Attenuating localized skeletal muscle fatigue that occurs during high-intensity exercise depends largely upon the body's preexisting metabolic buffering capacity (8,9). During such efforts, it was originally proposed that fatigue was induced by a progressive increase in proton (H+) concentration within the exercising muscle. Specifically, research in the mid-1990s proposed links between excessive H+ production and the inhibition of the rate-limiting enzyme glycogen phosphorylase (29,30). Recently, however, it has been suggested that the increase in H+ accumulation observed during prolonged high-intensity exercise above the metabolic buffering capacity may not directly influence skeletal muscle contraction as originally proposed, but rather have an adverse affect on calcium (Ca2+) release and resequestering in the sarcoplasmic reticulum (1,3,31). Regardless of whether the influence is direct or indirect, it may still be assumed that prolonging the maintenance of acid-base balance during high-intensity exercise, specifically in those events requiring either continuous supramaximal efforts or intermittent, high-intensity efforts, will ultimately improve performance by maintaining glycolytic flux (18,29).
These presupposed links between H+ accumulation and fatigue have provided continued justification for research into acid-base manipulation before exercise. Beginning in the late 1970s (7), researchers were documenting performance benefits by inducing a pre-exercise metabolic alkalosis with supplementation in the form of an exogenous buffer. Research into this area, most notably sodium bicarbonate (NaHCO3) supplementation, has become widespread, yet the efficacy of such practice remains equivocal (10,12,15). We have recently detailed potential reasons for discrepant findings in the literature, and to briefly summarize, these reasons may be linked not with the actual practice of loading NaHCO3, but rather the loading regimens, exercise requirements and training status of the participants (15). In addition, a majority of NaHCO3 research studies have been conducted on stationary cycle ergometers in controlled laboratory settings. Although this provides more internal control, the ecological validity and practical application are limited. Determining the practical benefits of NaHCO3 loading with other sports is warranted, as we and others have shown improvements in sport-specific performance in field-based settings (2,24).
One of the most difficult sports to quantify improvements through NaHCO3 loading may be that of swimming (as evidenced by the limited NaHCO3 research in the area) (4,11,19). The performance requirements are physiologically unique, and unlike cycling or running, also rely heavily on technical competencies (e.g., stroke efficiency ), which may attenuate the ergogenic potential of an induced pre-exercise alkalosis. An extensive literature search (Medline, PubMed, and SPORTDiscus) conducted before this study resulted in only 3 studies since 1988 that solely used NaHCO3 loading to enhance swim performance (4,11,19). All 3 studies reported an ergogenic benefit; however, direct comparison between these studies is problematic as 1 used a single effort (200 m) (11), and the other 2 used repeated intervals (between 100 and 200 yd) with recovery spanning from 2 to 20 minutes, respectively (4,19). These recovery time frames are generally longer than most repeated sprint studies, where smaller work-to-rest ratios are more likely to induce a greater degree of metabolic acidosis (15). Additionally, these studies also all incorporated performance distances of greater than one length of the pool. This approach may not only be suitable for elite-level swimmers but may also confound any ergogenic benefit from NaHCO3 for other populations (e.g., the use of swimming as an alternative training stimulus, non-weight bearing activity or rehabilitation procedure) because it requires the additional technical component of turning. One of these studies also employed different swimming strokes, which may have changed the total metabolic load requirement for each performance variable and limited the potential accuracy in quantifying the efficacy of NaHCO3 loading (19). Finally, other studies in this domain have failed to report pre and postswim acid-base status, have introduced lower than conventional NaHCO3 doses, or have combined the buffer with another supplement (16,19,21,26). Therefore, the purpose of this study was to observe the ergogenic potential and acid-base status of a standard 0.3 g·kg−1 NaHCO3 dose in competitive swimmers using a repeated swim sprint design that eliminated the technical component of turning.
Experimental Approach to the Problem
On a separate day 1 week before any testing, participants undertook a full familiarization session with the test protocol and were instructed as to the importance of nutritional intake and asked to control, record, and duplicate their food intake for all trials (collected and reviewed but not presented). The 2 trial conditions (NaHCO3 [BICARB] and NaCl placebo [PLAC]) were implemented in a randomized (counterbalanced), single blind manner, each separated by 1 week. Additionally, the subjects were paired by their coach according to swimming ability to provide a competitive environment during the sprint trials.
On each testing day, the participants reported to the laboratory at 14:00 to consume their prescribed drink (BICARB or PLAC) 4 hours postprandial. For the NaHCO3 trial, the buffer solution (0.3 g·kg−1) was diluted into 500 ml of a low calorie (9 kcals [1.2 g carbohydrate, 0.1 g protein]), flavored drink and consumed over a 15-minute period. For the placebo trials, 0.045 g·kg−1 of NaCl was substituted for NaHCO3. This ingestion protocol has been the most commonly reported in previous research (15,20). Additionally, we commenced exercise 2.5 hours postingestion, as we have recently documented that introducing the ingestion period within this time frame eliminates the commonly reported side effects associated with NaHCO3 while still maximizing the buffers potential (25).
Six male (181.2 ± 7.2 cm; 80.3 ± 11.9 kg; 50.8 ± 5.5 ml·kg−1·min−1O2max) and 8 female (168.8 ± 5.6 cm; 75.3 ± 10.1 kg; 38.8 ± 2.6 ml·kg−1·min−1O2max) members of a university swimming club (n = 14) 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 swimmers consisted of a mixed competitive ability and race history; however, all swimmers had a minimum of 5 years of racing experience. All swimmers were in the middle of their competitive season at the time of testing, training 3 times per week (ca. 7,500 m per week). In the 2 weeks leading up to the testing, the training was consistent (i.e., there was no change in the periodization program and within a mesocycle ), and there was nothing new or novel introduced that may have disrupted the training stimulus (i.e., changed the muscle buffering capacity). Additionally, the testing was only separated by 1 week (within a microcycle), with the training the week prior matched so that no additional training stimulus was introduced (28). All participants signed informed consent, and the study was approved by the Departmental Human Ethics Committee and following the principles outlined in the Declaration of Helsinki.
The sprint trials were administered in a 25-m pool, 2.5 hours postingestion. Initially, each swimmer completed a standard warm-up of mixed swimming drills (200-m front crawl, 200 m as 50-m ‘swim-kick-pull-swim’ and 200 m as 50-m individual medley). The predetermined swimming pairs were then assigned adjacent lanes and subsequently completed 8 25-m front crawl maximal effort sprints. Each sprint was individually timed using a standard stopwatch (the same investigator timed the same swimmer for both of the trial conditions) and recorded. Although hand-held timing has been shown to underestimate times when compared to electronic timing, the mean differences are consistent and well within a half second (−0.31 ± 0.07 seconds) with good reliability (13). After each 25-m sprint, the swimmers were allowed 5 seconds relative recovery before the next start (implemented to eliminate variation in turning ability and technique).
Blood Gas Analysis
The preingestion sample was collected immediately before beverage consumption in the laboratory and subsequently analyzed. The pre and postswim samples were collected at the poolside and stored on ice for 20 minutes until analyzed upon return to the laboratory. All blood samples were obtained aseptically via capillary finger sticks. Whole blood was collected in a balanced heparin 200 μl blood gas capillary tube for analysis of acid-base balance (pH, bicarbonate [HCO3 −], base excess [BE]), lactate (BLa) and strong ions (Na+, K+) using a clinical blood gas analyzer (OMNI 4 Blood Gas Analyzer, Roche Diagnostics Ltd, Sussex, United Kingdom). All measurements were done in duplicate, and the range of intraclass correlation coefficients were 0.85-0.97, p < 0.01 for all dependent variables, respectively.
Normality of data was checked using Q-Q plots and deemed plausible in each instance. Central tendency and dispersion of the sample data were described using the mean and SD. The differences between conditions for total swim times were analyzed using a paired t-test. Blood acid-base (pH, HCO3 −, BE), BLa and strong ions (Na+ and K+) were analyzed using 2-way (condition × time) analysis of variance for repeated measures. Post hoc analysis was conducted using Fisher's Least Significant Difference (LSD). Two-tailed significance was accepted at p < 0.05. When significant differences are stated, the mean difference plus the 95% confidence interval (95% CI) of the mean difference are provided, along with the Cohen effect size (d), which were calculated and interpreted as recommended by Hopkins et al. (5). Statistical analyses were completed using Statistica Software v.6 (Tulsa, OK, USA) and GraphPad Prism 4.0 (San Diego, CA, USA).
Total swim time was significantly different between conditions (p = 0.04), with the BICARB condition resulting in a 2% decrease in total swim time compared to the PLAC condition (159.4 ± 25.4 vs. 163.2 ± 25.6 seconds; mean difference = 4.4 seconds; 95% CI = 8.7-0.1; d = 0.15; Figures 1 and 3).
Blood Acid-Base and Lactate Response
Mean ± SD blood acid-base data are presented in Table 1. There were significant condition × time interaction effects for pH (F = 17.2; p < 0.001), HCO3 − (F = 57.2; p < 0.001), and BE (F = 49.5; p < 0.001). There were no differences between conditions preingestion, but elevated blood buffering potential and metabolic alkalosis were evident both pre and postswim (post hoc differences are depicted in Table 1). Significant main effects were also observed for the condition for pH (F = 84.9; p < 0.001), HCO3 − (F = 98.5; p < 0.001), and BE (F = 104.8; p < 0.001). The BICARB condition resulted in a significantly higher blood buffering potential compared to the PLAC condition for all 3 variables (pH: mean difference = 0.04; 95% CI = 0.06-0.03; d = 0.41; HCO3 −: mean difference = 2.8 mmol·L−1; 95% CI = 3.8-1.7; d = 0.55; BE: mean difference = 3.3 meq·L−1; 95% CI = 4.6-2.1; d = 0.51). Finally, there were also significant main effects for time for pH (F = 182.4; p < 0.001), HCO3 − (F = 331.3; p < 0.001), and BE (F = 233.1; p < 0.001). Again, blood alkalosis was evident preswim compared to preingestion for pH, HCO3 −, and BE (pH: mean difference = 0.04; 95% CI = 0.07-0.001; p = 0.044; d = 1.29; HCO3 −: mean difference = 2.7 mmol·L−1; 95% CI = 4.2-1.1, p = 0.001; d = 1.18; BE: mean difference = 2.7 meq·L−1; 95% CI = 5.1-0.3, p = 0.02; d = 1.13) and preingestion to postswim (pH: mean difference = 0.2; 95% CI = 0.2-0.1, p < 0.001; d = 3.17; HCO3 −: mean difference = 10.1 mmol·L−1; 95% CI = 11.6-8.5, p < 0.001; d = 4.93; BE: mean difference = 13.7 meq·L−1; 95% CI = 16.1-11.3, p < 0.001; d = 4.42). Preswim values were also elevated compared to postswim for all variables (pH: mean difference = 0.2; 95% CI = 0.25-0.2, p < 0.001; d = 3.58; HCO3 −: mean difference = 12.7 mmol·L−1; 95% CI = 14.3-11.2, p < 0.001; d = 4.32; BE: mean difference = 16.5 meq·L−1; 95% CI = 18.9-14.1, p < 0.001; d = 4.24).
A significant condition × time interaction was evident for BLa (F = 17.8; p < 0.001) (post hoc differences are depicted in Figure 2). Additionally, significant main effects were observed for BLa for condition (F = 19.8; p = 0.001), with the BICARB condition resulting in higher overall BLa values (mean difference = 1.0 mmol·L−1; 95% CI = 2.0-0.1; d = 0.13). Significant main effects were also observed for time (F = 184.1; p < 0.001), with postswim values being higher than both preingestion (mean difference = 14.3 mmol·L−1; 95% CI = 16.9-11.8, p < 0.001; d = 4.97) and preswim (mean difference = 14.4 mmol·L−1; 95% CI = 17.0-11.9, p < 0.001; d = 4.94).
Strong Ion Difference
Mean ± SD strong ion difference data are presented in Table 2. There were significant condition × time interaction effects for K+ (F = 13.9; p < 0.001) but not Na+ (F = 1.6; p = 0.23). There were no differences between conditions for K+ for preingestion, but both pre and postswim were different for each, respectively (post hoc differences are depicted in Table 2). Significant main effects were observed for condition for Na+ (F = 10.8; p = 0.008) and K+ (F = 10.5; p = 0.009). The PLAC condition resulted in lower Na+ levels (mean difference = −1.7 mmol·L−1; 95% CI = −3.6-0.3; d = 0.57), whereas K+ (mean difference = 0.3 mmol·L−1; 95% CI = 0.8-0.1; d = 0.2) was elevated compared to the BICARB condition for both variables. Finally, there were also significant main effects for time for Na+ (F = 20.8; p < 0.001) and K+ (F = 9.7; p = 0.001). Postswim Na+ was elevated compared to both preingestion (mean difference = 3.5 mmol·L−1; 95% CI = 5.2-1.8; d = 1.74) and preswim (mean difference = 2.8 mmol·L−1; 95% CI = 4.5-1.1; d = 1.23). Postswim K+ was also significantly decreased compared to preingestion values (mean difference = −0.4 mmol·L−1; 95% CI = −0.1 to −0.7; d = 1.02).
The aim of the present study was to determine the influence of NaHCO3 supplementation on repeated sprint swim performance in competitive, nonelite swimmers. The main finding of the study was that 0.3 g·kg−1 NaHCO3 administered 2.5 hours before competition improved total swim time in 8 repeated 25-m sprints. Ingestion of NaHCO3 also resulted in an elevated blood buffering potential before the swim, with that elevation being sustained throughout the 8 sprints. In addition, significant whole blood changes in strong ion concentrations were evident, as extracellular K+ was altered by ingesting the buffer solution.
As mentioned previously, accurately determining the influence of any intervention on swimming performance is made difficult by the inherent technical component of the sport (11). Of the limited number of published swim performance-related research papers, those that do exist almost exclusively have used high to elite-level swimmers (4,11,19). However, even these studies have reported discrepant findings, most likely because of the variation in methodology. For example, 1 of the first studies to use NaHCO3 supplementation was reported by Gao et al. and used a repeated bout protocol consisting of 5, 100-yd self-paced freestyle swims each separated by a 2-minute rest (4). Using a randomized mixed design, the authors reported significant improvements in the mean swim velocity (m·s−1) in bouts 4 and 5. Contrasting this, Pierce et al. reported no ergogenic benefit over a 7 event period designed to mimic ‘actual swimming competition’ (19). However, Pierce et al. incorporated distances twice that of the Gao study (200 vs. 100 yds) and substantially longer rest periods (20 vs. 2 minutes). In addition, the loading dose in the Pierce study was 0.2 vs. 0.3 g·kg−1 in the Gao study. The most plausible explanation to the discrepant reports, however, is the time course of the elevated blood buffering capacity after a bolus NaHCO3 load (20). We have also recently documented different peak buffering times between these 2 doses, with 0.2 g·kg−1 NaHCO3 loads occurring markedly earlier (∼40 to 50 minutes) than 0.3 g·kg−1 (∼80 to 90 minutes) (25). Our findings would suggest that to maximize the ergogenic potential of 0.2 g·kg−1 NaHCO3, exercise should commence no later than 50 minutes postingestion (25).
Using a more traditional single-bout design, Lindh et al. recently demonstrated performance improvements in 200-m freestyle swim times after 0.3 g·kg−1 NaHCO3 1 hour before the event (11). The authors reported an overall swim time improvement of approximately 1.6%, with 8 of the 9 swimmers decreasing their 200-m times (11). We felt that this study design could potentially be used to compare the ergogenic potential of NaHCO3 loading in elite vs. competitive, nonelite swimmers, with the exception being the elimination of the turning component. By introducing a minimal turning period (5 seconds), however, we maintained the high metabolic demand needed to induce performance enhancement during NaHCO3 supplementation as 11 of the 14 swimmers improved their total swim time (Figure 1 and 3). Because we believe that variation in participant populations is another causal factor in the discrepant findings regarding NaHCO3 supplementation, this provided additional justification and rationale for the study. However, in light of this disparity in swimming ability, we still observed improvements in swimming performance similar to that reported in the Lindh study (1.6 vs. 2% in the current study).
The blood buffering profile was also similar between the 2 studies, with HCO3 − and pH being significantly elevated before the swim (Table 1). This is an important finding, as with the inherent differences between the 2 participant populations, it could be assumed that there would be differences between the groups muscle buffering capacity (8). Among others, Juel et al. have demonstrated upregulation of BLa/H+, Na+/H+ or monocarboxylic transporters in trained muscle (8,17,22), and although not measured in the current study, it could be assumed that the H+ transport capacity was enhanced in the Lindh cohort. However, this would not explain the similar performance improvements with the addition of the NaHCO3. Another potential explanation may be in the changes in whole-blood strong ion concentrations with respect to the BICARB condition (Table 2), specifically the attenuated release of K+ into the extracellular medium. This may suggest not only the upregulation of Na+/H+ and BLa/H+ (as indicated by the elevated BLa in the BICARB condition [Figure 2]) cotransporters but also an upregulation of other skeletal muscle pumps perhaps not influenced by training such as Na+/K+, Na+-K+-Cl−, or K+/H+ exchangers and Na+/K+ ATPase activity (23,27). Unfortunately, we were unable to compare K+ concentrations because this variable was not measured in the Lindh study. Future research into the potential regulatory mechanisms and influence on training in these skeletal muscle pumps during high-intensity exercise is warranted.
In conclusion, the present study assessed the ergogenic potential of NaHCO3 loading before repeated swim sprints in nonelite swimmers. The findings suggest that a standard loading dose (0.3 g·kg−1) 2.5 hours before exercise enhances the blood buffering potential and may positively influence the performance outcome in terms of total swim times. Future study into the potential differences between elite and nonelite athletes skeletal muscle buffering capacity may aid in determining the specific physiological mechanisms responsible for improving performance during NaHCO3 supplementation.
Although the research literature regarding the efficacy of NaHCO3 supplementation remains equivocal (15), the practice of ‘soda loading’ is widespread, particularly in elite sport. There are numerous potential explanations for the discrepant findings illustrated in the research; however, of more practical importance may be whether or not the practice of soda loading may hinder performance in any manner. As the literature suggests, there is a large degree of intraindividual variability in terms of performance enhancement when introducing metabolic alkalosis through buffering agents such as NaHCO3 or sodium citrate (15). Indeed, this variability is present in the current study as indicated by the performance data in Figure 3. However, what is also apparent in Figure 3 is that although the ingestion protocol used in this study did improve performance in 11 of 14 swimmers (cohen's d = 0.15; minimal effect), it also did not hinder their performance (confidence limits −0.28 to 0.00 seconds). We would argue that this information is of practical significance to coaches, athletes, and practitioners (regardless of level) because it can provide them with the confidence to experiment with exogenous buffers during training without the apprehension of the buffer negatively influencing the training session.
Another issue of concern for the practitioner that commonly arises when supplementing with NaHCO3 is that of gastrointestinal (GI) distress or other feelings such as bloating, cramping, or upset stomach. We have recently documented the blood acid-base kinetics using various loading strategies (25) in an attempt to determine the optimum loading sequence as it relates to elevated blood buffering while concurrently minimizing subject discomfort. Interestingly, we observed that a common dose of NaHCO3 (0.3 g·kg−1) elicits a significantly elevated blood buffering capacity for approximately 4 hours after ingestion. A quick review of the NaHCO3 literature, however, will reveal that most exercise protocols are introduced after 1-1 ½ hours postingestion (15). We believe that 1 reason for this is based on early work in the 1980s that looked at the effects of various NaHCO3 doses on performance (6,14). These authors observed a performance benefit when introducing doses of 0.2-0.3 g·kg−1, however, did not assess whether or not this effect was evident over a longer ingestion time period. Subsequent studies over the course of the next 2 decades have based their ingestion protocols on the initial early work of these authors. However, using this ingestion protocol, it is our experience that most subjects are still feeling the residual effects of the NaHCO3 in either the stomach or the GI tract, which we also believe may have an impact on their subsequent performance effort (25). This issue is especially important when introducing this practice on elite athletes, as anything that may detract from their mental focus and physical preparation, whether during training or competition, will not be looked upon favorably. After documenting the 4-hour elevation in blood buffering, we began to implement this delayed exercise strategy to a successful degree in recent studies (24). Thus, it is our recommendation that if implementing this practice, to minimize the potential negative impact of the side effects of NaHCO3 supplementation, the ingestion time should to coincide with a minimum of 2 hours before exercise. Finally, and again in reference to athletic performance, we also recommend that athletes experiment with their tolerance to different loading strategies before competition.
The author's would like to thank all of those associated with the Hull City Council and Beverley Road Baths for their cooperation and the use of the training facility. The authors have no undisclosed professional relationships with companies or manufacturers that would benefit from the results of this study. The results of this study do not constitute endorsement of the product by the authors or the National Strength and Conditioning Association (NSCA).
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Keywords:© 2010 National Strength and Conditioning Association
metabolic alkalosis; ergogenic aid; buffering potential