Role of lactic acidosis as a mediator of sprint-mediated nausea.

This study aims to determine whether there is a relationship between nausea level and lactic acidosis during recovery from sprinting. In all, 13 recreationally active males completed a 60 s bout of maximal intensity cycling. Prior to and for 45 min following exercise, blood pH, pCO₂ , and lactate levels were measured together with nausea. In response to sprinting, nausea, lactate, and H⁺ concentrations increased and remained elevated for at least 10 min (p < .001), whereas pCO₂ increased only transiently (p < .001) before falling below pre-exercise levels (p < .001), with all these variables returning toward pre-exercise levels during recovery. Both measures of nausea adopted for analyses (nausea profile, NP; visual analogue scale, VAS), demonstrated significant repeated measures correlation (rmcorr) post-exercise between nausea and plasma lactate (VAS and NPr_rm > 0.595, p < .0001) and H⁺ concentrations (VAS and NPr_rm > 0.689, p < .0001), but an inconsistent relationship with pCO₂ (VAS r_rm = 0.250, p = .040; NP r_rm = 0.144, p = .248) and bicarbonate levels (VAS r_rm = -0.252, p = .095; NP r_rm = -0.397, p = .008). Linear mixed modeling was used to predict the trajectory of nausea over time, with both lactate and H⁺ concentrations found to be key predictors of nausea (p < .0001). In conclusion, this study reveals a strong positive relationship between nausea and both H⁺ and lactate concentrations during recovery from sprinting, a finding consistent with H⁺ and lactate being potential mediators of nausea post-sprinting. However, as the timing of the recovery of both H⁺ and lactate was delayed, compared to that of nausea, further research is required to confirm these findings and investigate other potential mechanisms.