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Human muscular mitochondrial fusion in athletes during exercise.
FASEB J. 33, 12087-12098 (2019)
The main objective of this work was to investigate whether mitochondrial fusion occurs in the skeletal muscle of well-trained athletes in response to high-intensity exercise. Well-trained swimmers (n = 9) performed a duration-matched sprint interval training (SIT) and high-intensity high-volume training (HIHVT) session on separate days. Muscle samples from triceps brachii were taken before, immediately after, and 3 h after the training sessions. Transmission electron microscopy (TEM) was applied to assess mitochondrial morphology. Moreover, expression of genes coding for regulators of mitochondrial fusion and fission were assessed by real-time quantitative PCR. In addition, mitofusin (MFN)2 and optic atrophy 1 (OPA1) were quantified by Western blot analysis. TEM analyses showed that mitochondrial morphology remained altered for 3 h after HIHVT, whereas SIT-induced changes were only evident immediately after exercise. Only SIT increased MFN1 and MFN2 mRNA expression, whereas SIT and HIHVT both increased MFN2 protein content 3 h after exercise. Notably, only HIHVT increased OPA1 protein content. Mitochondrial morphologic changes that suggest fusion occurs in well-adapted athletes during exercise. However, HIHVT appears as a more robust inducer of mitochondrial fusion events than SIT. Indeed, SIT induces a rapid and transient change in mitochondrial morphology.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Physical Activity ; Mitochondrial Fission ; Skeletal Muscle ; Mitofusin 2; Human Skeletal-muscle; Membrane Interactions; Fission; Protein; Reticulum; Adaptations; Activation; Fis1
Language
english
Publication Year
2019
HGF-reported in Year
2019
ISSN (print) / ISBN
0892-6638
e-ISSN
1530-6860
Journal
FASEB Journal
Quellenangaben
Volume: 33,
Issue: 11,
Pages: 12087-12098
Publisher
Wiley
Publishing Place
Bethesda, Md.
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)
POF-Topic(s)
30502 - Diabetes: Pathophysiology, Prevention and Therapy
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-553400-001
WOS ID
WOS:000507461600038
Scopus ID
85074379719
PubMed ID
31398297
Erfassungsdatum
2019-08-13