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

Abstract and Introduction

Purpose: Sodium bicarbonate was used to investigate the effect of blood pH on O2 kinetics during heavy exercise.
Methods: On separate days, 10 active subjects performed two 6-min cycling bouts (208 ± 12 W) at 25 W above their ventilatory threshold. Each subject ingested 0.3 g·kg-1 of sodium bicarbonate with ~1 L of water or water alone 1 h before exercise. O2 kinetics were examined by means of a three-component mono-exponential model.
Results: Bicarbonate ingestion caused a significant increase in the preexercise blood pH (7.512 ± 0.009 vs 7.425 ± 0.007; P < 0.001). In the bicarbonate trial, the time constant for the rapid component (27.9 ± 3.5 s) was slower than the control trial (20.8 ± 2.4 s; P = 0.017). The higher blood pH after bicarbonate ingestion would have diminished local blood flow and caused a leftward shift of the oxygen-hemoglobin dissociation curve both of which would slow oxygen delivery to working muscle. In addition, bicarbonate ingestion diminished the amplitude of the slow component 29% (463 ± 43 vs 649 ± 53 mL·min-1; P = 0.040). The primary cause of the slow component during heavy exercise is fatigue of working fibers and an accompanying increase of motor unit recruitment. Elevated plasma bicarbonate concentration is reported to stimulate the efflux of H+ from muscle fibers and to increase intramuscular pH.
Conclusions: The slower time constant during the rapid component suggested that oxygen delivery is a limiting factor of O2 kinetics during the onset of heavy exercise. Also, these results imply that bicarbonate ingestion diminished fatigue in working fibers during the slow component.

At the onset of moderate-intensity exercise, pulmonary O2 increases in a biexponential fashion to a steady-state level that reflects the amount of oxygen required for the exercise intensity. The rate at which O2 increases can be described by its kinetics. The first 15-25 s of exercise represents the cardiodynamic component (or phase 1) caused by increased pulmonary blood flow.[24] Thereafter, O2 rapidly increases at a first-order exponential rate until reaching steady state within 2-3 min and is referred to as the rapid phase (or phase 2). At exercise intensities above the ventilatory threshold (VT), however, O2 continues a slow rise, termed the slow component (or phase 3).

Various mechanisms have been proposed to explain the occurrence of the slow component during a constant work rate, although increased motor unit recruitment due to fatiguing fibers, is thought to be the most likely explanation.[6] Poole et al.[18] reported that 86% of the slow component resulted from increased muscle O2. Although the cause(s) of fatigue remains uncertain, one explanation may be intramuscular acidosis from lactic acid production.

If metabolic acidosis causes muscular fatigue, then bicarbonate ingestion may help diminish fatigue. Indeed, numerous studies have reported improved performances for maximal exercise lasting 1-7 min.[16] The increased plasma bicarbonate concentration is thought to increase the efflux of H+ and lactate from muscle and increase intramuscular pH.[15] Several groups have investigated the effect of bicarbonate ingestion on the slow component, which they described as the increase in O2 from minute 3 to the end of exercise.[20,25] After ingestion of 0.3 g·kg-1 of sodium bicarbonate, there was a nonsignificant trend of a smaller slow component when compared with the placebo trial during 6 min of cycling at 87% of O2max with active males[25] and 90% of O2max by professional male cyclists.[20] Similarly, the slow component was unaffected by bicarbonate during 30 min of cycling at ~80% of O2max.[8]

However, the difference in O2 between two arbitrary time points may not be the best approach to describing the slow component. As time delays for the start of the slow component have been reported from separate laboratories to be in the range of 70-130 s (for instance,[4,5,11]) establishing the beginning of the slow component at minute 3 might underestimate the actual magnitude of its amplitude. Rather, Bell et al.[1] recommended that the magnitude of the slow component be expressed as the increase in O2 from onset of the slow component and the end of exercise. This requires that O2 be analyzed using a three-component, nonlinear regression model in order to identify when the slow component begins.

Bicarbonate ingestion may also affect O2 kinetics in other ways. Two studies from the Whipp laboratory were the first to report that a warm-up bout of exercise above VT speeded O2 kinetics of subsequent exercise that was also above VT.[2,7] They speculated the faster kinetics were a consequence of increased oxygen delivery that resulted from the residual acidemia produced by the warm-up bout. The acidemia would have enhanced local vasodilation and caused a rightward shift of the oxygen-hemoglobin dissociation curve. Conversely, as bicarbonate ingestion would have an alkalotic effect on blood, we speculated that it would diminish local vasodilation and slow O2 kinetics.

The purpose of this study was to investigate the effects of bicarbonate ingestion on O2 kinetics. Unique to the study of bicarbonate's effects on O2 kinetics was the use of nonlinear regression modeling. This allowed for investigation of the effect of bicarbonate on the rapid component as well as identifying the start of the slow component. Furthermore, our design permitted the manipulation of blood pH without the use of prior exercise, which could have a residual effect on mitochondrial enzyme activity and influence O2 kinetics.[9] We hypothesized that bicarbonate ingestion would slow the time constant of the rapid component as well as diminish the amplitude of the slow component.