Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women

TLDR

The study examined how seven high‑intensity aerobic interval training sessions over two weeks affect skeletal muscle fuel content, mitochondrial enzymes, fatty‑acid transport proteins, peak oxygen consumption, and whole‑body metabolic, hormonal, and cardiovascular responses. Eight women performed a VO₂peak test and a 60‑min cycling trial at ~60 % VO₂peak before and after training, with each HIIT session consisting of ten 4‑min bouts at ~90 % VO₂peak interspersed with 2‑min rests. After two weeks of HIIT, VO₂peak rose 13 %, plasma epinephrine and heart rate fell during the last 30 min of a 60‑min cycling test, whole‑body fat oxidation increased 36 %, net glycogen use during exercise decreased, mitochondrial β‑hydroxyacyl‑CoA dehydrogenase and citrate synthase activities rose 32 % and 20 %, plasma‑membrane fatty‑acid‑binding protein increased 25 %, and overall capacity for fatty‑acid oxidation during exercise was markedly enhanced.

Abstract

Our aim was to examine the effects of seven high-intensity aerobic interval training (HIIT) sessions over 2 wk on skeletal muscle fuel content, mitochondrial enzyme activities, fatty acid transport proteins, peak O(2) consumption (Vo(2 peak)), and whole body metabolic, hormonal, and cardiovascular responses to exercise. Eight women (22.1 +/- 0.2 yr old, 65.0 +/- 2.2 kg body wt, 2.36 +/- 0.24 l/min Vo(2 peak)) performed a Vo(2 peak) test and a 60-min cycling trial at approximately 60% Vo(2 peak) before and after training. Each session consisted of ten 4-min bouts at approximately 90% Vo(2 peak) with 2 min of rest between intervals. Training increased Vo(2 peak) by 13%. After HIIT, plasma epinephrine and heart rate were lower during the final 30 min of the 60-min cycling trial at approximately 60% pretraining Vo(2 peak). Exercise whole body fat oxidation increased by 36% (from 15.0 +/- 2.4 to 20.4 +/- 2.5 g) after HIIT. Resting muscle glycogen and triacylglycerol contents were unaffected by HIIT, but net glycogen use was reduced during the posttraining 60-min cycling trial. HIIT significantly increased muscle mitochondrial beta-hydroxyacyl-CoA dehydrogenase (15.44 +/- 1.57 and 20.35 +/- 1.40 mmol.min(-1).kg wet mass(-1) before and after training, respectively) and citrate synthase (24.45 +/- 1.89 and 29.31 +/- 1.64 mmol.min(-1).kg wet mass(-1) before and after training, respectively) maximal activities by 32% and 20%, while cytoplasmic hormone-sensitive lipase protein content was not significantly increased. Total muscle plasma membrane fatty acid-binding protein content increased significantly (25%), whereas fatty acid translocase/CD36 content was unaffected after HIIT. In summary, seven sessions of HIIT over 2 wk induced marked increases in whole body and skeletal muscle capacity for fatty acid oxidation during exercise in moderately active women.