Aumento de la hipertermia en el estrés oxidativo inducido por el ejercicio.(In.)

S. R. McAnulty1, L. McAnulty2, D. D. Pascoe3, S. S. Gropper4, R. E. Keith4, J. D. Morrow5, L. B. Gladden3

1 Department of Health, Leisure, and Exercise Science, Appalachian State University, Boone, NC, USA
2 Department of Family and Consumer Sciences, Appalachian State University, Boone, NC, USA
3 Department of Health and Human Performance, Auburn University, Auburn, AL, USA
4 Department of Nutrition and Food Science, Auburn University, Auburn, AL, USA
5 Department of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, TN, USA


The purpose of this investigation was to examine oxidative markers after exercise in a hyperthermic environment (35 °C, 70 % RH) (Hot) versus a neutral environment (25 °C, 40 % RH) (Con). Hyperthermia may exacerbate oxidative stress by uncoupling the mitochondrial respiratory chain or by inhibiting antioxidant defense mechanisms, but this has not been assessed in vivo. Six male subjects performed low-intensity exercise (50 % VO2max) on a treadmill in Hot until a core temperature of 39.5 °C was reached, and for an equivalent time in Con. Blood samples were drawn before and immediately after exercise and at 8 min and 15 min following exercise. Samples were analyzed for F2 isoprostanes (FIP), lipid hydroperoxides (LPO), and lactate. A 2 × 4 repeated measures ANOVA was used to test for treatment, time, and interaction effects for FIP, LPO, and lactate. Differences in VO2 were tested with Student’s t-test. Significance was set at p < 0.05. Oxygen consumption was not significantly different between Hot and Con. The pattern of change of FIP and lactate in Hot was significant versus exercise in Con. LPO was significantly elevated over time in both Hot and Con, but the pattern of change was not significantly different. Ending core temperatures and heart rates were significantly elevated in Hot versus Con. These data indicate that hyperthermia increases oxidative stress and selectively affects specific lipid markers, independent of oxygen consumption.

Sports Med 2005; 26: 188-192.

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