Abstract

Mitochondrial ATP production is vital for meeting cellular energy demand at rest and during periods of high ATP turnover. We postulate that resting (Vrest) and maximal (Vmax) rates of mitochondrial ATP production reflect distinct aspects of mitochondrial function, and thus may respond to homeostatic perturbations differently. Short-term, high-intensity interval training (HIT) has been shown to increase markers of muscle Vmax, but little is known about the effects of HIT on mitochondrial ATP synthesis in vivo, particularly in resting muscle. PURPOSE: To examine the scope and timing of muscle bioenergetic adaptations in vivo during and following HIT. METHODS: Four young males performed 6 training sessions in a two-week period. Each session consisted of 4-6 bouts of 30-s sprints on a cycle ergometer. Pre- and post-training, whole-body VO2max was measured during cycling exercise. Following standardized meals and a 9 h fast, Vrest and Vmax of the vastus lateralis muscle were measured using phosphorus magnetic resonance spectroscopy at 4 Tesla. Measures were obtained at baseline, 15 h after the 1st training session, and 15 h after completion of the 6th session. Vrest was determined from the uni-directional flux between Pi and ATP, using the saturation transfer technique. The rate of phosphocreatine recovery (kPCr) following a maximal contraction was used to calculate Vmax. RESULTS: As expected, training increased VO2max, by ∼13% (Table 1, mean±SE). A single training session did not affect Vrest, kPCr, or Vmax. However, completion of all 6 training sessions increased each of these measures of muscle oxidative metabolism, by ∼8-15%.TABLECONCLUSIONS: High-intensity exercise training resulted in rapid (2 weeks), though not immediate (15 h), increases in both resting and maximal mitochondrial ATP production in vivo. The parallel time course and magnitude of these responses suggest that regulation of the adaptability of Vrest and Vmax to exercise may share a common regulatory process.This work was supported by NIH/NIA K02 AG023582.

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