The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man

The present experiment was designed to investigate whether a diet-induced metabolic acidosis was a major factor in the earlier onset of fatigue during high-intensity exercise. Six healthy males cycled to exhaustion at a workload equivalent to 95% of maximum oxygen uptake on four separate occasions. Exercise tests were performed after an overnight fast and each test was preceded by one of four experimental conditions. Two experimental diets were designed, either to replicate each subject's own normal diet [N diet, mean (SD) daily energy intake (E) = 13 (0.7) MJ, 14.5 (0.8)% protein (Pro), 37.5 (2.2)% fat (Fat) and 47.5 (2.1)% carbohydrate (CHO)], or a low-carbohydrate diet [E = 12.6 (0.8) MJ, 33.6 (1.3)% Pro, 64.4 (1.5)% Fat and 2.2 (0.4)% CHO]. These diets were prepared and consumed within the department over a 3-day period. Over a 3-period prior to the exercise trial subjects ingested either NaHCO₃ or CaCO₃ (3.6 and 3.0 mmol · kg body mass), thus giving four experimental conditions: N diet and treatment, N diet and placebo, low-CHO diet and treatment and low-CHO diet and placebo. Treatments were assigned using a randomised protocol. Arterialised venous blood samples were taken for the determination of acid-base status and metabolite concentrations at rest prior to exercise and at intervals for 30 min following exhaustion. Consumption of the low-CHO diet induced a mild metabolic acidosis which was reversed by the ingestion of NaHCO₃. Blood pH, bicarbonate (HCO₃ ^– ) and base excess (BE) were higher following NaHCO₃ ingestion after the normal diet than all of the other experimental conditions (P < 0.01). Exercise time following the low-CHO diet was less than on the normal diet conditions (P < 0.05): bicarbonate ingestion had no effect on exercise time on either of the diet conditions. Post-exercise blood pH, HCO₃ ^– and BE were higher following the ingestion of NaHCO₃ irrespective of the pre-exercise diet (P < 0.05). Blood lactate concentration was higher 2 min after exercise following the N diet with NaHCO₃ when compared to the low-CHO diets with either NaHCO₃ or placebo (P < 0.05). Plasma ammonia accumulation was not significantly different between experimental conditions. These data confirm previous data showing that the ingestion of a low-CHO diet reduces the capacity to perform high-intensity exercise, but it appears that the metabolic acidosis induced by the low-CHO diet is not the cause of the reduced exercise capacity observed during high-intensity exercise under these conditions.     

Sodium bicarbonate ingestion improves performance in interval swimming

Summary In an effort to determine the effects of bicarbonate (NaHCO₃) ingestion on exercise performance, ten male college swimmers were studied during five different trials. Each trial consisted of five 91.4m (100-yd) front crawl swims with a two-minute rest interval between each bout. The trials consisted of two NaHCO₃ treatments, two placebo trials and one test with no-drink. One hour before the onset of swimming, the subjects were given 300 ml of citric acid flavored solution containing either 17 mmol of NaCl (placebo) or 2.9 mmol of NaHCO₃ · kg^–1 body weight (experimental), or received no drink (no-drink). Performance times for each 91.4 m swim were recorded. Blood samples were obtained before and one hr after treatment, two min after warmup, and two min after the final 91.4 m sprint. Blood pH, lactate, standard bicarbonate (SBC) and base excess (BE) were measured. No differences were found for performance or the blood measurements between the placebo and no-drink trials. Bicarbonate feedings, on the other hand, produced a significant (P<0.05) improvement in performance on the fourth and fifth swimming sprints. Blood lactate, pH, SBC and BE were significantly higher (P<0.05) at post-exercise in NaHCO₃ treatments. These data are in agreement with previous findings that during repeated bouts of exercise pre-exercise administration of NaHCO₃ improves performance, possibly by facilitating the efflux of hydrogen ions from working muscles and thereby delaying the onset of fatigue.     

Sodium citrate ingestion and its effects on maximal anaerobic exercise of different durations

Summary The effects of an alkalising agent were studied in ten subjects who participated in anaerobic testing on a cycle ergometer to determine the effectiveness of sodium citrate (0.5 g·kg^–1 body mass) as an ergogenic aid during exercise of 10-s, 30-s, 120-s and 240-s duration. Blood was collected prior to, after ingestion of sodium citrate (NaHCO₃), and postexercise, from a heated (43–46°C) fingertip and analysed immediately postcollection for pH, partial pressure of oxygen and carbon dioxide, base excess and blood bicarbonate. Total work undertaken (kJ) and peak power (W) achieved during the tests was also obtained via a work monitor unit. The results indicated that a dose of 0.5 g sdkg^–1 body mass sodium citrate had no ergogenic benefit for exercise of either 10-s or 30-s duration. Blood bicarbonate concentrations, however, were significantly increased (P<0.05) following ingestion of the citrate during these trials. Exercise periods of 120 s and 240 s were significantly increased (P<0.05) above the control and placebo conditions following sodium citrate ingestion. Blood bicarbonate concentrations were again increased above control and placebo conditions and blood lactate concentrations were also increased following the citrate trials. The pH decreased significantly (P<0.05) in all trials below the control and placebo conditions. On the basis of the exercise undertaken in this study we would suggest that a dose of 0.5 g·kg^–1 body mass of sodium citrate could improve anaerobic exercise performance of 120-s and 240-s duration.     

The effect of induced alkalosis and acidosis on plasma lactate and work output in elite oarsmen

Summary In order to test the effect of artificially induced alkalosis and acidosis on the appearance of plasma lactate and work production, six well-trained oarsmen (age=23.8±2.5 years; mass=82.0±7.5 kg) were tested on three separate occasions after ingestion of 0.3 g·kg⁻¹. NH₄Cl (acidotic), NaHCO₃ (alkalotic) or a placebo (control). Blood was taken from a forearm vein immediately prior to exercise for determination of pH and bicarbonate. One hour following the ingestion period, subjects rowed on a stationary ergometer at a pre-determined sub-maximal rate for 4 min, then underwent an immediate transition to a maximal effort for 2 min. Blood samples from an indwelling catheter placed in the cephalic vein were taken at rest and every 30 s during the 6 min exercise period as well as at 1, 3, 6, 9, 12, 15, 18, 21, 25 and 30 min during the passive recovery period. Pre-exercise blood values demonstrated significant differences (p<0.01) in pH and bicarbonate in all three conditions. Work outputs were unchanged in the submaximal test and in the maximal test (p>0.05), although a trend toward decreased production was evident in the acidotic condition. Analysis of exercise blood samples using ANOVA with repeated measures revealed that the linear increase in plasma lactate concentration during control was significantly greater than acidosis (p<0.01). Although plasma lactate values during alkalosis were consistantly elevated above control there was no significant difference in the linear trend (p>0.05). During recovery, there was no significant difference in the rate of lactate disappearance amongst the three conditions. It is concluded that under this protocol artificial manipulation of the acid-base status of the blood does not significantly influence work production despite significantly reduced plasma lactate concentrations during acidosis. The inability of these pH changes to alter exercise performance emphasizes the relative importance of the intracellular and the extracellular buffer systems in well trained athletes.     

The CSF/Blood Potential in Sustained Acid-Base Changes in the Rat. With Calculations of Electrochemical Potential Differences for H+and HCO-3

The electrical D.C. potential difference between cisternal cerebrospinal fluid and external jugular blood was measured in rats during sustained acid-base changes. One group, serving as a control series, was given an artificial extracellular fluid i.p., while two other groups were made acidotic or alkalotic by means of i.p. injections of NH₄Cl or NaHCO₃ solutions. In the last two groups NH₄Cl or NaHCO₃ was given, but Con was simultaneously administered so as to keep either the plasma bicarbonate or the plasma pH constant. In all groups the CSF/ plasma potential was permanently changed in relation to the arterial plasma pH, but there was a larger potential change in alkalosis (about 50 mV/pH unit) than in acidosis (about 30 mV/pH unit). Calculations of electrochemical potential differences for H+and HCO₃^-between CSF and plasma showed no significant differences in nonrespiratory acidosis and alkalosis but significant increases in hypercapnia. The results do not support the theory that an active H+transport regulates the CSF pH to constancy.     

Sodium bicarbonate supplementation improves hypertrophy-type resistance exercise performance

The aim of the present study was to examine the effects of sodium bicarbonate (NaHCO₃) administration on lower-body, hypertrophy-type resistance exercise (HRE). Using a double-blind randomized counterbalanced design, 12 resistance-trained male participants (mean ± SD; age = 20.3 ± 2 years, mass = 88.3 ± 13.2 kg, height = 1.80 ± 0.07 m) ingested 0.3 g kg^?1 of NaHCO₃ or placebo 60 min before initiation of an HRE regimen. The protocol employed multiple exercises: squat, leg press, and knee extension, utilizing four sets each, with 10–12 repetition-maximum loads and short rest periods between sets. Exercise performance was determined by total repetitions generated during each exercise, total accumulated repetitions, and a performance test involving a fifth set of knee extensions to failure. Arterialized capillary blood was collected via fingertip puncture at four time points and analyzed for pH, [HCO₃ ^?], base excess (BE), and lactate [Lac^?]. NaHCO₃ supplementation induced a significant alkaline state (pH: NaHCO₃: 7.49 ± 0.02, placebo: 7.42 ± 0.02, P < 0.05; [HCO₃ ^?]: NaHCO₃: 31.50 ± 2.59, placebo: 25.38 ± 1.78 mEq L^?1, P < 0.05; BE: NaHCO₃: 7.92 ± 2.57, placebo: 1.08 ± 2.11 mEq L^?1, P < 0.05). NaHCO₃ administration resulted in significantly more total repetitions than placebo (NaHCO₃: 139.8 ± 13.2, placebo: 134.4 ± 13.5), as well as significantly greater blood [Lac^?] after the exercise protocol (NaHCO₃: 17.92 ± 2.08, placebo: 15.55 ± 2.50 mM, P < 0.05). These findings demonstrate ergogenic efficacy for NaHCO₃ during HRE and warrant further investigation into chronic training applications.     

Acute and chronic loading of sodium bicarbonate in highly trained swimmers

In the present study, 200-m swim time in highly trained male swimmers was measured on two consecutive days (Trial 1 and Trial 2) and under three conditions [(1) acute loading, AcL; (2) chronic loading, ChL; (3) Placebo, PLA]. No sodium bicarbonate (NaHCO₃) was administered between Trial 1 and Trial 2 under each condition. Blood lactate concentration ([La⁻]), base excess of extracellular fluid (BE_ecf), plasma bicarbonate concentration ([HCO₃ ⁻]) and pH were determined before and after capsule administration as well as at 0, 3, 5, 15 and 30 min after each 200-m swim trial. Swim time was not different among AcL, ChL or PLA for Trial 1 or 2 and we observed no change in 200-m swim time from Trial 1 to 2 under any condition (F = 0.48, P = 0.80). [HCO₃ ⁻], pH and BE_ecf measured after capsule administration was higher during AcL and ChL when compared with PLA (P < 0.05). We did not observe any difference in blood [La⁻] between the three conditions at any stage post-exercise (P > 0.05). The results indicate that acute and chronic loading of NaHCO₃ does not improve 200-m swim time in highly trained male swimmers.     

Effects of bicarbonate ingestion and high intensity exercise on lactate and H(+)-ion distribution in different blood compartments

Lactate (La) and H⁺-ions are unequally distributed in the blood between plasma and red blood cells (RBCs). To our knowledge there is no data concerning the effects of an oral ingestion of bicarbonate (HCO₃ ⁻) on repeated high intensity sprint exercise and La and H⁺ distribution between plasma and RBCs. Since an oral ingestion of HCO₃ ⁻ leads to a higher efflux of La from the working skeletal muscle to the plasma, as it was shown by previous studies, this would lead to a higher gradient of La between plasma and RBCs. Although a higher gradient leads to a higher uptake, it is even more difficult for the RBCs to take up La fast enough, due to the more stressed transport system. Since RBCs function to transport La from the working muscle and help to maintain a concentration difference between plasma and muscle, this potentially increases performance during repeated sprint exercise (e.g. 4 × 30 s). The major goal of the present investigation was to test this hypothesis. 11 male participants ingested either a solution of sodium bicarbonate (NaHCO₃) or placebo (CaCO₃). Thereafter all performed four maximal 30 s sprints with 5 min of passive rest. During the resting periods concentrations of HCO₃ ⁻, La and H⁺ where measured in both blood compartments (plasma and RBCs). There were no significant differences in the La-ratios between plasma and RBCs between both interventions. These results indicate that the La/H⁺ co-transport is not affected by an oral ingestion on NaHCO₃.     

Bicarbonate ingestion has no ergogenic effect on consecutive all out sprint tests in BMX elite cyclists

The aim of the present study was to examine the effect of sodium bicarbonate ingestion on consecutive "all out" sprint tests, analyzing the acid-base status and its influence on performance and perceived effort. Ten elite bicycle motocross (BMX) riders (20.7 ± 1.4 years, training experience 8-12 years) participated in this study which consisted of two trials. Each trial consisted of three consecutive Wingate tests (WTs) separated by 15 min recovery. Ninety minutes prior to exercise subjects ingested either NaHCO(3) (-) (0.3 g kg(-1) body weight) or placebo. Blood samples were collected for the assessment of blood acid-base status: bicarbonate concentration ([HCO(3) (-)]), pH, base excess (BE) and blood lactate concentration ([La(-)]). Performance variables of peak power (PP), mean power (MP), time to peak power and fatigue index were calculated for each sprint. Significant differences (p < 0.05) were observed in acid-base variables [pH before WT1: 7.47 ± 0.05 vs. 7.41 ± 0.03; [HCO(3) (-)] before WT1: 29.08 ± 2.27 vs. 22.85 ± 0.24 mmol L(-1) (bicarbonate vs. placebo conditions, respectively)], but there were not significant differences in performance variables between trials [PP WT1: 1,610 ± 373 vs. 1,599 ± 370 W; PP WT2: 1,548 ± 460 vs. 1,570 ± 428 W; PP WT3: 1,463 ± 361 vs. 1,519 ± 364 W. MP WT1: 809 ± 113 vs. 812 ± 108 W; MP WT2: 799 ± 135 vs. 799 ± 124 W; MP WT3: 762 ± 165 vs. 782 ± 118 W (bicarbonate vs. placebo conditions, respectively)]. Rating of perceived effort (RPE) was not influenced nor ratings of perceived readiness. Sodium bicarbonate ingestion modified significantly the blood acid-base balance, although the induced alkalosis did not improve the Wingate test performance, RPE and perceived readiness across three consecutive WTs in elite BMX cyclists.     

The effect of sodium bicarbonate and sodium citrate ingestion on anaerobic power during intermittent exercise

Summary The effect of sodium bicarbonate and sodium citrate ingestion on cycling performance in three 30 s Wingate Anaerobic Tests separated by 6 min recovery periods has been studied using 6 male subjects. Subjects ingested either sodium bicarbonate (B), sodium bicarbonate plus sodium citrate (BC), sodium citrate (C) or sodium chloride (P) 2.5 h prior to exercise in a dose of 0.3 g kg⁻¹ body weight. Pre-exercise blood pH was 7.44±0.06, 7.42±0.05, 7.41±0.05 and 7.38±0.04 in the C, BC, B and P conditions respectively. Mean and peak power output were significantly reduced by successive Wingate tests but not significantly affected by the treatments. Performance in the second and third tests was highest following C, BC and B ingestion. The total work done in the 3 tests was 103%, 102% and 101% of that achieved in the P condition after C, BC and B ingestion respectively. The increased alkali reserve recorded subsequent to bicarbonate and citrate treatment reduced mean post-exercise acidosis, although pH was significantly higher only in the C condition (p<0.05) compared to P after each exercise bout. No significant differences in plasma lactate concentration were recorded at any time. Citrate ingestion appears to be most effective in elevating blood pH and [HCO₃ ⁻], and in enhancing performance in short-term intermittent exercise. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood and has a small, but non-significant, effect on anaerobic power and capacity as measured in a series of 3 Wingate Anaerobic Tests.     

The effect of ammonium chloride and sodium bicarbonate ingestion on the physical working capacity at the fatigue threshold

Summary The purpose of this investigation was to examine the effect of ammonium chloride (NH₄Cl) and sodium bicarbonate (NaHCO₃) ingestion on the physical working capacity at the fatigue threshold (PWC_FT). Eighteen adult males (mean age, SD=23, 2 years) volunteered for two experiments (experiment 1,n=9 ; experiment 2,n=9). In both experiments, the subjects orally ingested 0.3 g · kg^–1 body weight of NH₄Cl and NaHCO₃ over a 3-h period in random order on days separated by 72 h or more. In experiment 1, following ingestion of the substance, the subjects performed a discontinuous incremental cycle ergometer test to the onset of PWC_FT which was estimated from integrated electromyography voltages at the vastus lateralis muscle. In experiment 2, the subjects performed a continuous PWC_FT test. The results of these experiments indicated that NH₄Cl and NaHCO₃ ingestion had no significant (P>0.05) effect on PWC_FT (experiment 1: NH₄Cl=257, SD 26 W; NaHCO₃=256, SD 22 W;t=0.06;r=0.866; experiment 2: NH₄Cl=231, 14 W; NaHCO₃=216, 16 W;t=1.78;r=0.857).     

Alkali Therapy Attenuates the Progression of Kidney Injury via Na/H Exchanger Inhibition in 5/6 Nephrectomized Rats

Metabolic acidosis is a cause of renal disease progression, and alkali therapy ameliorates its progression. However, there are few reports on the role of renal acid-base transporters during alkali therapy. We evaluated the effect of sodium bicarbonate therapy and the role of acid-base transporters on renal disease progression in rats with a remnant kidney. Sprague-Dawley rats consumed dietary sodium bicarbonate (NaHCO₃) or sodium chloride (NaCl) with 20% casein after a 5/6 nephrectomy. After being provided with a casein diet, the NaHCO₃-treated group had higher levels of serum bicarbonate than the control group. At week 4, the glomerular filtration rate in the NaHCO₃ group was higher than that in the NaCl group, and the difference became prominent at week 10. The glomerulosclerosis and tubulointerstitial damage indices in the NaHCO₃ group were less severe compared with controls at week 4 and 10. The expression of the Na/H exchanger (NHE) was decreased, and apical reactivity was decreased in the NaHCO₃ group, compared with the NaCl group. Endothelin-1 levels in the kidney were also decreased in the NaHCO₃ group. Dietary sodium bicarbonate has the effects of ameliorating renal disease progression, which may be related to the altered expression of NHE in the remaining kidney.

Graphical Abstract

相似文献   

Effect of oral administration of sodium bicarbonate on surface EMG activity during repeated cycling sprints

The purpose of this study was to determine the effect of oral administration of sodium bicarbonate (NaHCO₃) on surface electromyogram (SEMG) activity from the vastus lateralis (VL) during repeated cycling sprints (RCS). Subjects performed two RCS tests (ten 10-s sprints) interspersed with both 30-s and 360-s recovery periods 1 h after oral administration of either NaHCO₃ (RCS_Alk) or CaCO₃ (RCS_Pla) in a random counterbalanced order. Recovery periods of 360 s were set before the 5th and 9th sprints. The rate of decrease in plasma HCO₃⁻ concentration during RCS was significantly greater in RCS_Alk than in RCS_Pla, but the rates of decline in blood pH during the two RCS tests were similar. There was no difference between change in plasma lactate concentration in RCS_Alk and that in RCS_Pla. Performance during RCS_Alk was similar to that during RCS_Pla. There were no differences in oxygen uptake immediately before each cycling sprint and in SEMG activity between RCS_Alk and RCS_Pla. In conclusion, oral administration of NaHCO₃ did not affect SEMG activity from the VL. This suggests that the muscle recruitment strategy during RCS is not determined by only intramuscular pH.     

Effect of acute sodium bicarbonate ingestion on excess C02 output during incremental exercise

Summary The effect of bicarbonate ingestion on total excess volume of CO₂ Output (CO₂ excess), due to bicaronate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g · kg^–1 body mass) of CaCO₃ (control) and NaHCO₃ (alkalosis). The resting arterialized venous blood pH (P<0.05) and bicarbonate concentration ([HCO₃ ^–]_b;P<0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO₃ ^–]_b; 29.4 (SD 1.5) mmol·1^-1] than in the control [pH, 7.39 (SD 0.03); [HCO₃ ^–]_b, 25.5 (SD 1.0) mmol·1^–1]. The blood lactate concentrations ([la^–]_b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la^–]_b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol·1^–1,P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol · l^–1,P < 0.05] were found in AMA compared with the control. The CO₂ excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml;P < 0.05]. The CO₂ excess per body mass was found to be significantly correlated with both the increase of [la^–]_b from rest to 3 min after exercise ( [la^–]_b;r=0.926,P < 0.001) and with the decrease of [HCO₃ ^–]_b from rest to 3 min after exercise ( [HCO₃ ^–]_b;_r=0.872,P<0.001), indicating that CO₂ excess per body mass increased linearly with both [la^– _b and [HCO₃ ^–]_b. As a consequence, CO₂ excess per body mass per unit increase of [la^–]_b (CO₂ excess·mass^–1· [la^–]_b) was similar for the two conditions. The present results would suggest that the relationship between CO₂ excess and blood lactate accumulation was unaffected by acute metabolic alkalosis, because the relative contribution of bicarbonate buffering of lactic acid was the same as in the control.     

β-Alanine supplementation reduces acidosis but not oxygen uptake response during high-intensity cycling exercise

The oral ingestion of β-alanine, the rate-limiting precursor in carnosine synthesis, has been shown to elevate the muscle carnosine content. Carnosine is thought to act as a physiologically relevant pH buffer during exercise but direct evidence is lacking. Acidosis has been hypothesised to influence oxygen uptake kinetics during high-intensity exercise. The present study aimed to investigate whether oral β-alanine supplementation could reduce acidosis during high-intensity cycling and thereby affect oxygen uptake kinetics. 14 male physical education students participated in this placebo-controlled, double-blind study. Subjects were supplemented orally for 4 weeks with 4.8 g/day placebo or β-alanine. Before and after supplementation, subjects performed a 6-min cycling exercise bout at an intensity of 50% of the difference between ventilatory threshold (VT) and [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{2{\text{peak}}} . Capillary blood samples were taken for determination of pH, lactate, bicarbonate and base excess, and pulmonary oxygen uptake kinetics were determined with a bi-exponential model fitted to the averaged breath-by-breath data of three repetitions. Exercise-induced acidosis was significantly reduced following β-alanine supplementation compared to placebo, without affecting blood lactate and bicarbonate concentrations. The time delay of the fast component (Td₁) of the oxygen uptake kinetics was significantly reduced following β-alanine supplementation compared to placebo, although this did not reduce oxygen deficit. The parameters of the slow component did not differ between groups. These results indicate that chronic β-alanine supplementation, which presumably increased muscle carnosine content, can attenuate the fall in blood pH during high-intensity exercise. This may contribute to the ergogenic effect of the supplement found in some exercise modes.     

The physiological stress response to high-intensity sprint exercise following the ingestion of sodium bicarbonate

The purpose of this study was to investigate the effects of pre-exercise alkalosis on the physiological stress response to high-intensity exercise. Seven physically active males (age 22 ± 3 years, height 1.82 ± 0.06 m, mass 81.3 ± 8.4 kg and peak power output 300 ± 22 W) performed a repeated sprint cycle exercise following a dose of 0.3 g kg^?1 body mass of sodium bicarbonate (NaHCO₃) (BICARB), or a placebo of 0.045 g kg^?1 body mass of sodium chloride (PLAC). Monocyte-expressed heat shock protein 72 (HSP72) and plasma thiobarbituric acid reactive substances (TBARS) were significantly attenuated in BICARB compared to PLAC (p = 0.04 and p = 0.039, respectively), however total anti-oxidant capacity, the ratio of oxidised to total glutathione, cortisol, interleukin 6 and interleukin 8 were not significantly induced by the exercise. In conclusion, monocyte-expressed HSP72 is significantly increased following high-intensity anaerobic exercise, and its attenuation following such exercise with the ingestion of NaHCO₃ is unlikely to be due to a decreased oxidative stress.     

The effect of β-alanine and NaHCO3 co-ingestion on buffering capacity and exercise performance with high-intensity exercise in healthy males

Introduction

β-alanine (BAl) and NaHCO₃ (SB) ingestion may provide performance benefits by enhancing concentrations of their respective physiochemical buffer counterparts, muscle carnosine and blood bicarbonate, counteracting acidosis during intense exercise. This study examined the effect of BAl and SB co-supplementation as an ergogenic strategy during high-intensity exercise.

Methods

Eight healthy males ingested either BAl (4.8 g day^?1 for 4 weeks, increased to 6.4 g day^?1 for 2 weeks) or placebo (Pl) (CaCO₃) for 6 weeks, in a crossover design (6-week washout between supplements). After each chronic supplementation period participants performed two trials, each consisting of two intense exercise tests performed over consecutive days. Trials were separated by 1 week and consisted of a repeated sprint ability (RSA) test and cycling capacity test at 110 % Wmax (CCT_110 %). Placebo (Pl) or SB (300 mg kgbw^?1) was ingested prior to exercise in a crossover design to creating four supplement conditions (BAl-Pl, BAl-SB, Pl–Pl, Pl-SB).

Results

Carnosine increased in the gastrocnemius (n = 5) (p = 0.03) and soleus (n = 5) (p = 0.02) following BAl supplementation, and Pl-SB and BAl-SB ingestion elevated blood HCO₃ ^? concentrations (p < 0.01). Although buffering capacity was elevated following both BAl and SB ingestion, performance improvement was only observed with BAl-Pl and BAl-SB increasing time to exhaustion of the CCT_110 % test 14 and 16 %, respectively, compared to Pl–Pl (p < 0.01).

Conclusion

Supplementation of BAl and SB elevated buffering potential by increasing muscle carnosine and blood bicarbonate levels, respectively. BAl ingestion improved performance during the CCT_110 %, with no aggregating effect of SB supplementation (p > 0.05). Performance was not different between treatments during the RSA test.     

Haemodynamic changes induced by short- and long-term sodium chloride or sodium bicarbonate intake in deoxycorticosterone-treated rats

The contribution of chloride to the haemodynamic changes of salt-dependent deoxycorticosterone (DOC) hypertension was studied in young Wistar rats subjected to dietary loading with sodium chloride (NaCl) or sodium bicarbonate (NaHCO₃). Mean arterial pressure (MAP), cardiac output, systemic resistance (TPR) and arterial rigidity (estimated from pulse pressure/stroke volume ratio, PP/SV) were determined in conscious chronically cannulated rats. DOC-induced increase of MAP and TPR appeared earlier in NaCl-loaded than in NaHCO₃-loaded rats. After 4–6 weeks of hypertensive treatment MAP, TPR and PP/SV ratio were higher in DOC-treated rats fed NaCl diet than in those fed NaHCO₃ diet. In contrast, after a long-term hypertensive regimen (lasting for 7–9 weeks) there was no significant difference in either MAP or TPR between rats loaded with NaCl or NaHCO₃. On the other hand, DOC hypertension induced by a long-term feeding of NaHCO₃ diet was not associated with an increase of arterial rigidity which was characteristic for DOC-NaCl hypertensive rats. Thus, a sufficiently long selective dietary sodium loading is capable to increase the systemic resistance but not to alter the arterial rigidity. This was also confirmed by a comparison of blood pressure-matched DOC hypertensive rats fed NaCl or NaHCO₃ diets. These animals did not differ in the degree of systemic resistance elevation but the arterial rigidity was increased only in NaCl-loaded rats.     

Acid base status in unanesthetized,unrestrained guinea pigs

Acid-base status of arterial blood was measured in chronically cannulated, unanesthetized, unrestrained guinea pigs. Normal values were: pH=7.444±0.032,PaCO₂=35.7±4.4; HCO ₃ ^– =24.4±2.8; BE=+0.4±2.1 (n=69) andPaO₂=91.9±7.3 (n=25) (Values are mean±S.D.).Induction of light anesthesia with thiopentone caused a respiratory depression (decrease inPaO₂) accompanied by respiratory acidosis (increase inPaCO₂ and decrease in pH) and a development of slight metabolic acidosis (decrease in base excess and standard bicarbonate). Acid base parameters of guinea pigs are compared to those obtained from rats under identical experimental conditions.     

Sodium citrate ingestion and muscle performance in acute hypobaric hypoxia

Eight subjects were studied on four occasions following ingestion of a 300-ml solution containing either sodium citrate (C, 0.4g · kg^–1 body mass) or placebo (P, sodium chloride 0.045 g · kg^–1 body mass), at local barometric pressure (N, P _B approximately 740 mmHg, 98.7 kPa) or hypobaric hypoxia (HH, P _B = 463 mmHg, 61.7 kPa). At 2 h after ingestion of the solution, the subjects performed prolonged isometric knee-extension at 35% of the maximal voluntary contraction (MVC) measured either in N or HH. Results showed that ingestion of C led to an improvement in muscle endurance (P < 0.01). However, this increase in endurance time for knee extensor muscles was only significant in N ( +22%, P < 0.05, compared to + 15%, NS, at N and HH, respectively). Following ingestion of sodium citrate, pre-exercise bicarbonate concentrations and pH levels were significantly higher than those measured after P ingestion. A significant treatment effect was observed for blood lactate concentrations with values higher for C than for P after 4, 6 and 10 min of recovery (P < 0.05). Electromyographic signals (EMG) were obtained from the vastus lateralis muscle during the prolonged isometric contraction at 35% MVC. The mean power frequency (MPF) significantly decreased in time under both N-P and N-C conditions. In HH, no significant decrease in MPF was observed with time. The results suggest that C ingestion was an ergogenic aid enhancing endurance during a sustained isometric contraction. In addition, it is suggested that fatigue during prolonged isometric contraction in HH was not directly related to factors determining the EMG signs of fatigue.