If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
Oral sodium bicarbonate intake (NaHCO3) may improve performance in short maximal exercise by inducing metabolic alkalosis. However, it remains unknown whether NaHCO3 also enhances all-out performance at the end of an endurance competition. Therefore, the present study investigated the effect of stacked NaHCO3 loading on sprint performance following a 3-h simulated cycling race.
Eleven trained male cyclists (22.3 (18.3–25.3) year; 73.0 (61.5–88) kg; VO2max: 63.7 (57–72) ml kg−1 min−1) ingested either 300 mg kg−1 body weight NaHCO3 (BIC) or NaCl (PL). NaHCO3 or NaCl was supplemented prior to (150 mg kg−1) and during (150 mg kg−1) a 3-h simulated cycling race with a 90-s all-out sprint (90S) at the end. Capillary blood samples were collected for determination of blood pH, lactate and HCO3− concentrations. Analysis of variance (lactate, pH, HCO3−) and paired t-test (power) were applied to compare variables across condition (and time).
Results
NaHCO3 intake improved mean power during 90S by ∼3% (541 ± 59 W vs. 524 ± 57 W in PL, p = 0.047, Cohen’s D = 0.28, medium). Peak blood lactate concentration and heart rate at the end of 90S were higher (p < 0.05) in BIC (16.2 ± 4.1 mmol l 1, 184 ± 7 bpm) than in PL (12.4 ± 4.2 mmol l−1, 181 ± 5 bpm). NaHCO3 ingestion increased blood [HCO3−] (31.5 ± 1.3 vs. 24.4 ± 1.5 mmol l−1 in PL, p < 0.001) and blood pH (7.50 ± 0.01 vs. 7.41 ± 0.03 in PL, p < 0.05) prior to 90S.
Conclusions
NaHCO3 supplementation prior and during endurance exercise improves short all-out exercise performance at the end of the event. Therefore, sodium bicarbonate intake can be applied as a strategy to increase success rate in endurance competitions.
For the first time, it is shown that sodium bicarbonate loading prior to and during a simulated cycling race improves a 90-sec all-out sprint at the end of the race.
•
Stacked sodium bicarbonate loading of 0.3 g/kg body mass prior to and during cycling does not elicit gastrointestinal disturbances.
•
Coaches and athletes should test the supplementation protocol on training sessions before its application in competition.
1. Introduction
Success in prolonged endurance events such as road cycling, triathlon, long-distance running or cross-country skiing, often depends on the capacity to outperform residual competitors by short all-out exercise in the final stage of the race.
This requires aerobic endurance training to be combined with specific training to develop anaerobic power and capacity. The crucial role of late stage high power production to achieve success in endurance races justifies the use of nutritional interventions to enhance anaerobic capacity.
The spectrum of nutritional interventions to beneficially impact short all-out performance is narrow. It was previously demonstrated that oral creatine and β-alanine supplementation can improve sprint performance at the end of prolonged exercise.
the prevailing opinion is that intramyocellular proton (H+) accumulation plays an important role in the development of muscle fatigue during high-intensity muscle contractions.
There is ample evidence to indicate that NaHCO3 intake prior to exercise, by increasing extracellular buffer capacity, facilitates H+ as well as lactate− ion efflux from muscles,
However, findings with regard to the ergogenic effect of NaHCO3 loading in short maximal exercise are equivocal. This is at least partly explained by different reliability and duration (≤1 min
Surprisingly, it has never been investigated whether NaHCO3 intake during very prolonged endurance exercise can increase the HCO3− concentration to a sufficient degree to improve all-out performance in the final stage of the event. It was recently demonstrated that stacked NaHCO3 ingestion throughout the day, resulting in 400 mg kg−1 BW NaHCO3 intake over a 9-h period, significantly improved power output in a 2-min all-out exercise at the end of the loading period.
The present study investigated whether stacked sodium bicarbonate loading in the hours before and during a prolonged endurance exercise bout, can result in a higher HCO3− concentration by the time high anaerobic capacity is needed to be successful in a final all-out exercise bout or sprint. The authors hypothesize that stacked NaHCO3 loading by increasing extracellular buffer capacity can improve performance in a short all-out exercise bout at the end of a 3-h simulated cycling race.
2. Methods
Eleven male cyclists (age: 22.3(18.3–25.3) year; height: 1.83(1.67–1.95) m; weight: 73.0(61.5–88.0) kg; VO2max: 63.7(57.0–72.0) ml kg−1·min−1) who participated in regional competitions, volunteered to participate in the study. They were informed in detail on the aim and the procedures of the study protocol and signed a written informed consent as approved by the Ethics Committee Research at UZ/KU Leuven. All participants were non-smokers, abstained from dietary supplements for at least 3 months prior to the start of the study, and had a maximal oxygen uptake rate (VO2max) of at least 55 ml kg−1·min−1. Furthermore, participants were physically screened for contraindications to participate in maximal exercise. One week prior to the first experimental session an incremental cycling test was performed to determine the participant’s lactate threshold (LT) and VO2max. Initial workload was 60 W and was increased by 40 W per 8-min until volitional exhaustion (332 ± 42 W). Capillary blood was sampled from an earlobe at 4-min intervals throughout the test. LT (294 ± 42 W) was defined as the intensity at which blood lactate increased by 1 mmol·l−1 from min 4 to 8 within a given 8-min workload step. Following the incremental cycling test, the participants performed a cool down by cycling at 100 W for 15 min. Thereafter they performed a 90-s all-out isokinetic cycling bout as a familiarization for the same test to be performed in the later experimental sessions. Based on the results from the incremental cycling test (VO2max and peak power output) the participants were classified into performance level 1–5 according to De Pauw et al.
Three participants were ranked at level 3 (‘trained’, ‘competitive’), six at level 4 (‘highly trained’, ‘national cycling league’) and two participants at level 5 (‘professional cyclists’).
The double-blinded, placebo-controlled, randomized crossover study involved two experimental sessions (NaHCO3, BIC vs. placebo, PL supplementation) with a 1-week washout period in between. Treatment allocation was done by coin flipping by a local investigator who was otherwise not involved in the study, and assuring half of the participants to start with BIC vs. the others half with PL. All exercise testing was undertaken in an air-conditioned laboratory (18 °C and 60% relative humidity). During the experiments, the cycling ergometers were positioned in front of the cooling units, which were set at maximal airflow rate to obtain optimal cooling of participants during the exercise protocol. Participants were asked to abstain from strenuous exercise for at least 48 h prior to each session. All exercise testing was done on the participants’ personal race bicycle being mounted on an electromagnetically braked cycle ergometer (Avantronic® Cyclus 2, Leipzig, Germany) calibrated prior to the experiments.
The evening before the experimental sessions, participants received a standardized dinner (1200 kcal; 201 g CHO; 48 g protein; 22 g fat). After dinner they remained fasted until reporting to the laboratory next morning, yet were allowed to drink water at libitum. Upon arrival, they received a carbohydrate-rich breakfast (880 kcal; 154 g CHO; 32 g protein; 15 g fat), together with 90 mg kg−1 BW NaHCO3 or appearance-matched placebo delivering equimolar amounts of sodium. Forty-five and 90 min after breakfast two more doses of 30 mg kg−1 BW NaHCO3 were ingested. These supplements were administered in the form of 700 mg, the number of which was adjusted to match the prescribed dose kg−1 BW as close as possible. Two hours after breakfast the participants started a 3-h intermittent exercise bout (see below), during which they received 50 mg kg−1 BW NaHCO3 (#1370131000 Merck Millipore, Massachusetts, USA) per hour dissolved in 500 mL of a 6% maltodextrine (Body & Fit, Heerenveen, The Netherlands) solution, or taste and color-matched placebo (NaCl, #1064060500 Merck Millipore, Massachusetts, USA). In addition the participants received an energy bar containing 30 g of carbohydrates (6d Sports Nutrition, Oudenaarde, Belgium) in order to obtain a total oral carbohydrate intake at a rate of 60 g per hour. In total, from 2 h prior to the start until the end of the 3-h exercise bout, the participants ingested 300 mg kg−1 BW NaHCO3.
The exercise protocol included a 3-h intermittent exercise bout aimed to simulate a cycling race (RACE),
followed by a 90-s all-out ‘sprint’ (90S). All exercise was performed with the personal race bike of the participant mounted on calibrated cycling ergometers (Avantronic® Cyclus 2, Leipzig, Germany). To allow simultaneous participation of different subjects in the experiments, different ergometers were used for RACE, yet to avoid slight calibration differences between devices, the same ergometer was used for both experimental conditions in every participant. Conversely, all 90S tests were done on one single ergometer which was put into the isokinetic operation mode with cadence fixed at 100 rpm, and which was calibrated immediately prior to the experiments. RACE consisted of six consecutive 30-min blocks during which exercise intensity was varied per 5-min intervals between 60 and 90% of LT taken from the preliminary testing. Cadence during RACE was fixed at 85–95 rpm. Hereafter the participant’s race bike was moved to the isokinetic sprint ergometer while the participant rested for 2–3 min. Initial workload for 90S was set at 5 N kg−1 BW (330 ± 40 N) and no verbal encouragement was given during the test. Feedback was limited to the 90-s time countdown.
Capillary blood samples were collected from a hyperaemic earlobe into heparinized glass capillaries (70-μL; Clinitubes, Radiometer Medical ApS, Copenhagen, Denmark). Samples were taken prior to the supplementation, at the start, in the middle and at the end of RACE, and 3 min post 90S, and were immediately mixed for 15 s. Samples were then immediately analyzed for blood HCO3− content, blood pCO2 and pH using an automated acid–base laboratory (ABL90 Flex, Radiometer Medical ApS, Copenhagen, Denmark) and also blood lactate concentration was determined (Lactate Pro 2, Arkray, Japan). Heart rate (Polar, Kempele, Finland) and power output (Avantronic® Cyclus 2, Leipzig, Germany) were continuously measured during exercise. Heart rate data of one participant were lost due to technical issues. The fatigue index (%) was calculated as the [peak power − final power (last 10-s)]/peak power × 100. Rating of perceived exertion (RPE) was assessed immediately after RACE and following 90S by scoring a 15-point Borg-scale.
with 12 questions addressing GI discomfort at systemic, upper-abdominal and lower-abdominal level on a 9-point scale.
All data are presented as means ± SD, or mean and range in parentheses. The mean power output (MPO) of 90S was calculated per 10-s intervals as well as for the full exercise bout. The variables MPO, maximal PO, maximal blood lactate concentration, maximal heart rate, blood pH and fatigue index were normally distributed on all time points in both conditions (Kolmogorov–Smirnov test of normality; p > 0.05). Blood HCO3− was not normally distributed at the first time point in PL (Kolmogorov–Smirnov p = 0.036), but was normally distributed on the other four time points. Normally distributed data (and blood HCO3−) were analyzed with appropriate parametric statistical tests. Conditions were compared by repeated measures ANOVA across treatments (PL vs. BIC) and time, using Bonferroni post-hoc tests for multiple comparisons whenever a significant treatment × time interaction was found. The effect of BIC vs. PL on mean and peak power outputs, fatigue index, peak heart rate, and blood lactate concentration during 90S was evaluated by two-sided paired Student’s t-test. Delta (Δ) (±SD) values are provided to address the difference between BIC and PL (at a given time point). GI distress and RPE data were non-normally distributed (Kolmogorov–Smirnov p < 0.05) and were analyzed with the nonparametric Wilcoxon Signed Rank test to compare BIC vs. PL. Where relevant, Cohen’s D (D) was calculated as index of effect size (ES) for the t-tests (0.2 = small, 0.5 = medium, >0.8 = large), and eta-squared (η2) was used as index of ES for ANOVA (0.02 = small, 0.13 = medium, 0.26 = large). The ES of nonparametric data (GI, RPE) was calculated as r = z/ (0.1–0.3 = small, 0.3–0.5 = medium, >0.5 = large).
Significance was accepted for p < 0.05. All statistical analyses were performed using SPSS version 20 (IBM, Chicago, USA).
3. Results
Effect of bicarbonate intake on performance in 90S (Figs. 1B, 2 ) – During 90S power output peaked after ∼2.5 s, where after it gradually decreased until the end of the exercise bout. Peak power outputs were similar between the groups (PL: 864 ± 169; BIC: 853 ± 150 W; Δ11 ± 157 W; t = 0.238; df = 10; p = 0.817). But MPO over the full 90-sec bout was ∼3% higher in BIC (541 ± 59 W) than in PL (524 ± 57 W; Δ17 ± 25 W; t = −2.270; df = 10; p = 0.047; D = 0.29) (Fig. 2A). Eight out of 11 participants increased their MPO during BIC, with a 95% confidence interval at 0.3–33.7 W. Fatigue index was similar between conditions (−49.3 ± 11.7%; Δ1.7 ± 35.3 %; t = 0.310; df = 10; p = 0.763) though. RPE at the end of 90S was similar between PL (18.5 ± 1.3) and BIC (18.4 ± 1.2; z = −0.272; p = 0.785). Nonetheless, compared with PL (181 ± 5 bpm) peak heart rate elicited by 90S was higher in BIC (184 ± 7 bpm; Δ3.1 ± 2.6 bpm; t = −3.832; df = 9; p = 0.004; D = 0.52) (Fig. 1B).
Fig. 1Effect of sodium bicarbonate intake on blood lactate following and peak heart rate during a 90-s all out performance. Individual data points (n = 10–11) representing blood lactate (A) and peak heart rate (B). Participants first participated in a 3-h simulated cycling race. Immediately after, they performed a 90-sec all-out exercise bout. The participants received either oral sodium bicarbonate (BIC) or placebo (PL) supplements from baseline until the end of the 3-h cycling race. *P < 0.05 compared with PL.
Fig. 2Effects of sodium bicarbonate intake on 90-s all-out exercise performance at the end of a 3-h simulated cycling race. Participants participated in a 3-h simulated cycling race. Immediately after, they performed a 90-s all-out exercise bout (90S). Data (n = 11) represent the mean power output produced over the preceding 10-s time-interval (mean ± SD; A) and individual data points represent the mean power output during the first 60 s of 90S (B). The participants received either oral sodium bicarbonate (◼; BIC) or placebo (□; PL) supplements from baseline until the end of the 3-h cycling race. *P < 0.05 compared with PL.
Workload and fatigue during RACE – Total work done during RACE was 2266 (1587–2825) kJ. Workloads at 60, 70, 80 and 90% of LT were 176 (123–219), 205 (144–256), 234 (164–292) and 264 (185–329) W, respectively. These workloads corresponded to 74 (69–79), 76 (71–82), 81 (76–85) and 83 (79–88.1) % of peak heart rate taken from the VO2max test. Heart rates during RACE were similar between the experimental conditions at any time (F = 0.617; df = 4; pinteraction = 0.66; F = 0.839; df = 1; pcondition = 0.373). Blood lactate concentration values at 60% of LT were also similar at ∼1.2–1.4 mmol l−1 between conditions (F = 0.096; df = 2; pinteraction = 0.91; F = 2.134; df = 1; pcondition = 0.16). Accordingly, RPE at the end of RACE was 14.5 ± 1.2 in PL versus 13.8 ± 1.8 in BIC (z = −1.065; p = 0.29).
Effect of bicarbonate intake on blood-acid base balance (Fig. 3, Fig. 1A) – Compared with PL, NaHCO3 intake from baseline until the end of RACE increased blood HCO3− concentration by ∼30% (F = 108; df = 4; pinteraction < 0.001). Blood pH concomitantly increased by ∼0.1 unit in BIC, whilst it was stable in PL (F = 43.5; df = 4; pinteraction < 0.001; F = 47.8; df = 1; pcondition < 0.001). Thus at the start of 90S blood HCO3− concentration was 24.4 mmol l−1 (22.7–27.1) in PL, and was higher (31.5 (29.6–34.0) mmol l−1) in BIC (Δ7.2 ± 1.5 mmol l−1; F = 148.63; df = 1; p < 0.001). Corresponding blood pH values were 7.41 (7.39–7.48) in PL versus 7.50 (7.49–7.52) in BIC (Δ0.09 ± 0.02; F = 99.1; df = 1; p < 0.001). During 90S blood bicarbonate levels dropped more in BIC (−15.4 ± 3.0 mmol l−1) than in PL (−10.6 ± 2.5 mmol l−1; t = 8.529; df = 10; p < 0.001). Nonetheless, compared with PL, post 90S blood bicarbonate level was still higher in BIC (Δ2.3 ± 2.1 mmol l−1; F = 5.8; df = 1; p = 0.025). 90S decreased blood pH to the same degree in both groups, yet due to the higher pre-exercise value, blood pH post exercise remained higher in BIC than in PL (Δ0.07 ± 0.06; F = 6.7; df = 1; p = 0.018). The effect of NaHCO3 on HCO3− and pH levels can be considered very large, as ES values (η2) for both variables were ∼0.5 (before RACE), 0.8 (during RACE) and 0.9 (before 90S). After 90S, the ES was less pronounced, yet still high ∼0.24. Compared with PL (0.9 ± 0.1 mmol l−1) blood lactate concentration at the start of 90S was slightly higher in BIC (1.1 ± 0.2 mmol l−1; F = 3.1; df = 1; p = 0.095; η2 = 0.13). 90S increased blood lactate concentration more in BIC (+15.2 ± 4.0 mmol l−1) than in PL (+11.5 ± 4.2 mmol l−1; t = −4.142; df = 10; p = 0.002; D = 0.85), resulting in 16.2 (8.7–21.5) mmol l−1 post exercise blood lactate concentration in BIC vs. 12.4 (4.5–18.1) mmol l−1 in PL (F = 4.6; df = 1; p = 0.044; η2 = 0.19) (Fig. 1A). Prior to 90S, the arterial partial CO2 pressure (PaCO2) was higher in BIC (40.3 (36.0–42.7) mmHg) vs. PL (38.1 (35.4–40.5) mmHg; F = 9.613; df = 1; p = 0.006; η2 = 0.33), whereas this was not the case at the end of 90S (BIC: 32.2 (27.4–39) mmHg; PL: 31.2 (26.6–35.3) mmHg; F = 0.598; df = 1; p = 0.45). Consequently, although not significant (t = 1.9; df = 10; p = 0.09), compared to PL (−6.9 ± 3.2 mmHg), BIC induced a larger decrease of PaCO2 (ΔPaCO2) (−8.1 ± 3.5 mmHg; D = 0.34).
Fig. 3Effects of sodium bicarbonate intake on blood acid-base balance. Data are mean ± SD (n = 11) for blood bicarbonate (HCO3−) (A) and blood pH (B) at baseline and at the start, middle, and end of a 3-h simulated cycling race, followed by a 90-s all-out exercise bout (90S). Participants received either oral sodium bicarbonate (◼) or placebo (□) from baseline until the end of the 3-h race. *P < 0.05 compared with PL. §P < 0.05 compared with baseline.
Gastrointestinal discomfort – GI symptoms were negligible. In the total group of participants, and on a possible maximal score of 96, GI scoring was 2.0 (0–11) at the start, increasing to 4.1 (0–14) by the end of the exercise protocol (z = −2.388; p = 0.017; r = 0.51). However, values were not different between PL and BIC before (z = −1.4; p = 0.156) or after (z = −0.282; p = 0.778) the cycling protocol.
4. Discussion
An extensive number of studies over the last decades has investigated the effects of sodium bicarbonate supplementation on performance in short all-out exercise (for review see
In addition, all aforementioned studies only considered NaHCO3 loading prior to the start of exercise, with exception of the study by Mitchell et al. in which NaHCO3 or NaCl was infused intravenously during exercise.
However, the structure of a cycling race, which typically involves hours of mostly submaximal cycling preceding a high-intensity final phase, provides a window of opportunity to load sodium bicarbonate during the event in order to elevate blood HCO3− concentration in the approach of the final sprint. Furthermore, a stacked NaHCO3 loading protocol in conjunction with intermittent exercise throughout the day can gradually raise blood bicarbonate in the absence of GI distress.
Therefore, the present study evaluated a novel NaHCO3 supplementation strategy aiming to enhance buffering capacity and thereby improving performance in short all-out exercise at the end of a prolonged endurance exercise event. The time schedule applied in our protocol is relevant for real life road cycling competitions, i.e. early morning breakfast followed by the start of competition ∼2 h later. Stacked NaHCO3 loading from breakfast to the start of the event, delivering 150 mg kg−1 BW NaHCO3 (9.2–13.2 g), raised blood bicarbonate levels by ∼10%, resulting in a small initial increment in blood pH. Sustained NaHCO3 loading at a rate of 50 mg kg−1 BW per hour during RACE increased blood HCO3− by an additional ∼15%, resulting in ∼27% higher blood HCO3− at the start of the final 90-s all-out exercise bout (90S). In the conditions of the current study, the rise in blood HCO3− amounted to 6.7 (5.8–7.7) mmol l−1 in BIC. Others reported slightly greater increments in blood HCO3−, i.e. by 8.2 (6.0–12.3) mmol l−1 upon ingestion of a 0.3 g kg−1 NaHCO3 bolus.
whereas fewer measurements were done in the present study. Hence, we may have missed true peak blood HCO3− concentrations. Furthermore, in the present study, participants used some of the HCO3− load in H+-buffering during RACE whilst they were resting in the study by Jones et al.
Blood pH at the start of 90S eventually increased by ∼0.1 unit, reflecting a ∼20% reduction in free extracellular proton concentration. This is in agreement with earlier studies showing a single 0.3 g kg−1 NaHCO3 bolus to increase blood pH by ∼0.1.
Importantly, this stacked NaHCO3 loading procedure over the 5-h time-interval from breakfast to end of RACE was able to significantly increase the blood HCO3− concentration in the absence of any GI discomfort.
NaHCO3 loading also resulted in a better performance in 90S at the end of the RACE. Compared with PL, MPO on average was ∼3% higher in BIC. This magnitude of improved performance is in accordance with Bellinger et al.
Both studies concluded that acute NaHCO3 loading (0.3 and 0.4 g kg−1, respectively) improved MPO during a 4-min all-out sprint with ∼3% in trained cyclists.
McNaughton et al. suggested that more consistent ergogenic effects upon NaHCO3 ingestion in trained individuals might be due to a better reliability of exercise performance, hence facilitating the detection of small but pertinent ergogenic effects.
The magnitude of the performance effect observed (∼3%) was also greater than the coefficient of variation obtained by comparing performance between sessions 1 and 2 independent of the experimental conditions (1.47%), and indicating excellent reproducibility of the test procedure. In addition, eight of 11 participants exhibited a higher MPO during BIC than during PL, and confidence limits indicate 95% probability to experience a benefit in MPO ranging between 0.3 and 33.7 W. Furthermore, it is clear from Fig. 2A that this ergogenic effect was most prominent during the initial 60 s of 90S. In fact, when considering power outputs from 0 to 60 s, BIC stimulated power production in 9 out of the 11 participants (t = −2.138, df = 10; p = 0.058; D = 0.46; Fig. 2B). Interestingly, the increase in mean power output due to BIC (ΔMPO, calculated as MPO during BIC minus MPO during PL) was positively correlated with the greater drop in blood HCO3− (r = 0.77; p = 0.006) and with the increase in blood lactate concentration during 90S (r = 0.608; p = 0.047) in BIC compared with PL. This clearly indicates that the ergogenic effect generated by NaHCO3 supplementation was at least partly, if not entirely, due to increased extracellular buffering capacity by higher blood HCO3− availability during 90S.
This improved performance in 90S conceivably was directly due to a higher rate of extracellular bicarbonate utilization. Decrease of the blood bicarbonate pool during 90S was ∼50% greater in BIC (∼15 mmol l−1) than in PL (∼10 mmol l−1), which most likely reflects a higher efflux of both lactate ions and H+ from the active muscles. Support for such mechanism comes from the observation that the peak blood lactate concentration during 90S was substantially higher in BIC (∼16 mmol l−1) than in PL (∼12 mmol l−1). Lactate export in muscle cells is effected by membrane-bound monocarboxylate transporters which operate as a lactate∼H+ cotransport system.
Decrease of extracellular H+ concentration produced by high-dose HCO3− ingestion increases the outward gradient for H+ across the sarcolemma, which in turn stimulates the simultaneous export of lactate and H+ from muscle cells into the interstitial space. The ΔHCO3- in the present study was less pronounced than during a 4-min all-out sprint, during which blood HCO3− decreased with ∼20 mmol l−1, probably due to a longer time window during which HCO3− can be used.
Alternatively, due to limited blood HCO3− measurements, we may have missed true peak blood HCO3− concentrations, needed to calculate the total amount of HCO3− used during 90S. Between-subject variation in maximal blood lactate concentrations was relatively high (range: ∼13 mmol l−1). One subject reached a maximal blood lactate concentration of only 4.5 mmol l−1 in PL, conceivably due to low residual muscle glycogen content at the end of RACE. However, his response to NaHCO3 (8.7 mmol l−1; Δ + 4.2 mmol l−1) is in line with the other participants (Δ + 3.8 ± 3.0 mmol l−1). Furthermore, the low-end maximal blood lactate concentration was not associated with a low MPO, which was 73.5% higher than the power at his LT, similarly to the others, i.e. +88 ± 37%.
During 90S, ΔHCO3− was greater in BIC than in PL. Since ΔpH values were similar in both conditions, this suggests that ΔpCO2 was higher in BIC. Indeed, compared to PL (−6.9 mmHg), the 90S-induced ΔpCO2 tended to be greater in BIC (−8.1 mmHg), which can (partly) be explained by the increased buffering of H+ by HCO3−. It can be speculated that this would result in a higher VCO2 during 90S.
However, this should be confirmed in future studies.
To our knowledge, this is the first study to report an increase in peak heart rate during short all-out exercise due to BIC. During exercise, metabolites such as H+ accumulate in the working muscle and mainly stimulate the group IV afferents.
These eventually induce peripheral fatigue through regulation of the cardiovascular, hemodynamic and ventilatory responses to exercise, and prevent further metabolic disturbance by inhibition of neural output to muscles.
One might suggest that such inhibition is delayed due to prevention of premature muscular fatigue in BIC, which eventually allows greater cardiac sympathetic drive. There is also evidence indicating that acidosis blunts the sensitivity of cardiomyocytes to epinephrine,
which might explain a lower peak heart rate in PL compared with BIC. However, the latter mechanism is less likely to be responsible for the observed differences since vagal suppression is rather engaged in the initial heart rate response to exercise,
whereas sympathic activity is responsible for further increases in heart rate during more strenuous exercise, as was the case in 90S.
To maximize the ecological validity of the study, especially with regard to the incidence of GI symptoms, dietary recommendations for race days were simulated, i.e. a CHO-rich meal ∼2–3 h before RACE combined with consistent high-rate CHO intake during RACE (60 g per hour). In addition, combination of NaHCO3 with a high-carbohydrate meal can facilitate the development of blood alkalosis as well as reduce the incidence of GI symptoms.
In the current protocol the 3 h simulated cycling race consisted of mostly submaximal exercise bouts at workloads below the anaerobic threshold (60–90% of LT). However, in real competition the final sprint often is preceded by higher intensity exercise also involving repeated short all-out exercise bouts, or longer intervals at workloads exceeding the anaerobic threshold. Such exercises likely deplete the HCO3− concentration before the final sprint. Therefore, it remains to be established whether also under such conditions the rate of NaHCO3 used in the current protocol is able to maintain elevated buffering capacity until the final stage of the event.
5. Conclusion
This study evaluated the effect of stacked NaHCO3 loading before and during a prolonged endurance exercise bout (∼3 h) on all-out performance in the final stage of the event. Sodium bicarbonate loading delivering 300 mg kg−1 BW NaHCO3 before and during the exercise gradually elevated blood HCO3−. This translated into improved power output in a 90-sec all-out exercise bout.
Acknowledgements
The authors would like to thank Monique Ramaekers for her skillful technical assistance during the experiments. The authors declare no financial support for the project.
References
Padilla S.
Mujika I.
Santisteban J.
et al.
Exercise intensity and load during uphill cycling in professional 3-week races.
30770-2&id=gr1.jpg){kind=link}
30770-2&id=gr2.jpg){kind=link}
30770-2&id=gr3.jpg){kind=link}