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Cardiac Output During Exercise: Contributions of the Cardiac, Circulatory, and Respiratory Systems

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Abstract

The sections in this article are:

1 Intrinsic Properties of the Heart
1.1 Heart Rate (Exercise Response)
1.2 Stroke Volume (Exercise Response)
1.3 Determinants of Stroke Volume
2 Coupling of the Heart and Peripheral Circulation
2.1 Coupling of Left Ventricle to Arterial System
2.2 Ventricular Filling Pressure
2.3 Relation Between Cardiac Output and Filling Pressure at Rest
2.4 Relation Between Cardiac Output and Right Atrial Pressure in Dynamic Exercise
3 Respiratory System
3.1 Effects of Exercise on Respiratory Mechanics
3.2 Systemic Venous Return
3.3 Right Ventricular Output
3.4 Pulmonary Venous Return
3.5 Left Ventricular Output
3.6 Implications of Ventilatory Stresses during Exercise
Figure 1. Figure 1.

Schematic representation of the relationship between the heart and the respiratory and circulatory systems. The systemic arterial and venous circulations and the pulmonary circulation are conceptualized as extra‐ and intrathoracic reservoirs, respectively. The heart is depicted as two pumps coupled in series. R, right; L, left; A, atrium; V, ventricle.

Reprinted with permission from Janicki, J. S., S. G. Shroff, and K. T. Weber. Influence of extracardiac forces on the cardiopulmonary unit. In: Ventricular/Vascular Coupling, edited by F. C. P. Yin. New York: Springer‐Verlag, 1986, p. 262–287
Figure 2. Figure 2.

Heart rate responses to graded exercise before and after orthotopic cardiac transplantation. As a result of cardiac denervation, the resting heart rate is elevated and the response to exercise, being dependent primarily on the level of circulating catecholamines, is delayed and blunted.

Reprinted with permission from Squires, R. W. Exercise training after cardiac transplantation. Med. Sci. Sports. Exerc. 23: 686–694, 1991
Figure 3. Figure 3.

Heart rate (HR), stroke volume (SV), and cardiac output (CO) responses to incremental treadmill exercise obtained in a normal, untrained individual. Increased heart rate is responsibile for 63% of the augmented cardiac output. Larger stroke volumes account for the remainder, primarily from rest to moderate levels of work. Oxygen uptake () indicates the level of work.

Reprinted with permission from Weber, K. T. Gas transport and the cardiopulmonary unit. In: Cardiopulmonary Exercise Testing: Physiologic Principles and Clinical Application, edited by K. T. Weber and J. S. Janicki. Philadelphia: W. B. Saunders Company, 1986, p. 15–33
Figure 4. Figure 4.

For a given end‐diastolic pressure (EDP), heart rate, and contractile state, stroke volume is seen to be an inverse linear function of ejection pressure. Such a linear relation is obtained regardless of the EDP (left panel) and contractility (right panel). Data were obtained in an isolated, ejecting, canine heart preparation where, with a balloon in the left ventricle and a pressure servocontrol apparatus, it was possible to control the amount of filling volume at the end of diastole and to maintain a constant level of pressure (i.e., ejection pressure) during ejection.

Reprinted with modifications and permission from Weber, K. T., J. S. Janicki, W. C. Hunter, S. Shroff, E. S. Pearlman, and A. P. Fishman. The contractile behavior of the heart and its functional coupling to the circulation. Prog. Cardiovasc. Dis. 24: 375–400, 1982
Figure 5. Figure 5.

A, Brachial artery cuff systolic, mean, and diastolic blood pressure responses to progressive upright bicycle exercise for three age groups. All three pressures continually increase with elevations in work load. For any level of work, there is a tendency for systolic and mean pressures to be lower in the youngest group.

Reprinted with permission from Gerstenblith, G., D. G. Renlund, and E. G. Lakatta. Cardiovascular response to exercise in younger and older men. Federation Proc 46: 1834–1839, 1987.) B, Diastolic and systolic blood pressure responses to isometric exercise at 40% of maximal voluntary contraction (MVC) in normal individuals of different ages. These pressures were measured by auscultation of the noncontracting arm. Both pressures increase at the same rate and there is a significant correlation between systolic pressure and age. (Reprinted with permission from Petrofsky, J. S., and A. R. Lind. Aging, isometric strength and endurance, and cardiovascular responses to static‐effort. J. Appl. Physiol. 38: 91–95, 1975
Figure 6. Figure 6.

Heart rate (upper panel) and end‐diastolic volume (lower panel) as a function of cardiac output for three age groups of normal individuals performing progressive, upright bicycle exercise. Typically, end‐diastolic volume increases and then declines in the 25‐ to 40‐year group, while in the 45‐ to 64‐year group it initially increases and then becomes invariant and in the 65‐ to 80‐year group it continually increases. The heart rate at which the response differences become apparent (i.e., 115 bpm) is similar in the three age groups.

Reprinted with permission from Rodeheffer, R. J., G. Gerstenblith, L. C. Becker, J. L. Fleg, M. L. Weisfeldt, and E. G. Lakatta. Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac‐dilatation and increased stroke volume compensate for a diminished heart rate. Circulation 69: 203–213, 1984
Figure 7. Figure 7.

Ventricular pressure–volume loops obtained in the isolated heart preparation at varying end‐diastolic volumes. With constant contractility, ejection pressure, and heart rate, end‐systolic volume remains invariant and the increase in stroke volume is equal to the amount by which EDV is raised.

Reprinted with permission from Suga, H., K. Sagawa, and A. A. Shoukas. Load independence of the instantaneous pressure–volume ratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio. Circ. Res. 32: 314–322, 1973
Figure 8. Figure 8.

The left ventricular end‐diastolic pressure–volume relation over the physiologic range of end‐diastolic pressure is typically nonlinear, with the ventricle becoming stiffer as it is dilated. A nonparallel shift to the left or right indicates that ventricular stiffness has increased or decreased, respectively.

Figure 9. Figure 9.

End‐diastolic pressure (EDP) – end‐diastolic volume (EDV) relations obtained at constant contractility, heart rate, and ejection pressure (EP) or the isovolumetric state (P0). As EP (mm Hg) is increased, the EDP‐EDV relation is shifted downward or to the right, with the lowest curve obtained with the ventricle contracting isovolumetrically. Thus, the ventricle becomes less stiff as ejection pressure is raised. Numbers next to open circle EDP‐EDV data points represent corresponding peak isovolumetric pressures (mm Hg).

Reprinted with permission from Janicki, J. S., K. T. Weber, and L. L. Hefner. Ejection pressure and the left ventricular pressure–volume relation. Am. J. Physiol. 232 (Heart Circ. Physiol. 1): H545–H552, 1977
Figure 10. Figure 10.

The left ventricular pressure (EDP) – volume (EDV) relation obtained at two different levels of right ventricular (RV) volume (VOL). As a result of ventricular interdependence, the EDP‐EDV relation is shifted to the right as RV VOL is increased from RV VOL 1 to RV VOL 2. As depicted in the inset, this is the result of the septum being shifted toward the left ventricle and the outward movement of the RV free wall stretching the common muscle fibers and pericardium that surround both ventricles and causing an inward pull of the LV free wall.

Figure 11. Figure 11.

Summary of three exercise hemodynamic responses (R1, R2, and R3) to progressive upright treadmill exercise observed in heart failure patients with similar degrees of impairment. PCW, pulmonary capillary wedge pressure; RAP, right atrial pressure. In responses R2 and R3, the fact that PCW and RAP continue to rise with a slope of 1 despite an invariant stroke volume indicates pericardial constraint to further exercise‐induced ventricular expansion.

Reprinted with permission from Janicki, J. S. Influence of the pericardium and ventricular interdependence on left ventricular diastolic and systolic function in patients with heart failure. Circulation 81: III‐15–III‐20, 1990
Figure 12. Figure 12.

Doppler measured left ventricular (LV) peak early (E) and peak atrial systole (A) filling flow velocity values as a function of age. As a consequence of the ventricle becoming stiffer with age, the magnitude of the E wave decreases and that of the A wave increases.

Reprinted with permission from Iwase, M., K. Nagata, H. Izawa, M. Yokota, S. Kamihara, H. Inagaki, and H. Saito. Age‐related changes in left and right ventricular filling velocity profiles and their relationship in normal subjects. (Am. Heart J. 126: 419–426, 1993
Figure 13. Figure 13.

Left ventricular pressure–volume loops obtained at different levels of afterload and the peak isovolumetric pressure–volume relation (solid line) obtained in the isolated heart are depicted. As can be seen, the end‐systolic pressure–volume points lie on or near the peak isovolumetric pressure–volume curve. The slope of the peak isovolumetric or end‐systolic pressure–volume relations is an index of contractility.

Reprinted with permission from Weber, K. T., J. S. Janicki, and L. L. Hefner. Left ventricular force‐length relations of isovolumic and ejecting contractions. Am. J. Physiol. 231: 337–343, 1976
Figure 14. Figure 14.

Influence of cardiac output on central venous pressure during rest and treadmill exercise. Cardiac output was changed by changing ventricular pacing rate in conscious dogs with a surgically produced atrioventricular (AV) blockade. A, Responses after autonomic blockade with hexamethonium. Autonomic blockade (dashed lines) shifts curves downward (presumably owing to loss of peripheral sympathetic tone) with no change in slope compared to control (solid lines). Exercise shifts curves upward and rightward to an equal extent with no change in slope despite blockade of autonomic function. B, Reflexes intact. Filled circles depict normal flow and pressure; these data collected during AV‐linked pacing (ventricles stimulated after each atrial depolarization). Open circles, Data collected during periods in which pacing rate was reduced below normal AV‐linked values. Graded exercise shifts curves upward and right‐ward with no change in slope.

Reprinted with permission from Sheriff, D. D., X. P. Zhou, A. M. Scher, and L. B. Rowell. Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs. Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H316–H322, 1993
Figure 15. Figure 15.

Schematic representation of flow‐dependent and flow‐independent effects on central venous pressure (CVP). Line A, Effect on CVP when changes in blood flow to compliant regions occur as when cardiac output (CO) is changed at rest. Line B, Lack of change in CVP when changes in CO are directed to a noncompliant region (e.g., to muscle). Muscle pump, Effect on CVP of blood volume mobilized by the muscle pump. Additional increments in CVP related to increments in work rate may be of autonomic origin. Lines C‐E, Effects on CVP when CO is changed during graded exercise; these changes in CVP are attributed to changes in blood flow to compliant regions.

Reprinted with permission from Sheriff, D. D., X. P. Zhou, A. M. Scher, and L. B. Rowell. Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs. Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H316–H322, 1993
Figure 16. Figure 16.

Hemodynamic responses to exercise and to reductions in cardiac output imposed during exercise. Cardiac output (CO) changed by changing ventricular pacing rate in conscious dogs with a surgically produced atrioventricular (AV) blockade. A, Reflexes intact. Central venous pressure (CVP) and CO increase rapidly at start of exercise (AV‐linked pacing). Graded reductions in CO imposed during exercise are accompanied by graded increases in CVP. Inset, Plot of CVP vs. CO from the four steady‐state levels of CO during exercise. B, Responses after autonomic blockade with hexamethonium. CVP rises rapidly at start of exercise and a reduction in CO imposed during exercise is accompanied by an increase in CVP.

Reprinted with permission from Sheriff, D. D., X. P. Zhou, A. M. Scher, and L. B. Rowell. Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs. Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H316–H322, 1993
Figure 17. Figure 17.

Influence of cardiac output on central venous pressure during rest (line A) and bicycle exercise (line B). Cardiac output (CO) changed by changing ventricular pacing rate (numerical data labels) in heart‐block patients (dashed lines).

Data from Bevegard et al. .] Central venous pressure (CVP) and CO rise normally from rest to exercise (arrow, subjects recumbent). Decreases in CO are accompanied by increases in CVP in rest and exercise. Also shown is response to bicycle exercise in patients with congenital absence of venous valves (line C). Lack of change in CVP when CO rises indicates that CVP is maintained without an effective muscle pump when the rise in CO is directed to noncompliant skeletal muscle (data averaged from exercise in supine and sitting postures). [Data from Bevegard and Lodin
Figure 18. Figure 18.

Hemodynamic response to treadmill exercise when cardiac output is held constant at pre‐exercise level by ventricular pacing in a dog with a surgically produced atrioventricular block. Data collected while autonomic reflexes were blocked with hexamethonium. See text for interpretation of changes induced by exercise.

Reprinted with permission from Sheriff, D. D., L. B. Rowell, and A. M. Scher. Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump? Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H1227–H1234, 1993
Figure 19. Figure 19.

Model prediction of relationship between cardiac output and right atrial pressure during rest and exercise. Exercise is predicted to decrease the slope of the relationship between these two variables.

Adapted from Green and Jackman
Figure 20. Figure 20.

Influence of exercise intensity and of changes in cardiac output (CO) on the estimated fraction of cardiac output directed to active muscle (MBF/CO). Cardiac output was changed by changing ventricular pacing rate at rest and during 0% grade treadmill exercise in conscious dogs with a surgically produced atrioventricular block. A, MBF/CO rises with increasing exercise intensity. Direction of change in MBF/CO in response to a reduction in CO (arrows) depends on exercise intensity (e.g., MBF/CO falls when CO is reduced at rest but rises when CO is reduced during 4 mph exercise). B, Schematic illustration of potential effects of changes in cardiac output distribution on cardiac filling pressure. Changes in CO distribution (MBF/CO) change the slope of the relationship predicted between CO and filling pressure in (dashed lines A, B, C, and D). “Curve jumping” from line B to line A when CO is reduced at rest lowers the slope (circles), whereas “curve jumping” from line C to line D when CO is reduced during exercise increases the slope (squares). These directionally opposite changes in the distribution of cardiac output tend to equalize the slope of the curves relating CO to filling pressure measured in rest and exercise (solid lines). Arrow shows effect on filling pressure of diverting flow from a compliant to a noncompliant region when cardiac output does not change.

Adapted with permission from Sheriff, D. D., and X. P. Zhou. Influence of cardiac output distribution on cardiac filling pressure during rest and dynamic exercise in dogs. Am. J. Physiol. 267 (Heart Circ. Physiol. 36) H2378–2380, 1999
Figure 21. Figure 21.

Representation of pooled experimental data on the change in pulmonary vascular resistance with lung inflation in normal lungs. It is evident that pulmonary vascular resistance is minimal at point A, which corresponds to functional residual capacity. From that point, with either decreasing or increasing lung inflation, pulmonary vascular resistance increases.

Reprinted with permission from Nunn, J. F. Applied Respiratory Physiology London: Butterworth's 1977, p. 259
Figure 22. Figure 22.

Two consecutive respiratory cycles during partial inspiratory airway obstruction in an anesthetized dog postvagotomy. Vertical dashed lines indicate the two periods during which esophageal pressure (Pes) is reduced during inspiration. Both integrated mitral () and ascending aortic () flows diminish during inspiration and increase with expiration. There is a large expiratory increase in mitral flow preceding the large increase in aortic flow in both respiratory cycles. Although the rapid increase in esophageal pressure occurs during systole in the second breath, there is little effect on aortic flow. These two respiratory cycles demonstrate the dominance of mitral flow leading aortic flow during partial inspiratory obstruction. Pes, esophageal pressure; Pao, aortic pressure; Pla, left atrial pressure; Ppa, pulmonary artery pressure; Plv, left ventricular pressure.

Reprinted with permission from Robotham, J. L., R. S. Stuart, K. Doherty, M. A. Borkon, and W. Baumgartner. Mitral and aortic flows during spontaneous respiration in dogs. Anesthesiology 69: 516–526, 1988
Figure 23. Figure 23.

Diastolic phrenic nerve stimulation producing a transient decrease in esophageal pressure (PESO) confined to diastole in an acutely instrumented anesthetized dog during phrenic nerve stimulation. Steady‐state mitral () and ascending aortic () flows are observed prior to the transient fall in intrathoracic pressure. There is an immediate substantial decrease in peak and total mitral flow indicated by a vertical arrow pointing down. The subsequent LV stroke volume is similarly reduced at a time when intrathoracic pressure has returned to its baseline value such that there could be no effect on LV ejection. The subsequent mitral flow and LV stroke volume demonstrates compensatory increases. Of critical importance, LV end‐diastolic pressure (PLV), left atrial pressure (PLA) (at upward pointed vertical arrow), and right atrial pressure (PRA) are all increased relative to atmospheric pressure at end‐diastole when esophageal pressure has returned to baseline values. Since LV inflow has diminished, LV end‐diastolic volume is reduced and its pressure increased; thus, LV effective compliance must be reduced. The increase in right atrial pressure and pattern of change of mitral flow are consistent with ventricular interdependence being responsible for the reduction in LV preload. PAO, aortic pressure.

Reprinted with permission from Robotham, J. L., and J. Peters. Cardiorespiratory interactions. In: Adult Respiratory Distress Syndrome, edited by W. Zapol. New York: Marcel Dekker, Inc., 1991, p. 223–251
Figure 24. Figure 24.

Original recording with negative intrathoracic pressure confined to systole and the airway unobstructed, allowing lung volume to increase during phrenic nerve stimulation. The decrease in esophageal pressure (Peso) begins during isovolumic contraction (i.e., after diastolic mitral flow () has stopped) and is associated with a fall in ascending aortic flow () and LV stroke volume (integrated () indicated by the downward pointing arrow. An unchanged LV preload before the systolic negative intrathoracic pressure is indicated by constant (, end‐diastolic left ventricular (Plv) and atrial (Pla) pressures in the immediately preceding beats. In the diastolic period following the systolic fall in intrathoracic pressure, mitral inflow is decreased as indicated by the downward pointing arrow consistent with the increased end‐systolic volume. Thus, a fall in intrathoracic pressure during systole alone is sufficient to decrease LV stroke volume. PAO, aortic pressure; PRA, right artrial pressure.

Reprinted with permission from Peters, J., C. Fraser, R. S. Stuart, W. Baumgartner, and J. L. Robotham. Negative intrathoracic pressure decreases independently left ventricular filling and emptying. Am. J. Physiol. 257 (Heart Circ. Physiol. 26): H120–H131, 1989
Figure 25. Figure 25.

Recording with early systolic phrenic nerve stimulation (PNS) and the airway obstructed to keep lung volume constant in an anesthetized dog. The decrease of esophageal pressure (Peso) causes an increase in the systolic anteroposterior intrathoracic aortic diameter [DAo(AP)], indicated by the horizontal arrow, but a fall in left ventricular stroke volume derived from the ascending aortic blood flow (QAa), indicated by the lower horizontal arrow. Both systolic left ventricular (Plv) and aortic pressures (PAo) fall relative to atmospheric pressure. Neither the LV end‐diastolic pressure (recorded with a fluid‐filled catheter) immediately before phrenic nerve stimulation nor the R‐R interval change compared with the preceding cardiac cycle. Congruent with the increase in systolic DAo(AP), right‐to‐left aortic diameter [DAo(RL)] also increases. The decrease in LV stroke volume associated with increased DAo is compatible with an increased LV afterload. The same qualitative changes are observed when lung volume is allowed to increase with the fall in esophageal pressure, such that a decrease of intrathoracic pressure alone, with or without a change in lung volume, is sufficient to explain the fall in (QAa) and LV stroke volume and the increase in DAo.

Reprinted with permission from Peters, J., M. K. Kindred, and J. L. Robotham. Transient analysis of cardiopulmonary interactions. II. Systolic events. J. Appl. Physiol. 64: 1518–1526, 1988
Figure 26. Figure 26.

Tracings recorded in one dog during an increase in abdominal pressure (Pab) followed by maintenance of a quasisteady state and the acute release of abdominal compression. There were no arrhythmias in the ECG. Mean flow in both the ascending aorta () and descending aorta () decreased while flow in the innominate artery () increased. Airway pressure (PAW) measured at the trachea demonstrated a small peak inspiratory increase during abdominal compression. The expiratory airway pressure reflected transmission of 2 cm H2O of positive end‐expiratory pressure. The aortic pressure (PAO) and left atrial pressure (PLA) both increased as Pab increased.

Reprinted with permission from: Robotham, J. L., R. A. Wise, and B. Bromberger‐Barnea. Effects of changes in abdominal pressure on left ventricular performance and regional blood flow. Crit. Care Med. 13: 803–809, 1985


Figure 1.

Schematic representation of the relationship between the heart and the respiratory and circulatory systems. The systemic arterial and venous circulations and the pulmonary circulation are conceptualized as extra‐ and intrathoracic reservoirs, respectively. The heart is depicted as two pumps coupled in series. R, right; L, left; A, atrium; V, ventricle.

Reprinted with permission from Janicki, J. S., S. G. Shroff, and K. T. Weber. Influence of extracardiac forces on the cardiopulmonary unit. In: Ventricular/Vascular Coupling, edited by F. C. P. Yin. New York: Springer‐Verlag, 1986, p. 262–287


Figure 2.

Heart rate responses to graded exercise before and after orthotopic cardiac transplantation. As a result of cardiac denervation, the resting heart rate is elevated and the response to exercise, being dependent primarily on the level of circulating catecholamines, is delayed and blunted.

Reprinted with permission from Squires, R. W. Exercise training after cardiac transplantation. Med. Sci. Sports. Exerc. 23: 686–694, 1991


Figure 3.

Heart rate (HR), stroke volume (SV), and cardiac output (CO) responses to incremental treadmill exercise obtained in a normal, untrained individual. Increased heart rate is responsibile for 63% of the augmented cardiac output. Larger stroke volumes account for the remainder, primarily from rest to moderate levels of work. Oxygen uptake () indicates the level of work.

Reprinted with permission from Weber, K. T. Gas transport and the cardiopulmonary unit. In: Cardiopulmonary Exercise Testing: Physiologic Principles and Clinical Application, edited by K. T. Weber and J. S. Janicki. Philadelphia: W. B. Saunders Company, 1986, p. 15–33


Figure 4.

For a given end‐diastolic pressure (EDP), heart rate, and contractile state, stroke volume is seen to be an inverse linear function of ejection pressure. Such a linear relation is obtained regardless of the EDP (left panel) and contractility (right panel). Data were obtained in an isolated, ejecting, canine heart preparation where, with a balloon in the left ventricle and a pressure servocontrol apparatus, it was possible to control the amount of filling volume at the end of diastole and to maintain a constant level of pressure (i.e., ejection pressure) during ejection.

Reprinted with modifications and permission from Weber, K. T., J. S. Janicki, W. C. Hunter, S. Shroff, E. S. Pearlman, and A. P. Fishman. The contractile behavior of the heart and its functional coupling to the circulation. Prog. Cardiovasc. Dis. 24: 375–400, 1982


Figure 5.

A, Brachial artery cuff systolic, mean, and diastolic blood pressure responses to progressive upright bicycle exercise for three age groups. All three pressures continually increase with elevations in work load. For any level of work, there is a tendency for systolic and mean pressures to be lower in the youngest group.

Reprinted with permission from Gerstenblith, G., D. G. Renlund, and E. G. Lakatta. Cardiovascular response to exercise in younger and older men. Federation Proc 46: 1834–1839, 1987.) B, Diastolic and systolic blood pressure responses to isometric exercise at 40% of maximal voluntary contraction (MVC) in normal individuals of different ages. These pressures were measured by auscultation of the noncontracting arm. Both pressures increase at the same rate and there is a significant correlation between systolic pressure and age. (Reprinted with permission from Petrofsky, J. S., and A. R. Lind. Aging, isometric strength and endurance, and cardiovascular responses to static‐effort. J. Appl. Physiol. 38: 91–95, 1975


Figure 6.

Heart rate (upper panel) and end‐diastolic volume (lower panel) as a function of cardiac output for three age groups of normal individuals performing progressive, upright bicycle exercise. Typically, end‐diastolic volume increases and then declines in the 25‐ to 40‐year group, while in the 45‐ to 64‐year group it initially increases and then becomes invariant and in the 65‐ to 80‐year group it continually increases. The heart rate at which the response differences become apparent (i.e., 115 bpm) is similar in the three age groups.

Reprinted with permission from Rodeheffer, R. J., G. Gerstenblith, L. C. Becker, J. L. Fleg, M. L. Weisfeldt, and E. G. Lakatta. Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac‐dilatation and increased stroke volume compensate for a diminished heart rate. Circulation 69: 203–213, 1984


Figure 7.

Ventricular pressure–volume loops obtained in the isolated heart preparation at varying end‐diastolic volumes. With constant contractility, ejection pressure, and heart rate, end‐systolic volume remains invariant and the increase in stroke volume is equal to the amount by which EDV is raised.

Reprinted with permission from Suga, H., K. Sagawa, and A. A. Shoukas. Load independence of the instantaneous pressure–volume ratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio. Circ. Res. 32: 314–322, 1973


Figure 8.

The left ventricular end‐diastolic pressure–volume relation over the physiologic range of end‐diastolic pressure is typically nonlinear, with the ventricle becoming stiffer as it is dilated. A nonparallel shift to the left or right indicates that ventricular stiffness has increased or decreased, respectively.



Figure 9.

End‐diastolic pressure (EDP) – end‐diastolic volume (EDV) relations obtained at constant contractility, heart rate, and ejection pressure (EP) or the isovolumetric state (P0). As EP (mm Hg) is increased, the EDP‐EDV relation is shifted downward or to the right, with the lowest curve obtained with the ventricle contracting isovolumetrically. Thus, the ventricle becomes less stiff as ejection pressure is raised. Numbers next to open circle EDP‐EDV data points represent corresponding peak isovolumetric pressures (mm Hg).

Reprinted with permission from Janicki, J. S., K. T. Weber, and L. L. Hefner. Ejection pressure and the left ventricular pressure–volume relation. Am. J. Physiol. 232 (Heart Circ. Physiol. 1): H545–H552, 1977


Figure 10.

The left ventricular pressure (EDP) – volume (EDV) relation obtained at two different levels of right ventricular (RV) volume (VOL). As a result of ventricular interdependence, the EDP‐EDV relation is shifted to the right as RV VOL is increased from RV VOL 1 to RV VOL 2. As depicted in the inset, this is the result of the septum being shifted toward the left ventricle and the outward movement of the RV free wall stretching the common muscle fibers and pericardium that surround both ventricles and causing an inward pull of the LV free wall.



Figure 11.

Summary of three exercise hemodynamic responses (R1, R2, and R3) to progressive upright treadmill exercise observed in heart failure patients with similar degrees of impairment. PCW, pulmonary capillary wedge pressure; RAP, right atrial pressure. In responses R2 and R3, the fact that PCW and RAP continue to rise with a slope of 1 despite an invariant stroke volume indicates pericardial constraint to further exercise‐induced ventricular expansion.

Reprinted with permission from Janicki, J. S. Influence of the pericardium and ventricular interdependence on left ventricular diastolic and systolic function in patients with heart failure. Circulation 81: III‐15–III‐20, 1990


Figure 12.

Doppler measured left ventricular (LV) peak early (E) and peak atrial systole (A) filling flow velocity values as a function of age. As a consequence of the ventricle becoming stiffer with age, the magnitude of the E wave decreases and that of the A wave increases.

Reprinted with permission from Iwase, M., K. Nagata, H. Izawa, M. Yokota, S. Kamihara, H. Inagaki, and H. Saito. Age‐related changes in left and right ventricular filling velocity profiles and their relationship in normal subjects. (Am. Heart J. 126: 419–426, 1993


Figure 13.

Left ventricular pressure–volume loops obtained at different levels of afterload and the peak isovolumetric pressure–volume relation (solid line) obtained in the isolated heart are depicted. As can be seen, the end‐systolic pressure–volume points lie on or near the peak isovolumetric pressure–volume curve. The slope of the peak isovolumetric or end‐systolic pressure–volume relations is an index of contractility.

Reprinted with permission from Weber, K. T., J. S. Janicki, and L. L. Hefner. Left ventricular force‐length relations of isovolumic and ejecting contractions. Am. J. Physiol. 231: 337–343, 1976


Figure 14.

Influence of cardiac output on central venous pressure during rest and treadmill exercise. Cardiac output was changed by changing ventricular pacing rate in conscious dogs with a surgically produced atrioventricular (AV) blockade. A, Responses after autonomic blockade with hexamethonium. Autonomic blockade (dashed lines) shifts curves downward (presumably owing to loss of peripheral sympathetic tone) with no change in slope compared to control (solid lines). Exercise shifts curves upward and rightward to an equal extent with no change in slope despite blockade of autonomic function. B, Reflexes intact. Filled circles depict normal flow and pressure; these data collected during AV‐linked pacing (ventricles stimulated after each atrial depolarization). Open circles, Data collected during periods in which pacing rate was reduced below normal AV‐linked values. Graded exercise shifts curves upward and right‐ward with no change in slope.

Reprinted with permission from Sheriff, D. D., X. P. Zhou, A. M. Scher, and L. B. Rowell. Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs. Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H316–H322, 1993


Figure 15.

Schematic representation of flow‐dependent and flow‐independent effects on central venous pressure (CVP). Line A, Effect on CVP when changes in blood flow to compliant regions occur as when cardiac output (CO) is changed at rest. Line B, Lack of change in CVP when changes in CO are directed to a noncompliant region (e.g., to muscle). Muscle pump, Effect on CVP of blood volume mobilized by the muscle pump. Additional increments in CVP related to increments in work rate may be of autonomic origin. Lines C‐E, Effects on CVP when CO is changed during graded exercise; these changes in CVP are attributed to changes in blood flow to compliant regions.

Reprinted with permission from Sheriff, D. D., X. P. Zhou, A. M. Scher, and L. B. Rowell. Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs. Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H316–H322, 1993


Figure 16.

Hemodynamic responses to exercise and to reductions in cardiac output imposed during exercise. Cardiac output (CO) changed by changing ventricular pacing rate in conscious dogs with a surgically produced atrioventricular (AV) blockade. A, Reflexes intact. Central venous pressure (CVP) and CO increase rapidly at start of exercise (AV‐linked pacing). Graded reductions in CO imposed during exercise are accompanied by graded increases in CVP. Inset, Plot of CVP vs. CO from the four steady‐state levels of CO during exercise. B, Responses after autonomic blockade with hexamethonium. CVP rises rapidly at start of exercise and a reduction in CO imposed during exercise is accompanied by an increase in CVP.

Reprinted with permission from Sheriff, D. D., X. P. Zhou, A. M. Scher, and L. B. Rowell. Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs. Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H316–H322, 1993


Figure 17.

Influence of cardiac output on central venous pressure during rest (line A) and bicycle exercise (line B). Cardiac output (CO) changed by changing ventricular pacing rate (numerical data labels) in heart‐block patients (dashed lines).

Data from Bevegard et al. .] Central venous pressure (CVP) and CO rise normally from rest to exercise (arrow, subjects recumbent). Decreases in CO are accompanied by increases in CVP in rest and exercise. Also shown is response to bicycle exercise in patients with congenital absence of venous valves (line C). Lack of change in CVP when CO rises indicates that CVP is maintained without an effective muscle pump when the rise in CO is directed to noncompliant skeletal muscle (data averaged from exercise in supine and sitting postures). [Data from Bevegard and Lodin


Figure 18.

Hemodynamic response to treadmill exercise when cardiac output is held constant at pre‐exercise level by ventricular pacing in a dog with a surgically produced atrioventricular block. Data collected while autonomic reflexes were blocked with hexamethonium. See text for interpretation of changes induced by exercise.

Reprinted with permission from Sheriff, D. D., L. B. Rowell, and A. M. Scher. Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump? Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H1227–H1234, 1993


Figure 19.

Model prediction of relationship between cardiac output and right atrial pressure during rest and exercise. Exercise is predicted to decrease the slope of the relationship between these two variables.

Adapted from Green and Jackman


Figure 20.

Influence of exercise intensity and of changes in cardiac output (CO) on the estimated fraction of cardiac output directed to active muscle (MBF/CO). Cardiac output was changed by changing ventricular pacing rate at rest and during 0% grade treadmill exercise in conscious dogs with a surgically produced atrioventricular block. A, MBF/CO rises with increasing exercise intensity. Direction of change in MBF/CO in response to a reduction in CO (arrows) depends on exercise intensity (e.g., MBF/CO falls when CO is reduced at rest but rises when CO is reduced during 4 mph exercise). B, Schematic illustration of potential effects of changes in cardiac output distribution on cardiac filling pressure. Changes in CO distribution (MBF/CO) change the slope of the relationship predicted between CO and filling pressure in (dashed lines A, B, C, and D). “Curve jumping” from line B to line A when CO is reduced at rest lowers the slope (circles), whereas “curve jumping” from line C to line D when CO is reduced during exercise increases the slope (squares). These directionally opposite changes in the distribution of cardiac output tend to equalize the slope of the curves relating CO to filling pressure measured in rest and exercise (solid lines). Arrow shows effect on filling pressure of diverting flow from a compliant to a noncompliant region when cardiac output does not change.

Adapted with permission from Sheriff, D. D., and X. P. Zhou. Influence of cardiac output distribution on cardiac filling pressure during rest and dynamic exercise in dogs. Am. J. Physiol. 267 (Heart Circ. Physiol. 36) H2378–2380, 1999


Figure 21.

Representation of pooled experimental data on the change in pulmonary vascular resistance with lung inflation in normal lungs. It is evident that pulmonary vascular resistance is minimal at point A, which corresponds to functional residual capacity. From that point, with either decreasing or increasing lung inflation, pulmonary vascular resistance increases.

Reprinted with permission from Nunn, J. F. Applied Respiratory Physiology London: Butterworth's 1977, p. 259


Figure 22.

Two consecutive respiratory cycles during partial inspiratory airway obstruction in an anesthetized dog postvagotomy. Vertical dashed lines indicate the two periods during which esophageal pressure (Pes) is reduced during inspiration. Both integrated mitral () and ascending aortic () flows diminish during inspiration and increase with expiration. There is a large expiratory increase in mitral flow preceding the large increase in aortic flow in both respiratory cycles. Although the rapid increase in esophageal pressure occurs during systole in the second breath, there is little effect on aortic flow. These two respiratory cycles demonstrate the dominance of mitral flow leading aortic flow during partial inspiratory obstruction. Pes, esophageal pressure; Pao, aortic pressure; Pla, left atrial pressure; Ppa, pulmonary artery pressure; Plv, left ventricular pressure.

Reprinted with permission from Robotham, J. L., R. S. Stuart, K. Doherty, M. A. Borkon, and W. Baumgartner. Mitral and aortic flows during spontaneous respiration in dogs. Anesthesiology 69: 516–526, 1988


Figure 23.

Diastolic phrenic nerve stimulation producing a transient decrease in esophageal pressure (PESO) confined to diastole in an acutely instrumented anesthetized dog during phrenic nerve stimulation. Steady‐state mitral () and ascending aortic () flows are observed prior to the transient fall in intrathoracic pressure. There is an immediate substantial decrease in peak and total mitral flow indicated by a vertical arrow pointing down. The subsequent LV stroke volume is similarly reduced at a time when intrathoracic pressure has returned to its baseline value such that there could be no effect on LV ejection. The subsequent mitral flow and LV stroke volume demonstrates compensatory increases. Of critical importance, LV end‐diastolic pressure (PLV), left atrial pressure (PLA) (at upward pointed vertical arrow), and right atrial pressure (PRA) are all increased relative to atmospheric pressure at end‐diastole when esophageal pressure has returned to baseline values. Since LV inflow has diminished, LV end‐diastolic volume is reduced and its pressure increased; thus, LV effective compliance must be reduced. The increase in right atrial pressure and pattern of change of mitral flow are consistent with ventricular interdependence being responsible for the reduction in LV preload. PAO, aortic pressure.

Reprinted with permission from Robotham, J. L., and J. Peters. Cardiorespiratory interactions. In: Adult Respiratory Distress Syndrome, edited by W. Zapol. New York: Marcel Dekker, Inc., 1991, p. 223–251


Figure 24.

Original recording with negative intrathoracic pressure confined to systole and the airway unobstructed, allowing lung volume to increase during phrenic nerve stimulation. The decrease in esophageal pressure (Peso) begins during isovolumic contraction (i.e., after diastolic mitral flow () has stopped) and is associated with a fall in ascending aortic flow () and LV stroke volume (integrated () indicated by the downward pointing arrow. An unchanged LV preload before the systolic negative intrathoracic pressure is indicated by constant (, end‐diastolic left ventricular (Plv) and atrial (Pla) pressures in the immediately preceding beats. In the diastolic period following the systolic fall in intrathoracic pressure, mitral inflow is decreased as indicated by the downward pointing arrow consistent with the increased end‐systolic volume. Thus, a fall in intrathoracic pressure during systole alone is sufficient to decrease LV stroke volume. PAO, aortic pressure; PRA, right artrial pressure.

Reprinted with permission from Peters, J., C. Fraser, R. S. Stuart, W. Baumgartner, and J. L. Robotham. Negative intrathoracic pressure decreases independently left ventricular filling and emptying. Am. J. Physiol. 257 (Heart Circ. Physiol. 26): H120–H131, 1989


Figure 25.

Recording with early systolic phrenic nerve stimulation (PNS) and the airway obstructed to keep lung volume constant in an anesthetized dog. The decrease of esophageal pressure (Peso) causes an increase in the systolic anteroposterior intrathoracic aortic diameter [DAo(AP)], indicated by the horizontal arrow, but a fall in left ventricular stroke volume derived from the ascending aortic blood flow (QAa), indicated by the lower horizontal arrow. Both systolic left ventricular (Plv) and aortic pressures (PAo) fall relative to atmospheric pressure. Neither the LV end‐diastolic pressure (recorded with a fluid‐filled catheter) immediately before phrenic nerve stimulation nor the R‐R interval change compared with the preceding cardiac cycle. Congruent with the increase in systolic DAo(AP), right‐to‐left aortic diameter [DAo(RL)] also increases. The decrease in LV stroke volume associated with increased DAo is compatible with an increased LV afterload. The same qualitative changes are observed when lung volume is allowed to increase with the fall in esophageal pressure, such that a decrease of intrathoracic pressure alone, with or without a change in lung volume, is sufficient to explain the fall in (QAa) and LV stroke volume and the increase in DAo.

Reprinted with permission from Peters, J., M. K. Kindred, and J. L. Robotham. Transient analysis of cardiopulmonary interactions. II. Systolic events. J. Appl. Physiol. 64: 1518–1526, 1988


Figure 26.

Tracings recorded in one dog during an increase in abdominal pressure (Pab) followed by maintenance of a quasisteady state and the acute release of abdominal compression. There were no arrhythmias in the ECG. Mean flow in both the ascending aorta () and descending aorta () decreased while flow in the innominate artery () increased. Airway pressure (PAW) measured at the trachea demonstrated a small peak inspiratory increase during abdominal compression. The expiratory airway pressure reflected transmission of 2 cm H2O of positive end‐expiratory pressure. The aortic pressure (PAO) and left atrial pressure (PLA) both increased as Pab increased.

Reprinted with permission from: Robotham, J. L., R. A. Wise, and B. Bromberger‐Barnea. Effects of changes in abdominal pressure on left ventricular performance and regional blood flow. Crit. Care Med. 13: 803–809, 1985
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Joseph S. Janicki, Don D. Sheriff, James L. Robotham, Robert A. Wise. Cardiac Output During Exercise: Contributions of the Cardiac, Circulatory, and Respiratory Systems. Compr Physiol 2011, Supplement 29: Handbook of Physiology, Exercise: Regulation and Integration of Multiple Systems: 649-704. First published in print 1996. doi: 10.1002/cphy.cp120115