g. at the start

and during (final) sprints. In these occasions, i.e. when exercising above CP, W’ will be reduced. Consequently, a higher W’ can increase performance during tests of longer duration, especially if pacing strategies are implemented. We also found that five bolus intakes on five consecutive days did not result in an increase of T lim beyond the value observed after the first intake. Thus, multiday administration of NaHCO3 did not lead to a cumulative effect on endurance capacity. Accordingly, [HCO3 -], blood pH, and ABE after multiday NaHCO3 administration also remained unchanged relative to the initial rise after the first bolus. The most obvious explanation would be that during each CP-trial Nocodazole concentration a certain amount of NaHCO3 was used, leading to lower values for [HCO3 -], pH and ABE post vs. pre test. During the following 24 h of check details recovery, the body would then be expected to re-establish the resting values.

On the following day, the participants then would start the CP trial at similar (complete recovery) or lower [HCO3 -], blood pH, and ABE (incomplete recovery) relative to the first day, whereby an additional increase in performance would not be expected. Although we did not measure [HCO3 -], pH and ABE before supplementation on the following days, these two described cases can be most likely excluded. The reason for this is that [Na+] also did not increase during the consecutive 5 days MI-503 of NaHCO3 supplementation despite the fact that Na+, unlike HCO3 -, was not used as a buffer during the CP trials, and that the high amount of ingested Na+ could not be used completely through sweating. HAS1 The predicted sweating rate during exercise of 1 dm3∙ h-1 water, with a sweat [Na+] of 50 mEq∙ dm3[34] would have led to a Na+ loss of ~0.36 g. This calculated sweat-induced loss of Na+ corresponds to ~20% of the daily Na+ intake during the placebo intervention. Regarding the substantially higher Na+ intake during the NaHCO3 intervention, the sweat-induced loss of Na+ was negligible during

this intervention. As shown in this study, the NaHCO3 intervention led to an increase in [Na+] and plasma osmolality after the first bolus administration. This increase was counteracted by an expansion in PV. The increase in PV was to such an extent that pre-exercise blood [HCO3 -], pH, and ABE remained constant during the 5 days of testing. This proposed mechanism of PV expansion has already been described by Máttar et al.[35], who showed that plasma [Na+] and plasma osmolality were increased after NaHCO3 injections in acute cardiac resuscitation. Other mechanisms to counteract increases in [Na+] and plasma osmolality comprise a shift of fluid from the intra- to the extramyocellular compartment [36], a stimulation of arginine vasopressin secretion [37], which leads to an intensified water retention from the kidneys [38], and a stimulation of the thirst center whereby more fluid is consumed [37]. In accordance with our results, McNaughton et al.