The expansion of the tricarboxylic acid cycle intermediate (TCAi) pool during the transition from rest to exercise is enhanced by ingestion of glutamine (Bruce et al. 2001). However, there was no apparent reduction in substrate-level phosphorylation, and it may be that oxygen or acetyl group delivery is limiting. The aim of the present study was to determine the effect of glutamine upon pulmonary oxygen kinetics under conditions of normoxia and hyperoxia.

Four trained cyclists (aged 36 ± 4 years, ×_O2,max 5.3 ± 0.3 l min^-1; mean ± S.E.M.) completed four trials, each at least 10 days apart, with Ethical Committee approval. Subjects undertook a glycogen-depleting exercise protocol in the evening of day 1 and then consumed a low (30 %) carbohydrate diet (see Bruce et al. 2001). On day 2, overnight fasted subjects drank either 5 ml kg^-1 placebo or 0.125 g kg^-1 glutamine in 5 ml kg^-1 water 1 h before exercise in normoxia (CON and GLN trials), or in hyperoxia (50 % F_i,O2; HYP and HPG trials). Subjects cycled for 6 min at 70 ± 2 % ×_O2,max immediately before completing a performance test (time to complete an individualised set volume of work, equal to 4 min at 95 % W_max).

Breath-by-breath oxygen uptake data were obtained from a low inertia turbine and mass spectrometer system from which the time constant (t) of the oxygen uptake kinetics and the oxygen deficit (O_2,def) were calculated. Leg muscle tissue deoxygenation (HbH) was assessed using near-infrared spectrometry (NIRS). NIRS data were expressed as a percentage (relative to range induced by exercise or ischaemia), normalised for power output and integrated between 0 and 6 min. Data were analysed using a Friedman test and are presented in Table 1.

Glutamine tended to reduce O_2,def and t (in normoxia) and increase HbH relative to respective controls, but no statistical differences were found between trials for any variable. This suggests that enhanced anaplerosis via glutamine supplementation has no significant bearing on oxidative metabolism either in normoxia or hyperoxia. It may be that acetyl group availability rather than oxygen delivery limits oxidative metabolism in the situation of an expanded TCAi pool.

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All procedures accord with current local guidelines and the Declaration of Helsinki.