Muscle-damaging exercise increases heat strain during subsequent exercise heat stress.

PURPOSE: It remains unclear whether exercise-induced muscle damage (EIMD) increases heat strain during subsequent exercise heat stress, which in turn may increase the risk of exertional heat illness. We examined heat strain during exercise heat stress 30 min after EIMD to coincide with increases in circulating pyrogens (e.g., interleukin-6 [IL-6]) and 24 h after EIMD to coincide with the delayed muscle inflammatory response when a higher rate of metabolic energy expenditure (M˙) and thus decreased economy might also increase heat strain. METHODS: Thirteen non-heat-acclimated males (mean ± SD, age = 20 ± 2 yr) performed exercise heat stress tests (running for 40 min at 65% V˙O2max in 33°C, 50% humidity) 30 min (HS1) and 24 h (HS2) after treatment, involving running for 60 min at 65% V˙O2max on either -10% gradient (EIMD) or +1% gradient (CON) in a crossover design. Rectal (Tre) and skin (Tsk) temperature, local sweating rate, and M˙ were measured throughout HS tests. RESULTS: Compared with CON, EIMD evoked higher circulating IL-6 pre-HS1 (P < 0.01) and greater plasma creatine kinase and muscle soreness pre-HS2 (P < 0.01). The ΔTre was greater after EIMD than CON during HS1 (0.35°C, 95% confidence interval = 0.11°C-0.58°C, P < 0.01) and HS2 (0.17°C, 95% confidence interval = 0.07°C-0.28°C, P < 0.01). M˙ was higher on EIMD throughout HS1 and HS2 (P < 0.001). Thermoeffector responses (Tsk, sweating rate) were not altered by EIMD. Thermal sensation and RPE were higher on EIMD after 25 min during HS1 (P < 0.05). The final Tre during HS1 correlated with the pre-HS1 circulating IL-6 concentration (r = 0.67). CONCLUSIONS: Heat strain was increased during endurance exercise in the heat conducted 30 min after and, to a much lesser extent, 24 h after muscle-damaging exercise. These data indicate that EIMD is a likely risk factor for exertional heat illness particularly during exercise heat stress when behavioral thermoregulation cues are ignored.

The effects of two nights of sleep deprivation with or without energy restriction on immune indices at rest and in response to cold exposure.

The purpose of the study was to determine the effects of two nights of sleep deprivation with or without energy restriction on immune indices at rest and in response to cold exposure. On three randomised occasions ten males slept normally [mean (SD): 436 (21) min night(-1); CON], were totally sleep-deprived (SDEP), or were totally sleep-deprived and 90% energy-restricted (SDEP + ER) for 53 h. After 53 h (1200 h) participants performed a seated cold air test (CAT) at 0.0 degrees C until T (re) decreased to 36.0 degrees C. Circulating leucocyte counts, neutrophil degranulation, stress hormones and saliva secretory IgA (S-IgA) were determined at 0 h, 24 h, 48 h, pre-CAT, post-CAT, 1-h and 2-h post-CAT. One night on SDEP increased bacterially stimulated neutrophil degranulation (21%, P < 0.05), and two nights on SDEP and SDEP + ER increased S-IgA concentration (40 and 44%; P < 0.01). No other significant effects were observed for immuno-endocrine measures prior to CAT. CAT duration was not different between trials [mean (SD): 133 (53) min] and T (re) decreased to 35.9 (0.3) degrees C. Modest whole-body cooling decreased circulating lymphocyte counts (25%; P < 0.01), S-IgA concentration (36%; P < 0.01) and secretion rate (24%; P < 0.05). A neutrophilia occurred post-CAT on CON and SDEP and 2-h post-CAT on SDEP + ER (P < 0.01). Modest whole-body cooling also decreased neutrophil degranulation on CON (22%) and SDEP (18%; P < 0.05). Plasma cortisol and norepinephrine increased post-CAT (31 and 346%, P < 0.05), but modest whole-body cooling did not alter plasma epinephrine. In conclusion, two nights of SDEP or SDEP + ER did not compromise resting immune indices. However, modest whole-body cooling (T(re) 35.9 degrees C) decreased circulating lymphocytes, neutrophil degranulation and S-IgA, but responses were not amplified by prior SDEP or SDEP + ER.