ArticleThe Journal of physiology2001
Inhibition of creatine kinase reduces the rate of fatigue-induced decrease in tetanic [Ca(2+)](i) in mouse skeletal muscle.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 47 citations in OpenAlex.
- Serum agrin and talin are increased in major depression while agrin and creatine phosphokinase are associated with chronic fatigue and fibromyalgia symptoms in depression.Metabolic brain disease · 2020Article
- Fast skeletal muscle troponin activator CK-2066260 increases fatigue resistance by reducing the energetic cost of muscle contraction.The Journal of physiology · 2019Article
- Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular CaCold Spring Harbor perspectives in medicine · 2018Review
- Subcellular distribution of glycogen and decreased tetanic Ca2+ in fatigued single intact mouse muscle fibres.The Journal of physiology · 2014Article
- Proteomic screening of molecular targets of crocin.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2014Article
- The multiple roles of phosphate in muscle fatigue.Frontiers in physiology · 2012Article
- Muscle fatigue examined at different temperatures in experiments on intact mammalian (rat) muscle fibers.Journal of applied physiology (Bethesda, Md. : 1985) · 2009Article
- The effects of creatine pyruvate and creatine citrate on performance during high intensity exercise.Journal of the International Society of Sports Nutrition · 2008Article
- Regulation and function of Ca2+-calmodulin-dependent protein kinase II of fast-twitch rat skeletal muscle.The Journal of physiology · 2007Article
- Limited oxygen diffusion accelerates fatigue development in mouse skeletal muscle.The Journal of physiology · 2006Article
- Fatigue resistance of rat extraocular muscles does not depend on creatine kinase activity.BMC physiology · 2005Article
- Multiple sprint work : physiological responses, mechanisms of fatigue and the influence of aerobic fitness.Sports medicine (Auckland, N.Z.) · 2005Review
- Creatine kinase injection restores contractile function in creatine-kinase-deficient mouse skeletal muscle fibres.The Journal of physiology · 2003Article
- Role of phosphate and calcium stores in muscle fatigue.The Journal of physiology · 2001Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Ca(2+)-phosphate (P(i)) precipitation in the sarcoplasmic reticulum (SR) may cause reduced SR Ca(2+) release in skeletal muscle fatigue. To study this, we inhibited the creatine kinase (CK) reaction with 2,4-dinitro-1-fluorobenzene (DNFB). The hypothesis was that with inhibition of CK, phosphocreatine would not break down to creatine and P(i). Therefore P(i) transport into the SR would be limited and Ca(2+)-P(i) precipitation would not occur. 2. Intact single fibres from a mouse foot muscle were fatigued by repeated short tetani under control conditions or after exposure to DNFB (10 microM). The free myoplasmic concentrations of Ca(2+) ([Ca(2+)](i)) and Mg(2+) ([Mg(2+)](i)) were measured with indo-1 and mag-indo-1, respectively. Changes in [Mg(2+)](i) were assumed to reflect alterations in myoplasmic ATP concentration. 3. During the first 10 fatiguing tetani, tetanic [Ca(2+)](i) increased both in control and after DNFB exposure. Thereafter tetanic [Ca(2+)](i) fell and the rate of fall was about fourfold lower after DNFB exposure compared with control. 4. Under control conditions, there was a good relationship between declining tetanic [Ca(2+)](i) and increasing [Mg(2+)](i) during the final part of fatiguing stimulation. This correlation was lost after DNFB exposure. 5. In conclusion, the present data fit with a model where Ca(2+)-P(i) precipitation inhibits SR Ca(2+) release in fatigue produced by repeated short tetani. Furthermore, the results suggest that the rate of P(i) transport into the SR critically depends on the myoplasmic Mg(2+)/ATP concentration.
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