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

1  Human Muscle Metabolism Research Group, Loughborough University, Loughborough LE11 3TU; 2  School of Biomedical Sciences, Queens Medical Centre, Nottingham NG7 2UH; 3  Sunderland Royal Hospital, Sunderland SR4 7TP; and 4  Sport and Exercise Research Centre, South Bank University, London SE1 0AA,...

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Published inAmerican journal of physiology: endocrinology and metabolism Vol. 280; no. 4; pp. E669 - E675
Main Authors Bruce, Mark, Constantin-Teodosiu, Dumitru, Greenhaff, Paul L, Boobis, Leslie H, Williams, Clyde, Bowtell, Joanna L
Format Journal Article
LanguageEnglish
Published United States 01.04.2001
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Abstract 1  Human Muscle Metabolism Research Group, Loughborough University, Loughborough LE11 3TU; 2  School of Biomedical Sciences, Queens Medical Centre, Nottingham NG7 2UH; 3  Sunderland Royal Hospital, Sunderland SR4 7TP; and 4  Sport and Exercise Research Centre, South Bank University, London SE1 0AA, United Kingdom The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine -ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at ~70% maximal O 2 uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L- (+)-ornithine -ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L -glutamine dissolved 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 ( TCAI; citrate, malate, fumarate, and succinate, ~85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, TCAI (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 ± 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced ( P  < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of -ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise. tricarboxylic acid cycle intermediates; exercise; glutamate; phosphocreatine
AbstractList The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine alpha-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at approximately 70% maximal O2) uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine alpha-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved 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 (SigmaTCAI; citrate, malate, fumarate, and succinate, approximately 85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, SigmaTCAI (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 +/- 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of alpha-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.
1  Human Muscle Metabolism Research Group, Loughborough University, Loughborough LE11 3TU; 2  School of Biomedical Sciences, Queens Medical Centre, Nottingham NG7 2UH; 3  Sunderland Royal Hospital, Sunderland SR4 7TP; and 4  Sport and Exercise Research Centre, South Bank University, London SE1 0AA, United Kingdom The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine -ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at ~70% maximal O 2 uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L- (+)-ornithine -ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L -glutamine dissolved 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 ( TCAI; citrate, malate, fumarate, and succinate, ~85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, TCAI (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 ± 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced ( P  < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of -ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise. tricarboxylic acid cycle intermediates; exercise; glutamate; phosphocreatine
The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine α-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at ∼70% maximal O 2 uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wtl-(+)-ornithine α-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt l-glutamine dissolved 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 (ΣTCAI; citrate, malate, fumarate, and succinate, ∼85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, ΣTCAI (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 ± 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced ( P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of α-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.
The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine alpha-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at approximately 70% maximal O2) uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine alpha-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved 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 (SigmaTCAI; citrate, malate, fumarate, and succinate, approximately 85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, SigmaTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 +/- 0.61) than in the CON condition (3.74 +/- 0.38, P &lt; 0.05) and the OKG condition (3.85 +/- 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P &lt; 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of alpha-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.
The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine alpha -ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at similar to 70% maximal O sub(2) uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine alpha -ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved 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 ( capital 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, capital sigma TCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 plus or minus 0.61) than in the CON condition (3.74 plus or minus 0.38, P < 0.05) and the OKG condition (3.85 plus or minus 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of alpha -ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.
Author Williams, Clyde
Greenhaff, Paul L
Boobis, Leslie H
Bowtell, Joanna L
Bruce, Mark
Constantin-Teodosiu, Dumitru
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Snippet 1  Human Muscle Metabolism Research Group, Loughborough University, Loughborough LE11 3TU; 2  School of Biomedical Sciences, Queens Medical Centre, Nottingham...
The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity...
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StartPage E669
SubjectTerms Adult
Amino Acids - blood
Amino Acids - metabolism
Bicycling
Citric Acid Cycle - physiology
Energy Metabolism - drug effects
Glutamine - pharmacology
Humans
Male
Muscle, Skeletal - drug effects
Muscle, Skeletal - metabolism
Ornithine - analogs & derivatives
Ornithine - pharmacology
Oxidation-Reduction
Phosphocreatine - metabolism
Title Glutamine supplementation promotes anaplerosis but not oxidative energy delivery in human skeletal muscle
URI http://ajpendo.physiology.org/cgi/content/abstract/280/4/E669
https://www.ncbi.nlm.nih.gov/pubmed/11254475
https://search.proquest.com/docview/18117894
https://search.proquest.com/docview/18149238
https://search.proquest.com/docview/76981665
Volume 280
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