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Vigorous exercise may reverse cardiac effects of sedentary lifestyle
Two years of high-intensity exercise may reverse the effects of heart aging due to sedentary lifestyle and reduce the risk for HF with preserved ejection fraction by preventing the increase in cardiac stiffness that is often linked to sedentary aging, according to data published in Circulation.
According to a press release issued by the University of Texas Southwestern, if an exercise regimen consisting of 30-minute sessions plus warmup and cooldown performed four to five times per week is started early enough in life, the heart remains pliable enough to remodel itself.
In an interview with Cardiology Today, Benjamin D. Levine, MD, FACC, FAHA, FACSM, director of the Institute for Exercise and Environmental Medicine; S. Finley Ewing Jr. Chair for Wellness at Texas Health Presbyterian Dallas; Harry S. Moss Heart Chair for Cardiovascular Research; and professor of medicine and cardiology and distinguished professor of exercise science at the University of Texas Southwestern Medical Center, said the demonstration that patients at risk for HF can reverse the adverse effects of sedentary aging on the heart by intervening in the “sweet spot” of late middle age is critical to preserving functional capacity with aging and forestalling aging- related diseases such as HFpEF.
“We have already defined the optimal dose of exercise required to preserve the youthful structure of the heart as well as the time in the aging process when cardiovascular stiffening begins. However, in previous studies we were unable to reverse these effects if we started exercise much later in life,” Levine said. “So, our key question was whether there was indeed a sweet spot during which the atrophy and stiffening of the heart could be reversed if exercise was started at the right dose.”
To assess the effects of 2 years of supervised high-intensity exercise training on LV stiffness, Levine and colleagues enrolled 61 healthy, sedentary middle-aged participants who were randomly assigned to 2 years of exercise training or attention control.
To define LV end-diastolic pressure-volume relationships and Frank-Starling curves, researchers performed right heart catheterization and 3-D echocardiography with preload manipulations.
The researchers then calculated LV stiffness by curve fit of the diastolic pressure-volume curve and measured maximal oxygen uptake (VO2max) to quantify changes in fitness regimen.
Fifty-three participants completed the study.
Adherence to prescribed exercise sessions was 88 ± 11%.
The researchers observed an 18% increase in VO2max (exercise group: from 29 mL/kg/min to 34 mL/kg/min; controls: from 29.5 mL/kg/min to 28.7 mL/kg/min; P < .001 between groups) and a reduction in LV stiffness (from 0.072 to 0.051; P = .0018). There was, however, no change in controls (P = .83).
According to the researchers, exercise increased LV end-diastolic volume (P < .001 between groups); however, pulmonary capillary wedge pressure was unchanged. This provided greater stroke volume for any given filling pressure (P = .007).
Levine told Cardiology Today that understanding the basic mechanisms underlying the myocardial response to exercise training will not be simple, and future studies must address the complex stimulus of exercise in terms of duration, intensity, frequency and timing.
“Whether pharmacological approaches that could supplement exercise training could enhance the training response, perhaps push the sweet spot to older age ranges... would be very interesting,” Levine said. “The other key factor associated with aging hearts is slowing of relaxation. Intriguingly, this slowing of relaxation is not much affected by lifelong exercise training, even at very high doses, yet it remains an essential part of the CV response to exercise.”
According to Levine, the most important next question for researchers is whether the same outcomes can come from patients who are at especially high risk for HF, such as patients with hypertension, diabetes and obesity. – by Dave Quaile
For more information:
Benjamin D. Levine, MD, can be reached at Institute for Exercise and Environmental Medicine, 7232 Greenville Ave., Suite 435, Dallas TX 75231; email: benjaminlevine@texashealth.org.
Disclosure: The authors report no relevant financial disclosures.
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This is an excellent study. The authors are to be commended given the length of the study and the ability to maintain such great adherence. The power of the study, besides the length of the intervention, is the measurement of real cardiac physiology. This greatly improves our understanding of cardiac compliance and plasticity with aging as well as the power of exercise-induced cardiac remodeling. We certainly know that "exercise works" even beyond the simple parameters of weight, BP, glucose levels, insulin resistance, lipids, etc, and this study starts to elucidate some of the deeper mechanistic variables.
While the phrase "sweet spot" used by the authors for this age group I think is a bit misleading, as the value should be on lifelong exercise, their point is noted that it is not too late — at least based on this population— to gain valuable cardiac remodeling benefits from a quality exercise program. Note that this program was more than just get off the couch and walk the dog.
The next steps are to study higher-risk groups as well as various types of exercise programs, although given the adherence to the protocols in this study, one could argue that the authors’ approach simply to improve adherence is profound.