A myriad of factors determines skeletal muscle fatigue and exercise performance, which involve a complex interaction of central and peripheral components (30,47,57). The determinant(s) of fatigue, however, are dependent on the types, durations, and intensities of exercise undertaken by the individual. Central components are primarily mediated by afferent feedback to the central nervous system to maintain conscious and/or subconscious control of exercise to prevent catastrophic failure of homeostatic regulation (47,57). Peripheral fatigue, however, is often related to the excessive accumulation of metabolites, such as hydrogen ions (H+), potassium ions (K+), and phosphate ions (Pi+), and the availability of metabolic fuel sources (30).
Early work studying the etiology of fatigue proposed that exercise-induced acidosis (when the rate of hydrogen ion (H+) production surpasses the rate of removal) was a major contributing factor (29). Exercise can induce substantial perturbations to the acid-base balance through the generation of H+, the extent of which is dependent on exercise intensity and duration (12). Indeed, such circumstances are associated with the development of fatigue, and although the contributing mechanisms remain ambiguous, a number of methods have been proposed. These mechanisms include the dysfunction of the sarcoplasmic reticulum due to altered calcium ion sensitivity and handling (19,27), a reduced myosin-actin cross-bridge cycling activity, and increased potassium ion release (5), which together can impede muscular myofilament function and excitation-contraction coupling. Furthermore, glycolytic flux also is inhibited, with key glycolytic enzymes, such as phosphofructokinase, down-regulated under an acidic stress (37). Considering this association of exercise-induced acidosis and fatigue, the application of exogenous buffering agents, such as sodium bicarbonate (NaHCO3), to dampen the rate of H+ accumulation and attenuate the magnitude of metabolic acidosis may be warranted. Indeed, NaHCO3 has been investigated as an ergogenic aid for over 80 years, with recent evidence alluding to an ergogenic potential during short-duration high-intensity exercise (51). Early research from McNaughton (50) identified that NaHCO3 possessed ergogenic benefits during 120 and 240 s of “all-out” high-intensity exercise but not exercise of 10 and 30 s in duration. Other investigations of equivalent durations also reported a significant running sprint time improvement in 400 m (33) and 1,500 m (8).This ergogenic benefit is not however limited to short-duration exercise bouts, as performance improvements also have been reported during prolonged 60-min exercise bouts (48), repeated sprint exercises, and combat sports (3). The performance benefits observed with NaHCO3 ingestion are not synonymous in the literature, with studies also reporting no effect of NaHCO3 ingestion (26,69,81).
The aim of this review is to provide an update on the scientific literature relating to the supplementation of NaHCO3 from ca. 2008 to 2016, since the previous review of McNaughton et al. (51). More specifically, the review will address research relating NaHCO3 dosage strategies to the ergogenic influence on a range of exercise modalities. Beyond the exercise performance-related literature, emerging evidence has presented the potential use of NaHCO3 as a training aid and is suggested to have an effect on the physiological stress response to exercise; these aspects also will be explored in further detail. For an in-depth review of the literature pertaining to the performance effect of NaHCO3 before 2008, readers are directed to a previous review by McNaughton et al. (51); additionally, an overview of this research is presented in Table 1.
Mechanisms of Action
The ergogenic effect of NaHCO3 on exercise performance stems from the reinforced extracellular bicarbonate buffer capacity to regulate acid-base balance during exercise. Ingestion of NaHCO3 gives rise to bicarbonate ions (HCO3 −), thus contributing to an alkalotic environment in the extracellular fluid compartments (17). Concurrently, the elevated HCO3 − enlarges the gradient between extracellular and intracellular H+, which stimulates the lactate/H+ cotransporter (68). In turn, this leads to a greater efflux of H+ from intramuscular regions into the extracellular fluid, allowing HCO3 − and buffering compensatory systems to remove H+, therefore, increasing pH. The direct mechanism by which the inducement of alkalosis evokes an ergogenic response to exercise is however unclear. Numerous propositions surrounding both peripherally and centrally driven mediators of fatigue and exercise performance have been investigated (78). Such mechanisms include the attenuation of exercise-induced arterial oxygen desaturation allowing for enhanced oxygen delivery (56), delayed impairment of muscular contractile properties (88), and augmented glycolytic flux (38). More recently, research is indicative of an altered neuromuscular response to preexercise NaHCO3 administration (39,79). The neuromuscular response that is characterized by a reduced rate of force production declines during isometric contractions after a bout of submaximal exercise (39) and repeated bouts of high-intensity exercise (80). The suggestion therefore is that NaHCO3 modifies peripheral indices of fatigue to improve exercise performance. In addition, evidence also has alluded to a central derived contribution to NaHCO3 ergogenic effect (64). During a combination of ischemia and repeated maximal voluntary contractions, voluntary activation was preserved to a greater extent with prior alkalosis compared with control (76% ± 5% vs 57% ± 8%, P < 0.05 ). Voluntary activation is used as an indicator of a descending central drive, which is hypothesized to be preserved with NaHCO3 due to the reduced attenuation of groups III and IV afferent firing under dampened acidic conditions (64). The proposition of a centrally acting mechanism for NaHCO3 is however not new, as early work by Swank and Robertson (83,84) introduced the view of NaHCO3 lowering the subjective perception of exercise intensity. Such an observation aligns with the widely debated psychobiological model of fatigue (47) and suggests that the NaHCO3 mechanisms of action are centrally derived as a psychoactive drug. Nonetheless, further work is required to elucidate the mechanism by which NaHCO3 acts, although it is likely to be an interplay of peripheral and central components.
To attain the ergogenic benefit on performance from NaHCO3, it is recommended that a state of peak alkalosis is required, which refers to a postingestion peak in HCO3 − concentration (68,80). In theory, this will lead to a greater efflux of H+ from the intracellular to extracellular compartments to be buffered during high-intensity exercise compared with a resting HCO3 − concentration and attain maximum buffering capacity (see Mechanisms of Action). It would seem, however, that the point in time at which such a peak is achieved is abstruse. Indeed, Siegler et al. (80) identified within eight men that peak HCO3 − occurred at 60 min postingestion of 0.3 g·kg−1 body mass (BM) NaHCO3, supporting the 60- to 90-min recommendation by Price and Singh (68) to achieve a peak HCO3 −. Nevertheless, a study by Carr et al. (17), using various ingestion timings, fluid intake, coingestion of a small carbohydrate meal (1.5 g·kg−1 BM), and either a capsule or a solution of NaHCO3, displayed contrasting results. More specifically, peak HCO3 − was established at 150 min, a total of 90 min later than the Siegler et al. (80) study. Such a large difference may have been due to the coingestion of the carbohydrate meal, subsequently affecting the absorption rate of NaHCO3. Nevertheless, a study by Siegler and Marshall (79) with no coingestion strategy reported that peak HCO3 − was achieved at 180 min postsupplementation of 0.3 g·kg−1 BM NaHCO3. This shows that, currently, little consistency over the time until a peak HCO3 − is achieved exists within the literature, potentially leading to confusion over the most appropriate dosage strategy for athletes to utilize in competition or training.
Contrary to the popular belief that attaining peak HCO3 − concentration is essential to secure a performance enhancement, a study by Siegler et al. (80) displayed no effect on performance when exercise began at different time points (60, 120, and 180 min) after NaHCO3 supplementation. In more detail, eight recreationally active men performed ten 10-s maximal running sprints and displayed no difference in both peak power output (PPO) (60 min: 984 ± 208 W; 120 min: 916 ± 131 W; 180 min: 987 ± 228 W; P = 0.18) and distance covered (60 min: 456 ± 35 m; 120 min: 448 ± 32 m; 180 min: 448 ± 32 m; P = 0.22). A possible limitation to this study is the assumption that a particular level of alkalosis (i.e., HCO3 −) had been achieved at each time point when exercise commenced, and this also was based on group level data. Highlighted in these aforementioned studies, the dose-response shows a high variation, and thus, it is potentially difficult to ascertain whether each participant was at the respective peak the authors were attempting to replicate. Furthermore, in a recent study by Miller et al. (53), the authors mapped the time to individual peak pH after 0.3 g·kg−1 BM NaHCO3 supplementation and determined that the average time to peak pH was 68.2 ± 21.0 min, but with a population response range from 10 to 90 min postingestion. This demonstrates a high variability in the dose-response from NaHCO3 and possesses a considerable caveat to all previous research that have typically utilized a standard preingestion time of between 60 and 90 min and interpreted the response on a group level. A consideration, however, is that the Miller et al. (53) study was based on time to peak pH, not HCO3 −, which would be a greater indication of the NaHCO3 response. Nevertheless, these results may have considerable practical significance, as a more personalized approach to NaHCO3 supplementation can be utilized by athletes to elicit the ergogenic effects. Further research should look to adopt a personalized approach to ascertain the effects on various modes of exercise and identify the absorption characteristics in other populations.
A prominent determinant of NaHCO3’s use by athletes may arguably be the manipulation of dosage strategies to limit the onset of gastrointestinal (GI) discomfort. The negative GI symptoms caused by NaHCO3 are now well reported in the literature (13,40,74); however, the potential effect such instances can have on performance remains ambiguous. Indeed, Saunders et al. (74) reported a 4.7% improvement in the total work done (TWD) during a cycle to exhaustion at 110% PPO only when four participants that suffered from GI discomfort were removed from a group of 21 recreationally active men (all participants: placebo = 45.6 ± 8.4 kJ, NaHCO3 = 46.8 ± 9.1 kJ, P 0.16; d = 0.14; without GI discomfort: placebo = 46.2 ± 9.2, NaHCO3 = 48.4 ± 9.3 kJ, P < 0.05; d = 0.25). Similarly, Cameron et al. (13) reported a relationship, albeit weak, between the incidences of GI discomfort negatively affecting sprint performance (P = 0.90, r 2 = 0.12). Nonetheless, research has demonstrated that performance benefits and incidences of GI discomfort can coexist (50,53), and therefore, the relationship between the incidences of GI discomfort and the subsequent effect on performance remains unclear. Identifying strategies that reduce the incidences of GI discomfort is still a worthwhile area of investigation however, as incidences such as nausea, diarrhea, and vomiting are a serious practical consideration for athletes. If a dosage strategy could be identified that leads to an enhanced performance, while limiting the incidence of GI discomfort, this may enhance the prevalence of NaHCO3 in both training and competition.
Ergogenic Effect of NaHCO3 on “All-Out” and Supramaximal Exercise
Research assessing the ergogenic effect of NaHCO3 on short-duration high-intensity exercise has been equivocal, with improvements shown in some duration-based “all-out” performances with trained individuals (7,24,86), but not those investigated in an untrained, recreationally active cohort (61,87). A significant improvement in mean power output 4-min “all-out” exercise performance was reported with both serial (427.5 ± 43.6 W) and acute (431 ± 37.9 W) doses of NaHCO3 compared with the placebo (418.3 ± 41.5 W), representing up to a 3% improvement in performance (24). Equally, Bellinger et al. (7) found a 3% improvement in mean power output during 4-min “all-out” exercise performance in eight similarly trained individuals (<65 mL·kg−1· min−1), whereas a magnitude-based inference analysis revealed the 87% likelihood NaHCO3 having a positive performance effect on 4-min “all-out” exercise. This positive effect is not however representative in all investigations with both Vanhatalo et al. (88) and Peart et al. (62) observing unaltered performance during 3 and 4 min of high-intensity exercise bouts with NaHCO3 supplementation, respectively, in untrained participants. This difference in training status between the aforementioned studies indicates that the ergogenic properties of NaHCO3 supplementation during “all-out” high-intensity exercise performance may be more apparent in better trained individuals. This observation corresponds with a meta-analysis that discovered a moderate performance enhancement of 1.7% ± 2.0% (mean ± confidence interval) in athletic cohorts compared with a negative effect in nonathletic cohorts (−1.1% ± 1.1%). The reason for this observation remains unclear, although it is reasonable to postulate that a greater athletic status of participants may improve the reliability to detect the “true” ergogenic effect of NaHCO3, simply because they are able to replicate performance more reliably.
Numerous investigations assessing the ergogenicity of NaHCO3 during constant load supramaximal exercise at 110% to 120% PPO have demonstrated no change in mean performance (33,72,74). These investigations were conducted with recreationally active individuals, and as previously suggested, the training status of participants may account for the lack of detectable change. Alternatively, this lack of change could be attributed to emerging reports of a within-subject variability to the ergogenic effect of NaHCO3 reported within untrained individuals (22). In this study, 15 recreationally active participants conducted six 110% PPO trials to exhaustion, which involved four with NaHCO3 ingestion and two with placebo ingestion. Across the four NaHCO3 trials, blood acid-base response was consistent; that is, mean pH, base excess, and bicarbonate ion concentrations were not reported to be different in each NaHCO3 trial. Despite the blood response, performance across the four trials was not consistently improved after supplementation, with performance only significantly improved compared with placebo in one trial. Magnitude-based inference calculated across the four trials also indicated this mixed response, with the likelihood of an improvement reported to be 54% (possible), 7% (unlikely), 32% (possible), and 93% (likely) from NaCHO3 trials 1 to 4, respectively. Delving deeper, this study also observed an inconsistency in individual response to NaHCO3, as it was found that 10 participants improved performance in at least one of the four trials; however, five participants did not exhibit improved performance in any of the trials. This study therefore may allude to a responder/nonresponder phenomenon to the ergogenic potential of NaHCO3 (22). Aligned with the previously mentioned discussion of training status, it may be conceivable that the nature of the athletes used by Dias et al. (22) may account for some of the variability observed; therefore, further research is required to assess if this variability is present in a trained cohort.
Ergogenic Effect of NaHCO3 on High-Intensity Intermittent Exercise
The efficacy of NaHCO3 on various intermittent exercises, including sport-specific simulations, has been investigated in a range of exercise modalities, such as swimming (75,92), running (13,25,42,74), and cycling (31,53,77). With specific reference to repeated sprint ability, generally positive effects on performance have been demonstrated. Indeed, Miller et al. (53) reported a 17% and 11% improvement in TWD compared with control and placebo, respectively (69.8 ± 11.7 vs 59.6 ± 12.2 vs 630 ± 8.3 s, P < 0.05), during 6 × 10 s maximal cycling. Comparably, Krustrup et al. (41) also reported that the total running distance improved by 12% during a football-specific Yo-Yo intermittent recovery test (735 ± 61 vs 646 ± 46 m, P < 0.05). In contrast, Ducker et al. (25) reported a markedly lower improvement demonstrating that total sprint time was 2.2% faster to complete three sets of 6 × 20 m sprints with NaHCO3 supplementation 60 min before exercise (60.33 ± 2.62 vs 59.05 ± 2.83 s, P < 0.05). The differing intermittent activity patterns of the aforementioned studies do not allow for direct comparison, although the different supplementation methods used may explain the larger ergogenic effect noted by Krustrup et al. (42) and Miller et al. (53). A higher NaHCO3 dose of 0.4 g·kg−1 BM was used by Krustrup et al. (42), therefore increasing the availability of HCO3 − to buffer H+ to a greater extent during exercise. The authors, however, did not use a placebo treatment; therefore, some of the effect could be attributed to a placebo effect. The NaHCO3 treatment condition leads to an enhanced sodium ingestion that may cause an expansion in plasma volume, which also has been shown to possess ergogenic properties, thereby masking the true buffering potential of NaHCO3 to enhance performance. Conversely, Miller et al. (53) elicited an 11% improvement in TWD with the new personalized dosage method in comparison with an equimolar, taste-matched placebo treatment. This signifies the enhanced ergogenic influence that may be provoked from a personalized strategy.
Research investigating high-intensity intermittent-type exercise has produced equivocal performance responses to NaHCO3 supplementation. Swimming performance in eight well-trained competitive youth swimmers completing 4 × 50 m front crawl swims interspersed with 1-min passive rest periods was improved by 2.6% with NaHCO3 (112.9 s) compared with placebo (114.3 s). Likewise, a 2% improvement in total swim time was exhibited with NaHCO3 (159.4 ± 25.4 vs 163.2 ± 25.6) during 8 × 25 m front crawl, interspersed with 5-s rest (76). This was despite a presupplementation time of 2.5 h, substantially longer than previously reported mean peak alkalosis conditions at 60 to 90 min (68). Together, this indicates that NaHCO3 may be beneficial for intermittent swimming using different recovery periods. In a further study involving a hypoxic stimulus, encompassing a reduction in the fraction of inspired oxygen (FIO2) to 14.7% (approximately 3,000 m), no effect on performance was recorded after NaHCO3 supplementation against a placebo. In theory, hypoxia presents a substantial challenge to acid-base balance, subsequently offering ideal conditions to produce the ergogenic effects of NaHCO3; however, this has not been represented in the available literature. In more detail, 12 healthy participants cycled at 120% PPO for 30 s interspersed with 30-s active recovery at 30% PPO, until volitional fatigue. However, the cumulative time spent cycling at 120% PPO was not different between the placebo (133.3 ± 28.7 s) and the NaHCO3 (127.8 ± 27.9 s) conditions. Performance was greater under normoxic conditions; however, no significant differences existed between normoxic NaHCO3 and placebo supplementation protocols, despite performance improvement of 8.3% with NaHCO3 (183.8 ± 45 vs 199.1 ± 62 s). A single bout of 120% PPO exercise also has demonstrated no improvements in exercise performance after NaHCO3 ingestion in a similar recreationally active cohort (34,72). This suggests that the supramaximal intensity may be too severe to benefit from NaHCO3 and that the early termination of exercise at 120% PPO may, although speculated, be linked to the rate of change in pH. With such a severe change during 120% PPO, this may lead to the saturation of the muscle membrane transporters monocarboxylate transporter 1 and 4 or the sodium-hydrogen exchanger (46). Nevertheless, performance did improve under normoxic conditions at 120% PPO when performed intermittently, although nonsignificantly.
Empirical research also has investigated sport simulations within a range of sports including football (73), rugby (13), and water polo (85), with none reporting positive benefits from NaHCO3. A more sport-specific football simulation protocol, with incorporated 5 × 6 s maximal sprints before and after two football-specific intermittent treadmill protocols under acute hypoxia (FIO2, 15.5%; approximately 2,500 m), also revealed no difference in exercise performance (73). The lack of improvement, however, could be due to the NaHCO3 ingestion strategy, which entailed two discrete doses over a 4-h period (0.2 g·kg−1 BM, 4 h; 0.1 g·kg−1 BM, 2 h before exercise). More specifically, preexercise HCO3 − was 28.6 ± 1.6 mmol·L−1, which is lower than the peak HCO3 − reported in previous work (17,68), therefore not enhancing buffering capacity to its maximum and consequently obtaining no ergogenic benefit during exercise. Furthermore, the length of the protocol (>90 min in total) may have been a contributing factor to why no performance benefit was observed, as this was outside of the 1- to 10-min window suggested to elicit the largest ergogenic effects (15). Nevertheless, in a study supplementing 0.3 g·kg−1 BM NaHCO3 60 min before a “9-min” high-intensity rugby-specific exercise, no effect on performance was also recorded when compared with a placebo, within a group of 25 elite male rugby players. This study also entailed a 25-min warm-up before the performance, which may have already utilized the enhanced buffering capacity before the rugby-specific exercise, therefore failing to enhance the “9-min” exercise. Research that focused on water polo also mimics such findings. A group of 12 elite female water polo players completed a 59-min match simulation test entailing 56 × 10 m sprints, with no improvement in mean sprint time between the NaHCO3 and the placebo (NaHCO3 = 6.88 ± 0.28 vs placebo = 6.91 ± 0.31 s; d = 0.09). Similar to the study by Saunders et al. (73), it might be the case that the 59-min match simulation test was outside of the 1- to 10-min window for NaHCO3 to elicit an ergogenic effect. In summary, research simulating sport performance has shown no positive effects on performance from NaHCO3.
Ergogenic Effects of NaHCO3 on Distance-Based Time Trial Events
Research assessing the influence of NaHCO3 on distance-based time trial (TT) events has focused on rowing (14,16,20,35,43) and cycling (41,58). In relation to rowing, research has focused on determining the effect of NaHCO3 on 2-km TTs and has largely reported unequivocal results of unaltered performance (14,16,20,35,36,43). Carr et al. (16) reported no change in performance times with NaHCO3 compared with placebo within a group of eight well-trained rowers (NaHCO3 6: 44.4 ± 23.4 vs placebo 6: 43.8 ± 23.4). Results have been replicated after both acute and 3-d serial supplementations in well-trained rowers (14,43). These observations also were replicated among elite rowers (20) during a 6-min high-intensity bout, which is equivalent to the expected time to complete 2 km. Twelve international rowers completed similar distances with NaHCO3 and placebo at 1,860 ± 96 and 1,865 ± 104 m, respectively. Taken together, this research suggests that NaHCO3 may not be an effective ergogenic aid for trained rowers during simulated rowing performance. Hobson et al. (36), however, provides an interesting caveat to the previous outlined research, in that 500-m split times revealed a significantly faster performance during the second half of the 2-km row. Acute NaHCO3 ingestion stimulated a 0.5 ± 1.2-s improvement in the third 500-m split and a 1.1 ± 1.7-s improvement in the fourth 500-m split, with magnitude-based inferences representing likelihood of beneficial effect of NaHCO3 as possible and very likely during the third and fourth 500-m split, respectively. Despite this, overall performance did not change under the alkalotic conditions. This study does however provide an interesting insight into the potential pacing considerations when supplementing with NaHCO3; for example, the split times reported by Hobson et al. (36) are suggestive of a negative pacing strategy. Negative pacing strategies are often used within distance-based TTs as these allow for an intense burst toward the end of the event, which is driven by an enhanced utilization of anaerobic reserves (32), access to which may be facilitated by NaCHO3 due to the enhanced glycolytic flux (38). As such, NaHCO3 could potentially be beneficial for athletes utilizing such pacing strategies, although further work is required to test this initial observation.
In contrast to rowing, cycling TT research has been limited, with two studies investigating two distinctly different distances of 4 km (41) and 40 km (58). During 3-km TTs, performance was improved by 2.8% with NaHCO3 compared with placebo in 10 well-trained cyclists (225.9 ± 11.3 vs 228.7 ± 10.8 s), although mean differences were not significant (41). Despite the lack of statistical significance, magnitude-based inference analysis reported that NaHCO3 was very likely to have a positive influence on 3-km TT performance. Therefore, suggesting NaHCO3 may possess practical benefits to athletes competing over short TT distances. In contrast, Northgraves et al. (58) reported no benefits during 40-km TT distance from NaHCO3 supplementation, with a mean time to completion of 67.08 ± 5.04 min with NaHCO3 compared with 66.41 ± 4.04 min in the placebo trial. This opposes earlier work conducted by McNaughton et al. (48), during which well-trained cyclists (67.3 ± 3.3) performed an equivalent-duration (60 min) time-based TT and elicited a significant improvement in TWD with NaHCO3 compared with a placebo (950.9 ± 81.1 kJ vs 839.0 ± 88.6 kJ, P < 0.03). The ergogenic effect of NaHCO3 is dependent on the degree of metabolic acidity (51), and interestingly, the degree of metabolic acidity does not appear to be different between both studies (~7.32); therefore, the difference between studies is likely due to alternative factors. Time-based and distance-based TTs, although of similar duration, do exhibit discrete differences in an athlete’s perception of judging power output distribution (1). Therefore, the methodological difference may explain the difference observed between the two investigations. Moreover, trained individuals are suggested to elicit performance gains from NaHCO3 more readily (15); therefore, the use of untrained participants by Northgraves et al. (58) may account for the contrasting results. In addition, untrained participants may impede the reliability of the exercise protocol, thereby masking any ergogenic benefit. Based on current evidence, it may therefore be unwise to discount the use of a buffering agent during prolonged TT events at this early stage of research. Early research is indicative of a meaningful practical benefit of NaHCO3 on shorter duration high-intensity TT performance, although further work is required to clarify this initial observation.
Ergogenic Effect of NaHCO3 on Skill-Based Sports
Fatigue can have a deleterious effect on decision making and skill execution during sports performance. On this premise, emerging research has assessed the influence of NaHCO3 on a range of skill-based sports, including boxing (77), judo (28,87), and tennis (90). A study by Siegler and Hirscher (77), featuring 10 amateur boxers, investigated the effects of NaHCO3 before sparring bouts of 4 × 3 min rounds, interspersed with 1-min seated recovery. Compared with placebo, NaHCO3 evoked a significant 5% (P < 0.01) increase in overall punch efficacy (i.e., successful punches landed), along with improvements of 11.4% (88 ± 12 vs 79 ± 10) in round 1, 4.9% (86 ± 10 vs 82 ±) in round 3, and 7.5% (86 ± 13 vs 80 ± 10) in round 4 after NaHCO3 supplementation, but no difference in round 2. This study presents an encouraging area of investigation, but the test-retest reliability of such sparing protocols is unclear. Furthermore, the study makes no distinction between weight classes of participants and only evaluated four rounds when a typical boxing match lasts up to 12 rounds. Therefore, it is difficult to ascertain the true effect of NaHCO3 on a full bout. Another combat sport-related study assessed the efficacy of NaHCO3 in the special judo fitness test (SJFT) that comprised three sets (1 × 15 and 2 × 30 s), with performance assessed via the total number of judo throws. There was no difference in performance between the treatment and placebo conditions, although the reliability of such a protocol to detect change is unclear. Despite this, an upper body Wingate test (4 × 30 s interspersed with 3-min recovery) in nine judo and jujitsu athletes found that 7 d of chronic NaHCO3 (0.5 g·kg−1 BM) enhanced TWD by 8% (77).
Other skill-based sports, such as tennis, also are sensitive to the ergogenic benefits of NaHCO3 (90). There was tennis shot consistency during the Loughborough Tennis Skill Test (LTST), eliciting greater skill maintenance in nine male national level tennis players. More specifically, consistency of service declined by 34.3% in the placebo trial (16.9% ± 5.4% to 11.1% ± 6.0%), compared with 1.4% in the NaHCO3 trial (13.8% ± 5.1% to 13.6% ± 5.9%), and forehand shot consistency was reduced by 13.3% in the placebo trial (10.5% ± 2.8% to 9.1% ± 2.0%) but improved by 16% during NaHCO3 condition (8.0% ± 1.6% to 9.3% ± 2.6%). The mean differences in forehand and serve consistency skill execution were significantly maintained to a greater extent with NaHCO3. Together, this research suggests that NaHCO3 may be a promising ergogenic strategy to maintain skill execution throughout a fatiguing bout of exercise. However, it appears that further research would need to adopt reliable, or state the reliability of, the testing protocols.
The Potential Use of NaHCO3 as a Training Aid
Enhancing training-induced adaptations is a prominent area of sports nutrition research with two dietary approaches known as “training better” and “training smarter,” strategies that are often used by athletes to maximize training outcomes (10). The former involves the use of dietary strategies to enhance the quality of training, modulating training intensity and/or volume. In contrast, the latter “training smarter” approach is designed to result in enhanced training-induced molecular adaptations through dietary strategies without additional training stressors. These approaches typically involve carbohydrate manipulation during training; however, emerging evidence suggests that sodium bicarbonate supplementation has the potential to induce training adaptations through both methods.
Because of the ergogenic properties of NaHCO3 to improve a single bout of high-intensity exercise, it is conceivable that NaHCO3 could be used as a daily training supplement to enhance the quality of individual training bouts. Indeed, Mueller et al. (55) assessed five consecutive days of acute 0.3 g·kg−1 BM NaHCO3 on time to exhaustion during constant load cycling exercise at an intensity equivalent to critical power. Performance was greater each day after NaHCO3 supplementation compared with placebo, presenting a significant mean improvement of 23.5% (P = 0.001). Therefore, demonstrating daily acute supplementation is a viable nutritional strategy for athletes; however, the efficacy of NaHCO3 during a training intervention utilizing a “training better” approach has yet to be established.
Emerging evidence indicates that the regulation of acid-base balance, via NaHCO3, during high-intensity exercise bouts may stimulate oxidative molecular pathways and, in turn, promote aerobic capacity without inflicting further training stressors (9,26,63). Early work by Edge et al. (26) found that supplementation of NaHCO3 before training during an 8-wk (three sessions per week) supervised training program with moderately trained women (V˙O2peak: 42.1 ± 7.0 mL·kg−1·min−1) resulted in a significantly larger improvement in the lactate threshold (LT) and time to exhaustion by 42% and 25% (P < 0.05), respectively, compared with a matched exercise-only group. Training sessions between groups were matched for volume and intensity, thereby matching total training stress during interventions. Moreover, despite the reinforced buffering capacity with NaHCO3 during acute bouts of exercise, it did not translate to an altered intramuscular buffering capacity between groups, which is suggestive of an alternative mechanism for adaptation. LT is known to be a good indicator of aerobic capacity (52), which implies adaptations were likely to be aerobic in nature. Indeed, this assertion is supported in a latter investigation by Percival et al. (63), which reported an up-regulation of the peroxisome proliferator-activated receptor γ coactivator-1 alpha (PGC-1α) mRNA expression by 28% during recovery from a repeated high-intensity exercise bout with preexercise ingestion of NaHCO3 compared with exercise alone. Repeated up-regulation PGC-1α expression through a combination of exercise and NaHCO3 has been demonstrated to augment PGC-1α protein content and consequently stimulate mitochondrial biogenesis in a Wistar rat model (9). This improved muscular oxidative potential may explain, at least in part, the superior training-related adaptations in LT noted by Edge et al. (26). These performance enhancements were not however observed by Driller et al. (23) in six highly trained international rowing athletes following a 4-wk (two sessions per week) training period with NaHCO3 ingestion. It is unclear if PGC-1α was increased in these trained individuals since muscle biopsies samples were not obtained. Furthermore, it is conceivable that the low volume of exercise sessions with prior NaHCO3 ingestion in this study, compared with four exercise sessions over 8 wk by Edge et al. (26), may not be sufficient to elicit detectable improvements in performance. Consequentially, further research is required to determine whether preexercise alkalosis can induce oxidative adaptation in highly trained individuals and assess if it is an efficacious method to “train smarter.”
The Effect of NaHCO3 on Physiological Stress Response
Contemporary research has explored the influence of preexercise NaHCO3 ingestion on physiological parameters beyond the reputable ergogenic role during high-intensity exercise. More specifically, a series of investigations conducted by Peart et al. (59–62) has addressed the potential of pH regulation to attenuate cellular stress (e.g., heat shock protein (HSP)) experienced during exercise. The HSP-70 isoforms have been cited to have distinct importance during exercise because of their involvement in cytoprotective functions within cells in response to an exercise stressor (45,49,54). Heat shock proteins also possess an important exercise preconditioning response, whereby exposure to an initial exercise stressor can improve the tolerance to a subsequent exposure. As such, greater understanding of the response and role of HSP-70 isoforms during acute and repeated bouts of exercise may enhance our appreciation of the mechanisms of regular exercise that can induce adaptations for performance or protective function for health. A number of potential exercise-related stimuli have been proposed to instigate HSP-70 isoform response, including thermal, metabolic, oxidative, cytokine, and acidic stress (49,54), although the direct mechanism remains unclear as all these factors coincide during exercise.
The ingestion of NaHCO3 before a single bout of anaerobic (62) and high-intensity intermittent exercise (HIIE) (59,61) is shown to blunt intracellular HSP-72 response after an exercise bout. During recovery from a 4-min high-intensity “all-out” bout of exercise, HSP-72 is increased by 42% after 30 min postexercise, whereas prior NaHCO3 supplementation blunted HSP-72 response to the exercise bout (59). Similar results were observed after a HIIE bout, with HSP-72 significantly blunted postexercise with NaHCO3 ingestion compared with a peak 80% increase after exercise under the placebo treatment condition (59). Conversely, NaHCO3 was not found to attenuate HSP-72 after a 90-min submaximal intermittent exercise bout, despite a significant increase in HSP-72 with time, in treatment and placebo conditions (60). The reason for the contrasting results are unclear; however, it may be conceivable that a lower acidic stress from the prolonged submaximal bout (pH 7.31 ), compared with investigations employing high-intensity exercise (pH 7.16  and pH 7.15 ), may be a contributory factor, as the manipulation of the acid-base balance is the mechanism by which NaHCO3 typically mediates exercise performance. This implies that the expression of HSPs after high-intensity exercise is provoked by substantial disturbance to acid-base balance, although this may not be representative of a direct mechanistic relationship.
The attenuation of oxidative damage also was suggested to coexist with the dampened HSP-72 response after exercise observed with preexercise NaHCO3 ingestion. Delving deeper, lipid peroxidation was significantly reduced by 67% and 25% between 60 and 90 min after a single high-intensity and intermittent bout, respectively (59,62). The authors used thiobarbituric acid reactive substances to assess lipid peroxidation in this instance; however, this method is suggested to be an unreliable method of assessing lipid peroxidation (65). Further research is therefore required to determine the effect of NaHCO3 on more reliable markers of oxidative damage. Nonetheless, it unclear if the dampening of acidic stress directly contributes to the blunted HSP-72 response or if this is mediated via a reduced oxidative damage.
The biological and practical significance of the blunted HSP-72 expression to NaHCO3 before high-intensity exercise is unclear, although the same is asserted for the overall exercise-related implication of HSPs to health and training adaptation (54). The role in exercise preconditioning is one that is often cited in the literature with the HSPs deemed to be the central component in protecting the body from exercise stressors after an initial exposure. A recent study by Peart et al. (61) investigated the effect an initial blunted HSP-72 with NaHCO3 after high-intensity exercise had on the subsequent HSP-72 expression after a second bout of the same exercise stress without NaHCO3 ingestion. In comparison with placebo, the ingestion of NaHCO3 before the initial exercise stressor had no effect on HSP-72 expression during the subsequent exercise stressor. Sodium bicarbonate supplementation may not, therefore, interfere with the exercise preconditioning role of HSP, although the meaningfulness of this observation is not fully understood as further work is required to establish the importance HSP during regular exercise for adaptation and health outcome. This body of research related to NaHCO3 supplementation does however provide an important insight into the role of acidic stress to cellular stress manifestations during high-intensity exercise and also suggests that supplementation may not impede the role of HSP in the conditioning effects of acute exercise.
Research published since 2008 on the ergogenic effect of NaHCO3 has demonstrated improvements during high-intensity exercise, within a range of exercise modalities, such as a single bout of supramaximal exercise, high-intensity intermittent activity, and skill-based sports (summarized in Table 2). In particular, these benefits seem to be present to a greater extent within trained individuals. Despite this, a high intraindividual variability in response to NaHCO3 appears to exist; therefore, the ergogenic benefits may not be induced during every exercise bout. This response, however, has only been shown with untrained individuals, and further evidence is required to ascertain if this intraindividual response is prevalent within trained individuals. The development of a personalized dosage strategy enables individuals to exercise at their individualized peak alkalotic condition. This may produce greater performance enhancement and allow individuals to attain the ergogenic benefits of NaHCO3 more consistently. Contemporary research has alluded to benefits of acute NaHCO3 supplementation beyond performance alone. Preexercise alkalosis can alleviate physiological stress during high-intensity exercise, particularly in reference to HSP-72 response, whereas promising evidence is suggestive of an augmented molecular adaptation response to training.
The authors declare no conflict of interest and do not have any financial disclosures.
1. Abbiss CR, Thompson KG, Lipski M, et al. Pacing differs between time- and distance-based time trials in trained cyclists. Int. J. Sports Physiol. Perform.
2016 [Epub ahead of print].
2. Afman G, Garside RM, Dinan N, et al. Effect of carbohydrate or sodium bicarbonate ingestion on performance during a validated basketball simulation test. Int. J. Sport Nutr. Exerc. Metab.
2014; 24:632–44, 2014.
3. Artioli GG, Gualano B, Coelho DF, et al. Does sodium-bicarbonate ingestion improve simulated judo performance? Int. J. Sport Nutr. Exerc. Metab.
4. Atherton JC. Acid-base balance: maintenance of plasma pH. Anaest. Intens. Care Med.
5. Bangsbo J, Madsen K, Kiens BEA, Richter EA. Effect of muscle acidity on muscle metabolism and fatigue during intense exercise in man. J. Physiol.
6. Barber JJ, McDermott AY, McGaughey KJ, et al. Effects of combined creatine and sodium bicarbonate supplementation on repeated sprint performance in trained men. J. Strength Cond. Res.
7. Bellinger PM, Howe ST, Shing CM, Fell JW. Effect of combined β-alanine and sodium bicarbonate supplementation on cycling performance. Med. Sci. Sports Exerc.
8. Bird SR, Wiles J, Robbins J. The effect of sodium bicarbonate ingestion on 1500 m racing time. J. Sports Sci.
9. Bishop DJ, Thomas C, Moore-Morris T, et al. Sodium bicarbonate ingestion prior to training improves mitochondrial adaptations in rats. Am. J. Physiol. Endocrinol. Metab.
10. Burke LM. Fueling strategies to optimize performance: training high or training low. Scand. J. Med. Sci. Sports
11. Burke LM, Pyne DB. Bicarbonate loading to enhance training and competitive performance. Int. J. Sports Physiol. Perform.
12. Cairns SP. Lactic acid and exercise performance: culprit or friend. Sports Med.
13. Cameron SL, McLay-Cooke RT, Brown RC, et al. Increased blood pH but not performance with sodium bicarbonate supplementation in elite rugby union players. Int. J. Sport Nutr. Exerc. Metab.
14. Carr AJ, Gore CJ, Dawson B. Induced alkalosis and caffeine supplementation: effects on 2,000-m rowing performance. Int. J. Sport Nutr. Exerc. Metab.
15. Carr AJ, Hopkins WG, Gore CJ. Effects of acute alkalosis and acidosis on performance: a meta-analysis. Sports Med.
16. Carr AJ, Slater GJ, Gore CJ, Burke LM. Reliability and effect of sodium bicarbonate: buffering and 2000-m rowing performance. Int. J. Sports Physiol. Perform.
17. Carr AJ, Slater GJ, Gore CJ, et al. Effect of sodium bicarbonate on [HCO3 −
], pH and gastrointestinal symptoms. Int. J. Sport Nutr. Exerc. Metab.
18. Castell LM, Stear SJ, Burke LM. Nutritional supplements in sport, exercise and health: an A–Z guide
. London: Routledge, 2015.
19. Chin ER, Allen DG. The contribution of pH-dependent mechanisms to fatigue at different intensities in mammalian single muscle fibres. J. Physiol.
20. Christensen PM, Petersen MH, Friis SN, Bangsbo J. Caffeine, but not bicarbonate, improves 6 min maximal performance in elite rowers. Appl. Physiol. Nutr. Metab.
21. Christou H, Bailey N, Kluger MS, et al. Extracellular acidosis induces hemeoxygenase-1 expression in vascular smooth muscle cells. Am. J. Physiol. Heart Circ. Physiol.
22. Dias GFA, Painelli VS, Sale C, et al. (In)Consistencies in responses to sodium bicarbonate supplementation: a randomised, repeated measures, counterbalanced and double-blind study. PLoS One
23. Driller MW, Gregory JR, Williams AD, Fell JW. The effects of chronic sodium bicarbonate ingestion and interval training in highly trained rowers. Int. J. Sport Nutr. Exerc. Metab.
24. Driller MW, Gregory JR, Williams AD, Fell JW. The effects of serial and acute NaHCO3 loading in well-trained cyclists. J. Strength Cond. Res.
25. Ducker KJ, Dawson B, Wallman KE. Effect of beta-alanine supplementation on 2000-m rowing-ergometer performance. Int. J. Sport Nutr. Exerc. Metab.
26. Edge J, Bishop D, Goodman C. Effects of chronic NaHCO3
ingestion during interval training on changes to muscle buffer capacity, metabolism, and short-term endurance performance. J. Appl. Physiol.
27. Fabiato A, Fabiato F. Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiace and skeletal muscles. J. Physiol.
28. Fellippe LC, Lopes-Silva JP, Bertuzzi R, et al. Separate and combined effects of caffeine and sodium bicarbonate intake on judo performance. Int. J. Sports Physiol. Perform.
29. Fitts RH. The cross-bridge cycle and skeletal muscle fatigue. J. Appl. Physiol.
30. Fitts RH. The cross-bridge cycle and skeletal muscle fatigue. J. Appl. Physiol.
31. Flinn S, Herbert K, Graham K, Siegler JC. Differential effect of metabolic alkalosis and hypoxia on high-intensity cycling performance. J. Strength Cond. Res.
32. Foster C, DeKoning JJ, Hettinga F, et al. Effect of competitive distance on energy expenditure during simulated competition. Int. J. Sports Med.
33. Goldfinch J, McNaughton L, Davies P. Induced metabolic alkalosis and its effects on 400-m racing time. Eur. J. Appl. Physiol. Occup. Physiol.
34. Higgins MF, James RS, Price MJ. The effects of sodium bicarbonate (NaHCO3
) ingestion on high intensity cycling capacity. J. Sports Sci.
35. Hobson RM, Harric RC, Martin D, et al. Effect of beta-alanine, with and without sodium bicarbonate, on 2000-m rowing performance. Int. J. Sport Nutr. Exerc. Metab.
36. Hobson RM, Harris RC, Martin D, et al. Effect of sodium bicarbonate supplementation on 2000-m rowing performance. Int. J. Sports Physiol. Perform.
37. Hollidge-Horvat MG, Parolin ML, Wong D, et al. Effect of induced metabolic acidosis on human skeletal muscle metabolism during exercise. Am. J. Physiol.
38. Hollidge-Horvat MG, Parolin ML, Wong D, et al. Effect of induced metabolic alkalosis on human skeletal muscle metabolism during exercise. Am. J. Physiol. Endocrinol. Metab.
39. Hunter AM, De Vito G, Bolger C, et al. The effect of induced alkalosis and submaximal cycling on neuromuscular response during sustained isometric contraction. J. Sports Sci.
40. Kahle LE, Kelly PV, Eliot KA, Weiss EP. Acute sodium bicarbonate loading has negligible effects on resting and exercise blood pressure but causes gastrointestinal distress. Nutr. Res.
41. Kilding AE, Overton C, Gleave J. Effects of caffeine, sodium bicarbonate, and their combined ingestion on high-intensity cycling performance. Int. J. Sport Nutr. Exerc. Metab.
42. Krustrup P, Ermidis G, Mohr M. Sodium bicarbonate intake improves high-intensity intermittent exercise performance in trained young men. J. Int. Soc. Sports Nutr.
43. Kupcis PD, Slater GJ, Pruscino CL, Kemp JG. Influence of sodium bicarbonate on performance and hydration in lightweight rowing. Int. J. Sports Physiol. Perform.
44. Luetkemeier MJ, Thomas EL. Hypervolemia and cycling time trial performance. Med. Sci. Sports Exerc.
45. Madden LA, Sandström ME, Lovell RJ, McNaughton L. Inducible heat shock protein 70 and its role in preconditioning and exercise. Amino Acids
46. Messonnier L, Kristensen M, Juel C, Denis C. Importance of pH regulation and lactate/H+
transport capacity for work production during supramaximal exercise in humans. J. Appl. Physiol.
47. Marcora SM, Staiano W. The limit to exercise tolerance in humans: mind over muscle? Eur. J. Appl. Physiol.
48. McNaughton L, Dalton B, Palmer G. Sodium bicarbonate can be used as an ergogenic aid in high-intensity, competitive cycle ergometry of 1 h duration. Eur. J. Appl. Physiol. Occup. Physiol.
49. McNaughton L, Lovell R, Madden L. Heat shock proteins in exercise: a review. J. Exerc. Sci. Physiother.
50. McNaughton LR. Bicarbonate ingestion: effects of dosage on 60 s cycle ergometry. J. Sports Sci.
51. McNaughton LR, Siegler J, Midgley A. Ergogenic effects of sodium bicarbonate. Curr. Sports Med. Rep.
52. Midgley AW, McNaughton LR, Jones AM. Training to enhance the physiological determinants of long-distance running performance: can valid recommendations be given to runners and coaches based on current scientific knowledge? Sports Med.
53. Miller P, Robinson A, Sparks A, et al. The effects of sodium bicarbonate ingestion on repeated sprint ability. J. Strength Cond. Res.
54. Morton JP, Kayani AC, McArdle A, Drust B. The exercise-induced stress response of skeletal muscle, with specific emphasis on humans. Sports Med.
55. Mueller SM, Gehrig SM, Frese S, et al. Multiday acute sodium bicarbonate intake improves endurance capacity and reduces acidosis in men. J. Int. Soc Sports Nutr.
56. Nielsen HB, Bredmose PP, Strømstad M, et al. Bicarbonate attenuates arterial desaturation during maximal exercise in humans. J. Appl. Physiol.
57. Noakes TD, St Clair Gibson A, Lambert EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans: summary and conclusions. Br. J. Sports Med.
58. Northgraves MJ, Peart DJ, Jordan CA, Vince RV. Effect of lactate supplementation and sodium bicarbonate on 40-km cycling time trial performance. J. Strength Cond. Res.
59. Peart DJ, Kirk RJ, Hillman AR, et al. The physiological stress response to high-intensity sprint exercise following the ingestion of sodium bicarbonate. Eur. J. Appl. Physiol.
60. Peart DJ, Kirk RJ, Madden LA, et al. The influence of exogenous carbohydrate provision and pre-exercise alkalosis on the heat shock protein response to prolonged interval cycling. Amino Acids
61. Peart DJ, Kirk RJ, Madden LA, Vince RV. Implications of a pre-exercise alkalosis-mediated attenuation of HSP72 on its response to a subsequent bout of exercise. Amino Acids
62. Peart DJ, McNaughton LR, Midgley AW, et al. Pre-exercise alkalosis attenuates the heat shock protein 72 response to a single-bout of anaerobic exercise. J. Sci. Med. Sport
63. Percival ME, Martin BJ, Gillen JB, et al. Sodium bicarbonate ingestion augments the increase in PGC-1α mRNA expression during recovery from intense interval exercise in human skeletal muscle. J. Appl. Physiol.
64. Pollak KA, Swenson JD, Vanhaitsma TA, et al. Exogenously applied muscle metabolites synergistically evoke sensations of muscle fatigue and pain in human subjects. Exp. Physiol.
65. Powers SK, Smuder AJ, Kavazis AN, Hudson MB. Experimental guidelines for studies designed to investigate the impact of antioxidant supplementation on exercise performance. Int. J. Sport Nutr. Exerc. Metab.
66. Price MJ, Cripps D. The effects of combined glucose-electrolyte and sodium bicarbonate ingestion on prolonged intermittent exercise performance. J. Sports Sci.
67. Price MJ, Simons C. The effect of sodium bicarbonate ingestion on high-intensity intermittent running and subsequent performance. J. Strength Cond. Res.
68. Price MJ, Singh M. Time course of blood bicarbonate and pH three hours after sodium bicarbonate ingestion. Int. J. Sports Physiol. Perform.
69. Renfree A. The time course for changes in plasma [H+
] after sodium bicarbonate ingestion. Int. J. Sports Physiol. Perform.
70. Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. Am. J. Physiol. Regul. Integr. Comp. Physiol.
71. Roth DA, Brooks GA. Lactate and pyruvate transport is dominated by a pH gradient-sensitive carrier in rat skeletal muscle sarcolemmal vesicles. Arch. Biochem. Biophys.
72. Sale C, Saunders B, Hudson S, et al. Effect of β-alanine plus sodium bicarbonate on high-intensity cycling capacity. Med. Sci. Sports Exerc.
73. Saunders B, Sale C, Harris R, Sunderland C. Effect of sodium bicarbonate and beta-alanine on repeated sprints during intermittent exercise performance at hypoxia. Int. J. Sport Nutr. Exerc. Metab.
74. Saunders B, Sale C, Harris RC, Sunderland C. Sodium bicarbonate and high-intensity-cycling capacity: variability in responses. Int. J. Sports Physiol. Perform.
75. Siegler JC, Gleadall-Siddall DO. Sodium bicarbonate and repeated swim performance. J. Strength Cond. Res.
76. Siegler JC, Gleadall-Siddall DO. Sodium bicarbonate ingestion and repeated swim sprint performance. J. Strength Cond. Res.
77. Siegler JC, Hirscher K. Sodium bicarbonate ingestion and boxing performance. J. Strength Cond. Res.
78. Siegler JC, Marshall P. The effect of metabolic alkalosis on central and peripheral mechanisms associated with exercise-induced muscle fatigue in humans. Exp. Physiol.
79. Siegler JC, Marshall P. The effect of metabolic alkalosis on central and peripheral mechanisms associated with exercise-induced muscle fatigue in humans. Exp. Physiol.
80. Siegler JC, Marshall PWM, Bray J, Towlson C. Sodium bicarbonate supplementation and ingestion timing: does it matter. J. Strength Cond. Res.
81. Siegler JC, Marshall PWM, Raftry S, et al. The differential effect of metabolic alkalosis on maximum force and rate of force development during repeated, high-intensity cycling. J. Appl. Physiol.
82. Stephens TJ, McKenna MJ, Canny BJ, et al. Effect of sodium bicarbonate on muscle metabolism during intense endurance cycling. Med. Sci. Sports Exerc.
83. Swank A, Robertson RJ. Effect of induced alkalosis on perception of exertion during intermittent exercise. J. Appl. Physiol.
84. Swank AM, Robertson RJ. Effect of induced alkalosis on perception of exertion during exercise recovery. J. Strength Cond. Res.
85. Tan F, Polglaze T, Cox G, et al. Effects of induced alkalosis on simulated match performance in elite female water polo players. Int. J. Sport Nutr. Exerc. Metab.
86. Thomas C, Delfour-Peyrethon R, Bishop DJ, et al. Effects of pre-exercise alkalosis on the decrease in VO2max
at the end of all-out exercise. Eur. J. Appl. Physiol.
87. Tobias G, Benatti FB, de Salles Painelli V, et al. Additive effects of beta-alanine and sodium bicarbonate on upper-body intermittent performance. Amino Acids
88. Vanhatalo A, McNaughton LR, Siegler J, Jones AM. Effect of induced alkalosis on the power-duration relationship of “all-out” exercise. Med. Sci. Sports Exerc.
89. Verbitsky O, Mizrahi J, Levin M, Isakov E. Effects of ingested sodium bicarbonate on muscle force, fatigue, and recovery. J. Appl. Physiol. (1985)
90. Wu CL, Shih MC, Yang CC, et al. Sodium bicarbonate supplementation prevents skilled tennis performance decline after a simulated match. J. Int. Soc Sports Nutr.
91. Zabala M, Peinado AB, Calderón FJ, et al. Bicarbonate ingestion has no ergogenic effect on consecutive all out sprint tests in BMX elite cyclists. Eur. J. Appl. Physiol.
92. Zajac A, Cholewa J, Poprzecki S, et al. Effects of sodium bicarbonate ingestion on swim performance in youth athletes. J. Sports Sci. Med.