Comparative effects of thermal recovery strategies on strength, muscle soreness and molecular markers following exercise-induced muscle damage in healthy adults.

PURPOSE: This study investigated the effectiveness of three thermal recovery strategies; hot water immersion (HWI), cold water immersion (CWI), hot air exposure (HAE), to passive control (CON), on strength recovery following exercise-induced muscle damage in healthy adults. METHODS: A randomized, parallel group design (N = 40, N = 10 in each group) over four consecutive test days. Single bout of eccentric knee extensions, with baseline and post maximal voluntary contraction (MVC), followed by a thermal recovery strategy: hot water immersion (HWI; 30 min at 42°C), cold water immersion (CWI; 15 min at 9°C), hot air exposure (HAE; 30 min at 30°C, 30%RH) or control (CON: 30 min at 18°C, 30%RH). Restored strength (via MVC), and pain and muscle soreness (via visual analogue scales) were monitored over 72hr. Bloods were collected to analyse inflammatory marker interleukin 6 (IL-6), heat shock proteins (HSP72), and creatine kinase muscle-muscle isoenzyme (CK-MM). RESULTS: Maximal voluntary contraction (MVC) decreased by ∼36% immediately following exercise in all groups. A significant main effect of time (p = 0.001) and group (p = 0.032) was observed, with no time × group interaction (p = 0.93), indicating a similar recovery pattern across strategies. MVC progressively recovered over 72 h, reaching ∼88-89% of baseline in the HWI, HAE, and CON, and ∼82% in CWI; however, between-group differences at 72 h were not statistically significant. Markers of muscle damage (CK-MM) increased post-exercise in all groups (p < 0.05), with a significant time × group interaction (p = 0.02). CK-MM returned to baseline by 48 h in HWI and by 72 h in HAE and control, whereas values remained elevated in CWI at 72 h. Heat shock protein (HSP72) responses differed between conditions (time × group interaction, p = 0.001), with greater post-intervention increases observed following HWI and HAE compared with CWI. Interleukin-6 (IL-6) increased acutely in all groups post-exercise (p < 0.005), with a significant time × group interaction (p = 0.029). Following the recovery intervention, IL-6 was highest in HWI before declining more rapidly by 24 h relative to the other conditions. Pain and muscle soreness increased at 24 h and remained elevated at 72 h in all groups (p < 0.05), with no intervention fully restoring perceptual measures to baseline. CONCLUSION: Hot water immersion, hot air exposure, and passive control showed similar restoration of MVC by 72 h (88-89% of baseline), whereas cold water immersion remained lower at 82%. These patterns may be associated with the physiological responses observed following heat exposure, including elevated muscle temperature, increased HSP72 expression, and faster normalisation of markers of muscle damage and inflammation. However, functional recovery outcomes were comparable across strategies. None of the thermal recovery strategies were effective in alleviating pain and muscle soreness by 72 h.