Write
concisely on the cardiopulmonary changes in man in response to exercise.
Outline:
·
Changes in oxygen and
carbon dioxide levels
·
Tissue blood flow
·
Nervous control
·
Circulatory response
·
Stimulation of
ventilation
Essay:
Exercise is associated with very extensive alterations in the circulatory
and respiratory systems to meet the increased oxygen demand for muscle
contraction. The amount of oxygen is increased by increased blood flow and
ventilation rate. At the same time, the amount of carbon dioxide produced
increases due to increased tissue respiration and this too must be removed.
There is an increase in blood flow and ventilation before the onset of
exercise and this is probably due to psychic stimuli (thought of exercise) and
afferent impulses from proprioceptors in muscles, tendons, and joints which
relay the information to the vasomotor center. The vasoconstrictor area is
strongly stimulated while the activity of the cardiac inhibitory center is
highly attentuated. The heart is stimulated greatly to increase heart rate and
increasing pumping strength as a result of sympathetic discharge and inhibition
of the tonic parasympathetic discharge leading to an increase in stroke volume.
Most of the arterioles of the peripheral circulation are strongly constricted
except the arterioles in the active muscles, which are vasodilated by both the
actions of epinephrine on b2
receptors and local vasodilators. Thus, the heart is stimulated to supply the
increased blood flow required by the muscles and blood flow through most
nonmuscular areas of the body, with the exception of the heart and brain, is
temporarily reduced. This also leads to a pressure difference between the two
regions with the net result of blood flowing to the skeletal muscles. At the
same time, it prevents pooling of blood in the veins and pulmonary circulation,
shifting these ‘reservoirs’ of blood to the muscles.
Local mechanisms maintaining a high blood flow in exercising muscle
include a fall in tissue PO2, a rise in tissue PCO2, and
accumulation of K+ and other vasodilator metabolites. Dilation of the
arterioles and precapillary sphincters causes a 10-100 fold increase in the
number of open capillaries. The average distance between the blood and the
active cells – and the distance oxygen and metabolic products must diffuse is
thus greatly decreased. The decreased pH and increased temperature shift the
dissociation curve for hemoglobin to the right, so that more oxygen is given up
by the blood. Increased concentration of 2,3-DPG in the red blood cells further
decrease the oxygen affinity of hemoglobin and facilitates the extraction of
oxygen by the tissues. The net result is an up to 3-fold increase in the
arteriovenous oxygen difference, and the transport of carbon dioxide out of the
tissue is enhanced too. All these changes combine to make it possible for the
oxygen consumption of skeletal muscle to increase 100-fold during exercise.
The increase in the extraction of oxygen from the blood in exercising
muscles decreases the amount of oxygen in venous blood going to the lungs in the
pulmonary arteries. Therefore, there is a greater alveolar-capillary PO2
gradient is increased and this enhances the diffusion of oxygen from the alveoli
into the blood. At the same time, blood flow per minute is increased from
5.5L/min to as much as 20-35L/min. In less than one second, blood flowing
through the pulmonary capillaries becomes oxygenated. The total amount of oxygen
entering the blood therefore increases from 250 mL/min to as much as 8000 mL/min.
There is an abrupt increase in ventilation with the onset of exercise,
followed after a brief pause by a further, more gradual increase. The abrupt
increase at the start of exercise is presumably due to psychic stimuli (thought
of exercise) and afferent impulses from proprioceptors in muscles, tendons, and
joints. The arterial pH, PCO2 and PO2 remain constant
during moderate exercise and therefore there may be other factors involved in
stimulating ventilation. Exercise increases plasma K+ level, which
increases the discharge rate in chemoreceptor afferents, thereby increasing
ventilation. In addition, it may be that the sensitivity of the respiratory
center to carbon dioxide is increased or that the respiratory fluctuations in
arterial PCO2 increase so that, even though the mean arterial PCO2
does not rise, it is carbon dioxide that is responsible for the increase in
ventilation. As ventilation is increased, alveolar PO2 is
increased, facilitating the diffusion of oxygen into pulmonary blood.
When exercise becomes more vigorous, buffering of the increased amounts
of lactic acid that are produced liberates more carbon dioxide, and this further
increases ventilation. With further accumulation of lactic acid, the increase in
ventilation outstrips carbon dioxide production and alveolar and arterial PCO2
falls. The decline in arterial PCO2 provides respiratory compensation
for the metabolic acidosis produced by the additional lactic acid. The
respiratory rate after exercise does not reach basal levels until the oxygen
debt is repaid. This may take as long as 90 minutes.