Caffeine‐induced depolarization in amphibian skeletal muscle fibres: role of Na+/Ca2+ exchange and K+ release

Kotsias, Basilio A.; Venosa, R. A.

doi:10.1046/j.1365-201x.2001.00803.x

Cited by 4 publications

References 36 publications

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Effects of Verapamil and Gadolinium on Caffeine-Induced Contractures and Calcium Fluxes in Frog Slow Skeletal Muscle Fibers

et al. 2007

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In this work, we tested whether L-type Ca(2+ )channels are involved in the increase of caffeine-evoked tension in frog slow muscle fibers. Simultaneous net Ca(2+) fluxes and changes in muscle tension were measured in the presence of caffeine. Isometric tension was recorded by a mechanoelectrical transducer, and net fluxes of Ca(2+) were measured noninvasively using ion-selective vibrating microelectrodes. We show that the timing of changes in net fluxes and muscle tension coincided, suggesting interdependence of the two processes. The effects of Ca(2+)channel blockers (verapamil and gadolinium) were explored using 6 mM: caffeine; both significantly reduced the action of caffeine on tension and on calcium fluxes. Both caffeine-evoked Ca(2+) leak and muscle tension were reduced by 75% in the presence of 100 microM: GdCl(3), which also caused a 92% inhibition of net Ca(2+) fluxes in the steady-state condition. Application of 10 microM: verapamil to the bath led to 30% and 52% reductions in the Ca(2+)leak caused by the presence of caffeine for the peak and steady-state values of net Ca(2+) fluxes, respectively. Verapamil (10 microM): caused a 30% reduction in the maximum values of caffeine-evoked muscle tension. Gd(3+)was a more potent inhibitor than verapamil. In conclusion, L-type Ca(2+) channels appear to play the initial role of trigger in the rather complex mechanism of slow fiber contraction, the latter process being mediated by both positive Ca(2+)-induced Ca(2+ )release and negative (Ca(2+) removal from cytosol) feedback loops.

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Effects of Verapamil and Gadolinium on Caffeine-Induced Contractures and Calcium Fluxes in Frog Slow Skeletal Muscle Fibers

et al. 2007

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Caffeine-induced contracture in oesophageal striated muscle of normotensive and hypertensive rats

Sekiguchi¹,

Kawata²,

Komori³

et al. 2003

European Journal of Pharmacology

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Caffeine Use in Sports, Pharmacokinetics in Man, and Cellular Mechanisms of Action

Magkos

Kavouras

2005

Critical Reviews in Food Science and Nutrition

285

231

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Caffeine is the most widely consumed psychoactive 'drug' in the world and probably one of the most commonly used stimulants in sports. This is not surprising, since it is one of the few ergogenic aids with documented efficiency and minimal side effects. Caffeine is rapidly and completely absorbed by the gastrointestinal tract and is readily distributed throughout all tissues of the body. Peak plasma concentrations after normal consumption are usually around 50 microM, and half-lives for elimination range between 2.5-10 h. The parent compound is extensively metabolized in the liver microsomes to more than 25 derivatives, while considerably less than 5% of the ingested dose is excreted unchanged in the urine. There is, however, considerable inter-individual variability in the handling of caffeine by the body, due to both environmental and genetic factors. Evidence from in vitro studies provides a wealth of different cellular actions that could potentially contribute to the observed effects of caffeine in humans in vivo. These include potentiation of muscle contractility via induction of sarcoplasmic reticulum calcium release, inhibition of phosphodiesterase isoenzymes and concomitant cyclic monophosphate accumulation, inhibition of glycogen phosphorylase enzymes in liver and muscle, non-selective adenosine receptor antagonism, stimulation of the cellular membrane sodium/potassium pump, impairment of phosphoinositide metabolism, as well as other, less thoroughly characterized actions. Not all, however, seem to account for the observed effects in vivo, although a variable degree of contribution cannot be readily discounted on the basis of experimental data. The most physiologically relevant mechanism of action is probably the blockade of adenosine receptors, but evidence suggests that, at least under certain conditions, other biochemical mechanisms may also be operational.

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Caffeine‐induced depolarization in amphibian skeletal muscle fibres: role of Na⁺/Ca²⁺ exchange and K⁺ release

Cited by 4 publications

References 36 publications

Effects of Verapamil and Gadolinium on Caffeine-Induced Contractures and Calcium Fluxes in Frog Slow Skeletal Muscle Fibers

Effects of Verapamil and Gadolinium on Caffeine-Induced Contractures and Calcium Fluxes in Frog Slow Skeletal Muscle Fibers

Caffeine-induced contracture in oesophageal striated muscle of normotensive and hypertensive rats

Caffeine Use in Sports, Pharmacokinetics in Man, and Cellular Mechanisms of Action

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