ArticlePloS one2014
Effects of chronic administration of clenbuterol on contractile properties and calcium homeostasis in rat extensor digitorum longus muscle.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Chronic βThe Journal of physiology · 2018Trial
- Theaflavins decrease skeletal muscle wasting in disuse atrophy induced by hindlimb suspension in mice.Journal of clinical biochemistry and nutrition · 2021Article
- Muscle hypertrophy and muscle strength: dependent or independent variables? A provocative review.European journal of translational myology · 2020Article
- The β-arrestin-biased β-adrenergic receptor blocker carvedilol enhances skeletal muscle contractility.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Sympathomimetics regulate neuromuscular junction transmission through TRPV1, P/Q- and N-type CaMolecular and cellular neurosciences · 2019Article
- Role of β-adrenergic signaling in masseter muscle.PloS one · 2019Article
- β-arrestin 1 regulates β2-adrenergic receptor-mediated skeletal muscle hypertrophy and contractility.Skeletal muscle · 2018Article
- Role of phosphodiesterase 4 expression in the Epac1 signaling-dependent skeletal muscle hypertrophic action of clenbuterol.Physiological reports · 2016Article
- Chronic clenbuterol treatment compromises force production without directly altering skeletal muscle contractile machinery.The Journal of physiology · 2015Article
- The molecular basis for load-induced skeletal muscle hypertrophy.Calcified tissue international · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clenbuterol, a β2-agonist, induces skeletal muscle hypertrophy and a shift from slow-oxidative to fast-glycolytic muscle fiber type profile. However, the cellular mechanisms of the effects of chronic clenbuterol administration on skeletal muscle are not completely understood. As the intracellular Ca2+ concentration must be finely regulated in many cellular processes, the aim of this study was to investigate the effects of chronic clenbuterol treatment on force, fatigue, intracellular calcium (Ca2+) homeostasis and Ca2+-dependent proteolysis in fast-twitch skeletal muscles (the extensor digitorum longus, EDL, muscle), as they are more sensitive to clenbuterol-induced hypertrophy. Male Wistar rats were chronically treated with 4 mg.kg-1 clenbuterol or saline vehicle (controls) for 21 days. Confocal microscopy was used to evaluate sarcoplasmic reticulum Ca2+ load, Ca2+-transient amplitude and Ca2+ spark properties. EDL muscles from clenbuterol-treated animals displayed hypertrophy, a shift from slow to fast fiber type profile and increased absolute force, while the relative force remained unchanged and resistance to fatigue decreased compared to control muscles from rats treated with saline vehicle. Compared to control animals, clenbuterol treatment decreased Ca2+-transient amplitude, Ca2+ spark amplitude and frequency and the sarcoplasmic reticulum Ca2+ load was markedly reduced. Conversely, calpain activity was increased by clenbuterol chronic treatment. These results indicate that chronic treatment with clenbuterol impairs Ca2+ homeostasis and this could contribute to the remodeling and functional impairment of fast-twitch skeletal muscle.
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