training plans that are
characterized by the same basic periodization model (e.g., block) but may
differ based on how each person chooses to adjust the day-to-day execution
of the plan resulting from contingent factors such as schedule changes,
athlete subjective wellness, performance metrics, etc.

Periodization Model Selection

The periodization concept has a long and rich history of development going
back to ancient times (89). The concept has evolved so that currently two
base models of periodization are in use: traditional and block. Traditional
has two forms (typical and reverse), block periodization consists of two
subtypes, single-goal (single-factor) and multi-goal (multi-factor) (19, 89,
94).
Understanding the basic periodization concepts(s) is paramount for
appropriate selection. Periodization provides the overall concept of training
and deals with subdividing the training process into specific fitness phases
and timelines (25, 26, 60, 93). While various definitions have been created
and presented, these definitions often confuse programming with the
periodization concept or miss the inherent nonlinear nature of periodization
(19, 89). Indeed, the periodization concept and subsequent programming
(alterations in exercise selection, volume, and intensity) are designed to
occur in a cyclical manner and remove linearity. It should be noted here that
the recently coined terms such as “linear periodization,” “daily undulating
periodization,” and “weekly undulating periodization” are misnomers both
by definition and by concept (19, 89). Indeed, as previously noted, there are
only two types of periodization: traditional (classic) or block (19, 41, 89).
Periodization and appropriate programming are clearly not linear but rather
exploit the basic training principles, particularly variation. Furthermore,
general periodization terminology is not completely agreed upon and varies
somewhat from country to country and from author to author (24, 78, 93).
As a result, the following definition will be used for this discussion:

Periodization is a logical sequential, phasic method of manipulating

fitness and recovery phases in order to increase the potential for
achieving specific performance goals while minimizing the potential
for non-functional overreaching, overtraining and injury (25, 26, 89).

It is important to reiterate that periodization is a conceptual process of

training program management dealing with fitness phases and timelines
(19, 25, 26). This guideline allows the coach to project an approximate
timeline as for when fitness characteristics of different types (e.g.,
endurance, strength-endurance, strength, power, speed, taper, etc.) will be
emphasized, the order of the phases, and how long each of these phases will
last. The two types of periodization have similar fitness phases. Traditional
periodization typically consists of four fitness phases: general preparation,
special preparation, competition and taper, and active rest (25) (Table 10.1).

Table 10.1 Summary of traditional periodization and its phases

Phase Description
General Typically denotes a higher volume, lower intensity, relatively low task-specific
preparation phase designed to raise sport specific fitness, primarily concerned with altering body
composition and raising work capacity. (Block periodization: Accumulation block)
Special Volume decreases to moderately high levels, average training intensity begins to
preparation increase to moderate levels, exercise move toward greater task/mechanical
specificity. A portion of this phase often emphasizes the athletes’ ability to repeat
exercise with a greater task/mechanical specificity. Essentially this phase represents
a transition from higher volume, less-specific training to a higher-intensity, very
specific training phase associated with competition. (Block periodization:
Accumulation moving to the transmutation (or transition) block)
Competition Moderate-to-low volume phase with moderate to very high intensity that is markedly
task/mechanically specific. The purpose is to maintain fitness, stabilize technical
consistency/efficiency and engage in competition(s). The competition phase can last
several months, if volume reduction lasts more than 12–16 weeks, short periods of
mini-preparation take place (See Figure 10.6). These mini-preparation periods can
include periods (1 – 2 weeks) of functional overreaching which appear to enhance
competition performance if timed correctly. (Block periodization: Transition
moving to the realization block)
Peaking A competition phase segment lasting a short time (usually ≤ 4 weeks preceding
major competitions. Volume is reduced, average training intensity is increased for
some sports such as powerlifting or maintained at relatively high levels. Typically,
for most sports, intensity factors are also reduced shortly (≤2 days) before important
competitions to encourage adequate recovery. The later portion of a peaking phase
(typically 8–21 days), volume is markedly reduced, by as much as 60% in some
sports, and is referred to as a “taper.” A taper consists of a reduction of training
volume in order to reduce fatigue and take advantage of the fitness–fatigue paradigm
(66, 67, 78, 89, 93, 96). The taper can be integrated with planned overreaching in
order to push performance beyond that of a typical taper (2). (Block periodization:
Realization block)
Phase Description
Active rest A relatively short period of substantially reduce volume and intensity of training of
providing rest and recovery after peaking and major competitions (usually 1–2
weeks). The purpose of this phase is to allow for healing and rehabilitation of any
injuries that may have occurred as well as recovery from the psychological rigors of
competition. Although occasionally necessary, complete rest results in considerable
deterioration of sports-specific fitness and performance often to a degree from which
it is difficult to recover without extensive retraining, particularly in older athletes.
Compared to complete rest, active rest results in less deterioration of fitness and a
more rapid return to peak fitness during the next cycle or stage of training.
Occasionally, training can be re-directed into another activity (usually compatible
with sport specific characteristics) to improve the psychological/emotional recovery
aspects (i.e., make the training more recreational).

These phases can make up a macrocycle (several months to

approximately a year) or mesocycle (typically a few months). The phases
direct training from high to low volume and from low to high intensity
(general preparation to competition taper). The complexity and specificity
of exercises generally increase across phases. An important characterization
of traditional periodization is that during each phase, different components
of training tend to increase and decrease simultaneously. Thus, volume of
strength training, endurance training, etc., would rise together during
general preparation and tend to decrease together during the competition
phase. As noted by Matveyev and, particularly by Verkhoshansky and
Issurin, several problems were created. First – during some phases, the
volume of work becomes nearly, or completely, unmanageable and chronic
fatigue often becomes a substantial problem. Second – as the volume of all
fitness work decreased during the competition phase, maintaining overall
fitness was a problem. Third – optimum development, particularly for some
aspects such as strength-related variables (RFD, velocity, power), was
difficult or non-existent. This occurs because simultaneous use of non-
compatible exercises substantially reduced adaptation because of undue
chronic fatigue and compromises in underlying favorable physiological
mechanisms (44–46, 98, 99). Fourth – evidence indicates that a true peak
can only be held for, at most, approximately 3–4 weeks (29). As the
competition calendar has grown in complexity, it has become increasingly
difficult to peak at the right time and hold a peak through multiple
competitions (e.g., regionals, trials international competition). Block
periodization (BP) grew out of these observations (44, 46, 47). Although
not all agree, based on our own research and available evidence, BP appears
to be a superior method for producing alterations in sport and related
performance characteristics (25, 26), including strength-power alterations
(12, 13, 72, 73), endurance activities (64, 82), with individual (81, 82) and
team sports (58, 59, 77, 84, 88). Therefore, in selecting a periodization
model, it is recommended that the tenets of BP be adhered to in most
situations.
 Block Periodization and Phase Potentiation
Briefly, BP consists of a stage containing four defined periods (i.e., fitness
phases): accumulation, transmutation, realization, and active rest.
Typically, the first three blocks or phases last several weeks (≈4–8 weeks)
(though they can be longer or shorter) and represent a series of concentrated
loads. A concentrated load consists of “unidirectional” training with an
emphasis on one or two specific but compatible fitness characteristics (e.g.,
short interval sprints and power development). One or more related
concentrated loads can make up a periodization block. Concentrated loads
can take the form of summated microcycles. Summated microcycles
(typically 3–4 weeks) are a series of microcycles (e.g., 1 week) that are
linked together to emphasize a specific effect (89, 93). For example, a
strength training accumulation block could be made up of two summated
microcycles, the first emphasizing strength-endurance and the second
emphasizing basic strength (Figure 10.1).

Figure 10.1 Example of a stage of block periodization. Note that there

are three summated microcycles making up the three
periodization blocks. Two summated microcycles, one
emphasizing strength-endurance and the second
 emphasizing basic strength, make up the accumulation
block. Both microcycles result in the “accumulation” of
important physiological and physical attributes for
strength-power athletes. In this example, transmutation
and realization make up one summated microcycle in
which there is a marked volume reduction and shift to
more task specific, power-oriented exercises. Also note
that the initiation of the taper is preceded by an
overreaching microcycle, used to potentiate further
adaptation.
Source: Based on Stone et al. (89).

Development of additional characteristics during a concentrated load

(especially non-compatible characteristics (e.g., RFD and endurance) may
result in the temporary de-emphasis of certain qualities. The efficacy of
concentrated loads, in part, depends upon “residual effects” which carry
over into the next block or stage (45, 89). Each block can be extended if
necessary (e.g., additional initial fitness training, additional basic strength
training, etc.) by adding an additional concentrated load within a block.
Conceptually, BP depends upon “phase potentiation” programming, in
which each individual block theoretically potentiates the next, through
residual effects (19, 25, 26, 44, 89). Generally, during accumulation (as in
general preparation), the emphasis is on higher volume and less specific
training such that alterations in fitness-related characteristics (e.g., body
composition, work capacity, and basic strength), are emphasized. The initial
accumulation phase is used to prepare the athlete for higher intensity more
specific work occurring later in the training process. Although, there can be
some programming overlap with accumulation, the transmutation block
moves to more specific exercises with somewhat lower volumes and
somewhat higher intensities of training, and in references to strength-power
training, can result in substantial increases in maximum strength for specific
exercises. For strength-power athletes, realization usually deals with power-
oriented, task-specific exercises and typically involves a taper (reduction in
volume) to reduce accumulated fatigue and potentiate preparedness before a
competition. So, typically to develop strength and power, periodization
guides training from higher volume to lower volume and more general to
specific; programming is manipulated to make this occur. However, under
some conditions, for example, some endurance activities or team sports
with a high endurance component, a reverse paradigm may be useful (15–
17, 34). Regardless, a taper can bring the athlete’s preparedness to a peak
(66, 67). Often, a planned overreaching phase is used in conjunction with
the taper (7, 8, 13, 25, 26).
Active rest (AR) is the last block of a stage and usually takes the form of
low-volume and low-to-moderate intensity. Active rest is a short period
(≈1–2 weeks) of recovery usually taken after peaking and competition.
Peaking and competition can require both physical and emotional recovery.
Longer periods are sometimes necessary to accommodate individual
problems such as excessive fatigue, outside stressors, injury, etc. Absolute
rest can result in deterioration of sports-specific fitness to a degree such that
it is difficult to recover without substantial retraining. Compared to
complete rest, AR allows for less deterioration of fitness and therefore, a
faster return to optimum fitness levels during the next stage. Depending
upon the athlete, the type of sport, and the preceding competition,
particularly after a penultimate competition, it can be valuable at times to
re-directed training into a different but related fitness activity. Depending
upon individual athletes’ circumstances, a different training activity can be
considered. Redirection of activity, often allowing the AR training to be
more recreational in essence, may help to improve psychological/emotional
recovery aspects (52).
Due to modern issues of the competition calendar and depending upon
the sport, BP can take two forms: single target periodization (SBP) or a
multi-targeted form (MTBP) (48, 89, 94). SBP is primarily used when there
are single (or very few, very compatible) targets, such as weightlifting and
high jumping. MTBP should be used primarily with sports in which several
different factors must be developed simultaneously. For example, strength-
power, multiple changes of direction, shooting, and other attributes are
necessary to develop simultaneously for success in many team sports such
as football (soccer), basketball, and American football. MTBP attempts to
enhance or stabilize these attributes simultaneously; this means that a
specific fitness characteristic may not be as fully developed compared with
the use of concentrated loads in SBP. However, the goal for MTBP is more
“holistic” and while several characteristics may be trained in a block
simultaneously, attempts to control non-compatibility can be made through
programming choices. For example, it is known that long-slow distance
work and some types of interval exercise can substantially attenuate RFD,
power, and speed development (31, 79, 80, 101). However, evidence
indicates that high-intensity interval training can have a smaller interference
effect and produce superior performance effects compared to long-slow
distance (32, 71, 75, 85). So, during an accumulation block, endurance
might be developed substantially for a sport such as soccer using interval
work and short-sided games which may have a lower level of non-
compatibility (28).
However, a basic tenet of SBP is selecting and emphasizing fitness and
performance characteristics that are compatible during a particular block
(25, 48, 94). Non-compatible attributes should be de-emphasized. For
example, the simultaneous training of endurance and strength can decrease
adaptation for RFD and power. So, if RFD and power are the primary long-
term goal, the emphasis on high-intensity work (emphasizing RFD and
power) during an accumulation block may be de-emphasized in order to
concentrate on endurance activities until proceeding to a different block.
SBP is primarily used in sports in which there are relatively few tasks to
develop, especially those sports not necessitating development of tasks in a
simultaneous manner. Thus, SBP takes an approach somewhat opposed to
that of MTBP by targeting a single fitness (or a very few compatible)
characteristics during each periodization block of training through the
implementation and execution of “concentrated loads” (24, 48, 89).
Concentrated loads are unidirectional in content and promote specific
adaptations (e.g., hypertrophy, strength, etc.) that underpin a desired fitness
quality (e.g., maximal power) (99). Typically, with the exception of the
primary factor to be enhanced, higher volumes of compatible factors are
reduced, and non-compatible factors are greatly de-emphasized and often
non-existent during a concentrated load. Appropriate programming
characteristics for each “concentration” are applied over a series of
consecutive microcycles that display a similar pattern of volume and
intensity of loading, termed “summated microcycles” (Figure 10.1) (89, 92,
93). Despite accentuating a particular performance characteristic,
employing concentrated loads does not completely eliminate other
compatible fitness components during a training phase, but rather de-
emphasizes them through the use of retaining/maintenance loads (89, 93).
Thus, through a system of emphasis/de-emphasis, appropriate development
of desired characteristics can be fully developed over the course of an
annual plan (25, 26, 89, 93).
When compared to multi-targeted loading, concentrated loads used in
SBP appear to yield a superior supercompensation effect for the selected
emphasized characteristic following a period of restitution (63). This
delayed performance improvement is often referred to as the “delayed
training effect” (93, 99). Previous literature indicates that sequencing
concentrated loads in a typical order inherent to BP (e.g., strength-
endurance, maximal strength, strength-power, Figure 10.1) exploits the
delayed training effect, as the residual training effects from one phase serve
to enhance or “potentiate” the training effects of the subsequent phase (33,
44, 45, 48, 89, 99). This programming concept has been referred to as
“phase potentiation” (19, 25, 26). Therefore, when implemented correctly,
the conceptual effects of BP and the applied effects of phase potentiation
programming do not occur independently, but rather in a synchronous
fashion.

Training Process Components

An understanding of both conceptual and developmental factors of the
training process entails the major portion of constructing an appropriate
plan. Considering that training is multifaceted, the degree of success
achieved relates to how well coaches learn to plan conceptually,
subsequently creating comprehensive and precise subcomponents that can
be integrated and oriented into the process to produce superior results.
These factors of the training process include the development of the annual
plan, programming, integration of sport science (athlete monitoring), and
the integration of sport medicine.
Development of the Annual Plan
The first step in developing the annual plan is determining the performance
schedule, although modern forms of periodization have evolved beyond
simple calendar-centric models. Advances in scientific knowledge and
technology have permitted the consideration of biological timelines (e.g.,
physiological adaptation, fatigue decay, and skill acquisition) into the
planning process. This concept is promulgated in models such as the
fitness-fatigue paradigm, stimulus–fatigue–recovery–adaptation model, and
periodization of skills training framework for skill development. Thus,
identifying the performance schedule and available time between the start
of the plan and the performance schedule is the first step in identifying the
available timeline to elicit the desired training effects and configuration of
training phases and objectives. This step should be completed as far in
advance and with as much exactitude as possible, keeping in mind that
some dates and factors may change with or without notice. The time from
the onset of the plan until the (first) scheduled competition will dictate the
assigning and distribution of phases. Annual plans that include multiple
competition phases will recycle phases. Factors such as training status,
scheduled breaks or holidays, and relative placement within a multi-year
plan will influence the length of each phase. The sport demands, which
inform the practitioner in setting targeted objectives, will also influence
which periodization model is most appropriate. Based on the chosen
periodization model (i.e., block vs. traditional, single vs. multi-factor), the
coach may then proceed with determining the appropriate training content
to elicit the desired adaptations. Depending on organizational structure and
available resources, integration of ancillary components into the periodized
plan may also take place.
Though our discussion is primarily rooted in the creation of an annual
physical training plan, the inclusion of all interrelated training components
and emphases should be included in the annual plan (Figures 10.2 and
 10.3). It is popular (and necessary) within modern sport to consider the
athlete as a complex adaptive system. Though this is technically its own
scientific field, it is imperative that practitioners have an understanding so
that such principles may enhance planning. A full discussion of complex
adaptive systems is beyond the scope of this section, but there are a couple
of key characteristics that we will highlight due to their relevance to annual
planning. First, the annual plan has many parts and subsystems that have to
be managed in a complementary manner. This is because the interactions
between these components drive the emergent behavior (i.e., performance)
of the athlete. Though we cannot predict this behavior with precision – we
can predict it relatively well from a qualitative standpoint. Though
frustrating and even paradigm shifting in terms of constructing an annual
plan, the efficacious development and implementation of periodization have
progressed from complicated to complex through the advances in athlete
monitoring.

Figure 10.2 Example portion of an annual plan for a single-factor sport

athlete (weightlifting).
Figure 10.3 Example portion of an annual plan for a multi-factor sport
athlete (soccer).

Athlete monitoring is a crucial component for any periodized plan,

especially in the face of the modern complexities of sport and everyday life.
Even rudimentary forms of monitoring, such as keeping a training diary that
details training goals and activities, diet, sleep, injury, and basic health
markers like bodyweight and resting heart rate provide valuable information
to evaluate program efficacy, to potentially identify the onset of
maladaptation, and to make acute adjustments that are aligned with the
overall training objectives when faced with any contingent factors.
Additional personnel and resources may allow for more sophisticated
monitoring programs through the use of specialized equipment and
analysis. Applied sport science initiatives may include biomechanical
analysis, physiological testing, psychometrics, and predictive modeling.
Assessments may be scheduled within the annual plan in an isolated or
recurring fashion, depending on the assessment and intended application.
For example, baseline screening that includes a physical health evaluation,
range of motion testing, and a battery of physical performance tests may be
scheduled at the commencement of a preseason camp. Countermovement
jump testing and isometric strength tests may be included more regularly
such as at the beginning or conclusion of a phase, or even weekly, to
monitor neuromuscular status (Figure 10.4). Monitoring may also be
 incorporated on a daily basis such as through the use of hydration testing.
All forms of monitoring can be applied retrospectively to evaluate program
efficacy. However, well-integrated monitoring programs allow practitioners
to make acute programming decisions to address unexpected or emerging
scenarios while maintaining alignment with the objectives of the training
plan or to pivot toward new objectives such as when an athlete suffers a
catastrophic injury.

Figure 10.4 In-season weekly countermovement jump monitoring

illustrating changes in propulsion mean force and
propulsion time.
Programming
The annual plan also contains the programming for the periodized training
plan. Programming and periodization are often confused as they are clearly
not the same (19), programming “drives” the periodization phases in that
appropriate programming allows a specific fitness phase(s) attribute to be
developed. So, programming deals with creation of appropriate sets,
repetitions, exercise selections, rest periods, etc. Manipulation of these
programming factors make the different phases of training both efficient
and efficacious.
Separation of these two aspects (periodization and programming) within
the training process can sometimes be difficult. Programming is the primary
factor in directing training phases toward the desired goal(s) and for
managing fatigue. Indeed, alterations in programming variables, sometimes
subtle, can make substantial alterations in training adaptations and eventual
performance. Long periods of substantial training volumes or periods of
intensification creating excessive accumulative fatigue can inhibit
psychological and physiological adaptation to training stimuli, and can
increase the injury potential (50). Thus, a primary goal of programming is
concerned with manipulating programming variables (e.g., volume,
intensity, exercise selection, etc.) such that fatigue is controlled. This does
not mean that fatigue can be or should be completely obviated, but rather
controlled in a manner such that adaptation can be optimized.
Depending upon the model of periodization selected (traditional vs.
block), the programming can be substantially different. Regardless, creation
of the annual plan is the first and most important step in creating an
efficient and successful training process. Critically, the efficiency and
efficacy of a training plan often resides in the willingness and collaborative
efforts of the head coach and assistant coaches (and strength–conditioning
coaches) to learn and appreciate the intricacies of the planning process (42).
Unfortunately, willingness on the coaches’ part is a factor that does not
always occur. As can be expected, among coaches not accustomed to a
conceptual planning process, adjustment may be difficult, but hopefully,
temporary (42).
Although hereditary effects play a major role, an appropriate, critically
planned training program is still necessary to move the athlete toward their
genetic limits. Even though epigenetics play a role (relatively minor), not
much can alter your genetics (you’re stuck with it); so development of the
training process becomes paramount. However, in order to appropriately
develop a training process, an in-depth understanding of underlying
mechanisms and Training Principles are necessary. Fundamentally, it is the
appropriate manipulation of these mechanisms and principles that is critical
for training process development.
Block Programming Considerations
Block periodization and appropriate programming depends upon several
observations and training characteristics (11, 13, 45–47, 49, 63, 72, 73, 80,
89, 93). As previously noted, development of specific
physiological/performance characteristics, especially at high levels, cannot
be sustained for long periods of time. Furthermore, attempts to
simultaneously develop multiple characteristics can often be
counterproductive, particularly when total training volume is excessive and
the characteristics are non-compatible, such as long-term endurance, rate of
force development, and speed (37, 40, 101). Resulting from this
observation, emphasizing training variables at different points of the annual
plan can better develop specific performance characteristics, without
causing compromise in one or more of the developmental characteristics.
This tenet can be met through the use of a consecutive series of
“concentrated loads” that are sequenced together at the appropriate time in
order to produce superior results. In addition, abrupt short periods (1–3
weeks) of “planned” increases in training volume (and sometimes intensity)
can promote additional adaptation, possibly as a result of “functional
overreaching” (7, 8, 89). Collectively, the summating effects of
concentrated loads coupled with planned overreaching strategies may
positively affect future training through phase potentiation, as a result of the
accumulation of residual effects. While the differences between traditional
and block periodization may at times be subtle, coaches should understand
that the differences between winning and losing, a medal and no medal, are
often extremely small. For example, in the last nine Olympics, the
differences between 1st (Gold) and 4th (no medal) in sports with objective
outcomes (i.e., timing, weight lifted) has been less than 1.5% (18, 68, 97).
Thus, because of the nature of competitive sport, training advantages, even
those seemingly trivial, may in actuality be quite large. There is little doubt
that BP concepts and methods can offer training advantages for some
sports.

Additional Programming Considerations – Some Details and Nuances

Essentially, resulting from three primary factors, classic or traditional
periodization may not always produce desired effects (25–27, 89, 93).
These factors are:

1. Incompatibility with the modern training schedule.

2. For most sports, the simultaneous increase in non-compatible
variables.
3. Substantial and often excessive increases in training volume leading to
poor fatigue management.

Considerable evidence indicates that phase potentiation programming

strategies that are inherent in BP can produce superior results, particularly
as it relates to athletes (4, 5, 11, 13, 25, 26, 33, 38, 43, 45–47, 49, 58, 63,
72, 80, 82–84, 90, 91, 93, 100). There are substantial problems inherent in
the traditional periodization approach that can in part or whole, be obviated
by block methodology.

1. Modern competition schedules are not in concert with the typical

timelines afforded by traditional (classical) periodization methods,
particularly among collegiate sports in the USA. Some objective
evidence and considerable observation indicates that most athletes
cannot hold a true peak for more than 3 weeks (29, 66, 67, 69). This
short-term peak might work well if there is only one major competition
for each macrocycle; however, there may be multiple important
competitions, sometimes relatively close together. Thus, an approach
that requires long-term peaks or contains a number of closely spaced
peaks likely will not result in adequate outcomes.
2. Often coaches (not understanding all of the subtleties of periodization)
attempt to increase the volume of many different training variables
simultaneously. This approach can cause considerable difficulty in
fatigue management due to high volumes of training as well as create
physiological adaptations which may not support the goals of the
periodization phase (block):
Although necessary for some sports, care must be taken in the
simultaneous development of different physical characteristics,
especially if there is a degree of non-compatibility (i.e.,
endurance and explosiveness). Indeed, it can be burdensome and
potentially non-productive to attempt the simultaneous
development of different physical and physiological
characteristics or motor abilities (44, 46, 78, 89, 93). This loss of
timely development and fecundity can occur for several reasons
such as (a) the simultaneous training of fitness characteristics
typically results in a training volume increase, often considerable,
that can increase fatigue and recovery time (6, 9, 11, 62); (b) as a
result of non-compatibility, mixed training methods such as
combining endurance and strength-power-related training, can
reduce the effectiveness of training direction (i.e., achieving
specific goals) and retard gains in performance, often favoring
endurance over strength, power and particularly explosive
strength (RFD) (6, 11, 33, 49, 55, 61, 63, 80). Thus, the goals of
the training program could be compromised.
An aspect that can compound fatigue management problems
especially when associated with high volumes or mixed training
methods (i.e., simultaneously targeting multiple skill and fitness
variables) is training to failure or near failure (i.e., high absolute
or relative intensities) – a compounding problem that is
particularly associated with resistance training. Training to failure
has not been shown to provide a superior stimulus and has been
shown to increase training monotony and strain (13, 73) and
prolong recovery time (22, 35, 65, 74).
Some of these problems associated with traditional periodization were
recognized as early as the 1960s by Matveyev (60) and Matveyev and
Zdornyj (61). However, conceptual training paradigms attempting to
address these problems were not well constructed and systematized until the
1970s and 1980s. The foundation for BP was formalized during this time
period by Verkhoshansky (98, 99) and Issurin (47, 49) in Europe (Soviet
Union) and by Stone and colleagues (90, 91) in the USA, particularly for
strength-power training. Most importantly, these conceptual paradigms for
“BP” have continued to evolve over time, particularly as it concerns
appropriate programming (19, 89).
Integration of Sport Science (Athlete Monitoring)
Sport is the ultimate evaluator of processes. Typically, the efficacy of a
process is assessed using the wins accrued relative to losses, medal count,
or sustain a competitive rank. Though winning is important (it is the point
of sport, after all), using this myopically to evaluate the efficacy of a
preparation process may lead to an incorrect appraisal of a periodization
strategy. In a sense, winning does not necessarily confirm optimization as
there are many mediating factors (both positive and negative) that may
influence outcomes. However, the absence of winning (i.e., losing) does
verify that the training process was suboptimal and that adjustments should
be made.
Because of the difficult logic problem apparent in the “black box”
approach outlined above, “white box” approaches are strongly preferred in
modern sport. Now, the coach attempts to gain an understanding of the
inputs, outputs, and mediating factors using athlete monitoring. These types
of processes typically involve frequent measures of performance proxies.
The feedback afforded from these contextualized data equips the
performance practitioners with the information needed to make best
practice decisions regarding any modifications to the periodization structure
or contents of a training plan. This is not to say that “best practice”
decisions exclusively use monitoring data. Instead, as proposed by Sackett
(86) for the medical community, best practice performance training
strategies equally weight athlete monitoring data (i.e., context-specific
evidence), general scientific knowledge, and the preferences of the athlete.
Because the latter two are ever-present and continuously being refined, so
too should athlete monitoring data. In other words, the most valuable athlete
monitoring processes are those that permit frequent, longitudinal data
collection.
In order to have a discussion around the support that athlete monitoring
provides periodization during implementation, it is first important to spend
time discussing the differences between sports in relative contribution of
physical, psychological, technical, and tactical aspects on performance.
Because a discussion sport-by-sport would be exhaustive, the authors
instead provide three simplified examples of different relative contributions
of physical, technical, and tactical components – holding psychological
contributions constant for the sake of simplicity. The three scenarios of
sporting success can (i) involve equal contributions from physical,
technical, and tactical, (ii) be skill-intensive (i.e., more contribution from
technical and tactical relative to physical), or (iii) be physical-intensive (i.e.,
less contribution from technical and tactical relative to physical). These
differences in influence on elite performance undoubtedly dictate not only
the development and preparation strategies but what practitioners would be
most interested in measuring as augmentations to the periodization
structure.
These nuances impose a shifting of vantage point and require clarity in
deconstructing performance so that practitioners may select appropriate
metrics that inform performance potential. Physical-intensive sports (e.g.,
track and field) or positions within sports (e.g., bobsled push athlete) can be
deconstructed using key performance indicators (KPIs). KPIs are
measurable values that influence sporting success. In other words, they
allow practitioners to have a general idea on the competitive readiness or
preparation status of an athlete. In situations when sport scientists are
monitoring KPIs, there is typically a strong relationship between that
measurable variable and aspects of sport performance. KPIs are also
typically thought to possess a high transfer of training (20, 21, 56, 57, 102).
An example of KPIs in a physical-intensive sport would be sprint speed for
a bobsled push athlete. It is reasonable – all else equal – that improving a
push athlete’s sprint speed (e.g., assessed via 30 m timed sprint), would
have a favorable impact on that athlete’s push performance. Alternatively,
skill-intensive sports (e.g., baseball) or positions within sports (e.g.,
quarterback in American football) present significantly more nuance in
identifying metrics that matter for eventual performance potential. Even
with the same measurement of interest shared in the bobsled example
(sprint speed), a baseball player would not necessarily become a more
prolific base stealer or a football wide receiver a better pass catcher despite
the affordances that improvement in sprinting would provide. In other
words, because there are more predominant factors (i.e., technical, tactical),
what may be a KPI for one sport may not necessarily garner the same
classification (or to the same degree) within the context of other (more
skill-dominant) sports.
In skill-intensive sports, the number of identifiable KPIs may be limited
and the sport scientist may need to expand its athlete monitoring protocol to
include potential restraint factors (PRFs). PRFs can be thought of as
potential barriers to higher performance. They are measurable values that, if
a functional minimum is not met, have the potential (but is not guaranteed)
to negatively impact performance. In other words, the more that we
improve a certain measure, the less likely the related quality is contributing
to low performance. To provide an example, the higher a basketball point
guard scores on the YoYo IR1, the more confident that the practitioner can
be that a lack of aerobic fitness is not negatively impacting that athlete’s
ability to make free throws late in the game (14). Knowing the relationship
between fatigue and the regression of skill, the sport scientist may infer that
if the athlete has a low YoYo score that fatigue is a mediating factor in a
failed free throw attempt. It is also worth noting that there may never be a
clearly defined threshold, especially when attempting to make sense of the
physical development in a skill-dominant sport. This is because
occasionally, an athlete’s skill level supersedes any physical limitation to
the point where low performance never manifests. Though potentially
anomalies, they do exist and should not discourage the practitioner into
thinking that the measure selected is useless at the group level.
Furthermore, PRFs can be thought of as qualities that may serve as
physical, technical, or tactical prerequisites for elite performance. Maximal
strength provides a versatile example of applying the concept of a PRF in
this manner. For example, improving an athlete’s early acceleration ability,
regardless of sport, may require an athlete to first increase their maximal
strength, especially relative to body mass (23, 87, 95). Maximal strength
has also demonstrated the ability to reduce the risk of injury (53, 54) and
may therefore be a necessary prerequisite for skill-dominant athletes to
have enough availability to accumulate enough deliberate practice and
competitive exposures to reach elite status (1, 3, 70). In this regard, a lack
of sufficient maximal strength may indirectly prevent the athlete from
reaching elite status due to the removal of skill development that would
result from a serious injury. In situations where PRFs are used as gateway
qualities, it is reasonable for practitioners to use standards from the
literature in determining acceptable thresholds (e.g., IPFa of 280 N kg–2/3).
In the same manner that sport scientists are encouraged to leverage both
general scientific knowledge and context-specific evidence in design and
implementation of athlete monitoring processes, so too are they encouraged
to be inclusive to both KPIs and PRFs when identifying measurable targets
regardless of the skill- or physical-dominant nature of the sport or the
position. However, the relative emphasis placed on KPIs or PRFs may shift
depending on the scope of time being considered. How such a relationship
or sequence unfolds in practice will be largely unique to the sport, situation,
and even athlete’s development status.
Integration of Sport Medicine
Effective integration of sport medicine is important for the successful
implementation of a training plan and vital for handling disruptions to the
training process due to injury and other health concerns. The stark reality of
competitive sport, especially at the highest levels, is that health and
performance can be seemingly at odds. For example, in some extreme
examples, such as the super heavyweight category in weightlifting, linemen
in American football, and sumo wrestlers, athletes must carry excess body
fat in order to attain the size required to support specific performance
demands. Other sports expose athletes to high levels of repetitive trauma
that increase the susceptibility to overuse injuries. Furthermore, some sports
require grueling efforts that deplete the athlete’s energy stores, cause
excessive dehydration, or impose severe heat stress. So how do we
reconcile the often competing aspects of health and performance? Many of
these challenges can be managed through an interdisciplinary approach to
the training process that includes sport medicine, nutrition/dietetics, and
sport psychology.
Sport medicine is most directly concerned with the evaluation,
treatment, and rehabilitation of injuries. There are differences in the type
and etiology of injuries observed across sports. One of the most crucial
steps for the effective integration of sport medicine within the training
process is a comprehensive injury audit to determine injury incidence,
severity, and rate. The injury audit provides the basis to identify fixed and
modifiable risk factors, and any moderating interactions, within the various
domains of a high-performance program.
Strength and conditioning practitioners can take relevant information
from the injury audit to ensure that the annual plan appropriately addresses
any sport specific injury concerns. Licensed specialists from other
disciplines such as dietetics and psychology can provide interventions
suited to individual performance demands, as well as manage clinical
diagnoses and treatments.
Practitioners often take a reductionist approach to develop “injury
prevention programs.” While these programs are well-intentioned, they are
often overly simplistic and create challenges in evaluating program efficacy.
Firstly, injury rates in most contexts are relatively low so most datasets do
not provide adequate statistical power to create robust models for injury
prediction. Secondly, it is practically impossible to identify when an injury
has been prevented from happening!
Programs aimed at injury risk reduction or risk management are more
realistic and better suited to creating measurable outcomes to evaluate
program efficacy. These types of programs adopt a complex systems
approach that identify individual risk factors and how the interaction
between these risk factors may contribute to injury. The objective of these
programs is to positively influence these risk factors and their interactions.
The reality is that the risk for injury will never be zero, and the threshold
of injury risk tolerance is not static or universal. Thus, an athlete monitoring
program can provide critical information for stakeholders, including the
athlete, for the dynamic assessment of injury risk in training, availability,
and return to sport decisions. Furthermore, decision support systems can
help organizations to leverage information collected from the athlete
monitoring program to streamline decision making and interventions.
In cases of injury rehabilitation and return to sport, an emerging
paradigm is an outcome or criteria-based approach rather than a traditional
time-based approach. A criteria-based approach aligns outcome measures of
the rehabilitation process with task and sport-specific functional demands.
This approach also facilitates the coordination between departments to
support the rehabilitation process to ultimately minimize the time lost due
to injury and the risk of reinjury.
Implementation of the Plan
Though periodization has roots dating centuries ago, it is generally agreed
upon that the tenets of modern periodization start with Kotov in 1916 (51).
Kotov divided the year into cycles, phases, and stages – the structure still
generally implemented today. Shortly thereafter, Gorinewsky (36) and
Birsin (10) refined two of the primary training principles – overload and
specificity. Following the momentum gained in Russia, Western scientists
like Dyson and Pihkala (30, 76, 89) popularized periodization in the
Western world. What this globalization of periodization to the sport world
did more than anything is cause a key question to arise: “What are the rules
governing training periodization and the training process?” To answer this
question, it was obvious to the sport world that the training process must be
one subjected to the rigors of science. Though the calendar was important in
determining a periodization structure, physiology is an equally important
player in logical division of the calendar. Though we better understand this
now, this was an early acknowledgment of delayed training effects (e.g.,
phase potentation) and the impact that individual components can have on
larger scale adaptations (e.g., multi-factor).
As is the case with periodization in many instances, the advances
reflected those in other fields. For example, around this time, Henry Hazlitt
published his well-known book Economics in One Lesson (39) which took
on the economic fallacies of the time one-by-one. His “one lesson” is
relevant in the implementation of periodization. Also, his deconstruction of
economic fallacies is similar to how periodization continues to be a “first
principle” in the development of sport excellence despite attempted
criticisms, which will be discussed later. Hazlitt summarized his single
lesson in economics as follows: “The art of economics consists of looking
not merely at the immediate but at the longer effects of any act or policy; it
consists in tracing the consequences of that policy not merely for one group
but for all groups.”
 Periodization – whose advances followed a similar timeline as those of
economics – shares similar sentiment in its implementation. When
implementing a periodization structure, there is certainly art in making
decisions with immediacy – as both short- and long-term effects on sport
form must be considered. As will be discussed later in greater depth,
periodization is often criticized for its lack of flexibility for the unexpected
short-term circumstances – only following a rigid long-term plan. However,
just like Hazlitt’s economics, periodization done well equally respects the
influence of the short term and the long term. In doing so, a level of
flexibility is inherent – as one could not possibly navigate a training process
under such a construct if periodization were rigid. Furthermore, though
periodization does not have “groups” in the manner that Hazlitt’s
economics does, it does have co-active “clusters” of training types that have
to be managed simultaneously (i.e., physical, technical, tactical,
psychological). The interdependence of these aspects of preparation may
behave similarly to the “groups” to which Hazlitt refers to in his discussion
of economics. Therefore, in transferring Hazlitt’s sentiment to periodization
implementation, practitioners must not make decisions whose consequences
are siloed to one aspect of preparation – as any decision will have
ramifications on all these co-active components. Instead, periodization
permits a sort of “emphasis / de-emphasis” that may prioritize certain
aspects at different times of year, but never disregards the effects (direct or
indirect) on the other pieces. Also, through sound athlete monitoring
practices, the effects of these training decisions can quite literally be
“traced” back to all contributing factors of preparedness.
With this transfer of principle in mind, we now have the stage set to
discuss considerations in the implementation of the selected periodization
model. Though periodization does deal with the division of time with
respect to landmark events of an athlete’s calendar and career, the concepts
has long evolved beyond the rigidity of calendar-centric models. Though
this is still an often-used criticism of implementing periodization in modern
sport, this myopic application began to erode in the late 1950s. Though
Matveyev continued to push a relatively calendar-centric model in his texts
into the 1970’s, premier sport scientists like Verkhoshansky and Viru
dedicated most of their life’s work to give greater relative consideration or
physiology, pedagogy, and other aspects that may govern the training
process alongside the calendar.
Therefore, when implementing a periodization model, certainly the
annual competition calendar and long-term approach to an athlete’s
development must be considered. However, we must place substantial – if
not equal – weight on physiology, pedagogy, skill development, and other
timelines. Furthermore, mediating factors such as development or training
status may influence the relative contributions of the aforementioned
factors. For example, a developmental-level sprinter may implement a more
physiology and skill development-oriented periodization structure than an
advanced athlete. The advanced athlete – in the prime of their career and
positioning themselves for the opportunity to win medals – is going to be
more interested in “fitting” physiological timelines within the competitive
calendar since they must perform well at specific events (e.g., Olympic
qualifiers, finals). Because of the presence of these deliberate adjustments
that periodization affords, the concept itself can obviously handle schedule
changes as well. In fact, if you have not periodized, then how would you
know how to best navigate such a scenario? When implementing a
periodization model, we are doing two things: (i) dividing time into discrete
time blocks and (ii) assigning those discrete time blocks a particular goal or
objective. Therefore, schedule changes would actually become more
difficult to navigate without periodization implemented. When navigating
these changes, the practitioner now knows how much time they have to
course correct and what types of adjustments to programming would
maintain guidance of the training process towards the desired targeted
outcome. Therefore, when implementing our selected periodization model –
we must not fear schedule changes, as we have the tool in-hand to adjust
accordingly.
Chapter Summary
Periodization can be defined as a logical sequential, phasic method of
manipulating fitness and recovery phases in order to increase the potential
for achieving specific performance goals while minimizing the potential for
non-functional overreaching, overtraining, and injury. Evidence indicates
that a periodized training process coupled with appropriate programming
can produce superior athletic enhancement compared to non-periodized
methods. Periodization is cyclical in nature and deals with the macro-
management of timelines and fitness phases. Programming deals with the
micromanagement of the training process and deals with factors including,
exercise selection, rest periods, volume, and intensity. There are two models
of periodization: traditional and block. Block periodization has two
subtypes, single-factor (individual sports) and multiple-goal (team sports).
Both models have strengths and weaknesses but can be altered through
creative alterations in timelines and programming to produce superior
results for specific sports.
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Index

Note: Bold page numbers indicate tables; italic page numbers indicate
figures.

accumulation phase 229, 232, 233, 233, 236, 301, 302, 304
acetylcholine (ACh) 8, 13, 22, 34, 35; receptors (AChR) 36–37
actin 14, 16, 20, 21, 154; myofilaments 8, 18, 19, 20, 21, 22, 23–24,
253
actinin, α 20, 21, 21
action potential (AP) 23, 32–34, 33, 35
active rest 90, 229, 241, 242, 242, 300, 301, 302, 303
adenine 22, 60, 61
adenosine triphosphate see ATP
adipocytes 71, 72, 109
ADP (adenosine diphosphate) 22–23, 60, 60, 61, 62
aerobic exercise 39, 39, 66, 68, 79, 92, 93, 154; and carbohydrates
157, 160, 165; and cardiorespiratory adaptations 211; and endurance
training 210, 211; and ergogenic aids 186; and fats 161; and
hormones 116, 117, 118, 121, 125, 126, 127; and interference effect
212–213; and recovery 89–91, 148–149
aerobic system see oxidative (aerobic) system
alpha motor neurons (α-MN) 13, 23, 34–35, 37; and motor unit see
motor unit
altitude training see IHT
amino acids 60, 65, 71, 73, 81, 109, 154, 155, 156; essential (EAA)
151, 152, 153
ammonia 70, 71, 93, 156
AMP (adenosine monophosphate) 60, 61, 62, 70, 71, 81
anabolism 59, 151, 152
anaerobic exercise 39, 39, 67, 82, 84, 85, 154; and carbohydrates 157,
160, 165; and ergogenic aids 185, 186–187; and fats 161; and
hormones 117, 118, 121, 122, 126, 127; and recovery 149
androgens 115, 119–121
ankle joint 253, 256, 260
annual plans 305–307, 306
anthropometrics 203, 207–208, 254, 255; and athlete monitoring 265–
266, 265
antioxidants 161, 163, 182–183
ascorbic acid (vitamin C) 163, 183
astrocytes 30
athlete development see training principles/programs
athlete monitoring 169, 193–194, 240, 263–266, 275–296, 300; aims
of 279; and annual plans 306–307; and anthropometrics 265–266,
265; creating system of 289–290; and data handling 289, 290, 293,
310; and DSI 263; erroneous application of, effects of 294–296; and
force-velocity profiles 263–264; and injury prevention/risk
reduction 312–313; integration of 310–312; and KPIs/PRFs 311–
312; and outside stressors 285; overview of process 276; and poor
performance 280–282; as “post-dicting” 277–278; and preparedness
278, 279; and relative strength 264–265; and response variables
283–284; and scaling 279–280; and smart phone apps 285; and sport
organizations 292–294; and sport science 278, 283–284, 287, 289,
290–294; and subjectivity/objectivity 277; and testing 263–266,
283–284; and training cycles 278, 279, 280, 282, 283, 285; and
training dosage 282; and training volume/intensity 282, 283; and
validity/reliability 286–288
atlanto-occipital joint 252–253
ATP (adenosine triphosphate) 10, 14, 20, 22, 59–61, 60, 61, 112, 211,
231; depletion/recovery of 81–82; and glycolysis 63, 64, 70, 76, 78,
80, 80; hydrolysis 23, 28, 62, 93; and intensity of exercise 232, 234;
 and oxidative system 71, 72, 74; and phosphagen system (ATP-PCr)
62, 63, 81
ATPase 14, 16–17, 24, 28, 38, 39, 62, 207
axons 8, 30, 33, 35

B complex vitamins 163, 164

ballistic movements 203, 205, 208, 209, 221, 253
baseball 182, 256, 257, 265, 290
basketball 146, 147, 257, 265, 311
bench press 186, 233, 257
bicarbonate loading 185
biceps 4, 130
biocarbonate buffer system 65–66
bioenergetic systems 61–75; and depletion/recovery of ATP-
PCr/glycogen 81–83; and fuel efficiency 75–76; glycolytic see
glycolysis; and hormones 74, 75; limiting factors in 83–84, 84; and
maximum effort 61, 67, 79, 80, 81; oxidative see oxidative (aerobic)
system; phosphagen 31–33, 81–82; and production power/capacity
79–80, 80; and respiratory exchange ratio (RER) 77–79, 77, 78; and
substrate depletion/repletion 80–81; and training programs 231, 231
bioenergetics, defined 59
block periodization 92, 226, 229–230, 234, 243; and active rest 303;
and athlete monitoring 284; and concentrated loads 232, 241, 302,
304–305, 308; criticism of 242; implementation 314–315;
origin/development of 310; and phase potentiation 39, 302–305;
phases 301, 302–303; and programming 308–309; single/multi-
target (SBP/MTBP) 300, 304, 315; and summated microcycles 232,
233, 302, 303, 304; and traditional periodization, compared 229,
240, 241, 242, 243, 309
bobsled 311
bodybuilding 130, 162, 206, 230
bone growth 212
brain 40–42, 118, 203–204
buffer systems 65–66, 77, 185

C, vitamin 163, 183

caffeine 181, 186, 194
calcium (Ca) 13, 20, 21, 23, 25, 31–32, 210; channels 16, 22; and
osteoporosis 164, 165
calories 145, 148, 153
cAMP (cyclic adenosine monophosphate) 13, 109, 111, 112, 116, 118,
126, 128
carbohydrates 71, 78, 82, 83, 125, 129, 145, 148, 156, 157–160;
functions/benefits of 157, 158; groups 157; intake 159–160; loading
162; metabolism/control 158–159; and pre-/post-event meals 165–
166
cardiac muscle 3, 4, 70
cardiac output 84, 203, 210, 210–211, 213
catabolism 59, 151, 152, 154
catecholamines 108–109, 109, 116–117, 128, 129, 129, 211
cerebellum 41, 41
chloride 166–167
choline 12, 23, 37
circuit training 89–90, 146, 149
clothing 191–192, 192
CNS (central nervous system) 23, 29–32, 40, 71, 79; hierarchy of 40–
42, 41; and neurolemma 31–32; and neurons 30, 31; and RMP 31,
32 see also motor cortex
competition/realization phase 229, 232, 233, 234, 237, 301, 302, 303
concentrated loads 232, 241, 302, 304–305, 308
concurrent training 212–214; and interference effect 212–213, 214;
and periodization models 212; and separation of resistance/aerobic
training 213–214
cortisol 92, 118–119, 121, 122, 128, 129, 154, 157; functions of 159
countermovement jumping 260–261, 262, 307, 307
creatine (Cr) 184–185, 194
creatine kinase (CK) 20, 21, 62, 63
creatine phosphate (PCr) 62, 70, 80, 81, 211
cross bridges 18, 22, 23, 24, 27, 28, 63
Cushing’s disease 118, 119
cyclic adenosine monophosphate (cAMP) 13, 109, 111, 112, 116, 118,
126, 128
cycling 68, 146, 162, 166, 214; clothing/helmets 191, 192–193, 193;
exercise selection for 267–268
cytoskeletal system 14, 14
cytotubular systems 14–16

D, vitamin 162, 163, 181–182

de-training effect 232
deadlifting 254, 255
dehydration 166, 168
delayed training effects 188, 239, 304–305, 313
desmin 14, 21, 21
diet see nutrition
dietary recommended intake (DRI) 150, 153
DNA 60, 113, 222–223; mitochondrial (mtDNA) 10–11
dopamine 109
dynamic strength index (DSI) 263

E, vitamin 163, 183

electrolytes 166–167
electron transport system 70, 72, 73, 211
endocrine glands 108, 110, 114, 114–115, 133
endocrine system see NES
endurance training 38, 39, 40, 92, 93, 121, 231; adaptations resulting
from 210–212, 213, 213, 214; and cardiorespiratory adaptations
210–211; and ergogenic aids 183, 185, 188; and IHT 187–188; and
lactic acid 67, 68, 69; and metabolic adaptations 211; and metabolic
 changes 210; and musculoskeletal adaptations 211–212; and
nutrition 153, 155, 162, 164; training program for 233, 303, 304
energy 59, 145–147, 146, 147
environmental ergogenic aids 181, 187–188, 194
enzymes 10, 11, 20, 36, 38, 75, 93, 114, 163, 184, 223; glycolytic 64,
66, 210; and phosphagen system 62; see also specific enzymes
epigenetic influences 222–223, 222
epinephrine (EPI) 74, 115, 116, 117, 118, 126–127, 129, 154, 211; and
neurotransmitters 108–109
ergogenic aids 181–194; environmental 181, 187–188, 194;
mechanical see mechanical aids; physiological/pharmacological see
physiological/pharmacological aids; psychological 181, 193–194;
and regulations 181
estrogens 113, 115, 120, 124–125, 165
exercise selection 252–266; and anthropometrics 254, 255, 265–266,
265; and DSI 263; and force-velocity profiles 263–264; and
full/partial squats 261–262, 262; and levers see lever systems;
machine-based/free-weight exercises 255; and monitoring 263–266;
and phasic training goals 257–261, 257; and physiological
adaptations 254–255; and progressions/regressions 261–263; and
relative strength 264–265; and single-/multi-joint exercises 257–
258; and strength development phase 258–260; and strength-
endurance phase 257–258; and strength-power phase 260–261; and
task specificity 255, 256–257; and weightlifting derivatives 263
explosive performance 38, 185, 204, 207, 228, 241 see also RFD
extensor muscles 4, 189, 254, 256, 257
eye muscles 3, 4, 37

fast glycolysis 63–69, 80, 86, 87, 88; and buffer systems 65–66; fuel
efficiency of 75, 76
fatigue 91, 93, 157, 162, 232; accumulative 224, 225, 226, 239, 241,
308; and exercise selection 262, 264; and glycolytic system 63–65,
68, 71, 83, 117; and intensity of exercise 234, 235; management
 122, 227, 232, 235, 236, 240, 241, 279, 309, 310; and monitoring
288, 289; and substrate depletion 80–81; and training to failure 209
see also fitness–fatigue paradigm
fats 78, 79, 88, 118, 125, 145, 148, 155, 156, 160–162, 165; catabolism
of 59; groups/functions of 161, 161; metabolism 161–162, 211
fatty acids 10, 12, 59, 81, 116, 128, 161; free (FFA) 70, 71, 72, 74, 75,
76, 78, 90, 155, 211
fitness–fatigue paradigm 223, 225–226, 226, 305
football 146, 146, 166, 167, 311 see also soccer
footwear 188–191, 190, 191, 194
force-velocity relationships 27–29, 28, 29, 30; and athlete monitoring
263–264
free radicals 163, 182–183
fuel efficiency 75–76

gene derepression 112, 113–114, 118, 119, 122, 124

genetics 222–223, 222
glial cells 30
glucagon 74, 115, 118, 127–128, 129, 129, 154
gluconeogenesis 71, 115, 116, 118, 125, 159
glucose 63, 64, 69, 82, 127, 128, 129, 158, 165
glycerol 12, 59, 70, 71
glycogen 159, 161, 168, 211; depletion 82–83, 211; liver 80, 82, 84,
160; muscle 63, 64, 69, 80, 82, 83, 159, 160, 162; recovery 129,
159, 166, 185
glycogenolysis 14, 63, 66, 109, 117; liver 111, 116, 129; muscle 82,
83, 129
glycolysis 63–71, 72, 92, 129, 210; control of 70–71; and electron
transport system 70, 72, 73; energy yield from 70, 75–76, 79–80, 80;
fast see fast glycolysis; slow 63, 69–70, 72
Golgi tendon organs (GTO) 29, 41, 44, 45–47
growth hormone (GH) 74, 78, 110, 114, 126, 128, 129, 129, 153–154;
and carbohydrates 159; and protein 163–164
GTP (guanosine triphosphate) 13, 73, 74, 74, 75
gymnastics 182

hamstrings 253, 254, 255

heart 116; muscle 3, 4, 70
heart rate 29, 91, 93, 116, 210, 213
hemoglobin 88, 163, 187
heredity 222–223, 222
high-intensity training 9, 11, 42, 61–62, 63, 67, 80, 81, 84
hip joint 231, 253, 254, 255, 256, 260
homeostasis 13, 29, 66, 88, 89, 149, 224; and NES 108–109
hormones 13, 68, 71, 72, 74, 75, 90, 93, 108, 110–115, 154, 168;
action/regulation 111–115, 112–113, 114–115; negative effects of
117, 118; and protein metabolism 153–154; release 110–111, 211;
reproductive 120; and training 117, 118–119, 121–124, 125, 126,
128–132, 132, 133; vitamins as 163, 182; see also specific hormones
hydration 166–167
hypertrophy, muscle 6, 213, 214, 256; and endurance training 21; and
hormones 129, 130, 131–132, 159; and phosphagens 91–92; and
protein intake/synthesis 154, 156, 165; and resistance training 206,
207, 208–209, 208, 230–231; and satellite cells 9; and testosterone
119–121; and training specificity 92, 206, 247, 258, 266
hypoglycemic events 82–83
hypoxic training see IHT

IHT (intermittent hypoxic training) 187–188, 194

immune system 118, 129, 131, 159, 163
immunohistochemistry (IHC) 38–39, 40
injury prevention 312–313
insulin 82, 83, 109, 110, 111, 115, 116, 126–127, 128, 129, 129; and
carbohydrates 158–159, 160, 165; and protein 153–154
interference effect 212–213, 214
interval training 80, 86–88, 87, 91–92, 212; and ROC 89–91
involution 232
iron (Fe) 164
isometric twitches 24, 26, 38
isozymes 66, 67, 68, 79, 158

joint receptors 29, 44, 47, 206; and sensory ending types 47
judo 147, 167
jump squats 261
jumping 62, 210, 253, 288, 290; and force-velocity profiles 263–264;
interval 86

K, vitamin 163
key performance indicators (KPIs) 310, 311
kidneys 65, 66, 82, 110, 114, 115, 184
kinesthesis 44
kinetic chain exercises 230, 255
klapskates 189, 191, 194
knee joint 189, 253, 254, 256, 260
KPIs (key performance indicators) 310, 311
Krebs cycle 10, 11, 63, 66, 71, 72, 73, 74, 156, 161

lactic acid 63, 65, 66–69, 84, 211; accumulation of 66–67; post-
exercise 67–68, 88; threshold 68–69
LBM (lean body mass) 90, 122; and nutrition 146, 147, 151, 156, 167–
168
leg curls 254, 255, 257
length–tension relationships 23–27, 44; and isolated muscle
preparation 24, 25; and isometric contractions 24, 25, 26; and
sarcomere length 23–24, 24; and tetany 25
lever systems 252–254; 1st class 252–253; 2nd class 253; 3rd class
253; and force production 253–254; mechanical
advantage/disadvantage of 254
lipids/lipolysis 11–12, 13, 14, 30, 162; and antioxidants 161, 183; and
caffeine 186; and hormones 109, 111, 113, 118, 125, 127, 129, 161
see also fats
liver 74, 184; and NES 109, 110, 111
liver glycogen 80, 82, 84, 160
lunges 257
luteinizing hormone (LH) 110, 114, 119, 120

M-line 19, 20, 21

macrocycles 90, 234, 242, 242, 301, 309; and athlete monitoring 278,
279, 280, 282, 283, 285
magnesium (Mg) 31, 164
marathon running 80, 147, 151, 212; and footwear 188, 189
maximum effort 61, 67, 79, 80, 81, 87, 238–239, 239; limiting factors
on 83–84; and monitoring 286–287, 289
maximum strength 68, 92, 204, 205, 221, 223, 227–228, 229, 241,
312; and intensity of exercise 233
mechanical aids 181, 188–193, 194; attire 191–192; equipment 192–
193, 256; footwear 189–191, 190, 191
menstrual cycle 124–125, 124
mesocycles 233, 242, 242, 289, 301
metabolism 59–60, 60, 132; carbohydrate 158–159; and cost of
exercise 84–88, 85, 86, 87, 87; and endurance training 211; fat 161–
162; and hormones 74, 75; limiting factors in 83–84, 84; protein
151, 153–154; and ROC 88–91, 92; and specificity of training 91–
93; and sprinting 210
MHC (myosin heavy chains) 16–17, 17, 38–39, 40, 68, 207, 210
microcycles 229, 234; summated 232, 233, 302, 303, 304
minerals 145, 163, 164–165, 168; macro-/trace elements 163
mitochondria 9–11, 10, 36, 63, 66, 70, 208, 211, 213; DNA in
(mtDNA) 10–11; and fatty acids 161, 162; replication in 11, 12
monitoring see athlete monitoring
motor control see neuromotor control
motor cortex 22, 23, 34, 117, 204, 230; and voluntary movement 40,
41, 41, 203–204
motor end plate 8, 9, 13, 22, 36–37, 36
motor learning 41, 194, 209
motor neurons 13, 23, 34–35, 37, 44–45, 48
motor unit (MU) 37–40, 48, 76; classification 37–39, 39; and
immunohistochemistry (IHC) 38–39, 40; rate coding 42, 43, 44,
203, 204, 205; recruitment 42–44, 43, 203, 204, 205, 209, 221;
synchronization 44, 203, 205, 206; types 207
muscle, skeletal 3–48; and collagen 6, 7, 8; and compartmentalization
4–5, 7, 7; and connective tissue 6–7, 8, 9; constituents/properties of
3–4; and cross bridges 18, 22, 23, 24; cross-sectional area (CSA) of
4, 6, 119, 130, 133, 221, 227, 230–231, 232; and cytoskeletal system
14, 14; and cytotubular systems 14–16; diseases 8; and fiber
rotation/gear ratio 6; and force–velocity see force–velocity
relationships; force–velocity relationships 27–29, 28, 29, 30;
fusiform/pennate 5–6, 5; and length–tension see length–tension
relationships; as levers see lever systems; and nervous system 3, 22;
 and neuromuscular junction see NMJ; and RFD 6; and sarcolemma
see sarcolemma; and sarcomeres 4, 6; smooth/striated 3, 4;
structure/function 4–16
muscle biopsies 40, 81
muscle contraction 22–23, 45–46, 93, 163, 204; and ATP 60–61;
voluntary 40–42, 203–204 see also motor unit
muscle fibers 8–11, 34, 41, 48, 223; fast see type II (fast) muscle fiber;
molecular characteristics of 17; and motor unit see motor unit; and
sarcomere see sarcomere; slow see type I (slow) muscle fiber; stress
13
muscle glycogen 63, 64, 69, 80, 82, 83, 159, 160, 162, 186
muscle hypertrophy 6, 9, 81–82, 92
muscle relaxation 23
muscle spindles (MS) 34, 41, 44, 45, 45, 46
myelin sheath 30, 31, 35
myofibrils 4, 8, 9, 13, 14, 16, 20, 21; and ATPase 38; and resistance
training 207, 208
myofilaments 8, 13, 17, 18
myoglobin 9, 88, 89, 211, 213
myokinase 61, 62, 210
myosin 16–18, 17, 17, 18, 21, 22, 23–24, 27–28, 154, 253; heavy
chains (MHC) 16–17, 17, 38–39, 40, 68, 207, 210; and motor unit
38, 39; and phosphagen system 62
myototic (stretch) reflex 46

NADH 63, 66, 69, 70, 72, 74

NCAA intercollegiate sport 292–293
nebulin 20, 21
nervous system 3, 29–48; and action potential (AP) 32–34, 33, 35; and
axons 8, 30, 33, 35; and homeostasis 108; and motor unit see motor
unit; and muscle contraction 22; and
proprioception/kinesthesis/neuromotor control 44–47; and resistance
 training 203–207; and sprint training 209 see also CNS; neurons;
NMJ; PNS
neural inhibition 203, 206
neuroendocrine system (NES) 108–133, 208, 224; and catecholamines
108–109, 109, 116–117; and hormone action/regulation 111–115,
112–113, 114–115; and hormone release 110–111
neurolemma 31–32
neuromotor control 37, 42, 44–47, 203–204
neurons 30, 31, 32–35, 41, 47, 108; and action potential (AP) 32–34,
33; afferent/sensory 30, 46; efferent/motor 13, 23, 34–35, 37, 44–45;
structure/function of 34–35
neurotransmitters 22, 34, 35–36, 60, 108–109, 116
Nike running shoes 188–189
nitrogen balance 114, 126, 152, 153, 154, 156, 157
NMJ (neuromuscular junction) 8, 13, 22, 23, 35–37, 36
Nordic leg curls 255, 257
norepinephrine (NEPI) 11, 34, 109, 115, 116, 126–127, 211
nutrition 145–169, 214, 222; and calorie/nutrient density 148; and
DRI/RDA 150, 153, 155; and energy expenditure/intake 145–147,
146, 147; monitoring 169; and pre-/post event meals 165–166; and
recovery energy expenditure 148–149; and water/electrolytes 166–
167; and weight gain 167; and weight/fat loss 167–168 see also
carbohydrates; fats; minerals; proteins; vitamins

OPTIMAL motor learning theory 194

organelles 9, 14
osteogenesis 212
osteoporosis 164–165
overload 221, 224–225, 227–228, 313; intensity of 232–235, 235
overtraining/overreaching 91, 116, 117, 119, 145, 146, 212, 224–225,
241; and athlete monitoring 279, 281; and hypoglycemia 82–83; and
involution 232; and lactate concentrations 67; and nutrition 145,
 154, 155, 157, 159; planned/functional 212, 226, 227, 228, 229, 233,
237, 303
oxidative (aerobic) system 71–75, 185; and ATP production 72, 74;
and carbohydrate oxidation 72; control of 74; and fat oxidation 71–
72; fuel efficiency of 75, 76; and protein oxidation 71
oxidative phosphorylation 11, 11
oxygen deficit 84, 85, 86

peak power 79, 85, 86, 221, 309

pennate muscles 5–6, 5
peptides/polypeptides 18, 111
periodization 212, 226, 229, 232, 233, 234, 276, 279, 299–305;
accumulation phase 229, 232, 233, 233, 236, 302; and active rest
phase see active rest; and annual plans 305–307; block see block
periodization; defined/use of terms 300, 315; and delayed effects
239, 240; implementation 314–315; and intensity of overload 227–
228, 232–235; and intent of movement 238–239, 239; model
selection 300–302; origin/development of 299, 313–314; overview
of 239–243; phases 300–302, 301; and programming 307–310; and
rates of progression 237–238, 238; realization phase 229, 232, 233,
234, 237; and training density 236–237; and training session 236;
and training volume 235–236; transmutation phase 229, 233, 242;
and variation 228, 229 see also tapering
peripheral nervous system (PNS) 29, 30
phosphagen system 31–33, 71, 81–82, 86, 87, 88, 92, 185
phosphate buffer system 65
phosphocreatine 184, 210
phosphofructokinase (PFK) 64, 70–71, 78
phosphorus (P) 164
phosphorylation 11, 11, 14, 70, 72, 73, 74, 111–113, 208
physiological/pharmacological aids 181–187, 194; antioxidants 182–
183; bicarbonate loading 185; caffeine 181, 186; creatine 184–185;
vitamin D 181–182
plantar flexion see ankle joint
PNS (peripheral nervous system) 29, 30
post-exercise recovery see recovery
posture 38, 189, 253, 258
potassium (K) 118, 163, 164, 166–167, 185
potential restraining factors (PRFs) 310–311
potentiation 168, 221, 237, 264, 305, 309
preparedness 225, 226, 277, 278, 314
priority training 149–150
programming 307–310
proprioception 44
protein buffer system 65
proteins 145, 148, 150–157; complete/incomplete 151–152;
composition of 151–153, 152; contractile 16, 154; and cytoskeletal
system 14; degradation 154, 155, 159; effects of training on 154–
155; extrinsic/intrinsic 13–14; and hormones 110, 111, 118, 129,
153–154; intake 155–157; metabolism/function/control 151, 153–
154; and nitrogen balance 152, 153, 154, 156, 157; oxidation 71;
and pre-/post-event meals 165, 166; and sarcomere 16–21, 28; and
timing of meals 153; and vegetarians 152–153
psoas major 254, 256
psychological ergogenic aids 181, 193–194
puberty 125, 168
pyruvate 10, 63, 64, 70, 88

quadriceps 130, 231, 256

rapid force production 254, 259–260, 266

rate coding 42–44, 43, 203, 204
rate of force development see RFD
RDA (recommended dietary allowance) 150, 153, 155, 169
reactive oxygen species (ROS) 163, 183
realization phase see competition/realization phase
recovery 92, 93, 145, 159, 222, 303, 310; energy expenditure 88, 148–
149; and oxygen consumption (ROC) 88–91 see also active rest
recovery oxygen consumption (ROC) 88–91
redox balance 163, 182–183
reflex arcs 29
rehydration 167
relative strength 255, 264–265
RER (respiratory exchange ratio) 77–79, 77, 78
resistance training 69, 88, 89, 90, 92, 159, 161, 162, 168; adaptations
resulting from 203–209, 212; and anthropometrics 265–266; and
biochemical/anthropometric factors 207–208; and energy
expenditure 146; high-/low-intensity, compared 221; and hormones
116, 118, 125, 128–132; and intensity of exercise 233–234; and
loading 9, 208, 227; and maximum effort 238–239; and MU
recruitment/rate coding 204, 205, 209; and MU synchronization 44,
203, 205, 206; and neural factors 203–207; and neural inhibition
203, 206; and reversibility 232; and strength-shortening cycles 207;
and task specificity 205–206, 209; to failure 91, 92, 209; and
training dosage 282; training program for 233, 235; and training
volume 235; variable 229, 264
respiratory exchange ratio (RER) 77–79, 77, 78
resting membrane potential (RMP) 31, 32, 32, 34, 35
reversibility 227, 231–232
RFD (rate of force development) 6, 37, 92, 213, 221, 226, 228, 229,
232, 304; and monitoring 289; and overload 227; and periodization
234, 238, 241, 310 see also explosive performance
risk reduction/management 313
RMP (resting membrane potential) 31, 32, 32, 34, 35
ROC (recovery oxygen consumption) 88–91
ROS (reactive oxygen species) 163, 183
running 91, 146, 147, 164, 214, 231, 253; and footwear 188–189, 194
see also marathon running; sprinting
sarcolemma 11–14, 12, 14, 22; and intrinsic/extrinsic proteins 13–14;
and lipids 11–12, 13, 14; and TT network 12–13
sarcomere 16–21, 27, 48; and actin 16, 18, 19, 20; elements of 21;
length 23–24, 24; and M-line 19, 20, 21; and myosin 16–18, 17, 17,
18; and titin/nebulin 20–21, 28; and tropomyosin/troponin 18, 20;
and Z-disc 20–21
sarcoplasm 4, 9, 10, 11, 16, 22, 25, 36, 72, 208
sarcoplasmic reticulum (SR) 14–16, 15, 22, 23, 210
sartorius 4
Schwann cells 30, 35, 36
serotonin 34, 155–156
sleep 126, 222, 222, 285
slow glycolysis 63, 69–70, 72
soccer 69, 87, 212, 257, 304
sodium (Na) 166–167
sodium-potassium pump 3, 31, 32–33, 32, 47
softball 255, 256
somatotropin see growth hormone
specificity of training 41, 42, 47, 48, 205–206, 227, 230–231, 313; and
exercise selection 255, 256, 257; and transfer of training effect 209,
230, 255, 311
spectrin 14, 21, 21
speed skating 189, 191, 194
speed–strength training 241, 260
SPEG (sport performance enhancement group) 275, 276, 290, 292
spinal cord 29, 30, 35, 42, 204
sport medicine 240, 285, 299, 305, 312–313
sport organizations 292–294
sport science 145, 181, 189, 240; and medicine, compared 275–276
see also athlete monitoring
sports psychology 181, 193–194
sprinting 61, 82, 84, 89, 92, 146, 147, 182, 231; adaptations resulting
from 209–210, 231; exercise selection for 256–257, 257; and
 metabolic factors 210; and neural factors 209; phases 209
squats 160, 233, 237, 260; back 149, 256, 257, 257, 258; front 231,
256–257; full/partial 261–262, 262; jump 261
SSC (strength-shortening cycles) 207
steroids 110, 113, 113, 114
stimulus–fatigue–adaptation paradigm 223, 224–225, 224–225, 305
strength-endurance training 91, 186, 234, 257–258, 304
strength-power training 92, 93, 213, 310; and ergogenic aids 182, 183,
184, 186; and exercise selection 260–261; and motor unit types 207;
and muscle fibers 39, 40, 207; and neural inhibition 206; and
neuromotor control 204; and nutrition 151, 155, 156; and recovery
149; training program for 230, 233, 303, 310 see also weight
training
strength-shortening cycles (SSC) 207
stress 118, 119, 147, 183, 208, 223, 285
stretch reflex 46
summated microcycles 232, 233, 302, 303, 304
supercompensation 123, 124, 162, 224, 224–225
swimming 214, 229, 278
swimwear 192, 192, 194
synemin 14, 21, 21

tapering 90, 121, 123, 124, 207, 212, 226, 278, 303
task specificity see specificity of training
tennis 182
testing 263–266, 283–284, 307, 307
testosterone 92, 110, 115, 118, 119–124, 123, 125, 129, 132, 159, 223;
and nutrition 153–154, 157, 168
throwing 146, 147, 167, 253, 255, 257
thyroxin 110, 113, 128, 129, 129
titin 20–21, 21, 28
training aids see ergogenic aids
training density (TD) 236–237, 282
training dosage 282
training intensity (TI) 90, 122, 146, 149, 211–212, 214, 226, 234, 236,
237, 282; high/low, compared 221; of overload 232–235; and rates
of progression 237–238, 238; and training density 236–237
training principles/programs 221–243, 299–315; and annual plans
305–307; and athlete’s background 221; and exercise selection see
exercise selection; and fitness–fatigue paradigm 223, 225–226, 226;
genetic/training factors in 222–226, 222; and high-/low-intensity
programs 221; and monitoring see athlete monitoring; and overload
227–228, 232–235; overview of 239–240; and periodization see
periodization; and preparedness 225, 226; requirements of 221–222;
and reversibility 227, 231–232; and specificity see specificity of
training; and sport medicine 312–313; and stimulus–fatigue–
adaptation paradigm 223, 224–225, 224–225; and training intensity
see training intensity; and variation 227, 228–230
training to failure 91, 92, 209, 229, 235
training volume 91, 207, 214, 226, 282; and hormones 119, 122, 130;
and hypoglycemia 82; and periodization 235–236, 308, 309; and
protein intake 155, 156, 157
transmutation phase/block 229, 233, 242, 242, 301, 302–303, 303
transverse tubules (TT) network 5, 12–13, 14, 16, 22
triathletes 188
triglycerides 39, 59, 71–72, 74, 129, 161
tropomyosin 18–20, 21
troponin 18, 20, 21, 23
tryptophan 152, 152, 155
type I (slow) muscle fibers 13, 20, 21, 28, 39, 70, 209; efficiency of
76; and endurance athletes 40, 211, 223; and glucose 158; and
glycogen 121; and lactate accumulation 66; and MU recruitment 42,
43; and oxidative system 72; and phosphagens 62, 82; properties of
39
type II (fast) muscle fibers 13, 20, 28, 39, 70; efficiency of 76; and
endurance training 211–212; and glycogen 66, 82, 83, 92, 121;
 hypertrophy of 81–82, 92; and lactate accumulation 66, 68; and
loading 208–209; and motor unit recruitment 42, 43; and oxidative
system 72; and phosphagens 62, 66, 81–82, 92; properties of 39; and
sprinting 209, 210; and strength-power athletes 39, 40, 207, 223;
and vitamin D 182

ultraviolet radiation 182

validity, measurement 286–288

vastus lateralis 4, 83, 212
vegetarians 152–153, 164, 184
velocity of movement 47, 221
vimentin 14, 21
vitamins 145, 162–164, 168; water-/fat-soluble 163; see also specific
vitamins
VO2max 66, 68–69, 69, 79–80, 82, 85, 289; and IHT 188; and oxygen
deficit 84–85, 86
volleyball 146, 265, 290
voluntary movement 29

water 166–167
weight training 61, 66–67, 68, 69, 79, 81–82, 83, 84; and athlete
monitoring 286–287, 286, 287, 289; bilateral/unilateral exercises
258, 259, 266; and bone growth 212; deadlifting 254, 255;
derivatives 263; footwear for 189, 190; and hormones 121–124,
123, 127, 128; and lever systems 254; multi-/single joint exercises
257–258; and neuromotor control 204; and nutrition 146, 149–150,
154, 156, 166, 167; and overload 227, 235; and periodization 238,
241, 306; priority 149–150; and rapid force production 254, 259–
260, 266; and ROC 89–91; snatch/clean and jerk 255, 259, 260, 263;
squats see squats; and testosterone 121–122 see also resistance
training
window of adaptation 223
women 121, 123, 124–125, 124, 164–165, 261

Z-disc 14, 20–21, 21, 208