Age-related changes in skeletal muscle mitochondria: the role of exercise

Seo, Dongju; Lee, Sung Ryul; Kim, Nari; Ko, Kyung Soo; Rhee, Byoung Doo; Han, Jin

doi:10.1016/j.imr.2016.07.003

Cited by 66 publications

(43 citation statements)

References 41 publications

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“…For example, attenuation of muscle regeneration in satellite cells from old mice was shown to decrease when aged satellite cells were paired to young circulatory environments, indicating that repair can be influenced by the local cellular environment. Several studies have suggested that excess ROS generated from mitochondrial respiration can damage cellular structures and may contribute to cellular aging . It is possible, although speculative, that skeletal muscle containing high levels of SIRT1 may release more mitochondrial‐associated ROS than SIRT1 knockout models during injury and repair and thereby impair the proliferation capacity in satellite cells during muscle repair.…”

Section: Discussionmentioning

confidence: 99%

The role of SIRT1 in skeletal muscle function and repair of older mice

Myers

Shepherd

Durr

et al. 2019

J cachexia sarcopenia muscle

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Background Sirtuin 1 (SIRT1) is a NAD+ sensitive deacetylase that has been linked to longevity and has been suggested to confer beneficial effects that counter aging‐associated deterioration. Muscle repair is dependent upon satellite cell function, which is reported to be reduced with aging; however, it is not known if this is linked to an aging‐suppression of SIRT1. This study tested the hypothesis that Sirtuin 1 (SIRT1) overexpression would increase the extent of muscle repair and muscle function in older mice. Methods We examined satellite cell dependent repair in tibialis anterior, gastrocnemius, and soleus muscles of 13 young wild‐type mice (20–30 weeks) and 49 older (80+ weeks) mice that were controls ( n = 13), overexpressed SIRT1 in skeletal muscle ( n = 14), and had a skeletal muscle SIRT1 knockout ( n = 12) or a satellite cell SIRT1 knockout ( n = 10). Acute muscle injury was induced by injection of cardiotoxin (CTX), and phosphate‐buffered saline was used as a vector control. Plantarflexor muscle force and fatigue were evaluated before or 21 days after CTX injection. Satellite cell proliferation and mitochondrial function were also evaluated in undamaged muscles. Results Maximal muscle force was significantly lower in control muscles of older satellite cell knockout SIRT1 mice compared to young adult wild‐type (YWT) mice ( P < 0.001). Mean contraction force at 40 Hz stimulation was significantly greater after recovery from CTX injury in older mice that overexpressed muscle SIRT1 than age‐matched SIRT1 knockout mice ( P < 0.05). SIRT1 muscle knockout models (P < 0.05) had greater levels of p53 (P < 0.05 MKO, P < 0.001 OE) in CTX‐damaged tissues as compared to YWT CTX mice. SIRT1 overexpression with co‐expression of p53 was associated with increased fatigue resistance and increased force potentiation during repeated contractions as compared to wild‐type or SIRT1 knockout models ( P < 0.001). Muscle structure and mitochondrial function were not different between the groups, but proliferation of satellite cells was significantly greater in older mice with SIRT1 muscle knockout ( P < 0.05), but not older SIRT1 satellite cell knockout models, in vitro , although this effect was attenuated in vivo after 21 days of recovery. Conclusions The data suggest skeletal muscle structure, function, and recovery after CTX‐induced injury are not significantly influenced by gain or loss of SIRT1 abundance alone in skeletal muscle; however, muscle function is impaired by ablation of SIRT1 in satellite cells. SIRT1 appears to interact with p53 to improve muscle fatigue resistance after repair from muscle injur...

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Section: Discussionmentioning

confidence: 99%

The role of SIRT1 in skeletal muscle function and repair of older mice

Myers

Shepherd

Durr

et al. 2019

J cachexia sarcopenia muscle

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“…Physical activity and proper nutrition represent the best lifestyle measures to prevent and to retard age-related sarcopenia and progressive muscular weakness [115,116]. Remarkably, regular and controlled exercise with advancing age prolongs lifespan and improves skeletal muscle mass and performance [117,118].…”

Section: Exercise-an Anti-aging Strategy That Preserves Mitochondria mentioning

confidence: 99%

Impact of Melatonin on Skeletal Muscle and Exercise

Stacchiotti

Favero

Rodella

2020

Cells

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Skeletal muscle disorders are dramatically increasing with human aging with enormous sanitary costs and impact on the quality of life. Preventive and therapeutic tools to limit onset and progression of muscle frailty include nutrition and physical training. Melatonin, the indole produced at nighttime in pineal and extra-pineal sites in mammalians, has recognized anti-aging, anti-inflammatory, and anti-oxidant properties. Mitochondria are the favorite target of melatonin, which maintains them efficiently, scavenging free radicals and reducing oxidative damage. Here, we discuss the most recent evidence of dietary melatonin efficacy in age-related skeletal muscle disorders in cellular, preclinical, and clinical studies. Furthermore, we analyze the emerging impact of melatonin on physical activity. Finally, we consider the newest evidence of the gut–muscle axis and the influence of exercise and probably melatonin on the microbiota. In our opinion, this review reinforces the relevance of melatonin as a safe nutraceutical that limits skeletal muscle frailty and prolongs physical performance.

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“…Mitochondria are dynamic organelles that regulate cellular functions such as cellular respiration, calcium homeostasis, and reactive oxygen species (ROS) production. The most important role of mitochondria is energy metabolism, which involves production of adenosine triphosphate (ATP) through oxidative phosphorylation in skeletal muscle mitochondria [ 10 ]. In addition, mitochondria have a morphological and structural cycle referred to as mitochondrial dynamics (fusion, fission, and mitophagy) [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of exercise on obesity-induced mitochondrial dysfunction in skeletal muscle

Heo

Park

et al. 2017

Korean J Physiol Pharmacol

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Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all associated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dynamic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochondria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes. Obesity is associated with impairment of mitochondrial function (e.g., decrease in O2 respiration and increase in oxidative stress) in skeletal muscle. The balance between mitochondrial fusion and fission is critical to maintain mitochondrial homeostasis in skeletal muscle. Obesity impairs mitochondrial dynamics, leading to an unbalance between fusion and fission by favorably shifting fission or reducing fusion proteins. Mitophagy is the catabolic process of damaged or unnecessary mitochondria. Obesity reduces mitochondrial biogenesis in skeletal muscle and increases accumulation of dysfunctional cellular organelles, suggesting that mitophagy does not work properly in obesity. Mitochondrial dysfunction and oxidative stress are reported to trigger apoptosis, and mitochondrial apoptosis is induced by obesity in skeletal muscle. It is well known that exercise is the most effective intervention to protect against obesity. Although the cellular and molecular mechanisms by which exercise protects against obesity-induced mitochondrial dysfunction in skeletal muscle are not clearly elucidated, exercise training attenuates mitochondrial dysfunction, allows mitochondria to maintain the balance between mitochondrial dynamics and mitophagy, and reduces apoptotic signaling in obese skeletal muscle.

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Age-related changes in skeletal muscle mitochondria: the role of exercise

Cited by 66 publications

References 41 publications

The role of SIRT1 in skeletal muscle function and repair of older mice

The role of SIRT1 in skeletal muscle function and repair of older mice

Impact of Melatonin on Skeletal Muscle and Exercise

Effects of exercise on obesity-induced mitochondrial dysfunction in skeletal muscle

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