Effects of Sodium Bicarbonate on VO2 Kinetics During Heavy Exercise

Fred W. Kolkhorst; Robert S. Rezende; Susan S. Levy; Michael J. Buono


Med Sci Sports Exerc. 2004;36(11) 

In This Article


O2 at the beginning and end of exercise did not differ between trials. Regardless, bicarbonate ingestion altered the manner in which O2 increased during the 6 min of heavy exercise. The primary findings of this study were that sodium bicarbonate ingestion slowed the rapid component of O2 kinetics and also decreased the amplitude of the slow component. This is consistent with other reports in that the opposite effects were observed during heavy exercise while subjects were in a state of metabolic acidosis induced by a warm-up bout of heavy exercise.[14,19] Likewise, after blood pH was decreased from ingestion of ammonium chloride, Δ O2 6–3 was greater than the control trial.[26] However, those studies that have investigated the effect of sodium bicarbonate on O2 kinetics observed, as did we, a smaller but nonsignificant Δ O2 6–3 in the bicarbonate trial.[20,25] The use of Δ O2 6–3 to describe the slow component may have underestimated its actual magnitude, and when we used a three-component, nonlinear regression model to identify the beginning of the slow component, A'3 was 29% smaller in the bicarbonate trial. Our failure to observe significance between trials for Δ O2 6–3 in spite of significant differences in A'3 was influenced partly by differences in the TD3s of the two trials. The slow component of the bicarbonate trials started on average 29 s later than the control trial, and although this difference did not reach significance, a longer TD3 would tend to decrease A'3.

Nonetheless, this does not fully explain the difference in A'3 between the two trials. Rather, we speculated that the smaller slow component resulted from effects of bicarbonate on working muscle. Although muscle pH was not measured in the current study, it was likely affected by the bicarbonate dosage we administered. After bicarbonate infusion, there was an attenuation in the drop of muscle pH during handgrip exercise[17] as during a maximal ~60-min performance test after subjects received the same oral dosage administered in the present study.[22] The elevation of plasma bicarbonate concentration is thought to increase efflux of H+ from working muscle,[15] and we suggest that this mechanism was responsible for the smaller slow component observed in the bicarbonate trial. Although we have no explanation for the tendency of the slow component to begin later during the bicarbonate trial, it may also have been related to the delayed onset of fatigue, which would diminish increased motor unit recruitment during this period.

The second significant finding of this study was that bicarbonate ingestion slowed the rapid component. This observation is consistent with numerous investigations using varying exercise models in which prior heavy exercise speeded MRT,[2,3,7] or both τ2 and MRT [14,19,23] during a subsequent bout of heavy exercise. The residual acidemia at the onset of the second bout was postulated to have increased muscle perfusion and caused a rightward shift of the oxygen-hemoglobin dissociation curve.[2,7,14,23] These results were supported by two recent reports in which muscle O2 kinetics were determined through differences in arteriovenous O2 content of the exercising muscle. Muscle O2 was increased during the early phase in the second of two heavy bouts of forearm[13] and knee extensor exercise.[12] Both groups of investigators reported enhanced blood flow in exercising muscle before and during the early part of the second exercise bout. The mechanism(s) that explained the increased blood flow was uncertain, but as the differences in blood pH and flow occurred at similar time periods during the exercises, the acidemia may have been at least partly responsible for the improved perfusion[13] and increasing oxygen delivery.

The faster O2 kinetics observed in these studies suggested that oxidative metabolism is limited by oxygen delivery at the onset of heavy exercise.[2,3,12,13,23] However, the use of a warm-up bout of heavy exercise to induce metabolic acidosis may confound this hypothesis. Bohnert et al.[2] observed faster O2 kinetics during heavy leg exercise when preceded by heavy arm exercise, although the effect was less than when preceded by heavy leg exercise. Similarly, Fukuba et al.[5] reported faster O2 kinetics during heavy leg exercise when it was preceded by heavy leg exercise but not if preceded by heavy arm exercise. These results implied that prior exercise of the working muscle alters the metabolic status of the mitochondria and influences respiration. Recently, Hogan[9] observed faster adaptation to mitochondrial oxygen utilization in a frog muscle preparation during a second period of contractions. Oxygen availability was adequate during the onset of both contraction periods, and the faster mitochondrial adjustment to increased ATP demand may have been due to the pyruvate dehydrogenase complex being in a more active form at the start of the second contraction period.[9] MacDonald et al.[14] overcame this concern of repeated exercise bouts by exercising subjects in single bouts while breathing normoxic or hyperoxic air (FIO2 = 0.70). Oxygen delivery was increased during the hyperoxic trial, which sped up the MRT. Similarly, our experimental design attempted to manipulate oxygen delivery using a pharmacological approach while breathing normoxic air rather than the use of prior exercise.

A number of studies, though, have been unable to detect changes in τ2 or MRT during subsequent bouts of heavy exercise.[4,11,21] However, using a computer simulation model, Hughson et al.[10] illustrated the difficulty with simple O2 kinetics in detecting a significant physiological difference, even when present, in the rate of control of oxidative metabolism. Although we have no explanation for the contrasting results, these studies utilized similar curve-fitting methods and had comparable sample sizes as those studies that did observe differences in O2 kinetics.

In summary, we observed that bicarbonate ingestion before heavy exercise slowed the rapid component of O2 kinetics. We speculated that the induced alkalosis reduced muscle perfusion of working muscle, which suggests that oxygen delivery is a limiting factor of mitochondrial respiration at the onset of heavy exercise. Furthermore, bicarbonate ingestion decreased the magnitude of the slow component, which we theorized was the result of diminished fatigue. This supports the theory that metabolic acidosis is a contributing factor to fatigue during heavy exercise.

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