Hot exercise boosts IL-6 and hepcidin in female athletes, but gut permeability unchanged
Background
Endurance exercise is known to induce systemic inflammation and affect iron homeostasis, particularly through the acute phase reactant hepcidin, which regulates iron absorption. Environmental factors like heat stress can exacerbate physiological strain, potentially intensifying these responses and impacting recovery or performance. While exercise-induced immune activation is well-studied, the specific interplay of heat stress on gut permeability, systemic inflammation (e.g., IL-6, TNFα), and iron regulation in female athletes, especially with shorter-duration, high-intensity protocols, remains an area requiring further investigation.
Study Design
This randomized cross-over study enrolled 13 endurance-trained female athletes (age 26 years, VO2max 57.7 mL·kg-1·min-1). Each participant completed two treadmill exercise sessions at 70% VO2max until volitional exhaustion. Conditions included a hot environment (35°C and 40% RH) and a cool environment (11°C and 40% RH). Researchers measured LPS, TNFα, IL-6, and hepcidin concentrations at various time points post-exercise to assess gut permeability, systemic inflammation, and iron homeostasis, respectively, comparing responses between the two environmental conditions.
Results
Peak body core temperature was significantly higher in the hot condition, increasing by +2.1°C (95% CI: 1.8, 2.3) compared to +1.0°C (95% CI: 0.8, 1.3) in the cool condition (p < 0.01). While no changes were observed in LPS or TNFα concentrations at any time point, indicating no significant impact on gut permeability, the inflammatory and iron-regulatory responses differed.
The hot condition led to a greater rise in
IL-6concentration at 1 hour post-exercise, reaching 1.6 pg/mL (95% CI: 1.0, 2.2) compared to 1.0 pg/mL (95% CI: 0.8, 1.3) in the cool condition (p = 0.04). Furthermore,hepcidinconcentrations at 3 hours post-exercise were also significantly greater in the hot condition, measuring 15.1 ng/mL (95% CI: 8.8, 21.3) versus 7.9 ng/mL (95% CI: 3.5, 12.2) in the cool condition (p = 0.03).
Key Findings
- Peak core body temperature increased by +2.1°C in hot conditions vs. +1.0°C in cool conditions (p < 0.01).
- No significant changes in
LPSorTNFαconcentrations were observed in either condition. IL-6concentration at 1 hour post-exercise was higher in hot conditions (1.6 pg/mL) vs. cool (1.0 pg/mL) (p = 0.04).Hepcidinconcentration at 3 hours post-exercise was higher in hot conditions (15.1 ng/mL) vs. cool (7.9 ng/mL) (p = 0.03).
Why It Matters
This study highlights that training in hot environments significantly elevates inflammatory markers like IL-6 and iron-regulatory hormones like hepcidin in female athletes, even without affecting gut permeability. Athletes and coaches should consider environmental conditions when planning training and recovery strategies, especially for those prone to iron deficiency or aiming to optimize recovery. Elevated hepcidin can reduce iron availability, potentially impacting long-term iron status and performance. This suggests that post-exercise nutritional strategies or recovery protocols might need adjustment for heat-stressed training sessions to mitigate increased inflammatory load and manage iron metabolism more effectively, moving towards more personalized training regimens.
exercise
heat-stress
inflammation
iron-homeostasis
female-athletes
il-6