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Exercise: The best anti aging pill for your heart

by Luis Serratosa, EAPC Sports Cardiology Section

Risk Factors and Prevention


While sedentary aging is associated with deleterious effects in cardiovascular function including an increase in left ventricular (LV) stiffness, Masters athletes have large compliant LVs similar to those of much younger individuals.

In this interesting prospective randomized controlled study (1), the authors hypothesised that an optimised exercise training program, with ≥ 4 days/week including high intensity interval training, initiated in middle-age could reverse the LV stiffening process characteristic of heart failure with preserved ejection fraction (HFpEF).

Sixty one healthy sedentary middle-aged (53±5 years, 48% male) participants were randomly assigned to 2 years of supervised training 4 to 5 times/week (150-180 minutes, including 1-2 sessions of 4 x 4 minutes intervals of exercise at 95% of peak heart rate, 2 moderate intensity exercise sessions and 1-2 strength training sessions) or a yoga and balance training program (control group). A total of 53 participants completed the 2 year study (88% adherence). At 2 years, the exercise training group (n=28) showed an 18% increase in VO2max (29.0 to 34.4 mL·kg-1·min-1) and a decrease in LV stiffness, calculated by curve-fit of the diastolic pressure volume curve (stiffness constant from 0.072 to 0.051, p=0.0018). In contrast, the control group (n=24) showed a slight decrease in VO2max and no change in LV stiffness. Exercise training increased LV end-diastolic volume, while pulmonary capillary wedge pressure (PCWP) was unchanged, allowing for greater stroke volume for any given filling pressure.

Furthermore, the heart rate (HR) of the exercise training group decreased from 63 to 58 beats/min (p=0.0003), while remaining constant at 64 beats/min in the control group. The response to exercise training was not modified by sex.

As mentioned by the authors, the limitations of the study are the evaluation of LV pressure curves by use of mean PCWP as a surrogate for LV end-diastolic pressure; enrolling volunteers willing and able to participate in an intensive exercise regimen; and the predominantly white cohort (approx. 80%), which may limit generalizability of the findings to other racial groups.

According to the results, the authors conclude that regular exercise training may provide protection against the future risk of HFpEF by preventing the pathophysiological increase in cardiac stiffness attributable to sedentary aging. Compared to previous findings of this same group of researchers in older seniors, it is also suggested that intervening earlier (middle-age) in the aging process is necessary to preserve and possibly enhance ventricular compliance. These conclusions are still theoretical and further research is needed to determine whether similar exercise training programs translate into a true reduced risk of developing HFpEF, as well as major reductions in hospitalisations and mortality in this population.

Epidemiological evidence suggests that each 1-metabolic equivalent increase in exercise capacity is associated with a 13% and 15% reduction in all-cause and cardiovascular disease mortality, respectively. Lower HR also has been associated with reductions in mortality, independent of fitness levels. If this is true, it would mean a significant mortality reduction in the subjects of the exercise training group of the present study, who showed a VO2max increase of 5.4 mL·kg-1·min-1 and a HR reduction of 5 beats/min.

Although adherence was excellent in this study, adhering middle-aged sedentary adults to similar exercise training programs, including high intensity interval training sessions, for years might still be challenging.

Since HFpEF is such a common and problematic disease, efforts to reduce it in an aging population should be a priority. This is one more reason for both public and private medical and healthcare organisations to seriously consider investing in physical activity implementation.

Note: The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology

 

 

References

Luis Serratosa commented on this article:

1) Reversing the Cardiac Effects of Sedentary Aging in Middle Age—A Randomized Controlled Trial; Howden EJ, Sarma S, Lawley JS, et al.
Circulation. 2018;137:00–00. DOI: 10.1161/CIRCULATIONAHA.117.030617