That's how a new research paper poses the question, and its positive but still tentative results show: "Briefly we found that low intensity exercise training markedly delayed the onset of overt CHF without a reduction in antecedent hypertension. Additionally, we found that some, but not all, of the classic cellular and systemic physiological alterations normally associated with the development of overt CHF were attenuated with exercise training."
It's not an idle issue. The American Heart Association (AHA) 2005 Statistics Update reports that 65 million Americans have high blood pressure (hypertension) and nearly 5 million are suffering from CHF, where the chances of survival drop rapidly, as about 75% of patients die within 8 years after diagnosis.
"The key findings in this study," according to laboratory director Russell L. Moore, "are that (1) exercise can delay the onset of decompensated heart failure and improve survivability and (2) this effect is strongly dependent on the level of intensity of the exercise. You can push the level over the edge quickly," he added. "Not that long ago, clinicians were afraid to even suggest a little exercise in patients with CHF. However, our study, along with several human studies, shows a definite trend indicating that moderate intensity exercise has a potential role in stemming the downward spiral in heart failure," Moore said.
The paper, "Low-intensity exercise training delays the onset of decompensated heart failure in the spontaneously hypertensive heart failure (SHHF) rat," appears in the November edition of the American Journal of Physiology-Heart and Circulatory Physiology, published by the American Physiological Society. Research was Craig A. Emter, Sylvia A. McCune, Genevieve C. Sparagna, and Russell L. Moore at the University of Colorado at Boulder, and M. Judith Radin at Ohio State University.
Exercise could delay use of drug interventions, improve quality of life
Moore noted that the experiment was performed "on an animal model of CHF that shares many striking similarities to human CHF and we found that low-intensity exercise works in a way that is consistent with preliminary human results. Using exercise early in the disease might leave more expensive options like drug therapies until later, thus avoiding their inevitable side-effects. At the same time, it's likely that even low-level exercise has the additional potential of an improved life style."
Moore said the human equivalent of the exercise in the experiments would be a "brisk, but not taxing, walk." The paper noted that "our results underscore the importance of using low intensity exercise at a 'tolerable intensity'….(The) final training intensity was quite low as evidenced by the absence of a training-induced increase in skeletal muscle citrate synthase activity or body weight loss."
Model studies show decisive protection due to exercise, danger of over-exertion
The experiment involved three sedentary control groups (9 months, 15 months and 22 months of age) and two groups of rats that "trained" for six months; one group starting training at 9 months of age, the other at 16 months of age. The subjects were spontaneously hypertensive heart failure (SHHF) rats. True lean male SHHF rats develop hypertension at 3-4 months and spontaneously develop terminal overt CHF at 18-23 months, 100% of the time. The onset of hypertension preceding CHF in this model is particularly important because 75% of human CHF cases have antecedent hypertension, the 2005 AHA Update reports.
The exercise training started at 9 and 16 months of age, consisting of treadmill running three days a week, 45 minutes a day for six months. During the first month of training, the speed was increased from 10 meters/minute to 17.5 m/min. However three rats in the 9-month group experienced sudden death, though no animals in the 16-month group were adversely affected by the higher speed. Following the deaths of the younger rats, the speed was reduced to 14 m/min, and no further deaths occurred.
After six months of training, when the two oldest groups were 22 months of age, nine rats in the oldest sedentary group were near death in severe, end-stage decompensated heart failure (one had already died) and the experiment was terminated to allow for improved tissue analysis and comparison. Exercise improved survivability (p < 0.01) since all (nine) rats that started training at 16 months of age were still alive.
Exercise delays or suppresses many physiological changes associated with CHF
In addition to the delayed onset of CHF and increased mortality, the exercise regimen "prevented or suppressed alterations in myosin heavy chain isoform expression, cardiac cell morphology, proteinuria, plasma ANP, and body composition that normally occur with the development of overt heart failure," the paper reported. "Furthermore, the model of exercise training and heart failure described in this work may ultimately be of value in dissecting out the specific cellular and molecular processes that are influenced by training and that are required for improved survival in a setting of developing heart failure," the paper concluded.
Moore said the experimental results "are only the beginning" in trying to understand "how the heart interprets the exercise stimulus and what mechanisms are responsible for protecting the heart from going into heart failure." Moore outlined the following areas of interest:
Source and funding
The paper, "Low-intensity exercise training delays the onset of decompensated heart failure in the spontaneously hypertensive heart failure (SHHF) rat," appears in the November edition of the American Journal of Physiology-Heart and Circulatory Physiology, published by the American Physiological Society. Research was Craig A. Emter, Sylvia A. McCune, Genevieve C. Sparagna, and Russell L. Moore at the Department of Integrative Physiology, University of Colorado at Boulder, and M. Judith Radin at the Department of Veterinary Biosciences, Ohio State University, Columbus.
Research was supported by NIH/National Heart, Lung, and Blood Institute (Moore) and American Heart Association Pacific Mountain Affiliate (Sparagna and McCune).
Editor's note: The media may obtain a copy of Emter et al. by contacting Mayer Resnick, at the American Physiological Society, 301.634.7209, cell 301.332.4402 or firstname.lastname@example.org.
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