1.

The energetics of exercise

1.2 Principles in exercise physiology

1.3 Calorimetry and oxygen consumption

1.4 ATP and muscular work

1.5-1.6 Carbohydrate metabolism during exercise

1.7 Fat metabolism during exercise

1.6 Protein metabolism during exercise

2. Physiological systems during exercise

2.1 Skeletal muscle structure and function
In this module, we will examine the critical adjustments made by key physiological systems in
response to a single bout of exercise. This will include the muscular, respiratory, cardiovascular,
endocrine, and immune system.

Additionally, training adaptations in these systems will be addressed. I will begin by discussing the
muscular or skeletal system.

There are three types of muscles in the body: heart or cardiac muscle, skeletal muscle, and smooth
muscle such as the muscles surrounding your blood vessels that allow them to constrict or
dilate. This video will focus on skeletal muscle. 

First, let's review the three major types of contractions performed by skeletal muscle. I will provide
an example of each one. Isometric contractions are defined as no change in length of the muscle
while tension is being developed. 

In a concentric contraction the muscle shortens during tension development. Lastly, with eccentric
contractions, the muscle is actually lengthening while tension is being developed. Here's an
example of an isometric contraction. Pictured is a woman planking. 

As she holds this position, her muscles are not changing length yet tension must be employed in
the muscles recruited to prevent her from falling on her face. The most common type of muscle
contraction is concentric. 

Shown here is the basic arm curl where the bicep muscles are shortening as the weight is being
lifted up toward the shoulder. Finally, eccentric contractions involve the lengthening of the muscle
while it develops tension. A good example is that of downhill running. 
While you are running downhill your quadricep muscles are actually lengthening while developing
tension to resist gravity and prevent you from doing a faceplant. This type of contraction as we'll see
in Module 3 is the main cause of muscle soreness experienced 8 to 48 hours after exercise. 

It is very important to understand that skeletal muscle is composed of three very different types of
fibers that have a range of biochemical and physiological characteristics. Type 2x muscle fibers are
considered our power fibers. 

They are recruited when we need to generate a lot of force, such as in jumping, sprinting, and lifting
heavy weights. These fibers can also generate this force very quickly. 

Since they need to supply a large amount of ATP in a short period of time, they rely heavily on the
anaerobic pathways for energy production. As a reminder, this includes ATP and cretin phosphate
already present in the muscle plus the anaerobic breakdown of glucose to lactate. 

Also notice that since the bulk of their energy comes from the anaerobic pathways their
mitochondrial numbers are very low. Finally, as it is difficult to maintain this type of power output for
an extended period of time, Type 2x fibers fatigue rapidly. 

On the other extreme, Type 1 fibers can only generate moderate force at a much slower rate. 

These fibers are primarily recruited when we are engaging in submaximal exercise for an extended
period of time such as distance running, swimming, and cycling. 

These fibers are high in mitochondria and as such use the aerobic pathway for ATP
production. Also, as long as there is ample fuel, Type 1 fibers are slow to fatigue. Type 2a fibers are
a hybrid of Type 1 and Type 2x fibers. Thus, they demonstrate characteristics from both of these
fibers. 

Shown here are the motor units for each fiber type. A motor unit consists of the motor neuron and
all the muscle fibers that it enervates. Notice again that the Type 2x fibers can generate a great deal
of force quickly. As such, they are ideal for explosive exercises such as sprinting. 

However, as shown, they are quick to fatigue. On the other hand, Type 1 fibers generate a much
weaker force but are more resistant to fatigue. Let's look at how the various muscle fiber types
are recruited during exercise of increasing intensity. 

At the onset of exercise, when the workload is light intensity, the Type 1 fibers will be the primary
fiber type recruited. 
This should make sense since at the easy workloads only a small amount of force is required and
the Type 1 fibers are slow to fatigue, thus, an individual would be able to exercise at this intensity
for a long period of time. 

However, as the exercise intensity increases to moderate and heavy, Type 2a and Type 2x fibers
are also recruited to help generate the force required for these more difficult workloads. Please
notice that even at the higher workloads the Type 1 fibers are still being recruited.

At the highest workload we are dependent upon Type 2x fibers to provide the necessary
power required but we will not be able to maintain this intensity for very long as the 2x fibers will
soon fatigue. As a reminder, we discussed the crossover concept in Module 1. 

As the exercise intensity increases during the course of a graded exercise test, the reliance on
carbohydrates as a fuel also increases and at some point crosses over becoming the preferred
fuel. A major reason for this shift in fuel preference is the increasing recruitment of Type 2x fibers. 

As discussed, these fibers are low in mitochondria and rely heavily on the anaerobic utilization of
carbohydrates.

When we examine the fiber type composition of elite athletes, it is not surprising to find that distance
runners have a much greater percentage of Type 1 muscle fibers and a lower percentage of both
Type 2x and Type 2a fibers. 

The Type 1 fibers are ideal for distance athletes who compete at submaximal exercise intensities
for extended periods of time. On the other extreme, sprinters who repeatedly engage in high power
explosive exercise have a much greater percentage of both Type 2 fibers. 

An average individual will have a range of approximately 50 percent for Type 1 and Type 2 fibers
dependent upon genetic makeup and activity levels. With regular endurance training, these
individuals demonstrate a shift in their muscle fiber type from Type 2 to Type 1. 

Similarly, intense sprint training will result in a shift in the opposite direction from Type 1 to Type
2. Muscle fiber type can be determined from taking muscle biopsies from a specific muscle
group. The sample can then be stained to determine fiber types contained within the muscle. 
Shown here are results from two very different elite athletes, a sprinter and an endurance
athlete. As can be seen, the sprinter has a large percentage of Type 2 fibers shown in white
while the distance athlete has a much greater percentage of Type 1 fibers which stained black. 

Finally, regular involvement in intense strength or resistance training will produce very different
adaptations in muscle.

I will discuss these mechanisms in detail in Module 3 but for now realize this type of training will
result in an increase in the cross-sectional area, size, and strength of existing muscle fibers. 

This is called muscle hypertrophy and is defined as an increase in cross-sectional area of muscle
due to an increase in contractile proteins. This occurs to a greater extent in Type 2 fibers but also
occurs in Type 1 fibers. 

If you wish to review the 12 steps involved in the complete contraction of a skeletal muscle
beginning with the arrival of an action potential and ending with a complete contraction, I have
provided a link here. 

In summary:

 The three major types of contraction are isometric, concentric, and eccentric. The order of
fiber recruitment during progressively increasing exercise intensity is Type 1 initially
followed by Type 2a and Type 2x. 
 Type 1 fibers rely more on aerobic energy sources while Type 2x rely more on anaerobic
energy sources. Distance athletes have a greater percentage of Type 1 fibers while
sprinters have a greater percentage of Type 2 fibers.

2.2 Respiratory system responses to exercise.

This video will examine the adjustments made by the respiratory system, in response to a single
bout of exercise. We will also address other considerations related to lung function during exercise. 

The three major roles of the respiratory system during exercise are, one, to ensure that the partial
pressure of oxygen in our arteries is well-maintained allowing for adequate oxygen delivery to the
exercising muscles. Two, to eliminate both metabolic and non-metabolic carbon dioxide, thereby
maintaining the partial pressure of carbon dioxide in our arteries. And three, to assist in the
buffering of metabolic acids produced during intense exercise. 

Between inspiring oxygen, and ambient air, and it's eventually use in mitochondria of working
muscles, are the various components of oxygen transport. 

At sea level, the partial pressure of oxygen in the inspired air is 159 millimeters of mercury. 
By the time it reaches the alveolar sacs in the lungs, where gas exchange between the lungs and
the blood vessels occurs, this partial pressure has dropped to 105 millimeters of mercury. The
oxygen then diffuses down its concentration gradient into the lung capillaries, where it binds the
hemoglobin located within our red blood cells. 

Over 98% of the oxygen transported in blood, is bound to hemoglobin. From there, the oxygen-rich
blood is transported to the heart, where it can be pumped out via blood vessels to the exercising
muscles. As covered in a previous video, the oxygen will be consumed in the muscle mitochondria
for ATP production. 

During exercise, a decrease in pH or metabolic acidosis, plus an increase in body temperature will

facilitate the unloading of oxygen off hemoglobin into muscle. Also, during exercise, the partial
pressure of oxygen in the working muscles can drop to 20 millimeters of mercury, resulting in an
even greater unloading of oxygen from hemoglobin into muscle. 

Not surprisingly, increasing red blood cell numbers will improve the oxygen carrying capacity of
blood. This occurs to some extent as a result of endurance training. Further, this is the concept
behind the performance enhancing technique of blood doping, which will be discussed in module
three. 

A second important role for the respiratory system during exercise, is that of carbon dioxide
removal. 

Accumulation of carbon dioxide in blood and tissues would be toxic. Thus, the respiratory system
protects against this accumulation. 
Sources for carbon dioxide production can be both from metabolic and non-metabolic pathways. 

The metabolic sources come from the oxidative breakdown of our macronutrients for ATP
production. The carbon dioxide produced in this way in muscle, then diffuses into the blood and is
transported to the lungs for removal. 

As the name implies, non-metabolic carbon dioxide does not come from the metabolic breakdown
of our macronutrients, but instead, comes from the buffering of acids produced during a high-
intensity exercise. To help prevent the muscles and blood from becoming too acidic, the hydrogen
ions are buffered by bicarbonate, which is then converted to carbon dioxide. This non-metabolic
carbon dioxide is also transported to the lungs for removal. In this way, the respiratory system fulfills
its third major role, that of acid-base regulation during exercise. 

Obviously, when we go from rest to exercise, our ventilatory rate increases. This refers to the
mechanical process of moving air into and out of the lungs. This increase in ventilation will be
dependent upon the exercise intensity, and the need to get oxygen into and carbon dioxide out of
the body. 

The two ways to increase ventilation, are by increasing the tidal volume and breathing frequency. 

Notice that in this example when going from rest to maximal exercise, there is a 32 fold increase in
ventilation, measured in liters of air exchanged by the lungs per minute. This is accomplished by
increasing both tidal volume, measured in liters of air per breath and the breathing frequency
measured in breaths per minute. 

However, please take note that it is more efficient from an oxygen exchange standpoint, to increase
the tidal volume more than that of the breathing frequency. This allows for greater time for gas
exchange, as well as less repeated exchanges of air and the physiological dead space in the lungs
clamming. Increasing breathing frequency also contributes to the increase in ventilation during
exercise, but not nearly to the same extent as that for the increase in tidal volume. 

The increase in ventilation during exercise, is controlled by both neural and humoral or chemical
mechanisms. 

At the onset of exercise, the large and rapid increase in ventilation is primarily controlled by neural
pathways in the brain stimulating muscles involved in breathing. During submaximal steady state
exercise, the fine-tuning of ventilation is accomplished by blood borne substances such as carbon
dioxide, 

Oxygen and pH levels. During graded exercise, the generation of non-metabolic carbon dioxide will
result in a ventilatory threshold shown here. 

Basically, the exponential increase in lactic acid production results in a large increase in non-
metabolic carbon dioxide production from the buffering of the acid. This non-metabolic carbon
dioxide further stimulates the ventilatory response, resulting in this exponential increase or
threshold in ventilation. For this reason, researchers and clinicians frequently measure the
ventilatory threshold via indirect calorimetry to estimate the lactate threshold. 

Now let's discuss the few applied situations related to the respiratory system. I'm sure you've all
seen athletes wearing these nasal strips. Do they really improve performance. Conceptually, their
purpose is to reduce airway resistance in the nostrils which may increase airflow into the lungs. In
reality, there is no scientific evidence that they improve performance.

Because of the tremendous capacity of the lungs to increase ventilation even during maximal
exercise, ventilation is not considered to be a limiting factor in performance. Thus, marginally
reducing airway resistance in the nostrils will very likely have no effect on performance. The only
potential benefit nasal strips may have would be psychological in nature or the placebo effect. 

Next, if you've ever visited the weight room, you may have heard a lot of grunting and groaning, as
people are straining to lift very heavy weights. They are executing the Valsalva maneuver shown
here. 

Basically, they are performing a forced exertion with their mouth closed while holding their
breath. This results in a closed glottis which is part of the larynx. This maneuver creates
compressive forces that increases the intrathoracic pressure collapsing the inferior vena cava. This
can drastically reduce venous blood return to the heart, thereby decreasing the amount of blood
pumped by the heart. During a prolonged Valsalva maneuver, this can lower blood flow to the brain
resulting in dizziness and fainting. While young, healthy individuals can generally tolerate this state
for a brief period of time, older individuals, or those with heart conditions can actually suffer a
cardiac event, which can be lethal. So care must be taken in these populations to avoid the
Valsalva maneuver when lifting heavy weights. 

The final situation I would like to discuss pertains to exercise-induced asthma. This is more
common than you may think, affecting up to 20% of the general population, and 70 to 80% of
individuals suffering from persistent asthma. Symptoms include coughing, wheezing and shortness
of breath. Constriction of the smooth muscles surrounding the airways in the lungs, known as a
bronchospasm, along with inflammation and buildup of mucus in the lungs, are the main
mechanisms underlying exercise-induced asthma. 

Cold dry air is a common culprit, but air pollution, high pollen counts and other airborne chemicals
can contribute to exercise-induced asthma. Susceptible individuals should take the proper
precautions before exercising outdoors. 

In summary:

 Adjustments to all components of oxygen transport are essential during exercise to ensure

adequate oxygen delivery to muscles. 
 A decrease in pH and an increase in temperature, allow for more oxygen to be unloaded
from hemoglobin into muscles during exercise. 
 Ventilation also assists with exercise-induced metabolic acidosis. 
 Neural mechanisms are primarily responsible for the initial rapid rise in ventilation, while
humoral mechanisms do the fine tuning during submaximal steady-state exercise. 
 Care should be taken to avoid performing the Valsalva maneuver while lifting heavy
weights. 
 Also, individuals susceptible to exercise-induced asthma, should monitor environmental
conditions, and take the proper precautions.
2.3-2.4 Cardiovascular system responses to exercise.
Clearly, adjustments in the cardiovascular system are critical when engaging in aerobic activities
but they are also required for strength training as well. The three major adjustments made by the
cardiovascular system during exercise include one, an increase in cardiac output or the pumping
capacity of the heart, designed to enhance the delivery of oxygen and fuel to the working muscles.
Two, an increase in local blood flow to the working muscles, and three a decrease in blood flow to
other organs such as the kidneys, liver and stomach, thereby redirecting blood flow to the working
muscles. Cardiac output is the amount of blood pumped from the heart in one minute, generally
measured in liters per minute. It's simply calculated by heart rate, in beats per minute, times stroke
volume, or the amount of blood ejected by the heart with each beat. Thus in order to increase
cardiac output we can increase heart rate, stroke volume, or as it is the case during exercise, we
increase both. Let's examine the basic ways in which we can increase heart rate during exercise.
First, there is a reduction or withdrawal of the parasympathetic nerve activity to the heart. As
parasympathetic nerve activity causes a lowering of heart rate, its withdrawal will actually result in
an increase in heart rate. Second, an increase in sympathetic nerve activity to the heart will directly
cause an increase in heart rate. This increase in sympathetic nerve activity will be a function of the
exercise intensity. Lastly, an increase in the hormone epinephrine or adrenaline circulating in the
blood will also stimulate an increase in heart rate. These adjustments are also part of the fight or
flight response which you experience when nervous or frightened. You may actually feel your heart
pounding in your chest. This response is preparing the body for movement.

This figure demonstrates how densely the heart is innervated with sympathetic nerve fibers. Thus,
heart rate can be rapidly increased during exercise as a result of an increase in sympathetic nerve
activity.

Shown here is the typical heart rate response during a graded exercise test to max. Heart rate
increases linearly until approaching one's maximal heart rate. This will contribute to an increase in
cardiac output during the course of the test. Notice that endurance training results in lower, resting,
and submaximal heart rates with no change in maximal heart rate. I will discuss this in more detail
in the next video.
An increase in stroke volume also contributes to an increase in cardiac output during exercise. A
more forceful contraction of the ventricles of the heart, resulting in more blood being pumped per
beat, can be accomplished by both increasing sympathetic nerve activity and circulating
epinephrine. Shown here is the clear effect that an increase in sympathetic nerve stimulation has on
stroke volume. For a given amount of blood in the ventricles, sympathetic stimulation results in a
more forceful contraction, you'll get a significant increase in stroke volume. Here is the typical stroke
volume response during a graded exercise test to max. Stroke volume increases linearly at the
onset of the test, but can plateau at submaximal workloads. Again, please notice that endurance
training produces significantly greater stroke volumes both at rest and throughout the duration of the
test. Including a large increase in maximal stroke volume. The heart becomes a more forceful pump
after endurance training, this will be discussed in more detail in the next video. Taken together, the
increases in both heart rate and stroke volume result in a linear increase in cardiac output during
the course of a graded exercise test to exhausture. As mentioned in the calorimetry video, oxygen
consumption increases linearly during a graded exercise test until VO2 max is reached. Now let's
break down the cardiovascular factors responsible for this observation. The place to begin is with
the Fick equation which defines the the relationship between oxygen consumption with that for
cardiac output and the arterial venous oxygen difference. As indicated here, whether measured at
rest or during submaximal and maximal exercise, oxygen consumption is equal to one's cardiac
output times their arteriovenous oxygen difference. As we have already discussed the cardiac
output component here today, let's turn our attention to the arteriovenous oxygen difference.
Basically, the arteriovenous oxygen difference is the measure of oxygen uptake and utilization by a
cell, in our case a muscle cell. If we know the content of oxygen in an artery delivering oxygen to a
muscle and we know the content of oxygen leaving the muscle on the venous side, the difference
must be the amount of oxygen taken up and utilized by muscle for ATP production in mitochondria.
This measurement is abbreviated as (a-v)O2 Difference, with the little a representing the arterial
oxygen content, and the little v representing the venous oxygen content. Shown here is the
arteriovenous oxygen difference during a graded exercise test of VO2 max. As can be seen, the
arteriovenous oxygen difference increases progressively with increasing exercise intensity. This
indicates that the greater the exercise intensity, the greater extraction of oxygen from the blood and
utilization by muscle mitochondria. The two main factors responsible for the increase in
arteriovenous oxygen difference are a greater rate of oxygen delivery, accomplished by in an
increase in local muscle blood flow, and a greater rate of oxygen utilization, as mitochondria
consumed greater amounts of oxygen for ATP production at higher workloads. Thus, as per the
Fick equation, oxygen consumption can increase linearly as a function of exercise intensity due to
the contributions of both an increasing cardiac output as well as an increasing arteriovenous oxygen
difference until VO2 max is achieved. In summary, cardiac output is a function of heart rate and
stroke volume. Both factors increase in relation to exercise intensity and are regulated by both the
sympathetic nervous system as well as circulating epinephrine. Oxygen consumption is the function
of cardiac output and the arterial venous oxygen difference. The arteriovenous oxygen difference is
dependent upon both the rate of oxygen delivery as well as the rate of mitochondrial oxygen
utilization.

This video will continue with the second part of 

the Cardiovascular System's Responses to Exercise. 

I will examine the main ways in which blood flow is increased to the working muscles, 

as well as address a number of 

key training adaptations associated with endurance training, 

related to the cardiovascular system. 

There are three primary ways in which we can increase blood flow to the working muscles. 

The first way, is for the heart to pump more blood per minute. 

This increase in cardiac output was discussed in the previous video, 

and as such will not be addressed here. 

The second method to enhance muscle blood flow is known as vasodilation. 

Here, the smooth muscle surrounding blood vessels relaxes. 

In doing so, the blood vessels can now expand and open up, 

allowing for greater blood flow to the working skeletal muscles. 

Finally, the third method for increasing muscle blood flow is known as shunting. 

Basically, blood vessels and other tissues such as the kidneys, 

liver, and stomach, undergo vasoconstriction. 

In this case, the smooth muscle surrounding these blood vessels contract, 

thereby, narrowing the blood vessels resulting in a significant reduction in flow. 

The purpose of this response is to redirect or shunt 

blood flow away from these organs to the active muscles, where it is needed. 

This figure indicates just how powerful smooth muscle relaxation 

or constriction in a blood vessel can be in increasing or decreasing blood flow. 

In this example, if the radius of the vessel is reduced a mere 0.8 millimeters, 

blood flow through that vessel will be cut in half. 

This is exactly what happens during exercise in blood vessels of less active organs, 

thereby redirecting blood flow to the working muscles. 

On the other hand, the blood vessels to the working muscles relax, 

thus increasing their radius, 

allowing for greater blood flow. 

Let's examine the main factors that cause 

smooth muscle in the blood vessels of our working muscles to relax. 

At the local level of the muscle, 

we have several metabolic factors that increase or decrease, 

which reflect the exercise intensity, 

and thus, the need to enhance blood flow. 

As we have covered previously, 

there is an exercise intensity dependent increase 

in the production of carbon dioxide and metabolic acids. 

The increase in carbon dioxide and hydrogen ions in muscle, 

will cause smooth muscle of the local blood vessels to relax, 

thereby increasing muscle blood flow. 

Additionally, a decrease in oxygen levels, 

as muscle oxygen consumption increases, 

will also cause relaxation of smooth muscle, enhancing blood flow. 

This is known as functional or active hyperemia shown here. 

Basically, this refers to the fact that when 

the metabolic rate of skeletal muscle increases, 

as it does during exercise, 

the resulting changes in the local environment of the cell, 

reflect greater functional or metabolic needs. 

Thus, the metabolic byproducts associated with an increase in metabolism can be sensed, 

resulting in greater blood flow. 

Shown here is the typical cardiovascular response to intense exercise. 

Cardiac output increases approximately fivefold compared to rest. 

Please notice that despite 

this large increase in the amount of blood being pumped by the heart, 

blood flow to the kidneys, 

gastrointestinal tract, and other tissues such as liver, 

is actually reduced below resting levels. 

This represents vasoconstriction in the blood vessels of these tissues, 

thereby redirecting blood flow to the exercising muscles. 

Also notice that the bulk of the cardiac output, 

in this example 88%, 

is going to the exercising muscles. 

This represents vasodilation in blood vessels of these muscles, 

greatly enhancing blood flow. 

Lastly, I wish to point out that 

vasoconstriction in blood vessels of tissues such as the kidneys and liver, 

is primarily regulated by the sympathetic nervous system. 

As shown here, the arteries are elevated by sympathetic nerve fibers. 

During exercise, sympathetic nerve activity to 

the blood vessels in these tissues increases, 

causing smooth muscle contraction and vasoconstriction. 

Now, let's examine the blood pressure response during a bout of exercise. 

As indicated here, systolic blood pressure 

increases steadily with an increase in exercise intensity. 

Diastolic pressure remains stable. 

These are normal responses in healthy individuals. 

However, please notice that when individuals are 

engaging in intense or heavy weight training, 

involving large muscle groups, 

systolic blood pressure can increase to well above 250 millimeters of mercury. 

For young healthy individuals, 

this transient increase in blood pressure, 

is generally not a problem. 

However, for individuals with cardiovascular disease, 

such an elevation in blood pressure could be 

dangerous placing a great strain on the heart. 

Now let's examine the key training adaptations 

in the cardiovascular system associated with endurance training. 

A hallmark adaptation is a lower heart rate both at rest and during submaximal exercise. 

You can afford to have a lower heart rate because 

training results in an increase in stroke volume, 

both at rest and during exercise. 

Thus, resting and submaximal exercise cardiac output can be maintained. 

There is also an increase in maximal cardiac output, 

which is entirely due to an increase in maximal stroke volume, 

as maximal heart rate does not change with training. 

Also, the arteriovenous oxygen difference is greater during exercise after training. 

Together, the increase in maximal cardiac output and 

arteriovenous oxygen difference result in an increase in 

maximal oxygen consumption or VO2max. 

Now, let's examine these training adaptations more closely. 

In previously untrained individuals, 

the increase in VO2max with training, 

is due to an equal increase in 

maximal cardiac output and maximal arteriovenous oxygen difference. 

A range of 15 to 40% increase in 

VO2max can be achieved with training in previously untrained individuals. 

For already trained individuals, 

increasing their training volume or 

intensity will produce only modest increases in their VO2max, 

as it is already high to begin with. 

Not surprisingly, cross-country skiers who recruit a large muscle mass while training, 

both lower and upper body, 

demonstrate the highest values for VO2max. 

Distance runners are a close second. 

These values are approximately twice as great as their younger sedentary counterparts. 

Shown here, are the typical training adaptations related to the cardiovascular system. 

Notice that resting heart rate is significantly lower in trained men and women. 

This athletic bradycardia can occur because of the increase in resting stroke volume, 

thereby maintaining resting cardiac output. 

Now notice that at maximal exercise, 

training has no effect on maximal heart rate, 

if anything it's a tad lower. 

Thus, the increase in maximal cardiac output 

with training is entirely due to the increase in maximal stroke volume. 

The heart becomes a more forceful pump after training. 

The other component to the increase in VO2max with training, 

is the arteriovenous oxygen difference. 

An increase in red blood cell number will improve oxygen transport to muscles. 

An increase in the number of capillaries per muscle fiber, 

will enhance oxygen diffusion into muscles. 

Finally, more mitochondria will allow for 

greater utilization of the oxygen delivered to muscles. 

Together, these training adaptations result in a greater arteriovenous oxygen difference, 

at any given workload. 

In review, this figure highlights 

the significant endurance training adaptations associated with the cardiovascular system, 

and VO2max in particular. 

In summary, blood flow to muscles can increase dramatically, 

dependent upon the exercise intensity. 

Blood vessels and working muscles, 

will dilate allowing for greater blood flow. 

Blood flow to other organs will decrease, 

thereby redirecting blood flow to working muscles. 

Endurance training results in improvements in all components of the Fick Equation.

2.5-2.6 Endocrine system responses to exercise.

In this video and the next, I will address the role of the Endocrine System in regulating many
essential physiological and biochemical adjustments made by the body in response to exercise. The
Endocrine System is a collection of glands that produce and secrete specific hormones into the
blood. While there are numerous endocrine glands in the body, I will focus on only three. The
pancreas is responsible for the production and release of insulin and glucagon. Both of which play a
critical role in carbohydrate metabolism during exercise. The adrenal glands and specifically the
adrenal medulla produce epinephrine and norepinephrine which have multiple effects in the
regulation of many key physiological and biochemical adjustments made by the body in response to
exercise. Finally, I will adjust the role of the growth hormone released from the anterior pituitary
gland. First, let's briefly review some of the basic characteristics of hormones. Hormones are trace
substances produced and secreted by various endocrine glands which are then carried in the blood
to various target tissues. At this target tissues, hormones regulate a variety of physiologic and
metabolic functions as they react with their specific receptors present in or on target tissues. As
they circulate in the blood, hormones have the ability to reach all tissues in the body. Lastly, I wish
to emphasize that the endocrine system works closely with the nervous system to maintain
homeostasis during the physical stress of exercise. Let's begin with the hormone insulin. Insulin is
produced and secreted from the beta cells in the pancreas. It is responsive after a meal when the
blood is rich in macronutrients, with an elevation of blood glucose concentration be in a major
stimulus for its release. Shown here is the normal fasting range for blood glucose levels. Ideally in
healthy adults, blood glucose levels should be between 70 and 100 milligrams of glucose per 100
milliliters of blood. In this figure, the insulin response after a meal, when blood glucose levels are
high as indicated by the blue arrows. The increase in blood glucose levels directly stimulates the
pancreas to release insulin into the blood thereby elevating blood insulin levels. Insulin will now
promote glucose uptake in most cells for fuel. But in the case of skeletal muscle and the liver, the
glucose taken up will be primarily used to replenish your glycogen stores that have been somewhat
depleted since your last meal. This table demonstrates the metabolic effects of insulin on glucose
uptake and storage as glycogen in muscle and liver. Please notice that once these glycogen stores
have been completely replenished, any excess glucose from the meal will be converted into fat in
both liver and adipose tissue. We will revisit this concept when we discuss weight control and
obesity in module four. Whether you are engaging in sub-maximal steady state exercise, or a
graded exercise test to exhaustion, insulin levels decline during exercise. This decline in blood
insulin levels when coupled with the reduction in blood flow to not active tissue such as adipose and
inactive muscle, will minimize glucose uptake by these tissues. Thus the glucose in the blood can
be preferentially used by the active muscles where it's needed. Also, it is very important to realize
that although insulin levels are decreasing during exercise by as much as 50%, blood flow to the
active muscles can increase 10 to 15 fold. Thus, the active muscles actually see more insulin during
exercise. As insulin promotes glucose uptake in muscle, this will enhance the exercising muscle's
ability to extract glucose from the blood and use it for fuel. Lastly, exercise training results in a
significant improvement in insulin sensitivity. This has major implications for the treatment of type 2
diabetes. 90 to 95% of all diabetics have type 2 diabetes which is primarily caused by an increase in
insulin resistance. As we'll see in module four, there is no pill or technique more effective than
regular exercise to improve insulin sensitivity for the treatment of type 2 diabetes. As shown here,
the uptake of glucose from the blood during exercise can increase up to 20 fold when compared to
rest. As usual, the extent of glucose uptake will be dependent upon the exercise intensity, insulin
levels and muscle blood flow. The second hormone that plays a critical role in carbohydrate
metabolism, and glucose homeostasis during exercise, is glucagon. Glucagon is produced and
secreted by the alpha cells in the pancreas. Glucagon's primary function is to maintain blood
glucose concentration when levels drop below normal as is the case during time between meals,
fasting, and of course, during exercise. It accomplishes this functions by activating liver glycogen
breakdown resulting in the release of the newly formed glucose into the blood. Glucagons during
exercise is shown here, highlighted by the red arrows. At the onset of exercise, blood glucose levels
drop below normal, as working muscles extract glucose from the blood for fuel. This decrease in
blood glucose levels stimulates the release of glucagon from the pancreas. The elevation of
glucagon levels in the blood, will activate glycogen breakdown in the liver, resulting in a release of
glucose into the blood. As such, the working muscles will continue to have a source of glucose for
fuel and eventual ATP production as long as liver glycogen stores hold out. This table demonstrates
the metabolic effects of glucagon and glucose production and release by the liver. As can be seen
glucagons primary function is to break down liver glycogen supplying free glucose to be released
into the blood. However, a second role for glucagon is to stimulate gluconeogenesis in the liver.
This pathway allows the liver to make glucose from non-carbohydrate precursors, such as amino
acids and fats. This is particularly important during prolonged exercise, when liver glycogen stores
are depleting. This gives an individual a non-carbohydrate source for glucose production to
compensate for diminishing carbohydrate stores. Thus, during prolonged exercise, glucagon levels
rise to increase glucose output by the liver to match glucose uptake by active skeletal muscles,
thereby maintaining blood glucose concentrations. Notice that endurance trained individuals have a
blunted glucagon response to exercise when compared to untrained individuals. This is the result of
their greater ability to utilize fats and rely less on blood glucose. Thus, blood glucose levels will drop
less in trained individuals, so there's less of a need for a glucagon response. In summary, insulin
plays a major role in the significant increase in muscle glucose uptake during exercise. Glucagon
plays a major role in maintaining blood glucose levels during exercise. Together, both insulin and
glucagon ensure that working muscles have an adequate source of fuel for ATP production.

In this second video on the endocrine system, I will examine three additional hormones that play a
critical role in the adjustments made by the body in response to exercise. I will begin by discussing
the many contributions of epinephrine and norepinephrine. These hormones are released from the
adrenal glands and more specifically, the adrenal medulla. I will conclude the video examining the
role of the growth hormone plays during both exercise as well as into the post-exercise recovery
period. Based on their structure, epinephrine and norepinephrine belong to the chemical family of
catecholamines which also includes the neurotransmitter dopamine. Since epinephrine and
norepinephrine are synthesized in the adrenal glands they are also commonly referred to as
adrenaline and noradrenaline. Norepinephrine also functions as the major neurotransmitter for the
sympathetic nervous system, which as we discussed in the cardiovascular system videos, plays an
important role in the regulation of cardiac output and blood flow during exercise. The adrenal glands
are located on top of the kidneys. Shown here are the sympathetic nerve fibers directly enervating
the adrenal medulla. Thus, whenever sympathetic nerve activity is increased, as during exercise,
the adrenal medulla releases epinephrine and norepinephrine into the blood Where these hormones
will have a tremendous impact on a number of biochemical and physiological adjustments
necessary to sustain exercise. This sympathetic nervous system adrenal access is responsible for
the fight or flight response which occurs when you're frightened or nervous. It originates from the
animal kingdom, when a predator spots a prey. One animal gets excited for a chance at its next
meal while the other animal is frightened, not wanting to become the next meal. Both reactions elicit
a large sympathetic response. These stress hormones can actually prepare the body for exercise
prior to taking the first step. Shown here are the many biochemical and physiological variables
affected by these hormones. You may have felt your heart pounding in your chest when you
become frightened or nervous. This is the fight or flight response in action. This table demonstrates
the many physiological and metabolic effects of epinephrine required for exercise. As discussed in
our cardiovascular videos, epinephrine plays a major role in many physiological adjustments,
including an increase in heart rate and stroke volume, and thus cardiac output and an increase in
local muscle blood flow. All of these adjustments contribute to the increase in the delivery of oxygen
and fuel to the working muscles. From a metabolic standpoint, epinephrine regulates the breakdown
of glycogen in both muscle and liver. As well as stimulates fatty acid mobilization from adipose
tissue. Together, these metabolic functions ensure that the working muscles have adequate fuel for
ATP production. During the course of a graded exercise test to exhaustion, blood epinephrine and
norepinephrine levels will increase exponentially as maximal oxygen cup consumption is reached.
This represents the progressive increase in sympathetic nerve activity, resulting in adrenal
medullary release of epinephrine and norepinephrine. Not surprisingly, as shown here, the
epinephrine response to submaximal exercise will be dependent upon the exercise intensity. The
greater the exercise intensity, the greater is the sympathetic nerve activity and thus, epinephrine
release from the adrenal medulla. Before moving on to the next hormone I cannot emphasize
enough the critical role that both the sympathetic nervous system and the adrenal medullary
hormones, epinephrine and norepinephrine play in regulating multiple physiologic and metabolic
adjustments necessary to sustain physical activity. Next, I will discuss the contribution of the growth
hormone, both during exercise, as well as into the post exercise recovery period. The growth
hormone is synthesized and secreted by the anterior pituitary gland. While the growth hormone's
major effect is to promote protein synthesis in all tissues, during exercise it also plays a role in the
mobilization and utilization of free fatty acids. During exercise, there was a slow or delayed
response of growth hormone released into the blood. As just mentioned this will assist with the
mobilization and utilization of free fatty acids. However, notice that after relatively high-intensity
exercise, growth hormone levels continue to rise and can remain elevated up to over one hour post
exercise. As discussed in the video on protein metabolism, there is a very significant increase in the
rate of protein synthesis during the period immediately following exercise. This is a crucial time for
the initiation of training adaptations for both endurance and strength training. The elevation in
growth hormone is primarily responsible for the regulation of this increase in protein synthesis
during this post-exercise period. Many studies but not all suggest that as a result of training the
growth hormone responds to endurance training is more robust. This has potential implications for
not only future training adaptations but for healthy aging as well. The implications for aging will be
discussed in module four. For now, understand that both the frequency and magnitude of growth
hormone release from the anterior pituitary gland decreases with advancing age and sanitary men
and women. This can directly impact an individual's ability to maintain muscle mass and strength as
we get older and threaten one's independence and quality of life. In summary, shown here is the
typical response of the hormones that I have discussed in this and the previous video. Other
hormones, such as cortisol, contribute to the adjustments made by the body during the stress
imposed by a single bout of excercise. However, I have covered the five major players when it
comes to the regulation of the critical biochemical and physiological adjustments necessary to
sustain exercise.

2.7 Immune system responses to exercise.

This video will examine the impact that both a single bout of exercise, as well as regular training,
have on the immune system. The relatively new field of exercise immunology has emerged over
that past 20 years, and has generated some exciting results. As the immune system is extremely
complex, I will only address some of the key features as it pertains to exercise and one's
susceptibility to infections. Our bodies are constantly exposed to a number of infectious agents that
could potentially make us ill. Fortunately, for the most part, our immune system does an excellent
job of neutralizing these pathogens upon exposure. The two major branches of the immune system
are shown here. They are innate immunity and adaptive immunity. While exercise will affect both
branches, in the interest of time I will only focus on adaptive immunity. Adaptive immunity will
respond to a specific infectious agent such as a flu virus. And make immune cells specifically
designed to neutralize and kill that specific virus. The two arms of adaptive immunity include both a
humoral and cellular component. For the purpose of this video, the humoral arm is responsible for
making specific antibodies that circulate in the blood, neutralizing infectious agents. The cellular
arm is responsible for making t-cells that can kill cells that have all ready been infected. Thus when
we look at the responses to exercise, I will discuss the ability to make both antibodies as well as
these T killer cells. The impact that a single bout of exercise will have on the immune system will be
very much dependent upon the exercise intensity. A moderate bout of exercise has only a small or
marginal effect on immune function. However, heavy intense exercise can transiently suppress
immune function up to three hours post-exercise. Here is one of many studies demonstrating that
after an intense part of exercise. The humoral branch of adaptive immunity and specifically,
antibody production is transiently suppressed at least one hour post exercise. This study was
performed on eight well trained cyclists who exercised for two hours at 75% of their VOt max.
Shown here is the typical response of the cellular branch of adaptive immunity to a single bout of
intense exercise. Notice that after an intense training bout of exercise these marathon runners
demonstrated a significant reduction in their ability to produce T-cells up to three hours after
exercise. Again, this immunosuppression was transit as T-cell production returned to normal after
six hours. Taking together the suppression in both humoral and cellular immunity immediately post
exercise has lead to the Open Window Theory. Basically, this theory states that for several hours
after an intense bought of exercise your immune system is transitory suppressed. Giving any
opportunistic bacterial or virus the chance to get a foot hold leading to infection. You may have
already been exposed to these infectious agent before the bout of exercise, but your immune
system was effectively neutralizing them prior to the intense bout of exercise. Thus, one's
susceptibility to infection is likely greater during the post exercise recovery period. Possible
mechanisms for this transient suppression in immune function after exercise center around the
elevation of several stress hormones. These include the adrenal hormones of cortisol, epinephrine,
and norepinephrine, which are known to be immunosuppressive. Additionally, an increase in body
temperature as occurs during exercise may also play a role in immunosuppression. Shown here is
the cortisol and epinephrine response from those marathon runners described earlier in this video.
You'll had a significant reduction in T-cell production three hours after a bath of intense training.
Noticed that both cortisol and epinephrine levels remained elevated when compared to rest for
several hours into the recovery period. So does this transient suppression and immune function
actually translate into an increase susceptibility to infection? The answer appears to be yes. For the
weeks following a big racing competition such as a marathon, Iron Man, or Tour de France, the
incidents of infection is two to five fold greater an athletes who completed. When compared to
individuals of similar fitness, that did not compete. Shown here is just one of many studies that
demonstrates this point. Runners who competed in a 56-kilometer race had a two and a half-fold
increase in contracting upper respiratory tract infection, when compared to their roommates. As
their roommates were exposed to the same possible environmental infectious agents, this suggests
that it was the bout of intense exercise that made the runners more susceptible to infection. Other
factors that can contribute to an increased susceptibility to infection are shown here. I will briefly
discuss the interaction between exercise and stress at the end of this video. People frequently ask
me if they should exercise when they're sick. Some people believe that the work out will kill any
bacteria or viruses and rid the body of toxins. This is absolutely false. In fact, as stated above, a
single bout of exercise can suppress immune function during the post-exercise recovery period,
thus making the matter worse. The general rule of thumb is not to exercise, but rest if your
symptoms are below the neck. Such as muscle aches, fever, an upset stomach, and lung
congestion. If you have symptoms above the neck, such as a simple head cold, it is generally okay
to engage in light easy exercise as tolerated. However, if you find even easy exercise makes you
feel worse, then you should stop exercising and rest until you have recovered. As you start to feel
better, you can gradually return to your normal exercise pattern. Now let's examine how a training
can influence your baseline immune function. The majority of studies clearly indicate that
participation in regular moderate physical activity will improve overall immunity. Again, I will show
you just one representative study of many demonstrating this outcome. In this study, three months
of walking in previously sedentary individuals reduced the incidence of upper respiratory track
infections by approximately 50%. Over a 15 week window of observation. The mechanisms
responsible for this training adaptation remain to be determined, but likely involve both branches of
the immune system. While moderate training can boost immune function, involvement in repeated
high intensity training will have the opposite effect. As I've already stated in this video, a single bout
of high intensity exercise is immunosuppressive. Frequent engagement in these types of training
sessions will chronically suppress immune function, making the individual more susceptible to
infections. As shown here, this can result in a weakened immune system that puts the individual at
a greater risk for infection. Even when compared to their sedentary counterparts. The frequency of
infections is a common complaint among many distance athletes. In fact, one of the classic
symptoms of overtraining in athletes is an increase in the number of infections resulting from a
chronically suppressed immune system. Finally, I would like to discuss the interaction of stress,
immune function and regular exercise. It is well established that repeated or chronic stress can
weaken the immune system. And can contribute to the onset of illness and disease. Here is just one
example demonstrating that regular participation in moderate exercise can reduce the negative
effects of other life stressors on the immune system. When sedentary animals are exposed to a
stressor, their ability to mount an effective immune response is clearly blunted. However, endurance
trained animals when exposed to the exact same stressor, show no reduction or impairment in
immune function. Similar findings have been found in humans. Basically moderate exercise training
can provide a degree of immune resilience, or stress resistance, protecting you from the adverse
affects of other life stressors. In summary, a single bout of high-intensity exercise can transiently
suppress immune function allowing an opportunistic virus or bacteria to make you ill. Participation in
regular moderate exercise can improve baseline immune function, thereby, lowering the risk of
infection. Chronic high-intensity training and overtraining can lower immune function, thereby
increasing the rest risk of infection. Regular moderate exercise can reduce the negative effects of
other life stressors on the immune system and, thus, your susceptibility to infections.

3. Exercise for fitness and performance

3.1 Adaptations to endurance training

3.2 Adaptations to strength training

3.3 Nutritional considerations for exercise

3.4 Causes of muscle fatigue

3.5 Causes of muscle soreness

3.6-3.7 Performance enhancing drugs

4. Exercise in health, wellness and disease

4.1 Exercise is medicine

4.2 Diet, exercise and weight control

4.3 Exercise and risk factors for health disease

4.4 Exercise and risk factors for diabetes

4.5 Exercise and risk factors for cancer

4.6 Exercise and successful aging

4.7 Exercise and your brain