Excitation-induced cell damage and β2-adrenoceptor agonist stimulated force recovery in rat skeletal muscle
| Autor: | Torben Clausen, Hanne Gissel, Ulla Ramer Mikkelsen, Anne Fredsted |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Male
Long lasting medicine.medical_specialty Epinephrine Physiology Muscle Fibers Skeletal Calcitonin gene-related peptide Membrane Potentials Physiology (medical) Internal medicine medicine Animals Myocyte Albuterol Rats Wistar Na+/K+-ATPase Muscle Skeletal Ouabain Adrenergic beta-2 Receptor Agonists Cell damage Chemistry Sodium Skeletal muscle Anatomy β2 adrenoceptor agonist Adrenergic beta-Agonists medicine.disease Propranolol Rats Endocrinology medicine.anatomical_structure Potassium Calcium Female Receptors Adrenergic beta-2 |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 290:R265-R272 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.00392.2005 |
| Popis: | Intensive exercise leads to a loss of force, which may be long lasting and associated with muscle cell damage. To simulate this impairment and to develop means of compensating the loss of force, extensor digitorum longus muscles from 4-wk-old rats were fatigued using intermittent 40-Hz stimulation (10 s on, 30 s off). After stimulation, force recovery, cell membrane leakage, and membrane potential were followed for 240 min. The 30–60 min of stimulation reduced tetanic force to ∼10% of the prefatigue level, followed by a spontaneous recovery to ∼20% in 120–240 min. Loss of force was associated with a decrease in K+ content, gain of Na+ and Ca2+ content, leakage of the intracellular enzyme lactic acid dehydrogenase (10-fold increase), and depolarization (13 mV). Stimulation of the Na+-K+ pump with either the β2-adrenoceptor agonist salbutamol, epinephrine, rat calcitonin gene-related peptide (rCGRP), or dibutyryl cAMP improved force recovery by 40–90%. The β-blocker propranolol abolished the effect of epinephrine on force recovery but not that of CGRP. Both spontaneous and salbutamol-induced force recovery were prevented by ouabain. The salbutamol-induced force recovery was associated with repolarization of the membrane potential (12 mV) to the level measured in unfatigued muscles. In conclusion, in muscles exposed to fatiguing stimulation leading to a considerable loss of force, cell leakage, and depolarization, stimulation of the Na+-K+ pump induces repolarization and improves force recovery, possibly due to the electrogenic action of the Na+-K+ pump. This mechanism may be important for the restoration of muscle function after intense exercise. |
| Databáze: | OpenAIRE |
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