Why the study?
Does acetazolamide improve O2 uptake kinetics during constant-load exercise in men?
Does acetazolamide improve O2 uptake kinetics during constant-load exercise in men?
Acute carbonic anhydrase inhibition with acetazolamide lowers plasma lactate but does not affect O2 utilization kinetics at the onset of moderate or heavy exercise.
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Acetazolamide does not speed O2 uptake kinetics despite lowering lactate; leaves open effects in clinical populations with exercise intolerance.
Inhibition of carbonic anhydrase (CA) is associated with a lower plasma lactate concentration ([La-]pl) during fatiguing exercise. We hypothesized that a lower [La-]pl may be associated with faster O2 uptake (V(O2)) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz, 10 mg/kg body wt iv). On 6 separate days, each subject performed 6-min step transitions in work rate from 0 to 100 W (below ventilatory threshold, <VE(T)) or to a V(O2) corresponding to approximately 50% of the difference between the work rate at VE(T) and peak V(O2) (>VE(T). Gas exchange was measured breath by breath. Trials were interpolated at 1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (<VE(T)) or a three-component exponential model (>VE(T)). Arterialized venous blood was sampled from a dorsal hand vein and analyzed for [La-]pl. MRT was similar during Con (31.2 +/- 2.6 and 32.7 +/- 1.2 s for on and off, respectively) and Acz (30.9 +/- 3.0 and 31.4 +/- 1.5 s for on and off, respectively) for work rates <VE(T). At work rates >VE(T), MRT was similar between Con (69.1 +/- 6.1 and 50.4 +/- 3.5 s for on and off, respectively) and Acz (69.7 +/- 5.9 and 53.8 +/- 3.8 s for on and off, respectively). On- and off-MRTs were slower for >VE(T) than for <VE(T) exercise. [La-]pl increased above 0-W cycling values during <VE(T) and >VE(T) exercise but was lower at the end of the transition during Acz (1.4 +/- 0.2 and 7.1 +/- 0.5 mmol/l for <VE(T) and >VE(T) respectively) than during Con (2.0 +/- 0.2 and 9.8 +/- 0.9 mmol/l for <VE(T) and >VE(T), respectively). CA inhibition does not affect O2 utilization at the onset of <VE(T) or >VE(T) exercise, suggesting that the contribution of oxidative phosphorylation to the energy demand is not affected by acute CA inhibition with Acz.
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Scheuermann et al. (1998) studied this question.
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