Transient hyperpolarization of non‐contracting muscle fibres in anaesthetized rats.

Abstract

SUMMARY1. Following laminectomy, the L5 ventral roots of anaesthetized rats were split and approximately half of the nerve fibres were stimulated at 40 Hz. Resting membrane potentials were then measured in previously contracting and noncontracting soleus muscle fibres.2. In the non-contracting soleus fibres there was a post-tetanic increase in mean resting potential (from -822+ 7-1 (S.D.) to -91-6+ 87 mV) which was similar to that in contracting fibres (from -83-02 + 6-1 to -913 + 7.3 mV). In both types of fibres the hyperpolarizing responses (HRs) were evidently due to increased sodium pump activity since they could be abolished by the addition of ouabain (1 x 10-4 M) to the bathing fluid.3. The fl-adrenergic antagonist, propranolol, completely suppressed HRs in the non-contracting fibres and produced moderate reductions in the contracting ones. The a-adrenergic blocking agent, phentolamine, had no effect on the contracting fibres and only a modest, inhibitory, one on the non-contracting fibres.4. On the basis of the above drug actions it appeared that catecholamines were necessary for the full development of HRs in contracting and non-contracting fibres; noradrenaline, released from intramuscular sympathetic nerve endings, may have been involved.5. The increased sodium pump activity in the non-contracting fibres would serve to moderate the rise in interstitial [K+] caused by K+ efflux from the contracting fibres. By preventing passive depolarization, due to the rise in interstitial [K+], the sodium pump would also maintain the availability of non-contracting fibres for subsequent recruitment.

High-frequency submaximal stimulation over muscle evokes centrally generated forces in human upper limb skeletal muscles

“…Second, norepinephrine release from the muscle sympathetic fibres is one factor facilitating the active transport of Na ϩ -K ϩ that alters the excitability of the muscle fibre membrane (e.g., Refs. 34,39). This mechanism might explain some muscle potentiation with high-frequency trains and its abolition after nerve blocks.…”

Na+-K+Pump Regulation and Skeletal Muscle Contractility

“…In rat soleus, the early phase of electrical stimulation in vivo induced hyperpolarization and increased M-wave area, effects that were suppressed by ouabain (204,262). This hyperpolarization is likely to reflect the electrogenic action of the Na ϩ -K ϩ pump.…”

“…5) Following electrical stimulation in vivo, hyperpolarization of the fibers has been observed in 10-to 12-wk old mice (146) and large rats (204,262). This hyperpolarization was blocked by ouabain, indicating that it reflects the electrogenic contribution of the Na ϩ -K ϩ pump to the membrane potential.…”

“…The possible mechanism for the hyperpolarization induced by electrical stimulation in vivo was explored in an elegant experiment where the nerve supplying the soleus muscle of the rat was split so as to allow stimulation of about half the axons supplying the muscle, leaving the other half denervated and with no contractile response to stimulation of the nerve (262). The connection of the preserved axons to the muscle fibers was confirmed by the detection of action potentials elicited by stimulation of the nerve fibers.…”

The influence of contraction amplitude and firing history on spike‐triggered averaged trapezius motor unit potentials

“…The mechanism is increased Na + -K + pump activity due to elevated K + concentration in the interstitial fluid, causing membrane hyperpolarization and larger muscle fibre action potentials both in active and inactive muscle fibres (Hicks & McComas, 1989;Kuiack & McComas, 1992). Several studies indicate an increase of 10-30% following tetanic stimulation, assessed as transient increase in M-wave (West et al 1996;Harrison & Flatman, 1999) and in motor unit potentials elicited by nerve stimulation (Thomas et al 2004).…”