Author(s): CHAMBION-DIAZ, M., BOUTEN, J., TASCIOGULLARINDAN, T., BALLARIN, F., SIMIONI, G., LE GARREC, S., BRUNET, E., PISCIONE, J., HOSTEN, I., BILLAUT, F., MILLET, G.P., BROCHERIE, F., PIALOUX, V., Institution: CLAUDE BERNARD UNIVERSITY LYON 1, Country: FRANCE, Abstract-ID: 293

INTRODUCTION:
This study aimed to investigate the effects of repeated-sprint training performed under different environmental stressors on oxidative stress, inflammatory responses, and muscle damage in elite athletes.
METHODS:
22 elite athletes from the French national rugby sevens and cycling teams were randomly assigned to a repeated-sprint training program (3x 5, 7-10s sprints with 20-23s passive rest) conducted either in normobaric hypoxia (FiO₂ 14.5%, 20-22°C; RSHyp) or in hot conditions (FiO₂ 20.9%, 36°C; RSHot). The intervention consisted of three RSHyp/RSHot sessions per week over a 2-week intervention period. Blood samples were collected after 15 min of supine rest at rest before (Pre) and after (Post) the intervention. Biomarkers related to redox balance (antioxidant, pro-oxidant enzymes, oxidative damage markers), inflammation (TNF-α, IL-1β, IL-6, CRP), muscle damage (CK, Mb), hypoxic signaling (HIF-1α), cellular stress (HSP70, HSP90), nitrosative stress (nitrotyrosine) were analyzed.
RESULTS:
Following the intervention, HIF-1α and HSP70 concentrations increased in both groups, indicating activation of hypoxic and cellular stress pathways. In RSHyp , post-intervention increases were observed in catalase, XO, MPO, CK, TNF-α, and IL-6 (all p<0.05), reflecting enhanced oxidative and inflammatory responses. In contrast, RSHot showed a significant decrease in SOD and an increase in Mb levels (p<0.05), suggesting greater muscle membrane stress and lipid peroxidation.
CONCLUSION:
These findings support the existence of biological crosstalk between hypoxia and heat stress when combined with repeated-sprint training, particularly through HIF-1α and HSP signaling. However, in this special training modality, hypoxia preferentially amplified pro-oxidant and pro-inflammatory responses, whereas heat exposure predominantly increased lipid peroxidation. This highlights the stressor-specific nature of molecular adaptations to environmental training conditions.