High-intensity interval training increases in vivo oxidative capacity with no effect on Pi→ATP rate in resting human muscle

Abstract

Mitochondrial ATP production is vital for meeting cellular energy demand at rest and during periods of high ATP turnover. We hypothesized that high-intensity interval training (HIT) would increase ATP flux in resting muscle ( VPi→ATP) in response to a single bout of exercise, whereas changes in the capacity for oxidative ATP production ( Vmax) would require repeated bouts. Eight untrained men (27 ± 4 yr; peak oxygen uptake = 36 ± 4 ml·kg−1·min−1) performed six sessions of HIT (4–6 × 30-s bouts of all-out cycling with 4-min recovery). After standardized meals and a 10-h fast, VPi→ATPand Vmaxof the vastus lateralis muscle were measured using phosphorus magnetic resonance spectroscopy at 4 Tesla. Measurements were obtained at baseline, 15 h after the first training session, and 15 h after completion of the sixth session. VPi→ATPwas determined from the unidirectional flux between Piand ATP, using the saturation transfer technique. The rate of phosphocreatine recovery ( kPCr) following a maximal contraction was used to calculate Vmax. While kPCrand Vmaxwere unchanged after a single session of HIT, completion of six training sessions resulted in a ∼14% increase in muscle oxidative capacity ( P ≤ 0.004). In contrast, neither a single nor six training sessions altered VPi→ATP( P = 0.74). This novel analysis of resting and maximal high-energy phosphate kinetics in vivo in response to HIT provides evidence that distinct aspects of human skeletal muscle metabolism respond differently to this type of training.