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Difference between revisions of "Newsom 2021 Med Sci Sports Exerc"

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(Created page with "{{Publication |title=Newsom SA, Stierwalt HD, Ehrlicher SE, Robinson MM (2021) Substrate-specific respiration of isolated skeletal muscle mitochondria after 1 h of moderate cy...")
 
 
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{{Publication
{{Publication
|title=Newsom SA, Stierwalt HD, Ehrlicher SE, Robinson MM (2021) Substrate-specific respiration of isolated skeletal muscle mitochondria after 1 h of moderate cycling in sedentary adults.
|title=Newsom SA, Stierwalt HD, Ehrlicher SE, Robinson MM (2021) Substrate-specific respiration of isolated skeletal muscle mitochondria after 1 h of moderate cycling in sedentary adults. https://doi.org/10.1249/mss.0000000000002615
|info=Med Sci Sports Exerc 53:1375-84. [https://pubmed.ncbi.nlm.nih.gov/34127633 PMID: 34127633 Open Access]
|info=Med Sci Sports Exerc 53:1375-84. [https://pubmed.ncbi.nlm.nih.gov/34127633 PMID: 34127633 Open Access]
|authors=Newsom Sean A, Stierwalt Harrison D, Ehrlicher Sarah E, Robinson Matthew M
|authors=Newsom Sean A, Stierwalt Harrison D, Ehrlicher Sarah E, Robinson Matthew M
Line 7: Line 7:
|abstract=Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. Specific complexes oxidize lipid and nonlipid substrates. It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates.
|abstract=Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. Specific complexes oxidize lipid and nonlipid substrates. It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates.


We studied mitochondrial metabolism in sedentary male and female adults (n = 11F/4M) who were free of major medical conditions with mean ± SD age of 28 ± 7 yr, peak aerobic capacity of 2.0 ± 0.4 L·min-1, and body mass index of 22.2 ± 2 kg·m-2. Biopsies were collected from the vastus lateralis muscle on separate study days at rest or 15 min after exercise (1 h cycling at 65% peak aerobic capacity). Isolated mitochondria were analyzed using high-resolution respirometry of separate titration protocols for lipid (palmitoylcarnitine, F-linked) and nonlipid substrates (glutamate-malate, N-linked; succinate S-linked). Titration protocols distinguished between oxidative phosphorylation and leak respiration and included the measurement of reactive oxygen species emission (H2O2). Western blotting determined the protein abundance of electron transfer flavoprotein (ETF) subunits, including inhibitory methylation site on ETF-β.
We studied mitochondrial metabolism in sedentary male and female adults (n = 11F/4M) who were free of major medical conditions with mean ± SD age of 28 ± 7 yr, peak aerobic capacity of 2.0 ± 0.4 L/min, and body mass index of 22.2 ± 2 kg·m<sup>2</sup>. Biopsies were collected from the vastus lateralis muscle on separate study days at rest or 15 min after exercise (1 h cycling at 65% peak aerobic capacity). Isolated mitochondria were analyzed using high-resolution respirometry of separate titration protocols for lipid (palmitoylcarnitine, F-linked) and nonlipid substrates (glutamate-malate, N-linked; succinate S-linked). Titration protocols distinguished between oxidative phosphorylation and leak respiration and included the measurement of reactive oxygen species emission (H<sub>2</sub>O<sub>2</sub>). Western blotting determined the protein abundance of electron transfer flavoprotein (ETF) subunits, including inhibitory methylation site on ETF-β.


Aerobic exercise induced modest increases in mitochondrial respiration because of increased coupled respiration across F-linked (+13%, P = 0.08), N(S)-linked (+14%, P = 0.09), and N-linked substrates (+17%, P = 0.08). Prior exercise did not change P:O ratio. Electron leak to H2O2 increased 6% increased after exercise (P = 0.06) for lipid substrates but not for nonlipid. The protein abundance of ETF-α or ETF-β subunit or inhibitory methylation on ETF-β was not different between rest and after exercise.
Aerobic exercise induced modest increases in mitochondrial respiration because of increased coupled respiration across F-linked (+13%, P = 0.08), N(S)-linked (+14%, P = 0.09), and N-linked substrates (+17%, P = 0.08). Prior exercise did not change P:O ratio. Electron leak to H<sub>2</sub>O<sub>2</sub> increased 6% increased after exercise (P = 0.06) for lipid substrates but not for nonlipid. The protein abundance of ETF-α or ETF-β subunit or inhibitory methylation on ETF-β was not different between rest and after exercise.


In sedentary adults, the single bout of moderate-intensity cycling induced modest increases for intrinsic mitochondrial oxidative phosphorylation that was consistent across multiple substrates.
In sedentary adults, the single bout of moderate-intensity cycling induced modest increases for intrinsic mitochondrial oxidative phosphorylation that was consistent across multiple substrates.
|editor=[[Plangger M]]
|editor=[[Plangger M]]
|mipnetlab=US OR Corvallis Robinson MM
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration, Exercise physiology;nutrition;life style
|instruments=Oxygraph-2k
|organism=Human
|additional=2023-01
|tissues=Skeletal muscle
|preparations=Isolated mitochondria
|couplingstates=LEAK, OXPHOS, ET
|pathways=F, N, S, NS, ROX
|instruments=Oxygraph-2k, O2k-Fluorometer
|additional=2023-01, AmR
}}
}}

Latest revision as of 14:22, 4 January 2023

Publications in the MiPMap
Newsom SA, Stierwalt HD, Ehrlicher SE, Robinson MM (2021) Substrate-specific respiration of isolated skeletal muscle mitochondria after 1 h of moderate cycling in sedentary adults. https://doi.org/10.1249/mss.0000000000002615

» Med Sci Sports Exerc 53:1375-84. PMID: 34127633 Open Access

Newsom Sean A,  Stierwalt Harrison D,  Ehrlicher Sarah E, Robinson Matthew M (2021) Med Sci Sports Exerc

Abstract: Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. Specific complexes oxidize lipid and nonlipid substrates. It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates.

We studied mitochondrial metabolism in sedentary male and female adults (n = 11F/4M) who were free of major medical conditions with mean ± SD age of 28 ± 7 yr, peak aerobic capacity of 2.0 ± 0.4 L/min, and body mass index of 22.2 ± 2 kg·m2. Biopsies were collected from the vastus lateralis muscle on separate study days at rest or 15 min after exercise (1 h cycling at 65% peak aerobic capacity). Isolated mitochondria were analyzed using high-resolution respirometry of separate titration protocols for lipid (palmitoylcarnitine, F-linked) and nonlipid substrates (glutamate-malate, N-linked; succinate S-linked). Titration protocols distinguished between oxidative phosphorylation and leak respiration and included the measurement of reactive oxygen species emission (H2O2). Western blotting determined the protein abundance of electron transfer flavoprotein (ETF) subunits, including inhibitory methylation site on ETF-β.

Aerobic exercise induced modest increases in mitochondrial respiration because of increased coupled respiration across F-linked (+13%, P = 0.08), N(S)-linked (+14%, P = 0.09), and N-linked substrates (+17%, P = 0.08). Prior exercise did not change P:O ratio. Electron leak to H2O2 increased 6% increased after exercise (P = 0.06) for lipid substrates but not for nonlipid. The protein abundance of ETF-α or ETF-β subunit or inhibitory methylation on ETF-β was not different between rest and after exercise.

In sedentary adults, the single bout of moderate-intensity cycling induced modest increases for intrinsic mitochondrial oxidative phosphorylation that was consistent across multiple substrates.

Bioblast editor: Plangger M O2k-Network Lab: US OR Corvallis Robinson MM


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 


Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Isolated mitochondria 


Coupling state: LEAK, OXPHOS, ET  Pathway: F, N, S, NS, ROX  HRR: Oxygraph-2k, O2k-Fluorometer 

2023-01, AmR