The practice of inducing an alkalotic shift in acid-base balance to improve performance before supramaximal exercise has been widespread in elite sport for nearly 30 years (10,11,13). The most common method reported in the scientific literature, and perhaps the most effective, is via the ingestion of sodium bicarbonate (NaHCO3) (13). Ingesting an amount of 0.3 g·kg−1 body weight (BW) of this buffer will augment the concentration of the body's primary blood-buffering source, that is, bicarbonate (
), by approximately 5–6 mmol·L−1 (16,17,19). This increase in the concentration of blood
is considered to be sufficient to provide a supplemental blood-buffering pool, which in turn may enhance an individual's capacity to combat excessive proton (H+) production during prolonged high-intensity exercise. Improving the capacity for H+ removal from the contracting skeletal muscle cell corresponds with the maintenance of intracellular function, specifically adenosine triphosphate resynthesis and Ca2+ resequestering within the sarcoplasmic reticulum (1,20).
In practice, metabolic alkalosis via NaHCO3 ingestion is most commonly achieved via the oral administration of the buffer, either through encapsulation or mixing the substance in a palatable liquid (e.g., sport drinks, cordial, flat cola) (3,19). Often, however, inducing such dramatic alterations in acid-base balance is not without consequence. The physiochemical response to relatively large quantities of NaHCO3 entering the stomach results in Na+ absorption in the small intestine and increased plasma Na+ levels (6). This exchange of Na+ leads to an increase in the stomach PCO2 and diffusion of CO2 into plasma and increases the already acidic environment within the stomach (6). This temporary imbalance often results in unfavorable side effects such as stomach bloating, nausea, and diarrhea. The incidence of these side effects appears to vary widely between individuals, ranging from mild discomfort to extreme cases where exercise performance may be affected. For example, dosages of 0.3 g·kg−1 BW ingested as a single bolus have been reported to cause gastrointestinal (GI) disturbances in some individuals (12,16), whereas in 1992, McNaughton also reported that all subjects experienced side effects at dosages of 0.4 g·kg−1 BW and 0.5 g·kg−1 BW (12). Consideration of this issue is essential when preparing an athlete for competition under supplemental buffering conditions, because GI disturbances may reduce an individual's perceived physical and mental readiness to perform, and any potential ergogenic benefit of NaHCO3 may be diminished if an athlete is preoccupied or unfocused. With respect to the aforereferenced studies, documentation of the most common side effects associated with NaHCO3 ingestion has been sporadic in the literature (2,3,11,13), and a more objective representation of the relationship between GI discomfort, the loading and dosage sequence, and performance is needed.
One possible approach for reducing the likelihood of GI discomfort having a negative impact on performance might be to either prolong the ingestion time period or increase the time between ingestion and exercise. This practice is not evident in the literature, as a recent review of the NaHCO3 supplementation literature has indicated that a majority of studies (15 out of 16 since the year 2000) had ingestion protocols that required consumption 60–90 minutes before exercise (13). Within these studies, the authors commonly cited original work in this area that reported on the efficacy of various loading doses (8,12). For instance, Horswill et al. reported that dosages of ≤0.2 g·kg−1 BW were ineffective for improving sprint performance, whereas McNaughton reported that with dosages of 0.1, 0.2, 0.3, 0.4, and 0.5 g·kg−1 BW, only 0.1 g·kg−1 BW did not significantly enhance sprint performance (8,12). Both of these studies used 60 minutes postingestion as the commencing point for exercise and justified this by indicating that peak blood buffering occurred at this time (8,12). As a result, researchers have consistently presumed that commencing exercise at peak levels of blood buffering is of greater importance in terms of performance outcomes than delaying exercise because of any GI disturbances that may be present. However, to our knowledge, there is no evidence in the literature that suggests that performance is optimized at peak blood
concentrations after supplementation when compared with other time points throughout the loading period.
In light of this gap in the literature, we documented a sustained elevation in blood
after both 0.2 and 0.3 g·kg−1 BW for approximately 4 hours postingestion under resting conditions (19). Although slightly lower than peak levels (∼1 mmol·L−1), these levels were still 5–6 mmol·L−1 above preingestion values during hours 2–4 and well within the performance-enhancing buffering ranges reported by Matson and Tran (11). However, no evidence was provided to demonstrate that performance would still be enhanced 2–4 hours post NaHCO3 ingestion. Moreover, it is reasonable to believe that because symptoms of GI discomfort peak 60–90 minutes post NaHCO3 ingestion, a longer time period (i.e., 2–4 hours) between ingestion and physical performance may minimize GI discomfort while maintaining performance gains. As such, the primary aim of this study was to determine the influence of supplementation timing (60, 120, 180 minutes before) on repeated sprint ability (RSA) after a standard NaHCO3 load (0.3 g·kg−1·BW). A secondary aim was to profile both blood-buffering capacity and GI discomfort over these time periods to determine whether any relationship exists between the magnitude of GI discomfort, blood-buffering levels, and RSA. It was hypothesized that (a) RSA would be sustained regardless of the ingestion timing period and (b) peaks in blood-buffering capacity would correspond with maximal GI discomfort.
Experimental Approach to the Problem
The study used a randomized (counterbalanced), repeated measures design in which subjects reported to the temperature-controlled laboratory (19–23°C) at the same time of the day between 0900 and 1200 on 4 occasions, each separated by 1 week. The subjects were advised to limit strenuous exercise for 24 hours before testing and to attend each trial adequately hydrated (e.g., a minimum water consumption of 500 ml approximately 3 hours before the trial was recommended to all the subjects). On the initial visit, the subjects undertook a full familiarization session with the nonmotorized treadmill (NMT) and exercise protocol following the methods of Tong and coworkers (9,21). The subjects were also provided instruction on the subjective interpretation of GI discomfort using a visual analog scale (VAS). The VAS questionnaire has been used previously in the NaHCO3 literature (2) and is a commonly accepted tool for documenting subjective pain perception and discomfort (15). The 3 trial conditions (60 minutes NaHCO3 ingestion time [H1], 120 minutes NaHCO3 ingestion time [H2], and 180 minutes NaHCO3 ingestion time [H3]) were implemented in a randomized manner and each separated by 1 week. Because of the varying time ratios (ingestion sequence [60, 120, or 180 minutes] to commencement of exercise) between the 3 conditions, blinding the subjects was not possible. Additionally, including another 3 placebo trials to correspond with the 3 NaHCO3 conditions would have further confounded the repeated measures design with such a small sample size (n = 8 was determined sufficient a priori [>0.8] using previously published alkalotic changes in blood buffering after NaHCO3 supplementation [5,22]). Because the primary aim of the study was to distinguish whether different NaHCO3 loading protocols affected performance and not the efficacy of NaHCO3 ingestion, this methodological approach was chosen to best match the study objectives. For all trials, the buffer solution (0.3 g·kg−1 BW) was dispensed into gelatine capsules and consumed with 750 ml of water over a 15-minute period.
Eight recreationally active and healthy male subjects (mean ± SD: height, 180 ± 9 cm; body mass, 76.2 ± 9.1 kg; age, 22 ± 2 years) volunteered to take part in the study after being informed verbally and in writing as to the nature and risks associated with the study. The subjects were free of any cardiac or metabolic diseases, involved in regular aerobic training 3 times per week (∼4–6 hours total), did not smoke, and refrained from supplementation of all kinds (i.e., vitamins, ergogenic aids, etc.) during the testing period. All the subjects signed an informed consent, and the study was approved by the Departmental Human Ethics Committee and following the principles outlined by the Declaration of Helsinki.
Upon arriving at the laboratory for each trial, whole blood (preingestion sample) was collected in a balanced heparin 200-μL blood gas capillary tube for immediate analysis of acid-base balance (pH, bicarbonate [
], base excess [BE]) using a clinical blood gas analyser (OMNI 4 Blood Gas Analyser, Roche Diagnostics Ltd., Sussex, United Kingdom). All measurements were performed in duplicate, and the range of intraclass correlation coefficients (ICCs) were 0.85–0.97, p < 0.01 for all dependent blood variables, respectively. After the preingestion sample was obtained, the subjects were allowed 15 minutes to consume the gelatine capsules and were then required to sit quietly in the laboratory until their performance trial (e.g., either 60, 120, or 180 minutes).
During the ingestion period, the subjects were asked to rate any GI discomfort they were experiencing using the VAS every 30 minutes until the commencement of exercise. The symptoms provided to each participant consisted of the following: nausea, flatulence, stomach cramping, stomach bloating, stomach ache, belching, vomiting, bowel urgency, and diarrhea (2). The VASs consisted of 9 separate 100-mm scales, anchored at each end with ‘no symptom’ on the left hand and ‘severe symptom’ on the right hand. The subjects were instructed to indicate with a vertical mark the severity of each of the 9 symptoms presented on the scales.
Once the ingestion period concluded, a preexercise capillary sample was obtained, and the subjects completed a standardized warm-up consisting of a 10-minute series of short, high-intensity bouts on a motorized treadmill (Ergo ELG 55, Woodway GmbH, Weil am rhein, Germany) and light, active stretching. The performance trials required a standing start for ten, 10-second maximal efforts on an NMT (Woodway Force, Woodway GmbH, Weil am rhein, Germany). Each 10-second maximal effort was separated by 40 seconds of walking at 5 km·h−1, then 10-second standing in preparation for the next maximal effort (work-to-rest ratio 5:1). The performance data were acquired from the treadmill using a customized interface (XPV7 PCB, Interface, Fitness Technologies, Adelaide, Australia) and analyzed at 20 Hz using Force 3 Software (Innervations, Joondalup, Australia). A priori reliability measures for power and speed outputs on the NMT provided a range of ICCs between 0.88 and 0.99, p < 0.01, respectively. Upon completing the protocol, a final 1-minute postexercise capillary blood sample was obtained.
All statistical analyses were completed using Statistica Software, Tulsa, OK, USA, and GraphPad Prism 5.0, San Diego, CA, USA. A 2-way analysis of variance (ANOVA) for repeated measures (condition × time) was used to analyze the differences in blood acid-base balance (pH,
, BE). The performance (peak speed [PS] and average speed [AS] in meters per second, peak power [PP] and average power [AP] in watts, and total distance [TD] covered in meters) and GI discomfort (incidence and severity) data for each trial were analyzed using a 1-way ANOVA for repeated measures. The severity data were not normally distributed and thus analyzed using the Friedman statistic and where significant Dunn's posttest for comparison of the sum of ranks between groups. In all other instances, Tukey's honestly significant difference was performed in the event of a significant F ratio. Two-tailed statistical significance was accepted at p < 0.05. When significant differences are stated, the mean difference plus the 95% confidence interval (CI) of the mean difference are provided. The Cohen effect size (d) is also provided, which was calculated and interpreted as recommended by Hopkins (7). Briefly, Hopkins suggests that the effect size be interpreted as 0–0.19 (trivial), 0.20–0.59 (small), 0.60–1.19 (moderate), 1.20–1.99 (large), and 2.0 + (very large) (7).
Blood Acid-Base Response
Table 1 corresponds to the mean ± SD values for pH,
, and BE measured in the blood during each of the 3 experimental trials before NaHCO3 ingestion (Pre-Ing), before exercise (Pre-Ex), and 1 minute postexercise (Post-Ex). There were no significant interactions (p > 0.80) or main effects for condition (p > 0.74) for any of the acid-base variables (pH,
, BE); however, there was a main effect for time for all variables (p < 0.0001), respectively. At Pre-Ex time points, buffering capacity was significantly elevated from Pre-Ing as indicated by changes in pH (mean difference = 0.04; 95%CI = 0.08–0.01; d = 2.65; p < 0.05),
(mean difference = 4.8 mmol·L−1; 95%CI = 5.9–3.7; d = 3.86; p < 0.001), and BE (mean difference = 5.6 mEq·L−1; 95%CI = 7.1–4.1; d = 3.68; p < 0.001). As expected, Post-Ex acid-base balance was significantly depleted compared with Pre-Ex (pH: mean difference = 0.30; 95%CI = 0.34–0.27; d = 4.83; p < 0.001;
: mean difference = 18.2 mmol·L−1; 95%CI = 19.3–17.1; d = 9.48; p < 0.001; BE: mean difference = 23.1 mEq·L−1; 95%CI = 24.6–21.6; d = 8.99; p < 0.001).
There was no difference between trials for either PS (H1: 5.47 ± 0.45 m·s−1; H2: 5.54 ± 0.73 m·s−1; H3: 5.62 ± 0.65 m·s−1; p = 0.31) or PP (H1: 984 ± 208 W; H2: 916 ± 131 W; H1: 987 ± 228 W; p = 0.18). Although there was no significant interaction or difference between conditions (AS: p > 0.22; AP: p > 0.86), there was a decline over the 10 sprints in both AS (largest mean difference = 0.12; largest 95%CI = 0.01–0.21; d range = 0.3–0.5; p < 0.05; Figure 1) and AP (largest mean difference = 44; largest 95%CI = 0.9–80.1; d range = 0.3–0.5; p < 0.05; Figure 1). Similar to PS and PP, the TD covered over the 10 sprints for the 3 trials was not different (H1: 456 ± 35 m; H2: 448 ± 32 m; H3: 448 ± 32 m; p = 0.22).
The incidence of GI discomfort was significantly higher than the Pre-Ing values at all time points with the exception of 180 minutes (largest mean difference = 4.8; largest 95%CI = 0.3–7.3; d range = 1.6–2.1; p < 0.05; Figure 2). Although the Friedman test indicated a significant main effect for time (p < 0.001), after decomposition, the only difference appeared between 90 and 180 minutes (p < 0.01; Figure 2).
The primary aim of this investigation was to determine whether ingesting a standard 0.3 g·kg−1 BW of NaHCO3 at varying time points would influence RSA. The novel findings of this study were that (a) performance during repeated bouts of high-intensity exercise is not different when ingesting 0.3 g·kg−1·BW of NaHCO3 between 60 and 180 minutes before exercise; (b) metabolic alkalosis (as defined by an elevated blood [
] of ∼5 mmol·L−1) is maintained and not statistically different between 60 and 180 minutes postingestion; and (c) the incidence and severity of GI discomfort are reduced at 180 minutes compared with that at all previous time points postingestion, without compromising acid-base balance or performance. The finding that GI discomfort is reduced at 180 minutes postingestion with similar physical performance outcomes is an important consideration when recommending NaHCO3 as an ergogenic substance to athletes.
The proposed relationship between GI discomfort, NaHCO3 supplementation, and performance is arguably a deciding factor when considering the use of this buffer in a sporting context. The importance of understanding this association may be evidenced by the recent increase in NaHCO3 research related to this very question (2,3,16). At present, however, only the study of Carr et al. has gone beyond simply reporting the symptom-performance relationship to propose alternative loading strategies (e.g., consumption of carbohydrates in conjunction with NaHCO3) (3). In this study, instead of attempting to attenuate symptoms by introducing alternative dietary regimens, we delayed the onset of exercise beyond the typical 60–90 minutes ingestion time sequence (13). Our premise was based on the evidence that blood buffering remains elevated to ergogenic levels after NaHCO3 ingestion of 0.3 g·kg−1 BW for a period of 4 hours postingestion (19). Indeed, Pre-Ex blood-buffering levels in this study (∼4.8 mmol·L−1; 95%CI = 5.9–3.7) were within these predefined ergogenic ranges regardless of the Pre-Ex time point (60, 120, or 180 minutes) (11). If the approximate 5 mmol·L−1 increases in
are sufficient for invoking an ergogenic benefit, then this might also explain the similar fatigue pattern observed during the repeated sprint sequence (Figure 1).
The GI discomfort did not seem to have had a direct impact on RSA during this study. If the GI discomfort experienced by the subjects were to negatively impact the performance, then we would have expected to see an improvement in RSA as ingestion time was prolonged, particularly in the 180-minute condition in which symptoms had become negligible. Alternatively, reduced GI discomfort at 180 minute postingestion with no difference in physical performance subsequent to supplementation is a positive result for the recommendation of NaHCO3 supplementation to trainers and athletes who may otherwise be averse to performing strenuous exercise while symptoms are present. The GI discomfort data must be interpreted with caution, however, because there was a large degree of variability between subjects (as indicated by the large SDs in Figure 2). This idea that NaHCO3 supplementation causes differing levels of GI discomfort may also coincide with the often-mentioned ‘responders’ vs. ‘nonresponders’ issue in terms of performance (13,16,18). Why the temporary imbalance of carbon dioxide (CO2) levels in the stomach induced by the NaHCO3 ingestion causes discomfort in some individuals and not in others remains to be determined (6). However, this issue further illustrates the need to determine an optimal NaHCO3 loading sequence. Although it did not affect our participant population of recreationally trained athletes, this might not be the case for all populations (e.g., elite athletes), particularly when considering this application before competition where mental preparation may be just as influential to performance outcomes as a physiologically enhanced blood-buffering state (4,14).
In conclusion, performance during repeated bouts of high-intensity exercise was not different when ingesting 0.3 g·kg−1 BW of NaHCO3 between 60 and 180 minutes before exercise. This might have been a direct result of metabolic alkalosis remaining significantly elevated for up to 180 minutes postingestion. Finally, GI discomfort, even when elevated from 30 to 150 minutes postingestion, did not negatively impact performance or compromise the acid-base balance.
It is essential that both athletes and coaches define the energy requirements of their event before including alkalinizing agents into training and competition. For example, it may be appropriate to apply such practice to high-intensity events (e.g., 400 m up to middle distance) that induce large intracellular and extracellular H+ accumulation but not within more endurance-based activity (e.g., 4-hour endurance ride). Considering the optimal loading sequence will require a trial-and-error approach; however, as indicated in both this study (performance related) and other NaHCO3 loading studies (4,13,16,17), there appears to be approximately 3–4 hours after the initial supplementation where the ergogenic benefit will remain present. Delaying the onset of exercise will also minimize the likelihood of GI discomfort (Figure 2) and yet will still provide optimal blood-buffering potential.
Athletes and practitioners should approach this supplement with caution; however, because there is a large degree of within-subject variability in terms of responsiveness (Figure 1). We would advocate experimenting with different loading sequences and strategies before use in competition. We have also recently illustrated that, although not detrimental, it is very common to observe a ‘responder,’ ‘nonresponder’ phenomena (4). One reason for this may be that there are many different factors that can contribute to performance (and in this case fatigue); certain athletes may be more susceptible to decreases in pH (or becoming acidic) than are others (14). Another possible reason is the issue of ingestion timing. Getting the balance right between maximizing the extracellular buffering pool while minimizing any potential GI side effects is crucial to determining whether NaHCO3 can become an effective addition to an athlete's training or competition schedule.
The authors wish to thank the volunteers who participated in the study. The authors have no undisclosed professional relationships with any companies or manufacturers that would benefit them from the results of this study and therefore no conflicts of interest. There was no grant support for this study. The results of this investigation do not constitute endorsement of the product by the authors or the National Strength and Conditioning Association.
1. Bruton JD, Lannergren J, Westerblad H. Mechanisms underlying the slow recovery of force after fatigue: Importance of intracellular calcium. Acta Physiol Scand 162: 285–293, 1998.
2. Cameron SL, McLay-Cooke RT, Brown RC, Gray AR, Fairbairn KA. Increased blood pH but not performance with sodium bicarbonate supplementation in elite rugby union players. Int Sport Nutr Exerc Metab 20: 307–321, 2010.
3. Carr AJ, Slater GJ, Gore CJ, Dawson B, Burke LM. Effect of sodium bicarbonate on [HCO3−
], pH, and gastrointestinal symptoms. Int J Sport Nutr Exerc Metab 21: 189–194, 2011.
4. Dugdale JR, Eklund RC, Gordon S. Expected and unexpected stressors in major international competition: Appraisal, coping, and performance. Sport Psychol 16: 20–33, 2002.
5. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: A flexible statistical power analysis program for the social, behavioural, and biomedical sciences. Behav Res Methods Instrum Comput 39: 175–191, 2007.
6. Heigenhauser GJF. Ergogenics enhancement of performance in exercise and sport: Bicarbonate loading. In: Prospectives in Exercise Science and Sports Medicine (Vol. 4). Lamb D. R., Williams M. H., eds. Carmel, IN: Cooper Publishing Group LLC, 1991. pp. 183–212.
7. Hopkins WG, Batterham AM, Marshall SW. Progressive statistics. Sportscience 13: 55–70, 2009.
8. Horswill CA, Costill DL, Fink WJ, Flynn MG, Kirwan JP, Mitchell JB, Houmard JA. Influence of sodium bicarbonate on sprint performance: Relationship to dosage. Med Sci Sports Exerc 20: 566–569, 1998.
9. Hughes MG, Doherty M, Tong RJ, Reilly T, Cable NT. Reliability of repeated sprint exercise in non-motorised treadmill ergometry. Int J Sports Med 27: 900–904, 2006.
10. Linderman JK, Gosselink KL. The effects of sodium bicarbonate ingestion on exercise performance. Sports Med 18: 75–80, 1994.
11. Matson LG, Tran ZV. Effects of sodium bicarbonate ingestion on anaerobic performance: A meta-analytic review. Int J Sport Nutr 3: 2–28, 1993.
12. McNaughton LR. Bicarbonate ingestion: Effects of dosage on 60 s cycle ergometry. J Sports Sci 10: 415–423, 1992.
13. McNaughton LR, Siegler J, Midgley A. Ergogenic effects of sodium bicarbonate. Curr Sports Med Rep 7: 230–236, 2008.
14. Mellalieu SD, Neil R, Hanton S, Fletcher D. Competition stress in sport performers: stressors experienced in the competition environment. J Sports Sci 27: 729–744, 2009.
15. Price DP, McGrath PA, Rafil A, Buckingham B. The validation of visual analogue scales as ratio scale measures for chronic and experimental pain. Pain 17: 45–56, 1983.
16. Price MJ, Singh M. Time course of blood bicarbonate and pH three hours after sodium bicarbonate ingestion. Int J Sports Physiol Perf 3: 240–242, 2008.
17. Renfree A. The time course for changes in plasma [H+
] after sodium bicarbonate ingestion. Int J Sports Physiol Perf 2: 323–326, 2007.
18. Siegler JC, Gleadall-Siddall DO. Sodium bicarbonate ingestion and repeated swim sprint performance. J Strength Cond Res 24: 3105–3111, 2010.
19. Siegler JC, Midgley AW, Polman RC, Lever R. Effects of various sodium bicarbonate loading protocols on the time-dependent extracellular buffering profile. J Strength Cond Res 24: 2551–2557, 2010.
20. Stephenson DG, Lamb GD, Stephenson GM. Events of the excitation-contraction-relaxation (E-C-R) cycle in fast- and slow-twitch mammalian muscle fibres relevant to muscle fatigue. Acta Physiol Scand 162: 229–245, 1998.
21. Tong RJ, Bell W, Ball G, Winter EM. Reliability of power output measurements during repeated treadmill sprinting in rugby players. J Sports Sci 19: 289–297, 2001.
22. Vanhatalo A, McNaughton LR, Siegler J, Jones AM. Effect of induced alkalosis on the power-duration relationship for ‘all-out’ exercise. Med Sci Sports Exerc 42: 563–570, 2010.