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Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyltransferase I activity in human skeletal muscle during aerobic exercise.
J Physiol 2006; 571(Pt 1):201-10JP

Abstract

Mitochondrial fatty acid transport is a rate-limiting step in long chain fatty acid (LCFA) oxidation. In rat skeletal muscle, the transport of LCFA at the level of mitochondria is regulated by carnitine palmitoyltransferase I (CPTI) activity and the content of malonyl-CoA (M-CoA); however, this relationship is not consistently observed in humans. Recently, fatty acid translocase (FAT)/CD36 was identified on mitochondria isolated from rat and human skeletal muscle and found to be involved in LCFA oxidation. The present study investigated the effects of exercise (120 min of cycling at approximately 60% V(O2peak)) on CPTI palmitoyl-CoA and M-CoA kinetics, and on the presence and functional significance of FAT/CD36 on skeletal muscle mitochondria. Whole body fat oxidation rates progressively increased during exercise (P < 0.05), and concomitantly M-CoA inhibition of CPTI was progressively attenuated. Compared to rest, 120 min of cycling reduced (P < 0.05) the inhibition of 0.7, 2, 5 and 10 microM M-CoA by 16%, 21%, 30% and 34%, respectively. Whole body fat oxidation and palmitate oxidation rates in isolated mitochondria progressively increased (P < 0.05) during exercise, and were positively correlated (r = 0.78). Mitochondrial FAT/CD36 protein increased by 63% (P < 0.05) during exercise and was significantly (P < 0.05) correlated with mitochondrial palmitate oxidation rates at all time points (r= 0.41). However, the strongest (P < 0.05) correlation was observed following 120 min of cycling (r = 0.63). Importantly, the addition of sulfo-N-succimidyloleate, a specific inhibitor of FAT/CD36, reduced mitochondrial palmitate oxidation to approximately 20%, indicating FAT/CD36 is functionally significant with respect to LCFA oxidation. We hypothesize that exercise-induced increases in fatty acid oxidation occur as a result of an increased ability to transport LCFA into mitochondria. We further suggest that decreased CPTI M-CoA sensitivity and increased mitochondrial FAT/CD36 protein are both important for increasing whole body fatty acid oxidation during prolonged exercise.

Authors+Show Affiliations

Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Canada. ghollowa@uoguelph.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16357012

Citation

Holloway, Graham P., et al. "Mitochondrial Long Chain Fatty Acid Oxidation, Fatty Acid translocase/CD36 Content and Carnitine Palmitoyltransferase I Activity in Human Skeletal Muscle During Aerobic Exercise." The Journal of Physiology, vol. 571, no. Pt 1, 2006, pp. 201-10.
Holloway GP, Bezaire V, Heigenhauser GJ, et al. Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyltransferase I activity in human skeletal muscle during aerobic exercise. J Physiol (Lond). 2006;571(Pt 1):201-10.
Holloway, G. P., Bezaire, V., Heigenhauser, G. J., Tandon, N. N., Glatz, J. F., Luiken, J. J., ... Spriet, L. L. (2006). Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyltransferase I activity in human skeletal muscle during aerobic exercise. The Journal of Physiology, 571(Pt 1), pp. 201-10.
Holloway GP, et al. Mitochondrial Long Chain Fatty Acid Oxidation, Fatty Acid translocase/CD36 Content and Carnitine Palmitoyltransferase I Activity in Human Skeletal Muscle During Aerobic Exercise. J Physiol (Lond). 2006 Feb 15;571(Pt 1):201-10. PubMed PMID: 16357012.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyltransferase I activity in human skeletal muscle during aerobic exercise. AU - Holloway,Graham P, AU - Bezaire,Veronic, AU - Heigenhauser,George J F, AU - Tandon,Narendra N, AU - Glatz,Jan F C, AU - Luiken,Joost J F P, AU - Bonen,Arend, AU - Spriet,Lawrence L, Y1 - 2005/12/15/ PY - 2005/12/17/pubmed PY - 2006/4/28/medline PY - 2005/12/17/entrez SP - 201 EP - 10 JF - The Journal of physiology JO - J. Physiol. (Lond.) VL - 571 IS - Pt 1 N2 - Mitochondrial fatty acid transport is a rate-limiting step in long chain fatty acid (LCFA) oxidation. In rat skeletal muscle, the transport of LCFA at the level of mitochondria is regulated by carnitine palmitoyltransferase I (CPTI) activity and the content of malonyl-CoA (M-CoA); however, this relationship is not consistently observed in humans. Recently, fatty acid translocase (FAT)/CD36 was identified on mitochondria isolated from rat and human skeletal muscle and found to be involved in LCFA oxidation. The present study investigated the effects of exercise (120 min of cycling at approximately 60% V(O2peak)) on CPTI palmitoyl-CoA and M-CoA kinetics, and on the presence and functional significance of FAT/CD36 on skeletal muscle mitochondria. Whole body fat oxidation rates progressively increased during exercise (P < 0.05), and concomitantly M-CoA inhibition of CPTI was progressively attenuated. Compared to rest, 120 min of cycling reduced (P < 0.05) the inhibition of 0.7, 2, 5 and 10 microM M-CoA by 16%, 21%, 30% and 34%, respectively. Whole body fat oxidation and palmitate oxidation rates in isolated mitochondria progressively increased (P < 0.05) during exercise, and were positively correlated (r = 0.78). Mitochondrial FAT/CD36 protein increased by 63% (P < 0.05) during exercise and was significantly (P < 0.05) correlated with mitochondrial palmitate oxidation rates at all time points (r= 0.41). However, the strongest (P < 0.05) correlation was observed following 120 min of cycling (r = 0.63). Importantly, the addition of sulfo-N-succimidyloleate, a specific inhibitor of FAT/CD36, reduced mitochondrial palmitate oxidation to approximately 20%, indicating FAT/CD36 is functionally significant with respect to LCFA oxidation. We hypothesize that exercise-induced increases in fatty acid oxidation occur as a result of an increased ability to transport LCFA into mitochondria. We further suggest that decreased CPTI M-CoA sensitivity and increased mitochondrial FAT/CD36 protein are both important for increasing whole body fatty acid oxidation during prolonged exercise. SN - 0022-3751 UR - https://www.unboundmedicine.com/medline/citation/16357012/Mitochondrial_long_chain_fatty_acid_oxidation_fatty_acid_translocase/CD36_content_and_carnitine_palmitoyltransferase_I_activity_in_human_skeletal_muscle_during_aerobic_exercise_ L2 - https://doi.org/10.1113/jphysiol.2005.102178 DB - PRIME DP - Unbound Medicine ER -