How Exercise Reduces Heart Attack Risk

May 8, 2013 | Byron J. Richards, Board Certified Clinical Nutritionist

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 How Exercise Reduces Heart Attack Risk
Researchers from Emory University School of Medicine, University of Colorado at Boulder, and Johns Hopkins University School of Medicine set out to understand exactly how exercise benefits the heart and why regular exercisers who suffer a heart attack have improved survival compared to non-exercisers.

They found that a four-week voluntary exercise program1 in mice protected them from experimental induced heart injury, a benefit that was sustained for a full week following the last session of exercise. It is well known that aerobic exercise promotes the production of friendly nitric oxide, endothelial nitric oxide synthase (eNOS), by activating the enzyme that helps make eNOS. In turn, the extra eNOS helps the heart and circulation relax, improving blood flow. Interestingly, the researchers found that eNOS was converted by the heart and in the circulation and then stored as an eNOS savings account (eNOS was attached to a protein via sulfur, taking the form of nitrite and nitrosothiols). This stored eNOS could then be released out of the savings account as needed to improve cardiovascular function, even under stress.

Also of interest is that aerobic exercise activates fat burning almost immediately. This study found that the activation of adrenaline receptors within white adipose tissue (β3-adrenergic receptors) was essential for optimal eNOS production and storage, linking the health of white adipose tissue to the cardioprotective response of exercise.

“Our study provides new evidence that nitric oxide generated during physical exercise is stored in the bloodstream and heart, in the form of nitrite and nitrosothiols. These more stable nitric oxide intermediates, appear to be critical for the cardioprotection against a subsequent heart attack,” said senior author David Lefer, PhD, professor of surgery at Emory University School of Medicine.

There are several points to understand. The endorphin anti-inflammatory benefit from aerobic exercise tends to last about 48 hours, assuming a healthy response to exercise. The eNOS response is synergistic yet different. Once conditioned by regular aerobic exercise, a savings account of protective eNOS builds up, appearing to last for approximately one week after exercise is stopped. Both anti-inflammatory mechanisms are vital to health.

The animal study mentioned above showed that β3-adrenergic receptors were essential for the eNOS response. It is significant to note that the mice in this experiment were not overweight. Overweight humans exhibit “adrenaline resistance” in their white adipose tissue, which is likely to blunt a healthy eNOS response. On the other hand, as a person loses weight with aerobic exercise, adrenaline resistance diminishes and cardioprotective eNOS increases. This is yet another good reason for those who are overweight to commit to a good weight loss program. It also means that those who are significantly out of shape should build their fitness level gradually, as the inability to activate these β3-adrenergic receptors in white adipose tissue actually increases cardio stress from exercise.

Unfriendly and inflammatory nitric oxide (iNOS) wreaks havoc in the body, brain, and cardiovascular system. In healthy individuals, eNOS levels should surpass iNOS levels. An excellent way to boost eNOS is to exercise, assuming you have a healthy response to that exercise. Various nutrients enhance the exercise response and may be beneficial, especially for unfit people seeking a healthy path to recovering their fitness.

Referenced Studies

  1. ^ Exercise and eNOS Reserves  Circulation Research,  J. W. Calvert, M. Elston, J. Pablo Aragon, C. K. Nicholson, B. F. Moody, R. L. Hood, A. Sindler, S. Gundewar, D. R. Seals, L. A. Barouch, D. J. Lefer.
  2. ^ Resveratrol Boosts Endothelial Nitric Oxide Synthase  Br J Pharmacol.  Förstermann U, Li H.

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