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REVIEW |
Department of Endocrinology, Royal Free Hospital and Medical School, Pond Street, London NW3 2PF, UK
(Requests for offprints should be addressed to A M Solomon; Email: a.solomon{at}medsch.ucl.ac.uk)
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Abstract |
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 Top Abstract IntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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Introduction |
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TopAbstractIntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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Muscle cells function as a syncitium, with several nucleated cells fusing to form the muscle fibre – the key cellular activator of this process being the satellite cell (Wozniak et al. 2005). A sequence of transcription factors act on satellite cells – the myogenic regulatory factors (MRFs) –comprising myogenin, MRF4, MyoD and Myf5, which are expressed in an anatomical and time-dependent manner (Buckingham et al. 2003).
Satellite cells are located beneath the basal lamina of muscle fibres and are a distinct muscle cell subtype responsible for post-natal adaptation, growth and repair (Mauro 1961). They have a variety of potential fates, including proliferation, fusion or trans-differentiation (Zammit et al. 2004, Fig. 1
). Increasingly, observations are being made of stem cells adopting satellite cell status or vice versa – either locally derived, as muscle-derived stem cells (Mourkioti & Rosenthal 2005, Sinanan et al. 2004) or of bone marrow origin (Chen & Goldhamer 2003). Our present understanding of the factors affecting satellite cell biology has become increasingly sophisticated – of special interest are the influence of mechanical stimulation, ageing and endocrine factors (Dhawan & Rando 2005, Wagers & Conboy 2005, Wozniak et al. 2005, Scime & Rudnicki 2006, Sherwood & Wagers 2006).
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Muscle fibre type is a further level of skeletal muscle anatomy responsive to exercise and endocrine factors. Traditional classification has comprised slow-twitch (type I) and fast-twitch (type II) fibres further subdivided into type IIa and type IIb according to energy utilisation (although type IIb in humans is somewhat homologous to a further type IIx found in rodents). Testosterone induces hypertrophy of both type I and type II fibres (Kadi et al. 1999). There appear to be significant anatomical site, age and gender-specific differences in muscle fibre-type responses to resistance training in humans, the precise endocrine correlates of these observations are, as yet, not fully elucidated (Martel et al. 2006).
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Sarcopenia |
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TopAbstractIntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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Different inflammatory responses to equivalent exercise also occur in older versus younger muscle. Following 45-min downhill running at 75% VO2max muscle interleukin (IL)-6 and transforming growth factor (TGF)-ß1 concentrations did not increase in older (n=15) as much as in younger subjects (n=15; Carlson et al. 1999, Hamada et al. 2005, Carlson et al. 1999). These differences could reflect alterations in the adaptive cytokine response within the muscle – increasingly evidence points to a role for locally generated IL-6 in assisting with satellite cell proliferation during muscle regeneration following injury (Toumi et al. 2006). Decline in anabolic hormones and reduction in available myonuclei via inflammatory or apoptotic-like mechanisms represent alternative explanations for sarcopenia (Leeuwenburgh 2003).
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Muscle atrophy in disuse, denervation and medical disorders |
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TopAbstractIntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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Tumour necrosis factor (TNF)-
alone can induce musclecell atrophy in vitro, reversed by anti-TNF agents possibly via nuclear factor kappa B (NF-
B; Li & Reid 2000). An interaction between TNF- and IGF-I has been found to be therapeutically relevant where anti-TNF treatment was being provided to patients with rheumatoid arthritis, improving glucocorticoid-associated IGF-I resistance (Sarzi-Puttini et al. 2006).
Denervation of muscle (often with associated aberrant reinnervation) is regarded as a potent trigger to sarcopenia –both associated with ageing and neuromuscular disorders –and has recently been examined at the molecular level (Raffaello et al. 2006). The use of IGF-I electroporation, recombinant human IGF-I and the peptide representing mechano-growth factor (MGF) have all been considered for ameliorating such neuromuscular conditions, including muscular dystrophy and motor neuron disease (Lynch 2004).
In terms of HIV disease, muscle atrophy occurs both in untreated disease and in association with drug-induced lipodystrophy, endocrine deficiencies, altered protein intake and a cytokine-mediated catabolic state (Yarasheski et al. 2005). Using anti-TNF antibodies or receptor blockers represent a therapeutic avenue (Calabrese et al. 2004). Several studies have demonstrated a response to androgen therapy in such patients – studied most extensively not only in men (Bhasin et al. 2000, Grinspoon et al. 2000, Fairfield et al. 2001), but also in women (Dolan et al. 2004).
Attempts at reversing muscle atrophy in cardiac failure and chronic obstructive airways disease using anabolic therapies have confirmed the presence of hypogonadism, but no significant correlation with respiratory capacity (Laghi et al. 2005). In contrast, using a crossover design, short-term testosterone administration improved subjective and objective measures of exercise tolerance and metabolic factors in ten men with angina (Malkin et al. 2004). Muscle atrophy secondary to systemic disorders such as cardiac failure, has no unifying aetiology, although a cytokine-mediated process associated with TNF-, altered nitric oxide synthase expression and neuroendocrine alterations constitute plausible mechanisms (Strassburg et al. 2005).
Activation of the renin–angiotensin–aldosterone system, specifically angiotensin-II may also be involved in clinically relevant atrophy. Angiotensin-II infused into rats generates an atrophic response, apparently mediated via skeletal muscle IGF-I reduction; the AkT/mammalian Target of Rapamycin (mTOR)/p70S6K pathway may represent one target (Dalla et al. 2001). These changes are reversed upon transgenic IGF-I overexpression (Song et al. 2005). Prospective clinical trials examining the effects of manipulations of the renin–angiotensin system, on skeletal muscle in such patients are awaited.
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Specific endocrine systems |
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TopAbstractIntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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Calcium, vitamin D and phosphate levels all impact on muscle function most notably in deficiency states such as the myopathy seen in osteomalacia. This has been confirmed as a histological atrophy of muscle, predominantly type II fibres and is exacerbated by ageing (Janssen et al. 2002). Polymorphisms of the vitamin D receptor and vitamin D knockout models have a significant muscle phenotype (Demay 2003). Vitamin D null mice have smaller muscle fibres and raised levels of MRFs. These changes are reversed by treatment with vitamin D (Endo et al. 2003). Vitamin D-receptor polymorphisms associated with body composition and muscle strength have been reported in men and women. One study assessing older men showed variation in the vitamin D-receptor FokI polymorphism (Roth et al. 2004), with a different polymorphism linked with muscle strength in a further study of older women (Geusens et al. 1997). In a longitudinal study looking at sarcopenia in older men and women, low vitamin D was linked with increased risk (by approximately x2) of reduced muscle mass and strength. a similar relationship was found with raised parathyroid hormone levels (Visser et al. 2003). In functional terms, several trials have examined the relationship between vitamin D status and falls; these have been recently reviewed (Mosekilde 2005).
Glucocorticoids
Glucocorticoid-associated atrophyappears to be specific for type II or phasic muscle fibres. In a study of controlled hypercorti-solaemia in healthy men (Ferrando et al. 1999), experimental inactivity increased the catabolic effect of glucocorticoids, suggesting the absence of mechanical signals potentiates the glucocorticoid effect. The mechanism of glucocorticoid-induced atrophy may involve upregulation of myostatin and glutamine synthetase, the latter via glucocorticoid receptor interaction with the glutamine synthetase promoter (Carballo-Jane et al. 2004). Glucocorticoids inhibit the physiological secretion of growth hormone (GH) and appear to reduce IGF-I activity at target organs – alterations of steroid-induced glutamine synthetase represent a potential mechanism of action, and dose-dependent inhibition of glutamine synthetase was seen using IGF-I in rat L6 cells (Sacheck et al. 2004).
Growth hormone
GH has a variety of anabolic effects and has been shown to increase lean body mass, bone density and reduce fat mass in children, young adult or older adult with GH deficiency (Carroll et al. 2004) and those with Turner’s syndrome (Carel 2005). GH replacement also improves muscle mass in adult GH deficiency, without significant impact on muscle strength (Hoffman et al. 2004). With ageing, GH secretion and systemic IGF-I decrease and GH administration to elderly patients has resulted in changes in body composition seen in younger GH-deficient subjects (Borst 2004). Recombinant GH, when administered to young hypogonadal (Hayes et al. 2001) and ageing men (Brill et al. 2002), can increase IGF-I mRNA in muscle. In studies combining GH and exercise on muscle strength, a trend towards an increase in fat free mass and myosin heavy chain (MHC) isoforms has been demonstrated (Taaffe et al. 1996, Lange et al. 2002). Recent work focussing on the molecular adaptations to a 12-week training regime in older men found that GH and exercise together increased the IGF-I isoform MGF gene expression more than each individually (Hameed et al. 2004). The mechanisms of GH action and intracellular signalling are not fully understood. Evidence using a myoblast cell line has shown that exogenous GH appears to induce GH-receptor activation, IGF-I mRNA production, phosphorylation of JAK2, Stat5a, 5b and increases in suppressor of cytokine signalling-2 (SOCS-2; Sadowski et al. 2001, Frost et al. 2002).
Increasing evidence suggests that SOCS-2 is a key negative modulator of GH action (Leroith & Nissley 2005). There are eight SOCS proteins with conserved structural and functional domains (Greenhalgh & Alexander 2004). They appear to show differential responses to systemic insults (Johnson et al. 2001). SOCS-2 may have a biphasic concentration-dependent effect (Favre et al. 1999, Johnson et al. 2001), binding to the Tyr595 on the GH receptor with low levels inhibiting and higher concentrations enhancing GH effects. The SOCS-2–/– knockout mouse shows gigantism and deregulated growth. The mice demonstrate organomegaly, exuberant skeletal development and increased lean mass. The phenotype appears to be different to transgenic models of either GH or IGF-I excess, yet showing features of each (Metcalf et al. 2000, Johnson et al. 2001). However, a transgenic mouse overexpressing SOCS-2 was paradoxically, also moderately larger than average (Metcalf et al. 2000, Johnson et al. 2001, Greenhalgh et al. 2002).
In a combined GH and SOCS-2 knockout system (combining SOCS-2–/– knockout mice with lit/lit mice exhibiting a mutation in the GH-releasing hormone receptor), excessive growth only occurred upon GH administration (Greenhalgh et al. 2005). This implies a direct role for SOCS in early GH signalling. The SOCS-2 system may be a significant target for future research.
Insulin-like growth factors
There are two insulin-like growth factors, IGF-I and IGF-II. IGF-I is the only factor known to accelerate both satellite cell proliferation and differentiation and mice transgenically overexpressing IGF-I have significantly higher muscle mass than controls (Hayashi et al. 2004, Shavlakadze et al. 2005), whilst IGF-II appears to have an important developmental role and has higher specificity for the differentiating capacity of muscle (Florini et al. 1996).
IGF-I and IGF-II are both expressed during muscle regeneration and bind IGF-binding proteins (IGFBPs; Hayashi et al. 2004, Shavlakadze et al. 2005). A recent report has distinguished a mechanism for IGF-II in myogenesis from the classical IGF-I-mediated pathway – when fibroblast growth factor (FGF)-6–/–mice were given a regenerative stimulus to their muscle IGF-II and IGF-IIR were specifically upregulated (Armand et al. 2004).
In muscle, circulating IGF-I, paracrine generation of local IGF isoforms and IGFBPs may all play a role in myofibre function. It is presently unclear if each IGFBP performs an entirely unique role in skeletal muscle fibres, although several IGFBPs have been linked to time, load and age-dependent differences (Foulstone et al. 2003, Spangenburg et al. 2003). Evidence is accumulating for IGFBP-5 as a specific activator of myogenesis with independent activity at the muscle cell membrane (Cobb et al. 2004).
IGF-I isoforms and their distribution in muscle
Variation in IGF-I gene expression is based on site-specific alternative splicing of the gene. The gene has six exons, with promoter regions in exons 1 and 2. The mature peptide is found in exons 3 and 4. Transcripts containing exons 1, 3, 4 and 5 or 1, 3, 4 and 6 are called class I; those including 2, 3, 4 and 6 or 2, 3, 4 and 5 are termed as class II. Details of splice variants has recently been identified (Goldspink & Yang 2004), one of linked with mechanical stimuli has been named MGF. Known rat and human isoforms can be summarised as follows (Table 1 and Fig. 2).
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Androgens |
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TopAbstractIntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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The key cellular vector for androgen-associated muscle hypertrophy appears to be the satellite cell (Chen et al. 2005). Immunohistochemical examination has demonstrated the expression of androgen receptors (ARs) in CD34+ cells, fibroblasts, smooth muscle cells and satellite cells (Sinha-Hikim et al. 2004). Murine pluripotent C3H10T1/2 cells have been used to demonstrate increased MyoD+and MHC+myotubes following androgen administration, with dynamic effects of an AR antagonist (Artaza et al. 2005). The role of the androgen receptor has been studied using C2C12 myoblast satellite cells transfected with a flagged AR–accelerated myoblast cell differentiation was seen via enhanced myogenin expression (Lee 2002). Using C2C12 myoblasts transfected with wild-type or mutant ARs, testosterone induced a variable rate of cell differentiation or proliferation (Benjamin et al. 2004), androgen action using a gonadotrophin-releasing hormone agonist in young men resulted in a dose–response increase in satellite cell number in muscle biopsy samples (Sinha-Hikim et al. 2003).
Functionally important AR polymorphisms, including effects on body composition, have been recently associated with the cytosine adenine guanine (CAG) triplet repeat motif (Walsh et al. 2005). A pathological lengthening of CAG repeat is seen in Kennedy disease, an X-linked spinobulbar muscular atrophy (Merry 2005). When a cohort of patients with Kennedy disease were analysed in detail, a correlation was found between CAG repeat length and clinical manifestations with >60% subjects showing evidence of androgen insensitivity (Dejager et al. 2002).
There is increasing evidence of androgen action in muscle interacting with IGF-I. In rat diaphragmatic muscle, a dose-dependent increase in IGF-I mRNA expression occurred following exposure to androgen (Lewis et al. 2002). When harvested bovine male satellite cells were treated with various androgen concentrations (using trenbolone), a dose-dependent increase in IGF-I mRNA expression occurred (Kamanga-Sollo et al. 2004). As yet no data have been generated demonstrating a distinction in dynamics of specific IGF-I isoforms upon androgen administration. Androgenic activity may be directly linked to the IGF-I signalling system with p70s6kinase, found downstream of the Akt/mTOR pathway, a candidate for early evidence is emerging (Xu et al. 2004). A proportion of the anabolic effects of androgens may also be anti-catabolic via an anti-glucocorticoid action (Danhaive & Rousseau 1988, Zhao et al. 2004).
Clinical studies demonstrating the interaction of androgens and muscle
Androgens are associated with muscle size and strength, with a complex association between androgen levels and mechanical performance. In younger subjects, both androgens and exercise have been shown to increase muscle size and strength alone and in combination (Bhasin et al. 1996). More recently, effects have also been observed in older subjects, albeit of reduced magnitude (Bhasin et al. 2001, 2005). In a study of ten older men sequentially exposed to testosterone; GH or both, muscle IGF-I gene expression rose 1.9-fold in the GH group and by 2.3-fold in the testosterone+GH groups (Brill et al. 2002). More recently, larger (n=80) placebo-controlled randomised trial of GH versus testosterone or both, a statistically significant effect on muscle size and body composition was only found in the combination group (Giannoulis et al. 2006). However, only a fixed dose of testosterone was used. Therefore, future research may attempt to explore the mechanism of an androgen-mediated effect on the GH/IGF-I system.
Synthetic androgen modulators
Exogenous anabolic androgenic steroids such as oxandrolone have demonstrable efficacy, and are associated with increased AR mRNA and muscle protein synthesis (Sheffield-Moore et al. 1999). This effect was recently documented at the level of gene expression using microarray expression profiling where tetrahydrogestinone, a notorious synthetic anabolic androgen, was found to have a remarkably similar profile to dihydrotestosterone (Labrie et al. 2005).
A promising new androgen therapy 7-methyl-19-nortestosterone abbreviated as ‘MENT’ (also called trestolone) offers a number of clinical advantages when compared with conventional androgens. It can be delivered by several routes and is aromatisable, but not a substrate for 5-reductase. A study using MENT in orchidectomised rats showed anabolic effects on muscle and bone (Venken et al. 2005). Although the compound showed a dose-related action on the prostate, the higher doses tested caused both muscle gain and prostate hypertrophy the low to mid doses had divergent effects, with a smaller effect on the prostate. Therefore, dose-finding prospective randomised placebo-controlled clinical studies will be crucial (Anderson et al. 2003).
A further therapeutic mechanism in development is the use of selective AR modulators (SARMs), an exciting development aiming to provide anabolic effects without widespread adverse effects (Negro-Vilar 1999). Presently, the mechanism for tissue selectivity is still being explored (Gronemeyer et al. 2004). Initial development was derived from modification of the AR antagonists bicalutamide and flutamide. A study using orchidectomised rats using the ‘S-4’ compound demonstrated full agonist activity in muscle, but partial agonist action in the prostate providing improvements in muscle mass, strength and bone density without adverse prostatic effects (Gao et al. 2005). As yet, there are no convincing human data using orally available SARMs and examining muscle-related outcomes, although phase I/II trials are under way.
Myostatin
Myostatin was first discovered by McPherron et al.(1997) who demonstrated that a phenotype of exaggerated muscle hypertrophy correlated with mutations in the myostatin gene. Such knockout mutations of myostatin in animals (Grobet et al. 1997) – causing the so-called ‘double-muscled’ phenotype – and in one human child (Schuelke et al. 2004) have been described. Myostatin knockout mice show increased satellite cell proliferation compared with wild-type controls (Wagner et al. 2005), physiologically, it thus appears to be a gatekeeper maintaining satellite cells in reversible quiescence (Amthor et al. 2006).
The gene is highly conserved across species and polymorphisms of the myostatin gene are correlated with measures of muscle mass, strength and potentially athletic performance (Seibert et al. 2001). Also known as growth and differentiation factor 8, it is a member of the TGF superfamily. Myostatin acts through activin type I receptors, ActR2A and ActR2B. So far evidence suggests important binding properties to the propeptide itself and the follistatin-related gene protein (Hill et al. 2002). Follistatin appears to be a complementary antagonist to myostatin (Amthor et al. 2004). Myostatin acts as an inhibitor of muscle growth and promotes adipogenesis (Artaza et al. 2005). Myostatin signalling involves interaction with the MRFs, inhibiting the synthesis and activity of MyoD (Amthor et al. 2004, Guttridge 2004). At the cellular level, myostatin affects cell cycling by affecting the entry of satellite cells into S-phase (McCroskery et al. 2003, Amthor et al. 2004).
Endocrine targets of myostatin action
Myostatin appears to be sensitive to the anabolic actions of GH. Using the C2C12 myotube model, a dose-dependent reduction in myostatin expression was observed on exposure to GH, which was reversed by the GH antagonist pegvisomant (Liu et al. 2003).
In contrast, dexamethasone has been shown to increase myostatin expression that could be antagonised by RU-486 (Ma et al. 2001). The human myostatin gene promoter has been found to contain a number of potential glucocorticoid-response elements (Ma et al. 2001). Myostatin is also exercise responsive. In rats performing an exercise regime comprising 5 days of swimming, myostatin mRNA was significantly reduced in the exercise group compared with controls (Matsakas et al. 2005). In contrast, a clinical study using a 12-week resistance training protocol in young men found concomitant increases in glucocorticoid receptor and myostatin mRNA expressions (Willoughby 2004). Another report using a human training schedule demonstrated myostatin reduction (mean 20%) in the serum following heavy exercise (Lin et al. 2003, Walker et al. 2004). The explanation for these conflicting data is uncertain.
A variety of conditions causing muscle loss associated with observable increase in myostatin levels, including sarcopenia of ageing, HIV disease, disease disuse atrophy, glucocorticoid use and microgravity during spaced flight (Gonzalez-Cadavid et al. 1998, Baumann et al. 2003). In addition, male transgenic mice overexpressing myostatin had reduced muscle and higher fat mass than females (Reisz-Porszasz et al. 2003). Gender-specific evidence such as this leads to the suggestion that androgens could have a role in the mechanism.
Clinical trials involving myostatin inhibition
A recombinant human antibody to myostatin (MYO-029) is being utilised with the aim of improving states of muscle wasting in neuromuscular disease are in early phase trials. A second therapeutic approach now in development is a soluble activin type IIB receptor (ACVR2B/Fc) that binds to myostatin effectively causing reduced myostatin availability (Lee et al. 2005). These data are interesting in that normal animals were used, making this a transferable paradigm for sarcopenia research.
Figure 4 shows the differing endocrine influences on satellite cell function; Fig. 5 specifies effects on fibre types; Fig. 6 summarises endocrine factors influencing muscle-derived myostatin specifically.
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Muscle mass can also be influenced using plasmid gene transfer approaches to generate a variety of target endocrine molecules (Goldspink 2003, Reisz-Porszasz et al. 2003). MacColl et al.(2000) successfully employed this approach using GH as the target. The C2C12 model of murine muscle cells was used and GH secretion was measurable under several transfection conditions, including various stages of cellular differentiation into syncitial myotubes. This and other approaches may soon have a significant impact on the field of endocrine biology and a possible new source for anabolic hormones in deficiency states.
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Conclusion |
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TopAbstractIntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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Acknowledgements |
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Funding |
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References |
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TopAbstractIntroductionSarcopeniaMuscle atrophy in disuse,...Specific endocrine systemsAndrogensConclusionReferences |
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Received in final form 18 May 2006
Accepted 22 May 2006
Made available online as an Accepted Preprint 23 June 2006
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significant difference in percentage change between isoforms (P<0.05).
