3. Pulmonary ventilation
At rest: 6L/min
During maximum exercise, it increases by 20-25times to approx., 100L/min.
Pulmonary ventilation increases in parallel with increase on O2 consumption during
exercise.
Increases in parallel with increase in CO2 output except during heavy exercise when PV
increases disproportionately due to anaerobiosis of the working muscles, which
contributes an extra drive to respiratory centre.
The cause of such drive is: H+ concentration in the blood & CO2 release as a
consequences of high blood lactate level.
Increase in PV during maximum exercise is always of a lesser extent than MVV.
It shows that respiration is not main limiting factor in muscular exercise.
4. Control of PV during exercise
Psychic stimuli: stimulation of respiratory centre by increased activity in the motor
cortex.
Afferent stimuli from proprioceptors: in moving muscle, tendon and joints to the
brain.
Stimulation of carotid bodies: secondary to changes in blood chemistry (decrease
in arterial pO2, decrease in pH, increase in arterial pCO2, increase serum K+). These
changes increase the sensitivity of respiratory centre to CO2.
Accumulation of lactic acid in blood
Increased body temperature.
Increase in plasma potassium level.
5. Pulmonary diffusion capacity for oxygen
At rest: Do2 – 20-30ml/min/mmHg
During maximum exercise, Do2 increases above 3times due to:
Increased blood perfusion around air sacs in the lungs.
Opening of more capillaries.
These causes increases surface area of contact between alveoli and pulmonary
capillaries.
6. Oxygen consumption
Resting Vo2= 250ml/min.
During heavy exercise may increase to 15-20times due to:
3times increase in A-V O2 difference.
5times increase in O2 delivery to the tissues due to:
Increase in CO
Marked increase in alveolar ventilation
Increase in capillary density
Increase in RBCs count due to splenic contraction.
Vo2 max. Depends on muscle mass and functional dimensions of O2 transporting
system.
Vo2 max. Of an individual determines the max. Aerobic work capacity. It is the best
physiological indicator of aerobic work capacity in individual.
7. Pulmonary factors impose no limitation to O2 transport, therefore capacity of the
heart to increase the cardiac output may be the factor most frequently considered
as the main limiting factor.
The ability of the active tissues to extract O2 delivered by CVS or peripheral factors
are other possible limiting factors.
Criteria for establishing thatVo2 max. Has been achieved:
O2 consumption reaches a plateau.
Achievement of maximum heart rate with age after adulthood.
Respiratory quotient increase more than 1.15.
Blood lactic acid increases more than 70-80mg/dl.
8. Physiological effect of physical training
Physical performance is inversely related to O2 deficit.
In rhythmic dynamic muscular work, regardless of the level of exercise, O2 consumption
increases during first 2-4 min. Of exercise(adaptation phase), then reaches a plateau
(steady state level).
Causes of O2 deficit:
It takes few seconds for the circulation to deliver the extra O2 required by the working
muscles,
Therefore, during this period, ATP is primarily produced by anaerobic mechanism I.e,
breakdown of creatine phosphate and muscle glycogen.
This O2 deficit is repaid after stoppage of exercise, in the form of O2 dept (recovery
phase).
This extra O2 is used to regenerate depleted stores of ATP and creatine phosphate, to
resupply O2 to myoglobin in muscles and to resupply dissolved O2 in tissue fluids and
blood
Physical training decreases O2deficit. This can be achieved by warm up and training.
9. This Photo by Unknown Author is licensed under CC BY-SA-NC
10. Warm up effects
Increase the blood flow and nutrients to working muscles.
Increases level of mitochondrial enzymes and energy stores causing lesser use of
anaerobic work.
Prevents heart damage during 1st few seconds of heavy exercise, otherwise there
will be inadequate blood flow to heart.
Prevents muscular or connective tissue injuries.
11. Physical training effects
Psychology improves with training causing decrease in psychic stimuli to VMC and
respiratory centers.
Optimal blood flow distribution occurs I.e; cardiorespiratory response reaches a
steady-state early.
Greater fats are used for energy, sparing glycogen. RQ decreases causing oxidation
of more fats. Therefore, increased fatty acids are mobilized from tissues stores into
blood.
12. Higher Vo2 max can be achieved by:
Increase in max. CO. This is seen secondary to increase in stroke volume. SV
increases as EDV increases by better VR to heart.
Increase A-V O2 difference because capillary density increases, in crease in number
and size of mitochondria and myoglobin stores increases.
Less increase in both SBP&DBP because arterioles are opened more completely in
non working organs, thus, peripheral resistance decreases.
Less increase in PV because of less accumulation of metabolites and lactic acid.
Therefore, less stimulation to respiratory centre.
More increase in diffusion capacity of lungs for oxygen because pulmonary
capillary density increases.