scholarly journals Mitochondrial oxidative phosphorylation complexes exist in the sarcolemma of skeletal muscle

BMB Reports ◽  
2016 ◽  
Vol 49 (2) ◽  
pp. 116-121 ◽  
Author(s):  
Hyun Lee ◽  
Seung-Hyeob Kim ◽  
Jae-Seon Lee ◽  
Yun-Hee Yang ◽  
Jwa-Min Nam ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Oxidative Phosphorylation

P6277The impact of exercise training in combination with statin use on skeletal muscle mitochondrial oxidative phosphorylation and metabolomics in obese rats

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
I Urbaneck ◽  
F Lorenz ◽  
I Materzok ◽  
L Maletzki ◽  
M Pietzner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cytochrome C ◽  
Exercise Training ◽  
Oxidative Phosphorylation ◽  
Atp Synthase ◽  
Statin Treatment ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Complex Iv ◽  
Obese Rats ◽  
Statin Use

Abstract Background Exercise training (ET) and statin treatment both alter skeletal muscle function. Purpose We investigated the effects of a combined exercise and statin use on skeletal muscle mitochondrial oxidative phosphorylation (OxPhos) and metabolic alterations in obese rats. Methods Eight-week-old male Wistar rats were used. A total of 14 animals received standard chow, while 46 rats were fed a high-fat diet (HFD) for 20 weeks. After 8 weeks, the rats were randomized into 6 groups: sedentary (n=8), ET (n=6), sedentary with HFD (n=11), ET with HFD (n=11), statin with HFD (n=13) and ET with HFD and statins (n=11). Simvastatin (10mg/d/kg) was added to the drinking water. ET was performed for 12 weeks, 5 days/week for 1 h/day at 18 m/min in a motorized running wheel. OxPhos was assessed by complex-specific antibodies and targeted metabolomics using the Biocrates p180 kit. All experiments were done on frozen samples of the M. gastrocnemicus. An ANOVA with fixed effects for diet, exercise, statin treatment and statin-exercise interaction was used to identify significantly different metabolites. Results Statin use was associated with significantly lower cholesterol levels, but did not affect exercise duration and intensity compared to none-use. In sedentary animals, HFD increased OxPhos complex II (succinate dehydrogenase), complex IV (cytochrome-c-oxidase) and V (ATP synthase) while statin treatment diminished this increase in all complexes. HFD increased complex IV independent of statin treatment but had no effect on complex II and V in ET rats. Complex IV was increased due to ET only in HFD fed rats compared to rats on normal chow but decreased in contrast to sedentary animals on a HFD. With regards to metabolomics, we found 57 metabolites which were influenced by HFD while no metabolites were identified with a significant effect for ET. A significant statin-exercise interaction was found for three lysophosphatidylcholines (lysoPC a C26.0, lysoPC a C26.1, lysoPC a C24.0), one phosphatidylcholine (PC aa C42.6) and one sphingomyelin (SM C16.1). HFD decreased the concentration of all mentioned metabolites compared to standard chow fed animals. Likewise, ET increased the concentration of metabolites compared to sedentary animals on HFD. Statin treatment led to an increase, while statin in combination with ET did not rescue this effect. Conclusion HFD induced severely impaired skeletal muscle OxPhos independent of ET and statin treatment. Our findings suggest a limiting rate of NADH production in the tricarboxylic acid cycle as a potential mechanism. However, ET prevented the increase in cytochrome-c-oxidation while statins blocked the HFD induced increase in ATP synthase. Our metabolomics results imply that future research should consider the lipotoxic effects of a HFD when assessing skeletal muscle alterations due to ET or statins. Of particular interest could be the 5 metabolites that have been shown to be impacted by a statin-exercise interaction.

scholarly journals Skeletal muscle mitochondrial oxidative phosphorylation function in idiopathic pulmonary arterial hypertension: in vivo and in vitro study

2018 ◽  
Vol 8 (2) ◽  
pp. 204589401876829 ◽  
Author(s):  
Sasiharan Sithamparanathan ◽  
Mariana C. Rocha ◽  
Jehill D. Parikh ◽  
Karolina A. Rygiel ◽  
Gavin Falkous ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Pulmonary Arterial Hypertension ◽  
Oxidative Phosphorylation ◽  
Arterial Hypertension ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Pulmonary Vessels ◽  
Pulmonary Arterial

Mitochondrial dysfunction within the pulmonary vessels has been shown to contribute to the pathology of idiopathic pulmonary arterial hypertension (IPAH). We investigated the hypothesis of whether impaired exercise capacity observed in IPAH patients is in part due to primary mitochondrial oxidative phosphorylation (OXPHOS) dysfunction in skeletal muscle. This could lead to potentially new avenues of treatment beyond targeting the pulmonary vessels. Nine clinically stable participants with IPAH underwent cardiopulmonary exercise testing, in vivo and in vitro assessment of mitochondrial function by 31P-magnetic resonance spectroscopy (31P-MRS) and laboratory muscle biopsy analysis. 31P-MRS showed abnormal skeletal muscle bioenergetics with prolonged recovery times of phosphocreatine and abnormal muscle pH handling. Histochemistry and quadruple immunofluorescence performed on muscle biopsies showed normal function and subunit protein abundance of the complexes within the OXPHOS system. Our findings suggest that there is no primary mitochondrial OXPHOS dysfunction but raises the possibility of impaired oxygen delivery to the mitochondria affecting skeletal muscle bioenergetics during exercise.

scholarly journals Alteration of mitochondrial oxidative phosphorylation in aged skeletal muscle involves modification of adenine nucleotide translocator

2010 ◽  
Vol 1797 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Gilles Gouspillou ◽  
Isabelle Bourdel-Marchasson ◽  
Richard Rouland ◽  
Guillaume Calmettes ◽  
Jean-Michel Franconi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Adenine Nucleotide ◽  
Adenine Nucleotide Translocator ◽  
Mitochondrial Oxidative Phosphorylation

Age-associated deficit of mitochondrial oxidative phosphorylation in skeletal muscle: Role of carnitine and lipoic acid

2005 ◽  
Vol 280 (1-2) ◽  
pp. 83-89 ◽  
Author(s):  
S. Kumaran ◽  
Kavin S. Panneerselvam ◽  
S. Shila ◽  
K. Sivarajan ◽  
C. Panneerselvam
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Lipoic Acid ◽  
Mitochondrial Oxidative Phosphorylation
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