Short-term muscle disuse lowers myofibrillar protein synthesis rates and induces anabolic resistance to protein ingestion.
Level 3 - non-randomized controlled study
Prospective within-subject controlled physiological intervention trial without randomization between subjects.
PubMed 26578714 · doi:10.1152/ajpendo.00227.2015
What was done
Twelve healthy young men (mean age 22 ± 1 years) underwent 5 days of single-leg knee immobilization using a full leg cast. Quadriceps cross-sectional area (CSA) was measured before and after immobilization. Infusions of L-[ring-(2)H5]phenylalanine and L-[1-(13)C]leucine combined with ingestion of a 25 g bolus of intrinsically labeled dietary protein were used to determine postabsorptive and postprandial myofibrillar protein fractional synthetic rates in both the immobilized leg and the contralateral non-immobilized control leg.
What was found
Immobilization reduced quadriceps muscle CSA in the immobilized leg by 3.9 ± 0.6%. Using the phenylalanine tracer, postabsorptive myofibrillar protein synthesis rates were 41 ± 13% lower in the immobilized leg than the control leg (0.015 ± 0.002 vs. 0.032 ± 0.005%/h, P < 0.01). Postprandial synthesis rates were 53 ± 4% lower in the immobilized leg (0.020 ± 0.002 vs. 0.044 ± 0.003%/h, P < 0.01). Following protein ingestion, bound phenylalanine enrichment was 53 ± 18% lower in the immobilized leg compared to control (0.007 ± 0.002 vs. 0.015 ± 0.002 mole% excess, P < 0.05), with comparable results observed with the leucine tracer.
Why it matters
The findings demonstrate that even short-term disuse induces skeletal muscle atrophy by lowering basal myofibrillar protein synthesis and provoking anabolic resistance to dietary protein ingestion.
Limits
The sample size was small (n = 12) and included exclusively healthy young men, limiting generalizability to females, older individuals, or clinical populations. The study investigated only a 5-day disuse period and did not measure muscle protein breakdown.
Cited by
- supports A study by Luc van Loon's group led by Ben Wall showed that intracellular stable isotope tracer enrichment was higher after immobilization, indicating that disuse-induced protein synthesis decline is intracellular rather than caused by impaired membrane transport.