EXERCISE PHYSIOLOGY 2011

Dante G. Simbulan, Jr., PhD

I. The Different Muscular Capabilities During Exercise; Training Adaptations

II. Respiratory Responses During Exercise; Training Adaptations
III. Cardiovascular Responses During Exercise; Training Adaptations
IV. Thermoregulation; Fluid and Electrolyte Balance During Exercise

I. The Different Muscular Capabilities During Exercise; Training

Adaptations

A. Define muscle strength, power and endurance. Compare muscle

strength between men and women. What is the relationship between muscle size/ mass
and muscle strength ? What role does testosterone play in the differences in muscle mass ? Is there a
difference in muscle strength per cross-sectional area of muscle between men and women ? Can
muscle mass/ muscle strength be increased in men and women through training ?

B. Muscle Metabolism During Exercise /Work

(Read also Chapter 84: Sports Physiology , Guyton, “The Muscle Metabolic Systems in Exercise”; and
“Nutrients Used During Muscle Activity”;
Chapter 59, Exercise Physiology and Sports Science, Boron, “Conversion of Chemical Energy to
Mechanical Work” , p. 1244 – 1247; ).
Ganong, Ch 3: Excitable Tissue (Muscle) 21st edition, “Energy Sources & Metabolism”, pp. 74 – 76.

B.1 Three Energy Systems Involved in the Production of ATP for Exercise
i. Formation of ATP by phosphocreatine (PC) breakdown (PC/ phosphagen
pathway)
ii. Formation of ATP via the degradation of glucose or glycogen, leading to lactate
production (anaerobic glycolysis)
iii. Oxidative breakdown of substrates leading to formation of ATP (oxidative
phosphorylation/ Krebs cycle and the electron transport system)

Note: (i) and (ii) are also known as anaerobic metabolic pathways, while (iii) is an
aerobic metabolic pathway, utilizing O2 to generate ATP.

See also Boron, Medical Physiology, Figure 59-3, p. 1245.

B.2 Fuel Sources for the Three Energy Systems During Exercise

1. Phosphocreatine provides immediate source of phosphate for ATP

formation, during the first few seconds of intense exercise..
2. Glycogen in muscle provides a short-term source for ATP formation in
anaerobic glycolysis during the first minute or so of intense exercise.
Muscle lactate produced can be further metabolized in the liver to glucose
(gluconeogenesis).
3. Glycogen, blood glucose, and fatty acids become sources for ATP
formation during aerobic metabolism. Aerobic metabolism is dominant
metabolic system utilized during submaximal (low-intensity) prolonged
exercise.

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 The 3 Energy Systems During Exercise

See also Fig. 59-3. Energy Conversion in Skeletal Muscle., p. 1245, Boron.

B.3 Time course for involvement of the 3 energy systems.

Energy System Relative Rate of Time

maximum ATP
generation (M of
ATP / min)

1. Phosphagen system 4 8 – 10 SECONDS

(Phosphocreatine-ATP system;
anaerobic)

2. Glycogen-lactic 2.5 1.3 – 1.6 MINUTES

acid system
(Anaerobic )

3. Oxidative 1 Unlimited , as long

metabolism Nutrients last.
(aerobic)

Source: Guyton, Chapter 84.

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 B.4 Energy (Metabolic) System Utilitized for Different Types of Athletic Activities

Phosphagen Phosphagen & Glycogen-lactic Glycogen-lactic Aerobic system

entirely Glycogen-lactic acid mainly acid and aerobic
acid system
100 meter dash 200 meter dash 400 meter dash 800 meter dash Marathon run
Jumping basketball 100 meter swim 200 meter swim 10,000 m skating
Weight lifting Baseball home tennis 1,500 m skating Jogging
run
Diving Ice hockey soccer boxing Cross country
dashes skiing
Football dashes 2,000 m rowing
1.5 km run
1 mile run
400 m swim
Source: Guyton, Chapter 84

Questions: Know the difference between sprint-like activities and endurance type of activities in
work and exercise. Which energy system(s) favor(s) sprint-like components or types of athletic
activities or work ? Which energy system favors endurance components or type of athletic
activities or work.

C. Different Muscle Fiber Types ; Types of Athletic Activity the Different

Fiber Types Promote

[Read Ganong, Ch 3, 21st edition: Excitable Tissue: Muscle, “Fiber Types” (p. 73), “Protein Isoforms in
Muscle and their Genetic Control”, p. 74; “Properties of Skeletal Muscles in the Intact Organism” (pp.
76 – 78). Guyton, Chapter 84: Sports Physiology , “Fast Twitch and Slow Twitch Muscle Fibers”.
Boron, Ch. 9”Skeletal Muscle is Composed of Slow-Twitch and Fast-Twitch Fibers, pp. 251 – 253. See
also Table 9-1. “Isoform Expression of Contractile and Regulatory Proteins” (p. 252) and Table 9-2,
“Properties of Fast and Slow-Twitch Fibers”, (p. 252). Ch. 59 : Exercise Physiology and Sports Science,
“Muscle Work and Fatigue”, pp. 1242 – 1244.

From Boron:

Slow Twitch Fast Twitch Fast Twitch

Synonym Type 1 Type IIa Type IIb
Fatigue Resistant Resistant Fatigable
Color Red (myoglobin) Red (myoglobin) White (low)
myoglobin)
Metabolism Oxidative Oxidative Glycolytic
Mitochondria High Higher Fewer
Glycogen cont. Low Abundant High

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 From Rhoades and Tanner:

Metabolic Type IIb; Type IIa; Type I;

Properties Fast Twitch; Fast Twitch; Slow Twitch;
Fast Glycolytic Fast Oxidative- Slow Oxidative
(White) Glycolytic (Red) (Red)
ATPase activity High High Low

ATP sources Anaerobic Anaerobic Oxidative

glycolysis glycolysis/oxidative Phosphorylation
phosphorylation
[Glycolytic Enzyme ] High Moderate Low

No. of Mitochondria Low High High

Myoglobin content Low High High

Glycogen content High Moderate Low

Fatigue Resistance Low Moderate High

Mechanical Type IIb; Type IIa; Type I;

Fast Twitch; Fast Twitch; Slow Twitch;
And Neural
Fast Glycolytic Fast Oxidative- Slow Oxidative
Properties (White) Glycolytic (Red)
(Red)
Contraction Speed Fast Fast Slow

Force Capability High Medium Low

Sarcoplasmic High High Moderate

Reticulum: Ca+
ATPase activity
(pump)
Motor Axon velocity 100 m/sec 100 m/sec 85 m/sec
(bigger motor units) (bigger motor (smaller motor units)
units)

Structural Type IIb; Type IIa; Type I;

Properties Fast Twitch; Fast Twitch; Slow Twitch;
Fast Glycolytic Fast Oxidative- Slow Oxidative
(White) Glycolytic (Red)
(Red)
Fiber Diameter Large Moderate Small

No. of Capillaries Few Many Many

Type IIb ; Type IIa ; Type I ;

Fast Twitch; Fast Twitch; Slow Twitch;
Fast Glycolytic Fast Oxidative- Slow Oxidative
(White) Glycolytic (Red)
(Red)
Functional Role Rapid and Powerful Medium Postural/ Endurance
Movements Endurance
in Body
Typical Latissimus Dorsi In mixed-fiber Soleus
muscles, ex.
Example vastus lateralis
-

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What type of muscle fibers favor: (a) Sprint-like activities?
(b) Endurance type of exercises ?

From Berne and Levy:

Properties of Motor Nerve (alpha-motor neuron)

innervating Muscle Fiber Types

Characteristics Type I Type II

Cell diameter small Large

Conduction velocity Fast Very fast

Excitability High Low

FIBER TYPE COMPOSITION IN AN (A) UNTRAINED,

(B) ENDURANCE-TRAINED AND (C) SPRINT-TRAINED ATHLETES
(From Bijlani, 1995)
A. B. C.
80
70 80
Slow Twitch Fibers
% 75
60 %

50 Fast Twitch Fibers

% 40 55
%
45
30 %

20 20 25
% %
10
0
Untrained Distance Sprint
Control Runner Runner

What role does heredity/ genetics play in skeletal muscle fiber type composition ?

D. Training Adaptations: What is the effect of Training on Fiber Type

Composition and Muscular Capabilities ?
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D.1 What is the effect of Endurance or Strength training on fiber type composition and
muscular capabilities ? See Table below.

Human Biceps Sedentary After After After 4

Brachii Muscle Endurance Strength Months
Training Training Immobiliza
-tion
1. Total No.cells 300,000 300,000 300,000 300,000

2. Total Cross- 10 10 13 6
sectional Area

3. Isometric Strength 100 % 100 % 200 % 60 %

(% Control)

4. Fast-twitch fibers 50 % 50 % 50 % 50 %
(% by numbers)

5. Fast-twitch fibers, 67 67 87 40
average area (m2 x
102 )
6. Capillaries/ fiber 0.8 1.3 0.8 0.6

7. Succinate 100 150 77 100

dehydrogenase
activity/ unit area (%
control)

Questions on Effects of Training:

Based on experimental results shown above, which type of training (endurance or strength
training) :
(1) enhances muscle hypertrophy ?; which muscle fiber types undergo
hypertrophy (Type I or Type II) more in strength/ resistance training ?
(2) enhances muscle strength ? muscle endurance ? (obvious ?)
(3) enhances capillary growth around muscle fibers ? what type of training
enhances the oxidative capacitites of skeletal muscles (what is your
evidence)
(4) preferentially recruit Type I fibers ? What is low-frequency fatigue and
which muscle fibers are involved ? (Boron, p. 59)
(5) recruit both Type I and Type II fibers ? What is high-frequency fatigue and
which muscle fibers are involved ? (Boron, p. 59)

Are the total number of cells increased in muscle hypertrophy, based on the experimental
results shown above ? If the number of muscle cells are not increased in muscle hypertrophy
during appropriate forms of training, what underlies the increase in mass mass or size ?

D .2 Models to Explain Skeletal Muscle Hypertrophy

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 A. Stretch

Release of soluble factor(s) from muscle

Fiber or extracellular matrix

Activation of 2nd messenger systems in fiber

Arachidonic acid, phospholipases, PKC, tyrosine kinase, etc.

Induction of immediate early ( IEG) genes

Transcription of muscle genes MHC, MLC;

ACTIN, etc.

MUSCLE FIBER HYPERTORPHY

B.
Combined direct effects of stretching (autocrine
or paracrine mechanisms) and induced endocrine stimuli during
prolonged training resulting in muscle hypertrophy.

Blood Cytosol Nucleus

Plasmalemma Exercise Exercise Response
(autocrine or
paracrine)
Element
Exercise
(endocrine) Exercise transduction pathway(s)
DNA
IEG Transcription
coding
 [Hormone]
2nd
receptor Messenger mRNA
systems

Translation

Posttranslation control

New phenotype

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D.3 Other Biochemical Adaptations of Skeletal Muscle as a Result of Aerobic (Endurance)
Training

Endurance (aerobic) training improves the oxidative metabolism of both

carbohydrates and fats. On occasion where fat reserves are optimally
available, increased utilization during prolonged, low-intensity
(endurance) exercise.

[Source: Boron, Fig. 59.9, p. 1254]

Effects of Endurance Training: Increased number of

mitochondria and capillary density increase the rate
of free fatty-acid utilization, preserving plasma
glucose
Slower blood
flow in muscle
 Capillary Increased contact time for
density gas exchange
Increased uptake
 Mitochondria of FFA
number  FFA utilization

 Fatty acid cycle Spares plasma

enzymes and glucose for sprint
Carnitine transferase Activities; energy
reserves

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 Effects of Endurance training: Increased number of
mitochondria decreases lactate and H+ formation,
helping maintain blood pH
Decreased Pyruvate
FFA
formation
oxidation and
Decreased
Increased ‘H’ form of
PFK activity Lactate
dehydrogenase

 Decreased
lactate and H+
ion formation
 Mitochondria
number

mitochondrial Decreased
uptake of fluctuations in
pyruvate and NADH Blood pH
maintained.

RELATIONSHIP BETWEEN EXERCISE DURATION AND FUEL SOURCE:

Data below from highly-trained endurance athletes:
100
Muscle Triglycerides
80
% Plasma FFA
Energy 60
Expenditure
40 Plasma glucose
20
Muscle glycogen
O
0 1 2 3 4
Exercise time (hours)

As exercise duration increases, there is a shift from carbohydrate

metabolism to fat metabolism (Powers and Howley, p. 61).

RELATIONSHIP BETWEEN EXERCISE INTENSITY AND FUEL SOURCE:

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 (Powers and Howley, p.56)

100

80 % Fat
%
Energy 60
Expenditure
From Fat 40
Or
Carbohydrates 20 % Carbohydrate
O
0 20 40 60 80 100
Exercise Intensity ( % VO2 max)
Note that as the exercise intensity increases, there is a progressive
increase in the contribution of carbohydrate (CHO) as a fuel source,
especially when bursts of heavy activity are called for (utilizing both the
phosphagen, and the glycogen-lactic acid system).

Question: Is low or high intensity exercise best for burning fats ?

II. Respiratory Responses During Exercise; Training Adaptations

A. Acute Respiratory Responses to Exercise

[Remember that ventilation, or
Minute Ventilation (VE)= Tidal volume (ml) x Respiratory Rate (breaths per min) ]

A.1 Three Phases of Exercise Hyperpnea (moderate exercise)

Ventilation
(L/min)
I II III
40

30

20

10

0
Rest Exercise Recovery
Time

(adapted from : Ganong, Review of Medical Physiology, Fig. 37-2., p. 686., 21st edition; also from:
McArdle (2001), p. 289: Exercise Physiology, 5th edition.)

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During Exercise: No single factor controls ventilation during exercise. Rather, the combined and
perhaps simultaneous effects of several chemical and neural stimuli initiate and modulate exercise
alveolar ventilation.
The figure above shows the dynamic phases of minute ventilation during moderate exercise
and recovery.

Phase I : at the start of exercise, neurogenic stimuli from:

(a) the cerebral cortex (CENTRAL COMMAND, specifically the motor cortex),
(b) combined with peripheral (proprioceptive) feedback from the active limbs (muscles,
tendons and joints,) , stimulate the medulla to increase ventilation abruptly.
The initial increase in (minute) ventilation is mainly due to an increase in tidal volumes. In
more intense exercise, the increase in tidal volume is accompanied by an increase in respiratory
rate, leading to a pronounced increase in ventilation.
**Cortical and locomotor peripheral input continues throughout the exercise period (also in
Phase II and III.

Phase II: After a short plateau in Phase I (approximately 20 s), minute ventilation then
rises exponentially (in phase II) to reach a steady level related to the demands for metabolic gas
exchange. Central command input, including factors intrinsic to neurons of the respiratory control
system, regulates this phase of exercise ventilation. Continued activity of the respiratory neurons in
the medulla causes short-term potentiation that augments their responsiveness to the same continuing
stimulation. This brings minute ventilation to a new, higher level. In all likelihood, input from the
peripheral chemoreceptors in the carotid bodies also contributes to regulation during phase II.
{Ganong: The gradual increase is presumably humoral, even though arterial pH, PCO2, and
PO2 remain constant during moderate exercise.
i. The increase in ventilation is proportionate to the increase in O2 consumption, but the
mechanisms responsible for the stimulation of respiration are still the subject of much debate.
ii. The increase in body temperature may play a role in hyperpnea.
iii. Humoral factors in Phase II and III exercise hyperpnea:
- increase in plasma K+ level, and this increase may stimulate the peripheral
chemoreceptors.
- In addition, it may be that the sensitivity of the neurons controlling the response to CO 2
is increased or that the respiratory fluctuations in arterial PCO2 increase so that,
even though the mean arterial PCO2 does not rise, it is CO2 that is responsible for the
increase in ventilation.
- O2 seem to play some role despite the lack of a decrease in arterial PO 2, since during the
performance of a given amount of work, the increase in ventilation while breathing 100 % O2 is 10 –
20 % less than the increase while breathing air. Thus, it currently appears that a number of different
factors combine to produce the increase in ventilation seen during moderate exercise.)

Phase III : The final phase of control (phase III) involves a fine tuning of the steady-state
ventilation through peripheral sensory feedback mechanism. Modulation of alveolar gas pressures in
this phase results from central and reflex stimuli from the main by-products of increased muscle
metabolism – carbon dioxide and H+ concentration. These factors stimulate chemoreceptor group
IV unmyelinated neurons that communicate with regions of the central nervous system to regulate
cardiorespiratory function. The lactate anion itself, apart form lactate acidosis (excess H+) ,
contributes an additional stimulus to increase ventilation in strenuous exercise. Reflexes related to
pulmonary blood flow and the mechanical movement of the lung and respiratory muscles also
provide regulatory input. (Note similar factors involved in Phase II and III hyperpnea).
In recovery: The abrupt decline in ventilation when exercise stops reflects the removal of
both the central command drive and the sensory input from previously active muscles. More than
likely, the slower recovery phase results from:

(1) gradual diminution of the short-term potentiation of the respiratory center and
(2) re-establishment of the body’s normal metabolic, thermal and chemical milieau.

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 A.2 Acute Changes in Pulmonary Volumes, Pulmonary Blood Flow to Lungs,
Pulmonary Diffusing Capacities for Respiratory Gases; Recruitment of Respiratory Muscles

A.2.1 During moderate exercise, the increase in minute Ventilation (VE) is initially due to an
increase in tidal volume, later accompanied by an increase in respiratory rate. In more intense
activities, both TV and RR (TV x RR = VE) are increased leading to a more abrupt increase in
ventilation. Note in the figure above that arterial blood gases (partial pressures of O 2 and CO2) are
efficiently maintained under control, without much change, by the cardio- respiratory systems.
However, it has been suggested that minute fluctuations in arterial blood gases (above) can be
monitored by peripheral chemoreceptors, or that an increased sensitivity of medullary respiratory
neurons to minute fluctuations of respiratory blood gases may further enhance the ventilatory
response.

See also similar graph below, showing dependence of minute venitlation on intensity of
exercise. The sharper increase in minute ventilation (slope) during maximal exercise levels may be
due to increased chemoreceptor stimulation, particularly when anaerobic metabolism increases with
increased lactate and H+ production.

100

Minute
Ventilation
(L/min)
6

Rest Maximal
Exercise Intensity

More data below:

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 From Rest to Exercise: Changes in Pulmonary
Ventilation
Ex: 70 kg man
Rest* Exercise**
Tidal Volume 0.5 Liters
(VT), (L) 3 – 3.5 liters
Respiratory 15 breaths/min 40 – 50
Rate (f)
(breaths/min) breaths/ minute
Minute 7.5 L/min
Ventilation 120 – 175 L/min
(V) (L/min)
**Apex region as well as basal region
*Basal region of lungs receive more
receives Increased percentage of
Ventilation than apex, during quiet
total ventilation.
Breathing.

A.2.2 Acute Responses: Pulmonary Blood Flow

Pulmonary Vascular
Blood Flow (L/min) Resistance (mm Hg/ml/min)
25 0.0020
Exercise Exercise
20
0.0015 Normal,
15 At rest
0.0010
10 Normal,
At rest 0.0005
5

0 15 17 19 21
0 5 10 15 20 25

Mean Pulmonary Arterial Pressure (mm Hg)

At rest, pulmonary blood flow is higher at the base of the lungs or the apex of the lungs ?
As exercise duration and intensity progresses, what happens to pulmonary blood flow ? Why does
vascular resistance decline as mean pulmonary arterial pressure increases ? Describe the distribution
of blood flow in the base and apex of the lungs.

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 Recruitment & Apex of
Distention of lungs
pulmonary
capillaries

Base of lungs

A.2.3 Acute Responses: Changes in Pulmonary Diffusing Capacities from Rest to

Exercise Transitions

Pulmonary Diffusing Capacity = A x D x (P1 – P2);

T
A = Surface Area of capillary networks in contact
with blood and alveolar membrane;
T =is the thickness of the alveolar-blood gas barrier;
D is diffusion coefficient (constant);
P1 – P2 = difference in partial pressure across the
alveolar-blood gas barrier.

An increase in pulmonary blood flow recruits and distends more pulmonary capillaries,
including those in the apex of the lungs. This contributes to the increase in pulmonary diffusing
capacity for the respiratory gases as the surface area (A) for gas exchange increases,
increasing gassides
between two exhange across
of the the alveolar-blood gas barrier, leading to increased O2 uptake and
tissue.
exhalation of CO2 during exercise. Partial pressure gradients across the alveolar-blood gas barrier
also increases with increased oxygen consumption, and increased carbon dioxide production by the
tissues, contributing to the increased diffusing capacities (see formula above for diffusing capacity).
Guyton (8th edition, p. 946,below, data from table) presents data showing differences in
pulmonary diffusing capacities between untrained and trained persons (underwent regular exercise
training):
O2 diffusing capacity
ml/ min
80 Speed
70 skaters
Non- Oarsmen
60
athlete
50 Non- Swimmers
40 Athlete,
30 Rest
20
10 Maximal exercise
0

Is the increased oxygen diffusing capacity of athletes due to hereditary traits or a product of training ?

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 A.2.3 Acute Responses: Recruitment of Respiratory Muscles During Exercise

What are the principal and accessory respiratory muscles ? Describe their involvement during resting
respiration and breathing during exercise. Is there respiratory muscle fatigue, especially during
prolonged exercise ? Respiratory muscles at rest and exercise: The major muscle of inspiration is the
diaphragm. Air enters the pulmonary system due to intrapulmonary pressure being reduced below
atmospheric pressure (bulk flow). At rest, expiration is passive. However, during exercise, expiration
becomes active, using muscles located in the abdominal wall (e.g., rectud abdominis and internal
oblique).

A.2.4 Acute Responses: Sympathetic activation of the Adrenal Medulla and

Catecholamine Release

What is the effect of circulating catecholamines, principally epinephrine, on the

respiratory airway muscles ? How does this contribute to the acute respiratory response to exercise ?

B. Long-Term Respiratory Adaptations Due to Training (Regular

Exercise)

Take note of the decreased ventilatory response (10 – 20 % less, see graph above) in the post-
training period to the same work intensities compared to that of the pre-training period.
This decreased ventilatory response have been attributed to the increased oxidative capacities
of skeletal muscles as shown by graphs in biochemical adaptations (see sections above), and
specifically, the decreased lactate production in endurance- trained muscle systems of athletes (see
below).

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This results in decreased H+ stimulation of peripheral chemoreceptors, arising from decreased lactate
acidosis. The increasing production of CO2 from increased consumption of O2 by skeletal muscles
during exercise is easily buffered by NaHCO3- system in the blood, and arterial CO2 effectively
maintained at optimum levels by the exercise intensity-dependent and proportionate increase in
ventilation.

Do respiratory muscles also adapt to training, in the same way as locomotor skeletal
muscles ?

III. Cardiovascular Responses During Exercise; Training Adaptations

A. Acute Cardiovascular Responses to Exercise

[Source: Guyton, 8th edition, Fig.84-8, p. 947). Be able to discuss

Rest Exercise
25000
22000
1. Preferential increased blood flow to
20000 working Muscles, while blood flow to
resting muscles unchanged or reduced.
ml / min

15000 2. Also, coronary blood flow also

Increases in absolute amounts
During dynamic exercise
10000

5000 1400 1100

1200 1000 600
250 500 300 900 750 750
0
Muscles Heart Skin GIT Renal Brain
this.]

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 Cardiac Output, mean Arterial Pressure, and
Systemic Vascular Resistance Changes with
Exercise

120 105 Rest

93 15
100 Heavy Dynamic
Exercise
80
60
4
40 24
20 6
0
Cardiac Mean Arterial Systemic
Output Pressure vascular WHY ?
(L/min) (mm Hg) Resistance
(mm Hg/min/L)

Effects of active muscle mass on mean

arterial pressure in exercise
Isometric Exercise
Mean
160 Why ?
140
Arterial
120
Pressure Dynamic
(mm Hg) 100 (Isokinetic)
80 Exercise

+ + + + +
Rest 1 Hand 1 Arm 2 Arms 1 Leg 2 Legs

Muscle Mass

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 B. Cardiovascular Adaptations to Training

H e a rt R a te (b p m ) S tro k e V o lu m e (m l)
180 120
160
100
140
120 80
Rest
100
60 Rest
80 Maximal Maximal
60 Exercise 40
40
20
20
0 0
Before Training After Training Before Training After Training

Take note of HR, SV, and Cardiac Output before and after training period at
rest ? Take note of changes in HR, SV, and Cardiac Output before and after
training period during maximal exercise ? What is the effect of training on
HR, SV, and CO at rest and exercise ? The increased cardiac output during
maximal exercise after training is mainly due to what: increased heart rate
? increased stroke volume ? What advantage does this confer on the
athlete’s heart’s work performance and capacity to deliver blood supply ?

Cardiac Output (L/min)

25

20

15 Rest

10 M aximal
Exercise
5

0
Before Training After Training

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 Athletic Cardiac Hypertrophy due to Training;
Size returns to control levels with detraining
difference with pathologic hypertrophy
(disagreement with Guyton over types of exercise and hypertrophy)

“ECCENTRIC “CONCENTRIC
Large, HYPERTROPHY” HYPERTROPHY”
Venous
return

Preload

25% Larger volumes Volume (WHOLE HEART) Afterload

Sedentary = 800 ml
Endurance Non-endurance
Athletes Non-athlete (Sprint) Athletes
Source of figure above : Bowers and Fox (1991) , p. 255.

Comparative Average Cardiac Dimensions in College

Athletes, World Class Athletes and Normal Subjects

Dimension College College World College Wold Normals

Runners Swimmers Class Wrestlers Class (N= 16)
(N = 15) (N= 15) Runners (N = 12) Shot
(N = 10) putters
(N= 4)
Left Ventr. 54 51 48-59 48 43-52 46
Internl
dimens.
Left Ventr. 160 181 154 110 122 101
Volume, ml

Stroke 116 ------ 113 75 68 -----

Volume, ml

Left ventri. 11.3 10.6 10.8 13.7 13.8 10.3

wall, mm
Septum, mm 10.9 10.7 10.9 13.0 13.5 10.3

Left ventric. 302 308 283 330 348 211

Mass, g

Compare cardiac dimensions between endurance and resistance-trained

athletes.

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Source of data above : McArdle (2001), p. 469.

Compare left ventricular mass between endurance and resistance-trained

athletes.

IV. Thermoregulation; Fluid and Electrolyte Balance During Exercise

Be able to discuss thermoregulation and fluid-electrolyte regulation

during exercise.

V. My REFERENCES:

Guyton & Hall, Textbook of Medical Physiology (11th or earlier editions),

Chapter 84
Boron and Bolpaep, Medical Physiology (Chapt. 59)
Ganong’s Review of Medical Physiology (various chapters)
Berne and Levy 5th edition, (Chapter 12)
Rhoades and Tanner, Medical Physiology (Chapt. 32)
Biljani, Understanding Medical Physiology (Section 11, Chapter 11.8)
Bowers and Fox, Sports Physiology
McArdle et al, Exercise Physiology
Powers and Howley, Exercise Physiology
McNomas, Skeletal Muscle: Form and Function
Blooms and Fawcett, A Textbook of Histology

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