NaHCO3 Ingestion Research Articles

Mineral intake independent from gastric irritation or pica by cell-dehydrated rats

Gavage of 2M NaCl (IG 2M NaCl), a procedure to induce cell-dehydration—and water and 0.15M NaCl intake in a two-bottle choice test—is also a potential gastric irritant. In this study, we assessed whether mineral intake induced by IG 2M NaCl is associated with gastric irritation or production of pica in the rat. We first determined the amount of mineral solution (0.15M NaCl, 0.15M NaHCO3, 0.01M KCl and 0.05mM CaCl2) and water ingested in response to IG 2M NaCl in a five-bottle test. Then, we used mineral solutions (0.01M KCl and 0.15M NaHCO3), whose intakes were significantly increased compared to controls, and water in three-bottle tests to test the gastric irritation hypothesis. The IG 2M NaCl induced KCl and NaHCO3 intake that was not inhibited by gavage with gastric protectors Al(OH)3 or NaHCO3. IG 2M NaCl or gavage of 0.6N acetic acid induced mild irritation, hyperemia, of the glandular part of the stomach. A gavage of 50% ethanol induced strong irritation seen as pinpoint ulcerations. Neither ethanol nor acetic acid induced any fluid intake. Neither IG 2M NaCl nor acetic acid induced kaolin intake, a marker of pica in laboratory rats. Ethanol did induce kaolin intake. These results suggest that IG 2M NaCl induced a mineral fluid intake not selective for sodium and independent from gastric irritation or pica.

Increased Blood pH but Not Performance With Sodium Bicarbonate Supplementation in Elite Rugby Union Players

This study investigated the effect of ingesting 0.3 g/kg body weight (BW) of sodium bicarbonate (NaHCO₃) on physiological responses, gastrointestinal (GI) tolerability, and sprint performance in elite rugby union players. Twenty-five male rugby players, age 21.6 (2.6) yr, participated in a randomized, double-blind, placebo-controlled crossover trial. Sixty-five minutes after consuming 0.3 g/kg BW of either NaHCO₃ or placebo, participants completed a 25-min warm-up followed by 9 min of high-intensity rugby-specific training followed by a rugby-specific repeated-sprint test (RSRST). Whole-blood samples were collected to determine lactate and bicarbonate concentrations and pH at baseline, after supplement ingestion, and immediately after the RSRST. Acute GI discomfort was assessed by questionnaire throughout the trials, and chronic GI discomfort was assessed during the 24 hr postingestion. After supplement ingestion and immediately after the RSRST, blood HCO₃⁻ concentration and pH were higher for the NaHCO₃ condition than for the placebo condition (p < .001). After the RSRST, blood lactate concentrations were significantly higher for the NaHCO₃ than for the placebo condition (p < .001). There was no difference in performance on the RSRST between the 2 conditions. The incidence of belching, stomachache, diarrhea, stomach bloating, and nausea was higher after ingestion of NaHCO₃ than with placebo (all p < .050). The severity of stomach cramps, belching, stomachache, bowel urgency, diarrhea, vomiting, stomach bloating, and flatulence was rated worse after ingestion of NaHCO₃ than with placebo (p < .050). NaHCO₃ supplementation increased blood HCO₃⁻ concentration and attenuated the decline in blood pH compared with placebo during high-intensity exercise in well-trained rugby players but did not significantly improve exercise performance. The higher incidence and greater severity of GI symptoms after ingestion of NaHCO₃ may negatively affect physical performance, and the authors strongly recommend testing this supplement during training before use in competitive situations.

Effects of Induced Alkalosis on Simulated Match Performance in Elite Female Water Polo Players

This study investigated the effects of sodium bicarbonate (NaHCO3) ingestion on simulated water polo match performance. Twelve elite players from the Australian National Women's Water Polo Squad (age 23.7 +/- 3.0 yr, height 1.73 +/- 0.05 m, body mass 75.7 +/- 8.0 kg) participated in the study. In a randomized cross-over double-blind design, players ingested 0.3 g/kg of NaHCO3 or placebo 90 min before performing a 59-min match-simulation test (MST) that included 56 x 10-m maximal-sprint swims as the performance measure. Capillary blood samples were obtained preingestion, pre- and post-warm-up, and after each quarter of the MST. Preexercise ingestion of NaHCO3 was effective in enhancing extracellular pH from baseline levels of 7.41; +/- 0.01 (M; +/- 90% confidence limits) to 7.49; +/- 0.01 and bicarbonate levels from 24.4; +/- 0.3 to 28.5; +/- 0.5 mmol/L. The percentage difference in mean sprint times between trials showed no substantial effects of NaHCO3 (0.4; +/- 1.0, effect size = 0.09; +/- 0.23; p = .51). These findings are contrary to those of previous NaHCO3 studies on simulated team-sport performance, but this investigation is unique in that it examined highly trained athletes performing sport-specific tasks. In conclusion, water polo players should not expect substantial enhancement in intermittent-sprint performance from NaHCO3 supplementation.

Effect of Induced Alkalosis on the Power-Duration Relationship of "All-out" Exercise

We tested the hypotheses that sodium bicarbonate (NaHCO3) ingestion would result in no alteration in critical power (CP) but would improve performance in a 3-min all-out cycling test by increasing the total amount of work done above CP (W'). Eight habitually active subjects completed 3-min all-out sprints against fixed resistance in a blind randomized design after a dose of 0.3 g.kg body mass of NaHCO3 and 0.045 g.kg body mass of sodium chloride (placebo; PL trial). Blood acid-base status was assessed from arterialized fingertip blood samples before and after exercise. The CP was calculated as the mean power output during the final 30 s of the test, and the W' was estimated as the power-time integral >CP. The NaHCO3 dose was effective in inducing preexercise alkalosis as indicated by changes in blood pH (PL = 7.40 +/- 0.02 vs NaHCO3 = 7.46 +/- 0.01, P < 0.001), [bicarbonate] (PL = 21.9 +/- 3.0 vs NaHCO3 = 29.0 +/- 3.8 mM, P < 0.05), and base excess (PL = -1.9 +/- 2.5 vs NaHCO3 = 5.0 +/- 3.0 mM, P < 0.05). There were no significant differences in the total work done (PL = 62.8 +/- 10.1 vs NaHCO3 = 62.7 +/- 10.1 kJ), the CP (PL = 248 +/- 50 vs NaHCO3 = 251 +/- 51 W), or the W' (PL = 18.2 +/- 6.4 vs NaHCO3 = 17.5 +/- 6.0 kJ) estimates between treatments. Despite notably enhanced blood-buffering capacity, NaHCO3 ingestion had no effect on the W', the CP, or the overall performance during 3 min of all-out cycling. It is concluded that preexercise blood alkalosis had no influence on the power-duration relationship for all-out exercise.

Pre-Exercise Alkalosis and Acid-Base Recovery

The aim of this study was to observe the influence of pre-exercise sodium bicarbonate (NaHCO3) ingestion and varying recovery modes on acid-base recovery from a single bout of supramaximal exercise. Nine male subjects completed four separate, randomized cycle ergometer exercise trials to volitional fatigue at 120% maximum power output, under the following conditions: 0.3 g.kg(-1) BW NaHCO3 ingestion with passive recovery (BICARB P), 0.3 g.kg (-1) BW NaHCO3 ingestion with active recovery (BICARB A), placebo ingestion with passive recovery (PLAC P) and placebo ingestion with active recovery (PLAC A). Capillary blood samples were obtained every minute for 15 min during recovery. Significant main effects for pH were observed for time (F = 42.1, p < 0.001), intervention (BICARB and PLAC) (F = 1117.3, p < 0.001) and recovery condition (F = 150.0, p < 0.001), as the BICARB condition reduced acid-base perturbation. Significant interaction effects were observed between conditions (BICARB and PLAC) for active and passive recovery modes (F = 29.1, p < 0.001) as the active recovery facilitated H+ removal better than the passive condition. Pre-exercise alkalosis attenuates blood acid-base perturbations from supramaximal exercise to exhaustion, regardless of whether the recovery mode is active or passive. These findings suggest that individuals may benefit from introducing a pre-exercise alkalotic condition while including passive recovery during high-intensity training protocols.

Sodium Acetate Induces a Metabolic Alkalosis but Not the Increase in Fatty Acid Oxidation Observed Following Bicarbonate Ingestion in Humans

We conducted this study to quantify the oxidation of exogenous acetate and to determine the effect of increased acetate availability upon fat and carbohydrate utilization in humans at rest. Eight healthy volunteers (6 males and 2 females) completed 2 separate trials, 7 d apart in a single-blind, randomized, crossover design. On each occasion, respiratory gas and arterialized venous blood samples were taken before and during 180 min following consumption of a drink containing either sodium acetate (NaAc) or NaHCO3 at a dose of 2 mmol/kg body mass. Labeled [1,2-13C] NaAc was added to the NaAc drink to quantify acetate oxidation. Both sodium salts induced a mild metabolic alkalosis and increased energy expenditure (P < 0.05) to a similar magnitude. NaHCO3 ingestion increased fat utilization from 587 ± 83 kJ/180 min to 693 ± 101 kJ/180 min (P = 0.01) with no change in carbohydrate utilization. Following ingestion of NaAc, the amount of fat and carbohydrate utilized did not differ from the preingestion values. However, oxidation of the exogenous acetate almost entirely (90%) replaced the additional fat that had been oxidized during the bicarbonate trial. We determined that 80.1 ± 2.3% of an exogenous source of acetate is oxidized in humans at rest. Whereas NaHCO3 ingestion increased fat oxidation, a similar response did not occur following NaAc ingestion despite the fact both sodium salts induced a similar increase in energy expenditure and shift in acid-base balance.

Sodium Bicarbonate Ingestion Alters the Slow but Not the Fast Phase of V˙O2 Kinetics

The influence of metabolic alkalosis (ALK) on pulmonary O2 uptake (pVO2) kinetics during high-intensity cycle exercise is controversial. The purpose of this study was to examine the influence of ALK induced by sodium bicarbonate (NaHCO3) ingestion on pVO2 kinetics, using a sufficient number of repeat-step transitions to provide high confidence in the results obtained. Seven healthy males completed step tests to a work rate requiring 80% pVO2max on six separate occasions: three times after ingestion of 0.3 g x kg(-1) body mass NaHCO3 in 1 L of fluid, and three times after ingestion of a placebo (CON). Blood samples were taken to assess changes in acid-base balance, and pVO2 was measured breath-by-breath. NaHCO3 ingestion significantly increased blood pH and [bicarbonate] both before and during exercise relative to the control condition (P < 0.001). The time constant of the phase II pVO2 response was not different between conditions (CON: 29 +/- 6 vs ALK: 32 +/- 7 s; P = 0.21). However, the onset of the pVO2 slow component was delayed by NaHCO3 ingestion (CON: 120 +/- 19 vs ALK: 147 +/- 34 s; P < 0.01), resulting in a significantly reduced end-exercise pVO2 (CON: 2.88 +/- 0.19 vs ALK: 2.79 +/- 0.23 L x min(-1); P < 0.05). Metabolic alkalosis has no effect on phase II pVO2 kinetics but alters the pVO2 slow-component response, possibly as a result of the effects of NaHCO3 ingestion on muscle pH.

Dose-Related Effects of Prolonged NaHCO3 Ingestion during High-Intensity Exercise

Sodium bicarbonate (NaHCO3) ingestion may prevent exercise-induced perturbations in acid-base balance, thus resulting in performance enhancement. This study aimed to determine whether different levels of NaHCO3 intake influences acid-base balance and performance during high-intensity exercise after 5 d of supplementation. Twenty-four men (22 +/- 1.7 yr) were randomly assigned to one of three groups (eight subjects per group): control (C, placebo), moderate NaHCO3 intake (MI, 0.3 g x kg(-1) x d(-1)), and high NaHCO3 intake (HI, 0.5 g x kg(-1) x d(-1)). Arterial pH, HCO3(-), PO2, PCO2, K+, Na, base excess (BE), lactate, and mean power (MP) were measured before and after a Wingate test pre- and postsupplementation. HCO3(-) increased proportionately to the dosage level. No differences were detected in C. Supplementation increased MP (W x kg(-)) in MI (7.36 +/- 0.7 vs 6.73 +/- 1.0) and HI (7.72 +/- 0.9 vs 6.69 +/- 0.6), with HI being more effective than MI. NaHCO3 ingestion resulted postexercise in increased lactate (mmol x L(-1)) (12.3 +/- 1.8 vs 10.3 +/- 1.9 and 12.4 +/- 1.2 vs 10.4 +/- 1.5 in MI and HI, respectively), reduced exercise-induced drop of pH (7.305 +/- 0.04 vs 7.198 +/- 0.02 and 7.343 +/- 0.05 vs 7.2 +/- 0.01 in MI and HI, respectively) and HCO3(-) (mmol x L(-1)) (13.1 +/- 2.4 vs 17.5 +/- 2.8 and 13.2 +/- 2.7 vs 19.8 +/- 3.2 for HCO3 in MI and HI, respectively), and reduced K (3.875 +/- 0.2 vs 3.625 +/- 0.3 mmol x L(-1) in MI and HI, respectively). NaHCO3 administration for 5 d may prevent acid-base balance disturbances and improve performance during anaerobic exercise in a dose-dependent manner.

Sodium Bicarbonate Ingestion and its Effects on Blood Lactate and Judo-Related Performance

High intensity intermittent efforts are the main judo characteristics. In this kind of activity, muscular acidosis is one of the most important causes of fatigue. Since sodium bicarbonate (NaHCO3) decreases intramuscular acidosis and, therefore, delays the onset of fatigue in high intensity intermittent exercises, we hypothesized that NaHCO3 ingestion could improve judo-related performance. PURPOSE: to verify if NaHCO3 ingestion improves the performance in a specific judo test (Special Judo Fitness Test - SJFT). METHODS: nine judo competitors took part in this study (age: 21,5 + 3 years; weight: 68,7±7,7 kg; height: 1,7 ± 0,06 m; body fat: 6 ± 1,5%). They performed 3 series of SJFT, in two different days after NaHCO3 or placebo ingestion. Time recovery between series was 5 minutes. During recovery, blood samples were drawn for lactate analysis. The athletes ingested gelatinous capsules 2 hours prior to the trials. The dose was 0.3 g·kg−1 and the study was in a double-blind placebo-controlled fashion. They received a different treatment in counterbalanced order on each occasion RESULTS: ANOVA for repeated measures revealed a significant treatment effect for performance and lactate (p< 0,05), as showed in table 1. T-tests for dependent samples were used to locate differences between groups.TableCONCLUSION: sodium bicarbonate ingestion improves judo-related performance, especially when fatigue is more pronounced. The greater lactate concentration after NaHCO3 ingestion suggests that the ergogenic effect occurs due to an increase in glicolytic pathway activity. Supported by FAPESP (# 02/04497-2).

Sodium acetate ingestion perturbs substrate utilisation at rest and during the early stages of prolonged exercise in man

Sodium acetate administration has been shown to increase muscle acetyl-CoA and acetylcarnitine content at rest and during the early stages of exercise. We therefore investigated the effect of sodium acetate ingestion at rest on subsequent substrate utilisation during prolonged exercise. With local ethics approval six healthy males ingested either sodium acetate (NaAc) or sodium bicarbonate (NaHCO3) at a dose of 4 mmol.kg−1 body mass in a randomised order over 90 min prior to 120 min of exercise at 50% V̇O2max. NaAc ingestion decreased resting fat oxidation (0.09 ± 0.02 vs. 0.07 ± 0.02 g.min−1 pre- and post-ingestion respectively, P<0.05) with no effect upon carbohydrate utilisation. In contrast, NaHCO3 ingestion did not affect substrate utilisation at rest. Fat and CHO oxidation increased in both trials when exercise was undertaken, but fat oxidation was lower (0.16 ± 0.10 vs. 0.30 ± 0.10 g.min−1, P<0.05) and carbohydrate oxidation higher (1.75 ± 0.36 vs. 1.50 ± 0.23 g.min−1, P<0.05) in the NaAc compared with the NaHCO3 trial during the first 15 min of exercise. Plasma acetate concentration had returned to baseline after 30 min of exercise in the NaAc trial with no difference in either fat or carbohydrate utilisation between the trials over the last 90 min of exercise. These results demonstrate that increasing plasma acetate concentration suppresses fat oxidation at rest and at the onset of exercise possibly due to changes in acetyl group availability.

Effects of Induced Metabolic Alkalosis on Prolonged Intermittent-Sprint Performance

Previous studies have shown that induced metabolic alkalosis, via sodium bicarbonate (NaHCO3) ingestion, can improve short-term, repeated-sprint ability. The purpose of this study was to assess the effects of NaHCO3 ingestion on a prolonged, intermittent-sprint test (IST). Seven female team-sport athletes (mean +/- SD: age = 19 +/- 1 yr, VO2peak = 45.3 +/- 3.1 mL x kg(-1) x min(-1)) volunteered for the study, which had received ethics clearance. The athletes ingested two doses of either 0.2 g x kg(-1) of NaHCO3 or 0.138 g x kg(-1) of NaCl (placebo), in a double-blind, random, counterbalanced order, 90 and 20 min before performing the IST on a cycle ergometer (two 36-min "halves" of repeated approximately 2-min blocks: all-out 4-s sprint, 100 s of active recovery at 35% VO2peak, and 20 s of rest). Capillary blood samples were drawn from the ear lobe before ingestion, and before, during, and after each half of the IST. VO2 was also recorded at regular intervals throughout the IST. Resting plasma bicarbonate concentration ([HCO3-]) averaged 22.6 +/- 0.9 mmol x L(-1), and at 90 min post-ingestion was 21.4 +/- 1.5 and 28.9 +/- 2.8 mmol x L-1 for the placebo and NaHCO3 conditions, respectively (P < 0.05). Plasma [HCO3-] during the NaHCO3 condition remained significantly higher throughout the IST compared with both placebo and pre-ingestion. There was a trend toward improved total work in the second (P = 0.08), but not first, half of the IST after the ingestion of NaHCO3. Furthermore, subjects completed significantly more work in 7 of 18 second-half, 4-s sprints after NaHCO3 ingestion. The results of this study suggest that NaHCO3 ingestion can improve intermittent-sprint performance and may be a useful supplement for team-sport athletes.

SODIUM BICARBONATE AND SODIUM CITRATE

Numerous studies have used exogenous administration of sodium bicarbonate (NaHCO3) and sodium citrate (Na-citrate) in an attempt to enhance human performance. After ingestion of NaHCO3 and Nacitrate, two observations have been made: (a) There was great individual variability in the ergogenic benefit reached, which can be attributed to the level of physical conditioning of the subjects and to their tolerance of the buffer substance; and (b) the subjects who had ingested NaHCO3 and Na-citrate show higher levels of pH, bicarbonate, and lactate ions concentrations in their exercising blood than do the subjects who had ingested the placebo. A majority of the studies have suggested that the ingestion of both substances provides an ergogenic effect due to the establishment and maintenance of an elevated pH level during exercise. However, the exact mechanism by which the ergogenic effects occur has not been demonstrated conclusively. Sodium bicarbonate and Na-citrate seem to be effective in activities with a sufficient duration to generate a difference in the hydrogen ion gradient, characterized by a very high intensity and involving large muscular groups. However, in activities of equally high intensity, but with longer duration, the results obtained have been conflicting and inconclusive.

Dose-related Effects of Sodium Bicarbonate Ingestion on Acid-base Balance During Exhausting Anaerobic Exercise

1166 Anaerobic exercise causes significant acid-base balance perturbations. It has been suggested that sodium bicarbonate (NaHCO3) may prevent a significant pH drop during anaerobic exercise resulting in performance enhancement. PURPOSE: To determine whether two intake levels of short-term NaHCO3 supplementation alters acid-base balance and performance during an acute bout of anaerobic exercise. METHODS: Twenty-four men (22 ± 1.77 yrs, 77.5 ± 7.8 kg, 1.79 ± 6.6 m, and a VO2max of 51.03 ± 7.53 ml/kg/min) participated in the present study. Subjects were randomly assigned to one of 3 groups (n = 8/group): control (C, sugar-free mixed fruit placebo), moderate NaHCO3 intake (MI, 0.3 gr/kg), and high NaHCO3 intake (HI, 0.5 gr/kg). Participants consumed either placebo or NaHCO3 for 6 days. pH, HCO3, PO2, PCO2, and lactate in arterialised blood as well as mean cycling power were determined prior to and immediately following a Wingate test (before and following the supplementation period). Data were analysed by ANOVA repeated measures. RESULTS: There was a significant increase (p<0.001) in post blood bicarbonate in MI and HI, and the elevation was incrementally related to the dosage. Exercise in C caused a reduction (p<0.05) of pH (7.42 ± 0.01 at rest vs. 7.15 ± 0.02 post-exercise) and PCO2 (mmHg) (39.8 ± 2.3 at rest vs. 34.3 ± 1.9 post-exercise) and an increase (p<0.001) of lactate (mM) (0.9 ± 0.1 at rest vs. 10.9 ± 2.0 post-exercise). Mean power (W/kg) increased (p<0.05) after supplementation in MI (7.36 ± 1.33 vs. 6.73 ± 0.95) and HI (7.72 ± 1.24 vs. 6.69 ± 1.38) with HI being more effective (p<0.05) than MI. After NaHCO3 ingestion, blood lactate (mM) was higher (p<0.05) during exercise in MI (12.3 ± 1.5 vs. 10.3 ± 2.1) and HI (12.4 ± 1.8 vs. 10.2 ± 1.1). pH was significantly (p<0.05) elevated post-exercise when NaHCO3 was ingested (7.305 ± 0.03 vs. 7.198 ± 0.02 in MI and 7.343 ± 0.02 vs. 7.2 ± 0.01 in HI). HCO3 decreased (p<0.05) with NaHCO3 ingestion post-exercise (29.8 ± 3.3 vs. 17.56 ± 2.5 in MI and 19.8 ± 3.2 vs. 32.3 ± 4.1 in HI). PO2 (mmHg) increased (p<0.05) with NaHCO3 consumption post-exercise (113.3 ± 7.7 vs. 93.2 ± 6.9 in MI and 116.7 ± 8.2 vs. 92.7 ± 7.5 in HI) with HI being more effective (P<0.05) than MI. PCO2 declined (p<0.05) with NaHCO3 supplementation post-exercise (42.8 ± 3.3 vs. 36.2 ± 2.9 in MI and 44.2 ± 5.3 vs. 34.8 ± 4.1 in HI) with HI being more effective (P<0.05) than MI. CONCLUSIONS: Short-term NaHCO3 ingestion may be beneficial for protecting against acid-base balance disturbances and improve performance during acute anaerobic exercise. However, it appears that this NaHCO3-effect on acid-base balance and performance is dose-related with higher intakes being more effective.

Metabolic effects of induced alkalosis during progressive forearm exercise to fatigue.

Metabolic alkalosis induced by sodium bicarbonate (NaHCO(3)) ingestion has been shown to enhance performance during brief high-intensity exercise. The mechanisms associated with this increase in performance may include increased muscle phosphocreatine (PCr) breakdown, muscle glycogen utilization, and plasma lactate (Lac(-)(pl)) accumulation. Together, these changes would imply a shift toward a greater contribution of anaerobic energy production, but this statement has been subject to debate. In the present study, subjects (n = 6) performed a progressive wrist flexion exercise to volitional fatigue (0.5 Hz, 14-21 min) in a control condition (Con) and after an oral dose of NaHCO(3) (Alk: 0.3 g/kg; 1.5 h before testing) to evaluate muscle metabolism over a complete range of exercise intensities. Phosphorus-31 magnetic resonance spectroscopy was used to continuously monitor intracellular pH, [PCr], [P(i)], and [ATP] (brackets denote concentration). Blood samples drawn from a deep arm vein were analyzed with a blood gas-electrolyte analyzer to measure plasma pH, Pco(2), and [Lac(-)](pl), and plasma [HCO(3)(-)] was calculated from pH and Pco(2). NaHCO(3) ingestion resulted in an increased (P < 0.05) plasma pH and [HCO(3)(-)] throughout rest and exercise. Time to fatigue and peak power output were increased (P < 0.05) by approximately 12% in Alk. During exercise, a delayed (P < 0.05) onset of intracellular acidosis (1.17 +/- 0.26 vs. 1.28 +/- 0.22 W, Con vs. Alk) and a delayed (P < 0.05) onset of rapid increases in the [P(i)]-to-[PCr] ratio (1.21 +/- 0.30 vs. 1.30 +/- 0.30 W) were observed in Alk. No differences in total [H(+)], [P(i)], or [Lac(-)](pl) accumulation were detected. In conclusion, NaHCO(3) ingestion was shown to increase plasma pH at rest, which resulted in a delayed onset of intracellular acidification during incremental exercise. Conversely, NaHCO(3) was not associated with increased [Lac(-)](pl) accumulation or PCr breakdown.

Effect of sodium bicarbonate on muscle metabolism during intense endurance cycling

STEPHENS, T. J., M. J. McKENNA, B. J. CANNY, R. J. SNOW, and G. K. McCONELL. Effect of sodium bicarbonate on muscle metabolism during intense endurance cycling. Med. Sci. Sports Exerc., Vol. 34, No. 4, pp. 614–621, 2002. Introduction Sodium bicarbonate (NaHCO3) ingestion has been shown to increase both muscle glycogenolysis and glycolysis during brief submaximal exercise. These changes may be detrimental to performance during more prolonged, exhaustive exercise. This study examined the effect of NaHCO3 ingestion on muscle metabolism and performance during intense endurance exercise of ∼60 min in seven endurance-trained men. Methods Subjects ingested 0.3 g·kg−1 body mass of either NaHCO3 or CaCO3 (CON) 2 h before performing 30 min of cycling exercise at 77 ± 1% V̇O2peak followed by completion of 469 ± 21 kJ as quickly as possible (∼30 min, ∼80% V̇O2peak). Results Immediately before, and throughout exercise, arterialized-venous plasma HCO3− concentrations were higher (P < 0.05) whereas plasma and muscle H+ concentrations were lower (P < 0.05) in NaHCO3 compared with CON. Blood lactate concentrations were higher (P < 0.05) during exercise in NaHCO3, but there was no difference between trials in muscle glycogen utilization or muscle lactate content during exercise. Reductions in PCr and ATP and increases in muscle Cr during exercise were also unaffected by NaHCO3 ingestion. Accordingly, exercise performance time was not different between treatments. Conclusion NaHCO3 ingestion resulted in a small muscle alkalosis but had no effect on muscle metabolism or intense endurance exercise performance in well-trained men.

Effect of sodium bicarbonate on muscle metabolism during intense endurance cycling.

Sodium bicarbonate (NaHCO3) ingestion has been shown to increase both muscle glycogenolysis and glycolysis during brief submaximal exercise. These changes may be detrimental to performance during more prolonged, exhaustive exercise. This study examined the effect of NaHCO3 ingestion on muscle metabolism and performance during intense endurance exercise of approximately 60 min in seven endurance-trained men. Subjects ingested 0.3 g.kg-1 body mass of either NaHCO3 or CaCO3 (CON) 2 h before performing 30 min of cycling exercise at 77 +/- 1% .VO(2peak) followed by completion of 469 +/- 21 kJ as quickly as possible (approximately 30 min, approximately 80% .VO(2peak)). Immediately before, and throughout exercise, arterialized-venous plasma HCO3- concentrations were higher (P < 0.05) whereas plasma and muscle H+ concentrations were lower (P < 0.05) in NaHCO3 compared with CON. Blood lactate concentrations were higher (P < 0.05) during exercise in NaHCO3, but there was no difference between trials in muscle glycogen utilization or muscle lactate content during exercise. Reductions in PCr and ATP and increases in muscle Cr during exercise were also unaffected by NaHCO3 ingestion. Accordingly, exercise performance time was not different between treatments. NaHCO3 ingestion resulted in a small muscle alkalosis but had no effect on muscle metabolism or intense endurance exercise performance in well-trained men.

Role of skeletal muscle in plasma ion and acid-base regulation after NaHCO3 and KHCO3 loading in humans.

This paper examines the time course of changes in plasma electrolyte and acid-base composition in response to NaHCO3 and KHCO3 ingestion. It was hypothesized that skeletal muscle is involved in the correction of the ensuing plasma disturbance by exchanging ions, gasses, and fluids between cells and extracellular fluids. Five male subjects, with catheters in a brachial artery and antecubital vein, ingested 3.57 mmol/kg body mass NaHCO3 or KHCO3. While seated, blood samples were taken 30 min before ingestion of the solution, at 10-min intervals during the 60-min ingestion period, and periodically for 210 min after ingestion was complete. Blood was analyzed for gases, hematocrit, plasma ions, and total protein. With NaHCO3, arterial plasma Na+ concentration ([Na+]) increased from 143 +/- 1 to 147 +/- 1 (SE) meq/l, H+ concentration ([H+]) decreased by 6 +/- 1 neq/l, and PCO2 increased by 5 +/- 1 mmHg. There was no detectable net Na+ uptake by tissues. An increased plasma strong ion difference ([SID]) accounted fully for the decrease in plasma [H+]. With KHCO3, K+ concentration increased from 4.25 +/- 0.10 to 7.17 +/- 0.13 meq/l, plasma volume decreased by 15.5 +/- 2.3%, [H+] decreased by 4 +/- 1 neq/l, and there was no change in PCO2. The decrease in [H+] in the KHCO3 trial primarily arose in response to the increased [SID]. Net K+ uptake by tissues accounted for 37 +/- 5% of the ingested K+. In conclusion, ingestion of NaHCO3 and KHCO3 produced markedly different fluid and ionic disturbances and associated regulatory responses by skeletal muscle. Accordingly, the physicochemical origins of the acid-base disturbances also differed between treatments. The tissues did not play a role in regulating plasma [Na+] after ingestion of NaHCO3. In contrast, the net influx of K+ to tissues played an important role in removing K+ from the extracellular compartment after ingestion of KHCO3.

Effect of acid-base disturbances on aldosterone secretion in man.

The present study was carried out to elucidate whether changes in blood pH induced by administration of alkalinizing and acidifying agents influence aldosterone secretion in man. Since aldosterone secretion is known to be regulated by various factors such as the renin-angiotensin system, adrenocorticotropic hormone (ACTH), and serum potassium concentration, these indices were simultaneously measured during manipulation. Oral administration of tris hydroxymethyl aminomethane (THAM) resulted in a moderate but not significant decrease in serum aldosterone together with an increase in blood pH, whereas plasma renin activity (PRA) remained unchanged and serum potassium was elevated. ACTH and cortisol decreased significantly. Following CaCO3 ingestion, blood pH, serum potassium concentration, and hormones did not change significantly compared with before ingestion. NH4Cl ingestion showed a significant fall of blood pH and serum cortisol, on the other hand, aldosterone increased significantly compared with CaCO3 ingestion. Following NaHCO3 ingestion, serum aldosterone decreased with an increase in blood pH compared with before ingestion, while serum cortisol and PRA did not change significantly. The overall results of experiments using THAM, CaCO3, NaHCO3, and NH4Cl led to the conclusion that under acid-base disturbances a change in aldosterone can not be induced by either renin-angiotensin or ACTH. We suggest that under acid-base disturbances blood pH may be related, at least, in part to changes in aldosterone in humans.

Effect of ingested sodium bicarbonate on muscle force, fatigue, and recovery.

The influence of acute ingestion of NaHCO3 on fatigue and recovery of teh quadriceps femoris muscle after exercise was studied in six healthy male subjects. A bicycle ergometer was used for exercising under three loading conditions: test A, load corresponding to maximal oxygen consumption; test B, load in test A + 17%; test C, load in test B but performed 1 h after acute ingestion of NaHCO3. Functional electrical stimulation (FES) was applied to provoke isometric contraction of the quadriceps femoris. The resulting knee torque was monitored during fatigue (2-min chronic FES) and recovery (10-s FES every 10 min, for 40 min). Quadriceps torques were higher in the presence of NaHCO3 (P < 0.05): with NaHCO3 the peak, residual, and recovery (after 40 min) normalized torques were, respectively, 0.68 +/- 0.05 (SD), 0.58 +/- 0.05, and 0.73 +/- 0.05; without NaHCO3 the values were 0.45 +/- 0.04, 0.30 +/- 0.06, and 0.63 +/- 0.06. The increased torques obtained after acute ingestion of NaHCO3 indicate the possible existence of improved nonoxidative glycolysis in isometric contraction, resulting in reduced fatigue and enhanced recovery.

Light-chain-induced renal tubular acidosis: effect of sodium bicarbonate on sodium-proton exchange

We measured sodium-proton (Na+/H+) exchange in lymphocytes and platelets of a 46-year-old woman with the adult Fanconi syndrome before, during, and after treatment with NaHCO3. Kappa light chains in her urine and unique but rarely observed crystalline structures confirmed the presence of light-chain nephropathy. Her glomerular filtration rate was only moderately impaired at 72 ml/min. NaHCO3 at 1, 3, and 5 mmol/kg/day for 5 days increased her serum HCO3 and pH from 17 to 21 mmol/l and 7.28 to 7.39 respectively. Plasma renin and aldosterone values were decreased by NaHCO3. Na+/H+ exchange (delta Hi/min) was measured with the fluorescent marker BCECF after acidification of lymphocytes and platelets with sodium propionate at five (10-50 mM) doses. Na+/H+ exchange was accelerated in this patient compared to normal controls. NaHCO3 treatment significantly decreased Na+/H+ exchange in lymphocytes, but not in platelets. These findings suggest that Na+/H+ exchange can be influenced by NaHCO3 ingestion at doses that only modestly affect systemic pH. Since Na+/H+ exchange is involved in stimulus response coupling, cell growth regulation, cell differentiation, and perhaps the progression of nephrosclerosis, these observations may have clinical relevance.