Difference between revisions of "Pileggi 2018 Free Radic Biol Med"
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|journal=Free Radic Biol Med | |journal=Free Radic Biol Med | ||
|abstract=Extended periods of skeletal muscle disuse result in muscle atrophy. Following limb immobilization, increased mitochondrial reactive oxygen species (ROS) production may contribute to atrophy through increases in skeletal muscle protein degradation. However, the effect of skeletal muscle disuse on mitochondrial ROS production remains unclear. This study investigated the effect of immobilization, followed by two subsequent periods of restored physical activity, on mitochondrial H<sub>2</sub>O<sub>2</sub> emissions in adult male skeletal muscle. Middle-aged men (n = 30, 49.7 ± 3.84 y) completed two weeks of unilateral lower-limb immobilization, followed by two weeks of baseline-matched activity, consisting of 10,000 steps a day, then completed two weeks of three times weekly supervised resistance training. ''Vastus lateralis'' biopsies were taken at baseline, post-immobilization, post-ambulatory recovery, and post-resistance-training. High-resolution respirometry was used simultaneously with fluorometry to determine mitochondrial respiration and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) production in permeabilized muscle fibres. Mitochondrial H<sub>2</sub>O<sub>2</sub> emission with complex I and II substrates, in the absence of ADP, was greater following immobilization, however, there was no effect on mitochondrial respiration. Both ambulatory recovery and resistance training, following the period of immobilization, increased in mitochondrial H<sub>2</sub>O<sub>2</sub> emissions. These data demonstrated that 2 weeks of immobilization increases mitochondrial H<sub>2</sub>O<sub>2</sub> emissions, but subsequent retraining periods of ambulatory recovery and resistance training also led to in robust increases in mitochondrial H<sub>2</sub>O<sub>2</sub> emissions in skeletal muscle. | |abstract=Extended periods of skeletal muscle disuse result in muscle atrophy. Following limb immobilization, increased mitochondrial reactive oxygen species (ROS) production may contribute to atrophy through increases in skeletal muscle protein degradation. However, the effect of skeletal muscle disuse on mitochondrial ROS production remains unclear. This study investigated the effect of immobilization, followed by two subsequent periods of restored physical activity, on mitochondrial H<sub>2</sub>O<sub>2</sub> emissions in adult male skeletal muscle. Middle-aged men (n = 30, 49.7 ± 3.84 y) completed two weeks of unilateral lower-limb immobilization, followed by two weeks of baseline-matched activity, consisting of 10,000 steps a day, then completed two weeks of three times weekly supervised resistance training. ''Vastus lateralis'' biopsies were taken at baseline, post-immobilization, post-ambulatory recovery, and post-resistance-training. High-resolution respirometry was used simultaneously with fluorometry to determine mitochondrial respiration and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) production in permeabilized muscle fibres. Mitochondrial H<sub>2</sub>O<sub>2</sub> emission with complex I and II substrates, in the absence of ADP, was greater following immobilization, however, there was no effect on mitochondrial respiration. Both ambulatory recovery and resistance training, following the period of immobilization, increased in mitochondrial H<sub>2</sub>O<sub>2</sub> emissions. These data demonstrated that 2 weeks of immobilization increases mitochondrial H<sub>2</sub>O<sub>2</sub> emissions, but subsequent retraining periods of ambulatory recovery and resistance training also led to in robust increases in mitochondrial H<sub>2</sub>O<sub>2</sub> emissions in skeletal muscle. | ||
|keywords=Amplex Red in muscle fibers | |||
|editor=[[Kandolf G]] | |editor=[[Kandolf G]] | ||
|mipnetlab=NZ Auckland Hickey AJ | |mipnetlab=NZ Auckland Hickey AJ | ||
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|organism=Human | |organism=Human | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Permeabilized tissue | |||
|couplingstates=LEAK, OXPHOS, ET | |couplingstates=LEAK, OXPHOS, ET | ||
|pathways=N, NS, ROX | |pathways=N, NS, ROX | ||
|instruments=Oxygraph-2k, O2k-Fluorometer | |instruments=Oxygraph-2k, O2k-Fluorometer | ||
|additional= | |additional=2018-08, Amplex UltraRed, | ||
}} | }} |
Revision as of 08:40, 30 August 2018
Pileggi CA, Hedges CP, D'Souza RF, Durainayagam BR, Markworth JF, Hickey AJR, Mitchell CJ, Cameron-Smith D (2018) Exercise recovery increases skeletal muscle H2O2 emission and mitochondrial respiratory capacity following two-weeks of limb immobilization. Free Radic Biol Med [Epub ahead of print]. |
Pileggi CA, Hedges CP, D'Souza RF, Durainayagam BR, Markworth JF, Hickey AJR, Mitchell CJ, Cameron-Smith D (2018) Free Radic Biol Med
Abstract: Extended periods of skeletal muscle disuse result in muscle atrophy. Following limb immobilization, increased mitochondrial reactive oxygen species (ROS) production may contribute to atrophy through increases in skeletal muscle protein degradation. However, the effect of skeletal muscle disuse on mitochondrial ROS production remains unclear. This study investigated the effect of immobilization, followed by two subsequent periods of restored physical activity, on mitochondrial H2O2 emissions in adult male skeletal muscle. Middle-aged men (n = 30, 49.7 ± 3.84 y) completed two weeks of unilateral lower-limb immobilization, followed by two weeks of baseline-matched activity, consisting of 10,000 steps a day, then completed two weeks of three times weekly supervised resistance training. Vastus lateralis biopsies were taken at baseline, post-immobilization, post-ambulatory recovery, and post-resistance-training. High-resolution respirometry was used simultaneously with fluorometry to determine mitochondrial respiration and hydrogen peroxide (H2O2) production in permeabilized muscle fibres. Mitochondrial H2O2 emission with complex I and II substrates, in the absence of ADP, was greater following immobilization, however, there was no effect on mitochondrial respiration. Both ambulatory recovery and resistance training, following the period of immobilization, increased in mitochondrial H2O2 emissions. These data demonstrated that 2 weeks of immobilization increases mitochondrial H2O2 emissions, but subsequent retraining periods of ambulatory recovery and resistance training also led to in robust increases in mitochondrial H2O2 emissions in skeletal muscle. • Keywords: Amplex Red in muscle fibers • Bioblast editor: Kandolf G • O2k-Network Lab: NZ Auckland Hickey AJ
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, mt-Medicine
Stress:Oxidative stress;RONS Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET
Pathway: N, NS, ROX
HRR: Oxygraph-2k, O2k-Fluorometer
2018-08, Amplex UltraRed