Journal Logo

Clinical Sciences: Symposium: Resistance Training For Health And Disease

Acute responses to resistance training and safety


Editor(s): Pollock, Michael L.

Author Information
Medicine & Science in Sports & Exercise: January 1999 - Volume 31 - Issue 1 - p 31-37
  • Free


The circulatory responses to static (isometric) and dynamic exercise have been investigated extensively. Dynamic exercise invokes a "volume load" on the heart (29). Simply put, large increases in cardiac output are mediated by a rise in both stroke volume and heart rate together with reductions in peripheral vascular resistance; the attendant increases in mean arterial pressure are modest. In contrast, a sustained static contraction of even a small muscle group, such as the forearm muscles during handgrip dynamometry, presents a "pressure load" to the heart (29). This is characterized by a moderate increase in cardiac output, minimal change in peripheral vascular resistance, and a substantial rise in mean arterial pressure. Ventricular volumes show little change, and the increased cardiac output results from an accelerated heart rate (31).

Resistance, or weight-lifting exercise, is a combination of static and dynamic contractions, the proportions of each varying in accordance with the degree of effort required to lift the weight. At the initiation of the movement, there is a static contraction until the muscle force exceeds the weight of the object to be lifted. This is followed by a dynamic concentric (shortening) contraction to raise the weight, a dynamic eccentric (lengthening) contraction to lower it, and a variable relaxation phase between successive lifts. It is only during the past decade that the acute circulatory responses to resistance exercise have been investigated, using direct intra-arterial measurement techniques. Study populations have included healthy young and older subjects, uncomplicated postmyocardial infarction patients, and patients with congestive heart failure. This review will address the findings from those studies, outline the factors that influence the circulatory response to resistance exercise, and evaluate the safety of this form of activity.

Acute Circulatory Response to Resistance Exercise

The first investigation of the heart rate and intrabrachial artery pressures during heavy resistance exercise was in young subjects performing both single-arm, and single- and double-leg exercises to failure at intensities ranging from 80 to 100% of the one-repetition maximum (1-RM) (22). The data demonstrated large, pulsatile swings in arterial pressure throughout each repetition, and in one subject performing double-leg press the peak systolic and diastolic pressures reached 480/350 mm Hg. The major mechanisms underlying the dramatic increases in arterial pressure were assumed to be a potent pressor response, mechanical compression of the skeletal muscle vasculature, and an elevated intrathoracic pressure coincident with the Valsalva maneuver. Subsequent studies (14,20,23) have provided support for this contention and also acknowledged the modulating influence of the number of repetitions, the absolute and relative load, the muscle mass, and the joint angle.

The effects of the number of repetitions. The peak arterial pressures in the initial repetition of a set of lifts exceed those of the next two or three repetitions, then the pressures rise progressively, reaching the highest values during the final repetitions of a set ending in failure (Fig. 1). Over the same time period, heart rate may attain levels of 160-170 beats per min. Within 1-2 s after the final lift, the pressures decrease to resting values or below, confirming the inadequacy of postlifting measurements obtained by sphygmomanometry and auscultation (37).

Figure 1
Figure 1:
Tracings of intrabrachial artery blood pressure in one subject performing double-leg press exercise to failure at 95% of 1-RM (the maximum load that could be lifted throughout a complete range of motion once only). Inset: Subject's knee angle and direction of movement during lifting, lockout, and lowering phases of the exercise. Reprinted with permission from Lentini, A. C., R. S. McKelvie, N. McCartney, C. W. Tomlinson, and J. D. MacDougall. Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise. J. Appl. Physiol. 75:2703-2710, 1993.

The pattern of change in arterial pressure throughout a set of lifts may be explained as follows. In the first repetition the initial concentric contraction is not preceded by an eccentric contraction and thus does not benefit from the potentiating effects of the stretch-shortening cycle (18). In subsequent repetitions, the eccentric contraction reduces the voluntary effort (thus the motor unit activation) required in the following concentric contraction and the arterial pressure is lower (32,33). As the muscles become fatigued, the arterial pressure progressively rises, due most likely to a combination of factors: greater voluntary effort is needed to activate tired muscles to generate the same force; there is increased likelihood of recruitment of accessory muscles; there is increased use of the Valsalva maneuver; and feedback from muscle ergoreceptors and nociceptors to the cardiovascular control areas in the medulla (30) probably increases. The rapid drop in pressure postexercise may reflect an abrupt perfusion of the vasodilated exercising musculature, which may have been partially occluded previously, in addition to a temporary, baroreceptor mediated pressure undershoot responding to the very high pressures in the final lift (22).

The effects of absolute and relative load. Within subjects, the heart rate and arterial pressure responses increase in proportion to the load. The values attained during a single maximum lift, however, are less than those recorded in a set of heavy lifting to failure. Between-subject comparisons among individuals with markedly different lifting capacities indicate that it is the relative, rather than absolute load, that predicts the circulatory response (21)(Fig. 2). This lends support to the argument that it is a feed-forward central command mechanism, reflecting the central activity for the recruitment of motor units (30) that is the major contributor to the circulatory response during resistance exercise (21,23,32,33).

Figure 2
Figure 2:
Peak systolic and diastolic blood pressures graphed against total quadriceps cross-sectional area (A) and absolute weight lifted (B) during 10 repetitions to failure (10-RM). Regression lines indicate nonsignificant relationships (N = 11). Reprinted with permission from MacDougall, J. D., R. S. McKelvie, D. E. Moroz, D. G. Sale, N. McCartney, and F. Buick. Factors affecting blood pressure during heavy weightlifting and static contractions. J. Appl. Physiol. 73:1590-1597, 1992.

The effects of muscle mass. Within a given individual there appears to be a positive but nonlinear relation between the circulatory responses and the muscle mass engaged in the lifting. For example, the heart rate and arterial pressures are higher during bilateral-leg press than unilateral-leg press exercises but nowhere near double. A recent comparison of single- and double-arm exercises in our laboratory (unpublished observation) has shown that this relation does not extend to arm work, as the circulatory responses were the same despite the differences in activated muscle mass.

Comparisons between-subjects suggests that variations in muscle mass do not predict interindividual differences in the circulatory response to resistance exercise. A recent study by MacDougall and colleagues (21) revealed similar arterial pressures during a 10-RM of double-leg press lifting despite extremely large interindividual variability in total quadriceps cross-sectional area and the total weight lifted (Fig. 2). As before, this indicates that the circulatory responses to resistance exercise are determined in large part by the relative intensity of effort, as this would have been the same for each subject during the completion of an equal number of repetitions to failure.

The effects of joint angle. The effects of joint angle on the circulatory responses to resistance exercise have been investigated in studies of double-leg press exercise (20,21). At the beginning of the movement, the knee joint angle is 90°, and the leg extensors are at their weakest point on the strength curve. It is in this early phase that the rise in arterial pressure is the greatest. At lock-out, the knee joint angle is 170°, the strongest position for the leg extensors, and the arterial pressure is reduced almost to resting. During the eccentric lowering phase, the arterial pressures rise again, but significantly less than during the initial concentric contraction (Fig. 3). The most likely explanation for these observations is related to the relative effort required in each phase of the lift. Muscles can generate appreciably less force during a concentric contraction than when contracting eccentrically (19), so lifting a given weight will require a greater relative effort than lowering it, and this will be reflected in the magnitude of the circulatory response (21-23,32,33).

Figure 3
Figure 3:
Systolic and diastolic blood pressure responses to double-leg press exercise at different phases (preexercise, lifting, lockout, and lowering) of exercise. Data are means ± SE; ▪, systolic pressure; □, diastolic pressure; * P < 0.05 compared with preexercise; + P < 0.05 compared with lockout; # P < 0.05 compared with lowering. Reprinted with permission from Lentini, A. C., R. S. McKelvie, N. McCartney, C. W. Tomlinson, and J. D. MacDougall. Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise. J. Appl. Physiol. 75:2703-2710, 1993.

The effects of the Valsalva maneuver. It appears that subjects make little use of the Valsalva maneuver during lifting at intensities less than 80-85% of the 1-RM, in the absence of fatigue (21,22)(Fig. 4). At higher intensities of lifting, the Valsalva becomes almost obligatory, to stabilize the trunk and to facilitate the necessary force production (Fig. 4). In very heavy lifting to failure, the intrathoracic pressure may exceed 100 mm Hg, equivalent to 60% or more of the level that can be generated in a maximum voluntary Valsalva maneuver (21). During lifting to failure with submaximal loads, the Valsalva is used increasingly as the muscles become fatigued.

Figure 4
Figure 4:
Actual traces for intrabrachial artery pressure and intrathoracic pressure while a subject did dynamic leg presses. A, The weight is equal to ∼75% of the 1-RM, and elicits only an occasional Valsalva maneuver. B, The weight corresponds to ∼85% of 1-RM performed to failure, and a Valsalva maneuver is associated with each repetition. The magnitude of the Valsalva maneuver increases over repetitions and becomes greatest as the subject approaches failure. Reprinted with permission from MacDougall, J. D., R. S. McKelvie, D. E. Moroz, D. G. Sale, N. McCartney, and F. Buick. Factors affecting blood pressure during heavy weightlifting and static contractions. J. Appl. Physiol. 73:1590-1597, 1992.

The rise in intrathoracic pressure resulting from the Valsalva maneuver is transmitted directly to the arterial tree, causing an immediate increase in arterial pressure (12). For this reason, and because it may also reduce venous return, the Valsava is often contraindicated during resistance exercise and while performing isometric efforts (1,2,7). Recent evidence, however, suggests that an initial, brief Valsalva may be beneficial during resistance exercise. Lentini and colleagues (20) reported mean values of intrabrachial artery pressure of 270/183 mm Hg during the early concentric contraction phase of double-leg press exercise at 95% of 1-RM in healthy young men. At the same time, the intrathoracic pressure increased to 58 ± 25 mm Hg as a consequence of the Valsalva maneuver. Under most circumstances, the systolic pressure would be representative of the left-ventricular afterload, as intrathoracic pressure is usually low (4). In this investigation, however, it was concluded that the rise in intrathoracic pressure resulted in a lower left-ventricular transmural pressure, hence afterload, than would be predicted from the arterial pressure measurements alone (20). As increases in intrathoracic pressure are also transmitted directly to the cerebrospinal fluid (12), a brief Valsalva may also serve a protective effect by reducing the transmural pressure across cerebral vessels (21).

Acute left-ventricular response to resistance exercise. In a study by Miles and colleagues (28), 17 young men did 12 repetitions of leg extension exercise to fatigue (90 s), and cardiac function was assessed using impedance cardiography. There were significant increases in heart rate, arterial pressure, and total peripheral resistance, but the average cardiac output was unchanged. An analysis of the changes in stroke volume throughout different phases of the lift revealed a greater reduction during the concentric phase (∼35 mL) than in the eccentric phase (∼24 mL). The reason that cardiac output was unchanged throughout the exercise period was an apparent increase in myocardial contractility. A reduction in stroke volume during resistance exercise was also suggested by Brown et al. (5), but this conclusion was based on postexercise echocardiographic measurements, which may not be representative of the changes during the actual lifting (37).

A recent study (20) has extended previous observations by including a more detailed analysis of the changes in arterial pressure and left-ventricular volumes throughout the various phases of bilateral leg press exercise, done at 95% of the 1-RM to failure. During the initial concentric contraction the circulatory response was similar to that during a static effort. There were significant increases in mean arterial pressure (114 ± 3 to 212 ± 19 mm Hg) and total peripheral resistance (15 ± 1 to 19 ± 1 mm Hg·L·min−1), and end-diastolic volume and end-systolic volume declined by 30% and 50%, respectively. The 17-mL reduction in stroke volume was not significantly different from rest (Fig. 5), and an almost fourfold increase in the peak systolic pressure to end-systolic volume ratio indicated a notable enhancement of myocardial contractility (Fig. 6). In the lock-out phase, it was only the end-systolic volume that had not returned close to resting levels, remaining significantly lower (16 mL). Responses during the eccentric, lowering phase were qualitatively similar to those in the concentric phase, but of a lesser magnitude. Such rapid changes in arterial pressure, cardiac volumes, and myocardial contractility during the course of a single-repetition of leg press exercise were attributed to the varying degrees of effort (central command) required in each phase of the lift, being greatest in the concentric (weakest) phase and least during lock-out (strongest phase).

Figure 5
Figure 5:
Changes in left ventricular volumes during different phases of leg press exercise. Data are shown as mean ± SE; •, end-diastolic volume; □, stroke volume; ○, end-systolic volume. * P < 0.05 compared with preexercise; + P < 0.05 compared with lockout. Reprinted with permission from Lentini, A. C., R. S. McKelvie, N. McCartney, C. W. Tomlinson, and J. D. MacDougall. Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise. J. Appl. Physiol. 75:2703-2710, 1993.
Figure 6
Figure 6:
The ratio of intrabrachial artery mean peak-systolic pressure to end-systolic volume (peak SBP/ESV) response to double-leg press exercise at different phases of lifting. Data are means ± SE; * P < 0.05 compared with preexercise; + P < 0.05 compared with lockout. Reprinted with permission from Lentini, A. C., R. S. McKelvie, N. McCartney, C. W. Tomlinson, and J. D. MacDougall. Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise. J. Appl. Physiol. 75:2703-2710, 1993.

These findings in resistance exercise are in contrast to previous observations during the isometric deadlift, in which the end-systolic volume increased (34) and there was no improvement in indexes of myocardial contractility (31,34,36). It is therefore incorrect to equate resistance exercise with isometric exercise, as is sometimes done (3,13,30).

Acute Circulatory Response to Resistance Exercise in Patients with Coronary Artery Disease

Uncomplicated postmyocardial infarction. Over the past decade, supplementary resistance training has gained widespread acceptance in North American phase III and IV cardiac rehabilitation programs (1,2). Most of the studies of the arterial pressure (17,35) and left-ventricular responses (6) to this form of exercise have utilized postexercise measurements, which may provide limited information about the changes during the actual period of lifting. Arterial pressure has most often been measured indirectly by sphygmomanometry and auscultation. At rest, and during a set of resistance exercises, such indirect measures of arterial pressure may underestimate intrabrachial artery systolic pressure by 13-15% (37); immediately after exercise, the systolic pressure determined by auscultation may be more than 30% lower than the peak intra-arterial levels during lifting (37).

In the study by Haslam et al. (14), which utilized continuous intra-brachial artery recording of blood pressure during resistance exercise, the responses were qualitatively similar to those in healthy individuals. Arterial pressure increased over repetitions, there was a positive but nonlinear relation to muscle mass, and the pressures increased in proportion to the load. Only double-leg press exercise at 60% and single-and double-leg press exercise at 80% of the 1-RM elicited a peak rate-pressure product that exceeded the value recorded at 85% of the peak power output in cycle ergometer testing. The largest contributor to the rate-pressure product during resistance exercise was the systolic pressure, whereas in cycling it was the heart rate. The lower heart rate during resistance exercise, coupled with a much higher diastolic pressure, should facilitate more prolonged coronary artery filling at a higher perfusion pressure.

In a study by Featherstone and associates (9), the myocardial oxygen supply to demand was estimated in 12 patients who did arm and leg resistance exercises to failure at 40, 60, 80, and 100% of the 1-RM. The myocardial oxygen supply to demand balance was estimated from the ratio of the diastolic pressure-time index to rate-pressure product (DPTI:RPP). Compared with maximal treadmill exercise testing, the combination of reduced heart rates, higher diastolic pressures, and similar systolic pressures during resistance exercise produced a significantly increased DPTI:RPP, consistent with a more favorable myocardial oxygen supply to demand balance. The validity of the DPTI to estimate coronary artery perfusion in patients with atherosclerotic coronary artery disease may be questioned. Arterial pressure drops across a coronary lesion, being influenced by the length of the stenosis, the blood flow, and the arterial radius (8). In a stenotic coronary artery, the subendocardial perfusion reflects the gradient between the diastolic coronary pressure beyond the obstruction and the left-ventricular diastolic pressure (8). Therefore, in the presence of significant stenosis, the use of the pressure gradient between the aorta and the left ventricle to calculate the DPTI would tend to overestimate the subendocardial perfusion. Despite this caution, none of the patients in the study by Featherstone et al (9). exhibited any ECG evidence of ischemia during the resistance exercises, whereas 5 of the 12 had greater than 1 mm of ST-segment depression while on the treadmill.

The observation of reduced ischemic signs or symptoms during resistance training has been reported consistently (6,14,35). This suggests that the circulatory demands imposed by resistance exercise are not excessive for patients with coronary disease who are suitable candidates for cardiac rehabilitation programs. Data from patients with angina and left-ventricular dysfunction are scarce.

Congestive heart failure (CHF). It is only in recent years that aerobic exercise training has been demonstrated to be a safe and effective method to improve exercise tolerance in patients with CHF (27). These individuals are probably the most deconditioned of all cardiac patients, so theoretically may have the most to gain from resistance training. We recently (26) compared the intra-brachial artery pressure and the left-ventricular responses to single-leg press resistance exercise, with cycling, in 10 male CHF patients (ejection fraction 27 ± 2%). The patients did 10 repetitions of leg press at 70% of the 1-RM and 4 min of steady-state cycling, also at 70% of the peak power output. The heart rate, cardiac output, stroke volume, and rate-pressure product were significantly higher, and the total peripheral resistance was lower, during cycling compared with the leg press. The diastolic pressure was greater during the resistance exercise (98 ± 3.5 vs 86 ± 2.5 mm Hg), but there was no difference in end-diastolic volume, end-systolic volume, or ejection fraction. The peak systolic pressure to end-systolic volume ratio was more favorable in the cycling by a small, yet statistically significant amount, but it increased from rest in both exercise modalities. Taken together, these findings suggested that the myocardial oxygen demand was lower during the resistance exercise and the left-ventricular response was similar to that observed during cycling. Although the findings from this investigation could be interpreted to suggest that resistance training may be appropriate for CHF patients, the sample size was small, and more studies need to be done before this mode of exercise can be prescribed on a widespread basis.

The Effects of Resistance Training on the Acute Circulatory Response to Resistance Exercise

It is well established that even short-term resistance training results in significant increases in dynamic strength and muscle cross-sectional area. This being the case, when an individual lifts the same absolute weight as before training, it now represents a lower relative resistance. If the major influence on the circulatory changes during resistance exercise is indeed the degree of relative effort, or central motor command, then after a period of training the arterial pressure response to the same absolute load should be reduced. This hypothesis has been tested in two studies of young (32) and older (23) healthy male subjects. After 12 wk (23) and 19 wk (32) of training, the leg press 1-RM increased by 24% (23) and 26% (32). In both studies, during 10-20 repetitions of lifting with heavy submaximal loads, there were reductions in systolic pressure, diastolic pressure, and the rate-pressure product of 17-27%. There is limited evidence that highly trained weight lifters have a blunted circulatory response to resistance exercise compared with nontrained controls (10), but more research is needed in this area. It is tempting to speculate that increases in dynamic strength may reduce the circulatory demands during strength-related activities of daily living, but this has yet to be established.

The Safety of Resistance Training

Resistance training is widely utilized as part of fitness programs for individuals of all ages, and appears to be remarkably safe. There is one report of more than 26,000 maximal dynamic strength assessments done at the Cooper Clinic and at the University of Florida without a single cardiovascular event (11). The acute circulatory response seems to yield a favorable balance between myocardial oxygen supply and demand; in patients with coronary artery disease, this probably accounts for the observations of reduced signs and symptoms of ischemia, and fewer wall motion abnormalities, than during dynamic activities such as walking and cycling (6,14,35). The author is not aware of any reports in the literature of cardiac patients experiencing myocardial infarction or sudden death while engaged in resistance training.

Despite this impressive record of safety, there is some evidence that resistance training may be potentially hazardous for a small percentage of the population. Haykowsky and colleagues (15) have documented three cases of nonfatal subarachnoid hemorrhage associated with weight-lifting training. It is likely that these individuals harbored a previously innocuous intracranial aneurysm which ruptured in response to a significant increase in cerebral arterial transmural pressure precipitated by the lifting. For the estimated 1% of the population with an undetected intracranial aneurysm, resistance training may be inappropriate (15), but at the present time routine detection of this defect is unavailable.

In general, however, resistance training appears to be a safe and potentially beneficial form of exercise for the great majority of the population, even including categories of patients with heart disease (25), neuromuscular disorders (24), and end-stage renal disease (16). Nevertheless, there are little data on the acute circulatory responses to resistance exercise in these clinical populations, and this should be an area of future study. An examination of the responses of the transplanted, denervated heart to resistance exercise would also provide much useful information; such a study is currently underway in our laboratory.


1. American Association of Cardiovascular and Pulmonary Rehabilitation. Guidelines for Cardiac Rehabilitation Programs. Champaign, IL: Human Kinetics Publishers, 1995, pp. 44-50.
2. American College of Sports Medicine. Guidelines for Graded Exercise Testing and Prescription, 4th Ed. Philadelphia: Lea and Febiger, 1991, pp. 136-138.
3. Balady, G. J. Types of exercise: arm-leg and static-dynamic. Cardiol. Clin. 11:297-308, 1993.
4. Braunwald, E. Heart Disease a Textbook of Cardiovascular Medicine, 5th Ed. Philadelphia: W. B. Saunders, 1997, p. 428.
5. Brown, S. P., W. R. Thompson, M. Bean, L. Wood, K. Nayak, and J. Goff. The relationship of early versus two minute recovery echocardiographic values following maximal effort resistance exercise. Int. J. Sports Med. 12:241-245, 1991.
6. Butler, R. M., W. H. Beierwaltes, and F. J. Rogers. The cardiovascular response to circuit weight training in patients with cardiac disease. J. Cardiopulm. Rehabil. 7:402-409, 1987.
7. Effron, M. B. Effects of resistive training on left ventricular function. Med. Sci. Sports Exerc. 21:694-697, 1989.
8. Epstein, S. E., R. O. Cannon, and T. L. Talbot. Hemodynamic principles in the control of coronary blood flow. Am. J. Cardiol. 56:4E-10E, 1985.
9. Featherstone, J. F., R. G. Holly, and E. A. Amsterdam. Physiologic responses to weight lifting in coronary artery disease. Am. J. Cardiol. 71:287-292, 1993.
10. Fleck, S. J., and L. S. Dean. Resistance-training experience and pressor response during resistance exercise. J. Appl. Physiol. 63:116-120, 1987.
11. Gordon, N. F., H. W. Kohl III, M. L. Pollock, H. Vaandrager, L. S. Gibbons, and S. N. Blair. Cardiovascular safety of maximal strength testing in healthy adults. Am. J. Cardiol. 76:851-853, 1995.
12. Hamilton, W. F., R. A. Woodbury, and H. T. Harper, Jr. Arterial, cerebrospinal, and venous pressures in man during cough and strain. Am. J. Physiol. 141:42-50, 1944.
13. Hanson, P., and F. Nagle. Isometric exercise: cardiovascular responses in normal and cardiac populations. Cardiol. Clin. 5:157-170, 1987.
14. Haslam, D. R. S., N. McCartney, R. S. McKelvie, and J. D. Macdougall. Direct measurements of arterial blood pressure during formal weightlifting in cardiac patients. J. Cardiopulm. Rehabil. 8:213-225, 1988.
15. Haykowsky, M. J., J. M. Findlay, and A. P. Ignaszewski. Aneurysmal subarachnoid hemorrhage associated with weight training: three case reports. Clin. J. Sports Med. 6:52-55, 1996.
16. Horber, F. F., J. R. Scheidegger, B. F. Grunig, and F. J. Frey. Evidence that prednisone-induced myopathy is reversed by physical training. J. Clin. Endocrinol. Metab. 6:83-88, 1985.
17. Kelemen, M. H., K. J. Stewart, R. E. Gillilan, C. K. Ewart, S. A. Valenti, J. D. Manley, and M. D. Kelemen. Circuit weight training in cardiac patients. J. Am. Coll. Cardiol. 7:38-42, 1986.
18. Komi, P. V. Stretch-shortening cycle. In: Strength and Power in Sport, P. V. Komi (Ed.). London: Blackwell, 1992, pp. 169-179.
19. Komi, P. V. Relationship between muscle tension, EMG and velocity of contraction under concentric and eccentric work. In: New Development in Electromyography and Clinical Neurophysiology. Basel: Karger, 1973, pp. 596-606.
20. Lentini, A. C., R. S. McKelvie, N. McCartney, C. W. Tomlinson, and J. D. Macdougall. Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise. J. Appl. Physiol. 75:2703-2710, 1993.
21. MacDougall, J. D., R. S. McKelvie, D. E. Moroz, D. G. Sale, N. McCartney, and F. Buick. Factors affecting blood pressure during heavy weightlifting and static contractions. J. Appl. Physiol. 73:1590-1597, 1992.
22. MacDougall, J. D., D. Tuxen, D. G. Sale, J. R. Moroz, and J. R. Sutton. Arterial blood pressure response to heavy resistance exercise. J. Appl. Physiol. 58:785-790, 1985.
23. McCartney, N., R. S. McKelvie, J. Martin, D. G. Sale, and J. D. Macdougall. Weight-training induced attenuation of the circulatory response to weightlifting in older males. J. Appl. Physiol. 74:1056-1060, 1993.
24. McCartney, N., D. Moroz, S. H. Garner, and A. J. McComas. The effects of strength training in patients with selected neuromuscular disorders. Med. Sci. Sports Exerc. 20:362-368, 1988.
25. McCartney, N., and R. S. McKelvie. The role of resistance training in patients with cardiac disease. J. Card. Risk 3:160-166, 1996.
26. McKelvie, R. S., N. McCartney, C. W. Tomlinson, R. Bauer, and J. D. Macdougall. Comparison of hemodynamic responses to cycling and resistance exercise in congestive heart failure secondary to ischemic cardiomyopathy. Am. J. Cardiol. 76:977-979, 1995.
27. McKelvie, R. S., K. K. Teo, N. McCartney, D. Humen, T. Montague, and S. Yusuf. Effects of exercise training in patients with congestive heart failure: A critical review. J. Am. Coll. Cardiol. 25:789-796, 1995.
28. Miles, D. S., J. J. Owens, J. C. Golden, and R. W. Gotshall. Central and peripheral hemodynamics during maximal leg extension exercise. Eur. J. Appl. Physiol. 56:12-17, 1987.
29. Mitchell, J. H., and K. Wildenthal. Static (isometric) exercise and the heart: physiological and clinical considerations. Ann. Rev. Med. 24:369-381, 1974.
30. Mitchell, J. H. Cardiovascular control during exercise: central and reflex neural mechanisms. Am. J. Cardiol. 55:34D-41D, 1985.
31. Sagiv, M., P. Hanson, M. Besozzi, and F. Nagle. Left ventricular responses to upright isometric handgrip and deadlift in men with coronary artery disease. Am. J. Cardiol. 55:1298-1302, 1985.
32. Sale D. G., D. E. Moroz, R. S. McKelvie, J. D. Macdougall, and N. McCartney. Effect of training on the blood pressure response to weight lifting. Can. J. Appl. Physiol. 19:60-74, 1994.
33. Sale, D. G., D. E. Moroz, R. S. McKelvie, J. D. Macdougall, and N. McCartney. Comparison of blood pressure response to isokinetic and weight-lifting exercise. Eur. J. Appl. Physiol. 67:115-120, 1993.
34. Sullivan, J. P., P. Hanson, S. Rahko, and J. D. Folts. Continuous measurement of left ventricular performance during and after maximal isometric deadlift exercise. Circulation 85:1406-1413, 1992.
35. Vander, L. B., B. A. Franklin, D. Wrisley, and M. Rubenfire. Acute cardiovascular responses to Nautilus exercise in cardiac patients: implications for exercise training. Ann. Sports Med. 2:165-169, 1986.
36. Vitcenda, M. S., P. Hanson, J. D. Folts, and M. Besozzi. Impairment of left ventricular function during maximal isometric deadlifting. J. Appl. Physiol. 69:2062-2066, 1990.
37. Wiecek, E. M., N. McCartney, and R. S. McKelvie. Comparison of direct and indirect measures of systemic arterial pressure during weightlifting in coronary artery disease. Am. J. Cardiol. 66:1065-1069, 1990.


© 1999 Lippincott Williams & Wilkins, Inc.