Authors: Bogdan Mircea Petrescu1, Sorin Riga2, Octavian Vasiliu1, Andrei Gabriel Mangalagiu1
1 Psychiatry Department, “Carol Davila” Central Military Emergency University Hospital, Bucharest,
Romania; PhD student, “Carol Davila” University of Medicine and Pharmacy Bucharest, Romania
2 Department of Stress Research and Prophylaxis, “Prof. Dr. Alexandru Obregia” Clinical Hospital of
Psychiatry, Bucharest, Romania
Accumulation of dysfunctional and damaged cellular proteins and organelles occurs during aging, resulting in a perturbation of cell homeostasis and inexorable degeneration up to cellular death. Therefore, moderating these components may be a key in the promotion of longevity. Exercise is known to promote healthy aging and mitigate age-related pathologies, and recent studies suggest that exercise modulates the proteome. Autophagy is an evolutionary conserved recycling pathway managing degradation, and it declines during aging. The target of rapamycin complex 1 (TORC1), a central kinase involved in protein translation, is a negative regulator of autophagy, and inhibition of TORC1 enhances lifespan. As a consequence, the longevity effects of exercise may stem from the maintenance of the proteome by balancing the synthesis and recycling of intracellular proteins, and thus may promote longevity.
Participation in vigorous physical activity at a specific time point is an indicator of good fitness and health and is associated with a reduced risk of death. However, randomized controlled trials (RCTs) and translational models have not provided strong evidence to show that physical activity started during adulthood extends lifespan and promotes longevity. Physical activity improves fitness and physical function, and confers other health-related effects.
Key words: harmful binomial distress – aging, movement and physical activity, mTOR, stress, muscular contraction, autophagy, longevity.