The time to peak blood bicarbonate (HCO3–), pH, and the strong ion difference (SID) following sodium bicarbonate (NaHCO3) ingestion in highly trained adolescent swimmers

Josh W. Newbury; Matthew Cole; Adam L. Kelly; Richard J. Chessor; S. Andy Sparks; Lars R. McNaughton; Lewis A. Gough

doi:10.1371/journal.pone.0248456

Abstract

The timing of sodium bicarbonate (NaHCO₃) supplementation has been suggested to be most optimal when coincided with a personal time that bicarbonate (HCO₃^–) or pH peaks in the blood following ingestion. However, the ergogenic mechanisms supporting this ingestion strategy are strongly contested. It is therefore plausible that NaHCO₃ may be ergogenic by causing beneficial shifts in the strong ion difference (SID), though the time course of this blood acid base balance variable is yet to be investigated. Twelve highly trained, adolescent swimmers (age: 15.9 ± 1.0 years, body mass: 65.3 ± 9.6 kg) consumed their typical pre-competition nutrition 1–3 hours before ingesting 0.3 g∙kg BM^-1 NaHCO₃ in gelatine capsules. Capillary blood samples were then taken during seated rest on nine occasions (0, 60, 75, 90, 105, 120, 135, 150, 165 min post-ingestion) to identify the time course changes in HCO₃^–, pH, and the SID. No significant differences were found in the time to peak of each blood measure (HCO₃^–: 130 ± 35 min, pH: 120 ± 38 min, SID: 98 ± 37 min; p = 0.08); however, a large effect size was calculated between time to peak HCO₃^– and the SID (g = 0.88). Considering that a difference between time to peak blood HCO₃^– and the SID was identified in adolescents, future research should compare the ergogenic effects of these two individualized NaHCO₃ ingestion strategies compared to a traditional, standardized approach.

Citation: Newbury JW, Cole M, Kelly AL, Chessor RJ, Sparks SA, McNaughton LR, et al. (2021) The time to peak blood bicarbonate (HCO₃^–), pH, and the strong ion difference (SID) following sodium bicarbonate (NaHCO₃) ingestion in highly trained adolescent swimmers. PLoS ONE 16(7): e0248456. https://doi.org/10.1371/journal.pone.0248456

Editor: Caroline Sunderland, Nottingham Trent University, UNITED KINGDOM

Received: February 25, 2021; Accepted: June 17, 2021; Published: July 1, 2021

Copyright: © 2021 Newbury et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: We have now uploaded the data set as a S1 Data.

Funding: RJC contributed to this research by providing peer review from the perspective of a world-class performance nutritionist. British Swimming as an organisation had no role within any aspect of this research project. All funding and consumables were provided by Birmingham City University, and all participants were volunteers from a local high-performance swimming team (City of Birmingham Swimming Club).

Competing interests: The commercial affiliation of RJC does not alter our adherence to PLOS ONE policies on sharing data and materials.

Introduction

Sodium bicarbonate (NaHCO₃) is recommended to athletes based upon strong evidence of a performance enhancing effect [1]. It is well acknowledged that NaHCO₃ ingestion enhances buffering capacity by increasing bicarbonate (HCO₃^–) and pH concentrations within the blood, although the magnitude of these increases is variable between individuals [2, 3]. Increasing blood alkalosis alters the pH gradient between the intracellular and extracellular compartments, subsequently leading to the upregulation of the lactate–hydrogen ion (H⁺) co-transporter to efflux acidic H⁺ from the active musculature and into circulation [4, 5]. During exercise, accelerating the removal of H⁺ is purported to offset fatigue since intracellular acidosis is associated with debilitating effects on the capacity to sustain muscle force production [6–10]. Specifically, cellular acidosis is suggested to inhibit muscle shortening velocity and cross-bridge cycling by reducing calcium ion (Ca²⁺) sensitivity and myosin ATPase activity [10, 11]. Further impairments of key glycolytic enzymes [12, 13] and the strong ion difference (SID) [7, 14, 15] are also associated with exacerbated H⁺ accumulation, hence limiting the available ATP substrates and action potentials necessary to maintain muscular contractions, respectively. However, each of these fatiguing mechanisms are strongly contested [16–18]. Despite this, NaHCO₃ continues to provide an ergogenic benefit to exercise performance, subsequently requiring further investigation of the biochemical changes that occur following ingestion.

There is an apparent increase in the ergogenic potential of NaHCO₃ when baseline blood HCO₃^– is increased by +5 mmol∙L^-1, whereas increases above +6 mmol∙L^-1 are associated with almost certain performance enhancement [19, 20]. However, the time taken to reach these thresholds varies considerably between individuals when NaHCO₃ is consumed in either capsule (range: 40–240 min [3, 21, 22]) or solution form (range: 40–125 min [2, 23–25]), therefore highlighting a potential flaw in the current dosing guidelines (i.e., 60–150 min pre-exercise for all athletes [1]). Contemporary research is addressing this issue by timing exercise to coincide with an individual peak blood HCO₃^– concentration [21, 23–25], though at present, only Boegman et al. [21] has directly compared exercise performance between NaHCO₃ ingested at time to peak HCO₃^– (40–160 min pre-exercise) versus a traditional dosing protocol (60 min pre-exercise for all athletes). The individualized approach significantly improved the rowing performance (2000 m time-trial) of 18 of 23 world-class rowers (Individualized = 367.0 ± 10.5 s vs. Traditional = 369.0 ± 10.3 s), however, this result occurred with only a small difference in pre-exercise HCO₃^– (Individualized = +6 mmol∙L^-1 vs. Traditional = +5.5 mmol∙L^-1). It is therefore plausible that another mechanism besides those associated with increased HCO₃^– is involved with the ergogenic properties of NaHCO₃ supplementation.

Alternatively, NaHCO₃ may mitigate fatigue by altering the intracellular and extracellular balance of strong ions such as potassium (K⁺), sodium (Na⁺), chloride (Cl^–), and Ca²⁺ [26]. Specifically, NaHCO₃ increases the influx of K⁺ into the muscle following ingestion and attenuates losses in intramuscular K⁺ during exercise, subsequently improving the capacity to sustain muscle excitability [27–30]. A concomitant increase in muscular Cl⁻uptake is also observed post-ingestion [27, 29, 30], which is suspected to work synergistically with K⁺ to protect force and excitability when muscles begin to depolarize [31]. These effects are further strengthened by an increased plasma Na⁺ [2, 3, 27, 28], which together with changes in K⁺ and Cl^–, could indicate an upregulation of Na⁺/K⁺–ATPase and Na⁺/K⁺/2Cl^––ATPase activity to limit depolarization and preserve excitation-contraction coupling following NaHCO₃ ingestion [16, 30, 31]. Currently, only Gough et al. have reported changes in the collective SID following NaHCO₃ ingestion and whole-body exercise [24, 27]. Interestingly, both studies identified an ergogenic effect of NaHCO₃ (4 km cycling time-trial: 1.4% faster [24]; treadmill time-to-exhaustion: 28% further [27]) when blood HCO₃^– increases (+7.0 mmol∙L^-1 [24]; +8.8 mmol∙L^-1 [27]) were identified alongside an increased SID (+6 mEq∙L^-1 [24]; +10 mEq∙L^-1 [27]) prior to exercise. Given that the role of H⁺ accumulation is controversial within exercise fatigue [16–18], the resultant performance improvements could instead be attributed to an increased plasma SID. However, no study to date has purposely intended to identify a peak SID measurement. If a time difference exists between the time taken to reach peak blood HCO₃^– and the SID concentrations, then it is plausible that future NaHCO₃ dosing strategies based upon a time to peak SID could optimize the SID mechanisms associated with performance enhancement.

Adolescence (age: 15–19 years) is a critical time in an athlete’s career, whereby competitive success is essential for continued sports participation [32]. Young athletes are therefore attracted to nutritional ergogenic aids to support their performance, though in practice, these are not always ingested in an evidence-based fashion [33]. Moreover, whether NaHCO₃ supplementation is appropriate for trained adolescents is unclear, with there being little evidence to suggest that large increases in blood alkalosis occur following ingestion. For example, neither Zajac et al. (+3.4 mmol∙L^-1 [34]) or Guimarães et al. (+3.4 mmol∙L^-1 [35]) observed a blood HCO₃^– increase above the proposed +5 mmol∙L^-1 ‘ergogenic threshold’ when measured at 60 and 90 min post-ingestion, respectively. Despite similar HCO₃^– increases, however, both of these studies differed in performance outcomes (time to complete 4 x 50 m swimming sprints: 1.3% faster [34] vs. time to complete 6 x 35 m running sprints: no change [35]). Why this discrepancy occurred remains unknown, though the authors speculated that individual factors such as genetics and gastrointestinal (GI) physiology may have had a role [35]. Indeed, both studies did not account for individual differences since standardized ingestion strategies were employed and HCO₃^– changes were reported at the group level only. In order to optimize NaHCO₃ supplementation for adolescent athletes, it is therefore necessary to first understand the possible acid-base balance alterations that occur following ingestion. The purpose of this study was to explore the time course changes and peak blood concentrations of three acid-base balance variables (HCO₃^–, pH, and the SID) in highly trained adolescent swimmers following the ingestion of 0.3 g∙kg BM^-1 NaHCO₃.

Materials and methods

Participants

Twelve national level swimmers from a performance swim programme volunteered to participate in this study (Table 1). Three of the swimmers had recently represented Great Britain at either the European Junior Swimming Championships or the European Youth Olympic Festival in 2019, whilst seven had qualified for the senior British Swimming Championships in April 2020. At the time of the study, all swimmers were ranked within the top 25 in Great Britain in at least one event within their respected age group (mean FINA points = 696 ± 62) and were completing a minimum of 7 x 2.5 hours pool-based and 2 x 1-hour land-based training sessions per week. The study was granted institutional ethical approval (Birmingham City University Ethics Committee: Newbury/3649/R(B)/2019 /Nov/HELS FAEC) and both the swimmers and their parents/guardians provided written informed consent prior to their participation in the study.

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Table 1. Characteristics of study participants (± SD).

https://doi.org/10.1371/journal.pone.0248456.t001

Pre-experimental procedures

Each participant was required to attend the laboratory as per their usual training time (17:00–20:30 hrs) having eaten as they normally would prior to a competitive race (i.e., self-selected timing and meal composition). Previous studies have assessed time course changes in HCO₃^– and pH in a fasted state [2, 3, 36] or following a standardized meal [22], however, these conditions do not replicate the variance in nutritional intakes that would take place in competition. This ingestion method was selected to consider the effects of individualized nutrition on baseline acid-base balance, electrolyte status, and absorption rate that would occur in practice [37]. In addition, the ingestion of a meal has shown to reduce the occurrence and severity of potential GI side effects that are associated with NaHCO₃ ingestion [38]. Each swimmer completed a 24-hour dietary recall before NaHCO₃ ingestion, which was used to calculate diet composition (Table 2) using an online nutrition application (Nutritics, version 5.64, Dublin, Ireland). Similarly, water was permitted to be consumed ad libitum (mean intake: 1.2 ± 0.5 L, range: 0.5–2.0 L), though ingestion of further nutrients were restricted once NaHCO₃ had been consumed. Participants were also asked to refrain from additional exercise outside of their regular swim training programme in the 48 hours prior to participating in the study. No swimmers had ingested caffeine, although concurrent ingestion of creatine (participants 5, 8, 9, 10, and 11) and beta-alanine (participants 9 and 10) were reported. Neither of these supplements was expected to affect the blood acid-base balance alterations that would occur following NaHCO₃ ingestion [39, 40]. All trials were carried out between December 2019 and February 2020 during a specific race preparation training period (weekly swimming volume = 50.9 ± 3.4 km).

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Table 2. The dietary intake of the participant cohort in the 24 hours preceding NaHCO₃ ingestion.

https://doi.org/10.1371/journal.pone.0248456.t002

Protocol and measurements

Upon arrival to the laboratory, participants engaged in five min of seated rest before a baseline capillary sample of whole blood was collected from the fingertip into a 100 μL sodium-heparin coated glass clinitube (Radiometer Medical Ltd., Copenhagen, Denmark). Blood samples were immediately analysed using a blood gas analyser (ABL9, Radiometer Medical Ltd., Copenhgen, Denmark) for measurements of HCO₃^–, pH, K⁺, Na⁺, Ca²⁺, and Cl^–. An additional 5 μL sample was taken for the analysis of blood lactate (La^–) (Lactate Pro 2, Arkray, Japan) which was used in the following formula to calculate the apparent SID using a freely available spreadsheet: K⁺ + Na⁺ + Ca²⁺–Cl^––La⁻[41]. This method of calculating the apparent SID has been previously utilised in similar research investigating the SID alongside NaHCO₃ ingestion [24, 27]. Participants then ingested 0.3 g∙kg BM^-1 NaHCO₃ (Dr. Oetker, Bielefeld, Germany) contained in gelatine capsules (1 g NaHCO₃ per capsule; Size 00, Bulk Powders, Colchester, UK) within a five min period prior to 165 min of quiet seated rest. Blood samples were obtained and analysed on eight more occasions (60, 75, 90, 105, 120, 135, 150, and 165 min post-NaHCO₃ ingestion) with further samples taken at 180 (n = 4) and 195 min (n = 1) to ensure a peak HCO₃^– was found. No samples were taken within the first 60 min since 0.3 g∙kg^-1 BM NaHCO₃ in capsule form was not expected to display peak HCO₃^– concentrations in this time [3, 22].

Gastrointestinal side effects were monitored using nine 200 mm visual analogue scales (VAS) for nausea, flatulence, stomach cramping, belching, stomach ache, bowel urgency, diarrhoea, vomiting and stomach bloating consistent with previous NaHCO₃ research [2, 24, 25, 42]. The VAS scales were labelled “no symptom” on the left side and “severe symptom” on the right side.

Statistical analysis

Data was normally distributed (Shapiro-Wilks) and sphericity was assumed (Mauchly) prior to statistical analysis. If sphericity was violated, Huyn-Feldt (epsilon value >0.75) or Greenhouse-Geiser (epsilon value <0.75) corrections were applied. A repeated measures ANOVA was conducted to establish mean differences between the time to peak of the three alkalotic variables (HCO₃^–, pH, and the SID) and group mean differences for each blood metabolite (HCO₃^–, pH, SID, K⁺, Na⁺, Ca²⁺, and Cl^–) at each sampling time point. Post hoc comparisons were determined by the Bonferroni correction and effect sizes are reported as partial eta squared (Pη²). Additional effect sizes were calculated for each time course change using the Hedges’ g bias correction, which was selected based on the small sample size (n <20) included in this study [43]. Effect sizes were interpreted as trivial (g = <0.20), small (g = 0.20–0.49), medium (g = 0.50–0.79), and large (g = ≥0.80) [44]. Coefficient of variation (CV) was calculated using SD/mean*100 and described the inter-individual variance between participants for time course and absolute blood analyte changes. A Spearman’s rank-order correlation (r_s) was used to investigate associations between dietary intake (energy, macronutrients, and electrolytes consumed 24 and 3 hours before to NaHCO₃ ingestion) and the time to peak, absolute change, and baseline measures of blood HCO₃^–, pH, and the SID. This non-parametric correlation was selected due to violations in the sphericity of nutritional data. All statistical tests were completed using Statistical Package for the Social Sciences (SPSS), version 25 (IBM, Chicago, USA). All data are reported as mean ± SD with statistical significance set at p <0.05.

Results

Blood analyte changes

No statistical significance was found between the time to peak concentrations of each blood acid-base variable (HCO₃^– = 130 ± 34 min, pH = 120 ± 38 min, SID = 98 ± 37 min; p = 0.077, Pη² = 0.208). Despite this, a large effect size (g = 0.88) separated the time to peak SID and HCO₃^– following a mean difference of 33 min being observed between these two measures. A moderate effect size was also observed between time to peak SID and pH (23 min, g = 0.58), whereas the effect size was small between time to peak HCO₃^– and pH (10 min, g = 0.26). Large inter-individual variations were present in the time to peak (CV: HCO₃^– = 27%; pH = 32%; SID = 37%;) and absolute increase from baseline observed for each alkalotic measure (HCO₃^– = +6.8 ± 2.4 mmol∙L^-1, CV = 35%; pH = +0.10 ± 0.04 units, CV = 42%; SID = +3.7 ± 2.2 mEq∙L^-1, CV = 61%). Individual data for all blood acid-base balance variables is presented in Table 3, whereas the time course changes in HCO₃^– and the SID has been plotted in Figs 1 and 2 for four different participants to emphasise the individuality in blood responses.

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Fig 1.

The time course change in blood bicarbonate (HCO₃^–) over a 165 min period following NaHCO₃ ingestion for A) participant 1, B) participant 8, C) participant 7, and D) participant 5. The dotted line represents a +5 mmol∙L^-1 increase from baseline blood HCO₃^–.

https://doi.org/10.1371/journal.pone.0248456.g001

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Fig 2.

The time course change in blood strong ion difference (SID) over a 165 min period following NaHCO₃ ingestion for A) participant 10, B) participant 2, C) participant 12, and D) participant 3.

https://doi.org/10.1371/journal.pone.0248456.g002

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Table 3. Individual metabolite responses to 0.3 g∙kg BM^-1 sodium bicarbonate (NaHCO₃).

https://doi.org/10.1371/journal.pone.0248456.t003

Across the sampling timeframe, marked increases in acid-base variables were observed (HCO₃^–: p <0.001, Pη² = 0.609; pH: p <0.001, Pη² = 0.529; SID: p = 0.029, Pη² = 0.212; Fig 3). Blood bicarbonate was elevated 60 min post-ingestion (+3.2 ± 2.6 mmol∙L^-1, p = 0.046) and remained +4–6 mmol∙L^-1 until 165 min post-ingestion (all p <0.030). At 105 min mean blood HCO₃^– had increased by 5.2 ± 2.5 mmol∙L^-1 and remained elevated above the proposed +5 mmol∙L^-1 ergogenic threshold until the final 165 min time point (peak: 150 min, +5.9 ± 2.7 mmol∙L^-1, +23%). An increased pH occurred at 75 min post-ingestion (+0.06 ± 0.04 units, +0.8%, p = 0.010) and this level of increase was sustained at all remaining points in time (+0.06–0.08 units, all p <0.030). Peak pH occurred at 165 min post-ingestion (+0.08 ± 0.05 units, +1.1%). The SID increased by 2.0 ± 1.5 mEq∙L^-1 (+6%, p = 0.024) at 60 min post-ingestion and peaked at 135 min post-ingestion (+2.4 ± 2.6 mEq∙L^-1, +7%), however, this did not reach statistical significance.

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Fig 3.

Group mean time course changes in A) blood bicarbonate (HCO₃^–), B) pH, and C) the strong ion difference (SID) over a 165 min period following NaHCO₃ ingestion. * = a large effect size compared to baseline (g >0.80). ^# = a large effect size compared to 60 min post-ingestion (g >0.80).

https://doi.org/10.1371/journal.pone.0248456.g003

Ingestion of NaHCO₃ produced ionic shifts in the balance of strong ions (K⁺: p = 0.005, Pη² = 0.215; Na⁺: p = 0.044, Pη² = 0.160; Ca²⁺: p <0.001, Pη² = 0.562; Cl^–: p = 0.016, Pη² = 0.306). The electrolytes with the greatest absolute changes were K⁺ and Cl^–. Large inter-individual variations restricted the ability to detect statistical significances for all metabolites, therefore group level results are described using effect sizes (Fig 4). This analysis showed that K⁺ reduced gradually from baseline before reaching peak declines at 120 (–0.93 ± 1.07 mmol∙L^-1, –18%, g = 1.26) and 150 min (–1.03 ± 0.93 mmol∙L^-1, –20%, g = 1.64) post-ingestion. Large effect sizes were calculated for the reductions in Cl⁻from 105 to 165 min post-ingestion (all g >0.80) with the lowest point also occurring at 150 min post-ingestion (–3.5 ± 1.9 mmol∙L^-1, –3%, p = 0.002). The time that each individual participant reached their lowest values of K⁺ (133 ± 28 min, CV = 21%), Cl⁻(124 ± 27 min, CV = 21%), and Ca²⁺ (141 ± 32 min, CV = 23%) averaged within 20 min of one another, albeit with large inter-individual variances. Conversely, Na⁺ was largely unchanged throughout the sampling period. The absolute changes from baseline displayed high inter-individual variation for each variable (K⁺: –1.28 ± 0.88 mmol∙L^-1, CV = 69%; Cl^–: –4.5 ± 2.1 mmol∙L^-1, CV = 47%; Ca²⁺: –0.16 ± 0.07 mmol∙L^-1, CV = 43%; Na⁺: +1.6 ± 1.3 mmol∙L^-1, CV = 83%).

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Fig 4.

Group mean time course changes in A) blood sodium (K⁺), B) potassium (Na⁺), C) calcium (Ca²⁺), and D) chloride (Cl^–) over a 165 min period following NaHCO₃ ingestion. * = a large effect size compared to baseline (g >0.80). ^# = a large effect size compared to 60 min post-ingestion (g >0.80).

https://doi.org/10.1371/journal.pone.0248456.g004

The energy and macronutrient composition of the pre-ingestion meal had no statistically significant correlations with the increases observed in blood HCO₃^–, pH, or the SID (Table 4). However, the macronutrient consumption of the meal did affect the time course behaviour of blood HCO₃^–, with protein (r_s = –0.581) and fat intakes (r_s = –0.594) both having moderate, negative correlations with time to peak HCO₃^–. Conversely, protein intake had a strong, positive correlation (r_s = 0.711) with time to peak SID. The total energy content of the pre-ingestion also had a moderate, positive correlation with time to peak SID, although this did not reach statistical significance (r_s = 0.555, p = 0.061). The fat content of the pre-ingestion meal was associated with baseline blood acid-base balance, as both HCO₃^– (r_s = 0.609) and the SID (r_s = 0.639) displayed strong, positive correlations. The amount of Na⁺ consumed 1–3 hours before NaHCO₃ ingestion also had a strong, positive correlation with baseline HCO₃^– (r_s = 0.644, p = 0.024), but not with pH (r_s = –0.315, p = 0.318), or the SID (r_s = 0.171, p = 0.596). No other correlations were found between Na⁺, K⁺, Cl^–, or Ca²⁺ ingestion and time course changes in blood acid-base balance.

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Table 4. The associations between the composition of the pre-ingestion meal with the time course changes in acid-base balance variables following NaHCO₃ ingestion.

https://doi.org/10.1371/journal.pone.0248456.t004

Gastrointestinal discomfort

All participants reported at least one GI side effect, though the severity of these instances was rated ≤5/10 in 94% (29/31) of occurrences (Table 5). Of the reported side effects, 71% (22/31) of instances peaked in severity at 60 and 75 min post-ingestion. The most common symptom was belching (58%, 7/12), followed by stomach bloating and nausea (50%, 6/12).

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Table 5. The three most severe symptoms of gastrointestinal discomfort experienced following the ingestion of 0.3 g∙kg BM^-1 sodium bicarbonate (NaHCO₃).

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Discussion

This was the first study to compare the time to peak of three different methods of measuring peak alkalosis (i.e., HCO₃^–, pH, and the SID) following the ingestion of 0.3 g∙kg BM^-1 NaHCO₃ in highly trained adolescent male and female swimmers. Though no statistical significance was observed between the three measures, there was a 33 min difference between the average time that HCO₃^– and the SID peaked in the blood of trained adolescents. This study also identified large inter-individual variances in the time to peak of each alkalotic measure, whereby individual peak concentrations were identified across the sampling timeframe (between 60–180 min post-ingestion). It is possible that this difference was related to the protein content of a meal consumed 1–3 hours before NaHCO₃ ingestion, with this macronutrient positively and negatively correlated with time to peak SID and HCO₃^–, respectively. Finally, this study provides justification for utilising individualised NaHCO₃ dosing strategies in adolescents since some sustained HCO₃^– increases exceeding 5 mmol∙L^-1 for over 60 min (n = 6), whereas others either reached this threshold for a 30–60 min period (n = 4), or did not reach this threshold at all (n = 2). Based on the individuality in blood responses, future work should aim to clarify whether personalised NaHCO₃ strategies (i.e., time to peak HCO₃^– and time to peak SID) have a greater ergogenic effect for adolescents than standardised dosing procedures.

The average time that HCO₃^– and pH peaked within the blood of trained adolescents occurred within 10 min of one another, supporting the relationship between these two measurements when NaHCO₃ is consumed in gelatine capsules [3, 22, 38]. This discussion will therefore focus on the blood HCO₃^– time course since this measure displays less variance and greater reliability compared to pH [2, 21]. Time to peak blood HCO₃^– varied considerably within trained adolescents (75–180 min), which is in accordance with the blood responses of recreational adults following the ingestion of NaHCO₃ capsules in a fed or fasted state [3, 21, 22]. Whereas no comparisons can presently be made for the time course changes in the SID, the time to peak concentration was also highly variable between each individual (60–165 min). Interestingly, the average time that the SID peaked in trained adolescents occurred 33 min before time to peak HCO₃^–, which may have implications for NaHCO₃ timing in applied practice. Why this time difference occurred is currently unknown, though meal preference in the 1–3 hours prior to NaHCO₃ ingestion may be a contributing factor. Indeed, higher protein intakes were correlated (r_s = 0.711) with a delayed time to peak SID, whereas in contrast, higher protein intakes were also correlated (r_s = –0.581) with a faster time to peak blood HCO₃^–. Since NaHCO₃ will usually be supplemented with a pre-competition meal in practice, it is plausible that these two measurements will also be separated prior to performance. However, since this research did not measure a performance outcome, future work should aim to determine whether either of these individualised approaches (i.e., time to peak SID and HCO₃^–) has an enhanced ergogenic benefit versus a traditional, fixed ingestion method (i.e., 120 min pre-exercise).

The participants in the present study demonstrated a peak blood HCO₃^– concentration that exceeded the 5–6 mmol∙L^-1 threshold (+6.8 ± 2.4 mmol∙L^-1), contrasting previous studies when trained adolescents ingested NaHCO₃ prior to exercise [34, 35]. A possible explanation for this difference is that high-level swimmers often have an early maturation onset [45], which likely occurred in the current participants and aided their selection for the high-performance swimming programme in which they were recruited. For comparison, both the male (72 ± 11 kg) and female (60 ± 5 kg) swimmers from the present study carried considerably more body mass than the ‘well trained’ male swimmers (56 ± 1 kg) recruited by Zajac et al. [34], despite being the same age. Consequently, the current participants may have benefitted from maturity-related differences in gut physiology (i.e., caecal pH, distal microbiota) that potentially enhanced their capacity to uptake NaHCO₃ from the GI tract [46, 47]. Moreover, the advanced training age of the participants could have also enhanced muscle and blood buffering capabilities (e.g., monocarboxylate transporter density, Na⁺/HCO₃^– co-transport) [48–50], which could have enabled greater blood HCO₃^– increases to occur. However, it should be noted that two participants (both aged 15 years) did not increase their blood HCO₃^– concentrations above 3 mmol∙L^-1, therefore adding support to previous speculations that less biologically mature adolescents might have less capacity increase blood HCO₃^– by more than 5–6 mmol∙L^-1. Though it is unclear whether this range is necessary for performance enhancement in adolescents, it is perhaps appropriate to suggest that less biologically mature individuals do not require NaHCO₃ supplementation at their stage of development [51].

Highly trained adolescents also demonstrated an increased blood SID following NaHCO₃ ingestion. This supports contemporary evidence by Gough et al. [24, 27] whereby an elevated SID was reported prior to exercise in trained adults. Surprisingly, both studies by Gough et al. demonstrated greater group mean increases in the SID compared to the present study (+4 vs. +6–10 mEq∙L^-1), despite not purposely seeking to identify a peak concentration. The current study also observed lower baseline (33 vs. 36–38 mEq∙L^-1) and absolute peak SID concentrations (37 vs. 42–46 mEq∙L^-1), inferring that adolescents might also be limited with their capacity for strong ion movements (e.g., reduced Na⁺/K⁺ pump activity) [48]. Furthermore, these lower concentrations occurred despite food consumption 1–3 hours before NaHCO₃ ingestion, though the energy, macronutrient, or electrolyte (Na⁺, K⁺, Cl^–, and Ca²⁺) composition of this meal was not correlated with baseline SID or the absolute SID increases that were achieved. Since water was also permitted to be consumed ad libitum, it is possible that plasma volume also increased and masked some of the ionic movements that took place [52]. For example, the absolute increases observed in plasma Na⁺ were mitigated (+1.6 vs. +3.0 mmol∙L^-1) in comparison to previous research that investigated NaHCO₃ ingestion in a fasted state [2, 3, 27]. Nonetheless, large effect sizes were calculated for plasma reductions of K⁺, Ca²⁺, and Cl⁻between 120–150 min post-ingestion, therefore suggesting that an intramuscular uptake of these ions did occur at this time [53]. Given that this study did not consider changes in the intramuscular SID or plasma volume, however, future research is required in order to further elucidate the role of NaHCO₃ on the SID during exercise performance.

Comparable to adults, each blood analyte displayed a large inter-individual variance with regards to time to peak and absolute increases that occurred from baseline concentrations [2, 3, 22]. Why this phenomenon occurs remains elusive, though it is postulated that genetic differences in the rate of gastric emptying, intestinal motility, and GI blood flow may contribute to NaHCO₃ uptake characteristics [54, 55]. Despite the individual differences, the process of identifying a personal time to peak HCO₃^– measurement has recently been criticised [22]. Ingesting NaHCO₃ capsules has consistently been shown to produce increases in blood HCO₃^– (>5 mmol∙L^-1) that last for over 100 min in adults [3, 22, 23], therefore producing a long lasting ‘ergogenic window’ that undermines the necessity of a single ingestion time point. However, when considering the HCO₃^– time course on an individual basis, only half (n = 6) of the trained adolescent participants demonstrated a +5 mmol∙L^-1 HCO₃^– increase that lasted for more than 90 min. Moreover, the time that each participant spent above the +5 mmol∙L^-1 threshold occurred at completely separate periods within some individuals (i.e., 60–120 min, 135–165 min post-ingestion), whereas two participants had small reductions in blood HCO₃^– (~1 mmol∙L^-1) at 60–75 min post-ingestion before concentrations increased over the next 60–75 min. Due to these erratic time course differences, it is recommended that adolescents undergo time to peak testing prior to supplementation in order to identify a personal time frame for NaHCO₃ to elicit a sufficient blood HCO₃^– response. However, considering that this is an expensive procedure, adolescents should remain cautious since the effects of individualised ingestion methods on exercise performance are currently untested within this cohort.

There were minimal incidents of severe GI side effects when trained adolescents ingested NaHCO₃ capsules 1–3 hours after consuming a self-selected meal. Whilst each participant reported at least one side effect, the severity of these symptoms was rated less than 5 out of 10 on 94% (29/31) of occasions. This low level of GI disturbance therefore supports the findings of Carr et al. [38], whereby the co-ingestion of NaHCO₃ capsules with a meal provided the best mitigation against GI distress (vs. NaHCO₃ solution/fasted state). Both capsules and meal consumption are suggested to slow the reduction of NaHCO₃ to Na⁺ and carbonic acid (H₂CO₃), subsequently reducing the rate of acid-base disturbances that occur in the stomach (e.g., increases in carbon dioxide and water) [56, 57]. Alternatively, the age of the participants might have contributed to the lack of GI symptoms observed in this study, therefore supporting the lack of GI disturbances in adolescents from previous NaHCO₃ research [34, 35]. Whilst there is currently no clear explanation for the lack of GI disturbances in adolescents, it is plausible that a lower acidity of the GI fluids compared to adults may mediate the acid-base disturbances that occur in the stomach when an alkaline substance is ingested [58]. Another general observation is that athletes of a higher body mass (>75 kg) typically display greater GI distress than lighter individuals [42, 59]. Adolescents, being smaller in stature than their adult peers, may therefore experience less GI disturbances due to a reduced absolute NaHCO₃ dosage entering the stomach. However, this study did observe vomiting in one participant, which indicates that the severity GI side effects should be assessed on an individual basis.

The study methods were applied based on the logistical (e.g., taking highly trained swimmers out of training) and ethical considerations of the participant cohort (e.g., repeated blood analysis of young athletes). This limited the current study from including a placebo experiment or repeatability measures that could have altered the interpretation of results. Nonetheless, previous work found a placebo to cause no blood time course changes for either HCO₃^–, pH, or Na⁺ [2, 22], therefore it may be assumed that a placebo would not have altered baseline HCO₃^–, pH, or SID within an adolescent cohort. The repeatability of time to peak HCO₃^– is controversial, however, when 0.3 g∙kg BM^-1 NaHCO₃ capsules are ingested in a fed state. Indeed, Boegman et al. [21] reported an excellent repeatability (ICC = 0.77) within world-class rowers when NaHCO₃ was ingested alongside a standardised snack (energy: 682 kcal; protein: 20 g; carbohydrate: 140 g). Conversely, Oliveira et al. [22] found repeatability to be poor (ICC = 0.34) when recreational adults ingested NaHCO₃ 60 min following a standardised breakfast (energy: 563 kcal; protein: 9 g; carbohydrate: 90 g). Since both studies differed in meal composition, participant training status, time post-prandial, and blood analysis methods (capillary [21] vs. venous [22] samples), this leaves the repeatability of the current data unclear. However, the main purpose of this research was to identify the time course changes in three alternate blood acid-base balance variables following NaHCO₃ ingestion in a highly trained adolescent cohort. Since this was the first study to suggest that a difference in time to peak HCO₃^– and SID may exist in practice, future studies should therefore aim to determine the repeatability of these two measures under different competitive scenarios (e.g., pre-competition meal, after warm-up).

Conclusion

This study shows that highly trained adolescent swimmers have significant increases and highly individual time course changes in blood HCO₃^–, pH, and SID following the ingestion of NaHCO₃ capsules. Importantly, the post-ingestion time point in which the individual time to peak occurred for HCO₃^– and the SID was separated by a large effect size. Given that the effects of acidosis on exercise performance are controversial, future studies should seek to identify NaHCO₃ dosing strategies based upon a peak SID concentration could be more ergogenic than standardised ingestion strategies, or individualised approaches based upon a time to peak blood HCO₃^–. This study also suggests that highly trained adolescent athletes do not have a long lasting ‘ergogenic window’ following the ingestion of NaHCO₃ capsules, therefore supporting the practice of identifying an individualised time point whereby a peak alkalosis occurs. It is acknowledged that a lack of control surrounding pre-ingestion food and fluids may have influenced the findings of this study, however, these conditions better replicate the actual changes that would occur when athletes are in full competition preparation.

Supporting information

S1 Data.

https://doi.org/10.1371/journal.pone.0248456.s001

(XLSX)

Acknowledgments

We gratefully acknowledge all participants who volunteered for the study and the City of Birmingham Swimming Club for facilitating the research process.

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Figures

Abstract

Introduction

Materials and methods

Participants

Pre-experimental procedures

Protocol and measurements

Statistical analysis

Results

Blood analyte changes

Gastrointestinal discomfort

Discussion

Conclusion

Supporting information

S1 Data.

Acknowledgments

References