High-intensity aerobic interval training increases fat and carbohydrate metabolic capacities in human skeletal muscle

TLDR

HIIT offers a time‑efficient alternative to moderate‑intensity training, yet its effect on skeletal‑muscle fat and carbohydrate oxidation is poorly understood. The study examined whole‑body and skeletal‑muscle metabolic adaptations in previously untrained recreationally active adults after six weeks of HIIT. Participants completed a 6‑week HIIT program (10×4‑min intervals at ~90% VO₂peak, 3 d wk⁻¹) with pre‑ and post‑testing that included VO₂peak, a 90% VO₂peak exhaustion test, a 1‑h cycle at 60% VO₂peak, and muscle biopsies at rest, 5 min, and exhaustion during the exhaustion test. HIIT increased power output by 21% and VO₂peak by 9%, enhanced mitochondrial enzyme activities, transport proteins, and glycogen storage at rest, and during exercise it reduced early glycogenolysis and lactate accumulation, doubled time to exhaustion, and elevated fat oxidation at 60% VO₂peak, demonstrating a powerful boost in whole‑body and muscle oxidative capacity.

Abstract

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 × 4 min intervals at ~90% of peak oxygen consumption (VO 2 peak ), separated by 2 min rest, 3 d·week –1 ). A VO 2 peak test, a test to exhaustion (TE) at 90% of pre-training VO 2 peak , and a 1 h cycle at 60% of pre-training VO 2 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 VO 2 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%), β-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 VO 2 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.