The last article we discussed microtrauma and why it is essential for hypertrophy, as well as how load is linearly related to microtrauma. In this concluding part, we will look into the endocrine and metabolic factors that are often used to determine load guidelines for optimal hypertrophy.
Endocrine Factors
As the name connotes, growth hormone (GH) is anabolic in nature. The loss of strength and muscle mass characteristic of GH deficient folks, and the reversal in these performance indices upon GH supplementation, clearly reveals its anabolic role (1,2,3). This information, coupled with the presence of greater GH secretion following resistance training, leads to a barrage of GH studies which are worth discussing.
Interestingly, common to all these studies is a greater growth hormone response following moderate loads using shorter rest periods when compared with high loads using longer rest periods (4,5,6). Kraemer et al., for instance, showed that performing a 10 RM with 1 minute rest between sets showed greater GH response than performing a 5 RM with 5 minute rest periods (4). Another study reported that performance of 20 sets of 1RM produced a slight increase in GH, whereas a substantial increase in GH was observed following 10 sets of 10 repetitions with 70% of 1RM (5). Call it coincidence if you like, but the protocol that shows the greatest GH release appears to be that of a typical bodybuilding routine, while the program which showed the least GH response mirrored what we typically consider a powerlifting program.
Although researchers couldn’t find any causal evidence, this GH hypothesis was evidence enough to establish the current load and rest time guidelines for hypertrophy.
But is the evidence really enough? Let's see: one of the early processes involved in the secretions of GH is the accumulation of metabolic products like lactate (La) and proton (H) in the muscle. The acidic environment in the muscle stimulates sympathetic nerve activity through chemoreceptors, which may send signals to the hypothalamus-pituitary system, and in turn trigger the secretion of GH (6,7). Apparently, the changes in GH seen in most of the studies were in phase with changes in the lactate concentration (4,5). This suggests that metabolic accumulation during exercise is the primary stimulus influencing GH release. For example, Takarada showed a low intensity (20 RM) exercise to cause a 290-fold increase in the concentration of GH when the blood flow was blocked by occlusion (8). This magnitude of increase, even larger than that reported using heavier loads, reveals metabolic accumulation due to occlusion to be primarily responsible for GH release.
Activities that stress the metabolic pathways like hyperventilation, breath holding, hypoxia and even nicotinic acid ingestion have been shown to profoundly influence growth hormone release (9,10). The high correlation of GH and metabolic products is further supported by the decreased GH response following induced alkalosis during cycling (11). And, keep in mind that all these changes in GH are transient: the resting concentration of GH has never been altered by any sort of resistance training (12,13,14).
Researchers began to suspect that raising the resting concentration of GH through supplementation might be the key to inducing hypertrophy. After all, GH is a common ingredient in any bodybuilder's drug list. As expected, this let lose another flurry of GH supplementation studies. Surprisingly the majority of the studies, whether in young men, older men or athletes, showed little change in muscle fiber size or strength after GH supplementation (15,16,17). The inability of even supraphysiological doses to elicit a hypertrophic response clearly undermines the role these training-induced tiny spikes of GH play in hypertrophy.
The discovery of local growth factors and their central role in hypertrophy was the final blow which shifted the foundation of the growth hormone hypothesis. Studies showed muscle growth even after the depression of circulating GH and IGF-1 levels (19). Worse yet, substantial increase in muscle mass was observed even after the GH axis was surgically interrupted (20,21).
Ironically, after all these counter evidences the repetition bracket of 8-12 is still hailed as the optimum range for hypertrophy- and the same old GH hypothesis is still being quoted in its defense.
Metabolic Factors
Though mechanical factors are essential to resistance training adaptations, metabolic factors have also been shown to play a role in hypertrophy.
The feeling of "pump" or “burn” is associated with the build up of these metabolic products (H, La, P, Cr, and K) in the muscle; the higher the number of reps in a set, the greater their accumulation and effect. Traditionally, studies have used three methods to understand the influence of metabolites on hypertrophy and strength. And, all three methods have revealed conflicting roles for metabolites in hypertrophy.
Eccentric contractions recruit fewer fibers than concentric contractions when using the same load. This distinct metabolic characteristic of contractions is often exploited to examine the importance of high force stress versus metabolic stress on hypertrophy (1,2). The second method involves the manipulation of rest intervals between sets: shorter rest intervals are metabolically more taxing than longer rest intervals (3,4). The occlusion method uses a pressurized cuff to occlude or clog the blood flow to the exercising muscle and in turn also increases the metabolic fatigue (5,6).
Now let's delve deeper and look at the possible mechanisms by which the metabolic milieu can impact hypertrophy. One possibility is that the ischemic condition and/or the metabolic changes in the muscle could lead to a greater recruitment of the fast twitch muscle fibers (Type 2). This is quite evident from the greater EMG activity recorded in the occlusion studies. For instance, Moore and his team specifically investigated the neuromuscular activity accompanying occlusion and showed that there is an early activation of Type 2 fibers for the occlusive group compared to the non-occlusive group (5). Another study showed the EMG activity in the low intensity exercise (40% 1RM) with occlusion to be almost equal to that in the high intensity exercise (80% 1RM) without occlusion (6).