Until recently the common belief was that muscle growth is caused by the following mechanism:
- Stimulation by resistance exercise
- Release of testosterone and growth hormone
- Release of growth factors (especially IGF-I)
- Increased protein synthesis
This hypothesis has been increasingly questioned by various scientists. D.W. West and S.M. Phillips of McMaster University, Hamilton, Canada claims that: “…there is a persistent belief (both in scientific literature and among recreational weightlifters) that exercise-induced release of GH and testosterone underpins muscular hypertrophy with resistance training. This is a premature assumption because although pharmacological GH supplementation can increase muscle strength or size in individuals with clinical GH deficiency, there is no evidence that transient exercise-induced changes in GH have the same effects in individuals with normal GH levels. Exercise paradigms are designed based on the assumption (not necessarily evidenced-based mechanisms) that GH and testosterone facilitate anabolic processes that lead to skeletal muscle protein accretion and hypertrophy. Our recent work disputes this assumption. Instead, our data indicate that exercise-induced hormonal elevations do not enhance intracellular markers of anabolic signaling or the acute postexercise elevation of myofibrillar protein synthesis. Furthermore, data from our training study demonstrate that exercise-induced increases in GH and testosterone availability are not necessary for and do not enhance strength and hypertrophy adaptations. Instead, our data lead us to conclude that local mechanisms that are intrinsic to the skeletal muscle tissue performing the resistive contractions (ie, weightlifting) are predominant in stimulating anabolism.” (http://www.ncbi.nlm.nih.gov/pubmed/20959702 )
The importance of West’s research is chiefly in the observation of IGF-I. This growth factor is almost always associated with muscle growth but West claims that there is no direct link between higher IGF-I levels and increased protein synthesis in the muscles.
Another citation from a different study by West and colleagues: “However, while these hormones (testosterone, GH, IGF-I )are clearly anabolic during childhood and puberty, or when given at supraphysiological exogenous doses, the transient post-exercise elevations in hormone concentration are of little consequence to the either the acute protein synthetic response or to a hypertrophic phenotype after resistance training. Thus, the acute post-exercise increases in systemic hormones are in no way a proxy marker for anabolism since they do not underpin the capacity of the muscle to hypertrophy in any measurable way.” (http://www.ncbi.nlm.nih.gov/pubmed/20541030 )
So what are those intrinsic mechanisms?
“…the acute activation of intrinsically located signalling proteins such as p70(S6K) and the acute elevation of muscle protein synthesis are more reflective of the potential to increase in muscle mass with resistance training. Ultimately, local mechanisms are activated by the stress imposed by muscle loading and prime the muscle for protein accretion. Membrane-derived molecules and tension-sensing pathways are two intrinsic mechanisms implicated in upregulating the synthesis and incorporation of muscle proteins into the myofibre in response to mechanical stress derived from loaded contractions.” (http://www.ncbi.nlm.nih.gov/pubmed/20541030 )
This is a very important development in muscle growth-research. When we consider that such findings are relatively new (the citations are from studies published in 2010) we can expect many other teams trying to explain more closely those intrinsic mechanisms.