Yang Lee, M.S.

It has been reported that heart failure is the one of the leading cause of hospitalization for patients especially in the over-65 years aged population. Huge amounts of evidence indicate that impairment of myocardial structure and function through aging contribute to the development of heart failure. Age-related cardiac impairment is associated with left ventricular hypertrophy (increased cardiac cell size) and fibrosis (deposition of collagen) which induce diastolic dysfunction and heart failure. These age-related diastolic dysfunctions in the heart affect the elderly negatively in that impaired left ventricular filling reduces the quality of life by increasing the risk of cardiac disease.

In addition, this age-associated cardiac remodeling can cause the development of cardiac infraction in response to increased overload. Previously, we reported that 12 weeks of endurance exercise training reduced fibrosis, collagen accumulation, and geometrrical change in the aging heart. Increased linearity of the collagen network and decreased fibrosis following exercise training reduced internal work of the aging heart, such as lessening metabolic and blood flow requirements, alleviating arrhythmias, and improving heart function. Indeed, the underlying mechanism of the impairment is that the collagen and extra-cellular matrix degradation pathway is dysregulated concurrent with increased collagen deposition. We found that exercise reduced dysregulation of collagen degradation while reduced collagen synthesis. Our recent report confirms that after 12 weeks endurance exercise training, alterations in pathway signaling that elevate collagen degradation were protected. In addition, our current report revealed cellular mechanism underlying age-dependent fibrosis and how exercise ameliorates this process.

Studies with heart failure patients suggest a protective role of exercise training on cardiac function, compliance, and diastolic filling. In addition, master athletes tend to maintain high cardiovascular function, including compliance and stroke volume even at 70 years of age. Most interestingly, people who have been involved in habitual exercise showed protection against age-related filling and relaxation abnormalities, diastolic dysfunction, and stiffness. Indeed, similar to aging, physical inactivity can cause cardiac function impairment. In the elderly, physical inactivity exacerbates risk of heart disease. Therefore, the clinical significance of habitual exercise in the protection of cardiac function especially in elderly is profound.

A question can be raised as to which exercise or what type of exercise will be beneficial. Traditionally, the primary means of improving cardiovascular function and structure is endurance exercise. However, several laboratories suggested that age-related decline partially due to skeletal muscle weakness and strength loss. After 12 weeks resistance training, Frontera et al. from US Department of Agriculture Human Nutrition Research Center reported strength gain accompanied by increased capillary density and aerobic capacity. Therefore, the most important factor is habitual exercise or physical activity with the proper intensity regardless of the type of exercise for elderly populations.

Further Reading

1. Biernacka, A., & Frangogiannis, N. (2011). Aging and Cardiac Fibrosis. Aging and disease, 2(2), 158-173.
2. Kwak, H.-B., Kim, J.-h., Joshi, K., Yeh, A., Martinez, D. A., & Lawler, J.M. (2010). Exercise training reduces fibrosis and matrix metalloproteinase dysregulation in the aging rat heart. The FASEB Journal, 25(3), 1106-1117.
3. Lee, Y., Hord, J. M., Kwak, H.-B., Kim, J.-H., & Lawler, J. M. (2011). Exercise Training Reduces Age-Dependent Elevation of Angiotensin II Type 1 receptor and NAD(P)H Oxidase. The FASEB J., 25(lb), 549.