No effect of acute oral glutamine on glutathione status and lipid peroxidation during and in recovery from exercise

University of Central Lancashire / University of Liverpool (2002) J Physiol 543P, S202

Communications: No effect of acute oral glutamine on glutathione status and lipid peroxidation during and in recovery from exercise

J.L. Bowtell, S. Marwood, M. De Vito, H. Uusi-Hakala and L. Zaidell

Sport and Exercise Science Research Centre, South Bank University, London SE1 0AA, UK

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Glutathione (GSH) is the major endogenous intracellular anti-oxidant system, which protects the cell against oxidative damage. GSH is synthesised predominantly in the liver from cysteine, glycine and glutamate (via glutamine); and it has been shown that 4 days intravenous glutamine (gln) elevated plasma GSH in rats (Denno et al. 1996). Our aim was to determine whether oral glutamine would alter total GSH status and hence the extent of oxidative damage during and in recovery from exercise.

Seven male untrained subjects (24 ± 1 years, 73.1 ± 3.5 kg, ×O2,max 3.17 ± 0.28 l min-1) completed two trials, with Ethical Committee approval, receiving either 3 ml kg-1 flavoured water (CON) or 0.125 g kg-1 gln in 3 ml kg-1 flavoured water (GLN). Overnight fasted subjects consumed a drink, then after 30 min rest cycled at 68.8 ± 1.9 % ×O2,max for 45 min, and rested for a further 30 min. Blood and expired air samples were taken at baseline and regular intervals throughout. Whole blood was analysed for total GSH concentration (OXIS Research), and plasma was analysed for lipid hydroperoxides (LPO) (OXIS Research). Data are presented as means ± S.E.M., and were analysed by two-way repeated measures ANOVA.

Whole blood total GSH concentration did not differ between trials at any time point, although there was a significant elevation at the end of exercise relative to baseline in the CON trial (927.9 ± 46.8 vs. 1051.2 ± 50.4 mM, P < 0.05) but not GLN trial (969.5 ± 67.7 vs. 955.0 ± 90.9 mM). Except at the end of exercise (6.0 ± 1.8, CON vs. 6.7 ± 1.4, GLN; both mM), plasma LPO concentration tended to be higher in the CON than the GLN trial throughout, particularly after 30 min recovery (6.2 ± 1.6, CON vs. 4.7 ± 1.7, GLN, mM).

In conclusion, a single bolus of oral glutamine did not enhance blood total GSH status, nor were significant differences in a marker of oxidative damage evident. Possible explanations are that glutamine does not limit biosynthesis of GSH in healthy human beings under conditions of exercise-induced metabolic stress, or that chronic glutamine supplementation may be required to achieve any such benefit.

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



Where applicable, experiments conform with Society ethical requirements.

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