Exercise Performance Response to Active Dehydration: A Metabolomics Study

Abstract

Background: Dehydration through exercise induces physiological and metabolic changes which may impair health, limit exercise capacity, and negatively affect athletic performance. However, our understanding of the underlying mechanisms driving dehydration-induced exercise impairment is limited. Furthermore, there appears to be a high inter-individual variability in physiological response to hypohydration. Metabolomics analysis can provide valuable insight into cellular signaling pathways and biochemical processes that underlie the physiological and practical impacts of dehydrating exercise, providing the foundation for personalized exercise and hydration recommendations based on an individual’s metabolic profile. Study Design: Accordingly, we subjected 10 male athletes to a dehydrating exercise protocol while measuring exercise performance, hydration status and body morphometrics. We metabolically profiled blood samples taken before and after a dehydrating exercise, and again after a rehydration period. Salivary and plasma osmolality were used as indicators of dehydration status; A VO2max test and cognitive measures (Trail Making Test and Stroop Test) were used to define the extent of performance deficit. Results: Salivary osmolality and plasma osmolality both increased throughout the dehydration protocol (Salivary: 92.9 ± 30.2 mmol/kg at Baseline vs 341.6 ± 129.3 mmol/kg at Post-Exercise, p = 0.0033; Plasma: 302.5 ± 8.7 mmol/kg at Baseline vs 315.4 ± 8.8 mmol/kg at Post-Exercise, p = 0.0122), and returned to baseline levels after rehydration (Salivary: 93.8 ± 21.3 mmol/kg at Post-Hydration vs 92.9 ± 30.2 mmol/kg at Baseline, p > 0.9999; Plasma: 302.6 ± 8.0 mmol/kg at Post-Hydration vs 302.5 ± 8.7 mmol/kg at Baseline, p > 0.9999), indicating that the body fluid loss during exercise significantly impaired body fluid balance. VO2max, on average, showed a significant decrease (-7.7 ± 6.7%) from Baseline to the Post-Exercise time point (43.7 ± 6.4 mmol O2/min/kg vs 40.6 ± 7.6 mmol O2/min/kg, p = 0.0318), with minimal changes in VO2 at ventilatory threshold (VT) across these time points that did not reach significance (24.4 ± 3.8 mmol O2/min/kg at Baseline vs 26.5 ± 5.3 mmol O2/min/kg at Post-Exercise, p = 0.0895). After the rehydrating period, VO2max increased back to near baseline levels (42.8 ± 8.4 mmol O2/min/kg at Post-Hydration vs 43.7 ± 6.4 mmol O2/min/kg at Baseline, p = 0.7309). Additionally, we observed strong correlations of VO2max deficit and recovery with several metabolites, including arachidonic acid, which is heavily involved in exercise-induced inflammation. Conclusions These results indicate impaired aerobic capacity due to hypohydration, and recovery upon rehydration, as well as a potential for the utility of individual athlete metabolite profiles to inform personalized recommendations for the mitigation of hypohydration-induced performance deficits, and as predictors of physiological response to variable hydration status. Future studies should investigate the precise nature of the relationship between aerobic capacity and the associated metabolites.