Christensen 2016 J Appl Physiol (1985): Difference between revisions
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|year=2016 | |year=2016 | ||
|journal=J Appl Physiol (1985) | |journal=J Appl Physiol (1985) | ||
|abstract=The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (VΜo<sub>2</sub>) kinetics following a short period of high-intensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 Β± 2 yr; mean Β± SD) performed six HIT sessions (8-12 Γ 60 s at incremental test peak power; 271 Β± 52 W) over a 2-wk period. Before and after the HIT period, VΜo<sub>2</sub> kinetics was modeled during moderate-intensity cycling (110 Β± 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, VΜo<sub>2</sub> kinetics became faster (Ο: 20.4 Β± 4.4 vs. 28.9 Β± 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 VΜo<sub>2</sub> kinetics (low Ο values) was associated with large values for ETFP, electron transport system capacity ( | |abstract=The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (VΜo<sub>2</sub>) kinetics following a short period of high-intensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 Β± 2 yr; mean Β± SD) performed six HIT sessions (8-12 Γ 60 s at incremental test peak power; 271 Β± 52 W) over a 2-wk period. Before and after the HIT period, VΜo<sub>2</sub> kinetics was modeled during moderate-intensity cycling (110 Β± 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, VΜo<sub>2</sub> kinetics became faster (Ο: 20.4 Β± 4.4 vs. 28.9 Β± 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 VΜo<sub>2</sub> kinetics (low Ο values) was associated with large values for ETFP, electron transport system capacity (ET-pathway), 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 VΜo<sub>2</sub> kinetics and better markers than maximal oxidative enzyme activity in describing the speed of the VΜo<sub>2</sub> response during moderate-intensity exercise. | ||
Copyright Β© 2016 the American Physiological Society. | Copyright Β© 2016 the American Physiological Society. | ||
|keywords=OXPHOS, Cycling economy, Enzyme activity, High-intensity training, Oxygen uptake | |keywords=OXPHOS, Cycling economy, Enzyme activity, High-intensity training, Oxygen uptake | ||
|mipnetlab=CH Zurich Gassmann M, CH Zurich Lundby C, US CO Colorado Springs Jacobs | |mipnetlab=CH Zurich Gassmann M, CH Zurich Lundby C, US CO Colorado Springs Jacobs RA | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
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|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Permeabilized tissue | |preparations=Permeabilized tissue | ||
|couplingstates=LEAK, OXPHOS, | |couplingstates=LEAK, OXPHOS, ET | ||
| | |pathways=F, N, S, CIV, NS, Other combinations, ROX | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2016-09 | |additional=2016-09, MiR05, MitoEAGLE muscle buffer, | ||
}} | }} |
Latest revision as of 21:47, 8 March 2020
Christensen PM, Jacobs RA, Bonne T, FlΓΌck D, Bangsbo J, Lundby C (2016) A short period of high-intensity interval training improves skeletal muscle mitochondrial function and pulmonary oxygen uptake kinetics. J Appl Physiol (1985) 120:1319-27. |
Christensen PM, Jacobs RA, Bonne T, Flueck D, Bangsbo J, Lundby C (2016) J Appl Physiol (1985)
Abstract: The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (VΜo2) kinetics following a short period of high-intensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 Β± 2 yr; mean Β± SD) performed six HIT sessions (8-12 Γ 60 s at incremental test peak power; 271 Β± 52 W) over a 2-wk period. Before and after the HIT period, VΜo2 kinetics was modeled during moderate-intensity cycling (110 Β± 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, VΜo2 kinetics became faster (Ο: 20.4 Β± 4.4 vs. 28.9 Β± 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 VΜo2 kinetics (low Ο values) was associated with large values for ETFP, electron transport system capacity (ET-pathway), 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 VΜo2 kinetics and better markers than maximal oxidative enzyme activity in describing the speed of the VΜo2 response during moderate-intensity exercise.
Copyright Β© 2016 the American Physiological Society. β’ Keywords: OXPHOS, Cycling economy, Enzyme activity, High-intensity training, Oxygen uptake
β’ O2k-Network Lab: CH Zurich Gassmann M, CH Zurich Lundby C, US CO Colorado Springs Jacobs RA
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET
Pathway: F, N, S, CIV, NS, Other combinations, ROX
HRR: Oxygraph-2k
2016-09, MiR05, MitoEAGLE muscle buffer