Abstract
This study aimed to assess the effect of a marathon running at a hot environmental temperature on the baseline skin temperature (Tsk) of the posterior day and to analyze the relationship between Tsk response and muscle damage markers variation. The Tsk, creatine kinase, and lactate dehydrogenase of 16 marathon runners were assessed four times before (15 days and 45 min) and after (24 h and 6 days) a marathon in a hot environment (thermal stress index = 28.3 ± 3.3 °C and humidity ~81%). The Tsk of thirteen different body regions of both right and left lower limbs were analyzed. Higher values after the marathon were observed than 45 min before in creatine kinase (174.3 ± 136.4 UI/L < 1159.7 ± 699.7 UI/L, p < 0.01 and large effect size) and lactate dehydrogenase (362.6 ± 99.9 UI/L < 438 ± 115.5 UI/L, p = 0.02 and moderate effect size). Generally, Tsk was higher the day after the marathon than at the other three moments (e.g., rectus femoris region, 6 days before vs. the day after, 95% confidence interval of the difference (0.3, 1.6 °C), p = 0.04 and large effect size). No relationship or correlation was observed between the variation of Tsk and muscle damage markers (p > 0.05). In conclusion, performing a marathon in a hot environmental condition results in a higher Tsk the day after the marathon. This increase in Tsk could be because of the heat generated by the marathon and its subsequent physiological processes (e.g., increase in endothelial nitric oxide, glycogen resynthesis, or increase of systemic hormones), which would be reflected in the Tsk due to the peripheral vasodilation promoted by the hot environment. However, among these processes, muscle damage does not seem to be of great importance due to the lack of an observed relationship between Tsk and muscle damage markers.
Highlights
Endurance competition such as marathon running is recognized for having a high physical and physiological demand [1]
Tsk was higher at Post24h than at the other three moments (e.g., rectus femoris: Post24 vs. Pre15d 95%CI (0.9, 2.0◦ C), p < 0.001 and ESd = 1.6; difference Post24 vs. Pre0h 95%CI (0.4, 1.4 ◦ C), p < 0.01 and
It was hypothesized that the high thermal stress caused by a marathon in a high environmental temperature could result in Tsk increments 24 h after the marathon and could have a direct relationship with muscle damage markers
Summary
Endurance competition such as marathon running is recognized for having a high physical and physiological demand [1]. Marathon running could lead to muscle damage due to the cumulus of the high volume of concentric–eccentric muscle contractions [2]. Muscle fibers damage may provoke leakage of the muscle proteins into the bloodstream and later to subsequent complications, including but not limited to delayed onset muscle soreness (DOMS), rhabdomyolysis, and acute kidney injury [2,3,4]. Muscle damage induced by exercise is commonly assessed by quantifying blood markers such as serum creatine kinase (sCK), serum lactate dehydrogenase (sLDH), myoglobin, magnesium, among others [7,8,9,10]. SCK and sLDH are considered good indicators of muscle damage [11], other indirect tools have been used to decrease the invasive procedure during blood collection, such as using visual analog scales to measure DOMS [12]
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