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 a14% 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.