The beneficial effect of myostatin deficiency on maximal muscle force and power is attenuated with age

Schirwis, Elija; Agbulut, Onnik; Vadrot, Nathalie; Mouisel, Etienne; Hourdé, Christophe; Bonnieu, Anne; Butler-Browne, Gillian; Amthor, Helge; Ferry, Arnaud

doi:10.1016/j.exger.2012.11.008

Cited by 23 publications

(17 citation statements)

References 47 publications

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“…Schirwis et al [54] reported that the effects of myostatin deficiency on maximal force and power are greater in young (as compared to old) and female (as compared to male) mice. Bergen et al [33] showed that older females compared to younger have higher myostatin levels and older men have lower myostatin levels compared to younger ones.…”

Section: Discussionmentioning

confidence: 99%

Relationship of muscle function to circulating myostatin, follistatin and GDF11 in older women and men

et al. 2018

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BackgroundMyostatin, its inhibitor follistatin, and growth/differentiation factor 11 (GDF11) have been proposed as factors that could potentially modify biological aging. The study aimed to test whether there is a relationship between these plasma circulating proteins and muscle strength, power and optimal shortening velocity (υopt) of older adults.MethodsThe cross-sectional study included 56 women and 45 men aged 60 years and older. Every participant underwent examination which included anthropometric and bioimpedance analysis measurements, functional and cognitive performance tests, muscle strength of upper and lower extremities, muscle power testing with two different methods and blood analyses.ResultsWomen had higher plasma levels of myostatin and GDF11 than men. Men had higher plasma level of follistatin than women. In women, plasma level of myostatin was negatively correlated with left handgrip strength and υopt. Follistatin was negatively correlated with maximum power output (Pmax), power relative to kg of body mass (Pmax∙kg− 1) (friction-loaded cycle ergometer) and power at 70% of the 1-repetition maximum (1RM) strength value (P70%) of leg press (Keiser pneumatic resistance training equipment), and positively correlated with the Timed Up & Go (TUG) test. GDF11 was negatively correlated with body mass, body mass index, waist circumference, fat mass and the percentage of body fat. In men, there were no significant correlations observed between circulating plasma proteins and muscle function measures.ConclusionsThe circulating plasma myostatin and follistatin are negatively associated with muscle function in older women. There is stronger relationship between these proteins and muscle power than muscle strength. GDF11 has a higher association with the body mass and composition than muscle function in older women.

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Section: Discussionmentioning

confidence: 99%

Relationship of muscle function to circulating myostatin, follistatin and GDF11 in older women and men

et al. 2018

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“…Among them, myostatin is a regulator of skeletal muscles, and it plays a key role in the development and the maintenance of muscles. Myostatin levels increase with muscle atrophy due to neuromuscular inactivity, and with severe muscle wasting in elderly and myoatrophy patients [29]. Therefore, increased myostatin level in human muscles potentially explains the underlying mechanism of decrease muscle mass in sarcopenia.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, myostatin is known to affect myocytes proliferation [6]. It was reported that the beneficial effect of myostatin deficiency is greater in elderly mice [29]. …”

Section: Discussionmentioning

confidence: 99%

Aerobic Exercise Affects Myostatin Expression in Aged Rat Skeletal Muscles: A Possibility of Antiaging Effects of Aerobic Exercise Related With Pelvic Floor Muscle and Urethral Rhabdosphincter

Jeong

Kim

et al. 2014

Int Neurourol J

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PurposeAging-induced loss of muscle mass and subsequent reduction of strength is a fundamental cause of frailty, functional decline, and disability. And this may lead to muscular dysfunction, voiding dysfunction, or urinary incontinence due to pelvic muscle weakness induced by aging. Physical exercise has been recommended for the prevention and the treatment of these age-related frail states. We investigated the effects of treadmill exercise on muscle strength, myostatin mRNA and protein expression, and gastrocnemius myocytes proliferation in aged rats to investigate the possible antiaging effects of aerobic exercise on skeletal muscles such as pelvic floor muscles and urethral rhabdosphincter muscle.MethodsIn this study, 5-month-old male Sprague-Dawley rats were used as the young-age group (n=20) and 24-month-old rats were used as the old-age group (n=20). Each group was randomly divided into two groups (n=10 in each group): the sedentary and the treadmill exercise group. The rats in the exercise groups were forced to run on a motorized treadmill for 30 minutes, once a day, for 6 weeks. For this study, a weight load test, hematoxylin and eosin staining, real-time and reverse transcription polymerase chain reaction for myostatin mRNA, myostatin western blot, and 5-bromo-2'-deoxyuridine immunohistochemistry were performed in the gastrocnemius muscle.ResultsThe age-induced reduction of muscle mass and strength was associated with a decrease in myocyte proliferation and an increase in myostatin mRNA and protein expression in the gastrocnemius. However, treadmill exercise improved muscle mass and strength through suppression of myostatin mRNA and protein expression, and myocyte proliferation increase in the gastrocnemius against the aging process.ConclusionsAerobic exercise is a useful strategy for enhancing muscle function against aging-induced loss of skeletal muscle mass and functions.

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“…A member of the TGF-β superfamily of secreted growth factors, myostatin is produced by skeletal muscle and adipose tissue, functioning as a negative regulator of muscle mass [48]. Its clinical relevance has been confirmed in rodent models whereby myostatin infusion has resulted in marked muscle wasting [49].…”

Section: Pharmacologic Therapymentioning

confidence: 99%

Sarcopenic obesity

Bouchonville

Villareal

2013

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

123

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Purpose of review The increasing prevalence of sarcopenic obesity in older adults has heightened interest in identifying the most effective treatment. This review highlights recent progress in management with an emphasis on lifestyle interventions and pharmacologic therapy aimed at reversing sarcopenic obesity. Recent findings While weight loss and exercise independently reverse sarcopenic obesity, they act synergistically in combination to improve body composition and physical function beyond which is observed with either intervention alone. Optimizing protein intake appears to have beneficial effects on net muscle protein accretion in older adults. Myostatin inhibition is associated with favorable changes in body composition in animal studies, though experience in humans is relatively limited. Testosterone and growth hormone offer improvements in body composition but the benefits must be weighed against potential risks of therapy. GHRH-analog therapy shows promise but further studies are needed in older adults. Summary At present, lifestyle interventions incorporating both diet-induced weight loss and regular exercise appear to be the optimal treatment for sarcopenic obesity. Maintenance of adequate protein intake is also advisable. Ongoing studies will determine whether pharmacologic therapy such as myostatin inhibitors or GHRH-analogs have a role in the treatment of sarcopenic obesity.

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The beneficial effect of myostatin deficiency on maximal muscle force and power is attenuated with age

Cited by 23 publications

References 47 publications

Relationship of muscle function to circulating myostatin, follistatin and GDF11 in older women and men

Relationship of muscle function to circulating myostatin, follistatin and GDF11 in older women and men

Aerobic Exercise Affects Myostatin Expression in Aged Rat Skeletal Muscles: A Possibility of Antiaging Effects of Aerobic Exercise Related With Pelvic Floor Muscle and Urethral Rhabdosphincter

Sarcopenic obesity

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