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