Natural Testosterone Levels Not Important For Muscle Growth

Yes, this is another study pointing out that acute fluctuations in hormones such as testosterone and growth hormone do not contribute meaningfully to muscle hypertrophy. For those that are perhaps less familiar with the issue, here is an excerpt from something I wrote up a while ago. For the sake of space, I will not include a reference list. Enjoy :)

Resistance exercise can acutely increase serum concentrations of hormones such as growth hormone (GH), IGF-1, and testosterone. A long held theory is that exercise that leads to a buildup of anaerobic metabolites which increases systemic anabolic hormonal concentrations, thereby enhancing the anabolic milieu and subsequent muscle hypertrophy (Goto, Ishii, Kizuka, & Takamatsu, 2005; Hansen, Kvorning, Kjaer, & Sjøgaard, 2001; Kraemer, et al., 1990). Metabolically-induced spikes in GH, IGF-1, and testosterone in particular, have been implicated as having a positive effect on post-exercise myofibrillar protein synthesis. What follows is a brief description of each hormone followed by the evidence for its role in resistance exercise induced muscle hypertrophy.

GH, also known as somatotropin, is a superfamily of polypeptide hormones that act as repartitioning agents that modulate fat metabolism, as well as stimulate cellular uptake and incorporation of amino acids into various proteins (Chikani & Ho, 2013). The direct hypertrophic actions of GH on muscle protein metabolism appear to be negligible, with anabolic effects seemingly limited to synthesis of non-contractile tissue (i.e. collagen) (Doessing, et al., 2010; Boesen, et al., 2014). Nevertheless, a large body of research demonstrates a strong correlation between exercise-induced metabolic stress and increased acute hypophyseal GH secretion (Hakkinen & Pakarinen, 1993; Gordon, Kraemer, Vos, Lynch, & Knuttgen, 1994; Gotshalk, et al., 1997; Goto, Ishii, Kizuka, & Takamatsu, 2005; Pierce, Clark, Ploutz-Snyder, & Kanaley, 2006; Stokes, Tyler, & Gilbert, 2008). IGF-1 is a homologous peptide hormone that has both mitogenic and anabolic effects on skeletal muscle and is the primary mediator of the effects of GH. IGF-1 is part of the IGF-1/PI3K/Akt signaling pathway which plays a key role in the regulation of muscle mass by promoting myofibrillar protein synthesis (Coleman, et al., 1995; Barton-Davis, Shoturma, Musaro, Rosenthal, & Sweeney, 1998; Musaro, et al., 2001; Dardevet, Sornet, Vary, & Grizard, 1996; Rommel, et al., 2001). Similar to GH, training routines that generate extensive metabolic buildup have been found to result in significantly greater elevations of circulating IGF-1 levels compared with high-intensity protocols that cause minimal metabolite accumulation (Kraemer, et al., 1990; Kraemer, et al., 1991; Gregory, et al., 2013; Kraemer & Ratamess, 2005). Notwithstanding this correlation, it has been shown that blockade of the IGF-1/PI3K/Akt pathway during mechanical loading does not prevent the activation of mTOR or muscle hypertrophy (Goodman, 2014; Miyazaki, McCarthy, Fedele, & Esser, 2011).

Testosterone is a steroid hormone important for developmental growth and is responsible for secondary sexual characteristics in males. Testosterone has well known anabolic effects on muscle tissue (Bhasin, et al., 2001; Herbst & Bhasin, 2004) during growth and acute elevations in testosterone have also been seen following metabolically demanding resistance exercise (Kraemer, et al., 1990; Kraemer, et al., 1991; Kraemer & Ratamess, 2005; Ahtiainen, Pakarinen, Alen, Kraemer, & Häkkinen, 2003).

Although a strong correlation exists between resistance exercise that is known to induce muscle hypertrophy and the acute elevation of anabolic hormones, resistance exercise trials comparing protocols that produce either high or low acute hormonal responses show equivalent effects when looking more specifically at myofibrillar protein synthesis and muscle hypertrophy (West, et al., 2009; West , et al., 2010; West & Phillips, 2012; Wilkinson, Tarnopolsky, Grant, Carreia, & Phillips, 2006). West et al (2009) compared the acute change in myofibrillar protein synthesis following exercise of the elbow flexors under low (i.e. basal) hormone levels, to the same exercise under high hormone levels. GH, IGF-1, and testosterone levels were increased in the high hormone condition by performing high-volume leg resistance exercise immediately following elbow flexor exercise. Exercise stimulated a rise in myofibrillar protein synthesis in the biceps brachii with no effect of elevated hormones. Phosphorylation of p70S6K also increased post-exercise with no differences between conditions. This same research group followed the acute study with a long term study using a similar protocol. They measured the chronic effects of acute elevations in GH, IGF-1, and testosterone on muscle fiber CSA and strength following 15 weeks of training under low or high hormone conditions. Again, no difference was found between groups in either CSA or muscle strength after 15 weeks. These data provide multiple lines of evidence that exercise-induced elevations of purportedly anabolic hormones are not necessary for, and do not enhance, muscle anabolism following resistance exercise.