Cited by 207Muscle Physiology and DisordersAdipokines, Inflammation, and Metabolic DiseasesTGF-β signaling in diseases

Expression and function of myostatin in obesity, diabetes, and exercise adaptation

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ALLEN, DAVID L., HITTEL, DUSTIN S., MCPHERRON, ALEXANDRA C.·2011·Medicine & Science in Sports & Exercise

Abstract

Myostatin is a member of the transforming growth factor-β/bone morphogenetic protein (TGF-β/BMP) superfamily of secreted factors that functions as a potent inhibitor of skeletal muscle growth. Moreover, considerable evidence has accumulated that myostatin also regulates metabolism and that its inhibition can significantly attenuate the progression of obesity and diabetes. Although at least part of these effects on metabolism can be attributable to myostatin's influence over skeletal muscle growth and therefore on the total volume of metabolically active lean body mass, there is mounting evidence that myostatin affects the growth and metabolic state of other tissues, including the adipose and the liver. In addition, recent work has explored the role of myostatin in substrate mobilization, uptake, and/or utilization of muscle independent of its effects on body composition. Finally, the effects of both endurance and resistance exercise on myostatin expression, as well as the potential role of myostatin in the beneficial metabolic adaptations occurring in response to exercise, have also begun to be delineated in greater detail. The purpose of this review was to summarize the work to date on the expression and function of myostatin in obesity, diabetes, and exercise adaptation.

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  • Inhibition of myostatin upregulates oxidative metabolism in skeletal muscle.

    “On the contrary, inhibition of myostatin upregulates oxidative metabolism in SkM [115].”

    From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [115]

    The Myostatin and Endurance Exercise Adaptation section (page unavailable) reports that untrained myostatin-null mice have more fast, glycolytic muscle fibers and poorer endurance performance, contrary to a general claim that inhibition upregulates skeletal-muscle oxidative metabolism. It also says their muscle oxidative potential increases with endurance training comparably to wild-type mice, not that myostatin inhibition itself causes the increase. (LLM, conf=0.78)

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  • Myostatin was the first identified muscle-secreted factor and is known to promote skeletal muscle atrophy.

    “Myostatin was the first identified muscle-secreted factor and is known to promote SkM atrophy [115].”

    From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [115]

    The Introduction says myostatin is secreted and that its overexpression is associated with dramatic muscle atrophy in mice. It describes myostatin’s identification in 1997 but does not say it was the first muscle-secreted factor identified. Page numbers are not available in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Myostatin is the only myokine known to be downregulated by acute and chronic endurance- and resistance-type exercise in both rodents and humans.

    “It is the only myokine known to be downregulated by acute and chronic endurance- and resistance-type exercise in both rodents and humans [115].”

    From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [115]

    The Endurance Exercise Adaptation section reports decreased muscle myostatin expression after acute and chronic endurance exercise, including training in rodents and humans. The Resistance Exercise Adaptation section reports decreases after acute and chronic resistance exercise in humans, but also describes studies finding an increase or no change. The copy does not establish that myostatin is the only myokine with this response or document the full combination of exercise types and durations in both species; page numbers were not available. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Myostatin expression increases in skeletal muscle due to obesity and insulin resistance, and it could favor the loss of skeletal muscle in sarcopenic obesity.

    “Myostatin expression increases in skeletal muscle due to obesity and IR. Thus, it could favor the loss of skeletal muscle in SO [14, 61, 62].”

    From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [61]

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Authors
ALLEN, D. L., HITTEL, D. S., & MCPHERRON, A. C.
Affiliations
  • University of Colorado Boulder (US)
  • University of Calgary (CA)
  • National Institutes of Health (US)
Venue
Medicine & Science in Sports & Exercise
Published
2011-10
Volume
43
Issue
10
Pages
1828-1835
ISSN
0195-9131 (ISSN-L)
OpenAlex
W2008438711
Cited by
207
References
75
Citations by year
2026: 9 · 2025: 13 · 2024: 19 · 2023: 17 · 2022: 24 · 2021: 16 · 2020: 13 · 2019: 14 · 2018: 12 · 2017: 13 · 2016: 7 · 2015: 11 · 2014: 17 · 2013: 9 · 2012: 9
FWCI
1.10
Type
journal article
Language
en
Open access
Locations
  • Medicine & Science in Sports & Exercise (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (ZIADK056020, ZIADK075048)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
myostatin, obesity, diabetes mellitus, exercise adaptation, skeletal muscle growth, adipose tissue, liver, substrate mobilization, lean body mass, endurance exercise, resistance training, metabolic adaptation
MeSH terms
Adaptation, Physiological, Adipose Tissue, Animals, Diabetes Mellitus, Type 2, Female, Humans, Liver, Male, Obesity, Exercise, Muscle, Skeletal, Mice, Rats, Myostatin

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