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, pCO(2), 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 pCO(2) 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 pCO(2) (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.