Skeletal muscle immobilization has been demonstrated to induce atrophy and strength loss. Research utilizing animal models posits that the application of heat therapy may serve as a protective mechanism against skeletal muscle atrophy during injuries. The purpose was to investigate the effect of whole-body heat therapy on preventing muscle deconditioning during immobilization and rehabilation in humans. Methods: Following four weeks of supervised training, 20 male participants (33.6±2.8 years, 83.8±9.2 kg, 182±6 cm) were tested before (PRE-IMMO) and after (POST-IMMO) two weeks of single-lower leg immobilization, as well as at return to sport following two weeks of supervised rehabilitation (RTS). Testing included measures of muscle force and volume as well as muscle biopsies. Participants were split into two groups, receiving whole-body heat therapy (HEAT) or a sham treatment (SHAM) throughout the immobilization and rehabilitation periods. Maximal isometric strength of the plantarflexors was lower at RTS than PRE-IMMO in SHAM (p=0.027), but not HEAT (p=0.301). Isokinetic strength during a fatigue test was higher at RTS than PRE-IMMO in HEAT (p=0.039) but not SHAM (p=0.245). Pennation angle and muscle thickness were lower POST-IMMO than PRE-IMMO only in SHAM (p=0.027). Muscle cross-sectional area measured by magnetic resonance imagery was decreased in Soleus and Gastrocnemius medialis and lateralis (all p≤0.035) in SHAM, but only in Gastrocnemius medialis in HEAT. There was a large (d=0.91) but not significant (p=0.054) decrease in the ratio of phosphorylated/total NFκB from PRE-IMMO to POST-IMMO in HEAT only. There was an increase in phosphorylated FoxO only in HEAT (p=0.034), suggesting a decrease in FoxO activity. Caspase 3 expression increased from PRE-IMMO to POST-IMMO in SHAM only (p=0.004). Using heat therapy throughout immobilization and rehabilitation reduces skeletal muscle atrophy and maintains plantarflexors strength in humans. Moreover, heat therapy leads to the inactivation of the FoxO and NFκB signaling pathways involved in atrophy.
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Labidi et al. (2024) studied this question.
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