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Cardiac output and its components

This is an excerpt from Advanced Cardiovascular Exercise Physiology-2nd Edition by Denise L. Smith & Bo Fernhall.

Cardiac output increases modestly during mild dynamic exercise involving lifting and extending the leg (Elstad et al., 2009). Participants performing 2 min of dynamic leg exercise that involved alternating contracting and relaxing the quadriceps for 2 s at 25% of MVC increased heart rate by approximately 40% (from 55.3 to 78.0 beats/min), and stroke volume decreased by about 5% (from 86.5 to 82.2 mL). Consequently, cardiac output increased by about 35% (from 4.59 to 6.18 L/min). The increase in cardiac output was solely a function of the increased HR as SV decreased slightly.

Dynamic re­sis­tance exercise at higher intensities may produce larger decreases in SV, but still results in modest increases in cardiac output due larger increases in HR (Miles et al., 1987; Howlett et al., 2020). For instance, SV was evaluated in healthy male subjects who performed a double leg press to failure at 95% of their maximum dynamic strength. Stroke volume was evaluated at the end of the lift phase, during the “lockout,” and during the lowering phase of the lift. Cardiac output increased significantly during the lifting phase and increased further during the lockout phase (figure 11.1a). The increase in cardiac output, however, is modest compared to that with aerobic exercise—­and is due almost entirely to an increase in heart rate, which reached approximately 140 beats/min, as stroke volume was relatively unchanged or decreased slightly during the exercise (figure 11.1b).

More recent research has added to our understanding of cardiac output changes during dynamic re­sis­tance exercise. The change in cardiac output is dependent on muscle mass, as dynamic leg re­sis­tance exercise produces greater increases compared to dynamic arm re­sis­tance exercise. Furthermore, in a 5-­repetition set of dynamic re­sis­tance exercise, the highest cardiac output was recorded during the fifth repetition for both leg and arm exercise (Howard et al., 2018). This increase in cardiac output was a function of an increase in HR as SV did not change from rest. HR also increased with each successive repetition for both leg and arm exercise. However, the changes in cardiac output (approximately 130% for leg exercise and 90% for arm exercise) and HR (approximately 128% for leg exercise and 95% for arm exercise) ­were much larger than ­those reported in the ­earlier studies. The likely reason is the difference in the exercise intensity between the studies. Additional recent work also shows that eccentric muscle contractions produces smaller changes in HR, and thus presumably also in cardiac output, at similar exercise intensities as previously reported for concentric muscle contractions (Howlett et al., 2020). Although few data exist to date, it appears that cardiac output changes during dynamic re­sis­tance exercise may be lower in older compared to younger individuals (Rosenberg et al., 2020) due primarily to a reduced HR response in the older individuals.

Heart rate responses to re­sis­tance exercise have been more widely reported than changes in stroke volume and cardiac output. Most studies indicate that heart rate increases modestly during dynamic re­sis­tance exercise to volitional fatigue. Dynamic leg exercise at 80%-95% of 1RM or MVC typically result in a peak heart rate of 140-160 beats/min. When taken to volitional failure, submaximal re­sis­tance exercise results in a larger volume of work and produces heart rates that are higher than for a single 1RM (Falkel, Fleck, and Murray, 1992; Fleck and Dean, 1987; Howard et al., 2018). However, peak heart rates as high as 170 beats/min have been reported during per­for­mance of bilateral and unilateral lifts of the upper and lower body using weights equivalent to 80%, 90%, 95%, and 100% of maximum, with the highest heart rates occurring just before muscle fatigue prevented further contractions (MacDougall et al., 1985). Heart rate increases during acute re­sis­tance exercise are due to vagal withdrawal and stimulation of the sympathetic ner­vous system. It is likely that the sympathetic ner­vous system is stimulated by central command and from muscle chemo-­ and mechanoreceptors. The higher heart rates observed during dynamic re­sis­tance exercise at submaximal intensities to fatigue (exercise at some ­percent of 1RM) than during 1RM lifts is likely due to the increased amount of time the exercise is performed, allowing for greater influence of sympathetic activation and from the muscle chemo-­ and mechanoreceptors.

The relatively unchanged or decreased stroke volume that has been reported during re­sis­tance exercise is due to a combination of decreased preload, increased afterload, and enhanced contractility. Preload may be lower than baseline ­because of decreased filling time (due to increased heart rate) and a decrease in venous return. Venous return is likely decreased due to mechanical occlusion to the muscle during contraction and the per­for­mance of the Valsalva maneuver (see side bar). High intramuscular pressure generated during contraction can temporarily occlude flow through the active muscles, thus decreasing venous return and leading to a reduction in stroke volume. Supporting the hypothesis that high intramuscular pressure may occlude venous return and thus blunt stroke volume during re­sis­tance exercise, Miles and coworkers (1987a) reported that stroke volume and cardiac output ­were significantly lower during the concentric phase of the exercise than during the eccentric phase. Lentini and colleagues (1993) found that end-­diastolic ventricular volume decreased during both the lifting and lowering phase of the exercise at 95% of 1RM. However, a recent study found no significant change in ­either end-­diastolic or end-­systolic volume during dynamic re­sis­tance exercise at ­either 30% or 60% of 1RM (Stöhr et al., 2017). Taken together, ­these data suggest that exercise intensity may influence the cardiac response to dynamic re­sis­tance exercise. High intrathoracic pressure associated with performing the Valsalva maneuver also impedes venous return and thus leads to a decrease in stroke volume during re­sis­tance exercise (Haykowsky et al., 2018). Although participants are usually told to avoid the Valsalva maneuver during studies described above, this is not always pos­si­ble. Weightlifters commonly perform the Valsalva maneuver during heavy lifting, and this may be beneficial for both the heart and for providing structural support.

The large increase in blood pressure that is associated with re­sis­tance exercise (discussed in the following section) results in an increase in afterload, which makes it more difficult for the heart to eject blood. Si­mul­ta­neously, activation of the sympathetic ner­vous system during re­sis­tance increases heart contractility, which helps to maintain SV. Lentini and colleagues (1993) showed a decrease in end-­systolic volume during the lifting and lowering phase of the exercise, and an increase in ejection fraction. However, ­others have found no change in systolic function during high-­intensity dynamic re­sis­tance exercise (Haykowsky et al., 2001). More recent work using tissue Doppler and cardiac strain imaging suggest no change in systolic function and an ­actual decrease in cardiac dynamics during dynamic re­sis­tance exercise, evidenced by a decrease in left ventricular twist mechanics (Stöhr et al., 2017). Although stroke volume also decreased, this decrease was smaller than expected, likely as a result of increased diastolic function. Interestingly, the high intrathoracic pressure developed during dynamic re­sis­tance exercise with the Valsalva maneuver does not increase left ventricular wall stress, despite the apparent increase in afterload. This is ­because the increased intrathoracic pressure puts external pressure on the heart, essentially pushing on the heart wall from the outside, thus preventing an increase in end-­systolic pressure and preserving left ventricular wall stress (Haykowsky et al., 2001, 2018). The small-­to-­modest increase in cardiac output during re­sis­tance exercise is the result of a modest increase in heart rate and an unchanged or decreased stroke volume, without changes in ventricular wall stress (figure 11.2).

The acute cardiovascular responses to re­sis­tance exercise just described are in stark contrast to ­those seen during aerobic exercise. Cardiac output increases dramatically during heavy aerobic exercise (five-­ to sevenfold) but modestly during re­sis­tance exercise (20%-100%). More specifically, during aerobic exercise, both heart rate and stroke volume increase to achieve a greater cardiac output, which is accomplished through increased venous return, increased contribution of the Frank-­Starling effect, and increased contractility and diastolic function. During re­sis­tance exercise, heart rate increases modestly but stroke volume decreases as explained above; thus cardiac output is only modestly increased. ­Table 11.1 shows a comparison of the expected hemodynamic and cardiac responses to dynamic exercise compared to dynamic re­sis­tance exercise.

The Valsalva Maneuver

The Valsalva maneuver, defined as forcefully exhaling against a closed glottis, is almost impossible to avoid during re­sis­tance exercise at higher intensity (Gaffney, Sjøgaard, and Saltin, 1990; Sale et al., 1993). As intrathoracic pressure is dramatically increased to stabilize the spine, force is more efficiently transferred through the flexible spinal column, thus assisting the lift. Both intrathoracic and intra-­abdominal pressure increase substantially, particularly when the Valsalva maneuver is performed during re­sis­tance exercise (Blazek et al., 2019). The increase in intrathoracic pressure and intrabdominal pressure reduces venous return. During the rapid exhale following the strain period, ­there is a sudden decrease in BP, which can lead to lightheadedness or dizziness. The sudden drop in blood pressure is primarily explained by a rapid refilling of the aorta, which temporarily decreases systemic arterial flow, coupled with a drop in central venous pressure, thus decreasing peripheral venous pressure. ­These two ­factors cause a very rapid drop in BP (Pstras et al., 2016).

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