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

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 ( V Pi→ATP ) in response to a single bout of exercise, whereas changes in the capacity for oxidative ATP production ( V max ) 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, V Pi→ATP and V max of 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. V Pi→ATP was determined from the unidirectional flux between P i and ATP, using the saturation transfer technique. The rate of phosphocreatine recovery ( k PCr ) following a maximal contraction was used to calculate V max . While k PCr and V max were 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 V Pi→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.