High-intensity aerobic interval training increases fat and carbohydrate metabolic capacities in human skeletal muscle.
High-intensity aerobic interval training (HIIT) is a compromise between time-consuming moderate-intensity training and sprint-interval training requiring all-out efforts. However, there are few data regarding the ability of HIIT to increase the capacities of fat and carbohydrate oxidation in skeletal muscle. Using untrained recreationally active individuals, we investigated skeletal muscle and whole-body metabolic adaptations that occurred following 6 weeks of HIIT (~1 h of 10 x 4 min intervals at ~90% of peak oxygen consumption (VO2 peak), separated by 2 min rest, 3 d.week-1). A VO2 peak test, a test to exhaustion (TE) at 90% of pre-training VO2 peak, and a 1 h cycle at 60% of pre-training VO2 peak were performed pre- and post-HIIT. Muscle biopsies were sampled during the TE at rest, after 5 min, and at exhaustion. Training power output increased by 21%, and VO2 peak increased by 9% following HIIT. Muscle adaptations at rest included the following: (i) increased cytochrome c oxidase IV content (18%) and maximal activities of the mitochondrial enzymes citrate synthase (26%), beta-hydroxyacyl-CoA dehydrogenase (29%), aspartate-amino transferase (26%), and pyruvate dehydrogenase (PDH; 21%); (ii) increased FAT/CD36, FABPpm, GLUT 4, and MCT 1 and 4 transport proteins (14%-30%); and (iii) increased glycogen content (59%). Major adaptations during exercise included the following: (i) reduced glycogenolysis, lactate accumulation, and substrate phosphorylation (0-5 min of TE); (ii) unchanged PDH activation (carbohydrate oxidation; 0-5 min of TE); (iii) ~2-fold greater time during the TE; and (iv) increased fat oxidation at 60% of pre-training VO2 peak. This study demonstrated that 18 h of repeated high-intensity exercise sessions over 6 weeks (3 d.week-1) is a powerful method to increase whole-body and skeletal muscle capacities to oxidize fat and carbohydrate in previously untrained individuals.
Perry
Christopher G R
CG
Department of Human Health and Nutritional Sciences, University of Guelph, ON N1G 2W1, Canada. perryc@uoguelph.ca
Heigenhauser
George J F
GJ
Bonen
Arend
A
Spriet
Lawrence L
LL
D000328:Adult; D024442:Aspartate Aminotransferase, Mitochondrial / Q000378:metabolism; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D001706:Biopsy; D001786:Blood Glucose / Q000032:analysis; D015153:Blotting, Western; D050260:Carbohydrate Metabolism / Q000502:physiology*; D002950:Citrate (si)-Synthase / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D015444:Exercise / Q000502:physiology*; D005223:Fats / Q000378:metabolism*; D005260:Female; D005990:Glycerol / Q000097:blood; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000097:blood; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D010807:Physical Endurance / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D055815:Young Adult
D015415:Biomarkers; D001786:Blood Glucose; D005223:Fats; D011768:Pyruvate Dehydrogenase Complex; D019344:Lactic Acid; D006003:Glycogen; D003576:Electron Transport Complex IV; D002950:Citrate (si)-Synthase; D024442:Aspartate Aminotransferase, Mitochondrial; D005990:Glycerol