Extracellular Ca2+-induced force restoration in K+-depressed skeletal muscle of the mouse involves an elevation of [K+]i: implications for fatigue
| Autor: | Amanda Higgins, John P. Leader, Denis S. Loiselle, Simeon P. Cairns, Wei Lin, Jean-Marc Renaud |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Male
Physiology Muscle Fibers Skeletal Action Potentials chemistry.chemical_element Calcium Mice Sarcolemma Physiology (medical) medicine Extracellular Animals Potential mechanism Fiber type Muscle fatigue Skeletal muscle Articles Anatomy medicine.anatomical_structure chemistry Muscle Fatigue Potassium Biophysics Female medicine.symptom Muscle Contraction Muscle contraction |
| Zdroj: | Journal of Applied Physiology. 118:662-674 |
| ISSN: | 1522-1601 8750-7587 |
| Popis: | We examined whether a Ca2+-K+ interaction was a potential mechanism operating during fatigue with repeated tetani in isolated mouse muscles. Raising the extracellular Ca2+ concentration ([Ca2+]o) from 1.3 to 10 mM in K+-depressed slow-twitch soleus and/or fast-twitch extensor digitorum longus muscles caused the following: 1) increase of intracellular K+ activity by 20–60 mM (raised intracellular K+ content, unchanged intracellular fluid volume), so that the K+-equilibrium potential increased by ∼10 mV and resting membrane potential repolarized by 5–10 mV; 2) large restoration of action potential amplitude (16–54 mV); 3) considerable recovery of excitable fibers (∼50% total); and 4) restoration of peak force with the peak tetanic force-extracellular K+ concentration ([K+]o) relationship shifting rightward toward higher [K+]o. Double-sigmoid curve-fitting to fatigue profiles (125 Hz for 500 ms, every second for 100 s) showed that prior exposure to raised [K+]o (7 mM) increased, whereas lowered [K+]o (2 mM) decreased, the rate and extent of force loss during the late phase of fatigue (second sigmoid) in soleus, hence implying a K+ dependence for late fatigue. Prior exposure to 10 mM [Ca2+]o slowed late fatigue in both muscle types, but was without effect on the extent of fatigue. These combined findings support our notion that a Ca2+-K+ interaction is plausible during severe fatigue in both muscle types. We speculate that a diminished transsarcolemmal K+ gradient and lowered [Ca2+]o contribute to late fatigue through reduced action potential amplitude and excitability. The raised [Ca2+]o-induced slowing of fatigue is likely to be mediated by a higher intracellular K+ activity, which prolongs the time before stimulation-induced K+ efflux depolarizes the sarcolemma sufficiently to interfere with action potentials. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|