Exercise Science and Sport Management
Accumulation of dysfunctional and damaged cellular proteins and organelles occursduring aging, resulting in a disruption of cellular homeostasis and progressive degen-eration and increases the risk of cell death. Moderating the accrual of these defunctcomponents is likely a key in the promotion of longevity. While exercise is knownto promote healthy aging and mitigate age‐related pathologies, the molecular under-pinnings of this phenomenon remain largely unclear. However, recent evidencessuggest that exercise modulates the proteome. Similarly, caloric restriction (CR), aknown promoter of lifespan, is understood to augment intracellular protein quality.Autophagy is an evolutionary conserved recycling pathway responsible for thedegradation, then turnover of cellular proteins and organelles. This housekeepingsystem has been reliably linked to the aging process. Moreover, autophagic activitydeclines during aging. The target of rapamycin complex 1 (TORC1), a central kinaseinvolved in protein translation, is a negative regulator of autophagy, and inhibitionof TORC1 enhances lifespan. Inhibition of TORC1 may reduce the production ofcellular proteins which may otherwise contribute to the deleterious accumulationobserved in aging. TORC1 may also exert its effects in an autophagy‐dependentmanner. Exercise and CR result in a concomitant downregulation of TORC1 activityand upregulation of autophagy in a number of tissues. Moreover, exercise‐inducedTORC1 and autophagy signaling share common pathways with that of CR. There-fore, the longevity effects of exercise and CR may stem from the maintenance ofthe proteome by balancing the synthesis and recycling of intracellular proteins andthus may represent practical means to promote longevity.
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