A study has recently been published, which indicates that (transient) exercise-induced changes in growth hormone and testosterone are neither necessary or sufficient to increase size and strength. What this means, is that the testosterone/GH elevation you get from a hard workout probably isn’t going to be “the thing” that boosts your size and strength.
This doesn’t mean that “test and GH don’t work” or “they don’t do anything,” but rather that the natural training-induced spike probably isn’t the causative factor behind size and strength (although I’d wager that a training protocol that boosts test/gh will be effective, while one which lowers those hormones will likely be ineffective).
Phys Sportsmed. 2010 Oct;38(3):97-104.
Anabolic processes in human skeletal muscle: restoring the identities of growth hormone and testosterone.
West DW, Phillips SM.
Exercise Metabolism Research Group, Department of Kinesiolgy, McMaster University, Hamilton, Ontario, Canada.
Testosterone supplementation acts via numerous mechanisms as a highly potent anabolic agent to skeletal muscle. Although growth hormone (GH) strongly affects collagen synthesis and lipolysis, as well as increasing lean body mass, it is not anabolic toward the contractile (ie, myofibrillar) muscle tissue in healthy individuals. However, 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. The purpose of this article is 1) to provide a brief overview of the mechanisms of action of testosterone and GH; 2) to discuss the inability of physiological exercise-induced elevations in these hormones to have a measurable impact on skeletal muscle anabolism; and 3) to describe factors that we believe are more important for stimulating hypertrophy in human skeletal muscle. Clarifying both the role of hormones in regulating muscle mass as well as the underlying basis for adaptation of skeletal muscle to resistance exercise will hopefully enhance and support the prescription of resistance exercise as an integral component of a healthy lifestyle.
PMID: 20959702 [PubMed – in process]