The measurement of pulmonary oxygen uptake (pV˙O2) kinetics during exercise provides a noninvasive window into the rate of oxidative metabolism in skeletal muscle (mV˙O2). Specifically, after an abrupt increase in work rate, the time constant (τ) associated with the fundamental or fast exponential rise in pV˙O2 in phase II has been demonstrated to be within ± 10% of the τ describing the exponential rise in mV˙O2 towards the required steady state (6). Furthermore, for exercise engendering a significant lactic acidosis (i.e., at work rates above the so-called lactate threshold, LT), the slow component of pV˙O2 originates predominantly from an increased energy turnover and O2 consumption within the contracting muscles (25,28). The careful measurement and interpretation of pV˙O2 kinetics can therefore be used to provide insight into the control of, and limitations to, muscle oxidative metabolism-insight that is likely to be of both scientific interest and practical value (35). Indeed, studies have shown that pV˙O2 kinetics are influenced by maturation and aging, training status, disease conditions, prior exercise, muscle fiber type, motor unit-recruitment patterns, exercise modality, O2 availability, and a variety of nutritional and pharmacological interventions (24).
The phase II τ has been reported to be similar or somewhat longer for exercise performed above as compared with below the LT, and the pV˙O2 slow component is normally associated with an elevation of blood [lactate] (24). However, whether the lactic acidosis is a cause or a consequence of these alterations in the pV˙O2 response profiles is not clear. Several studies have attempted to investigate these issues by acutely altering muscle and blood acid-base status through the ingestion of sodium bicarbonate (NaHCO3), but the results have been equivocal. For example, the results of two recent studies that investigated the influence of NaHCO3 ingestion on pV˙O2 kinetics during cycle exercise requiring approximately 75-85% pV˙O2peak were diametrically opposed (14,37). Specifically, Kolkhorst et al. (14) reported that NaHCO3 ingestion resulted in a 34% longer τ (i.e., slower phase II pV˙O2 kinetics) compared with the control condition; in contrast, Zoladz et al. (37) reported that NaHCO3 ingestion was associated with a 32% shorter τ. The results of these two studies are difficult to reconcile because they involved subjects with similar characteristics and employed similar experimental procedures. The influence of NaHCO3 ingestion on the magnitude of the pV˙O2 slow component is no less ambiguous. In two studies, NaHCO3 ingestion was reported to reduce either the pV˙O2 slow component (14) or the slow component of intramuscular phosphocreatine concentration ([PCr]; a proxy for mV˙O2 in healthy subjects) (5). However, in three other studies, NaHCO3 ingestion had no effect on the pV˙O2 slow component (9,29,36). Clearly, the influence of induced alkalosis on pV˙O2 kinetics requires clarification.
One possible shortcoming of all the previous studies that have examined the influence of induced alkalosis on pV˙O2 kinetics is that subjects only completed step exercise tests on two occasions (i.e., once after the ingestion of NaHCO3 and once in the control or placebo condition). Because breath-by-breath pV˙O2 data possess inherent variability, it is recommended that the pV˙O2 responses to several like transitions are averaged together before analysis to reduce noise and increase statistical confidence in the parameters, such as τ, derived from the exponential model fits (16,35). The purpose of the present study, therefore, was to investigate the influence of NaHCO3 ingestion on pV˙O2 kinetics during high-intensity cycle exercise using a sufficient number of repeat transitions to provide high confidence in the results obtained. We hypothesized that induced metabolic alkalosis would have no significant effect on the phase II τ but that it would reduce the amplitude of the pV˙O2 slow component.
Seven healthy males (mean ± SD: age 26 ± 5 yr, height 1.83 ± 0.06 m, body mass 81.7 ± 7.1 kg) volunteered and gave written informed consent to participate in this study, which had received approval from the local research ethics committee. The subjects, who were familiar with the exercise testing procedures employed in the study, were occasionally active in recreational sports activities but were not highly trained. The subjects were instructed to arrive at the laboratory at the same time of day (± 1 h) in a rested (no heavy exercise during the previous 24 h), well-hydrated state, having consumed no food, caffeine, or alcohol during the previous 3 h.
All testing was completed in a well-ventilated laboratory at a temperature of 20-22°C. The subjects attended the laboratory on up to seven occasions during a 3-wk period to perform exercise tests on an electronically braked cycle ergometer (Ergoline E800, Jaeger, Höchberg, Germany). The first visit was used to establish pV˙O2max and to estimate the gas exchange threshold (GET). On each of the subsequent visits, subjects completed a single bout of exercise at a work rate that was calculated to require 60% of the difference between the GET and pV˙O2max (60%Δ; severe-intensity exercise) (26). In six subjects, the exercise was preceded by the ingestion of NaHCO3 on three occasions and by the ingestion of a placebo (see below) on another three occasions; the remaining subject completed a total of four exercise bouts (two after NaHCO3 ingestion and two after placebo ingestion). The experimental and placebo conditions were presented to the subjects in random order, and each trial was separated by 1-4 d.
During the first visit to the laboratory, the ergometer was adjusted so that each subject was comfortable, and the settings were recorded and replicated during all subsequent exercise tests. After measurement of height and body mass, subjects performed a ramp incremental exercise test to determine pV˙O2max and GET. This test consisted of 3 min of unloaded pedaling, and then a continuous ramped increase in work rate of 30 W·min−1 until the limit of tolerance. The pedal rate selected by each of the subjects in this test (typically 80-85 rpm) was employed during all subsequent tests. All gas exchange and ventilatory variables were averaged and displayed every 10 s. The pV˙O2max was determined as the highest pV˙O2 measured for 30 s, and the GET was estimated from a cluster of gas exchange indices, including a nonlinear increase in carbon dioxide output (pV˙CO2) when plotted against pV˙O2, and an increase in the ventilatory equivalent for O2 with no increase in the ventilatory equivalent for CO2 (34). The work rate corresponding to 60%Δ was calculated using linear regression of pV˙O2 versus work rate, with account taken of the lag in pV˙O2 relative to work rate that exists during ramp incremental exercise (34).
On each of the subsequent laboratory visits, the subjects were asked to consume either 0.3 g·kg−1 body mass of NaHCO3 in 1 L of orange squash (ALK; on three occasions) or 0.1 g·kg−1 body mass of sodium chloride in 1 L of orange squash (CON; on three occasions) over a 10-min period. The step exercise test protocol commenced 60 min after consumption of the CON or ALK beverage. The step test began with 3 min of pedaling at 20 W (the lowest work rate available on the ergometer), after which the 60% change in work rate was abruptly applied and subjects continued exercising for a further 6 min.
During two of the exercise bouts (once for CON and once for ALK), arterialized capillary blood samples were collected to document the effects of NaHCO3 ingestion on blood acid-base status. Blood samples were collected shortly after first entry to the laboratory, 60 min after ingestion of CON or ALK, during the last 30 s of the baseline period of cycling, and at 1, 2, 3, and 6 min of exercise. On each occasion, blood was collected into heparinized glass capillary tubes for subsequent determination of acid-base status (AVL Omni 4, Roche Diagnostics, Lewes, UK) and whole blood [lactate] (YSI 1500, Yellow Springs Instruments, Yellow Springs, OH). Blood lactate accumulation was calculated as the difference between the blood [lactate] measured at 6 min of exercise and the blood [lactate] measured at baseline, at 2 min of exercise, and at 3 min of exercise. During another two of the exercise bouts (again once for CON and once for ALK), arterial O2 saturation (SaO2) was monitored continuously throughout exercise using a pulse oximeter positioned on the index finger of the left hand (model 8000AA, Nonin, UK). During these tests, subjects were also asked to provide a rating of perceived exertion (RPE) at 3 and 6 min of exercise by pointing to a 6-20 graded Borg scale (4). Heart rate (HR) was measured every 5 s in all tests using short-range radio telemetry (Polar S610, Polar Electro Oy, Kempele, Finland).
Pulmonary gas exchange and ventilation were measured breath-by-breath with subjects wearing a nose clip and breathing through a low-dead space, low-resistance mouthpiece and impeller turbine assembly (Jaeger Triple V). The inspired and expired gas volume and gas concentration signals were continuously sampled at 100 Hz, the latter using paramagnetic (O2) and infrared (CO2) analyzers (Jaeger Oxycon Pro, Höechberg, Germany) via a capillary line connected to the mouthpiece. The gas 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). The volume and concentration signals were time aligned by accounting for the delay in the capillary gas transit and the analyzer rise time relative to the volume signal. Pulmonary V˙O2, VCO2, and minute ventilation (V˙E) were calculated and displayed breath-by-breath.
The breath-by-breath data from the step exercise tests were used to estimate the pV˙O2 kinetics. The data were first manually filtered to remove outlying breaths, defined as breaths deviating by more than three standard deviations from the preceding five breaths. The data were subsequently interpolated to provide second-by-second values and, for each individual, the data sets from the CON and ALK conditions were time aligned and averaged. However, in the present study, we also modeled the pV˙O2 response to each of the individual transitions to examine the between-test variability in the estimated phase II τ.
The first 20 s of data after the onset of exercise (i.e., the phase I response) were deleted, and a nonlinear least-square algorithm was used to fit the data as described in the following biexponential equation:
where pV˙O2 baseline (t) represents the absolute pV˙O2 at a given time t; pV˙O2 baseline represents the mean pV˙O2 in the final 2 min of the baseline period; Ap, TDp, and τp represent the amplitude, time delay, and time constant, respectively, describing the fundamental or primary increase in pV˙O2 above baseline; and As, TDs, and τs represent the amplitude, time delay, and time constant describing the development of the pV˙O2 slow component. An iterative process was used to minimize the sum of the squared errors between the fitted function and the observed values. Because the asymptotic value (As) of the exponential term describing the pV˙O2 slow component may represent a higher value than is actually reached at the end of the exercise, the actual amplitude of the pV˙O2 slow component at the end of exercise was used and defined as As′. The pV˙O2 slow component was also estimated by calculating the difference between the mean pV˙O2 during the last 20 s of exercise and the mean pV˙O2 during the 20-s period centered on 3 min of exercise, that is, pV˙O2 (6 to 3 min).
A repeated-measures ANOVA (treatments (2) × time (7)) was used to determine whether there were statistical differences in the blood data for each of the individual variables (e.g., pH, [bicarbonate], base excess, [lactate]). Where the data were significant and when there was no interaction effect, individual ANOVAs were undertaken on the relevant data with post hoc comparisons between the various times using a Fisher's PLSD. Paired t-tests were used to determine the existence of significant differences in the parameters of the pV˙O2 kinetics between the CON and ALK conditions. Statistical significance was accepted at P < 0.05. Data are presented as mean ± SD, unless otherwise indicated.
The pV˙O2max of the subjects measured during the ramp incremental test was 3.92 ± 0.26 L·min−1 (48.3 ± 4.9 mL·kg−1·min−1), and the highest work rate attained was 384 ± 37 W. The GET occurred at a mean pV˙O2 of 2.07 ± 0.23 L·min−1 or 52 ± 3% pV˙O2max. The work rate equivalent to 60%Δ was 283 ± 31 W.
The repeated-measures ANOVA revealed that NaHCO3 ingestion had a significant effect on pH for both treatment (P < 0.005) and time (P < 0.0001), although there was no interaction effect (P > 0.064; Fig. 1). There was a significant interaction between treatment and time for blood [bicarbonate] (P < 0.0001), and each variable was also significant (treatment: P < 0.0005; time: P < 0.0001; Fig. 2). Consistent with this, there was a significant interaction between treatment and time for base excess (P < 0.0001), and each variable was also significant (treatment: P < 0.001; time: P < 0.0001; Fig. 3).
There was a significant interaction between treatment and time for blood [lactate] (P < 0.005), and each variable was also significant (treatment: P < 0.05; time: P < 0.0001; Fig. 4). At the final measurement point (6 min), blood lactate level in the experimental condition was significantly higher (P < 0.0001) than in the placebo condition. The accumulation of blood lactate was significantly greater after NaHCO3 ingestion when computed as the difference in blood [lactate] between 6 min of exercise and baseline (CON: 5.0 ± 0.7 vs ALK: 6.1 ± 0.8 mM; P < 0.01), 6 and 2 min of exercise (CON: 3.3 ± 0.5 vs ALK: 4.3 ± 0.9 mM; P < 0.05), and 6 and 3 min of exercise (CON: 2.1 ± 0.4 vs ALK: 2.9 ± 0.7 mM; P < 0.005).
Heart rate was not different between the conditions before, during, or at the end of exercise (CON: 166 ± 9 vs ALK: 165 ± 10 bpm; P = 0.64). RPE tended to be lower after NaHCO3 ingestion both at 3 min (CON: 14.3 ± 1.1 vs ALK: 13.3 ± 1.3; P = 0.06) and at 6 min (CON: 15.9 ± 1.6 vs ALK: 15.3 ± 1.3; P = 0.17) of exercise. Arterial O2 saturation (as estimated by pulse oximetry) remained high (> 96%) throughout exercise in the control condition and was not altered by NaHCO3 ingestion.
The model parameters for the pV˙O2 kinetics in the two conditions are shown in Table 1, whereas the pV˙O2 responses of a representative subject are shown in Figure 5. The parameters describing the pV˙O2 response over the fundamental phase of the response were not significantly different between the conditions. Of particular interest in relation to the experimental hypotheses was that the phase II τ was not changed by NaHCO3 ingestion (CON: 29 ± 6 vs ALK: 32 ± 7 s; P = 0.21). The 95% confidence interval (95% CI) surrounding the estimation of the phase II τ was 3 ± 1 s for both conditions. The pV˙O2 slow component emerged significantly later (CON: 120 ± 19 vs ALK: 147 ± 34 s; P < 0.01) and tended to be smaller (CON: 0.59 ± 0.15 vs ALK: 0.48 ± 0.14 L·min−1; P = 0.08) after NaHCO3 ingestion. However, the pV˙O2 (6 to 3 min) was not significantly different between the conditions (Table 1). The end-exercise pV˙O2 was significantly reduced after NaHCO3 ingestion (CON: 2.88 ± 0.19 vs ALK: 2.79 ± 0.23 L·min−1; P < 0.05).
The estimated phase II τ, along with the corresponding 95% CI, derived from each of the individual exercise bouts are shown in Table 2. There was appreciable intrasubject variability in the phase II τ when the latter was estimated from single transitions. The coefficient of variation was approximately 28% (range: 8-52%) in the CON condition and approximately 20% (range: 7-43%) in the ALK condition. The mean 95% CI for single transitions was 7 ± 4s (range: 3-23 s) compared with 3 ± 1 s (range: 2-6 s) when the responses to the repeat transitions for each subject were ensemble averaged.
The principal findings of this study were that NaHCO3 ingestion, which significantly altered blood acid-base balance, had no significant effect on the phase II pV˙O2 kinetics but resulted in alterations in the pV˙O2 slow component such that the pV˙O2 was significantly reduced after 6 min of exercise. These results are consistent with some previous studies that have reported reductions in the magnitude of the pV˙O2 or [PCr] slow component (5,14), but they disagree with two previous studies that have suggested that the phase II τ is either significantly longer (14) or significantly shorter (37) after NaHCO3 ingestion.
Influence of NaHCO3 ingestion on blood acid-base balance
As expected, NaHCO3 ingestion resulted in significant alterations to blood pH, bicarbonate, base excess, and lactate, before and during exercise (Figs. 1-4). The magnitude of the changes in blood acid-base status was similar to those reported in other studies that had used similar dosing protocols (3,9,10,12,14,29,37). The ingestion of NaHCO3 increases blood-buffering capacity and enables a greater efflux of H+ from the active muscles during exercise (10,20), effects that have been shown to be performance enhancing, particularly during activities that rely to an appreciable extent on anaerobic glycolysis for energy supply (3,12,21). The significantly higher blood [lactate] at 6 min of exercise is also consistent with some previous reports (3,12,21,23,30) and indicates that the energy derived from anaerobic glycolysis during exercise is increased (possibly as a result of an attenuated reduction in intracellular pH), and/or that muscle lactate efflux is enhanced, and/or that lactate clearance by inactive tissue is reduced, after NaHCO3 ingestion (3,10,30,31).
Influence of NaHCO3 ingestion on phase II p V˙O2 kinetics
To our knowledge, only two previous studies have examined the influence of NaHCO3 ingestion on phase II pV˙O2 kinetics (14,37). Confusingly, these studies, which used similar experimental procedures, resulted in impressive, but directionally opposite, effects: NaHCO3 ingestion resulted in a 34% longer phase II τ in the study of Kolkhorst et al. (14) and a 32% shorter phase II τ in the study of Zoladz et al. (37). The experimental procedures used in our study including the NaHCO3 dosing regimen (0.3 g·kg−1 body mass), the cycle exercise protocol (requiring approximately 80% pV˙O2max), and the type of subject recruited (recreationally active young males) were similar to those used in these other studies (14,37). However, in the present study, we were unable to discern any significant effect of NaHCO3 ingestion on the phase II τ (mean values of 29 and 32 s in the CON and ALK conditions, respectively). Our results therefore disagree with those of both Kolkhorst et al. (14) and Zoladz et al. (37).
In discussing their results, Zoladz et al. (37) argued that initial alkalinization of the muscle cells after NaHCO3 ingestion (23,27,30) should alter the creatine kinase equilibrium such that more ADP would be available to stimulate mitochondrial respiration (19), resulting in a speeding of mV˙O2 kinetics. However, they also suggested that the paradoxical reduction in pH after NaHCO3 ingestion that has been reported in some studies (10) could also result in a speeding of mV˙O2 kinetics because of the inhibitory effect of hydrogen ions (H+) on ATP supply through anaerobic glycolysis. Although controversial (2,15), there is some evidence that the rate of mitochondrial respiration in skeletal muscle can be influenced by cell pH (5,7,13,32). However, the direction and extent to which an alteration in blood acid-base balance invoked by NaHCO3 ingestion might impact intracellular pH is by no means clear (3,5,10,23,27,30). Recently, Forbes et al. (5) used 31P magnetic resonance spectroscopy (MRS) techniques to examine the influence of NaHCO3 ingestion on muscle metabolism during wrist-flexion exercise. These authors reported that NaHCO3 ingestion had no effect on intracellular [H+] at rest or during moderate-intensity exercise, but that it reduced H+ accumulation, [PCr] depletion, and free [ADP] during the last 3 min of high-intensity exercise. Muscle [PCr] kinetics (a proxy for mV˙O2 kinetics (19,28)) were not significantly altered by NaHCO3 ingestion either in the transition from rest to moderate-intensity exercise (CON: 52.2 vs ALK: 52.0 s) or in the transition from moderate- to high-intensity exercise (CON: 56.9 vs ALK: 63.6 s). Our results are therefore consistent with Forbes et al. (5) in indicating that NaHCO3 ingestion does not significantly alter the kinetics of oxidative metabolism after the onset of high-intensity exercise.
Kolkhorst et al. (14) suggested that the significantly slower pV˙O2 kinetics they observed after NaHCO3 ingestion could be explained by a leftward shift of the oxyhemoglobin (O2Hb) dissociation curve, which would inhibit O2 offloading at the muscle capillary. Consistent with this suggestion, respiratory alkalosis caused by hyperventilation has been reported to result in somewhat slower pV˙O2 kinetics (8,33), although recent evidence suggests that respiratory alkalosis might also have independent effects on muscle metabolism (18). Another effect of a left-shifted O2Hb-dissociation curve with NaHCO3 ingestion would be an enhanced loading of Hb with O2 in the lung. This effect has been reported to attenuate arterial O2 desaturation, at least in highly trained subjects performing high-intensity exercise (22). Therefore, the potential for an inhibition of diffusive O2 delivery to muscle to slow pV˙O2 kinetics with NaHCO3 ingestion might be offset by better oxygenation of the arterial blood in subjects who are susceptible to arterial hypoxemia during such exercise. In the present study, there was no evidence of arterial O2 desaturation (as estimated from pulse oximetry) during the control condition, as might be expected given the training status of the subjects and the exercise intensity studied (22). Our results therefore do not support the suggestion that a leftward shift of the O2Hb-dissociation curve caused by NaHCO3 ingestion results in a significant slowing of the phase II pV˙O2 kinetics.
A key strength of the present study was the averaging together of several like transitions in each of the experimental conditions, a process that resulted in tight 95% CI of 3 ± 1 s for the estimation of the phase II τ in each of the conditions. Breath-by-breath pulmonary gas exchange is inherently noisy and, for this reason, it is recommended that a number of transitions are averaged together to enhance the signal-to-noise ratio and hence improve confidence in the outputs derived from the modeling procedures (16,35). This is particularly important in situations where higher-order models (i.e., those containing more parameters) are required to adequately fit the data (35). To illustrate this point, Table 2 shows the estimates of the phase II τ in each of the subjects when the pV˙O2 responses to individual bouts were modeled and also when the bouts were ensemble averaged before modeling. It is clear from this analysis that there can be substantial intrasubject variability in the estimated phase II τ when it is derived from single exercise bouts. For example, the group mean phase II τ was 22% longer in CON bout 1 compared with ALK bout 1 (P = 0.14), but 44% shorter in CON bout 2 compared with ALK bout 3 (P = 0.04). Clearly, estimating the phase II τ from single transitions (as was done in the studies of Kolkhorst et al. (14) and Zoladz et al. (37)) is hazardous in that the inherently greater data variability has the potential to result in spurious results. It seems that the use of single transitions might at least partly explain the disparate results reported in previous studies. Table 2 also reports the 95% CI for the estimation of the phase II τ for the single transitions and when the data were ensemble averaged before modeling. The mean 95% CI for single transitions was 7 ± 4 s (range: 3-23 s), whereas the mean 95% CI when two to three transitions were ensemble averaged was 3 ± 1 s (range: 2-6 s). Therefore, although both Kolkhorst et al. (14) and Zoladz et al. (37) reported statistically significant differences between the mean values for the phase II τ after NaHCO3 ingestion (i.e., CON: ~21 vs ALK: ~28 s; CON: ~33 vs ALK: ~25 s), the use of single transitions makes it possible that the 95% CI surrounding the estimates in the CON and ALK conditions overlapped, at least in some subjects. This further highlights the importance of averaging together a sufficient number of like transitions to provide greater confidence in the results and their interpretation (16,35).
Influence of NaHCO3 ingestion on the p V˙O2 slow component
In the present study, NaHCO3 ingestion had some significant effects on the development of the pV˙O2 slow component. Specifically, the appearance of the pV˙O2 slow component (TDs) was significantly delayed. Its amplitude was reduced by an average of 19% (not significant), and the increase in pV˙O2 above baseline at the end of exercise was significantly reduced by NaHCO3 ingestion. Although the reduction in the amplitude of the pV˙O2 slow component with NaHCO3 ingestion did not attain statistical significance (P = 0.08), this might be a function of the relatively small sample size in the present study. Six of the seven subjects demonstrated substantial reductions in the pV˙O2 slow-component amplitude after NaHCO3 ingestion (150 mL·min−1, on average, or 25%). It is unclear why this same effect was not observed in the one remaining subject, although it is of interest that NaHCO3 ingestion did not alter the accumulation of blood lactate during exercise in this individual, suggesting that he had a diminished response to the treatment.
Several previous studies have investigated the influence of NaHCO3 ingestion on the pV˙O2 (or [PCr]) slow component (5,9,14,29,37). Of those, Kolkhorst et al. (14) reported that the pV˙O2 slow component was delayed and significantly reduced (by 29%), whereas Forbes et al. (5) also reported that the [PCr] slow component was significantly attenuated (by 40%) after NaHCO3 ingestion. Our results seem to be generally consistent with these previous studies. Three other studies reported no significant difference in the magnitude of the pV˙O2 slow component with NaHCO3 ingestion compared with the control condition (9,29,37). These studies estimated the pV˙O2 slow component by calculating the difference in pV˙O2 between that measured at 3 min and that measured at 6 min (or the end of exercise). This approach, although useful in providing an approximation of the pV˙O2 slow-component magnitude, is likely to underestimate the true amplitude of this phase of the response because the pV˙O2 slow component typically commences before 3 min of exercise have elapsed (Table 1). This approach also does not account for possible differences in the time at which the pV˙O2 slow component is first discerned between experimental conditions. For example, the higher-order model applied in the present study indicates that NaHCO3 ingestion delayed the appearance of the pV˙O2 slow component by 23% (TDs, CON: 120 s vs ALK: 147 s, on average). It is also of note that blood [lactate] during exercise was increased to a greater extent in the present study than in those in which no effect on the pV˙O2 slow component after NaHCO3 ingestion had been reported (9,29,37).
There is compelling evidence from a variety of sources that the pV˙O2 slow component is related, in some manner, to the recruitment of low-efficiency type II fibers in the active muscles (24). The pV˙O2 slow component is typically associated with an elevated blood [lactate], although whether this is the cause or the consequence of increased type II fiber recruitment is unclear. It is recognized, however, that blood [lactate] per se is not causally related to the pV˙O2 slow component (24). Consistent with this view, the greater accumulation of lactate during the last 3-4 min of exercise after NaHCO3 ingestion was associated with a smaller pV˙O2 slow component in the present study. One popular explanation for the development of the pV˙O2 slow component during high-intensity exercise is that initially recruited fibers that become fatigued are replaced by fibers that are higher in the recruitment hierarchy and that have a higher ATP and O2 cost of force generation (24). Alternatively, the accumulation of metabolites or ions (i.e., H+, Pi, K+) in fatiguing muscle might increase the ATP (and O2) cost of contractions by increasing Ca2+ or Na+-K+ pump activity (24). In either case, a greater extrusion of H+ after NaHCO3 ingestion and, consequently, a higher intracellular pH (5,23,27) could be envisaged to reduce muscle fatigue (1,17) and therefore attenuate the mV˙O2 and pV˙O2 slow components by one or both of the mechanisms described above. Consistent with this suggestion, it is notable that similar results to those of the present study (i.e., a significantly longer time delay before the appearance of the pV˙O2 slow component, and a lower end-exercise pV˙O2) were reported after the infusion of dichloroacetate, a pharmacological agent that is known to reduce muscle "anaerobic&" energy transfer (11).
It is well known that NaHCO3 ingestion can be performance enhancing, particularly during activities that rely to an appreciable extent on anaerobic glycolysis for energy supply (3,12,21). Although we did not directly measure exercise performance, the results of the present study (i.e., delayed pV˙O2 slow component, reduced pV˙O2 after 6 min of exercise, and tendency for RPE to be reduced), along with previous reports of a significant attenuation of the pV˙O2 or [PCr] slow components (5,14), suggest that NaHCO3 ingestion might also be ergogenic during endurance events where these are performed above the critical power (CP). Exercise above the CP is associated with an inexorable increase in blood [lactate] and a continued rise of pV˙O2 with time until pV˙O2max is reached and exhaustion ensues (26). Exercise in this state can typically be sustained for a maximum of 30-40 min. Future research might usefully investigate the influence of NaHCO3 on exercise performance during such events.
This study has shown that NaHCO3 ingestion has no significant effect on phase II pV˙O2 kinetics but delays the appearance of the pV˙O2 slow component and reduces end-exercise pV˙O2 during cycle exercise in healthy young males. We were careful to include a sufficient number of like transitions in our experimental design to provide high confidence in the parameters derived from the model fits to the pV˙O2 data, and our results cohere with a recent report that NaHCO3 ingestion had no effect on [PCr] kinetics in the fundamental phase of the response but reduced the intramuscular [PCr] slow component during wrist-flexion exercise (5). Our results therefore suggest that NaHCO3 ingestion does not impact sufficiently on intramuscular pH to significantly alter the fundamental mV˙O2 kinetics (as reflected by pV˙O2 kinetics). We speculate that the effects of NaHCO3 on the slow phase of the pV˙O2 response might be related to a greater efflux of H+ from muscle to blood in this condition (3,10,20), which might attenuate the rate of fatigue development and delay or reduce the recruitment of higher-order muscle fibers as exercise proceeds.
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Keywords:©2006The American College of Sports Medicine
METABOLIC ALKALOSIS; PULMONARY GAS EXCHANGE; O2 DYNAMICS; PHASE II TIME CONSTANT; V˙O2 SLOW COMPONENT