Whereas resistance exercise (RE) has long been accepted as means of developing and maintaining muscular strength, endurance, power, and muscle mass in healthy adults, its beneficial role in the prevention and management of various chronic conditions (eg, low back pain, osteoporosis, sarcopenia, susceptibility to falls, and impaired function in frail elderly persons) has only recently been recognized. In 1990, The American College of Sports Medicine was the first to recognize RE as a significant component of a comprehensive fitness program for healthy adults of all ages. 1 Subsequently, numerous professional and government health associations and agencies 2-4 now include resistance training in their current recommendations and guidelines for healthy adults. Despite the application of RE to a variety of clinical populations, historically this mode of training had not been indicated for patients with heart disease due to unsubstantiated concerns over the potential for myocardial ischemia, hemodynamic abnormalities, or complex ventricular arrhythmias. Numerous studies (summarized in Wenger et al 5), although conducted largely in men already participating in aerobic exercise training programs, have demonstrated that RE testing and training (often "circuit training") are safe for "clinically stable" cardiac patients. The extent to which the safety and efficacy demonstrated by these studies can be extrapolated to other "cardiac" populations, including those with left ventricular (LV) dysfunction remains unclear. 2 While RE is now an established component of a comprehensive cardiac rehabilitation/secondary prevention program, current professional guidelines 6 at the present do not recommend this mode of training for patients with heart failure and reduced LV function due to lingering safety concerns.

Left ventricular systolic and/or diastolic dysfunction, can result in the pathophysiologic "syndrome" of heart failure (HF) that includes derangement in skeletal muscle, vascular, and pulmonary structure and function as well as alterations in neurohormal responses. 7 The diminished skeletal muscle blood flow, secondary to an attenuated cardiac output, has a negative impact on skeletal muscle mass, morphology, enzymology, and contractile properties. Consequently, abnormal skeletal muscle function is a major component of the exercise intolerance and reduced physical function common among patients with HF. 8 Despite initial concerns over the safety of physical activity in this population, a variety of studies over the past 20 years have shown that aerobic exercise (AE) training can improve the physical function of HF patients, often through improvement in skeletal muscle structure and function. Despite the potential for RE to stimulate greater improvements in skeletal muscle mass, strength, and endurance as compared AE, RE training is not currently indicated for patients with reduced LV function or HF. Before RE (or any intervention) becomes widely accepted and recommended in national guidelines, the safety and efficacy of this mode of training must be firmly established.

Fortunately, we are beginning to see the emergence of studies, such as the one published in the current issue of JCR, 9 attempting to provide support for the hypothesis that RE is a safe and effective mode of training for patients with LV dysfunction or heart failure. The few previously published studies 10-12 examining RE in HF, although generally positive, have been limited by small sample sizes, methodological issues including combining RE with AE (eg, circuit weight training), limited assessments of LV function, and patient selection issues. The authors of the present study 9 are to be congratulated for a timely and carefully performed assessment of strength testing and RE on LV performance in a complex patient population. In addition to confirming observations from earlier investigations, this study contributes unique information to this important area of research as it is the first study to evaluate LV function during 1 RM testing and to evaluate wall motion abnormalities during RE testing and training in patients with mild-moderate LV dysfunction.

In this study, LV performance during strength testing and RE was assessed via transthoracic two-dimensional echocardiography and consequently needs to be viewed cautiously. Due to inherent subjectivity and potential for operator error with echocardiography, direct measurement of cardiac hemodynamics by right heart catheter, although highly invasive, would have been more desirable. Echocardiographic measurements during the GXT (reflecting AE responses) were taken 30 seconds after exercise and therefore reflect recovery rather than peak exercise. In contrast, it appears that RE testing and training measurements were actually recorded during exercise. Furthermore, post-GXT echocardiographic measurements were obtained in the "left decubitus position" (which is recumbent); it is not clear what posture the subjects held for the RE assessments, but presumably it was more upright. Given these limitations, this study did agree with previous reports indicating that hemodynamic responses (heart rate, systolic blood pressure, ejection fraction, cardiac output, LV end-diastolic volume) are actually higher during GXT than during 1RM RE testing or training (at least up to 15 repetitions at up to 60% 1RM). This reinforces the premise that a symptom-limited GXT is a useful screening test for 1RM testing and RE training to 60% 1RM.

Another unique aspect of this study was the attempt to evaluate wall motion abnormalities during RE testing and training. Although similar occurrences of wall motion abnormalities were observed during RE testing and GXT, there was a "moderate" increase in new wall motion abnormalities during RE training (particularly during lower body exercise) as the exercise intensity increased to 60% 1RM. The authors conclude that these findings were "small in magnitude and do not suggest reduced cardiac performance" but fail to provide any further meaningful discussion on the clinical implications of these findings. From these data, it appears that the hemodynamic responses to RE increases as a function of the intensity (%1RM), number of the repetitions, and size of muscle mass involved, yet no discussion of the interaction between these factors was provided. While concerns about RE historically relate to its isometric component, it appears the hemodynamic response to combined isometric and dynamic contractions, typical of RE, appear to create a scenario that improves the myocardial oxygen supply/demand balance at a given rate pressure product through an increased diastolic pressure-time index. Surprisingly, there was no mention of the occurrence or frequency of ventricular arrhythmias or blood pressure abnormalities during RE testing or training. Reporting either the presence or absence of these potential risks would provide the evidence necessary to support or dismiss these common concerns of RE in this population.

As the case with most investigations, study design and methodological issues limit the generalizability of the results from the present study 9 and leave important questions yet unanswered. For instance, the subjects who participated had a fairly mild to moderate degree of LV dysfunction with ejection fractions ranging from 30% to 49% (mean = 42%). Furthermore, these subjects appear to be relatively free of HF signs and symptoms as all were classified as NYHA class I or II. This study was also limited by the homogeneity of the group as all subjects were male and the underlying cause of LV dysfunction for each was ischemic in nature (as opposed to idiopathic etiology-the other major cause of HF). Additionally, the patients used in this investigation had a relatively high functional capacity (mean peak oxygen uptake of 21 mL/kg/min) and were pre-conditioned by participating in an AE program for an average of 2.5 years (range of 3 months to 6 years) before participating in the RE study. Consequently, these findings may not be representative and/or applicable to those with more severe forms of LV dysfunction just entering a rehabilitation program. The sample size of this study was small, but it may have still been useful to stratify the group based on EF to evaluate the possibility of an interaction between the severity of LV dysfunction and the presence of hemodynamic or wall motion abnormalities.

This study was very well done and provides meaningful insight on LV hemodynamics and wall motion abnormalities, in patients with mild-moderate LV dysfunction, during RE testing and training. However, it is likely that most cardiac rehabilitation programs already recommend RE for the type of patients evaluated in this study (ie, aerobically trained, clinically stable with only mild-moderate LV dysfunction). At minimum, this study does demonstrate the safety of 1RM testing and RE up to 60% 1RM for this patient population and provides adequate support to continue this practice. There are several important limitations to this study, though, particularly the generalizability of these findings to a more heterogeneous group of heart failure patients, particularly those with lower EF or more symptomatic heart failure. These patients are presently excluded from RE programs 6 and this study provides no justification to alter this position. Resistance exercise would likely be beneficial for patients with more severe LV dysfunction or heart failure, or both, particularly as a means of increasing functional capacity through changes to skeletal muscle structure and function; however, the safety of this practice has yet to be established and will have to wait until further data is generated.

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