Several new findings have been observed in this randomized, placebo-controlled, double-blind interventional crossover investigation. First, multiday NaHCO3 supplementation for 5 days increased Tlim at CP on each day relative to placebo in highly trained athletes. Second, there was no difference in the increased Tlim over the 5 days of supplementation with NaHCO3 or NaCl. Third, the increase in Tlim was paralleled by increases in [HCO3-], pH and ABE. Fourth, [HCO3-] and [Na+] in the blood stabilized over time in the NaHCO3 condition. Fifth, calculated PV increased during the NaHCO3 more than in the placebo intervention.
We found that NaHCO3 supplementation led to an increase in Tlim at CP and that the improvement in Tlim was paralleled by an increase in blood [HCO3-], pH and ABE, indicating that the alteration in Tlim appears to be linked to an elevated extracellular buffer capacity. In fact, it has been shown that an increased [HCO3-] gradient between the intra- and extramyocellular compartment leads to an amplified H+-efflux from the muscle cell and delays the fall in intramyocellular pH [8, 14]. We observed a trend for higher [La-] during the constant-load tests following NaHCO3 supplementation (P = 0.070, data not shown), supporting the notion that the increased H+-concentration resulted from a lactate-proton symport. A fall in intramyocellular [H+] is associated with muscle fatigue due to 1) an inhibition of glycogenolysis and glycolysis , 2) increased muscular K+ release, 3) lesser contractility of the heart muscle , 4) inhibition of the sarcoplasmatic calcium release  and 5) inhibition of the actin-myosin interactions . Thus, delaying the fall in intramyocellular pH might postpone the fatigue process and prolong intact muscle function. Indeed, our results showed that the ingestion of NaHCO3 induced metabolic alkalosis, which in turn enhanced Tlim at CP and thus improved high-intensity exercise in the range of 10 to 20 min duration.
As hypothesized, Tlim at CP could be increased with NaHCO3 supplementation. This is in contrast to the theoretical model, which states that an intramyocellular metabolic steady state exists at exercise intensities up to CP. However, our results support the notion that CP overestimates the metabolic steady state [4, 5]. Furthermore, our result that NaHCO3 increased Tlim at CP extends previous findings showing that NaHCO3 supplementation increases exercise above CP relative to placebo [14, 29]. In the latter studies, short high-intensity tests, during which intramyocellular pH falls rapidly from the beginning of exercise, were completed. During these types of tests, the finite work capacity above CP (W′) is drawn on after the start of exercise and becomes reduced. In light of our findings, these results might be interpreted to mean that NaHCO3 simply increases W’. However, Vanhatalo et al. showed that NaHCO3 does not increase W’ during a 3-min all-out test, and concluded that changes in intramyocellular pH might not influence W’ in this particular test setting, and that for short all-out exercise, [PCr] dynamics is more important in determining W’. In our constant-load trials at CP, W’ was supplied to a large extent by anaerobic glycolysis. Therefore, we assume that NaHCO3 supplementation increases W’ in conditions where acidification occurs during exercise. Our result that the estimated V̇ O2 slow component was not different between the two interventions lends further credence to this notion, although the influence of NaHCO3 on the V̇ O2 slow component remains ambiguous (reduction: ; no change: ). In our study, the identical V̇ O2 slow component for both, the NaHCO3 and placebo condition, indicated that V̇ O2peak was attained at the same point in time. Based on the fact that the depletion of W’ coincides with the attainment of V̇ O2peak, our results indicate that NaHCO3 ingestion did not increase the rate of W’ utilization but rather W’ itself. Further support for our assumption comes from another study, where average power in a 60 min cycling time trial was found to be higher with NaHCO3 as compared to placebo . During a 60 min time trial, power output will fluctuate around CP with power peaks occurring e.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 Tlim 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 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 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 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. The predicted sweating rate during exercise of 1 dm3∙ h-1 water, with a sweat [Na+] of 50 mEq∙ dm3 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., 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 , a stimulation of arginine vasopressin secretion , which leads to an intensified water retention from the kidneys , and a stimulation of the thirst center whereby more fluid is consumed . In accordance with our results, McNaughton et al. found an increase in plasma [Na+] after the first of five doses of NaHCO3 but no further increase of plasma [Na+] on the following days. The elevation of PV in the present study is mirrored by the measured increase in DXA whole-body lean mass. In the DXA two-component soft tissue model, lean mass comprises water, proteins, glycogen and non-bone minerals . As increases in protein, glycogen and non-bone minerals can virtually be excluded (see below), the increase in whole-body lean mass must have resulted from an increase in whole body water, which led to an expansion in PV. Our findings are in accordance with the report of Lands et al. who found a significantly higher value for DXA-derived whole-body lean mass after saline infusion given to healthy male participants. Finally, our finding that HRCLT was reduced lends further credence to our result that PV increased as a consequence of NaHCO3 supplementation, because PV expansion simultaneously increases stroke volume and reduces sympathetic nervous activity, leaving V̇ O2,CLT unaffected .
In our study, DXA-derived leg lean mass did neither change between interventions nor over time (Table 2). As with each gram of glycogen stored in muscle tissue 3–4 g of water is bound , and body water is present within the lean soft tissue compartment , a decrease in leg lean mass in such a short time (2 days) would indicate a loss of glycogen. In turn, glycogen loss would implicate incomplete regeneration, which would manifest itself in a reduced anaerobic work capacity and, accordingly, decreased performance . Since our participants displayed neither a reduction in leg lean mass nor performance, the provided regeneration drink and the participants’ daily nutritional intake were sufficient to restore glycogen from day to day, allowing them to perform maximally on each day.
Our results have at least two practical implications. First, since the [HCO3-] gradient between intramyocellular compartment and blood did not decrease over time, NaHCO3 can be taken daily in multiday competitions or tournaments lasting ≤ 5 d without the risk of reducing performance. Second, the apparent PV expansion in response to the high ion intake (see above) blunted any further increase in [HCO3-]. If the same mechanism would be true for the chronic supplementation protocol, the effectiveness of this protocol should be questioned, as it seems that [HCO3-] cannot be increased limitlessly, i.e. that it probably reaches a ceiling. The observed ceiling effect was probably based on a metabolic compensation mechanism preventing a disproportionate increase in [HCO3-]. A respiratory compensation mechanism is unlikely to have occurred in our study because there were no differences between the NaHCO3 and placebo intervention for V̇ CO2 (P = 0.903, data not shown) and RER (P = 0.556, data not shown) during the resting measurements before the constant-load tests. Of further note is that the standard chronic protocol comprises a daily dose of 0.5 g NaHCO3 kg-1 body mass , which might accentuate the increase in PV and possible side effects. Thus, one adequate dose of NaHCO3 administered before the competition should be effective in mediating all of the performance-enhancing effects without the need of a “loading phase”. In this context, our results expand the findings of McNaughton and Thompson  as well as Siegler et al., who compared different acute and chronic protocols and found that there are no differences between these ingestion protocols with respect to exercise performance.
It may be argued that the present findings could be limited by 1) differences in performance ability throughout the study period and 2) decreasing motivation. Regarding the first point we have shown that CP was neither different between the first and second intervention period nor before the NaHCO3 and placebo condition. An increase in CP from the first to the second intervention would have indicated a training effect, whereas a decrease in CP would have indicated incomplete recovery. Hence, we can assume that the participants had the same performance ability throughout the study, allowing a comparison of Tlim between the two conditions. Regarding the second point, decreasing motivation in a single participant would be evident from a decrease in Tlim within or between interventions. Considering the single variations in Tlim irrespective of condition, during which no distinct increases or decreases in Tlim over time (i.e. from the second to the fifth test day) were identified, a decreasing motivation can be excluded for all participants. In addition, V̇ O2,CLT, V̇ CO2,CLT and RERCLT were not different between conditions and days of testing. This indicates that the participants’ effort was constant during the whole study period.