Effects of glutamine and hyperoxia on pulmonary oxygen uptake and muscle deoxygenation kinetics

Abstract

The aim of the present study was to determine whether glutamine ingestion, which has been shown to enhance the exercise-induced increase in the tricarboxylic acid intermediate (TCAi) pool size, resulted in augmentation of the rate of increase in oxidative metabolism at the onset of exercise. In addition, the potential interaction with oxygen availability was investigated by completing exercise in both normoxic and hyperoxic conditions. Eight male cyclists cycled for 6 min at 70% VO2max following consumption of a drink (5 ml kg body mass(-1)) containing a placebo or 0.125 g kg body mass(-1) of glutamine in normoxic (CON and GLN respectively) and hyperoxic (HYP and HPG respectively) conditions. Breath-by-breath pulmonary oxygen uptake and continuous, non-invasive muscle deoxygenation (via near infrared spectroscopy: NIRS) data were collected throughout exercise. The time constant of the phase II component of pulmonary oxygen uptake kinetics was unchanged between trials (CON: 21.5 +/- 3.0 vs. GLN: 18.2 +/- 1.3 vs. HYP: 18.9 +/- 2.0 vs. HPG: 18.6 +/- 1.2 s). There was also no alteration of the kinetics of relative muscle deoxygenation as measured via NIRS (CON: 5.9 +/- 0.7 vs. GLN: 7.3 +/- 0.8 vs. HYP: 6.5 +/- 0.9 vs. HPG: 5.2 +/- 0.4 s). Conversely, the mean response time of pulmonary oxygen uptake kinetics was faster (CON: 33.4 +/- 1.2 vs. GLN: 29.8 +/- 2.3 vs. HYP: 33.2 +/- 2.6 vs. HPG: 31.6 +/- 2.6 s) and the time at which muscle deoxygenation increased above pre-exercise values was earlier (CON: 9.6 +/- 0.9 vs. GLN: 8.7 +/- 1.1 vs. HYP: 8.5 +/- 0.8 vs. HPG: 8.4 +/- 0.7 s) following glutamine ingestion. In normoxic conditions, plasma lactate concentration was lower following glutamine ingestion compared to placebo. Whilst the results of the present study provide some support for the present hypothesis, the lack of any alteration in the time constant of pulmonary oxygen uptake and muscle deoxygenation kinetics suggest that the normal exercise induced expansion of the TCAi pool size is not limiting to oxidative metabolism at the onset of cycle exercise at 70% VO2max.

No effect of glutamine supplementation and hyperoxia on oxidative metabolism and performance during high-intensity exercise

“…Full details of preliminary testing and pre-experimental procedures can be found elsewhere (Marwood & Bowtell, 2007). In brief, a submaximal test and a maximal ramp test to determine 2 o V  max, were completed.…”

“…Continuous, non-invasive measurements of muscle deoxygenation via the deoxyhaemoglobin signal (Hb) were made via near infrared spectroscopy (NIRO 500, Hamamatsu, Japan) throughout rest and exercise periods (see Marwood & Bowtell, 2007 for full details of these procedures). Muscle deoxyhaemoglobin data were normalised to the physiological range which inflation and release of a cuff (see above) around the interrogated thigh produced (%Hb), (Marwood & Bowtell, 2007).…”

“…Muscle deoxyhaemoglobin data were normalised to the physiological range which inflation and release of a cuff (see above) around the interrogated thigh produced (%Hb), (Marwood & Bowtell, 2007).…”

No acetyl group deficit is evident at the onset of exercise at 90% of maximal oxygen uptake in humans

“…produces maximum and minimum changes in Hb and allowed normalisation of the near infrared spectroscopy data to the physiological range (%Hb), (Marwood & Bowtell, 2007). To allow for individual differences and some day-to-day variability relating to the placement of the optodes, this procedure was conducted for each individual trial.…”

“…Using custom written software and the "Solver" function in Microsoft Excel, the fitting window was widened by 1 s intervals from 60 s until the end of exercise with the time constant of the curve of best fit for each time window plotted against time (Marwood & Bowtell 2007). The goodness of fit was determined by the maintenance of a flat profile for the residual plot and minimisation of the sum of the error squared data (Solver, Microsoft Excel).…”