Enteric-coated sodium bicarbonate supplementation improves high-intensity cycling performance in trained cyclists

High-intensity exercise bouts are impaired by peripheral fatigue (Thomas et al. 2015), typically as a result of disturbances to intramuscular homeostasis (Jones et al. 2008). Significant decreases in muscle and blood potential hydrogen (pH) have been reported (Hollidge-Horvat et al. 2000) as a result of the glycolytic contribution during high-intensity exercise (Baker et al. 2010; Gastin 2001). While the mechanisms responsible for the decline in muscular force across the neuromuscular junction are equivocal (Fitts 2016; Westerblad 2016), reductions in muscle pH are associated with simultaneous declines in muscle excitability (Cairns and Lindinger 2008), contractility (Spriet et al. 1989), glycolytic enzyme activity (MacLaren 1989), and exercise performance (Raymer et al. 2004). Exercise training and nutritional strategies that offset these perturbations to acid–base balance have, therefore, received considerable attention.

Inducing metabolic alkalosis prior to exercise, which can be achieved by oral ingestion of sodium bicarbonate (NaHCO₃), has been shown to improve various performance measures (e.g., power, speed, and performance time) during single bouts of high-intensity exercise (Matson and Tran 1993; Peart et al. 2012; Lancha Junior et al. 2015). Through increases in extracellular bicarbonate ion concentration ([HCO₃^–]), NaHCO₃ supplementation can augment buffering capacity (Siegler et al. 2010) and strong ion handling (Raymer et al. 2004), both of which favour high-intensity exercise performance. Although 0.2–0.4 g∙kg^–1 body mass NaHCO₃ is generally regarded as ergogenic during high-intensity exercise (McNaughton et al. 2016), gastrointestinal (GI) symptoms can be a problematic side-effect, with some individuals reporting severe symptoms (e.g., vomiting and diarrhoea) at the onset of exercise (Burke and Pyne 2007; Kahle et al. 2013). While some studies have shown that NaHCO₃ can improve exercise performance despite GI distress (Price and Simons 2010), there is evidence to suggest that symptoms may compromise the performance-enhancing effects of supplementation (Cameron et al. 2010; Saunders et al. 2014; Deb et al. 2018). Furthermore, there is evidence to suggest that athletes may be deterred from supplementing with NaHCO₃ due to the risk of GI symptoms during training and/or competition (Heibel et al. 2018).

Novel ingestion strategies are being investigated to alleviate GI symptoms, such as the administration of NaHCO₃ in gastro-resistant capsules (Hilton et al. 2019a). Through the application of an enteric coating, which resists dissolution at a low pH (e.g., stomach), acid-sensitive ingredients such as NaHCO₃ can bypass the stomach (Barbosa et al. 2017). Consequently, this reduces the neutralisation of gastric acid and minimises adverse side-effects (e.g., GI symptoms associated with elevated carbon dioxide tension in the GI tract). Indeed, delayed-release NaHCO₃ has been shown to reduce the incidence and severity of GI symptoms compared with an aqueous solution, whilst increasing blood [HCO₃^–] and pH to comparable levels. In a recent study, enteric-coated NaHCO₃ was shown to attenuate GI symptoms beyond encapsulation in gelatin and delayed-release capsules, which may be more favourable for those who experience GI symptoms post-ingestion (Hilton et al. 2019b). Nevertheless, changes in blood [HCO₃^–] and pH were lower with enteric-coated NaHCO₃, potentially due to the absorption of bicarbonate across the intestinal mucosa (Turnberg et al. 1970) and less time available for absorption. Given that the degree of alkalosis can modulate the effects of NaHCO₃ ingestion on exercise performance (Carr et al. 2011a), enteric-coated formulations may not favour performance improvements compared with alternative ingestion strategies. While enteric-coated NaHCO₃ can reduce GI symptoms post-ingestion, no study to date has investigated the effects of supplementation on exercise performance. Therefore, it is unknown whether ingesting NaHCO₃ in enteric-coated capsules alters the overall ergogenicity of supplementation. Furthermore, knowledge of the performance-enhancing potential of enteric-coated NaHCO₃ would help to elucidate the impact of GI symptoms and acid–base balance on exercise performance, as well as improve the practical recommendations for athletes. The aim of the present study, therefore, was to determine whether enteric-coated NaHCO₃ improves high-intensity exercise performance using an acute loading protocol.

This is the first study to investigate the effect of enteric-coated NaHCO₃ supplementation on exercise performance, specifically that which would typically benefit from extracellular buffering agents. The main finding of this study was that ingesting enteric-coated NaHCO₃ prior to exercise improved (~ 2.3%) subsequent 4 km cycling TT performance among trained cyclists. Despite inducing a lower degree of metabolic alkalosis with enteric-coated NaHCO₃ (Fig. 3), there were no differences in exercise performance compared with a standard ingestion form (i.e., gelatin capsules). Furthermore, enteric-coated NaHCO₃ reduced GI symptoms experienced immediately before exercise compared with gelatin capsules (Table 2), although subjective ratings of GI symptoms in this sample were low. When taken together, these data suggest that enteric-coated NaHCO₃ improves high-intensity cycling performance in those with mild-to-moderate GI symptoms. However, the effects of enteric-coated NaHCO₃ on exercise performance could be greater in those who experience more severe GI symptoms at the onset of exercise, although this warrants further investigation. Enteric-coated NaHCO₃ supplementation may, therefore, offer an alternate strategy to improve high-intensity exercise performance and mitigate GI symptoms associated with acute bicarbonate loading.

Numerous studies have investigated the effects of NaHCO₃ on simulated high-intensity TT events with equivocal outcomes (Callahan et al. 2017; Gough et al. 2018). Where some studies have reported performance improvements (Gough et al. 2018), others have reported no benefit (Callahan et al. 2017; Correia-Oliveira et al. 2017) following supplementation. This disparity between studies could be explained by the timing of supplementation, given that the current study demonstrated positive outcomes when exercise was timed with peak alkalosis. Studies that have reported no effect of NaHCO₃ ingestion during similar exercise protocols have administered the supplement at a standardised time (Callahan et al. 2017; Correia-Oliveira et al. 2017) despite considerable variability in the time taken to reach metabolic alkalosis (Jones et al. 2016). Time between ingestion and the onset of exercise largely determines the degree of metabolic alkalosis in terms of blood [HCO₃^–] and pH (Heibel et al. 2018), which, in turn, may influence the ergogenicity of NaHCO₃ supplementation (Carr et al. 2011a). Interestingly, the effect of NaHCO₃ on exercise performance in the present study was mediated by the ingestion form, with a small-to-moderate effect on performance time (2.3–2.6%) with enteric-coated and gelatin NaHCO₃, respectively. The present study reported a mean 5.6 mmol L^–1 increase in blood [HCO₃^–] with gelatin compared to placebo, which is lower than the 3.8 mmol L^–1 increase shown with the enteric-coated capsules. This finding is consistent with the previous studies that have investigated the acid–base kinetics following NaHCO₃ ingestion (Hilton et al. 2019b), which could account for the difference in effect size reported in the present study. Nevertheless, exercise performance still improved with enteric-coated NaHCO₃ supplementation, which questions the 5–6 mmol L^–1 threshold suggested to improve performance (Carr et al. 2011a; Heibel et al. 2018). Furthermore, the improvements in 4 km cycling TT performance in the present study are similar to the previous studies, despite higher pre-exercise blood [HCO₃^–] reported by others (Gough et al. 2018). Given this disparity between studies, it is unlikely that timing is the only factor modulating the ergogenicity of NaHCO₃ during high-intensity exercise.

Whilst an individualised ingestion strategy may increase the likelihood of commencing exercise with greater blood buffering capacity, it is not clear whether this optimises the ergogenicity of NaHCO₃ supplementation. Individualising the timing of supplementation may also not be practical at present, for some athletes, given that this requires access to a blood-gas analyser. In the current study, however, mean ingestion timings corresponded to those that have been previously suggested with enteric-coated NaHCO₃ (Hilton et al. 2019b). Furthermore, it is important to note that enteric-coated capsules delay the time-to-reach peak blood [HCO₃^–] following NaHCO₃ ingestion, suggesting that the current recommendations (e.g., 60–90 min before exercise) are not appropriate for this ingestion form. Instead, the current study adds to the growing body of evidence, suggesting that enteric-coated NaHCO₃ should be ingested ~ 120 min prior to exercise to maximise blood [HCO₃^–] if a standardised ingestion timing strategy is adopted (Hilton et al. 2019b). Whilst participants ingested the capsules in a fasted state in the present study, co-ingestion with food may delay gastric emptying and alter the release of NaHCO₃ (Davis et al. 1986). Further research should look to compare the effects of an individualised and standardised ingestion time on subsequent performance, including the effects of prandial state on acid–base responses and GI symptoms following NaHCO₃ ingestion.

Given that enteric-coated NaHCO₃ improves exercise performance among those with mild-to-moderate GI symptoms, the effects on exercise performance may be enhanced among those with more severe GI symptoms at the onset of exercise. Indeed, GI distress was significantly reduced in some individuals in the current study (Table 2), although numerous individuals did not report symptoms at the onset of exercise. Although ergogenic doses (~ 0.3 g kg^–1 body mass) of NaHCO₃ may induce GI symptoms, these may not necessarily be timed with exercise performance. This is consistent with the previous studies (Hilton et al. 2019a, b) demonstrating the reduced incidence of GI symptoms at the time of peak alkalosis, despite severe symptoms at other timepoints. It is, therefore, difficult to elucidate whether GI symptoms can negate the ergogenic effects of NaHCO₃ supplementation from the current data, since the overall incidence and severity of GI symptoms was low. Nevertheless, GI symptoms may hinder high-intensity exercise performance or dampen the ergogenic effects of NaHCO₃ supplementation (Saunders et al. 2014). Further research should, therefore, examine the effects of enteric-coated NaHCO₃ supplementation in those who typically report moderate-to-severe GI symptoms at the onset of exercise, as the effects may be greater among these individuals. Given that only few participants reported GI symptoms following enteric-coated NaHCO₃ supplementation, future studies could consider increasing the dose (> 0.3 g·kg^–1 body mass), which may also increase blood [HCO₃^–].

Whilst psychological indicators of perceived exertion and fatigue increased during exercise, no differences were reported between the placebo and NaHCO₃ conditions (Table 1), suggesting an alternative mechanism other than reductions in afferent feedback to the central nervous system (Siegler and Marshall 2015). Nevertheless, this finding indicates the enhancements in power output were attained at a relatively similar RPE when supplementing with NaHCO₃. Similarly, despite distinct changes in blood [Na⁺] and [K⁺] during exercise, no differences were shown between NaHCO₃ and placebo (Fig. 3). Changes in these strong ions can impair muscle excitability (Cairns and Lindinger 2008), therefore, suggesting that improvements in performance were not due to ionic shifts in [Na⁺] and [K⁺] associated with enhanced contractility. Nevertheless, enhanced muscle contractile function cannot be dismissed as a potential mechanism, as altered calcium handling can improve mechanical efficiency (Siegler et al. 2016), although this cannot be elucidated from the current study. Alternatively, given that pre-exercise blood [HCO₃^–] and pH were greater in the NaHCO₃ conditions compared to placebo, the performance improvements shown in the current study may be attributed to increases in extracellular buffering capacity. Reinforced extracellular concentrations of bicarbonate are suggested to promote H⁺ efflux from intramuscular to extracellular regions through increases in monocarboxylate transporter activity, which maintains muscle pH during exercise (Bishop et al. 2006). Given the delayed onset of intramuscular acidosis, NaHCO₃ promotes glycolytic enzyme activity and flux, as indicated through increases in muscle glycogen utilisation and lactate concentrations (Hollidge-Horvat et al. 2000; Siegler et al. 2016). Although muscle pH and lactate were not measured in the current study, increases in muscle pH and lactate efflux have been shown during exercise following NaHCO₃ supplementation (Costill et al. 1984). Augmenting glycolytic flux may have, therefore, permitted exercise at higher intensities and could explain the performance improvements reported in the current study. This would account for the greater blood [La^–] shown with gelatin NaHCO₃, although the increases reported with enteric-coated capsules did not reach significance (Fig. 4a). Given that monocarboxylate transporters 1- and 4 are stimulated by the intra- to extracellular [H⁺] gradient, the greater extracellular pH shown with gelatin capsules may have upregulated the co-transport of H⁺ and lactate to a greater extent, and could account for differences in the ergogenic effect size (0.3%). This may also explain why power output was greater when NaHCO₃ was given in gelatin capsules (Fig. 2), although this did not result in greater overall performance times compared to enteric-coated capsules. Therefore, the current evidence suggests that while pre-exercise blood [HCO₃^–] does not determine the overall ergogenicity of NaHCO₃ supplementation, the magnitude of such effects may be increased by a greater degree of metabolic alkalosis.

In summary, this study is the first to demonstrate that 0.3 g∙kg^–1 body mass of enteric-coated NaHCO₃ improves high-intensity exercise performance when timed with peak alkalosis. This study also provides novel data, highlighting that ingestion form (e.g., gelatin or enteric-coated capsules) can mediate the effects on exercise performance, potentially through the degree of induced alkalosis. To understand the implications of GI symptoms on exercise performance, further research should compare the effects of enteric-coated NaHCO₃ supplementation on exercise performance in those who experience severe symptoms immediately before exercise, particularly as GI distress may be ergolytic among these individuals. Furthermore, given the growing range of ingestion forms commercially available to athletes (e.g., liquid, gelatin capsules, and enteric-coated capsules), future studies should compare the effects on exercise performance. Nonetheless, acute enteric-coated NaHCO₃ consumption improves 4 km cycling TT performance and, therefore, may offer an appropriate ergogenic strategy for those who experience GI side-effects following supplementation.