During exercise, there is a release of oxygen (O2) from the blood. This release is facilitated by the shift in the oxyhemoglobin dissociation curve. The high concentration of carbon dioxide (CO2) and the formation of lactic acid during exercise cause a decrease in tissue pH and an increase in muscle temperature. These factors shift the oxyhemoglobin dissociation curve to the right, resulting in less O2 being held by hemoglobin in red blood cells. As a result, more O2 is available for the tissues. Oxygen consumption can increase significantly during exercise, even with a relatively smaller increase in muscle blood flow. Myoglobin in the muscles can act as a limited O2 store and can also facilitate O2 transport from capillaries to mitochondria.

During exercise, the sympathetic drive is enhanced and parasympathetic inhibition of the sinoatrial node is reduced, leading to persistent tachycardia. If the workload is moderate and constant, the heart rate reaches a certain level and remains stable throughout the exercise. However, as the workload increases, the heart rate also increases until it reaches a plateau of around 180 beats per minute during strenuous exercise. In contrast to the significant increase in heart rate, the increase in stroke volume is relatively smaller, typically ranging from 10% to 35%. Well-trained distance runners can have stroke volume approximately twice the resting value, resulting in a cardiac output that is six to seven times higher than at rest.

The size of cardiac muscles is directly related to the amount of work imposed on them. During development and endurance exercise, cardiac growth occurs in relation to systolic blood pressure and the ratio of wall thickness to ventricular chamber radius. Relative wall thickness, measured using echocardiography, can help differentiate between physiological and pathological hypertrophy. In physiological hypertrophy, left ventricular mass and radius increase proportionately, without significant changes in relative wall thickness. Physiological hypertrophy is commonly observed in endurance athletes and pregnant women, where left ventricular enlargement occurs due to volume overload, maintaining a constant relative wall thickness. In physiological hypertrophy, arterial diameter increases, and capillary density increases proportionally to the degree of hypertrophy. Unlike pathological hypertrophy, physiological hypertrophy does not exhibit myocardial fibrosis or rearrangement of muscle fiber orientation.

The increase in cardiac output during exercise is primarily correlated with an increase in heart rate. In individuals with denervated baroreceptors, the cardiac output and heart rate responses to exercise are relatively small compared to those with normally innervated baroreceptors. However, even in cases of total cardiac denervation, exercise still increases cardiac output to a similar extent as in normal individuals, primarily through an elevated stroke volume. However, when dogs with denervated hearts are administered a β-adrenergic receptor antagonist, their exercise performance is impaired. This antagonist prevents the cardiac acceleration and enhanced contractility caused by increased levels of circulating catecholamines. Therefore, the maximal increase in cardiac output required for optimal exercise performance is limited.
Fig. 19.17 ). This release of O2 from blood is facilitated by the shift in the oxyhemoglobin dissociation curve during exercise. During exercise, the high concentration of CO2 and the formation of lactic acid cause a reduction in tissue pH. This decrease in pH, in addition to the increase in temperature in the contracting muscle, shifts the oxyhemoglobin dissociation curve to the right (see ). Therefore, at any given PO2, less O2 is held by the hemoglobin in the red blood cells, and consequently more O2 is available for the tissues. Oxygen consumption may increase as much as 60-fold, with only a 15-fold increase in muscle blood flow. Muscle myoglobin may serve as a limited O2 store during exercise, and it can release the attached O2 at very low partial pressures. However, myoglobin can also facilitate O2 transport from capillaries to mitochondria by serving as an O2 carrier.
Because the enhanced sympathetic drive and the reduced parasympathetic inhibition of the sinoatrial node continue during exercise, tachycardia persists. If the workload is moderate and constant, the heart rate reaches a certain level and remains there throughout the period of exercise. However, if the workload increases, the heart rate increases concomitantly until a plateau of approximately 180 beats per minute is reached during strenuous exercise. In contrast to the large increase in heart rate, the increase in stroke volume is only approximately 10% to 35%, the larger values occurring in trained individuals (see
Fig. 19.17 ). In well-trained distance runners, whose cardiac output can reach six to seven times the resting level, stroke volume attains approximately twice the resting value.
Cardiacmusclesize(growth)isdirectlyrelatedtotheamountofworkthatisimposeduponit.Duringdevelopmentandinenduranceexercise,cardiacgrowthisachievedataconstantrelationbetweensystolicbloodpressureandtheratioofwallthicknesstoventricularchamberradius.Anechocardiographicmeasurementusedtodistinguishphysiologicalfrompathologicalhypertrophyisrelativewallthickness(ratioofleftventricularwallthicknesstochamberradius).Inphysiologicalhypertrophy,leftventricularmassandradiusincreaseproportionatelysothatrelativewallthicknessdoesnotchangesignificantly.Examplesofphysiologicalhypertrophyoccurinenduranceathletesandinpregnantwomen,inwhomleftventricularenlargementoccurswithvolumeoverloadatconstantrelativewallthickness.Physiologicalhypertrophyisassociatedwithanincreasedarteriolardiameterinexperimentalanimals.Also,capillarydensityincreasesinproportiontothedegreeofhypertrophy.Thisisincontrasttothesituationinpathologicalhypertrophy,inwhichareductionofcapillarydensity(rarefaction)canoccur.Neithermyocardialfibrosisnorderangementofmusclefiberorientationisdetectedinphysiologicalhypertrophy,incontrasttothefindingsinpathologicalhypertrophy.
Thus the increase in cardiac output observed during exercise is correlated principally with an increase in heart rate. If the baroreceptors are denervated, the cardiac output and heart rate responses to exercise are small in comparison with those in individuals with normally innervated baroreceptors. However, with total cardiac denervation, exercise still increases cardiac output as much as it does in normal individuals. This increase in cardiac output is achieved chiefly by means of an elevated stroke volume. However, if a β-adrenergic receptor antagonist is given to dogs with denervated hearts, exercise performance is impaired. The β-adrenergic receptor antagonist prevents the cardiac acceleration and enhanced contractility caused by increased amounts of circulating catecholamines. Therefore, the increase in cardiac output necessary for maximal exercise performance is limited.