Hormones, such as human growth hormone (GH) and testosterone, have been shown to play a role in the muscle hypertrophy and strength gains. Men suffering from either GH deficiency or testosterone deficiency have increased fat mass, reduced muscle mass, and reduced muscle force production. The anabolic effects of testosterone on muscle mass are dose and concentration dependent . Bhasin et al. demonstrated that supraphysiological doses of testosterone can induce increases in muscle size and strength in younger men without exercise.
Testosterone-induced increase in muscle mass is associated with a dose-dependent increase in cross-sectional areas of both type I and type II muscle fibers . However, the mechanisms by which testosterone increases muscle mass are not well understood. The prevalent dogma for the past 50 years has been that testosterone increases muscle mass by stimulating fractional muscle protein synthesis. Testosterone administration primes skeletal muscle for growth by increasing net protein synthesis, even in the fasted state [6,7]
The logical extrapolation of a continued increase in net protein synthesis results in an increase in lean body mass and strength. Additionally, testosterone stimulates many other pathways besides just increasing protein synthesis rates to stimulate of muscle hypertrophy. Testosterone administration also results in increases in GH secretion, androgen receptor number, satellite cell activity, and increased IGF-I expression in skeletal muscle . It has also been demonstrated that the increase in muscle anabolism is associated with an increase in the expression of intramuscular mRNA IGF-I .
GH is also highly recognized for its role in muscle growth. Resistance exercise stimulates the release of GH from the anterior pituitary gland, with released levels being very dependent on exercise intensity. GH helps to trigger fat metabolism for energy use in the muscle growth process. As well, GH stimulates the uptake and incorporation of amino acids into protein in skeletal muscle. GH is an anabolic hormone capable of increasing muscle mass . In humans, GH administration is known to increase both whole-body and muscle protein synthesis [10,11] and almost unequivocally to increase lean body mass and decreased fat mass. GH-also stimulates hepatic production of circulating IGF-1 concentrations and may also stimulate IGF-1 production in other tissue such as skeletal muscle [12,13].
It is well established that testosterone and GH are important for muscle hypertrophy and strength, but what about the acute increases that occur during resistance exercise? Are they important? Researchers at the Exercise Metabolism Group at McMaster’s University reported this month that muscle hypertrophy took place without acute increases in anabolic hormone concentrations . 10 healthy young male subjects performed unilateral resistance training for 8 week (3 days/week). Unilateral resistance exercise is basically where you train one arm or in this case leg, while the other arm or leg is used as a control or untrained muscle. Exercises performed in the study included knee extensions and leg press performed at 80-90% of the subject’s single repetition maximum (1RM). Blood samples were collected before, immediately after, 30, 60, 90, and 120 minutes post-exercise. The first training bout and following the last training bout were analyzed for total testosterone, free-testosterone, GH, and insulin-like growth factor-1, along with other hormones. Thigh muscle cross sectional area (CSA) and muscle fiber CSA by biopsy (vastus lateralis) were also measured pre- and post-training.
Acutely, no changes in GH, testosterone, or IGF-1 concentrations were observed in the 90 min period following exercise and there was no influence of training on the anabolic hormones measured. GH did show a moderate increase 30 minutes post-exercise but returned to baseline values by 90 minutes. Training-induced increases were observed in type IIb and IIa muscle fiber CSA. No changes were observed in fiber CSA in the untrained leg. Whole muscle CSA increased in the trained leg and remained unchanged in the untrained leg. In conclusion, unilateral training induced local muscle hypertrophy only in the exercised limb, which occurred in the absence of testosterone, GH, or IGF-1 circulating levels.
Muscle Hypertrophy without Anabolic Hormones
Back in the early 70’s researchers quickly realized that if you took a rat and had him walk downhill on a treadmill or induced tension overload by putting a muscle on stretch (eccentric contractions) that they could do all sorts of nasty things to try and blunt muscle hypertrophy but it did not stop muscle hypertrophy from occurring: they removed their pituitary so they could not produce GH or IGF-1, castrated them so they could not produce testosterone, removed their thyroid, or just didn’t feed them…despite this punishment, the rats still had increases in muscle hypertrophy in their legs . In his research, Dr. Goldberg noted, “Maximal tension development leads to increases in muscle hypertrophy. Unlike normal developmental growth, work-induced hypertrophy can be induced in hypophysectomized (rats that can’t produce GH) or diabetic animals. This process thus appears independent of growth hormone and insulin as well as testosterone and thyroid hormones. Hypertrophy can also be induced in fasting animals, in which there is a generalized muscle wasting. Thus muscular activity takes precedence over endocrine influences on muscle size. The increase in muscle weight reflects an increase in protein, especially sarcoplasmic protein, and results from greater protein synthesis and reduced protein breakdown.
The ‘Intramuscular Growth Factor’ Camp
Elevated testosterone levels have been reported to occur in some studies whereas several studies have shown no difference [19,20,21] or even reductions . Some researchers have even gone on to argue that the gains in strength and size are all related to “intramuscular growth factors” that are independent of testosterone and GH. A paper presented by Dr. Goldberg in 1975 stunned scientists about the relationship between muscle growth and testosterone. In his research, he castrated rats so that they could not produce testosterone and put their leg muscle on tension overload. Surprisingly, the rats’ leg muscles grew in size suggesting that mechanical overload increases muscle hypertrophy independent of testosterone . Research scientists are now discovering the signaling pathway by which mechanical stimulation of contracting muscle and intramuscular growth factors as IGF-1 activity leads to changes in satellite cells, muscle DNA content, increased muscle protein synthesis, increased muscle mass, and strength. Other recent research has demonstrated that IGF-1 increases intracellular calcium ion concentrations leading to the activation of the muscle growth signaling pathway, and subsequent muscle fiber hypertrophy. For example, in one study 10 healthy men completed eight sets of maximal eccentric squats. The intramuscular IGF-I mRNA concentration increased 62% but serum testosterone showed little change . The results of the study suggest that maximal muscle tension is more important than acute increases in testosterone.
An increase in muscle hypertrophy can lead to greater increases in muscle strength. Reports in the literature have suggested that the insulin-like growth factor I protein plays a major role in strength training-induced skeletal muscle hypertrophy and strength improvements. Some people due to differences in genetics express higher levels of IGF-1 than others, what we call ‘lucky bastards’. One study compared those that expressed high levels of IGF-1 levels in muscle to those that did not. After 10 weeks of training, with a single-leg knee-extension strength training program, 1-repetition maximum, muscle volume, and muscle quality increased significantly for all exercising groups. Subjects that expressed higher natural levels of IGF-1 levels gained significantly more strength than those whom did not. Thus the data suggest that the IGF-1 may influence the strength response to strength training.
In conclusion, there is debate as to whether the increases in acute anabolic hormone responses are important for muscle hypertrophy. Look at the muscle hypertrophy of some powerlifters, elite powerlifters have considerable muscle hypertrophy yet they take prolonged rest periods and more than likely have very small increases in anabolic hormones when they train. It seems that direct muscle tension and muscle fiber damage leads to increases in muscle hypertrophy. Resistance training leads to trauma or injury of the cellular proteins in muscle. This prompts cell-signaling messages to activate satellite cells to begin a cascade of events leading to muscle repair and muscle growth. Several growth factors are involved that regulate the mechanisms of change in protein number and size within the muscle. The acute increases in anabolic hormones are temporary and may not be as important for muscle growth as the direct stress placed on muscle fibers during exercise.
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