Understanding the factors that effect maximal fat oxidation

Troy Purdom, Len Kravitz, Karol Dokladny, Christine Mermier, Troy Purdom, Len Kravitz, Karol Dokladny, Christine Mermier

Abstract

Lipids as a fuel source for energy supply during submaximal exercise originate from subcutaneous adipose tissue derived fatty acids (FA), intramuscular triacylglycerides (IMTG), cholesterol and dietary fat. These sources of fat contribute to fatty acid oxidation (FAox) in various ways. The regulation and utilization of FAs in a maximal capacity occur primarily at exercise intensities between 45 and 65% VO2max, is known as maximal fat oxidation (MFO), and is measured in g/min. Fatty acid oxidation occurs during submaximal exercise intensities, but is also complimentary to carbohydrate oxidation (CHOox). Due to limitations within FA transport across the cell and mitochondrial membranes, FAox is limited at higher exercise intensities. The point at which FAox reaches maximum and begins to decline is referred to as the crossover point. Exercise intensities that exceed the crossover point (~65% VO2max) utilize CHO as the predominant fuel source for energy supply. Training status, exercise intensity, exercise duration, sex differences, and nutrition have all been shown to affect cellular expression responsible for FAox rate. Each stimulus affects the process of FAox differently, resulting in specific adaptions that influence endurance exercise performance. Endurance training, specifically long duration (>2 h) facilitate adaptations that alter both the origin of FAs and FAox rate. Additionally, the influence of sex and nutrition on FAox are discussed. Finally, the role of FAox in the improvement of performance during endurance training is discussed.

Keywords: Carnitine; Cpt-1; Crossover concept; Dietary fat oxidation; Fat adaptation; Fat oxidation; Ketogenic diet; Maximal fat oxidation; PDH activity; Substrate oxidation.

Conflict of interest statement

1) TP is an assistant professor of exercise science at Longwood University specializing in metabolic adaptation to exercise with an emphasis in sport nutrition. TP currently has accepted abstracts with ACSM, NSCA, and ISSN in the area of fat metabolism, athletic performance evaluation, energy expenditure, and body composition. 2) LK’s research interests include energy metabolism, exercise product evaluation, energy expenditure and exercise program measurement and assessment. LK has published in Medicine & Science in Sports & Exercise, Journal of Strength and Conditioning Research, Perceptual and Motor Skills, Dance Medicine & Science, IDEA Fitness Journal, Journal of Exercise Physiology online, ACSM’s Health & Fitness Journal, and Journal of Sports Science and Medicine. 3) KD’s research interests include the heat shock protein and autophagy response to stress. KD is published in the Molecular Medicine, Journal of Applied Physiology, Cell Stress & Chaperones, The American Journal of Pathology, Journal of Applied Toxicology, The British Journal of Sports Medicine, and The International Journal of Endocrinology and Metabolism. 4) CM’s research interests include physiological responses to exercise in all populations including athletes and those with chronic disease or disability, as well as non-traditional athletes such as dancers and rock climbers. CM has published original research in journals including Medicine & Science in Sports & Exercise, British Journal of Sports Medicine, Journal of Dance Medicine & Science, International Journal of Sport Nutrition & Exercise Metabolism, and The Journal of Bone and Joint Surgery.Not applicable.Not applicable.Not applicable.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Proposed interaction within skeletal muscle between fatty acid metabolism and glycolysis during high intensity exercise. During high intensity exercise the high glycolytic rate will produce high amounts of acetyl CoA which will exceed the rate of the TCA cycle. Free carnitine acts as an acceptor of the glycolysis derived acetyl groups forming acetylcarnitine, mediated by carnitine acyltransferase (CAT). Due to the reduced carnitine, the substrate for CPT-1 forming FA acylcarnitine will be reduced limiting FA transport into the mitochondrial matrix. This limits B-oxidation potential reducing overall FAox. OMM: outer mitochondrial membrane; IMM: inner mitochondrial membrane; CPT-1: carnitine pamitoyltransferase; FA: fatty acid; CPT-II: carnitine palmitoyltransferase II; PDH: pyruvate dehydrogenase; CAT: carnitine acyltransferase. Adapted from Jeppesen and Kiens 2012
Fig. 2
Fig. 2
The crossover concept. The relative decrease in energy derived from lipid (fat) as exercise intensity increases with a corresponding increase in carbohydrate (CHO). The crossover point describes when the CHO contribution to substrate oxidation supersedes that of fat. MFO: maximal fat oxidation. Adapted from Brooks and Mercier, 1994

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