Resistance exercise is seldom used with the expressed purpose of enhancing cardiovascular function, but it does result in acute and chronic cardiovascular changes. This section details the acute cardiac responses to resistance exercise.
A recent study showed that cardiac output increased during mild dynamic exercise involving lifting and extending the leg (Elstad et al., 2009). Researchers had participants perform 2 min of dynamic leg exercise that involved alternating contracting and relaxing the quadriceps for 2 s. As the quadriceps were contracted, the knee was extended and the heel lifted 3 to 5 cm. During the exercise, one leg was contracted while the other leg was relaxed. Bilateral weights of 2 to 5.5 kg (equal to 25% of maximal voluntary contraction force) were added to the ankles to increase muscular work. Throughout the leg exercise, heart rate was recorded and stroke volume was measured using Doppler ultrasound. In this study, heart rate increased 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). Thus, cardiac output increased by about 35% (from 4.59 to 6.18 L/min). Therefore, in this study, mild dynamic exercise with a light resistance caused a small increase in cardiac output resulting from a small decrease in stroke volume that was more than offset by the increase in heart rate.
Miles and colleagues (1987) reported that stroke volume decreased significantly (~20%) during leg extension exercises that involved 12 repetitions to fatigue (lasting about 90 s). In this study, the leg extension included a 3 s lifting motion, a 1 s pause, and a 3 s lowering motion, and stroke volume was assessed using impedance cardiography. Heart rate increased approximately 50 beats/min (from 70 to 120 beats/min), and cardiac output increased from approximately 5.4 to 6.3 L/min (17%), although this increase did not achieve statistical significance.
Cardiac output responses to more intense resistance training have been reported by Lentini and colleagues (1993), who had healthy male subjects perform a double leg press to failure at 95% of their maximum dynamic strength. Stroke volume was determined using echocardiography and was reported preexercise, 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).
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 resistance exercise to volitional fatigue. In the study just cited, double leg press performed to failure with 95% of maximal strength resulted in a peak average heart rate of 143 beats/min. When taken to volitional failure, low-intensity 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). Some authors, however, have reported greatly elevated heart rates during high-intensity resistance exercise. 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 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. High intramuscular pressure generated during contraction can temporarily occlude flow through the active muscles, thus decreasing 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. High intrathoracic pressure associated with performing the Valsalva maneuver can also impede venous return and thus lead to a decrease in stroke volume during resistance exercise. In the studies mentioned here, participants were told to avoid the Valsalva maneuver and were watched to confirm that they did so. Weightlifters, however, commonly perform the Valsalva maneuver during heavy lifting.
The Valsalva maneuver, defined as forcefully exhaling against a closed glottis, is performed as a natural tendency to stabilize the torso during resistance exercise (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. Because the lungs remain inflated against a closed glottis, the pressure within the thorax increases dramatically, providing additional rigidity for the spine. Concurrently, the pressure in and around the heart increases and venous return is decreased. Upon release of the air that has been temporarily trapped in the lungs, participants may feel light-headed because of a sudden decrease in blood pressure. The decrease in blood pressure may also be partly explained by a baroreceptor-mediated drop in heart rate and vasodilation. Although there are few data on post-Valsalva decreases in blood pressure, the sudden drop in blood pressure may be the result of rapid redistribution of blood to the periphery after the pressure within the thorax has been released. Any rapid redistribution of blood could result in syncope or light-headedness until the systemic pressure has been
The large increase in blood pressure that is associated with resistance exercise (discussed in the following section) results in an increase in afterload, which has a lowering effect on stroke volume. Activation of the sympathetic nervous system during resistance exercise would be expected to increase heart contractility. Evidence for increased contractility comes from the study by Lentini and colleagues (1993) that showed a decrease in end-systolic volume during the lifting and lowering phase of the exercise, and an increase in ejection fraction. The stroke volume response is a result of the balance of changes in preload, afterload, and contractility. 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.
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. During resistance exercise, heart rate increases modestly but stroke volume decreases; thus cardiac output is only modestly increased.
The rate–pressure product (RPP) or double product ([HR 3 SBP]/100) has been used as an indirect measure of myocardial oxygen consumption. The RPP has been shown to correlate well with myocardial oxygen consumption under both static and dynamic exercise conditions (Nelson et al., 1974). Because of increases in both heart rate and systolic blood pressure, the RPP can rise to high levels during intense resistance exercise (MacDougall et al., 1985). However, many authors have found that RPP does not reach extremely high levels because heart rate increases are generally modest. Fleck and Dean (1987) assessed heart rate and blood pressure responses to one-knee extension exercises performed to volitional fatigue in trained bodybuilders, novice bodybuilders, and sedentary controls. In this study, the subjects achieved a RPP less than 250 3 102. Furthermore, the results indicated that the trained bodybuilders had a lower RPP than novice lifters or sedentary controls.
Historically, the high RPP was a primary reason that intense resistance exercise was considered contraindicated for persons with known cardiovascular disease (McCartney, 1999). However, revised guidelines from the American Heart Association suggest that resistance training may indeed be beneficial for those with known cardiovascular disease if contemporary prescriptive guidelines are employed with close supervision (Thompson et al., 2007). In a statement published by the American Heart Association (Braith and Stewart, 2006) regarding the use of resistance exercise in those with and without cardiovascular disease, the authors detail what is currently known about the safety of resistance exercise. They acknowledge that “excessive” blood pressure elevations have been documented with high-intensity resistance exercise (80-100% of 1RM performed to exhaustion), but note that such elevations are generally not a concern with low- to moderate-intensity resistance training performed with correct breathing technique and avoidance of the Valsalva maneuver. Furthermore, there is indirect evidence that resistance exercise results in a more favorable balance in myocardial oxygen supply and demand than aerobic exercise because of the lower heart rate and higher myocardial (diastolic) perfusion pressure (Braith and Stewart, 2006).
In a study comparing the physiological responses to weightlifting and aerobic exercise, Featherstone and coworkers (Featherstone, Holly, and Amsterdam, 1993) tested 12 men with known cardiovascular disease. Participants performed both a maximal treadmill exercise and maximal resistance exercise at intensities of 40%, 60%, 80%, and 100% of maximal voluntary contraction. During the treadmill test, over 40% of the subjects experienced ST depression, whereas no such ischemia was observed during any of the resistance exercises. The RPP was higher during the treadmill test as compared to any of the lifting conditions. Although systolic pressures were similar between the conditions, the heart rates achieved during weightlifting were significantly lower than during the treadmill exercise.
Public health guidelines also suggest that resistance training is appropriate for older adults and should be part of an overall exercise program (Williams et al., 2007).