High-intensity sprints of short duration interspersed with short recoveries are commonly performed during most team sports. Therefore, the ability of the team-sport athlete to recover and to be able to reproduce a high power output in subsequent sprints is an important fitness requirement. This fitness component has been termed repeated-sprint ability (RSA). Despite its importance, little is known about what factors limit RSA and how best to improve RSA.
Maximal sprint exercise requires a high skeletal muscle adenosine triphosphate (ATP) turnover rate. As intramuscular ATP storage is able to sustain muscular activity for only 1–2 s, ATP must continually be resynthesized for activity to continue. It has been reported that the majority of the energy required to resynthesize ATP for a 6-s maximal sprint is provided by phosphocreatine (PCr) degradation and anaerobic glycolysis (11). Anaerobic glycolysis is associated with the intracellular accumulation of hydrogen ions (H+), which have been implicated as a cause of muscular fatigue (27). Although recent evidence suggests that, at physiological temperatures, direct inhibition of force production by acidification is not as great as previously thought (30), interventions that minimize intracellular H+ accumulation may improve RSA.
H+ accumulation depends on both the production and removal of H+. The intra- and extracellular buffer systems act to reduce the build up of free H+ during high-intensity exercise and may therefore be important in maintaining repeated-sprint performance. Indeed, we have reported a significant relationship between RSA and both change in blood pH (3) and in vivo muscle buffer capacity (βin vitro) (8). The intracellular accumulation of H+ also depends on the extracellular H+ concentration. H+ efflux out of the muscle cell has been reported to be inhibited by extracellular acidosis (16) and enhanced by a greater extracellular buffer concentration (21). It may therefore be hypothesized that increases in the extracellular buffer concentration, via the ingestion of an alkaline solution such as sodium bicarbonate (NaHCO3), may improve H+ efflux out of the muscle cell and improve repeated-sprint performance.
Consistent with the above hypothesis, research investigating the influence of NaHCO3 ingestion on repeated bouts of high-intensity exercise has reported significant improvements in performance (7,25). However, in these studies the duration of both the sprints (30–60 s) and recovery periods (0.5–2.0 min) were longer than what is likely to be encountered in a team-sport context. For example, in soccer the reported mean duration of high-intensity movements is 3.7–4.4 s and the time between high-intensity efforts has been reported to average 40 s (23). It is, therefore, doubtful whether these results can be extrapolated to the performance of repeated sprints of shorter duration interspersed with shorter recoveries more typical of team-sport performance.
The results of studies investigating the effects of induced alkalosis on repeated-sprint performance more typical of team-sport performance have been equivocal. Lavender and Bird (19) reported that NaHCO3 ingestion significantly improved the performance of ten, 10-s cycle sprints with 50-s recovery between each sprint. However, a small improvement in the performance of 10, 6-s running sprints (on a nonmotorized treadmill), separated by 30-s recovery periods, was not significant after NaHCO3 ingestion (10). It is unclear why there is a discrepancy in these previous findings. However, an investigation of intracellular changes is important to determine the effects of induced alkalosis on repeated-sprint performance more typical of team-sport performance. Whereas other studies investigating the effects of NaHCO3 ingestion have incorporated muscle biopsies (17), this is the first study to investigate potential mechanisms by which induced alkalosis may improve repeated-sprint performance. It was hypothesized that increases in the extra-cellular buffer concentration, via the ingestion of NaHCO3, would improve H+ efflux out of the muscle cell and increase the anaerobic energy contribution to repeated sprints and therefore improve repeated-sprint performance.
Ten recreational, team-sport playing females (mean ± SD: age 19 ± 1 yr; mass 64.3 ± 10 kg; O2max 49.4 ± 12.8 mL·kg−1·min−1; lactate threshold 34.5 ± 10.2 mL·kg−1·min−1) volunteered to participate in this study. Subjects were informed of the study requirements, benefits, and risks before giving written informed consent. Approval for the study’s procedures was granted by the Research Ethics Committee of the University of Western Australia.
In addition to a familiarization session for all tests, the main experiment required the subjects to be tested on three separate occasions. On day one, subjects performed a graded exercise test (GXT) to determine both their lactate threshold (LT) and O2max. At least 48 h later, in a random, counterbalanced order, subjects performed the 5 × 6-s test of repeated-sprint ability (RSA) 90 min after the ingestion of either sodium bicarbonate (NaHCO3) or a placebo substance (NaCl). A week separated the two RSA testing sessions and both RSA tests were conducted at the same time of day to control for diurnal effects. Capillary blood was sampled after each intensity increment throughout the GXT. Capillary blood was also taken before ingestion of the test substance, 60 min postingestion, 90 min postingestion (i.e., immediately preexercise), and immediately after the 5 × 6-s test. Muscle biopsies from the vastus lateralis were also taken before (i.e., 90 min postingestion) and immediately after each 5 × 6-s cycle test. Subjects were asked to maintain their normal diet and training throughout the study. Subjects were required to consume no food or beverages (other than water) 2 h before testing and were asked not to consume alcohol or perform vigorous exercise in the 24 h before testing.
Subjects ingested either 0.3 g·kg−1 NaHCO3 or 0.207 g·kg−1 of NaCl (CON), contained within 8–14 gelatin capsules, with 500 mL of water 90 min before performing the RSA test. Treatment was assigned in a counterbalanced, randomized, double-blind manner.
Graded exercise test.
The GXT was performed on an air-braked track-cycle ergometer (Evolution Pty. Ltd., Adelaide, Australia) and consisted of graded exercise steps (4-min stages), using an intermittent protocol (1-min passive rest between stages). The test commenced at 50 W and thereafter, intensity was increased by 30 W every 4 min until volitional exhaustion. Subjects were required to maintain the set power output, which was displayed on a computer screen in front of them. The test was stopped when the subject could no longer maintain the required power output. Strong verbal encouragement was provided to each subject as they came to the end of the test. Both LT and O2max were determined from the GXT. The LT was calculated using the modified Dmax method (2). This is determined by the point on the polynomial regression curve that yields the maximal perpendicular distance to the straight line connecting the first increase in lactate concentration above resting level and the final lactate point.
5 × 6-s cycle test.
Subjects performed a pretest warm up consisting of 5-min cycling at approximately 80 W, followed by three practice sprint starts. The practice starts required the subject to pedal close to maximal for 2–3 s, interspersed with 20-s slow pedaling. A 90-s rest followed this. Each subject then performed a 10-s maximal sprint test on a front access cycle ergometer (Model Ex-10, Repco, Australia). The total work recorded in the first 6 s of the 10-s sprint was used as the criterion score during the subsequent 5 × 6-s cycle test. Upon completion of the 10-s test, subjects rested for 5 min before performing the 5 × 6-s cycle test.
The 5 × 6-s cycle test consisted of five, 6-s maximal sprints departing every 30 s. During the first sprint, subjects were required to achieve at least 95% of their criterion score, as a check on pacing. If 95% of the criterion score was not achieved, the subject rested for a further 5 min and then recommenced the 5 × 6-s cycle test. During the 24-s recovery between sprints, subjects rested completely. Five seconds before starting each sprint, subjects were asked to assume the ready position and await the start signal. Strong verbal encouragement was provided to each subject during all sprints. All sprints were performed in the standing position. This test has previously been reported to be both a valid (4) and reliable (9) test of repeated-sprint ability.
Gas analysis (GXT).
During the GXT, expired air was continuously analyzed for O2 and CO2 concentrations using Ametek gas analyzers (Applied Electrochemistry, SOV S-3A11 and COV CD-3A, Pittsburgh, PA). Ventilation was recorded every 15 s using a turbine ventilometer (Morgan, 225A, Kent, UK). The gas analyzers were calibrated immediately before and verified after each test using three certified gravimetric gas mixtures (BOC Gases, Chatswood, Australia); the ventilometer was calibrated preexercise and verified postexercise using a 1-L syringe in accordance with the manufacturer’s instructions. The ventilometer and gas analyzers were connected to an IBM PC that measured and displayed variables every 15 s. The sum of the four highest consecutive 15-s values was recorded as the subject’s O2max.
Capillary blood sampling and analysis.
A hyperemic ointment (Finalgon, Boehringer Ingelheim, Germany) was applied to the earlobe 5–7 min before initial blood sampling. Glass capillary tubes were used to collect 50 μL of blood during the GXT (GMRD-054, Analox Instruments Ltd., London, UK) and 100 μL of blood for the RSA test (478 600, Chiron Diagnostics, Norwood, MA). Capillary blood samples were taken at rest and immediately after each 4-min stage of the GXT. Capillary blood samples were also taken at rest and immediately after the 5 × 6-s cycle test.
Whole blood lactate concentration ([La−]) during the GXT was determined using a Micro Stat LM3 (Analox Instruments Ltd., London, UK). The Micro Stat was regularly calibrated using precision standards and routinely assessed by external quality controls. Whole blood pH and [La−] for the RSA test was determined using a Ciba Corning blood gas analyzer (#865, Chiron Diagnostics).
Muscle sampling and analysis.
On the day of the 5 × 6-s cycle test, one incision was made under local anesthesia (2.5 mL, 1% Xylocaine) into the skin, surrounding fascia, and sheath of the vastus lateralis of each subject. The incision was used for the pretest biopsy and then closed with a steri strip and subsequently used for the posttest biopsy. The first muscle sample (50–80 mg wet mass per sample) was taken (before warm-up) during supine rest. The second muscle sample (50–80 mg) was taken immediately after the cessation of the 5 × 6-s test, while the subject remained on the cycle ergometer. Mean time for the preexercise and postexercise (time from cessation of pedaling) muscle sample to be placed in liquid nitrogen was 6.9 ± 1.7 s and 17.5 ± 5.8 s, respectively. The samples were then removed from the biopsy needle and stored at −80°C until subsequent analysis. The frozen muscle samples were weighed on a microbalance (HM202 Lab Supply Pty Ltd., Sydney, Australia) and freeze dried. The freeze-dried muscle was then dissected free from visible blood and connective tissue.
Muscle buffering capacity; titration method (βin vitro).
Freeze-dried, resting muscle samples (1.8–2.3 mg) were homogenized on ice for 2 min in a solution containing sodium fluoride (NaF) (10 mM) at a dilution of 30 mg dry muscle·mL−1 of homogenizing solution. The muscle homogenate was then placed in a circulating water bath at 37°C for 5 min before and during the measurement of pH. The pH measurements were made with a microelectrode (MI-415, Microelectrodes Inc, Bedford, NH) connected to a pH meter (SA 520, Orion Research Inc, Cambridge, MA). After initial pH measurement, muscle homogenates (rest samples) were adjusted to a pH of ~ 7.2 with a sodium hydroxide (NaOH) (0.02 M) solution and then titrated to a pH of ~ 6.2 by the serial addition of 2 μL of hydrochloric acid (HCl) (10 mM). From the fitted titration trend line, the number of moles of H+ (per gram of dry muscle) required to change the pH from 7.1 to 6.5 were interpolated. This value was then normalized to the whole pH unit for final display as millimoles H+ per gram dry muscle per unit pH (μmol H+·g−1 muscle dw·pH−1) and determined as the subject’s βin vitro.
Muscle lactate concentration and βin vitro determination.
Freeze-dried, rest, and postexercise muscle samples (3.5–4.5 mg) were enzymatically assayed for [La−] according to the methods of Harris et al. (14). Muscle buffer capacity (βin vitro) was estimated from changes in [La−]i and pHi; βin vitro = Δ [La−]i/Δ pHi.
All values are reported as mean ± SEM. One-way ANOVA (1 group × 2 treatments), with repeated measures for treatment, were used to compare blood, muscle, and performance data. Where appropriate, posthoc comparisons were employed (Student-Newman-Keuls test). The alpha level for statistical significance was set at P < 0.05.
Plasma H+ and HCO3− concentrations were not different preingestion for the two treatments (Fig. 1; P > 0.05). NaHCO3 ingestion decreased plasma H+ concentration (37.2 ± 0.5 vs 31.5 ± 0.8 nmol·L−1; P < 0.05) and raised plasma HCO3− concentration (23.6 ± 1.1 vs 30.0 ± 3.0 mmol·L−1; P < 0.05) compared with preingestion after both 60 and 90 min. Ingestion of NaCl (CON) did not change these resting parameters (Fig. 1; P > 0.05). After the 5 × 6-s test of RSA, plasma H+ concentration increased and plasma HCO3− concentration decreased such that values were different from the three preexercise values (i.e., −90 min, −60 min, and pretest) (P < 0.05). In addition, posttest plasma H+ and HCO3− concentrations were lower and higher, respectively, compared with CON (P < 0.05). There was no difference between treatments for preingestion (−90 min) or preexercise (i.e., −60 min and pretest) blood La− concentration (Fig. 2; P > 0.05). After the 5 × 6-s test of RSA, blood La− concentration increased in both treatments (P < 0.05). In addition, posttest blood La− concentration was ~ 28% higher in NaHCO3 than CON (P < 0.05).
There was no treatment effect for either resting muscle La− or H+ concentration (Fig. 3; P > 0.05). Muscle H+ concentration increased (P < 0.05) during the 5 × 6-s test in both treatments to a similar extent. These muscle H+ concentrations were equivalent to a pH in CON of 7.12 at rest and 6.89 at the end of exercise, and in NaHCO3 of 7.11 and 6.89 respectively. After the 5 × 6-s test, muscle La− concentration also increased from rest in both treatments (Fig. 3; P > 0.05). Posttest muscle La− concentration was ~ 72% higher in NaHCO3 than CON (P < 0.05). Although there was no significant difference in βin vitro between treatments (P > 0.05), βin vitro was significantly greater in NaHCO3 than CON (Fig. 4; P < 0.05).
Compared with CON, the NaHCO3 treatment resulted in a significant increase in total work for the five, 6-s sprints (CON vs NaHCO3: 15.7 ± 3.0 vs 16.5 ± 3.1 kJ; P < 0.05). This increase in total work was largely a result of significant increases in the work done in sprints 3, 4, and 5 in the NaHCO3 treatment compared with CON; there was also a significant increase in peak power output during these sprints (Fig. 5; P < 0.05). There was no treatment effect for either percent work decrement (CON vs NaHCO3: 8.9 vs 8.2%) or percent peak power decrement (CON vs NaHCO3: 7.3 vs 6.8%).
The present study is the first to examine the effects of induced alkalosis on the metabolic responses of skeletal muscle to repeated high-intensity sprint efforts (5 × 6-s all-out sprints every 30 s). The major finding was that despite there being no significant difference in posttest muscle pH between trials, the NaHCO3 trial resulted in significantly greater posttest muscle lactate concentration. A second major finding was that NaHCO3 ingestion improved repeated-sprint ability (i.e., total work over five sprints and work and peak power for sprints 3, 4, and 5) in the population tested.
Efficacy of NaHCO3 ingestion.
The efficacy of the NaHCO3 ingestion protocol was demonstrated through the elevation of blood [HCO3−] and the reduction in blood [H+] at rest (−60 min and pretest;Fig. 1). These changes were of similar magnitude to previous studies (7,10,28). Further-more, the increase in blood [HCO3−] (5.4 mmol·L−1) was similar to the mean increase of 5.3 mmol·L−1 reported in a meta-analysis of human NaHCO3-loading studies that have used a 0.3 g·kg−1 dose (22). Consistent with previous research, there was no change in resting blood lactate concentration (7,10,28).
There was also no change in resting muscle lactate or [H+]. This is consistent with the results of other studies in humans (7). However, our results contrast with those of Stephens et al. (28) who reported a similar reduction in plasma [H+] after NaHCO3 ingestion (~ 4 nM) being associated with ~ 9 nM reduction in resting muscle [H+]. There were two main differences between the present study and the study by Stephens et al. (28). Whereas subjects ingested an identical dose of NaHCO3 (0.3 g·kg−1), it was ingested 2 h before the exercise test (vs 90 min in the present study). However, the nonsignificant change in blood [HCO3−] from 60 to 90 min in the present study suggests that this is unlikely to explain the discrepant findings. Another difference was that Stephens et al. (28) used calcium carbonate (CaCO3) as their control substance (vs NaCl in the present study). As a result, there was a significant elevation of resting plasma sodium concentration ([Na+]) in the NaHCO3 group only. The authors hypothesized that there may have been a corresponding increased muscle [Na+] with alkalosis and a subsequent removal of H+ by the skeletal muscle Na+/H+ exchanger. In addition, an increase in muscle [Na+] after NaHCO3 ingestion may have decreased muscle [H+] via an increase in the strong ion difference (15). However, in the present study, the control substance (0.207 g·kg−1 NaCl) contained an equimolar amount of Na+. Although we did not measure [Na+] in the muscle or the blood, it is likely that the [Na+] did not differ between conditions. This may explain why we did not see a decrease in muscle [H+] after NaHCO3 ingestion. Again, this is consistent with previous research that has used NaCl as the control substance (7). Our results are also consistent with the previous observation that induced alkalosis does not affect intramuscular pH (pHi) until blood pH is above 7.55 (~ 7.5 in the present study) (1).
Consistent with previous research (18), there was no significant difference between groups for βin vitro. This was expected due to the relative impermeability of the sarcolemma to bicarbonate (20). As a result, the ergogenic benefit of alkalosis is believed to be derived from greater buffering of H+ released by muscle during contraction, in tandem with a more rapid efflux of muscle La− and H+.
Effects of metabolic alkalosis on postexercise lactate concentration.
Postexercise muscle lactate concentration was ~ 72% higher in NaHCO3 than in CON (P > 0.05). This is the first study to report the effects of metabolic alkalosis on muscle lactate concentration after brief, repeated sprints. However, an increase in muscle lactate concentration (~ 90%) has also been reported with alkalosis after continuous exercise at 95% O2max (29) and 125% O2max (5). An increase in muscle lactate accumulation with alkalosis could be the result of changes in lactate production and/or clearance.
The results of Stephens et al. (28) suggest that alkalosis does not affect muscle metabolism during exercise at 80% O2max. However, these results contrast with Hollidge-Horvat et al. (17), who reported that metabolic alkalosis resulted in a significant increase in muscle glycogen use and higher muscle lactate accumulation during 15 min of exercise at 75% O2max Although both of these studies required subjects to exercise at 75–80% O2max it is possible that the untrained subjects in the study by Hollidge-Horvat et al. (17) were exercising above their LT, whereas the well-trained subjects in the study by Stephens et al. (28) were not exercising above their LT. As there is a disproportionate increase in muscle lactate concentration at intensities above the lactate threshold (6), alkalosis may only affect lactate accumulation at intensities above the LT. In support of this, alkalosis has been reported to result in significantly greater muscle glycogen use and higher intramuscular lactate concentration at 75% O2max, but not 30% O2max (17). As the peak power during the sprint efforts in the present study were performed at > 300% O2max, this intensity may have been sufficient for alkalosis to affect the rate of glycogenolysis and hence, muscle lactate production.
Changes in muscle lactate accumulation with alkalosis may also be the result of changes in clearance of lactate from muscle to the blood. However, impaired lactate clearance appears unlikely to be the cause of higher muscle lactate accumulation with alkalosis. Most researchers have reported that lactate efflux from muscle is higher as a result of extracellular alkalosis (21). Thus, the significantly greater increase in muscle lactate concentration after exercise in the present study after alkalosis is likely to be attributable to increased muscle glycogen use rather than impaired lactate clearance.
Consistent with previous research (28), there was also a significant increase in postexercise blood lactate concentration after induction of a metabolic alkalosis. The elevated blood lactate concentration observed in the present study after alkalosis is likely to be largely attributable to a greater rate of lactate entry into the blood as a result of the higher muscle lactate to blood lactate concentration gradient and/or an increased rate of lactate release from the muscle into the blood (21). It is possible, however, that a reduction in blood lactate clearance by inactive tissues may also have contributed to the higher blood lactate concentration in the NaHCO3 trial. Granier et al. (12) have previously reported that arteriovenous lactate difference across the inactive forearm was reduced during repeated-sprint cycling exercise (6-s sprints with 5-min recovery) after NaHCO3 infusion, suggesting less lactate removal. However, as neither arteriovenous lactate difference or lactate kinetics were measured in the present study, the exact mechanism(s) responsible for the greater postexercise blood lactate concentration in the present study require further investigation.
Effects of metabolic alkalosis on postexercise [H+].
In addition to increasing postexercise blood lactate concentration, NaHCO3 ingestion also resulted in an increase in postexercise blood pH (decreased [H+]). This is consistent with the results of most previous studies (7,17,28), although some have reported no treatment effect (5,24). It should be noted, however, that both studies reporting no significant effect of alkalosis on postexercise pH values recruited low subject numbers (N = 6) and a trend for higher postexercise blood pH was apparent. In the present study, and in most previous studies, the postexercise blood pH difference between NaHCO3 and CON trials appears to parallel the preexercise difference produced by NaHCO3 ingestion (Fig. 1). The similar change in postexercise blood [H+], coupled with a greater reduction in blood [HCO3−] and a greater increase in blood lactate concentration suggests that the buffer capacity of the blood was enhanced in the NaHCO3 trial.
NaHCO3 ingestion also resulted in a significant increase in βin vitro (Fig. 4). That is, there was a greater change in muscle lactate concentration for the same change in muscle pH. Although this contrasts with a previous study in greyhounds (18), an increase in βin vitro is consistent with the results of previous research reporting that alkalosis increases the rate of proton release from the muscle into the blood (21). An increase in βin vitro could delay the fall in muscle pH and thus its inhibitory effects on glycogenolysis/glycolysis and thereby facilitate the greater postexercise muscle lactate accumulation observed in the NaHCO3 trial.
The increase in total work for the same final [H+] suggests that alkalosis was associated with a delayed increase in postexercise muscle [H+]. Similarly, Costill et al. (7) reported that in a series of five, 1-min cycling bouts (separated by 1-min rest) muscle pH after the fifth bout (which continued to exhaustion) was similar in both the NaHCO3 and CON trials. This was despite the fact that subjects in the NaHCO3 trial performed ~ 47% more work. The results of both these studies raise the possibility that the performance of repeated-sprint exercise is limited, in part, by a critical muscle pH.
Effects of metabolic alkalosis on performance.
In the present study, there was a significant effect of NaHCO3 ingestion before exercise on repeated-sprint performance (five, 6-s all-out sprints every 30 s). Compared with CON, the NaHCO3 trial resulted in a significant increase in total work for the five, 6-s sprints and in work and peak power output in the final three sprints. This is consistent with the results of previous studies that have reported significant improvements in repeated-sprint performance after NaHCO3 ingestion (7,19,25). However, in most of the previous studies, the duration of both the sprint efforts (30– 60 s) and the recovery periods (0.5–2.0 min) were considerably longer than what is likely to be encountered in a team-sport context. For example, in soccer, the reported mean duration of high-intensity movements is 3.7– 4.4 s (23), and the time between high-intensity efforts has been reported to be 40 s (23). Similarly, we have reported that a typical repeated-sprint bout within an elite field-hockey match consists of approximately four, 4-s sprints performed every 15–20 s (26). This is therefore, the first study to show that NaHCO3 ingestion is able to improve the performance of repeated-sprint bouts typical of team-sport performance.
In the only other study to use a similar protocol, Gaitanos et al. (10) reported that NaHCO3 ingestion failed to improve repeated-sprint running performance (10, 6-s sprints every 36 s) in male subjects. There was, however, a 2% increase in total work done in the alkaline condition. It is unlikely that these differences are related to differences in the reliability of the two protocols as running and cycling repeated-sprint tests have previously been reported to have similar reliability (9). These differences are more likely to be associated with the relatively small change in blood pH post NaHCO3 ingestion (7.38–7.43) compared with the present study (7.42–7.50). As the dose was identical (0.3 g·kg−1) in the two studies, this difference may be due to the greater time delay between ingestion and exercise in the previous study (150 min) compared with the present study (90 min). These contrasting results may also reflect a subject effect (e.g., fitness or gender). Further research is required to examine factors that influence both the alkalizing and ergogenic effects of NaHCO3 ingestion.
Further research is also required to elucidate the mechanisms by which NaHCO3 ingestion may improve repeated-sprint ability. Repeated-sprint exercise (6 s), interspersed with a brief recovery (<30 s), results in a significant decline in power output (3). Furthermore, those individuals who have the greatest fall in power output have been reported to have the greatest glycolytic rate during the first sprint (r = 0.89; (10)) and the greatest change in both blood pH (r = 0.66–0.82; (3,10)) and muscle pH (r = 0.51; (8)). It therefore seems that H+ accumulation resulting from maximal glycogenolysis/glycolysis may be associated with the observed reduction in power output during repeated-sprint exercise. Furthermore, the significant increase in posttest muscle [La−] in the NaHCO3 trial suggests that increased glycogenolysis/glycolysis is one mechanism by which NaHCO3 ingestion may have improved RSA. Although force decline during fatiguing work has also been related to percentage of fast-twitch fibers (13,30), this would not have been altered by NaHCO3 ingestion.
In summary, despite no significant difference in posttest muscle pH between conditions, the NaHCO3 trial resulted in greater posttest muscle lactate concentration and improved repeated-sprint ability (i.e., total work across the five sprints and work and peak power for sprints 3, 4, and 5). As NaHCO3 ingestion does not increase resting muscle pH or βin vitro, it is likely that the improved performance was a result of the greater extracellular buffer concentration increasing H+ efflux from the muscles into the blood. The significant increase in posttest muscle lactate concentration in the NaHCO3 trial suggests that an increased anaerobic energy contribution is one mechanism by which NaHCO3 ingestion improved repeated-sprint ability.
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Keywords:©2004The American College of Sports Medicine
BUFFER CAPACITY; CYCLING; INTERMITTENT EXERCISE; TEAM SPORTS