The relationship between power output and the tolerable duration of high-intensity exercise is characterized by a hyperbolic function, which is defined by the power asymptote (critical power, CP) and the curvature constant (W′) (11,27,31). The CP represents the boundary between the "heavy" and "severe" exercise intensity domains and is closely associated with the "maximal lactate steady state" (31). Exercise within the severe domain (>CP) is associated with limited exercise tolerance and non-steady-state responses of blood lactate concentration ([lactate]) and also pulmonary oxygen uptake (V˙O2), which reaches its maximum value (V˙O2max) at, or shortly before, volitional exhaustion (13,31). The W′ parameter represents a fixed amount of work that can be performed above the CP, irrespective of the rate of its expenditure (11,41). The physiological correlates of the W′ remain elusive and are likely to include several interrelated factors. The W′ has been classically described as an "anaerobic work capacity" that is sensitive to changes in intramuscular concentrations of phosphocreatine (PCr) (25,38) and glycogen (26), but which is unaffected by hypoxia (28). However, it is also acknowledged that the magnitude of the W′ might be limited by the accumulation of fatigue-related metabolites such as hydrogen ions (H+) and inorganic phosphate (Pi) within the contracting muscles (6,17).
The power-duration relationship is conventionally established by performing three to five exhaustive high-intensity constant-work-rate exercise trials on separate days (13,31). The recent demonstration that the CP and W′ can be estimated from a single 3-min all-out cycle exercise test, therefore, has considerable practical appeal (5,40,41). The rationale for the all-out protocol derives from the two-parameter CP model, which posits that the magnitude of the W′ remains constant regardless of the rate of its expenditure >CP (11,27,31). During all-out exercise, the W′ is expended rapidly, and the power output falls until none of the W′ remains (40,41). It has been demonstrated that the highest power output that can be elicited by voluntary effort during the final 30 s of the 3-min all-out test closely approximates the CP (coefficient of variation = 2%), whereas the W′ can be estimated as the power-time integral above the end-test power output (coefficient of variation = 12%) (41). In recent studies, the parameter estimates derived from the all-out protocol have been shown to be unaffected by dietary creatine loading (39) but to be sensitive to changes in the power-duration relationship after training and prior exercise interventions (38,40).
Supra-CP exercise results in a progressive reduction in intramuscular [PCr] and concomitant increase in [Pi] and also [H+] (17), all factors that have been associated with the fatigue process (10). An acidic pH is believed to impair muscle function by inhibiting the key regulatory enzyme, phosphofructokinase, and by interfering with Ca2+ release from the sarcoplasmic reticulum and its binding to troponin (7,10,12). It is presently not known whether the W′ parameter, which defines exercise tolerance >CP, is sensitive to acute manipulation of the acid-base balance.
Ingestion of sodium bicarbonate (NaHCO3) or sodium citrate (Na-citrate) 1-2 h before exercise is a commonly used intervention to increase the buffering capacity of the blood (24,32). The induced state of alkalosis may improve high-intensity exercise performance by facilitating enhanced energy supply through anaerobic glycolysis (4,14). Higher plasma and muscle pH and higher plasma concentrations of bicarbonate and lactate have been reported after NaHCO3 and Na-citrate supplementation (9,21,30,35). Although these data are consistent in indicating enhanced efflux of H+ from the active muscle after buffer ingestion, the reported effects of induced alkalosis on "all-out" exercise performance have been equivocal and argely limited to sprint durations of 30-60 s (9,43). Whereas some investigations have reported improved performance during a single bout, as well as repeated bouts, of maximal exercise with buffer ingestion (4,8,21,42), others have shown no effect (9,30,43). It has been suggested that a beneficial effect of induced alkalosis on performance requires a sufficient time for the H+ gradient between the intramuscular and vascular compartments to develop (32), and therefore, a more pronounced ergogenic effect might be expected for exercise durations greater than ∼1 min (23,42).
Given that the W′ parameter has been classically considered to represent a work capacity comprising the energy available from the "anaerobic" energy pathways (25,26,28), it would be expected that any intervention that enhances the glycolytic flux by attenuating the fall in muscle pH during supra-CP exercise would increase the W′. Conversely, alterations in glycolytic metabolism should have no effect on the CP parameter, which has been defined as the highest sustainable rate of aerobic energy transfer (27,28). We hypothesized that acute NaHCO3 ingestion would enable greater total work done during the 3-min all-out test because of an increased work done >CP (W′) with no alteration in the CP itself.
Eight habitually active male participants (mean ± SD; age = 29 ± 9 yr, stature = 1.81 ± 0.05 m, body mass = 77.0 ± 9.4 kg) volunteered to take part in this study that had been approved by the local research ethics committee and was conducted in accordance with the Declaration of Helsinki. Testing procedures were fully explained before written informed consent was obtained from each participant. All participants had previous experience of high-intensity exercise testing in the same laboratory. Participants were instructed to be adequately hydrated and not to have consumed alcohol for 24 h and food or caffeine for 3 h before each test.
The testing sessions took place in a well-ventilated laboratory at a temperature of 20-22°C. Participants made four visits to the laboratory during a period of 3 wk, and tests were separated by a minimum of 24 h. The first visit was used to establish the V˙O2peak and the gas exchange threshold (GET) using a ramp incremental test. During the second visit, the participants performed a 3-min all-out test that served as a familiarization trial and was not included in the subsequent data analyses. During the third and fourth visits, participants performed a 3-min all-out test, 60 min after having ingested 0.3 g·kg−1 body mass of NaHCO3 (BC trial) or 0.045 g·kg−1 body mass of sodium chloride (placebo; PL trial). Each supplement was mixed in 0.75 L of low-calorie squash that subjects were asked to consume during a 15-min period. Both supplements were tolerated well by all subjects. The supplements were administered in a blind, randomized order, and no feedback on test performance was given until all experimentation had been completed. The test-retest reliability of the 3-min all-out test has been established previously, with a coefficient of variation of 3% for CP (5) and 9% for the W′ between repeated trials (37).
Determination of V˙O2peak and GET.
All exercise testing was conducted using an electromagnetically braked cycle ergometer (Lode Excalibur Sport, Groningen, the Netherlands). The ergometer seat and handlebar were adjusted for comfort, and settings were replicated for subsequent tests. The ramp protocol consisted of 3 min of unloaded baseline pedaling, followed by a ramp increase in power output of 30 W·min−1 until volitional exhaustion. Participants were instructed to maintain their chosen preferred cadence (80 rpm, n = 6; 90 rpm, n = 2) for as long as possible. The test was terminated when pedal rate fell more than 10 rpm below the chosen cadence for more than 5 s despite strong verbal encouragement.
Pulmonary gas exchange was measured breath-by-breath during the incremental test. The participants wore a nose clip and breathed through a low-dead space, low-resistance mouthpiece, and a digital volume transducer (DVT) turbine assembly. The inspired and expired gas volume and gas concentration signals were continuously sampled, the latter using electrochemical cell (O2) and infrared (CO2) analyzers (MetaMax 3B; Cortex Biophysik, Leipzig, Germany) through a capillary line connected to the mouthpiece. These analyzers were calibrated before each test with gases of known concentration, and the turbine volume transducer was calibrated using a 3-L syringe (Hans Rudolph, Kansas City, MO). Gas exchange data were reduced to 10-s averages for the estimation of GET using the V-slope method (2), and the V˙O2peak was determined as the highest average V˙O2 during a 10-s period.
Three-minute all-out tests.
Subjects performed a total of three 3-min all-out tests: one familiarization, one PL, and one NaHCO3-supplemented trial. These tests were performed against fixed resistance using the linear mode of the Lode Excalibur Sport cycle ergometer. The test began with 3 min of unloaded baseline pedaling at preferred cadence, followed by a 3-min all-out effort. Participants were asked to accelerate to 110-120 rpm during the last 5 s of the baseline period. The fixed resistance on the flywheel during the 3-min all-out test was normalized so that the participant would attain the power output halfway between the GET and V˙O2peak (50%Δ) on reaching their preferred cadence (linear factor = power/cadence2). Strong verbal encouragement was provided throughout the test, but participants were not informed of the elapsed time to prevent pacing. To ensure an all-out effort, participants were instructed to attain their peak power output as quickly as possible at the start of the test and to maintain the cadence as high as possible at all times throughout the 3 min. The CP was calculated as the mean power output during the final 30 s of the test, and the W′ was calculated as the power-time integral above CP.
During the PL and NaHCO3-supplemented trials, arterialized capillary blood samples were collected from a warmed fingertip for the assessment of blood acid-base status. Blood samples were drawn 1) on subjects' arrival in the laboratory, 2) 60 min after ingestion of the supplement (within 5 min of the start of the 3-min test), 3) immediately on completion of the 3-min test, and 4) after 10 min of recovery. Blood was collected into heparinized capillary tubes for subsequent determination of acid-base status (AVL Omni 4; Roche Diagnostics, Lewes, United Kingdom) and whole blood [lactate] (Stat 2300; YSI, Yellow Springs, OH). Blood lactate accumulation (Δblood [lactate]) was calculated as the difference between blood [lactate] at the end of exercise and blood [lactate] at rest. Pulmonary gas exchange was measured breath-by-breath throughout the all-out tests as described above for the ramp incremental test. The V˙O2peak was determined as the highest 10-s average measured during the test.
A repeated-measures ANOVA across treatments (PL and NaHCO3) and time (on arrival, 60 min after ingestion, end of exercise, and 10 min after exercise) was used to assess differences in pH, blood [NaHCO3], base excess, and [lactate]. A one-way ANOVA was used to compare the V˙O2peak values measured during the ramp test and the 3-min trials. Parameter comparisons between the PL and BC trials were analyzed using a Student's t-test. Statistical significance was accepted at P < 0.05 level, and data are presented as mean ± SD.
The V˙O2peak measured in the ramp incremental test was 4.05 ± 0.83 L·min−1 with the GET occurring at 1.87 ± 0.60 L·min−1. These values corresponded to work rates of 380 ± 66 and 116 ± 35 W, respectively.
The ingestion of NaHCO3 had the expected effect on blood acid-base status. The repeated-measures ANOVA revealed a significant effect on pH for treatment (P < 0.001) and time (P < 0.001) as well as an interaction effect (P < 0.001; Fig. 1A). The pH values measured after ingestion, before the start of the 3-min all-out tests, were 7.40 ± 0.02 (PL) and 7.46 ± 0.01 (NaHCO3; P < 0.001). There was also a significant effect on blood [NaHCO3] across treatment (P < 0.05) and time (P < 0.001), with a significant treatment × time interaction (P < 0.01; Fig. 2). The blood [NaHCO3] at the start of the 3-min test was 21.9 ± 3.0 mM in PL and 29.0 ± 3.8 mM in the BC trial (P < 0.05; Fig. 1B). The effect on base excess response was significant for time (P < 0.001), treatment (P < 0.001), and the treatment × time interaction (P < 0.05). The base excess was significantly higher in the NaHCO3 (5.0 ± 3.0 mEq·L−1) than in the PL (−1.9 ± 2.5 mEq·L−1, P < 0.05) condition after ingestion and remained elevated (nonsignificant) immediately after exercise and 10 min into the recovery (Fig. 1C). The effect on blood [lactate] was significant across treatment (P < 0.05) and time (P < 0.001), with a significant treatment × time interaction (P < 0.05). Blood [lactate] was not different after ingestion (i.e., within 5 min of the commencement of the 3-min test) between PL (0.9 ± 0.3 mM) and NaHCO3 (0.9 ± 0.2 mM; P > 0.05), but postexercise blood [lactate] was higher in the NaHCO3 (12.3 ± 1.8 mM) than in the PL (10.5 ± 1.3 mM, P < 0.05) and remained elevated 10 min into the recovery (Fig. 1D).
The induced alkalosis had no effect on performance during the 3-min all-out test. There were no significant differences in total work done, the CP, or the W′ between the PL and the BC trials (Table 1). The coefficients of variation between PL and BC trials were 3% for CP and 5% for the W′. The peak power output was also unaffected by NaHCO3 ingestion (Table 1). The group mean power output and the power profiles of a representative individual are presented in Figure 2.
The highest V˙O2 values measured during the all-out trials were not different from the ramp test-determined V˙O2peak, equaling 99 ± 12% V˙O2peak in PL and 99 ± 10% V˙O2peak in the BC trial (F7,2 = 0.22, P = 0.75). The NaHCO3 supplementation resulted in no alterations in the overall V˙O2 response during the 3-min all-out test (Fig. 3A). Whereas the V˙CO2peak values were not significantly different between treatments (Table 1; Fig. 3C), V˙CO2 was significantly elevated during the final ∼120 s in the BC trial in comparison to PL, with the mean V˙CO2 during 60-180 s being 4.92 ± 0.84 L·min−1 in the PL trial and 5.21 ± 0.93 L·min−1 in the BC trial (P < 0.05). Consistent with this, the mean RER was significantly higher during 60-180 s of the test in the NaHCO3 (1.38 ± 0.08) compared with that in the PL trial (1.30 ± 0.08, P < 0.05), and the peak RER was also higher in the NaHCO3 (1.60 ± 0.14) than in the PL trial (1.49 ± 0.10, P < 0.05; Fig. 3B). There were no marked differences in V˙E between treatments (Fig. 3D).
To our knowledge, this is the first study to investigate the effect of NaHCO3 ingestion on the power-duration relationship and all-out sprint performance during a single exercise bout of greater than 60 s in duration. The principal novel finding of this study was that, although the blood acid-base balance was significantly altered after NaHCO3 ingestion, the induced alkalosis did not improve the purportedly "anaerobic" component of the power-duration relationship (i.e., W′). It was also shown that the CP, which has been characterized as the highest metabolic rate that is sustainable without a progressive reduction in the muscle energy charge and its systemic sequelae, was not affected by the induced alkalosis. Overall, NaHCO3 ingestion did not improve performance (as indicated by the total work done) in a single 3-min bout of all-out cycling against fixed resistance (Fig. 2). Therefore, although the present results supported the hypothesis of unaltered CP, they were contrary to the hypothesis that NaHCO3 ingestion would improve the W′ and 3-min all-out cycling performance.
The loading dose of 0.3 g of NaHCO3 per kilogram body mass was effective in altering the blood pH, bicarbonate, and base excess before the 3-min all-out test (Fig. 1), which is consistent with several previous investigations (4,14,18,35,42). Also consistent with earlier studies (9,35), V˙CO2 and RER were markedly elevated during the last 2 min of the test (Fig. 3, B and C), which is likely a consequence of an elevated rate of bicarbonate buffering in the blood, resulting in CO2 release via carbonic acid. Although the 0.3 g·kg−1 dose used in the present study was sufficient to induce a significant preexercise alkalosis, it is not known whether an even greater increase in buffering capacity might have resulted in improved performance. However, in our experience, doses exceeding 0.3 g·kg−1 greatly increase the occurrence of gastrointestinal distress and do not result in a demonstrable additional ergogenic effect during maximal-intensity exercise (22).
The present findings are in agreement with some previous studies that have reported no ergogenic effect on high-intensity exercise performance despite significant preexercise alkalosis (9,30,35,43) but are in contrast with others that have reported performance improvements (4,8,18,21,36,42). These latter studies suggest that high-intensity constant-work-rate exercise (95%-125% V˙O2max) may be continued for longer with induced alkalosis when the high-intensity performance bout is preceded by several shorter bouts at the same high-intensity (8,21) or by prolonged submaximal exercise (40 min at 20%-60% V˙O2max (18,36)). Only one study (42) has shown improved time to exhaustion during a single constant-work-rate bout lasting ∼90 s. In contrast, evidence for any tangible ergogenic effects on "all-out" exercise performance resulting from preexercise alkalosis is scant. Bishop et al. (4) reported a significant 5% increase in total work done during five 6-s sprints separated by 30-s recoveries, whereas others have shown no performance improvement in repeated 30-s (30), 45-s (43), and 60-s all-out exercise bouts (9). The present results extend these findings in showing that preexercise alkalosis does not improve performance in a single all-out exercise bout lasting 3 min.
To our knowledge, no previous study has investigated the effects of preexercise alkalosis on the power-duration parameters as measured using the conventional protocol of multiple separate prediction trials. As hypothesized, the CP was not affected by an alteration in blood-buffering capacity. This finding is in agreement with earlier studies that have reported no improvement in prolonged exercise performance at 80% V˙O2max (35) and no alteration in the so-called neuromuscular fatigue threshold (16) after administration of NaHCO3. However, given that the CP is considered to represent a boundary above which intramuscular pH (among other physiological variables) cannot be stabilized (17), it might be argued that an intervention that facilitates H+ efflux from the muscle might, in fact, have increased the CP. That this did not occur might indicate that the induced blood alkalosis did not alter the intramuscular pH. Indeed, significant changes in blood-buffering capacity by increased [NaHCO3] may not directly translate into the intracellular environment which relies predominantly on phosphate and protein buffers in the regulation of pH (19,20). The actual effects of induced blood alkalosis on the intracellular pH remain controversial, with some studies reporting elevated pH (29,35) and others showing no effect (4,8,15).
The lack of effect of NaHCO3 ingestion on the W′ may be interpreted in light of both methodological and physiological factors. It should firstly be considered whether the 3-min all-out test is sufficiently sensitive to detect potentially small changes in performance. In the present study, the coefficient of variation for the W′ between PL and BC trials was 5%, which is within the previously established test-retest variation of 9% (37). The power output profiles were virtually indistinguishable between the two treatments in all eight subjects without any indication of a trend for altered performance (Fig. 2). Furthermore, we have previously used the same protocol in identifying changes in the CP after a 4-wk training intervention (40) and in the W′ after a previous sprint exercise (38). We are therefore confident that the 3-min all-out protocol possesses the necessary sensitivity to detect any meaningful changes in the power-duration parameters invoked by NaHCO3 ingestion.
The present findings may also be considered in light of the complex metabolic consequences of induced alkalosis (14,34,35). If the finite work capacity >CP is to a large extent derived from nonoxidative metabolism as has been suggested (26,28), an intervention that might be expected to increase the glycolytic contribution during exercise (4,14) should increase the W′. The possible beneficial effect of preexercise alkalosis on muscular performance is thought to stem from a greater efflux of H+ from the active muscle, thereby attenuating the rate at which intracellular pH falls and facilitating a greater glycolytic contribution to energy turnover (4,18,32,36). Support for this contention has been provided by a report of an elevated rate of glycogen utilization during high-intensity exercise after induced metabolic alkalosis (14). However, Bangsbo et al. (1) demonstrated that the relative contribution of aerobic and anaerobic metabolic pathways to total ATP turnover during exhaustive high-intensity exercise was not related to preexercise muscle pH. It should therefore be noted that whereas the NaHCO3 ingestion was demonstrably effective in increasing the blood pH in the present study, and might have altered the muscle pH (see earlier discussion), changes in the glycolytic rate may not be the mechanism by which any putative performance-enhancing effects (e.g., [4,8,18]) of preexercise alkalosis are manifested.
Whereas the effect of pH on glycolytic rate is unclear, it has been established that the inability to continue exercise at a given supra-CP work rate is associated with a low muscle pH (17). If preexercise alkalosis can attenuate the rate of fall in pH, the attainment of a "critically low" pH could be delayed, enabling improved exercise tolerance >CP and thereby increased W′ (31). It has been proposed that the magnitude of the W′ is limited both by the depletion of intramuscular [PCr] (in accordance with the classic interpretation of W′ as an "anaerobic energy store" [25-28]) and also by the accumulation of metabolites such as Pi and H+, which are known to impair muscle contractility (10,17). In a recent study, Raymer et al. (33) reported that induced alkalosis delayed intramuscular acidification during exhaustive incremental wrist-flexion exercise but without altering the rate of PCr breakdown. If a similar effect occurred in the present study, it might be speculated that the [PCr] dynamics play a more important role in determining the magnitude of the W′ than does changes in muscle pH (and, by inference, the rate or magnitude of glycolytic metabolism). Consistent with this suggestion, we have recently reported that the magnitude of the W′ measured in the 3-min all-out test was closely related to the estimated muscle [PCr] when the latter was manipulated using previous sprint exercise and varying recovery durations (38). Moreover, exercise tolerance during >CP exercise seems to be more closely correlated with the attainment of a critically low muscle [PCr] than with muscle pH or [Pi] (17). However, in the absence of direct information on the effects of NaHCO3 ingestion on muscle metabolism in the present study, and given the difficulty in quantifying the relative contribution from the oxygen-independent energy sources during dynamic high-intensity exercise (1), the precise physiological determinants of W′ remain obscure.
It has recently been suggested that the W′ is closely related to the same factors that regulate the V˙O2 response to high-intensity exercise, such that the W′ may be defined by an interplay of intramuscular [PCr] and glycolytic flux, the rate at which O2 uptake projects toward the end-exercise value, and the maximal rate of O2 uptake that can be achieved during supra-CP exercise (6). Consistent with this suggestion, neither the V˙O2 response (Fig. 3A) nor the W′ during the 3-min test was altered by NaHCO3 ingestion in the present study. That NaHCO3 ingestion did not alter the V˙O2 response to all-out exercise is consistent with the unchanged fundamental component V˙O2 kinetics reported by Berger et al. (3) during severe-intensity constant-work-rate exercise after NaHCO3 loading.
In summary, preexercise alkalosis has no effect on the finite capacity for work above CP (W′) or the CP during all-out exercise. Although NaHCO3 ingestion resulted in a significant preexercise alkalosis, the total work done during 3 min of all-out cycling was not altered. These results indicate that any putative changes in the rate of "anaerobic" glycolysis or in muscle H+ accumulation as a result of preexercise blood alkalosis do not influence the parameters of the power-duration relationship as established during all-out exercise.
This research was not sponsored by any funding body external to University of Exeter. The results of the present study do not constitute endorsement by American College of Sports Medicine.
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