Effect of muscle glycogen on glucose, lactate and amino acid metabolism during exercise and recovery in human subjects

Citation
E. Blomstrand et B. Saltin, Effect of muscle glycogen on glucose, lactate and amino acid metabolism during exercise and recovery in human subjects, J PHYSL LON, 514(1), 1999, pp. 293-302
Citations number
21
Categorie Soggetti
Physiology
Journal title
JOURNAL OF PHYSIOLOGY-LONDON
ISSN journal
00223751 → ACNP
Volume
514
Issue
1
Year of publication
1999
Pages
293 - 302
Database
ISI
SICI code
0022-3751(19990101)514:1<293:EOMGOG>2.0.ZU;2-0
Abstract
1. Eight subjects performed two-legged exercise, one leg with low and the o ther with normal muscle glycogen content. The purpose was to study the effe ct of low initial muscle glycogen content on the metabolic response during 1 h of exercise and 2 h of recovery. This model allows direct comparison of net fluxes of substrates and metabolites over the exercising legs receivin g the same arterial inflow. 2. Muscle glycogen breakdown during exercise was 60% lower in the leg with a reduced preexercise glycogen concentration and the rate of glucose uptake during exercise was 30% higher. 3. The amount of pyruvate that was oxidized during exercise was calculated to be approximately 450 mmol in the low-glycogen leg and 750 mmol in the no rmal-glycogen leg, which suggests more fat and amino acid oxidation in the low-glycogen leg. 4. During exercise, there was a significant release of amino acids not meta bolized in the muscle, e.g, tyrosine and phenylalanine, only from the low-g lycogen leg, suggesting an increased rate of net protein degradation in thi s leg. 5. The release of tyrosine and phenylalanine from the low-glycogen leg duri ng the exercise period and the change in their muscle concentrations yield a net tyrosine and phenylalanine production rate of 1.4 and 1.5 mmol h(-1), respectively. The net rate of protein degradation was then calculated to b e 7-12 g h(-1). 6. The results suggest that the observed differences in metabolism between the low-glycogen and the normal-glycogen leg are induced by the glycogen le vel per se, since the legs received the same arterial supply of hormones an d substrates.