High-intensity interval training (HIIT) involves near maximal exercise bouts (>80–100% maximum heart rate) separated by brief recovery periods (1). The high anaerobic demand associated with maximal efforts results in the accumulation of hydrogen cations (H⁺) within the cytosol (2). Whilst these are mostly removed by intramuscular and/or extracellular buffering mechanics, production overwhelms neutralization, and this contributes toward a reduced intramuscular pH (3), causing exercise-induced acidosis. Such a biochemical state has been suggested to reduce glycolytic energy production and may disrupt calcium ion cross-bridge formation (4). A common strategy to mitigate these deleterious effects of exercise is to enhance circulating level of extracellular blood bicarbonate (HCO3−), which subsequently allows for sustained efflux of H⁺ from intramuscular environments during high-intensity exercise (5). Increases in [HCO3−] of ~5.0–6.0 mmol.l⁻¹ are suggested to be ergogenic and can be achieved via the ingestion of extracellular buffers, such as sodium bicarbonate (NaHCO₃) in doses of 0.2–0.3 g.kg⁻¹ BM, respectively (6, 7).

Common practice is to ingest 0.3 g.kg⁻¹ BM NaHCO₃ at 60–90 min prior to exercise, which is based on historical research showing time to peak pH or HCO3− occurs at this time point at the group mean level (6, 8). It is, however, likely that through following this strategy the dissociation of NaHCO₃ within stomach acid will cause gastrointestinal (GI) upset (9), which may impair performance or dissuade athletes from using NaHCO₃ (10, 11). Whilst, some authors have observed ergogenic benefits despite moderate GI upset (12, 13), in some cases the upset has been severe or the participant has not been able to continue with the study procedures (14, 15). The administration of smaller NaHCO₃ doses (0.2 g.kg⁻¹ BM) might therefore be preferable, as it can mitigate GI upset and also reduce the sodium load per dose which might alleviate the health risks of ingesting this supplement; although these risks are more associated with long term use of NaHCO₃ (12, 16). McNaughton (17) reported exacerbated GI upset following higher NaHCO₃ doses, while Gough et al. (12) observed reduced occurrence of bowel urgency and bloating for 0.2 g.kg⁻¹ compared to 0.3 g.kg⁻¹ BM NaHCO₃. Reducing the dose is a simple strategy that might remove some of the negative connotations of ingesting this supplement, whilst it is far more cost effective than some of the recent strategies employed to reduce the GI upset following NaHCO₃ ingestion, such as in enteric-coated capsules (18, 19).

Contemporary research has administered NaHCO₃ using an individualized time-to-peak pH or HCO3− approach, which is in response to studies showing that time-to-peak pH or HCO3− can vary between 10 and 180 min within individuals, regardless of the ingestion method (i.e., capsule vs. fluid) (7, 12–14). In using the individual time-to-peak approach, this ensures that peak [HCO3−] is achieved immediately before exercise, which does seem to lead to a more consistent ergogenic response (12, 14). The identification of this time-to-peak HCO3− response presents a logistical challenge to athletes however, as the financial cost is high and requires specialist equipment and staff. It is plausible to suggest further research is therefore required to simplify this strategy, and to assess whether ergogenic benefits still exist for smaller NaHCO₃ doses following administration at a standardized time point. This, in turn, could increase the practical application of this supplement, whilst also potentially limiting GI upset.

The ergogenic benefits associated with NaHCO₃ ingestion are somewhat related to the increased activation of glycolytic energy pathways (20, 21). Whilst this is debated (22), NaHCO₃ ingestion attenuates muscle acidosis during exercise thus preventing the allosteric inhibition of glycogen phosphorlyase and phosphofructokinase (5). This has been shown to increase estimated glycolytic contribution during HIIT protocols (20), while there is robust evidence suggesting enhanced glycolytic flux within the muscle (23). Strategies that elevate glycolytic energy system contribution may enhance exercise capacity during HIIT, however, research is yet to determine whether smaller NaHCO₃ doses elicit a similar physiological response.

The purpose of this study therefore was to investigate the effect of 0.2 and 0.3 g.kg⁻¹ BM NaHCO₃ ingested at 60 min pre-exercise on estimated energy contribution during a high-intensity, interval cycling test (HICT), and time-to-exhaustion (TTE) cycling performance.

Performance was greater for SBC2 (136.4 ± 43.5 s) and SBC3 (158.7 ± 63.3 s) compared to PLA (116.2 ± 46.6 s) (Figure 2). These increases were significant for SBC2 (+20.2 s; CI: 0.4, 39.9; p = 0.045; g = 0.77) and SBC3 (+31.9 s; CI: 10.8, 53.1; p = 0.004; g = 1.13). A total of 8 out of 12 participants improved their performance above the SWC following SBC2, whilst 11 participants (out of 12) improved above this threshold following SBC3 (Figure 3). There was an 11.7 s mean difference in favor of SBC3 vs. SBC2, but this increase was not significant (p = 0.303; g = 0.48). Nonetheless, seven of the participants (out of 12) improved their performance above the SWC for SBC3 vs. SBC2, whilst this was only in favor of SBC2 for a single participant.

Grouped mean ± SD data for [BLa⁻] and RER are presented in Table 1. No significant differences were displayed during the HICT protocol (p > 0.05). Post-TTE [BLa⁻] was elevated for SBC2 (+2.35 mmol.l⁻¹; CI: 0.06, 4.64; p = 0.04; g = 0.77) and SBC3 (+3.13 mmol.l⁻¹; CI: 1.44, 4.82; p = 0.001; g = 1.40) compared to PLA. There was a small effect size for SBC3 vs. SBC2 (+0.78 mmol.l⁻¹; p = 0.34; g = 0.46). Peak RER was also increased for SBC2 (+0.09 AU; CI: 0.03, 0.15; p = 0.005; g = 1.14) and SBC3 (+0.11 AU; CI: 0.03, 0.19; p = 0.011; g = 0.98) compared to PLA.

Total energy demand and contribution of the oxidative and glycolytic energetic systems during the HICT are presented in Table 2. No significant differences were displayed for energy demand or contribution from W_AER or W_[LA] (p > 0.05), although W_[LA] contribution was moderately increased for SBC2 (+3.71 kJ; p = 0.09; g = 0.66) and SBC3 (+7.12 kJ; p = 0.14; g = 0.60) compared to PLA (23.40 ± 8.93 kJ). There was a small effect size for W_[LA] contribution when comparing SBC3 vs. SBC2 (+3.41 kJ; p = 0.99; g = 0.27). Energy contribution from W_AER was greater during the second 60 s bout for PLA vs. SBC2 (+4.16 kJ; CI: 0.50, 7.81; p = 0.03; g = 0.86). No significant differences were observed for energy contribution from W_AER or W_[LA] during TTE cycling (p > 0.05; Figures 4A,B), although W_[LA] was moderately increased for SBC2 (+7.77 kJ; p = 0.10; g = 0.65) and SBC3 (+7.95 kJ; p = 0.07; g = 0.70) compared to PLA (15.62 ± 9.27 kJ). No difference was reported for W_[LA] when comparing SBC3 vs. SBC2 (+0.18 kJ; p = 1.00; g = 0.01).

Treatments were successfully single-blinded and taste-matched (Fisher's exact test, p = 0.28). One subject identified all three beverages, eight only correctly perceived one of the three beverages, and the remaining three were unsure on all treatments. Eight participants reported their severest symptom after either SBC2 (4/12) or SBC3 (4/12), although some reported no difference between treatments (3/12), whereas one experienced the severest symptom following PLA (Table 3). No intervention or time interaction was observed at 30- or 60-min post-ingestion for any GI symptom (p > 0.05), or at post-exercise for vomiting, flatulence, GF, BUR, or diarrhea (p > 0.05). Nonetheless, symptom severity was increased post-exercise following SBC3 compared to PLA for nausea (10.0 vs. 1.0 mm; Z = −2.197; p = 0.028) and belching (8.0 vs. 1.0 mm; Z = −2.371; p = 0.018), but not for SBC2 compared to PLA (p > 0.05). Increases in the severity of nausea post-exercise was also observed following SBC3 compared to SBC2 (Z = 2.366; p = 0.018; Figure 5A), but not belching (Z = 1.352; p = 0.176; Figure 5B). There was no difference between aggregate GI upset between SBC2 and SBC3 at any time point (all p > 0.05).

This study is the first to explore the dose-response effects of NaHCO₃ ingestion when administered at a standardized time point on estimated energy system contribution and performance during intermittent cycling exercise. Both 0.2 and 0.3 g.kg⁻¹ BM NaHCO₃ improved cycling TTE and estimated glycolytic contribution during HICT, therefore both doses can be employed as an ergogenic strategy. Only minimal dose-dependent differences in GI upset were observed, although the smaller dose mitigated severity of post-exercise nausea and belching. The key finding of this study therefore is that 0.2 g.kg⁻¹ BM of NaHCO₃ can increase estimated glycolytic system contribution and be ergogenic for intermittent exercise performance.

Improvements in cycling TTE were observed for SBC2 and SBC3, with the moderate-to-large effect sizes reflective of previous findings employing a similar TTE protocol (26). The present study adds to previous work (17, 38), however, that ergogenic benefits can also be observed with a lower dose of NaHCO₃. Importantly, however, more participants improved over the SWC for SBC3 vs. SBC2, and a small effect size between treatments was observed in favor of SBC3 at the group level. This contradicts findings by McKenzie et al. (38) that displayed a 4 s difference in TTE for 0.15 and 0.3 g.kg⁻¹ BM NaHCO₃, and Gough et al. (12) where only a 0.1% variation in 4-km cycling time trial performance was present for 0.2 and 0.3 g.kg⁻¹ BM doses. This discrepancy could be explained by differences in administration approach (standardized time point vs. time-to-peak), or the high-degree of inter-individual variation present in acid base balance following NaHCO₃ ingestion. Nonetheless, based on seven participants improving their performance following SBC3 vs. SBC2 (based on SWC), it is likely the athlete will secure the largest benefit from this higher dose. These dose-dependent differences in performance could also be attributed to the timing of exercise protocols. The cycling TTE protocol commenced ~75 min after NaHCO₃ ingestion accounting for both the warm-up and HICT, however it is expected that [HCO3−] will continue to rise until ~80 min post-ingestion for SBC3, by which point [HCO3−] will have started to decline for SBC2 in most individuals (12, 14). Nonetheless, athletes unable to pre-determine their time-to-peak HCO3− can still employ either dosing strategy of the present study to obtain performance benefits during high-intensity cycling exercise.

Moderate, albeit non-significant, increases were observed for W_[LA] during the HICT without altering energy demand or contribution from W_AER, which is in agreement to findings from recent studies (20, 21, 31). Despite not achieving statistical significance, these increases were considered substantial for both SBC2 (+15.8%) and SBC3 (+30.3%) when compared to PLA, with the relatively small absolute changes in W_[LA] attributed to the controlled total mechanical work during the HICT (20). The most novel finding, however, was that there may be a dose-response effect of NaHCO₃ ingestion on changes in energy system contributions, with a small effect size present for W_[LA] in favor of SBC3. Considering that enhanced HCO3− buffering capacity is responsible for elevating glycolytic contribution, one explanation for these dose-dependent results could relate to the total amount of H⁺ that can be neutralized. Assuming that total blood volume is ~5 L and that [HCO3−] was as small as ~1.0 mmol.l⁻¹ higher for SBC3 vs. SBC2, then the higher dose could have allowed the neutralization of an extra ~5 mmoles of H⁺ (based on the 1:1 stoichiometry of HCO3− and H⁺ reaction), in theory eliciting a greater up-regulation of glycolytic contribution (20). It is important to note, however, that as the current methodology only indirectly assesses glycolytic flux (i.e., from changes in [BLa⁻]), these increases in W_[LA] contribution may overestimate glycolytic activation, instead reflecting greater lactate efflux from working muscles (5). Nonetheless, previous research has corroborated the findings of the present study following NaHCO₃ ingestion (23), therefore it seems plausible that both dosing strategies partially up-regulate glycolytic activation during high-intensity cycling.

The ingestion of NaHCO₃ resulted in mild-to-moderate GI symptoms, although both doses were well-tolerated, which agrees with previous research (14). Minimal dose-dependent differences were observed for GI upset, though the reduced post-exercise nausea and belching for SBC2 agrees with Gough et al. (12) where belching was exacerbated for the higher dose. The reduced severity of GI upset from this study could be attributed to the body mass of the participants in the present study (mean = 68 ± 6 kg) compared to those that have reported greater severity of GI upset in healthy males (15) and trained rugby players (10) (90 ± 6 and 95 ± 13 kg). Relative dosing protocols were derived during early laboratory studies to normalize post-exercise base deficit (39), and therefore fail to account for physiological differences such as body mass and the total absolute NaHCO₃ dose. Athletes with high body mass administer a greater absolute NaHCO₃ dose despite minimal differences in gut absorption rates, particularly for the first 60 min post-ingestion (14), which most likely exacerbates GI upset. There might be an upper threshold for absolute NaHCO₃ doses, with doses above this exacerbating GI upset. At present, 0.2 g.kg⁻¹ BM NaHCO₃ is a suitable strategy for mitigating GI upset; however, future research could examine the effect of absolute dosage on symptom severity and exercise performance.

There are methodological limitations in the present study that future research should address. Firstly, the single-blind design of this study is a limitation that is important to note. Important methodological choices were adopted, however, to mitigate any potential impact of this design. This included the standardized verbal encouragement during exercise, and the use of a supplement belief questionnaire, as per previous research (12). The findings from the latter methodological decision suggested that the supplement was blinded from the participants and therefore the single-blind design has no impact on the efficacy of NaHCO₃ ingestion. Moreover, our inability to quantify changes in absolute demand and contribution from the ATP-PCr energetic system is a limitation. This was due to the relatively short recovery period (90 s) between each bout of the HICT that did not allow a clear EPOC curve to form and therefore, it was decided that the ATP-PCr energy contribution calculations should be excluded from our analysis. Lastly, it was not possible to measure changes in [HCO3−] following NaHCO₃ ingestion in the present study. Evidence suggests, however, that the HCO3− response is similar for 0.2 and 0.3 g.kg⁻¹ BM NaHCO₃ doses within ~60 min, therefore participants were likely at a similar level of alkalosis irrespective of dose (12, 14). This timing of NaHCO₃ ingestion employed in this study was selected to assess of the potential ergogenic effects for athletes unable to adopt an individualized time-to-peak HCO3− approach, or access a blood gas analyser. Based on the observed ergogenic benefits for both doses vs. PLA, it should further enhance the practical application of NaHCO₃ supplementation to the athlete with limited funding.

Ingestion of 0.2 and 0.3 g.kg⁻¹ BM elevated glycolytic contribution to high intensity exercise and are ergogenic strategies to improve exercise performance. It is likely that athletes will gain increased benefit from SBC3, despite the occurrence of higher GI upset. Nonetheless, some athletes may still opt for the lower dose if this displays greater tolerability, whilst still securing an ergogenic benefit. The present study also shows that the contemporary time to peak alkalosis strategy might not be required when ingested 60 min prior to exercise, however direct comparisons between these two methods of ingestion are required.

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

The studies involving human participants were reviewed and approved by University of Essex. The patients/participants provided their written informed consent to participate in this study.

KR, WG, and LG designed the study. WG completed the data collection, whilst WG and LG completed the majority of the manuscript, MF, SS, and KR also contributed. All authors reviewed the paper and provided feedback. LG and WG completed the preparation of the manuscript.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.