Exercise Is Muscle Mitochondrial Medicine

Oliveira, Ashley N.; Richards, Brandon J.; Slavin, Mikhaela; Hood, David A.

doi:10.1249/jes.0000000000000250

Cited by 16 publications

(13 citation statements)

References 89 publications

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“…Similar findings have been reported in numerous other forms of muscle inactivity (reviewed in [25,27,79]). Indeed, evolving evidence suggests that mitochondrial fission and remodeling of mitochondria play a contributory role in skeletal muscle atrophy due to inactivity, aging, and several chronic diseases [25,27,53,79,80].…”

Section: Mitochondrial Dysfunction Resulting In Increased Mitochondrial Ros Emission Promotes Inactivity-induced Muscle Atrophysupporting

confidence: 87%

“…For example, muscle inactivity resulting from denervation is associated with changes in the expression of key fission and fusion proteins that results in the disruption of the mitochondrial network [78]. Similar findings have been reported in numerous other forms of muscle inactivity (reviewed in [25,27,79]). Indeed, evolving evidence suggests that mitochondrial fission and remodeling of mitochondria play a contributory role in skeletal muscle atrophy due to inactivity, aging, and several chronic diseases [25,27,53,79,80].…”

Section: Mitochondrial Dysfunction Resulting In Increased Mitochondrial Ros Emission Promotes Inactivity-induced Muscle Atrophysupporting

confidence: 63%

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Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity

Hyatt

Powers

2021

Antioxidants

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Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions can promote skeletal muscle wasting, including several chronic diseases, cancer chemotherapy, aging, and prolonged inactivity. Although the mechanisms responsible for this loss of muscle mass is multifactorial, mitochondrial dysfunction is predicted to be a major contributor to muscle wasting in various conditions. This systematic review will highlight the biochemical pathways that have been shown to link mitochondrial dysfunction to skeletal muscle wasting. Importantly, we will discuss the experimental evidence that connects mitochondrial dysfunction to muscle wasting in specific diseases (i.e., cancer and sepsis), aging, cancer chemotherapy, and prolonged muscle inactivity (e.g., limb immobilization). Finally, in hopes of stimulating future research, we conclude with a discussion of important future directions for research in the field of muscle wasting.

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Section: Mitochondrial Dysfunction Resulting In Increased Mitochondrial Ros Emission Promotes Inactivity-induced Muscle Atrophysupporting

confidence: 87%

Section: Mitochondrial Dysfunction Resulting In Increased Mitochondrial Ros Emission Promotes Inactivity-induced Muscle Atrophysupporting

confidence: 63%

Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity

Hyatt

Powers

2021

Antioxidants

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“…Regular endurance exercise improves cardiorespiratory fitness and skeletal muscle function and has well-documented health effects, including reduced all-cause mortality [ 9 ]. It furthermore importantly influences mitochondrial health [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

The Muscle-Brain Axis and Neurodegenerative Diseases: The Key Role of Mitochondria in Exercise-Induced Neuroprotection

Burtscher

Millet

Place

et al. 2021

IJMS

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Regular exercise is associated with pronounced health benefits. The molecular processes involved in physiological adaptations to exercise are best understood in skeletal muscle. Enhanced mitochondrial functions in muscle are central to exercise-induced adaptations. However, regular exercise also benefits the brain and is a major protective factor against neurodegenerative diseases, such as the most common age-related form of dementia, Alzheimer’s disease, or the most common neurodegenerative motor disorder, Parkinson’s disease. While there is evidence that exercise induces signalling from skeletal muscle to the brain, the mechanistic understanding of the crosstalk along the muscle–brain axis is incompletely understood. Mitochondria in both organs, however, seem to be central players. Here, we provide an overview on the central role of mitochondria in exercise-induced communication routes from muscle to the brain. These routes include circulating factors, such as myokines, the release of which often depends on mitochondria, and possibly direct mitochondrial transfer. On this basis, we examine the reported effects of different modes of exercise on mitochondrial features and highlight their expected benefits with regard to neurodegeneration prevention or mitigation. In addition, knowledge gaps in our current understanding related to the muscle–brain axis in neurodegenerative diseases are outlined.

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“…Regular endurance exercise improves mitochondrial health, mitochondrial plasticity, and mitochondrial biogenesis and respiration [ 286 , 287 ]. It also enhances antioxidant capacities and the affinity of mitochondria for oxygen, improving healthy aging ([ 288 , 289 , 290 , 291 ] and references therein).…”

Section: Lifestyle Modificationsmentioning

confidence: 99%

Disentangling Mitochondria in Alzheimer’s Disease

Johri

2021

IJMS

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Alzheimer’s disease (AD) is a major cause of dementia in older adults and is fast becoming a major societal and economic burden due to an increase in life expectancy. Age seems to be the major factor driving AD, and currently, only symptomatic treatments are available. AD has a complex etiology, although mitochondrial dysfunction, oxidative stress, inflammation, and metabolic abnormalities have been widely and deeply investigated as plausible mechanisms for its neuropathology. Aβ plaques and hyperphosphorylated tau aggregates, along with cognitive deficits and behavioral problems, are the hallmarks of the disease. Restoration of mitochondrial bioenergetics, prevention of oxidative stress, and diet and exercise seem to be effective in reducing Aβ and in ameliorating learning and memory problems. Many mitochondria-targeted antioxidants have been tested in AD and are currently in development. However, larger streamlined clinical studies are needed to provide hard evidence of benefits in AD. This review discusses the causative factors, as well as potential therapeutics employed in the treatment of AD.

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Exercise Is Muscle Mitochondrial Medicine

Cited by 16 publications

References 89 publications

Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity

Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity

The Muscle-Brain Axis and Neurodegenerative Diseases: The Key Role of Mitochondria in Exercise-Induced Neuroprotection

Disentangling Mitochondria in Alzheimer’s Disease

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