A short period of high-intensity interval training improves skeletal muscle mitochondrial function and pulmonary oxygen uptake kinetics

TY - JOUR

T1 - A short period of high-intensity interval training improves skeletal muscle mitochondrial function and pulmonary oxygen uptake kinetics

AU - Christensen, Peter Møller

AU - Jacobs, Robert A

AU - Bonne, Thomas Christian

AU - Flück, Daniela

AU - Bangsbo, Jens

AU - Lundby, Carsten

N1 - CURIS 2016 NEXS 154

PY - 2016/6/1

Y1 - 2016/6/1

N2 - The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (VO2) kinetics following a short period of highintensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 ± 2 yr; mean ± SD) performed six HIT sessions (8-12 × 60 s at incremental test peak power; 271 ± 52 W) over a 2-wk period. Before and after the HIT period,VO2 kinetics was modeled during moderateintensity cycling (110 ± 19 W). Mitochondrial function was assessed with high-resolution respirometry (HRR), and maximal activities of oxidative enzymes citrate synthase (CS) and cytochrome c oxidase (COX) were accordingly determined. In response to HIT,VO2 kinetics became faster (τ: 20.4 ± 4.4 vs. 28.9 ± 6.1 s; P < 0.01) and fatty acid oxidation (ETFP) and leak respiration (LN) both became elevated (P < 0.05). Activity of CS and COX did not increase in response to training. Both before and after the HIT period, fast VO2 kinetics (low τ values) was associated with large values for ETFP, electron transport system capacity (ETS), and electron flow specific to complex II (CIIP) (P < 0.05). Collectively, these findings support that selected measures of mitochondrial function obtained with HRR are important for fast VO2 kinetics and better markers than maximal oxidative enzyme activity in describing the speed of theVO2 response during moderateintensity exercise.

AB - The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (VO2) kinetics following a short period of highintensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 ± 2 yr; mean ± SD) performed six HIT sessions (8-12 × 60 s at incremental test peak power; 271 ± 52 W) over a 2-wk period. Before and after the HIT period,VO2 kinetics was modeled during moderateintensity cycling (110 ± 19 W). Mitochondrial function was assessed with high-resolution respirometry (HRR), and maximal activities of oxidative enzymes citrate synthase (CS) and cytochrome c oxidase (COX) were accordingly determined. In response to HIT,VO2 kinetics became faster (τ: 20.4 ± 4.4 vs. 28.9 ± 6.1 s; P < 0.01) and fatty acid oxidation (ETFP) and leak respiration (LN) both became elevated (P < 0.05). Activity of CS and COX did not increase in response to training. Both before and after the HIT period, fast VO2 kinetics (low τ values) was associated with large values for ETFP, electron transport system capacity (ETS), and electron flow specific to complex II (CIIP) (P < 0.05). Collectively, these findings support that selected measures of mitochondrial function obtained with HRR are important for fast VO2 kinetics and better markers than maximal oxidative enzyme activity in describing the speed of theVO2 response during moderateintensity exercise.

U2 - 10.1152/japplphysiol.00115.2015

DO - 10.1152/japplphysiol.00115.2015

M3 - Journal article

C2 - 26846547

SN - 8750-7587

VL - 120

SP - 1319

EP - 1327

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

IS - 11

ER -