Glutamine supplementation promotes anaplerosis but not oxidative energy delivery in human skeletal muscle

The aims of the present study were twofold: first to investigate whether TC A cycle intermediate (TCAI) pool expansion at the onset of moderate-intensi ty exercise in human skeletal muscle could be enhanced independently of pyr uvate availability by ingestion of glutamine or ornithine alpha -ketoglutar ate, and second, if it was, whether this modification of TCAI pool expansio n had any effect on oxidative energy status during subsequent exercise. Sev en males cycled for 10 min at similar to 70% maximal O-2 uptake 1 h after c onsuming either an artificially sweetened placebo (5 ml/kg body wt solution , CON), 0.125 g/kg body wt L-(+)-ornithine alpha -ketoglutarate dissolved i n 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L- glutamine dissol ved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (Sigma TCAI; citrate, malate, fumarate, and succinate, similar to 85% of total TCAI pool) was not different between conditions 1 h postsupplement . However, after 10 min of exercise, STCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 +/- 0.61) than in the CON condition (3.74 +/- 0 .38, P < 0.05) and the OKG condition (3.85 <plus/minus> 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduce d (P < 0.05) in all conditions, but there was no significant difference bet ween conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of g lutamine carbon at the level of <alpha>-ketoglutarate. However, this increa sed expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.