Research Perspective Volume 14, Issue 23 pp 9388—9392

Figure 1. Late-in-life exercise training boosts autophagic flux to an extent that rejuvenates cardiac function. Accrual of ubiquitinated proteins that is, in part, secondary to impaired autophagic flux occurs over time and contributes to age-associated myocardial dysfunction (red lines and arrows). In mice, lifestyle (e.g., caloric restriction), nutraceutical (e.g., spermidine ingestion), and pharmacological (e.g., rapamycin-treatment) interventions initiated late-in-life boost cardiac autophagy and preserve myocardial function (blue lines and arrows). Cho et al. demonstrate that a physiological intervention (i.e., exercise-training), even when initiated late-in-life, improves autophagic flux, clears ubiquitinated proteins, reduces oxidant stress, and enhances cardiac function vs. results obtained from age-matched mice that did not train. These data provide the first evidence that habitual physical exercise, even when initiated late-in-life, is a viable adjunct “therapy” to improve/maintain myocardial performance during the inevitable process of aging.