Growth factors, muscle function and doping.
ABSTRACT Recently much interest has been shown in developing a treatment of muscle wasting associated with a range of diseases as well as in ageing, which are major medical and socioecomonic problems. Emerging molecular techniques have made it possible to gain a better understanding of the growth factor genes involved and how they are activated by physical activity including the IGF-I gene that can be spliced to give rise to different isoforms, one of which is called MGF that activates muscle progenitor cells that provide the extra nuclei required for muscle hypertrophy, repair and maintenance. This fact that MGF 'kick starts' the hypertrophy process clearly has potential for abuse and has already attracted the attention of body builders.
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ABSTRACT: It has traditionally been believed that resistance training can only induce muscle growth when the exercise intensity is greater than 65 % of the 1-repetition maximum (RM). However, more recently, the use of low-intensity resistance exercise with blood-flow restriction (BFR) has challenged this theory and consistently shown that hypertrophic adaptations can be induced with much lower exercise intensities (<50 % 1-RM). Despite the potent hypertrophic effects of BFR resistance training being demonstrated by numerous studies, the underlying mechanisms responsible for such effects are not well defined. Metabolic stress has been suggested to be a primary factor responsible, and this is theorised to activate numerous other mechanisms, all of which are thought to induce muscle growth via autocrine and/or paracrine actions. However, it is noteworthy that some of these mechanisms do not appear to be mediated to any great extent by metabolic stress but rather by mechanical tension (another primary factor of muscle hypertrophy). Given that the level of mechanical tension is typically low with BFR resistance exercise (<50 % 1-RM), one may question the magnitude of involvement of these mechanisms aligned to the adaptations reported with BFR resistance training. However, despite the low level of mechanical tension, it is plausible that the effects induced by the primary factors (mechanical tension and metabolic stress) are, in fact, additive, which ultimately contributes to the adaptations seen with BFR resistance training. Exercise-induced mechanical tension and metabolic stress are theorised to signal a number of mechanisms for the induction of muscle growth, including increased fast-twitch fibre recruitment, mechanotransduction, muscle damage, systemic and localised hormone production, cell swelling, and the production of reactive oxygen species and its variants, including nitric oxide and heat shock proteins. However, the relative extent to which these specific mechanisms are induced by the primary factors with BFR resistance exercise, as well as their magnitude of involvement in BFR resistance training-induced muscle hypertrophy, requires further exploration.Sports medicine (Auckland, N.Z.). 09/2014;
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ABSTRACT: Inter-individual variation in muscle mass and muscular fitness is broad; being at the upper tail of the distribution not only contributes to improve elite sport performance, but is also associated with longer independent living and higher quality-of-life in the aging population. Heritability estimates of muscle phenotypes are substantial and warrant the search for genetic components underlying this individual variability. The 'kinesiogenomics' field is young, but genetic associations with muscle strength-related phenotypes have been reported already for more than 40 candidate genes, and genome-wide scans revealed several additional regions of interest in the genome. Although genetic findings may reveal attractive targets for novel muscle atrophy therapy, the benefit of exercise as a major stimulus for natural muscle mass enhancement or maintenance cannot be underestimated.Current Opinion in Pharmacology 03/2012; 12(3):355-62. · 5.44 Impact Factor
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ABSTRACT: In rehabilitation, immobilization of skeletal muscles in the elongated position is performed as a countermeasure in order to reverse the effects of severe muscle shortening and postoperative events. The return to normal functional activities is believed to stimulate mechanotransducers capable of reorganizing the normal muscle cytoarchitecture, but few data describing the histopathological changes relating to these procedures are available in the literature. To assess and quantify histological abnormalities induced by immobilization of the extensor digitorum longus (EDL) muscle in elongation and to compare them with free movement of the animal after this procedure. Eighteen female Wistar rats were used, divided into the following groups: Control; Immobilized in plantar flexion (EDL in an elongated position) for 14 days (GI); Immobilized for 14 days and released for 10 days (GIL). EDL fragments were frozen, sectioned and processed through immunohistochemical reactions for collagens I and III and histochemical methods for myofibrillar adenosine triphosphatase using hematoxylin-eosin. GI animals presented slight increases in collagen I and fiber expression in a degenerative/necrotic process, and reductions in the proportion of FT2A fibers and in the diameters of all fiber types, compared with the controls. In GIL, the quantity of collagen I returned to control conditions; the proportion of FT2D decreased; the number of centralized nuclei increased; and the fiber diameter was smaller than in GI. However, FT2B and FT2D expression did not reach the reference values. The data presented show that the recovery of function over a 10-day period was partially efficient with regard to recuperation of the characteristics of the EDL muscle after the period of immobilization. If the data are extrapolated to physiotherapeutic clinical practice, use of procedures directed towards primary dysfunctions of the muscle may favor a morphofunctional response in the segment and its full recovery.Revista Brasileira de Fisioterapia 01/2011; 15(1):73-9. · 1.00 Impact Factor