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THE PHYSIOLOGY OF TRAINING:

EFFECTS ON VO2 MAX,


PERFORMANCE, HOMEOSTASIS &
STRENGTH
PRINCIPLES OF TRAINING
 Overload
 Specificity
Overload
PRINCIPLES OF TRAINING
OVERLOAD:
 Overload refers to the observation that a system or

tissue must be exercised at a level beyond which it is


accustomed in order for a training effect to occur.

 The system or tissue gradually adapts to this


overload.

 This pattern of progressively and systematically


overloading a system or tissue as adaptations occur
results in improved function over time.
PRINCIPLES OF TRAINING
 The typical variables that constitute the overload
include the

 Intensity,
 Duration, and
 Frequency (days per week) of exercise.

 The principle of reversibility, simply indicates that the


gains are quickly lost when the overload is removed.
Specificity
Specificity

 Specificity also refers to the types of adaptations


occurring in muscle as a result of training
Specificity
 If a muscle is engaged in endurance types of
exercise, the primary adaptations are in capillary and
mitochondria number, which increase the capacity of
the muscle to produce energy aerobically

 If a muscle is engaged in heavy resistance training,


the primary adaptation is an increase in the quantity
of the contractile proteins; the mitochondrial and
capillary densities may actually decrease
Specificity
The training effect is
 Specific to the muscles involved,

 The fiber types recruited,

 The principal energy system involved (aerobic versus anaerobic),

 The velocity of contraction, and

 The type of muscle contraction (eccentric, concentric, or isometric)

 Tenweek iogging program


 An individual participates in a long, slow, distance
 Running program that utilizes the slow-twitch muscle fibers, there is
little or no training effect taking place in those fast-twitch fibers in the
same muscle
 Cycle or run training, but had their lactate threshold (LT)
evaluated before and after training on both the cycle and
treadmill.

 Run training increased the LT 58% and 20% for the treadmill
and cycle, respectively

 The cycle training increased the cycle LT 39%, with no


measured improvement in the treadmill LT.

 Training effects were clearly specific to the type of training


Research Designs to Study Training

 Cross-sectional studies
 Examine groups of differing physical activity at one
time
 Record differences between groups

 Longitudinal studies
 Examine groups before and after training
 Record changes over time in the groups
ENDURANCE TRAINING
AND V02 MAX
VO2 Max
 Also maximal oxygen consumption

 The maximum rate of oxygen consumption as measured during 


incremental exercise, most typically on a motorized treadmill 

 Maximal oxygen consumption reflects the aerobic 


physical fitness of the individual

 An important determinant of endurance capacity during


prolonged, sub-maximal exercise.
 Expressed as

 Litres of oxygen per minute (L/min)

 Millilitres of oxygen per kilogram of bodymass


per minute mL/(kg·min))
Range of VO2max Values in the Population
Cardiac Output & Arteriovenous O2 Difference

 Best described by maximal oxygen consumption (VO2max)

 VO2= Q ×avO2diff (also note that Q = HR ×SV)Where: VO2= oxygen consumption; volume
of O2consumed per minute
 Q = cardiac output; volume of blood ejected from the left ventricle per minute
 SV= stroke volume; volume of blood ejected from the left ventricle per heartbeat
 HR = heart rate; cardiac contractions per minute
 avO2diff = arteriovenousO2difference; volume of O2extracted per liter of blood

 Cardiorespiratory fitness is the product of the ability to transport and utilize oxygen.

 The greater the peak exercise VO2value, the higher an individual’s cardiorespiratory
fitness.
 Differences in VO2max in different populations
 Due to differences in SVmax

 Improvements in VO2max
 50% due to SV
 50% due to a-vO2
Factors Increasing Stroke Volume
Increased VO2max With Training
1. Increased Svmax

  Preload (EDV):

End volumetric pressure that stretches the right or left ventricle of


the heart to its greatest dimensions

…therefore preload = initial stretching of the cardiac muscles before


contraction.

*Preload = Volume (If the volume is low, the blood pumped out of the heart will be a
trickle. If the volume is too high, it will back up the cardiac system (right-sided
heart failure, edema etc)

*Afterload = Pressure/Resistance (Afterload = pressure or resistance. If there is a


narrowing in the veins/arteries, the volume will back up AND the cardiac output
will drop.) 
Increased VO2max With Training
1. Increased Svmax (cont…)

Preload is increased by increasing the end-diastolic volume


(this occurs with increased venous pressure)

As ventricle contracts = develop greater pressure & eject blood


more rapidly
(because the Frank Starling Mechanism = activated by the
increased preload.) 
Because  venous pressure:
(pressure exerted on the walls of the veins by the circulating
blood)

Plasma volume (yellowish solution ±91% water & other 9%


= nutrients: glucose, amino acids; sodium, potassium; antibodies)

Venous return (volume of blood flowing back to the heart


through the veins.)

 Ventricular volume
Increased VO2max With Training
2.  Afterload (TPR):
Tension or stress developed in the wall of the left ventricle
during ejection.

 end load (pressure) against which the heart contracts to eject


blood.

 Afterload is broken into components:


aortic pressure and/or the pressure the ventricle must
overcome to eject blood.
Increased VO2max With Training

2.  Afterload (TPR):

 Arterial constriction
 Maximal muscle blood flow with no change in
mean arterial pressure

3.  Contractility
Increased VO2max With Training

4. a-vO2max
  Muscle blood flow =  O2 to active muscles
 Therefore  SNS vasoconstriction

[= vasodilation to  blood flow to muscles]

Improved ability of the muscle to extract oxygen from the blood

 Capillary density
 Mitochondial number (therefore  ATP produced)
Factors Causing Increased VO2max
Detraining and VO2max
 Decrease in VO2max with stopping
training

  SVmax
 Rapid loss of plasma volume

  Maximal a-vO2 difference


  Mitochondria
  Oxidative capacity of muscle (ability to produce ATP)

  Type IIa fibers [red  myoglobin]


[long term anaerobic  slow fatigue]
  type IIx fibers [white  no myoglobin]
[short term aerobic  quicker to fatigue]
Detraining and Changes in VO2 Max and
Cardiovascular Variables
Summary
 The large differences in VO2 max in the normal
population are due to differences in maximal stroke
volume.
 The training-induced increase in maximal stroke
volume is due to both an increase in preload and a
decrease in afterload.
 The decrease in VO2 max with cessation of training is
due to both a decrease in maximal stroke volume and a
decrease in oxygen extraction, the reverse of what
happens with training.
Effects of Endurance Training on Performance
& Homeostasis

 Maintenance of homeostasis
 More rapid transition from rest to steady-state

 Reduced reliance on glycogen stores

 Cardiovascular and thermoregulatory adaptations

 Neural and hormonal adaptations


 Initial changes in performance

 Structural and biochemical changes in muscle


  Mitochondrial number

  Capillary density
Structural and Biochemical
Adaptations to Endurance Training
 Increased capillary density
 Increased number of mitochondria
 Increase in oxidative enzymes
 Krebs cycle (citrate synthase)
 Fatty acid (-oxidation) cycle

 Electron transport chain

 Increased NADH shuttling system


 NADH from cytoplasm to mitochondria

 Change in type of LDH


 M4 -> M3H-> M2H2->MH3->H4
 The combination of the increase in the density of
capillaries and the number of mitochondria per muscle
fiber increases the capacity to transport FFA from the
plasma ~ cytoplasm ~ mitochondria.

 The increase in the enzymes of the fatty acid cycle


increases the rate of formation of acetyl CoA from FFA
,for oxidation in the Krebs cycle. This increase in fat
oxidation in endurance trained muscle spares both muscle
glycogen and plasma glucose.
Time Course of Training/Detraining
Mitochondrial Changes
 Training
 Mitochondria double with five weeks of training
 Detraining
 About 50% of the increase in mitochondrial content was
lost after one week of detraining
 All of the adaptations were lost after five weeks of
detraining
 It took four weeks of retraining to regain the adaptations
lost in the first week of detraining
Time Course of Training/Detraining Mitochondrial
Changes
Physiological Effects of Strength Training

 Strength training results in increased muscle size and


strength
 Neural factors
 Increased ability to activate motor units
 Strength gains in initial 8-20 weeks
Physiological Effects of Strength Training

 Muscular enlargement
 Mainly due enlargement of fibers

 Hypertrophy
 May be due to increased number of fibers

 Hyperplasia
 Long-term strength training
Neural and Muscular Adaptations
to Resistance Training
Training to Improve Muscular Strength

 Traditional training programs


 Variations in intensity, sets, and repetitions

 Periodization
 Volume and intensity of training varied over time
 More effective than non-periodized training for

improving strength and endurance


 Periodization is the program design strategy that
governs planned, systematic variations in training
specificity, intensity, and volume.
 The goal with periodization is to maximize your
gains while also reducing your risk of injury.
 For quick questions and answers about physiology
of training please visit the following link.
 http://quizlet.com/60211439/exercise-physiology-ch-1
3-flash-cards/
THANK
YOU

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