ArticleThe Journal of physiology2003
Mitochondrial function in intact skeletal muscle fibres of creatine kinase deficient mice.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular CaCold Spring Harbor perspectives in medicine · 2018Review
- Development of a high-throughput method for real-time assessment of cellular metabolism in intact long skeletal muscle fibre bundles.The Journal of physiology · 2016Article
- Primary Murine Myotubes as a Model for Investigating Muscular Dystrophy.BioMed research international · 2015Article
- Subcellular distribution of glycogen and decreased tetanic Ca2+ in fatigued single intact mouse muscle fibres.The Journal of physiology · 2014Article
- Sphingomyelinase promotes oxidant production and skeletal muscle contractile dysfunction through activation of NADPH oxidase.Frontiers in physiology · 2014Article
- Mitochondrial calcium uptake.Proceedings of the National Academy of Sciences of the United States of America · 2013Review
- Mitochondrial Ca2+-handling in fast skeletal muscle fibers from wild type and calsequestrin-null mice.PloS one · 2013Article
- Comparative proteomics of skeletal muscle mitochondria from myostatin-null mice.Cell biology international reports · 2011Article
- Rearrangement of energetic and substrate utilization networks compensate for chronic myocardial creatine kinase deficiency.The Journal of physiology · 2011Article
- Ryanodine receptor oxidation causes intracellular calcium leak and muscle weakness in aging.Cell metabolism · 2011Article
- Faster O₂ uptake kinetics in canine skeletal muscle in situ after acute creatine kinase inhibition.The Journal of physiology · 2011Article
- Altered contractility of skeletal muscle in mice deficient in titin's M-band region.Journal of molecular biology · 2009Article
- Sarcoplasmic reticulum calcium uptake and speed of relaxation are depressed in nebulin-free skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008Article
- In situ detection and measurement of intracellular reactive oxygen species in single isolated mature skeletal muscle fibers by real time fluorescence microscopy.Antioxidants & redox signaling · 2008Article
- Impaired voluntary running capacity of creatine kinase-deficient mice.The Journal of physiology · 2005Article
- Ca2+-activated myosin-ATPases, creatine and adenylate kinases regulate mitochondrial function according to myofibre type in rabbit.The Journal of physiology · 2005Article
- In vivo monitoring of Ca(2+) uptake into mitochondria of mouse skeletal muscle during contraction.The Journal of cell biology · 2004Article
- Contraction-mediated glycogenolysis in mouse skeletal muscle lacking creatine kinase: the role of phosphorylase b activation.The Journal of physiology · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Creatine kinase (CK) has a central role in skeletal muscle, acting as a fast energy buffer and shuttle between sites of energy production (mitochondria) and consumption (cross-bridges and ion pumps). Unexpectedly, isolated fast-twitch skeletal muscle cells of mice deficient in both cytosolic and mitochondrial CK (CK-/-) are highly fatigue resistant during stimulation protocols that stress aerobic metabolism. We have now studied different aspects of mitochondrial function in CK-/- skeletal muscle. Intact, single fibres of flexor digitorum brevis (FDB) muscles were fatigued by repeated tetanic stimulation (70 Hz, 350 ms duration, duty cycle 0.14). Under control conditions, CK-/- FDB fibres were more fatigue resistant than wild-type fibres. However, after mitochondrial inhibition with cyanide, force declined markedly faster in CK-/- fibres than in wild-type fibres. The rapid force decline in CK-/- fibres was not due to decreased myoplasmic [Ca2+] during tetani (measured with indo-1), which in these fibres remained virtually constant during fatigue in the presence of cyanide. Intact, single fibres of highly oxidative soleus muscles were fatigued by repeated tetani (50 Hz, 500 ms duration, duty cycle 0.5). All CK-/- soleus fibres tested (n = 9) produced > 40 % force at the end of the fatiguing stimulation period (500 tetani), whereas force fell to < 40 % before 500 tetani in two of three wild-type fibres. Mitochondrial [Ca2+] (measured with rhod-2 and confocal microscopy) increased during repeated tetanic stimulation in CK-/- but not in wild-type FDB fibres. In conclusion, mitochondria and energy shuttling operate effectively in CK-/- fibres and this is associated with an increase in mitochondrial [Ca2+].
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