Acute Endocrine and Lipid Responses to Extreme Ultramarathon Running Across 100, 308, and 622 km Events

Extreme ultramarathon running provides a unique human model for examining physiological responses under sustained metabolic stress. This study compared acute endocrine and lipid responses across 100, 308, and 622 km ultramarathon events, with particular attention to whether these responses were uniformly amplified with increasing race distance or differed according to event characteristics. Forty-four experienced male ultramarathon runners participated in the study (100 km group: n = 17; 308 km group: n = 18; 622 km group: n = 9). Venous blood samples were collected within 2 h before race start and generally within 5 min after race completion, and post-race biochemical concentrations were corrected for participant-specific plasma volume changes. Insulin and triglycerides decreased significantly across all three events, whereas T3 and HDL-C increased across all events. FSH and C-peptide decreased significantly in the 100 and 308 km groups, and FT4 increased significantly in these two groups. LH showed a significant time × event group interaction, with a significant reduction in the 100 km group and no significant within-group change in the 308 or 622 km groups. Because LH secretion is pulsatile and only one venous sample was obtained at each pre- and post-race time point, these findings should be interpreted as acute differences in circulating LH concentrations rather than evidence of altered gonadotropin regulation or hypothalamic-pituitary-gonadal axis suppression. Total cholesterol decreased significantly only after the 622 km event, whereas LDL-C decreased after the 308 and 622 km events. The observed endocrine and lipid response patterns differed across ultramarathon events characterized by distinct cumulative durations, pacing characteristics, nutritional exposure, hydration conditions, and recovery opportunities. Extreme ultramarathon running may therefore serve as a useful physiological model for investigating context-dependent endocrine and lipid responses to prolonged endurance stress.