No significant differences were found for [BLa] at 30 minutes after each WT ([BLa]30min) between both conditions. However, for [BLa] at 3 minutes after each WT ([BLa]3min), a significant increase was observed in the NaHCO3− condition after WT2 (p = 0.014) and tendency to be greater after WT3 (p = 0.07) (Figure 4). For both placebo and NaHCO3− trials, [BLa]3min was significantly higher after WT2 when compared with WT1, but it was not different between WT2 and WT3 (Figure 4). A similar response was observed in [BLa]30min in the placebo condition. However, in the NaHCO3− condition, [BLa]30min was significantly increased after each successive WT.
The absence of any ergogenic effect in the first WT performed in the protocol is in agreement with those studies that have analyzed the effect of NaHCO3− administration before one WT (7,23,24,30). Only Inbar et al. (13) and Douroudos et al. (7) observed significant increases in WT mean power subsequent to bicarbonate loading, but they showed no effects on other WT parameters measured. Douroudos et al. (7) compared three treatment conditions (PLC, 0.3 g·kg−1 body mass, and 0.5 g·kg−1 body mass taken during 5 days) and suggest that the improvement in performance depends on the doses used, as just the greater amount of NaHCO3− was be clearly effective. However, this research used a Monark 834E ergometer to measure WT performance, which has been reported not to provide a correct calculation of power because of incomplete load transmission to the flywheel (19). In contrast to the results obtained by Douroudos et al., McNaughton (24), testing the effects of five different doses of NaHCO3− (from 0.1 to 0.5 g·kg−1 body mass), reported no differences in 60-second maximal cycling performance and venous blood pH when increasing the dose to more than 0.3 g·kg−1 body mass. Moreover, the highest value of cycling work and peak power were achieved with the dose of 0.3 g·kg−1 body mass. For the present study, we chose a dose of 0.3 g·kg−1 body mass dissolved in 1 L of flavored mineral water and ingested 90 minutes before the first WT. Although an important limitation of the present study was that blood pH and [HCO3−] values were not monitored, the protocol selected has been extensively analyzed previously (17,22,24,25,33,34,40) and proposed by several authors (10,17,40) as the most appropriate to obtain a blood alkalosis in humans without side effects (i.e., gastrointestinal distress). In this regard, an NaHCO3− intake of 0.3 g·kg−1 body mass at rest produced an increase of approximately 4-5 mmol·L−1 of the [HCO3−] and 0.03-0.06 pH units in venous plasma for approximately 3 hours after ingestion (8,24), with a peak in pH and [HCO3−] at 100-120 minutes. Thus, the lack in WT performance observed in the present study may consequently not be attributable to the NaHCO3−-administration protocol used.
In the present study, we selected elite sprint cyclists well familiarized with WT, and we hypothesized that in these subjects the effects of NaHCO3− ingestion over WT should be more significant than those published previously in sedentary subjects. It is known that sprinters have an increased ability to activate high-threshold motor units during maximal voluntary contractions (16) and a greater percentage of type II fibers in their muscles than endurance trained or untrained subjects (9). Fast-twitch fibers are characterized by a greater intramuscular acidosis during their activation (nearly fourfold difference in the maximum mechanical power output and the ATP hydrolysis rate) than slow-twitch fibers (44). Moreover, fast-twitch fibers are more susceptible to force depression with acidosis (3). On the contrary, one of the principal mechanisms proposed to explain why the induced blood alkalosis may enhance exercise performance is an improved H+ efflux out of the muscle cell, thereby limiting the effects of the decreased pHi (17,33,34,41), especially in the face of increasing metabolic demand (33,41). It is known that the fatiguing effects of a declining pHi during exercise include allosteric inhibition of the rate-limiting enzymes phosphofructokinase and glycogen phosphorylase, decreased release of Ca2+ from the sarcoplasmatic reticulum, and a reduction in the number and force of muscle cross-bridge activations (17,37). In this sense, induced alkalosis has been shown to increase muscle phosphorylase, phosphofructokinase, and pyruvate dehydrogenase activities during high-intensity exercise, resulting in enhanced glycogen use with a concomitant increase in pyruvate production, increased intramuscular Lac− accumulation, and enhanced Lac− efflux from the activated fibers (10). Indeed, in the present study we found an enhanced [BLa] at 3 minutes after WT2 and WT3 in the NaHCO3− trial. However, the mechanisms responsible for the reduced muscle [H+] during alkalosis are unclear. Proposed mechanisms include increased skeletal muscle Lac−/H+ cotransporter activity, increased Na+/H+ exchange, and/or an increased intracellular strong ion difference (33,40). An attenuated intracellular acidosis in alkalosis compared with a control condition has been found during 5 minutes of dynamic, high-intensity handgrip exercise (27), 9 minutes and until to volitional fatigue (8) of moderate to heavy-intensity wrist-flexion exercise, and after a 1-hour cycling time trial (33). On the basis of these results, an enhanced ergogenic benefit from induced blood alkalosis should be expected in subjects with higher percentages of fast-twitch fibers in their muscles during activities in which those fibers should be recruited. However, the results found in the present study did not support our hypothesis; instead, they are in agreement with previous studies that have suggested that when exercise protocols of short duration (30-40 seconds) are used, alkaline agents have minor or no effects on performance (7,12,23,24,26,30). Nevertheless, although we did not obtain a significant enhancement in WT performance in the whole group tested, it is important to point out that in our sample, the more powerful subjects got the greater the gains after alkalinizant ingestion (i.e., for subject 1, PP was 1833 vs. 1936 W in WT1, 1672 vs. 1847 W in WT2, and 1698 vs. 1814 W in WT3, comparing PLC and NaHCO3−-ingestion conditions). In this regard, significant correlations between PP in both conditions and the gain in performance (W) after NaHCO3− ingestion (r = 0.40-0.87; p < 0.01) were obtained (see Figure 3). Further research is needed to find out whether subjects with greater percentages of fast-twitch fibers in their working muscles are better “responders” to induced blood alkalosis in high-intensity, short-term exercises (less than 1 minute).
In the present study, we did not perform arterial/venous blood sampling, measurements of leg blood flow, or muscle biopsy that would permit us to elucidate which mechanisms underlie the lack of WT improvement after NaHCO3− intake. On the basis of the literature reviewed, the failure of alkalosis to increase WT performance may be explained by an insufficient time during the exercise to allow a significant difference in H+ ion efflux from the muscle fibers or an inability to generate a sufficient difference in H+ ion gradient to produce a difference between trials (8,17,20,22,23,41). Both of these could result in insignificant differences in pHi, in which case muscle performance would be expected to be similar (10,22). In apparent contrast with this possible explanation, recent studies have shown that induced intramuscular acidosis has limited effects on muscle contractile function at body temperatures (2,34) and may even exert a protective effect on excitability and performance (32). On the basis of these studies, Sostaric et al. (39) have proposed that the major beneficial effect of alkalosis on muscle performance might be the preservation of muscle membrane excitability by its integrated effects on K+, Na+, Cl−, and Lac− homeostasis. However, in this study pHi was not monitored. Moreover, a number of in situ and in vivo 31P-MRS studies have demonstrated a strong correlation between declines in pHi and force production (8,31). A controversy exists about the role of intramuscular acidosis on muscle fatigue, especially when it is conceivable and not well studied that H+ may interact with some other factors that change during intense exercise (as Na+, Cl−, or phosphate metabolites) to impair exercise performance (2,35). Similarly, a controversy exists regarding which mechanisms underlie the enhancement in human performance after NaHCO3− intake. Induction of a metabolic alkalosis may result in a complex series of metabolic effects such as lower intramuscular acidosis (8,33,40), changes in the activity of key regulatory enzymes and fuel use (8,10), or preservation of muscle cell membrane excitability (39) during exercise that may permit, under certain conditions of exercise intensity and duration, increases in muscle performance.
The authors gratefully acknowledge the team manager of BMX Spanish National Team, Mr. Miguel Hernández-Pariente, for his interest and help, and Mr. Pablo Fernández-Gálvez (Sportlab, Granada, Spain) for the technical support.
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