Alterations of protein turnover underlying disuse atrophy in human skeletal muscle.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic physiological literature without systematic methodology
PubMed 19608931 · doi:10.1152/japplphysiol.00452.2009
What was done
This narrative review summarizes human in vivo metabolic studies using arterial-venous balance, tracer dilution, and tracer incorporation to evaluate muscle protein turnover during disuse atrophy, contrasting these human dynamic measurements with animal, cell culture, and disease-related inflammatory wasting models.
What was found
The abstract presents no quantitative data. It reports that muscle disuse atrophy in humans is driven primarily by a depression of muscle protein synthesis in both postabsorptive and postprandial states (termed anabolic resistance), whereas muscle proteolysis itself is not elevated, leading to disrupted diurnal protein balance.
Why it matters
It differentiates uncomplicated mechanical unloading from inflammatory muscle wasting and questions the direct translation of rodent proteolysis models to humans, clarifying that human disuse interventions should focus on overcoming anabolic resistance.
Limits
This is a narrative review with no systematic search criteria, meta-analytic synthesis, or risk-of-bias grading. The abstract provides no quantitative effect sizes, patient counts, or disuse durations.
Cited by
- supports Disuse muscle atrophy occurs primarily because of a reduction in muscle protein synthesis rates in both the fasted state and in response to amino acid feeding.