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Respiratory adjustments to
exercise
Objectives
 Pulmonary ventilation
 Pulmonary diffusion capacity for oxygen(Do2)
 Oxygen consumption (Vo2)
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.
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.
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.
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.
 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.
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.
This Photo by Unknown Author is licensed under CC BY-SA-NC
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.
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.
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.
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respiratory adjustments during exercise.pptx

  • 2. Objectives  Pulmonary ventilation  Pulmonary diffusion capacity for oxygen(Do2)  Oxygen consumption (Vo2)
  • 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.