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Effects of membrane depolarization and changes in extracellular [K(+)] on the Ca (2+) transients of fast skeletal muscle fibers. Implications for muscle fatigue.

Quiñonez M, González F, Morgado-Valle C, DiFranco M - J. Muscle Res. Cell. Motil. (2010)

Bottom Line: Similar effects were found for the Ca(2+) transients elicited by the first pulse of 100 Hz trains.Changes in Ca(2+) transients along the trains were associated with impaired or abortive APs.The effects of 10 mM K(+)(O) on Ca(2+) transients, but not those of 15 mM K(+)(O), could be fully reversed by hyperpolarization.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio de Fisiología y Biofisíca del Músculo, IBE, UCV, Caracas, Venezuela. mquinonez@mednet.ucla.edu

ABSTRACT
Repetitive activation of skeletal muscle fibers leads to a reduced transmembrane K(+) gradient. The resulting membrane depolarization has been proposed to play a major role in the onset of muscle fatigue. Nevertheless, raising the extracellular K(+) K(+)(O) concentration ([K(+)](O)) to 10 mM potentiates twitch force of rested amphibian and mammalian fibers. We used a double Vaseline gap method to simultaneously record action potentials (AP) and Ca(2+) transients from rested frog fibers activated by single and tetanic stimulation (10 pulses, 100 Hz) at various [K(+)](O) and membrane potentials. Depolarization resulting from current injection or raised [K(+](O) produced an increase in the resting [Ca(2+)]. Ca(2+) transients elicited by single stimulation were potentiated by depolarization from -80 to -60 mV but markedly depressed by further depolarization. Potentiation was inversely correlated with a reduction in the amplitude, overshoot and duration of APs. Similar effects were found for the Ca(2+) transients elicited by the first pulse of 100 Hz trains. Depression or block of Ca(2+) transient in response to the 2nd to 10th pulses of 100 Hz trains was observed at smaller depolarizations as compared to that seen when using single stimulation. Changes in Ca(2+) transients along the trains were associated with impaired or abortive APs. Raising [K(+)](O) to 10 mM potentiated Ca(2+) transients elicited by single and tetanic stimulation, while raising [K(+)](O) to 15 mM markedly depressed both responses. The effects of 10 mM K(+)(O) on Ca(2+) transients, but not those of 15 mM K(+)(O), could be fully reversed by hyperpolarization. The results suggests that the force potentiating effects of 10 mM K(+)(O) might be mediated by depolarization dependent changes in resting [Ca(2+)] and Ca(2+) release, and that additional mechanisms might be involved in the effects of 15 mM K(+)(O) on force generation.

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Effects of membrane potential on AP and Ca2+ transients parameters. A Peak Ca2+ transient as a function of membrane potential. The dashed line represents the peak Ca2+ transient at −100 mV. B FDHM of Ca2+ transients recorded at various membrane potentials. C Depression of AP overshoot with membrane depolarization. D FDHM of AP’s elicited from various membrane potentials. Symbols and bars represent the mean ± ES (n = 5)
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Fig5: Effects of membrane potential on AP and Ca2+ transients parameters. A Peak Ca2+ transient as a function of membrane potential. The dashed line represents the peak Ca2+ transient at −100 mV. B FDHM of Ca2+ transients recorded at various membrane potentials. C Depression of AP overshoot with membrane depolarization. D FDHM of AP’s elicited from various membrane potentials. Symbols and bars represent the mean ± ES (n = 5)

Mentions: The effects of membrane depolarization on some features of APs and Ca2+ transients are summarized in Fig. 5. The biphasic dependence of Ca2+ transient amplitude on membrane potential is clearly seen in Fig. 5A. It can be observed that the Ca2+ transient potentiation changes smoothly with depolarization between −90 and −65 mV, while a steep relationship between Ca2+ transient amplitude depression and membrane potential is seen in the range of −60 to −55 mV. The fact that the potentiation region of the plot is not correlated with the expected effects of changes in the overshoot (Fig. 5C) and FDHM of the AP (Fig. 5D), suggests that Ca2+ transient potentiation results from another voltage-dependent parameter, such as the resting [Ca2+]. In fact, a significant potentiation is still seen at about −60 mV, while the AP amplitude and overshoot are highly depressed. Figure 5A is highly reminiscent of the effect of raising on twitch tension (Renaud and Light 1992). On the other hand, the depression region of the plot is correlated with a pronounced reduction in the overshoot and a large increased of the FDHM of the AP.Fig. 5


Effects of membrane depolarization and changes in extracellular [K(+)] on the Ca (2+) transients of fast skeletal muscle fibers. Implications for muscle fatigue.

Quiñonez M, González F, Morgado-Valle C, DiFranco M - J. Muscle Res. Cell. Motil. (2010)

Effects of membrane potential on AP and Ca2+ transients parameters. A Peak Ca2+ transient as a function of membrane potential. The dashed line represents the peak Ca2+ transient at −100 mV. B FDHM of Ca2+ transients recorded at various membrane potentials. C Depression of AP overshoot with membrane depolarization. D FDHM of AP’s elicited from various membrane potentials. Symbols and bars represent the mean ± ES (n = 5)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2908756&req=5

Fig5: Effects of membrane potential on AP and Ca2+ transients parameters. A Peak Ca2+ transient as a function of membrane potential. The dashed line represents the peak Ca2+ transient at −100 mV. B FDHM of Ca2+ transients recorded at various membrane potentials. C Depression of AP overshoot with membrane depolarization. D FDHM of AP’s elicited from various membrane potentials. Symbols and bars represent the mean ± ES (n = 5)
Mentions: The effects of membrane depolarization on some features of APs and Ca2+ transients are summarized in Fig. 5. The biphasic dependence of Ca2+ transient amplitude on membrane potential is clearly seen in Fig. 5A. It can be observed that the Ca2+ transient potentiation changes smoothly with depolarization between −90 and −65 mV, while a steep relationship between Ca2+ transient amplitude depression and membrane potential is seen in the range of −60 to −55 mV. The fact that the potentiation region of the plot is not correlated with the expected effects of changes in the overshoot (Fig. 5C) and FDHM of the AP (Fig. 5D), suggests that Ca2+ transient potentiation results from another voltage-dependent parameter, such as the resting [Ca2+]. In fact, a significant potentiation is still seen at about −60 mV, while the AP amplitude and overshoot are highly depressed. Figure 5A is highly reminiscent of the effect of raising on twitch tension (Renaud and Light 1992). On the other hand, the depression region of the plot is correlated with a pronounced reduction in the overshoot and a large increased of the FDHM of the AP.Fig. 5

Bottom Line: Similar effects were found for the Ca(2+) transients elicited by the first pulse of 100 Hz trains.Changes in Ca(2+) transients along the trains were associated with impaired or abortive APs.The effects of 10 mM K(+)(O) on Ca(2+) transients, but not those of 15 mM K(+)(O), could be fully reversed by hyperpolarization.

View Article: PubMed Central - PubMed

Affiliation: Laboratorio de Fisiología y Biofisíca del Músculo, IBE, UCV, Caracas, Venezuela. mquinonez@mednet.ucla.edu

ABSTRACT
Repetitive activation of skeletal muscle fibers leads to a reduced transmembrane K(+) gradient. The resulting membrane depolarization has been proposed to play a major role in the onset of muscle fatigue. Nevertheless, raising the extracellular K(+) K(+)(O) concentration ([K(+)](O)) to 10 mM potentiates twitch force of rested amphibian and mammalian fibers. We used a double Vaseline gap method to simultaneously record action potentials (AP) and Ca(2+) transients from rested frog fibers activated by single and tetanic stimulation (10 pulses, 100 Hz) at various [K(+)](O) and membrane potentials. Depolarization resulting from current injection or raised [K(+](O) produced an increase in the resting [Ca(2+)]. Ca(2+) transients elicited by single stimulation were potentiated by depolarization from -80 to -60 mV but markedly depressed by further depolarization. Potentiation was inversely correlated with a reduction in the amplitude, overshoot and duration of APs. Similar effects were found for the Ca(2+) transients elicited by the first pulse of 100 Hz trains. Depression or block of Ca(2+) transient in response to the 2nd to 10th pulses of 100 Hz trains was observed at smaller depolarizations as compared to that seen when using single stimulation. Changes in Ca(2+) transients along the trains were associated with impaired or abortive APs. Raising [K(+)](O) to 10 mM potentiated Ca(2+) transients elicited by single and tetanic stimulation, while raising [K(+)](O) to 15 mM markedly depressed both responses. The effects of 10 mM K(+)(O) on Ca(2+) transients, but not those of 15 mM K(+)(O), could be fully reversed by hyperpolarization. The results suggests that the force potentiating effects of 10 mM K(+)(O) might be mediated by depolarization dependent changes in resting [Ca(2+)] and Ca(2+) release, and that additional mechanisms might be involved in the effects of 15 mM K(+)(O) on force generation.

Show MeSH
Related in: MedlinePlus