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The existence of an acetyl group deficit at or above 90% of maximal oxygen uptake (VO(2max)) has proved controversial, with contradictory results likely relating to limitations in previous research. The purpose of the present study was to determine whether the "acetyl group deficit" occurs at the start of exercise at 90%VO(2max) in a well-controlled study. Eight male participants (age: 33.6 +/- 2.0 years; VO(2max): 3.60 +/- 0.21 litres . min(-1)) completed two exercise bouts at 90%VO(2max) for 3 min following either 30 min of saline (control) or dichloroacetate (50 mg . kg(-1) body mass) infusion, ending 15 min before exercise. Muscle biopsies were obtained immediately before and after exercise while continuous non-invasive measures of pulmonary oxygen uptake and muscle deoxygenation were made. Muscle pyruvate dehydrogenase activity was significantly higher before exercise following dichloroacetate infusion (control: 2.67 +/- 0.98 vs. dichloroacetate: 17.9 +/- 1.1 mmol acetyl-CoA . min(-1) . mg(-1) protein, P = 0.01) and resulted in higher pre- and post-exercise muscle acetylcarnitine (pre-exercise control: 3.3 +/- 0.95 vs. pre-exercise dichloroacetate: 8.0 +/- 0.88 vs. post-exercise control: 11.9 +/- 1.1 vs. post-exercise dichloroacetate: 17.2 +/- 1.1 mmol . kg(-1) dry muscle, P < 0.05). However, substrate-level phosphorylation (control: 125 +/- 20 vs. dichloroacetate: 113 +/- 13 mmol adenosine triphosphate . kg(-1) dry muscle) and VO(2) kinetics (control: 19.2 +/- 2.2 vs. dichloroacetate: 22.8 +/- 2.5 s), were unaltered. Furthermore, dichloroacetate infusion blunted the slow component of VO(2) and muscle deoxygenation and slowed muscle deoxygenation kinetics, possibly by enhancing oxygen delivery during exercise. These data support the hypothesis that the "acetyl group deficit" does not occur at or above 90%VO(2max).

Mechanical models of cycling time-trial performance have indicated adverse effects of variations in external power output on overall performance times. Nevertheless, the precise influences of the magnitude and number of these variations over different distances of time trial are unclear. A hypothetical cyclist (body mass 70 kg, bicycle mass 10 kg) was studied using a mathematical model of cycling, which included the effects of acceleration. Performance times were modelled over distances of 4-40 km, mean power outputs of 200-600 W, power variation amplitudes of 5-15% and variation frequencies of 2-32 per time-trial. Effects of a "fast-start" strategy were compared with those of a constant-power strategy. Varying power improved 4-km performance at all power outputs, with the greatest improvement being 0.90 s for ± 15% power variation. For distances of 16.1, 20 and 40 km, varying power by ± 15% increased times by 3.29, 4.46 and 10.43 s respectively, suggesting that in long-duration cycling in constant environmental conditions, cyclists should strive to reduce power variation to maximise performance. The novel finding of the present study is that these effects are augmented with increasing event distance, amplitude and period of variation. These two latter factors reflect a poor adherence to a constant speed.

Glutamine enhances the exercise-induced expansion of the tricarboxylic acid intermediate pool. The aim of the present study was to determine whether oral glutamine, alone or in combination with hyperoxia, influenced oxidative metabolism and cycle time-trial performance. Eight participants consumed either placebo or 0.125 g kg body mass(-1) of glutamine in 5 ml kg body mass(-1) placebo 1 h before exercise in normoxic (control and glutamine respectively) or hyperoxic (FiO(2) = 50%; hyperoxia and hyperoxia + glutamine respectively) conditions. Participants then cycled for 6 min at 70% maximal oxygen uptake (VO(2max)) immediately before completing a brief high-intensity time-trial (approximately 4 min) during which a pre-determined volume of work was completed as fast as possible. The increment in pulmonary oxygen uptake during the performance test (DeltaVO(2max), P = 0.02) and exercise performance (control: 243 s, s(x) = 7; glutamine: 242 s, s(x) = 3; hyperoxia: 231 s, s(x) = 3; hyperoxia + glutamine: 228 s, s(x) = 5; P0.01) were significantly improved in hyperoxic conditions. There was some evidence that glutamine ingestion increased DeltaVO(2max) in normoxia, but not hyperoxia (interaction drink/FiO(2), P = 0.04), but there was no main effect or impact on performance. Overall, the data show no effect of glutamine ingestion either alone or in combination with hyperoxia, and thus no limiting effect of the tricarboxylic acid intermediate pool size, on oxidative metabolism and performance during maximal exercise.