Hypo-activity induced skeletal muscle atrophy and potential nutritional interventions: A review

Abstract

Periods of hypo-activity result in profound changes in skeletal muscle morphology and strength. This review primarily addresses the differential impact of de-training, bed-rest, limb immobilisation and unilateral lower limb suspension on muscle morphology, strength and fatigability. The degree of muscle atrophy differs depending on the hypo-activity model and the muscles in question, with the leg and postural muscles being the most susceptible to atrophy. Hypo-activity also results in the dramatic loss of strength that often surpasses the loss of muscle mass, and consequently, the nervous system and contractile properties adapt to adjust for this excessive loss of strength. In addition, the degree of muscle strength loss is different depending on the hypo-activity model, with immobilisation appearing to have a greater impact on strength than unloaded models. There is a step-wise difference in the magnitude of muscle loss so that, even after accounting for differential durations of interventions immobilisation ≥ unilateral lower limb suspension ≥ bed-rest ≥ de-training. Muscle fatigability varies between hypo-activity models but the results are equivocal and this may be due to task-specific adaptations. This review also addresses potential nutritional interventions for attenuating hypo-activity induced muscle atrophy and strength declines, in the absence of exercise. Essential amino acid supplementation stands as a strong candidate but other supplements are good contenders for attenuating hypo-activity induced atrophy and strength losses. Several potential nutritional supplements are highlighted that could be used to combat muscle atrophy but extensive research is needed to determine the most effective.

Keywords: Immobilisation; Disuse; Muscle size; Muscle strength; Nutrition supplementation; Muscle fatigability

Core tip: This review summarises and compares the morphological, strength and fatigability changes in response to different models of hypo-activity. The hypo-activity models include de-training, bed-rest, immobilisation and unilateral lower limb suspension. There is a step-wise difference in the magnitude of muscle and somewhat strength losses so that, even after accounting for differential durations of interventions immobilisation ≥ unilateral lower limb suspension ≥ bed-rest ≥ de-training. Muscle fatigability varies between hypo-activity models but the results are equivocal and this may be due to task-specific adaptations. This review also highlights several potential nutritional interventions for attenuating hypo-activity induced changes.