Effect of Chronic Stimulation on Cation Distribution and Membrane Potential in Fast-Twitch Muscles of Rabbit

doi:10.1515/9783110837483-035

Cited by 8 publications

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“…Previous studies have shown that electrical stimulation increases the influx and accumulation of Ca 2+ in skeletal muscle (Bianchi & Shanes, 1959;Curtis, 1966;Sreter et al 1980;Everts et al 1993;Gissel & Clausen, 1999. A maximum of only 20% of the excitationinduced Ca 2+ influx occurs via L-type Ca 2+ channels, the remaining possibly occurring through voltage gated Na + channels (Gissel & Clausen, 1999).…”

Section: Ca Uptake and Ca 2+ Contentmentioning

confidence: 99%

“…During muscle excitation, the influx of Ca 2+ is markedly increased, leading to a progressive intracellular accmulation of Ca 2+ both in vitro (Bianchi & Shanes, 1959; Curtis, 1966; Gissel & Clausen, 1999, 2000) and in vivo (Sreter et al 1980; Everts et al 1993). Ca 2+ may enter normal, contracting muscle cells through voltage gated Na + channels, through voltage gated L‐type Ca 2+ channels (Gissel & Clausen, 1999, 2001) and through stretch‐activated channels (Belcastro et al 1996; McBride et al 2000).…”

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confidence: 99%

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Excitation‐induced Ca²⁺ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Mikkelsen

Fredsted

Gissel

et al. 2004

The Journal of Physiology

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Prolonged or unaccustomed exercise leads to loss of contractility and muscle cell damage. The possible role of an increased uptake of Ca 2+ in this was explored by examining how graded fatiguing stimulation, leading to a graded uptake of Ca 2+ , results in progressive loss of force, impairment of force recovery, and loss of cellular integrity. The latter is indicated by increased [14 C]sucrose space and lactic acid dehydrogenase (LDH) release. Isolated rat extensor digitorum longus (EDL) muscles were allowed to contract isometrically using a fatiguing protocol with intermittent stimulation at 40 Hz. Force declined rapidly, reaching 11% of the initial level after 10 min and stayed low for up to 60 min. During the initial phase (2 min) of stimulation 45 Ca uptake showed a 10-fold increase, followed by a 4-to 5-fold increase during the remaining period of stimulation. As the duration of stimulation increased, the muscles subsequently regained gradually less of their initial force. Following 30 or 60 min of stimulation, resting 45 Ca uptake, [ 14 C]sucrose space, and LDH release were increased 4-to 7-fold, 1.4-to 1.7-fold and 3-to 9-fold, respectively (P < 0.001). The contents of Ca 2+ and Na + were also increased (P < 0.01), a further indication of loss of cellular integrity. When fatigued at low [Ca 2+ ] o (0.65 mM), force recovery was on average twofold higher than that of muscles fatigued at high [Ca 2+ ] o (2.54 mM). Muscles showing the best force recovery also had a 41% lower total cellular Ca 2+ content (P < 0.01). In conclusion, fatiguing stimulation leads to a progressive functional impairment and loss of plasma membrane integrity which seem to be related to an excitation-induced uptake of Ca 2+ . Mechanical strain on the muscle fibres does not seem a likely mechanism since very little force was developed beyond 10 min of stimulation. Intense exercise, such as extended periods of running, strength training, sprinting or eccentric exercise, disrupts the normal ultrastructure of skeletal muscle (Waterman-Storer, 1991;Belcastro, 1993;Belcastro et al. 1998). Impaired force recovery seen after intense exercise can be due to structural damage such as myofibrillar and cytoskeletal disruptions often leading to Z-disc streaming (Hoppeler, 1986; WatermanStorer, 1991;Appell et al. 1992;Gibala et al. 1995), as well as disturbances to mitochondria and the SR-T-tubular system (Hoppeler, 1986;Gibala et al. 1995). Loss of sarcolemmal integrity has also repeatedly been reported after prolonged or unaccustomed exercise (e.g. Stupka et al. 2001;Clarkson & Hubal, 2002), contributing to the functional impairment.Several mechanisms have been proposed to explain the functional impairment and it is unlikely to be caused by one single factor. The causes of functional impairment could be either mechanical damage due to eccentric contractions (Armstrong, 1986(Armstrong, , 1990, loss of excitability (Nielsen & Overgaard, 1996;Clausen, 1996;Overgaard et al. 1999;Carlsen & Villarin, 2002), or Ca 2+ -induced damage (Gissel & Cl...

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Section: Ca Uptake and Ca 2+ Contentmentioning

confidence: 99%

mentioning

confidence: 99%

Excitation‐induced Ca²⁺ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Mikkelsen

Fredsted

Gissel

et al. 2004

The Journal of Physiology

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“…Continuous stimulation at 10 Hz Ion contents. In order to allow comparison with earlier reports (Sreter 1963, Sreter et al 1980, the study was initiated by a pilot experiment, where the Na+ and K' contents in SOL, EDL and T A muscle were determined after 24 h or 7 d of continuous stimulation at 10 Hz. As shown in Figure 1, 24 h of stimulation produced a decrease in K+ content and an increase in Na+ content in all three muscles.…”

Section: R E S U L T Smentioning

confidence: 99%

Changes in K+, Na⁺ and calcium contents during in vivo stimulation of rat skeletal muscle

Everts

Lømo

Clausen

1993

Acta Physiologica Scandinavica

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The effects of in vivo stimulation via the sciatic nerve on Na+, K+ and calcium contents in slow-twitch and fast-twitch muscles were compared. Whereas intermittent stimulation for 24 h at 20 Hz caused only minor changes in soleus (SOL), a considerable loss of K+ (around 24%) and gain of Na+ (around 84%) was observed in extensor digitorum longus (EDL) and tibialis anterior (TA) muscles. These changes could be detected within 0.5 h and a plateau was maintained from 2 to 24 h. Total calcium content increased progressively, reaching values 245 and 382% above the control level in EDL and TA muscle, respectively, after 24 h of 20 Hz stimulation. Whereas the Na+ and K+ content recovered within a few hours, calcium content did not return towards control level until after 48 h of rest. In a pilot study performed with continuous stimulation at 10 Hz, the changes in Na+ and K+ contents in SOL, EDL and TA muscle were comparable to those at 20 Hz. The concentration of the Na(+)-K+ pumps was highest in the fast-twitch EDL and TA muscles and was unaffected by 10 Hz stimulation. It is concluded that a stimulation pattern leading to a rise in intracellular Na+ and a loss of K+ may cause a marked accumulation of calcium. These events seem to be related to insufficient activation of the Na-K+ pump rather than to variations in the total Na(+)-K+ pump capacity.

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“…A large increase in total Ca 2+ content of hindlimb muscle has been observed following long-term electrical stimulation at low-frequency in vivo in both rabbit (Sreter et al 1980) and rat (Everts et al 1993). Recently, it has been reported that in rat muscle also in vitro longterm low-frequency stimulation was associated with an increase in the total muscle Ca 2+ content (Gissel and Clausen 1999).…”

Section: Introductionmentioning

confidence: 99%

“…The larger uptake of 45 Ca observed in EDL compared to soleus muscle was well in keeping with earlier reports showing that prolonged electrical stimulation at low frequency favoured the accumulation of Ca 2+ only in muscles mainly composed of fast-twitch ®bres, such as peroneus, EDL and tibialis anterior. In soleus muscle which is mainly composed of slow-twitch ®bres, no accumulation of Ca 2+ has been observed (Everts et al 1993;Sreter et al 1980). The reason for the dierence between the two types of muscle ®bres is not yet understood.…”

Section: Introductionmentioning

confidence: 99%

Ca 2+ accumulation and cell damage in skeletal muscle during low frequency stimulation

Gissel

2000

European Journal of Applied Physiology

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Electrical stimulation has been shown to produce a marked increase in Ca2+ influx and Ca2+ content in rat skeletal muscle. Long-term low-frequency stimulation (1 Hz, 240 min) increased 45Ca uptake by 30% and 154% in soleus and extensor digitorum longus muscles, respectively. Studies using Ca2+-fluorescent dyes have shown that intracellular concentrations of free Ca2+ are increased up to threefold during long-term low-frequency stimulation, suggesting that muscle cells have difficulties in handling the Ca2+ taken up during stimulation. Furthermore, long-term low-frequency stimulation induces leakage of the intracellular enzyme lactate dehydrogenase from the muscles. This leakage may reflect degradation of membrane proteins by the Ca2+-activated neutral protease calpain. This, in turn, leads to further influx of Ca2+ and further acceleration of protein breakdown. Membrane leakages are likely to result in sensations of pain in the damaged muscle. It is suggested that Ca2+ plays a central role in the development of muscle fibre injury during prolonged muscle activity of workers using a computer mouse.

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Effect of Chronic Stimulation on Cation Distribution and Membrane Potential in Fast-Twitch Muscles of Rabbit

Cited by 8 publications

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Excitation‐induced Ca²⁺ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Excitation‐induced Ca²⁺ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Changes in K+, Na⁺ and calcium contents during in vivo stimulation of rat skeletal muscle

Ca 2+ accumulation and cell damage in skeletal muscle during low frequency stimulation

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Effect of Chronic Stimulation on Cation Distribution and Membrane Potential in Fast-Twitch Muscles of Rabbit

Cited by 8 publications

References 0 publications

Excitation‐induced Ca2+ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Excitation‐induced Ca2+ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Changes in K+, Na+ and calcium contents during in vivo stimulation of rat skeletal muscle

Ca 2+ accumulation and cell damage in skeletal muscle during low frequency stimulation

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Resources

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Excitation‐induced Ca²⁺ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Excitation‐induced Ca²⁺ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery

Changes in K+, Na⁺ and calcium contents during in vivo stimulation of rat skeletal muscle