Venous return is facilitated not only by sympathetically mediated constriction of capacitance vessels in both active and inactive parts of the body but also by the supplementary pumping action of working skeletal muscles and respiratory muscles. The contracting muscles intermittently compress the veins that pass through them, causing blood to be pumped back towards the right atrium due to the orientation of venous valves. During exercise, the flow of venous blood to the heart is further assisted by deeper and more frequent respirations, which increase the pressure gradient between abdominal and thoracic veins. This leads to a more negative intrathoracic pressure.

Contrary to popular belief, blood reservoirs make minimal contributions to the overall circulating blood volume in humans. In fact, blood volume typically decreases slightly during exercise, as indicated by an increase in the hematocrit ratio. This reduction in blood volume is primarily due to external water loss through sweating and increased ventilation, as well as fluid movement into the contracting muscles. However, fluid loss is counteracted through various mechanisms. As interstitial fluid pressure rises, it opposes the heightened hydrostatic pressure in capillaries of the active muscle, resulting in a plateau in fluid loss from the vascular compartment into the contracting muscles. Additionally, fluid loss is partially offset by the movement of fluid from inactive muscle and splanchnic regions into the bloodstream. This occurs as hydrostatic pressure in the capillaries of these tissues decreases and plasma osmolarity increases due to the movement of osmotically active molecules from the contracting muscle into the blood. The kidneys also play a role in conserving body water by reducing urine formation.

The substantial volume of venous blood that returns to the heart is efficiently pumped through the lungs and out into the aorta, thereby maintaining a relatively constant pulmonary venous pressure. Consequently, the Frank-Starling mechanism, which involves a greater initial fiber length, does not account for the increased stroke volume observed during moderate exercise. However, radiographs of individuals at rest and during exercise reveal a decrease in heart size during exercise. In situations of maximal or near-maximal exercise, right atrial pressure and end-diastolic ventricular volume do increase, and the Frank-Starling mechanism contributes to the enhanced stroke volume observed during highly vigorous exercise.

During strenuous exercise, both the cardiac and vascular function curves undergo significant alterations, enabling a fourfold to fivefold increase in cardiac output. The operating point of the cardiovascular system shifts from point A to point B. The cardiac function curve during strenuous exercise is the result of increased heart rate, stroke volume, and contractility. Conversely, the vascular function curve reflects a considerable decrease in total peripheral resistance and an increase in mean circulatory pressure. These changes arise from increased venous constriction (tone) in the skeletal muscle "pump" and the respiratory "pump." At the new operating point (point B), cardiac output is more than quadrupled, while filling pressure experiences only a slight increase.

In active, healthy individuals who are untrained, the mechanisms described above typically lead to a fourfold to fivefold increase in cardiac output during intense exercise. This increase in cardiac output is the primary mechanism by which more oxygen is delivered to exercising muscles. The cardiac function curve during exercise demonstrates an elevation in stroke volume (up to approximately 1.5-fold) and heart rate (up to approximately 3-fold). The vascular function curve during dynamic exercise reveals a significant reduction in peripheral resistance (slope change) and an increase in mean circulatory filling pressure (intercept change). These alterations result from increased venous constriction in the skeletal muscle "pump" and the respiratory "pump." As a result of these systemic changes in vascular function, the cardiovascular system is able to operate at a new point (point B in the graphical analysis), where cardiac output is increased while filling pressure remains relatively unchanged. Without these alterations, even a strong and fast-beating heart would only produce a minimal increase in cardiac output.
In addition to the contribution made by sympathetically mediated constriction of the capacitance vessels in both exercising and nonexercising parts of the body, venous return is aided by the auxiliary pumping action of the working skeletal muscles and the muscles of respiration (see also ). The intermittently contracting muscles compress the veins that course through them. Because the venous valves are oriented toward the heart, the contracting muscle pumps blood back toward the right atrium (see ). In exercise, the flow of venous blood to the heart is also aided by the deeper and more frequent respirations that increase the pressure gradient between the abdominal and thoracic veins (intrathoracic pressure becomes more negative during exercise).
In humans, blood reservoirs do not contribute much to the circulating blood volume. In fact, blood volume is usually reduced slightly during exercise, as evidenced by a rise in the hematocrit ratio. This decrease in blood volume is caused by water loss externally through sweating and enhanced ventilation and by fluid movement into the contracting muscle. However, fluid loss is counteracted in several ways. Fluid loss from the vascular compartment into the contracting muscles eventually reaches a plateau as interstitial fluid pressure rises and opposes the increased hydrostatic pressure in capillaries of the active muscle. Fluid loss is partially offset by movement of fluid from the splanchnic regions and inactive muscle into the bloodstream. This influx of fluid results from (1) a decrease in hydrostatic pressure in the capillaries of these tissues and (2) an increase in plasma osmolarity because of movement of osmotically active molecules into blood from the contracting muscle. Reduction in urine formation by the kidneys also helps conserve body water.
The large volume of venous blood returning to the heart is so effectively pumped through the lungs and out into the aorta that Pv remains essentially constant. Thus the Frank-Starling mechanism of a greater initial fiber length does not account for the greater stroke volume in moderate exercise. Radiographs of individuals at rest and during exercise reveal a decrease in heart size during exercise. However, during maximal or near-maximal exercise, right atrial pressure and end-diastolic ventricular volume do increase, and the Frank-Starling mechanism contributes to the enhanced stroke volume in very vigorous exercise.
•Fig. 19.18 Cardiacandvascularfunctioncurvesaregreatlyalteredduringstrenuousexercise,whichallowscardiacoutputtoincreasefourfoldtofivefold.TheoperatingpointofthecardiovascularsystemmovesfrompointAtopointB.Thecardiacfunctioncurveduringstrenuousexerciseistheresultofincreasedheartrate,strokevolume,andcontractility.Thevascularfunctioncurvereflectsgreatlydecreasedtotalperipheralresistanceandincreasedmeancirculatorypressure.Atthenewoperatingpoint(pointB),cardiacoutputisincreasedmorethanfourfold,butfillingpressureisincreasedonlyslightly.
In an active, healthy (untrained) individual, the mechanisms previously described typically lead to a fourfold to fivefold increase in cardiac output during vigorous exercise (
Fig. 19.18 ). Increased cardiac output is the fundamental means by which more O2 is delivered to exercising muscles (see
Fig. 19.17 ). The cardiac function curve during exercise reflects increased stroke volume (up to ≈1.5-fold) and heart rate (up to ≈3-fold). The vascular function curve during dynamic exercise reflects a marked decrease in peripheral resistance (changed slope) and an increase in mean circulatory filling pressure (changed intercept), which result from increased venous constriction (tone) in the skeletal muscle “pump,” and the respiratory “pump.” In these conditions, the cardiovascular system is able to operate at a new point (point B in
Fig. 19.18 ), in which cardiac output is increased while filling pressure is little changed. The graphical analysis (see
Fig. 19.18 ) shows that without the systemic changes in vascular function, even a heart beating strongly and fast would be able to produce only a small increase in cardiac output.