Post on 28-Mar-2015
1
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.
2
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.
Source: Guyton, Chapter 84.
1.3 – 1.6 MINUTES2.52. Glycogen-lactic
acid system
(Anaerobic )
Unlimited , as long
Nutrients last.
13. Oxidative
metabolism
(aerobic)
8 – 10 SECONDS41. Phosphagen system
(Phosphocreatine-ATP system;
anaerobic)
TimeRelative Rate of
maximum ATP
generation (M of
ATP / min)
Energy System
1.3 – 1.6 MINUTES2.52. Glycogen-lactic
acid system
(Anaerobic )
Unlimited , as long
Nutrients last.
13. Oxidative
metabolism
(aerobic)
8 – 10 SECONDS41. Phosphagen system
(Phosphocreatine-ATP system;
anaerobic)
TimeRelative Rate of
maximum ATP
generation (M of
ATP / min)
Energy System
3
B.4 Energy (Metabolic) System Utilitized for Different Types of Athletic Activities
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:
400 m swim
1 mile run
1.5 km run
2,000 m rowingFootball dashes
Cross country
skiing
boxingsoccerIce hockey
dashes
Diving
Jogging1,500 m skatingtennisBaseball home
run
Weight lifting
10,000 m skating200 meter swim100 meter swimbasketballJumping
Marathon run800 meter dash400 meter dash200 meter dash100 meter dash
Aerobic systemGlycogen-lactic acid and aerobic system
Glycogen-lactic acid mainly
Phosphagen & Glycogen-lactic acid
Phosphagen entirely
400 m swim
1 mile run
1.5 km run
2,000 m rowingFootball dashes
Cross country
skiing
boxingsoccerIce hockey
dashes
Diving
Jogging1,500 m skatingtennisBaseball home
run
Weight lifting
10,000 m skating200 meter swim100 meter swimbasketballJumping
Marathon run800 meter dash400 meter dash200 meter dash100 meter dash
Aerobic systemGlycogen-lactic acid and aerobic system
Glycogen-lactic acid mainly
Phosphagen & Glycogen-lactic acid
Phosphagen entirely
High Abundant Low Glycogen cont.
Fewer Higher High Mitochondria
Glycolytic Oxidative Oxidative Metabolism
White (low)
myoglobin) Red (myoglobin) Red (myoglobin) Color
Fatigable Resistant Resistant Fatigue
Type IIb Type IIa Type 1 Synonym
Fast Twitch Fast Twitch Slow Twitch
4
From Rhoades and Tanner:
-
HighModerateLowFatigue Resistance
LowModerateHighGlycogen content
HighHighLowMyoglobin content
HighHighLowNo. of Mitochondria
LowModerateHigh[Glycolytic Enzyme ]
Oxidative
Phosphorylation
Anaerobic
glycolysis/oxidative
phosphorylation
Anaerobic
glycolysis
ATP sources
LowHighHighATPase activity
Type I;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa;
Fast Twitch;
Fast Oxidative-
Glycolytic (Red)
Type IIb;
Fast Twitch;
Fast Glycolytic
(White)
Metabolic
Properties
HighModerateLowFatigue Resistance
LowModerateHighGlycogen content
HighHighLowMyoglobin content
HighHighLowNo. of Mitochondria
LowModerateHigh[Glycolytic Enzyme ]
Oxidative
Phosphorylation
Anaerobic
glycolysis/oxidative
phosphorylation
Anaerobic
glycolysis
ATP sources
LowHighHighATPase activity
Type I;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa;
Fast Twitch;
Fast Oxidative-
Glycolytic (Red)
Type IIb;
Fast Twitch;
Fast Glycolytic
(White)
Metabolic
Properties
85 m/sec
(smaller motor units)
100 m/sec
(bigger motor
units)
100 m/sec
(bigger motor units)
Motor Axon velocity
ModerateHighHighSarcoplasmic
Reticulum: Ca+
ATPase activity
(pump)
LowMediumHighForce Capability
SlowFastFastContraction Speed
Type I;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa;
Fast Twitch;
Fast Oxidative-
Glycolytic
(Red)
Type IIb;
Fast Twitch;
Fast Glycolytic
(White)
Mechanical
And Neural
Properties
85 m/sec
(smaller motor units)
100 m/sec
(bigger motor
units)
100 m/sec
(bigger motor units)
Motor Axon velocity
ModerateHighHighSarcoplasmic
Reticulum: Ca+
ATPase activity
(pump)
LowMediumHighForce Capability
SlowFastFastContraction Speed
Type I;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa;
Fast Twitch;
Fast Oxidative-
Glycolytic
(Red)
Type IIb;
Fast Twitch;
Fast Glycolytic
(White)
Mechanical
And Neural
Properties
ManyManyFewNo. of Capillaries
SmallModerateLargeFiber Diameter
Type I;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa;
Fast Twitch;
Fast Oxidative-
Glycolytic
(Red)
Type IIb;
Fast Twitch;
Fast Glycolytic
(White)
Structural
Properties
ManyManyFewNo. of Capillaries
SmallModerateLargeFiber Diameter
Type I;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa;
Fast Twitch;
Fast Oxidative-
Glycolytic
(Red)
Type IIb;
Fast Twitch;
Fast Glycolytic
(White)
Structural
Properties
SoleusIn mixed-fiber
muscles, ex.
vastus lateralis
Latissimus DorsiTypical
Example
Postural/ EnduranceMedium
Endurance
Rapid and Powerful
Movements
Functional Role
in Body
Type I ;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa ;
Fast Twitch;
Fast Oxidative-
Glycolytic
(Red)
Type IIb ;
Fast Twitch;
Fast Glycolytic
(White)
SoleusIn mixed-fiber
muscles, ex.
vastus lateralis
Latissimus DorsiTypical
Example
Postural/ EnduranceMedium
Endurance
Rapid and Powerful
Movements
Functional Role
in Body
Type I ;
Slow Twitch;
Slow Oxidative
(Red)
Type IIa ;
Fast Twitch;
Fast Oxidative-
Glycolytic
(Red)
Type IIb ;
Fast Twitch;
Fast Glycolytic
(White)
5
What type of muscle fibers favor: (a) Sprint-like activities?
(b) Endurance type of exercises ?
From Berne and Levy:
FIBER TYPE COMPOSITION IN AN (A) UNTRAINED,
(B) ENDURANCE-TRAINED AND (C) SPRINT-TRAINED ATHLETES (From Bijlani, 1995)
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 ?
0
10
20
30
40
50
60
70
80
Untrained
Control
Distance
Runner
Sprint
Runner
Slow Twitch Fibers
Fast Twitch Fibers%
45
%
55
%
80
%
20
%
25
%
75
%
0
10
20
30
40
50
60
70
80
Untrained
Control
Distance
Runner
Sprint
Runner
Slow Twitch Fibers
Fast Twitch Fibers
Slow Twitch Fibers
Fast Twitch Fibers%
45
%
55
%
80
%
20
%
25
%
75
%
LowHighExcitability
Very fastFastConduction velocity
LargesmallCell diameter
Type II Type ICharacteristics
LowHighExcitability
Very fastFastConduction velocity
LargesmallCell diameter
Type II Type ICharacteristics
Properties of Motor Nerve (alpha-motor neuron)
innervating Muscle Fiber Types
A. B. C.
6
D.1 What is the effect of Endurance or Strength training on fiber type composition and
muscular capabilities ? See Table below.
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
50 %50 %50 %50 %4. Fast-twitch fibers
(% by numbers)
408767675. Fast-twitch fibers,
average area (m2
x
102
)
0.60.81.30.86. Capillaries/ fiber
100771501007. Succinate
dehydrogenase
activity/ unit area (%
control)
60 %200 %100 %100 %3. Isometric Strength
(% Control)
300,000300,000300,000 300,0001. Total No.cells
61310102. Total Cross-
sectional Area
After 4
Months
Immobiliza
-tion
After
Strength
Training
After
Endurance
Training
SedentaryHuman Biceps
Brachii Muscle
50 %50 %50 %50 %4. Fast-twitch fibers
(% by numbers)
408767675. Fast-twitch fibers,
average area (m2
x
102
)
0.60.81.30.86. Capillaries/ fiber
100771501007. Succinate
dehydrogenase
activity/ unit area (%
control)
60 %200 %100 %100 %3. Isometric Strength
(% Control)
300,000300,000300,000 300,0001. Total No.cells
61310102. Total Cross-
sectional Area
After 4
Months
Immobiliza
-tion
After
Strength
Training
After
Endurance
Training
SedentaryHuman Biceps
Brachii Muscle
7
Combined direct effects of stretching (autocrine
or paracrine mechanisms) and induced endocrine stimuli during
prolonged training resulting in muscle hypertrophy.
Stretch
Release of soluble factor(s) from muscle
Fiber or extracellular matrix
Activation of 2nd messenger systems in fiber
Induction of immediate early ( IEG) genes
Transcription of muscle genes
Arachidonic acid, phospholipases, PKC, tyrosine kinase, etc.
MUSCLE FIBER HYPERTORPHY
MHC, MLC;
ACTIN, etc.
Blood
Plasmalemma
Cytosol Nucleus
Exercise
(endocrine)
[Hormone]
receptor2
nd
Messenger
systems
Exercise
(autocrine or
paracrine)
Exercise transduction pathway(s)
Translation
Posttranslation control
New phenotype
Exercise Response
Element
IEG
DNA
Transcription
coding
mRNA
A.
B.
8
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
Fatty acid cycle
enzymes and
Carnitine transferase
Mitochondria
number FFA utilization
Spares plasma
glucose for sprint
Activities; energy
reserves
Capillary
density
Slower blood
flow in muscle
Increased contact time for
gas exchange
Increased uptake
of FFA
9
RELATIONSHIP BETWEEN EXERCISE DURATION AND FUEL SOURCE:
Data below from highly-trained endurance athletes:
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:
Effects of Endurance training: Increased number of
mitochondria decreases lactate and H+ formation,
helping maintain blood pH
mitochondrial
uptake of
pyruvate and NADH
Mitochondria
number
Decreased
lactate and H+
ion formation
Decreased
fluctuations in
Blood pH
maintained.
FFA
oxidation and
Decreased
PFK activity
Decreased Pyruvate
formation
Increased ‘H’ form of
Lactate
dehydrogenase
Plasma glucose
Plasma FFA
Muscle glycogen
Muscle Triglycerides
Exercise time (hours)
%
Energy
Expenditure
0 1 3 420 1 3 42O
20
40
60
80
100
O
20
40
60
80
100
10
(Powers and Howley, p.56)
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)
(adapted from : Ganong, Review of Medical Physiology, Fig. 37-2., p. 686., 21st edition; also from:
McArdle (2001), p. 289: Exercise Physiology, 5th edition.)
IIII IIIIIIII
Ventilation
(L/min)
0
20
10
30
40
Rest Exercise Recovery
Time
Exercise Intensity ( % VO2 max)
%
Energy
Expenditure
From Fat
Or
Carbohydrates
0 20 80 10040O
20
40
60
80
100
O
20
40
60
80
100
60
% Fat
% Carbohydrate
11
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 CO2
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 PO2, 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.
12
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 O2 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.
More data below:
MinuteVentilation(L/min)
6
100
Rest Maximal
Exercise Intensity
13
A.2.2 Acute Responses: Pulmonary Blood Flow
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.
Pulmonary
Blood Flow (L/min)
0 5 10 15 20 25
0
5
10
15
25
20
Pulmonary
Blood Flow (L/min)
0 5 10 15 20 25
0
5
10
15
25
20
Mean Pulmonary Arterial Pressure (mm Hg)
Normal,
At rest
Normal,
At rest
Normal,
At rest
Exercise
Vascular
Resistance (mm Hg/ml/min)
15 17
Exercise
19 21
Normal,
At rest
0.0005
0.0010
0.0015
0.0020
Vascular
Resistance (mm Hg/ml/min)
15 17
Exercise
19 21
Normal,
At rest
0.0005
0.0010
0.0015
0.0020
From Rest to Exercise: Changes in Pulmonary
Ventilation
15 breaths/minRespiratory
Rate (f)
(breaths/min)
Minute
Ventilation
(V) (L/min)
Tidal Volume
(VT), (L)
0.5 Liters
7.5 L/min
Exercise**Rest*
15 breaths/minRespiratory
Rate (f)
(breaths/min)
Minute
Ventilation
(V) (L/min)
Tidal Volume
(VT), (L)
0.5 Liters
7.5 L/min
Exercise**Rest*
Ex: 70 kg man
3 – 3.5 liters3 – 3.5 liters
40 – 50
breaths/ minute
40 – 50
breaths/ minute
120 – 175 L/min120 – 175 L/min
**Apex region as well as basal region
receives Increased percentage of
total ventilation.
*Basal region of lungs receive more
Ventilation than apex, during quiet
Breathing.
14
A.2.3 Acute Responses: Changes in Pulmonary Diffusing Capacities from Rest to
Exercise Transitions
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 gas exhange across the alveolar-blood gas barrier, leading to increased O2 uptake and
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):
Is the increased oxygen diffusing capacity of athletes due to hereditary traits or a product of training ?
Recruitment &
Distention of
pulmonary
capillaries
Base of lungs
Apex of
lungs
Base of lungs
Apex of
lungs
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.
between two sides of the tissue.
0
10
20
30
40
50
60
70
80
ml/ min
Maximal exercise
Non-
athlete
Non-
Athlete,
Rest
Speed
skaters
Swimmers
Oarsmen
O2
diffusing capacity
0
10
20
30
40
50
60
70
80
ml/ min
Maximal exercise
Non-
athlete
Non-
Athlete,
Rest
Speed
skaters
Swimmers
Oarsmen
0
10
20
30
40
50
60
70
80
ml/ min
Maximal exercise
Non-
athlete
Non-
Athlete,
Rest
0
10
20
30
40
50
60
70
80
ml/ min
Maximal exercise
0
10
20
30
40
50
60
70
80
ml/ min
0
10
20
30
40
50
60
70
80
0
10
20
30
40
50
60
70
80
ml/ min
Maximal exercise
Non-
athlete
Non-
Athlete,
Rest
Speed
skaters
Swimmers
Oarsmen
O2
diffusing capacity
15
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).
16
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
this.]
25025010001000
500500600600
14001400
300300
11001100900900 750750750 7507507501200
0
1200
0
5000
10000
15000
20000
250002200022000
Muscles Heart Skin GIT Renal BrainMuscles Heart Skin GIT Renal Brain
RestRest ExerciseExercise
1. Preferential increased blood flow to
working Muscles, while blood flow to
resting muscles unchanged or reduced.
1. Preferential increased blood flow to
working Muscles, while blood flow to
resting muscles unchanged or reduced.
2. Also, coronary blood flow also
Increases in absolute amounts
During dynamic exercise
2. Also, coronary blood flow also
Increases in absolute amounts
During dynamic exercise
ml / m
in
17
Cardiac Output, mean Arterial Pressure, and
Systemic Vascular Resistance Changes with
Exercise
0
20
40
60
80
100
120
0
20
40
60
80
100
120
Cardiac
Output
(L/min)
Cardiac
Output
(L/min)
Mean Arterial
Pressure
(mm Hg)
Mean Arterial
Pressure
(mm Hg)
Systemic
vascular
Resistance
(mm Hg/min/L)
Systemic
vascular
Resistance
(mm Hg/min/L)
Rest
Heavy Dynamic
Exercise
Rest
Heavy Dynamic
Exercise
2424
6
93105105
15
44
WHY ?WHY ?
Effects of active muscle mass on mean
arterial pressure in exercise
Rest
+
1 Hand
+
1 Arm
+
2 Arms
+
1 Leg
+
2 Legs
MeanArterialPressure(mm Hg)
80
100
120
140
160Isometric Exercise
Dynamic
(Isokinetic)
Exercise
Muscle Mass Muscle Mass
Why ?
18
B. Cardiovascular Adaptations to 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 ?
0
20
40
60
80
100
120
140
160
180
Before Training After Training
Rest
Maximal
Exercise
0
20
40
60
80
100
120
Before Training After Training
Rest
Maximal
0
20
40
60
80
100
120
140
160
180
Before Training After Training
Rest
Maximal
Exercise
0
20
40
60
80
100
120
Before Training After Training
Rest
Maximal
H e a rt R a te (b p m ) S tro ke V o lu m e (m l)
0
5
10
15
20
25
Before Training After Training
Rest
Maximal
Exercise
Cardiac Output (L/min)
19
Source of figure above : Bowers and Fox (1991) , p. 255.
Compare cardiac dimensions between endurance and resistance-trained
athletes.
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)
Non-athleteEndurance
Athletes
Non-endurance
(Sprint) Athletes
Large,
Venous
return
PreloadPreload
AfterloadAfterload
“ECCENTRIC
HYPERTROPHY”“CONCENTRIC
HYPERTROPHY”
Volume (WHOLE HEART)
Sedentary = 800 ml25% Larger volumes
Comparative Average Cardiac Dimensions in College
Athletes, World Class Athletes and Normal Subjects
211348330283308302Left ventric.
Mass, g
10.313.513.010.910.710.9Septum, mm
10.313.813.710.810.611.3Left ventri.
wall, mm
-----6875113------116Stroke
Volume, ml
101122110154181160Left Ventr.
Volume, ml
4643-524848-595154Left Ventr.
Internl
dimens.
Normals
(N= 16)
Wold
Class
Shot
putters
(N= 4)
College
Wrestlers
(N = 12)
World
Class
Runners
(N = 10)
College
Swimmers
(N= 15)
College
Runners
(N = 15)
Dimension
211348330283308302Left ventric.
Mass, g
10.313.513.010.910.710.9Septum, mm
10.313.813.710.810.611.3Left ventri.
wall, mm
-----6875113------116Stroke
Volume, ml
101122110154181160Left Ventr.
Volume, ml
4643-524848-595154Left Ventr.
Internl
dimens.
Normals
(N= 16)
Wold
Class
Shot
putters
(N= 4)
College
Wrestlers
(N = 12)
World
Class
Runners
(N = 10)
College
Swimmers
(N= 15)
College
Runners
(N = 15)
Dimension
20
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