Part 1: Exercise Induced ĎAnabolicí Hormones and the Hormone Hypothesis
Hormones are discussed a lot in bodybuilding circles. If rumours are to be believed, some hormones are the be all and end all of promoting hypertrophy and others are catastrophic and tear your muscle apart. In this series we will tackle some of the major hormone topics in natural bodybuilding, from the hormonal response to exercise, to the effectiveness and ethical considerations of pro-hormone supplementation. In this first article, we will look at the myths surrounding the importance of resistance exercise induced anabolic hormones for hypertrophy.
So what are anabolic hormones?
Anabolic hormones are biochemicals, secreted by glands, which in part function to promote anabolism, the technical term given to processes that essentially builds big stuff from small stuff. The primary anabolic hormones are testosterone, growth hormone (GH), insulin and insulin-like growth factor 1 (IGF-1). These hormones have typically been defined as anabolic either because they have a well defined role in developmental processes, because chronic supraphysiological (beyond what occurs normally) administration has anabolic properties or because a bunch of molecular studies looking at cells in a dish have said so. It therefore follows that because anabolism is one known function of these hormones, they must play a role in exercise-induced hypertrophy. As we will see, this is likely not the case.
What is the hormone hypothesis?
Resistance exercise has been shown to be capable of increasing the concentration of circulating Ďanabolicí hormones within the physiological range, for a short time period after exercise (1). This phenomenon led to the development of something called the Ďhormone hypothesisí, which essentially states that the acute elevation in circulating hormones post-resistance exercise contributes to hypertrophy developments (1). It has been well established that to maximise this hormonal response, compound exercises should be performed at moderate intensities with short rest intervals for high volumes (1) i.e. your typical bodybuilding routine. Despite some studies in the literature supporting the Ďhormone hypothesisí, they have generally been of poor quality. Therefore, one research group in particular set out to delineate the role this exercise induced Ďanabolicí hormone response really plays in skeletal muscle hypertrophy.
So what does the science actually say?
One of the suspected primary drivers of muscle hypertrophy is the resistance exercise induced increase in muscle protein synthesis (MPS). The metabolic mechanism for increasing muscle mass is that the acute increase in MPS post-exercise Ďaddsí a small amount of new muscle after each exercise bout. Over time, these additions summate and eventually lead to measurable increases in muscle mass. Therefore, acute studies that assess an interventions short-term effect on MPS can be insightful. With this in mind, researchers had healthy young men perform two exercise trials (2). In one trial, only unilateral cable preacher curl exercise was performed, producing a low Ďanabolicí hormone condition. Whereas in the other trial, the same exercise was performed (in the other arm) but was followed by high volume, intense, heavy leg-exercise with short rest periods, therefore producing a high Ďanabolicí hormone condition. A protein drink was ingested after exercise in both trials. It was found that MPS in the biceps brachii was increased in both conditions with no difference between the two, despite marked differences in circulating GH, IGF-1 and testosterone concentrations (2). So this study showed that producing a high anabolic hormonal response through resistance training does not augment MPS.
Now, this study didnít directly measure hypertrophy, because it was an acute study. These types of studies make the assumption that they reflect long-term adaptation. To address this however, the same researchers then performed a follow up 12-week training study in untrained subjects where they did directly measure hypertrophy (3). They used the same exercise protocols as in the previous acute study, such that one arm was trained in a high hormone condition, and the other arm was trained in a low hormone condition. They found that the arm trained in the high hormone condition DID NOT show greater increases in muscle size or strength following training than the arm trained in the low hormone condition (3).
Interestingly, the same group (really trying to put this myth to rest) published two other papers looking at the associations between post-exercise hormones and training adaptations such as strength and hypertrophy (4,5). They found that testosterone and IGF-1 had no association with any training adaptation (4,5). However, cortisol, and GH in one of the studies were positively correlated with some measures of hypertrophy (4). Before this is considered evidence that the acute GH rise is important for hypertrophy, bear in mind that the association was weak, associations are inherently flawed anyway, and GH is known not to be anabolic toward myofibrillar proteins (the contractile proteins bodybuilders want to grow). GH and cortisol might associate with hypertrophy for other reasons than the fact they are required to drive hypertrophy. Interestingly, the researchers did find that Ďlocalí factors within the muscle cells being activated by exercise did correlate with muscle growth (5). This knowledge, when combined with the ever growing literature on the molecular signals that occur within the muscle group trained, point to the fact that hypertrophy is an intrinsic process and specific to the muscle group activated (6).
So why are these hormones increased by exercise?
It seems logical to argue that as the exercise-induced hormone release is a well-characterised phenomenon, it must surely serve some function. Truth is, scientists arenít entirely sure what this function might be. Itís possible this phenomenon is part of some acute stress response to mobilise fuel, to help provide energy for the working muscle (6). Itís also possible that some of these hormones have an effect on tissue other than skeletal muscle such as connective tissue (6). The bottom line for bodybuilders however, is that the circulating Ďanabolicí hormone increase induced by a weight training session does not likely function to promote skeletal muscle growth. Even if it truly did, the effect is so small itís almost immeasurable and certainly not replicable. Therefore, programmes should not necessarily focus on designing sessions that elicit the greatest hormonal response. Other factors such as volume and frequency, incorporated into a non-linear or undulated periodization scheme are far more important considerations.
Compound, short rest period, moderate intensity, high volume resistance training leads to increased circulating concentrations of supposedly Ďanabolicí hormones.
The hormone hypothesis postulates that these hormones play a role in regulating hypertrophy.
Both acute and long-term studies have shown however that circulating anabolic hormones do not enhance muscle protein synthesis or hypertrophy.
In addition, correlation studies have shown circulating levels of Ďanabolicí hormones do not associate with long-term muscle growth.
Remember that short term, small elevations in hormones are NOT the same thing as chronic supraphysiological administration.
Hypertrophy is an intrinsic or Ďlocalí process, specific to the muscle trained, whereby mechanical stress on the working muscle is Ďsensedí and translated into molecular events that lead to adaptation of the trained muscle.
Do not necessarily focus your training program on sessions that elicit a large circulating anabolic hormonal response. The type of weight training that induces a large hormonal response is effective and excellent for hypertrophy, so should be incorporated, but not because of its hormonal properties.
Instead, while not explicitly mentioned in this article, focus on proper programming within a non-linear or daily undulating periodised scheme by manipulating several training variables such as rep scheme, intensity, volume, frequency and rest periods.
(1) Schoenfeld B. Post-exercise hypertrophic adaptations: A re-examination of the hormone hypothesis and its applicability to resistance training program design. Journal of Strength and Conditioning Research. 2013
(2) West DWD, Kujbida GW, Moore DR, Atherton P, Burd NA, Padzik JP, De Lisio M, Tang J, Parise G, Rennie MJ, Baker SK and Phillips SM. Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men. Journal of Physiology. 587 (21): 5239-5247, 2009.
(3) West DWD, Burd NA, Tang J, Moore DR, Staples AW, Holwerda AM, Baker SK and Phillips SM. Elevations in ostemsibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. Journal Applied Physiology. 108: 60-67, 2010.
(4) West DWD and Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. European Journal of Applied Physiology. 112: 2693-2702, 2012.
(5) Mitchell CJ, Churchward-Venne TA, Bellamy L, Parise G, Baker SK and Phillips SM. Muscular and systemic Correlates of Resistance Training-Induced Muscle Hypertrophy. Plos One. 8 (10), 2013.
(6) West DWD and Phillips SM. Anabolic Processes in Human Skeletal Muscle: Restoring the Identities of Growth Hormone and Testosterone. The Physician and Sports Medicine. 3 (38), 2010.