Control of the Size of the Human Muscle Mass

Rennie, Michael J.; Wackerhage, Henning; Spangenburg, Espen E.; Booth, Frank W.

doi:10.1146/annurev.physiol.66.052102.134444

Cited by 343 publications

(288 citation statements)

References 165 publications

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“…IL-1b and IL-6) are also reported to decrease the expression of skeletal muscle insulin-like growth factor 1, 41 a hormone central to post natal muscle growth. 34 With elevated levels of adipokines present in obese mice, 6 this might further contribute to the obesity-related decrements in skeletal muscle mass observed in this study.…”

Section: Iiamentioning

confidence: 80%

“…32 Furthermore, glucocorticoids upregulate myostatin expression, 33 a growth factor that acts as a negative regulator of skeletal muscle mass. 34 Increased myostatin expression in rats through dexamethasone administration has been shown to lead to muscle atrophy, 35 whereas in ob/ob mice lacking the myostatin gene, muscle mass was twice that of conventional ob/ob mice at 3 months of age. 36 Taken together, these data suggest that an amplified glucocorticoid presence might be involved in the smaller skeletal muscle mass common to obese rodents.…”

Section: Iiamentioning

confidence: 99%

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Morphological and biochemical alterations of skeletal muscles from the genetically obese (ob/ob) mouse

et al. 2009

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Background: Knowledge of the morphological and biochemical alterations occurring in skeletal muscles of obese animals is relatively limited, particularly with respect to non-limb muscles and relationship to fibre type. Objective: Sternomastoid (SM; fast-twitch), extensor digitorum longus (EDL; fast-twitch), and soleus (SOL; mixed) muscles of ob/ob mouse (18-22 weeks) were examined with respect to size (mass, muscle mass-to-body mass ratio, cross-sectional area (CSA)), fibre CSA, protein content, myosin heavy chain (MHC) content, MHC isoform (MHC i ) composition, MHC i -based fibre type composition, and lactate dehydrogenase isoenzyme (LDH iso ) composition. Results: Compared with (control) muscles from lean mice, all the three muscles from ob/ob mice were smaller in size (by 13-30%), with SM and EDL being the most affected. The CSA of IIB and IIB þ IID fibres (the predominant fibre types in SM and EDL muscles) was markedly smaller (by B30%) in ob/ob mice, consistent with differences in muscle size. Total protein content (normalised to muscle mass) was significantly lower in EDL (À9.7%) and SOL (À14.1%) muscles of ob/ob mice, but there were no differences between SM, EDL, and SOL muscles from the two animal groups with respect to MHC content (also normalised to muscle mass). Electrophoretic analyses of MHC i composition in whole muscle homogenates and single muscle fibres showed a shift towards slower MHC i content, slower MHC i containing fibres, and a greater proportion of hybrid fibres in all the three muscles of ob/ob mice, with a shift towards a more aerobic-oxidative phenotype also observed with respect to LDH iso composition. Conclusion: This study showed that SM, EDL, and SOL muscles of ob/ob mice display size reductions to an extent that seems to be largely related to fibre type composition, and a shift in fibre type composition that may result from a process of structural remodelling, as suggested by the increased proportion of hybrid fibres in muscles of ob/ob mice.

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Section: Iiamentioning

confidence: 80%

Section: Iiamentioning

confidence: 99%

Morphological and biochemical alterations of skeletal muscles from the genetically obese (ob/ob) mouse

et al. 2009

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“…Furthermore, the acute increase of GH to strength training has been found to correlate with the magnitude of muscle fiber hypertrophy (McCall et al 1999). It has been suggested that GH and cortisol are involved in the regulation of the mRNA expression of IGF-I and myostatin (Rennie et al 2004). This is in line with the findings of increased IGF-IEa and mechano growth factor expression after GH treatment in older subjects (Hameed et al 2004) and myostatin has been shown to be up regulated in response to elevated serum glucocorticoids (Lang et al 2001;Ma et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Physiological elevation of endogenous hormones results in superior strength training adaptation

Rønnestad¹,

Nygaard²,

Raastad

2011

Eur J Appl Physiol

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This file was dowloaded from the institutional repository Brage NIH -brage.bibsys.no/nih Rønnestad, B. R., Nygaard, H., Raastad, T. (2011) ABSTRACTThe purpose of this study was to determine the influence of transiently elevated endogenous hormone concentrations during exercise on strength training adaptations. Nine subjects performed four unilateral strength training session per week on the elbow flexors for 11 weeks. During two of the weekly sessions, leg exercises were performed to acutely increase the systemic anabolic hormone concentration immediately before the exercises for one of the elbow flexors (L+A). On the two other weekly training sessions, the contralateral elbow flexors were trained without prior leg exercises (A). By randomizing one arm of the subjects to serve as a control and the other as experimental, both conditions have the same nutritional and genetic environment. Serum testosterone and growth hormone was significantly increased during the L+A training session, while no hormonal changes occurred in the A session. Both A and L+A increased 1RM in biceps curl, peak power in elbow flexors at 30% and 60% of 1RM, and muscle volume of the elbow flexors (p<0.05). However, only L+A achieved increase in CSA at the part of the arm flexors with largest cross sectional area (p<0.001), while no changes occurred in A. L+A had superior relative improvement in 1RM biceps curl and favorable muscle adaptations in elbow flexors compared to A (p<0.05). In conclusion, performing leg exercises prior to arm exercises, and thereby increasing the levels of serum testosterone and growth hormone, induced superior strength training adaptations compared to arm training without acute elevation of hormones.

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“…the imbalance between protein anabolism and catabolism. There are a number of recent reviews which detail mechanisms associated with muscle loss to which the reader can refer (3,10,30,(89)(90)(91)(92) . In terms of muscle anabolism, protein as amino acids is essential for muscle (93) .…”

Section: Overview Of Mechanisms Associated With Nutrition and Muscle mentioning

confidence: 99%

“…In terms of muscle anabolism, protein as amino acids is essential for muscle (93) . The mechanism that controls entry of branched chain amino acids into metabolic pathways is the mTOR pathway (originally 'mammalian TOR', now referred to as 'mechanistic TOR') (91,(93)(94)(95) . mTOR is a kinase downstream of insulin and nutrient-sensing pathways that is required for cell growth (89) .…”

Section: Overview Of Mechanisms Associated With Nutrition and Muscle mentioning

confidence: 99%

Nutritional influences on age-related skeletal muscle loss

2013

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Age-related muscle loss impacts on whole-body metabolism and leads to frailty and sarcopenia, which are risk factors for fractures and mortality. Although nutrients are integral to muscle metabolism the relationship between nutrition and muscle loss has only been extensively investigated for protein and amino acids. The objective of the present paper is to describe other aspects of nutrition and their association with skeletal muscle mass. Mechanisms for muscle loss relate to imbalance in protein turnover with a number of anabolic pathways of which the mechanistic TOR pathway and the IGF-1-Akt-FoxO pathways are the most characterised.

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Control of the Size of the Human Muscle Mass

Cited by 343 publications

References 165 publications

Morphological and biochemical alterations of skeletal muscles from the genetically obese (ob/ob) mouse

Morphological and biochemical alterations of skeletal muscles from the genetically obese (ob/ob) mouse

Physiological elevation of endogenous hormones results in superior strength training adaptation

Nutritional influences on age-related skeletal muscle loss

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