PMID- 12864750 OWN - NLM STAT- MEDLINE DCOM- 20030826 LR - 20211203 IS - 0001-6772 (Print) IS - 0001-6772 (Linking) VI - 178 IP - 4 DP - 2003 Aug TI - Regulatory mechanisms in the interaction between carbohydrate and lipid oxidation during exercise. PG - 443-52 AB - At the onset of exercise, signals from inside and outside the muscle cell increase the availability of carbohydrate (CHO) and fat to provide the fuel required for ATP production. CHO and fat oxidation are the dominant sources of aerobic ATP production and both pathways must be heavily upregulated during exercise to meet the increased energy demand. Within this paradigm, there is room for shifts between the proportion of energy that is provided from CHO and fat. It has long been known that increasing the availability of endogenous or exogenous CHO can increase the oxidation of CHO and decrease the oxidation of fat. The opposite is also true. While descriptive studies documenting these changes are numerous, the mechanisms regulating these shifts in fuel use in the face of constant energy demand have not been thoroughly elucidated. It would be expected, for example, that any fat-induced shift in CHO metabolism would target the enzymes that play key roles in regulating CHO metabolism and oxidation. Inside the muscle these could include glucose uptake (GLUT4) and phosphorylation (hexokinase), glycogenolysis (glycogen phosphorylase), glycolysis (phosphofructokinase) and conversion to acetyl CoA (pyruvate dehydrogenase). The same would be expected for a CHO-induced down regulation of fat metabolism and oxidation and might target transport of long chain fatty acids into the cell (fatty acid translocase CD36), release of fatty acids from intramuscular triacylglycerol (hormone sensitive lipase) and transport into the mitochondria (carnitine palmitoyl transferase complex). This review summarizes the work describing the interaction between CHO and fat metabolism in human skeletal muscle during exercise and presents the theories that may account for CHO/fat interaction during exercise. FAU - Spriet, L L AU - Spriet LL AD - Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada. FAU - Watt, M J AU - Watt MJ LA - eng PT - Journal Article PT - Review PL - England TA - Acta Physiol Scand JT - Acta physiologica Scandinavica JID - 0370362 RN - 0 (Fats) RN - 0 (Fatty Acids, Nonesterified) RN - 0 (Insulin) RN - 0 (Pyruvate Dehydrogenase Acetyl-Transferring Kinase) RN - 0U46U6E8UK (NAD) RN - EC 2.7.- (Protein Kinases) RN - EC 2.7.11.1 (Protein Serine-Threonine Kinases) RN - IY9XDZ35W2 (Glucose) SB - IM MH - *Carbohydrate Metabolism MH - Energy Metabolism MH - Exercise/*physiology MH - Fats/metabolism MH - Fatty Acids, Nonesterified/metabolism MH - Glucose/metabolism MH - Humans MH - Insulin/metabolism MH - *Lipid Metabolism MH - Mitochondria/metabolism MH - NAD/metabolism MH - Oxidation-Reduction MH - Protein Kinases/metabolism MH - Protein Serine-Threonine Kinases MH - Pyruvate Dehydrogenase Acetyl-Transferring Kinase RF - 60 EDAT- 2003/07/17 05:00 MHDA- 2003/08/27 05:00 CRDT- 2003/07/17 05:00 PHST- 2003/07/17 05:00 [pubmed] PHST- 2003/08/27 05:00 [medline] PHST- 2003/07/17 05:00 [entrez] AID - 1152 [pii] AID - 10.1046/j.1365-201X.2003.01152.x [doi] PST - ppublish SO - Acta Physiol Scand. 2003 Aug;178(4):443-52. doi: 10.1046/j.1365-201X.2003.01152.x.