With the right plan and the right discipline, you can get seriously shredded in just 28 days.Read article
Hormones such as human growth hormone (GH), testosterone, and IGF-1 have been shown to play a role in muscle hypertrophy and strength gains. Many of the great bodybuilders in the early ’90s trained with short rest periods between sets, as earlier research found that short rest periods in conjunction with intense training led to significant increases in GH and testosterone. The anabolic effects of testosterone on muscle mass are dose and concentration dependent. The prevalent dogma for the past 50 years has been that testosterone increases muscle mass by stimulating fractional muscle protein synthesis. Testosterone administration also results in increases in GH secretion, androgen receptor number, satellite cell activity, and increased IGF-I expression in skeletal muscle. It’s 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. In humans, GH administration is known to increase both whole-body and muscle protein synthesis and almost unequivocally to increase lean body mass and decreased fat mass. Human growth hormone also stimulates hepatic production of circulating IGF-1 concentrations and may also stimulate IGF-1 production in other tissue such as skeletal muscle. So it’s 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 University reported that muscle hypertrophy took place without acute increases in anabolic hormone concentrations. Ten healthy young male subjects performed unilateral resistance training for eight weeks (three days/week). Unilateral resistance exercise is basically where you train one arm or leg, while the other arm or leg is used as a control or untrained muscle. Exercises performed in the study were knee extensions and leg presses performed at 80–90% of the subject’s single-repetition maximum (1RM). Blood samples were collected before, immediately aﬅ er, 30, 60, 90, and 120 minutes post-exercise. The first training bout and 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 preand post-training.
Acutely, no changes in GH, testosterone, or IGF-1 concentrations were observed in the 90-minute period following exercise and there was no influence of training on the anabolic hormones measured. Human growth hormone 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. To further support the evidence that acute anabolic hormones have little impact on muscle growth, an excellent review was published in Medicine in Sports Science and Exercise, which further supports the notion, that acute anabolic hormones have little to do with muscle hypertrophy. The reviewers suggested that the interpretation of the current literature to support that post-exercise hormone levels have an effect on the extent of muscular hypertrophy is lacking.