ArticleThe Journal of physiology2007
KATP channel deficiency in mouse flexor digitorum brevis causes fibre damage and impairs Ca2+ release and force development during fatigue in vitro.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Glucose and glycogen affects CaPhysiological reports · 2024Article
- Novel loss-of-function variants expand ABCC9-related intellectual disability and myopathy syndrome.Brain : a journal of neurology · 2024Article
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- Skeletal muscle delimited myopathy and verapamil toxicity in SUR2 mutant mouse models of AIMS.EMBO molecular medicine · 2023Article
- A New Unified Theory of Trigger Point Formation: Failure of Pre- and Post-Synaptic Feedback Control Mechanisms.International journal of molecular sciences · 2023Article
- Consequences of SUR2[A478V] Mutation in Skeletal Muscle of Murine Model of Cantu Syndrome.Cells · 2021Article
- Pathophysiological Consequences of KATP Channel Overactivity and Pharmacological Response to Glibenclamide in Skeletal Muscle of a Murine Model of Cantù Syndrome.Frontiers in pharmacology · 2020Article
- KATP channel deficiency in mouse FDB causes an impairment of energy metabolism during fatigue.American journal of physiology. Cell physiology · 2016Article
- Disruption of ATP-sensitive potassium channel function in skeletal muscles promotes production and secretion of musclin.Biochemical and biophysical research communications · 2016Article
- ATP Sensitive Potassium Channels in the Skeletal Muscle Function: Involvement of the KCNJ11(Kir6.2) Gene in the Determination of Mechanical Warner Bratzer Shear Force.Frontiers in physiology · 2016Review
- MicroRNA-431 accelerates muscle regeneration and ameliorates muscular dystrophy by targeting Pax7 in mice.Nature communications · 2015Article
- Disruption of KATP channel expression in skeletal muscle by targeted oligonucleotide delivery promotes activity-linked thermogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- Properties of single FDB fibers following a collagenase digestion for studying contractility, fatigue, and pCa-sarcomere shortening relationship.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Changes in myoplasmic Ca2+ during fatigue differ between FDB fibers, between glibenclamide-exposed and Kir6.2-/- fibers and are further modulated by verapamil.Physiological reports · 2015Article
- Sarcolemmal ATP-sensitive potassium channels modulate skeletal muscle function under low-intensity workloads.The Journal of general physiology · 2014Article
- Muscle uncoupling protein 3 overexpression mimics endurance training and reduces circulating biomarkers of incomplete β-oxidation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Loss of cIAP1 attenuates soleus muscle pathology and improves diaphragm function in mdx mice.Human molecular genetics · 2013Article
- Effect of temperature on crossbridge force changes during fatigue and recovery in intact mouse muscle fibers.PloS one · 2013Article
- Wnt7a treatment ameliorates muscular dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Glibenclamide increases post-fatigue tension in slow skeletal muscle fibers of the chicken.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the K(ATP) channels results in faster fatigue rates as the channels depress action potential amplitude, whereas abolishing the channel activity has no effect in whole extensor digitorum longus (EDL) and soleus muscles. In this study, we examined the effects of abolished K(ATP) channel activity during fatigue at 37 degrees C on free intracellular Ca(2+) (Ca(2+)(i)) and tetanic force using single muscle fibres and small muscle bundles from the flexor digitorum brevis (FDB). K(ATP) channel deficient muscle fibres were obtained (i) pharmacologically by exposing wild-type fibres to glibenclamide, and (ii) genetically using null mice for the Kir6.2 gene (Kir6.2(-/-) mice). Fatigue was elicited using 200 ms tetanic contractions every second for 3 min. This study demonstrated for the first time that abolishing K(ATP) channel activity at 37 degrees C resulted in faster fatigue rates, where decreases in peak Ca(2+)(i) and tetanic force were faster in K(ATP) channel deficient fibres than in control wild-type fibres. Furthermore, several contractile dysfunctions were also observed in K(ATP) channel deficient muscle fibre. They included partially or completely supercontracted single muscle fibres, greater increases in unstimulated Ca(2+)(i) and unstimulated force, and lower force recovery. We propose that the observed faster rate of fatigue in K(ATP) channel deficient fibres is because the decreases in peak Ca(2+)(i) and force caused by contractile dysfunctions prevail over the expected slower decreases when the channels do not depress action potential amplitude.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.