West · The Journal of physiology 2009 · within-subject crossover trial · n=8

Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men.

Cited 288 times in the scientific literature.

Level 2 - randomized trial

Within-subject crossover experimental trial

PubMed 19736298 · doi:10.1113/jphysiol.2009.177220 · record verified 2026-08-31

What was done

Eight young men (age 20 +/- 1.1 years, BMI 26 +/- 3.5 kg m(-2)) completed two exercise protocols: a low-hormone protocol (LH) consisting of unilateral elbow flexor resistance exercise alone, and a high-hormone protocol (HH) consisting of contralateral elbow flexor exercise followed immediately by high-volume leg resistance exercise. Participants consumed 25 g of protein after arm exercise. Muscle biopsies from the biceps brachii and blood samples were collected to measure serum testosterone, growth hormone (GH), and IGF-1, along with myofibrillar protein synthesis (MPS) and p70S6K phosphorylation.

What was found

Serum testosterone, GH, and IGF-1 did not change after the LH protocol, but were markedly elevated after the HH protocol (testosterone, P < 0.001; GH, P < 0.001; IGF-1, P < 0.05). Biceps brachii MPS increased following exercise (rest = 0.040 +/- 0.007% h(-1), LH = 0.071 +/- 0.008% h(-1), HH = 0.064 +/- 0.014% h(-1); P < 0.05), with no difference between hormone conditions (P = 0.72). Phosphorylation of p70S6K also increased post-exercise (P < 0.05) with no differences between conditions.

Why it matters

This study demonstrates that transient, exercise-induced spikes in endogenous anabolic hormones do not augment fed-state muscle protein synthesis or anabolic signalling. It highlights that local intramuscular mechanisms, rather than systemic hormone fluctuations, are the primary drivers of post-exercise muscle protein synthesis.

Limits

The study is limited by a very small sample size (n = 8) restricted to young healthy men. It measured acute, short-term protein synthesis and signalling responses rather than chronic muscle hypertrophy, and examined endogenous physiological hormone elevations rather than exogenous administration.

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