EXERCISE

PHYSIOLOGY
Muscle Metabolic Systems
Types of Exercise
Grading of Exercise
Phases of muscular exercise
Respiratory adaptations
EXERCISE
It is the period of enhanced energy expenditure by skeletal
muscles due to repetitive contraction & relaxation process of
skeletal muscles, which is met by many complex adjustments of
metabolism, respiration, circulation & temperature regulation.
ENERGY SOURCES AND METABOLISM
 Muscle Metabolic Systems in Exercise
1. Phosphocreatine – creatine system
2.

3.

4. Carbohydrate & lipid breakdown

- Aerobic gycolysis
- Anearobic glycolysis
IMMEDIATE
SOURCE OF
ENERGY:

PHOSPHORYL
CREATINE

ULTIMATE SOURCE
CARBOHYDRATE
(GLUCOSE & GLYCOGEN)
AND LIPIDS (FREE FATTY
ACIDS)
 Types of exercise
1) Dynamic exercise
Involves isotonic muscle
contraction
External work is done
Eg : walking, jumping, jogging

2) Static exercise
Involves isometric muscle
contraction
No external work is done
Eg: lifting a heavy weight,
pushing against a wall
 OXYGEN CONSUMPTION (VO2 max)
Maximum amount of O2 consumed by a person while performing severe
exercise
Normal O2 consumption during rest: 250 ml/min
VO2 max in Adult: 3L/min (15-20 times increase)
Product of max CO & max O2 extraction by tissues. Both increase with
athletic training.
In trained athlete it is 5L/min

Factors: Cardiac output

O2 extraction by tissues
Muscle mass
Significance: Physiological indicator of maximum aerobic work capacity
PHASES OF EXERCISE
 ADAPTATION PHASE
First 2 -5 min
O2 consumption increases linearly to its VO2max level
O2 consumption much less than its demands of the body-
O2 deficit
O2 deficit occurs at the beginning and continues throughout
the exercise
Energy supply above VO2max is filled by the anaerobic
pathway
 STEADY PHASE
Characterized by plateau state : VO2max is at its max and
steady state
Excess energy is met with by anaerobic pathway like
breakdown of Creatine phosphate and muscle glycogen
Lactate accumulate
pH decrease
Buffered by HCO3 - increased CO2 production and
hyperventilation.
Sharp rise in lactic acid levels which decreases blood pH –
more CO2 – Hyperventilation
 Recovery phase
Period after cessation of exercise during which extra amount
of O2 is consumed (O2 debt)

Degree of O2 debt is proportionate to O2 deficit

Oxygen debt- importance

To remove excess lactate
To replace the ATP & phosphoryl creatine store
To replace the oxygen that come from myoglobin
RESPIRATORY
RESPONSES
 Respiratory adaptations
Increase in pulmonary ventilation
Increase in O2 uptake in lungs
Changes at tissue level
Pulmonary ventilation
At rest, RR-12/min ; TV – 500ml ; Pul venti – 6L/min

During exercise,

RR – 40 to 45/min
TV increases from 10 -15% to 50% of VC ;
PV – increases 20 to 25 times
Ventilation increases abruptly at the beginning of exercise
followed by a brief pause & gradual increase to reach a steady
state as the exercise is continued

When exercise ceases, there is an abrupt decrease in ventilation

followed by a brief pause & a more gradual decline to pre exercise
values
 Cause for abrupt increase
i) Psychic stimuli from
higher centers to
respiratory muscles
ii) Afferent impulses from
proprioceptors in muscle,
tendons & joints
iii)

Cause for pause -

increased CO2 wash out
 Cause for gradual increase
i) Fluctuations in pO2
ii) Increase in chemoreceptor
sensitivity to pCO2
iii) Decrease in pH (Isocapnic
buffering)
iv) High K+ levels – peripheral
chemoreceptor stimulation
v) Increase in body temperature
 Vigorous exercise

Lactate accumulation

Buffering

Increase in CO2

Increases ventilation

CO2 wash out (arterial & alveolar CO2 changes little)

Isocapnic buffering
The stimulus to ventilation after exercise is not the

arterial Pco2, which is normal or low, or the arterial Po2,

which is normal or high, but the elevated arterial H+

concentration due to the lactic acidemia.

Increase in O2 uptake
From 250ml/min at rest to 4L/min in severe exercise.
Mechanisms:
1. Increased alveolar to arterial gradient of PO 2 : decreased
oxygen content of venous blood due to more
consumption.
2.

3. Increased perfusion of lungs: Increase pulmonary flow due

to increased cardiac output.
4.

5. Increased diffusion capacity of alveolo-capillary membrane:

Opening of capillaries, so increase Surface area
Amount of CO2 removed from each unit of blood is

increased.

CO2 excretion increases from 200mL/min to

8000mL/min.
Changes in the tissues
1.Increased blood flow to skeletal muscles-
Because the capillary bed of contracting
muscle is dilated and many previously
closed capillaries are open.
2.Increased pO2 gradient-More O2 diffuses from
the blood, the blood Po2 in the muscles
drops, and more O2 is removed from
hemoglobin
3.Right shift of ODC-

accumulation of CO2
rise in temperature in active tissues
rise in red blood cell 2,3diphosphoglycerate
(2,3-DPG)
 Fatigue
Subjective sensation of exhaustion.

Causes
(i) Bombardment of brain by neural impulses from muscle
(ii) Decline in blood pH by lactic acidosis.
(iii) Hypoglycemia
(iv) Depletion of muscle glycogen

Dyspnea & uncomfortable sensation are produced by activation

of receptors in lungs.
 Effects of training
Increase in VO2 max

Increase in pulmonary O2 diffusing capacity

Increase in maximal minute ventilation

Increases breaking point of lactate

Cardiovascular Adaptations
CARDIOVASCULAR RESPONSES
Increase in skeletal muscle blood flow
Systemic changes
Redistribution of blood flow in the body
Increase in cardiac output
Blood pressure changes
Changes in blood volume
 Skeletal muscle blood flow
At rest – 2 -4 ml/100g/min

During exercise – increase up to 25 times

( 50 – 80ml/100g/min)

Exercise hyperemia

arteriolar dilatation
opening up of capillaries
Mechanisms increasing blood flow
1. Neural mechanisms
Increases blood flow even before exercise begins
Impulses in sympathetic vasodilator system

2. Local mechanisms
Fall in pO2 , rise in pCO2
Accumulation of local metabolites
( K+ , H+ ,lactic acid)
Local rise in temperature
local vasodilation
( by 10 – 100 fold
in open capillaries)
Role of K+

Dilates arterioles in exercising muscles. In K+ depleted

individuals, muscle blood flow increases to lesser degree

greater tendency for severe disintegration of muscles (Exertional

Rhabdomyolysis )
Intermittent blood flow through calf muscle during rhythmic contraction
Redistribution of Blood Flow
Visceral Blood Flow:
Sympathetic discharge to visceral organs ( Alpha receptors)
causes vasoconstriction.
Decrease the flow
Divert blood flow to skeletal muscles
Kidney:
Decrease RBF by 50-80% in severe exercise.
Athletic Pseudonephritis
Prolonged & severe exercise
Decreased RBF- hypoxia- increased permeability to large
molecules resulting in proteinuria.
Splanchnic blood flow: Decrease by 80% in severe exercise.
Cutaneous Blood Flow: Adipose tissue blood flow:
Initial decrease- reflex Increase 4 times
vasoconstriction Lipolysis: Mobilize FA
Prolonged exercise- from TG stores to working
Increase due to muscles.
thermogenic vasodilation.
 Increase in Cardiac Output
At rest – 5L/min
Exercise – increase by 5 -6 times
CO = Heart rate x Stroke volume
Increase in Heart rate
Increase linearly with severity of exercise
Maximum heart rate – determined by age of the subject.
Anticipatory tachycardia
Reasons – increased sympathetic discharge
- decreased vagal tone
- hormonal mechanism
- thermogenic stimulation
Increase in stroke volume – increases twice the normal value
stroke volume during isometric (same) & isotonic
exercise ( increase)
Increased sympathetic discharge
Increased EDV
-Thoracic pump
-Muscle pump
 Blood Pressure changes
Isometric exercise – both SBP & DBP rises ( due to increased PR
as contracting muscle compresses blood vessels & thereby
diminish its blood flow )

Isotonic exercise – SBP increases

DBP decreases / unaltered

(Marked fall in PR due to extensive vasodilation )

 Changes in Blood Volume

Reduced by 15% - haemoconcentration

Reasons

(i) Increased hydrostatic pressure in capillaries

(ii) Increased tissue fluid osmotic pressure

SYSTEMIC CIRCULATORY CHANGES
Changes in trained Athletes
Cardiac hypertrophy ( by 40%)
Decrease in resting heart rate due to increase in vagal tone
Increase in stroke volume at rest due to increase in force
of contraction.
Cardiac output
Changes in skeletal muscles with training
Increases in the number of mitochondria and the enzymes
involved in oxidative metabolism.

Increase in the number of capillaries, with better

distribution of blood to the muscle fibers.

Less increase in lactate production.

Increase in blood flow to muscles is less and, because of

this, less increase in heart rate and cardiac output than in
an untrained individual. This is one of the reasons that
exercise is of benefit to patients with heart disease.
Endocrine responses to Exercise
ADH

ACTH &Cortisol

Catecholamines
 Therapeutic benefits of training
Slows down ageing
Reduces insulin sensitivity
Reduces sympathetic tone
Improves coronary perfusion
Reduces body fat mass
Psychological benefits
 Respiratory

CVS Endocrine
EXERCISE

Training