We propose the beneficial effects of exercise are in part mediated through the prevention and elimination of senescent cells. Exercise counters multiple forms of age-related molecular damage that initiate the senescence program and activates immune cells responsible for senescent cell clearance. Preclinical and clinical evidence for exercise as a senescence-targeting therapy and areas needing further investigation are discussed.
Retrotransposons are gene segments that proliferate in the genome, and the Long INterspersed Element 1 (LINE-1 or L1) retrotransposon is active in humans. Although older mammals show enhanced skeletal muscle L1 expression, exercise generally reverses this trend. We hypothesize skeletal muscle L1 expression influences muscle physiology, and additional innovative investigations are needed to confirm this hypothesis.
In this review, we highlight recent studies from our group and others that have characterized the cardiovascular adjustments that occur after acute heat exposure. Special emphasis will be placed on underlying mechanisms and clinical implications. Finally, we postulate that these acute cardiovascular adjustments may predict the long-term adaptive response to chronic heat therapy.
Specific nervous system functions and the regulating roles of oxytocin have evolved because of the necessity to negotiate increasingly complex social systems. We hypothesize that acute and long-term physical activity and exercise have the potential to benefit social cognitive abilities, such as emotion recognition and regulation, by operating on these functions.
Approximately 6 million individuals have heart failure in the United States alone and 15 million in Europe. Left ventricular assist devices (LVAD) improve survival in these patients, but functional capacity may not fully improve. This article examines the hypothesis that patients supported by LVAD experience persistent reductions in functional capacity and explores mechanisms accounting for abnormalities in exercise tolerance.
Aging induces physiological and molecular changes in the heart that increase the risk for heart disease. Several of these changes are targetable by exercise. We hypothesize that the mechanisms by which exercise improves cardiac function in the aged heart differ from those in the young exercised heart.
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