Abstract
Oxidative damage is one mechanism linking aging with chronic diseases including the progressive loss of skeletal muscle mass and function called sarcopenia. Thus, mitigating oxidative damage is a potential avenue to prevent or delay the onset of chronic disease and/or extend healthspan. Mitochondrial hormesis (mitohormesis) occurs when acute exposure to stress stimulates adaptive mitochondrial responses that improve mitochondrial function and resistance to stress. For example, an acute oxidative stress via mitochondrial superoxide production stimulates the activation of endogenous antioxidant gene transcription regulated by the redox sensitive transcription factor Nrf2, resulting in an adaptive hormetic response. In addition, acute stresses such as aerobic exercise stimulate the expansion of skeletal muscle mitochondria (i.e., mitochondrial biogenesis), constituting a mitohormetic response that protects from sarcopenia through a variety of mechanisms. This review summarized the effects of age-related declines in mitochondrial and redox homeostasis on skeletal muscle protein homeostasis and highlights the mitohormetic mechanisms by which aerobic exercise mitigates these age-related declines and maintains function. We discussed the potential efficacy of targeting the Nrf2 signaling pathway, which partially mediates adaptation to aerobic exercise, to restore mitochondrial and skeletal muscle function. Finally, we highlight knowledge gaps related to improving redox signaling and make recommendations for future research.
Highlights
In the half century, the world’s population of individuals aged over 65 years will significantly increase
Nrf2, resulting in an adaptive hormetic response. Acute stresses such as aerobic exercise stimulate the expansion of skeletal muscle mitochondria, constituting a mitohormetic response that protects from sarcopenia through a variety of mechanisms
This review summarized the effects of age-related declines in mitochondrial and redox homeostasis on skeletal muscle protein homeostasis and highlights the mitohormetic mechanisms by which aerobic exercise mitigates these age-related declines and maintains function
Summary
In the half century, the world’s population of individuals aged over 65 years will significantly increase. Often touted as a beneficial health behavior, exercise is somewhat underappreciated as a means to target many of the hallmarks of aging and slow age-related declines in function. One of the suspected primary mechanisms by which aerobic exercise confers beneficial health adaptations is through mitohormesis. We describe the age-related decline in mitochondrial function, the concomitant decline in redox homeostasis, and their combined deleterious effect on skeletal muscle function. We discuss the mitohormetic effect of an acute bout of aerobic exercise as a means to improve redox homeostasis and mitochondrial function. We highlight the mitohormetic adaptations to lifelong aerobic exercise as a means to prevent age-related declines in mitochondrial function and redox homeostasis to maintain skeletal muscle health with age
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