2019
DOI: 10.3390/sports7070170
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Exercise-Induced Mitohormesis for the Maintenance of Skeletal Muscle and Healthspan Extension

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 mit… Show more

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Cited by 48 publications
(48 citation statements)
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References 142 publications
(181 reference statements)
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“…The cellular antioxidant capacity is stimulated by low ROS levels that promote an adaptation mechanism leading to increased expression of the detoxifying enzymes and accumulation of antioxidant molecules (see the Exercise Counteracts Cachexia Modulating the Redox Homeostasis section for further details). Among the signaling regulatory factors that sense intracellular ROS, the nuclear factor-kappaB (NF-jB), the activator protein-1 (AP-1), the heat shock transcriptional factor-1 (HSF-1), and the nuclear respiratory factor (Nrf)2 regulate several muscle homeostatic processes and trigger the increased expression of antioxidant enzymes (84).…”
Section: Role Of Oxidative Stress In Muscle Wasting and Dysfunctionmentioning
confidence: 99%
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“…The cellular antioxidant capacity is stimulated by low ROS levels that promote an adaptation mechanism leading to increased expression of the detoxifying enzymes and accumulation of antioxidant molecules (see the Exercise Counteracts Cachexia Modulating the Redox Homeostasis section for further details). Among the signaling regulatory factors that sense intracellular ROS, the nuclear factor-kappaB (NF-jB), the activator protein-1 (AP-1), the heat shock transcriptional factor-1 (HSF-1), and the nuclear respiratory factor (Nrf)2 regulate several muscle homeostatic processes and trigger the increased expression of antioxidant enzymes (84).…”
Section: Role Of Oxidative Stress In Muscle Wasting and Dysfunctionmentioning
confidence: 99%
“…Whereas regular and nonstrenuous exercise leads to low ROS production inducing metabolic adaptations poised to improve muscle function, strenuous exercise leads to excessive ROS levels, resulting in muscle damage (119). Among the adaptations induced by regular exercise, the reduction of systemic inflammation, the improvement of mitochondrial function, and the increase of the antioxidant defenses play a pivotal role in modulating the muscle redox homeostasis (84,116), producing a potentially anticachexia response.…”
Section: Exercise Counteracts Cachexia Modulating the Redox Homeostasismentioning
confidence: 99%
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“…Exercise is widely known to improve mitochondrial health, potentially by providing a hormetic challenge that induces mitochondrial biogenesis [10]. Another potential intervention strategy for enhancing the metabolic flexibility of the mitochondria is intermittent fasting (IF), or more specifically, time-restricted feeding (TRF) [11].…”
Section: Introductionmentioning
confidence: 99%
“…This assumption is made upon the mitohormesis theory. The sublethal stress promoted by gestational CR and consequent improved mitochondrial function observed in latter ages may lead to life span extension and global health improvement (Musci et al, 2019).…”
Section: Discussionmentioning
confidence: 99%