The Effects of Heat Therapy During Immobilization and Rehabilitation on Muscle Atrophy and Strength Loss at Return to Sports in Healthy Humans

Abstract

Background: Animal research suggests that repeated heat exposures may stimulate skeletal muscle protein synthesis and downregulate protein degradation.

Hypothesis: Repeated heat exposures during ankle immobilization and rehabilitation would preserve human muscle strength and mass.

Study design: Controlled laboratory study.

Methods: A total of 20 male participants (age, 33.6 ± 2.8 years; weight, 83.8 ± 9.2 kg; height, 182 ± 6 cm) underwent 4 weeks of supervised training, 2 weeks of single-lower leg immobilization, and 2 weeks of supervised rehabilitation before return to sports (RTS). Participants were split into 2 groups: (1) whole-body heat therapy (HEAT) and (2) sham treatment (SHAM) throughout the immobilization and rehabilitation periods. Measures of muscle strength (isometric and isokinetic), volume (magnetic resonance imaging and ultrasound), and muscle biopsies were obtained preimmobilization, postimmobilization, and at RTS.

Results: Maximal isometric strength of the plantarflexors was lower at RTS compared with preimmobilization in SHAM (P = .027) but not HEAT (P = .301). Isokinetic strength during a fatigue test was higher at RTS compared with preimmobilization in HEAT (P = .039) but not SHAM (P = .245). Pennation angle and muscle thickness were lower at postimmobilization compared with preimmobilization only in SHAM (P≤ .027). Muscle cross-sectional area decreased in soleus and both gastrocnemius medialis and lateralis (all P≤ .035) in SHAM, but only in gastrocnemius medialis in HEAT. There was a large (d = 0.91) but not significant (P = .054) decrease in the ratio of phosphorylated/total nuclear factor-kappa B (NFκB) from preimmobilization to postimmobilization in HEAT only. There was an increase in phosphorylated fork head box O proteins (FoxO) only in HEAT (P = .034), suggesting a decrease in FoxO activity. Caspase 3 expression increased from preimmobilization to postimmobilization in SHAM only (P = .004).

Conclusion: These results indicate that using heat therapy throughout immobilization and rehabilitation reduces skeletal muscle atrophy and maintains plantarflexor strength in healthy humans. Moreover, heat therapy may lead to the inactivation of the FoxO and NFκB signaling pathways involved in atrophy.

Clinical relevance: Repeated heat exposures should be considered a novel therapeutic intervention to counteract muscle atrophy during immobilization.

Keywords: ankle; athletic training; biologic healing enhancement; muscle injuries; muscle physiology; physical therapy modalities; physical therapy/rehabilitation.

Figure 1.

General procedure for the 8-week protocol. The training phase lasted for 4 weeks, the immobilization for 2 weeks, and the rehabilitation postimmobilization for 2 weeks. The HEAT group was in an environmental chamber set at 50ºC for the passive heat exposures (ie, immobilization) and 35ºC for the active heat exposures (ie, rehabilitation). The SHAM group was in an altitude chamber set to a simulated altitude of 200 m. MRI, magnetic resonance imaging; POST-IMMO, postimmobilization; PRE-IMMO, preimmobilization; Res., resistance; RTS, return to sports.

Figure 2.

Individual and mean maximal torque during (A) iMVC and (B) isokinetic fatigue tests of the HEAT and control (SHAM) groups preimmobilization (PRE-IMMO), postimmobilization (POST-IMMO), and after rehabilitation (RTS). *P < .05. iMVC, isometric maximal voluntary contraction; ns, nonsignificant; RTS, return to sport.

Figure 3.

Ultrasound of the GM. Individual and mean (±SD) of (A) muscle thickness, (B) pennation angle, and (C) fascicle length of the SHAM (control) and HEAT groups preimmobilization (PRE-IMMO), postimmobilization (PRE-IMMO), and after rehabilitation (RTS). *P < .05. (D) Representative ultrasound image; muscle thickness was calculated as the mean of the vertical distances between points 1 and 3, and 2 and 4; pennation angle and fascicle length were calculated using the f1:0 and f1:1 markers. GM, gastrocnemius medialis; ns, nonsignificant; RTS, return to sport.

Figure 4.

Individual and mean (±SD) cross-sectional areas were obtained from MRI scans for the (A) GL, (B) GM, and (C) SOL muscles. Data are shown for the SHAM and HEAT groups preimmobilization (PRE-IMMO), postimmobilization (PRE-IMMO), and after rehabilitation (RTS). (D) Representative image. *P < .05. GL, gastrocnemius lateralis; GM, gastrocnemius medialis; MRI, magnetic resonance imaging; ns, nonsignificant; RTS, return to sport; SOL, soleus.

Figure 5.

Results of muscle biopsies. Representative protein blot (phosphorylated and total when applicable) and analyses for (A) protein kinase B (AKT), (B) fork head box O proteins (FoxO), (C) nuclear factor-kappa B (NFκB), and (D) caspase 3. Data are shown for the SHAM group and HEAT groups preimmobilization (PRE-IMMO), postimmobilization (PRE-IMMO), and after rehabilitation (RTS). Differences with PRE-IMMO: *P < .05, (*)P = .054. ns, nonsignificant; RTS, return to sport.