Is interstitial K+accumulation a key factor in the fatigue process under physiological conditions?

Autor: Nicolas Place
Rok vydání: 2008
Předmět:
medicine.medical_specialty
Epinephrine
Physiology
Calcitonin Gene-Related Peptide
Skeletal Muscle And Exercise
Potassium/*metabolism/pharmacology
Stimulation
In Vitro Techniques
Contractile protein
Muscle
Skeletal/drug effects/innervation/*metabolism
ddc:616.9802
Physical Conditioning
Animal/physiology
Physical Conditioning
Animal
Exercise/physiology
medicine
Insulin
Animals
Humans
Albuterol
Letters
Muscle Strength
Rats
Wistar
Muscle
Skeletal
Exercise
Muscle force
Soleus muscle
Muscle Fatigue/drug effects/*physiology
Dose-Response Relationship
Drug
Muscle fatigue
Chemistry
Endoplasmic reticulum
Sodium
Adrenergic beta-Agonists
Muscle endurance
Oxygen/metabolism
Electric Stimulation
Rats
Surgery
Oxygen
Muscle Fatigue
Physical Endurance
Potassium
Biophysics
Sodium-Potassium-Exchanging ATPase/physiology
Sodium-Potassium-Exchanging ATPase
Myofibril
Muscle Contraction/physiology
Muscle Contraction
Zdroj: The Journal of Physiology, Vol. 586, No 4 (2008) pp. 1207-1208; author reply 1209
ISSN: 0022-3751
DOI: 10.1113/jphysiol.2007.150292
Popis: Muscle fatigue, i.e. the decrease in muscle force in response to prolonged or repeated contractions, can originate from any impairment along the neuromuscular system, from a reduction in central neural drive to impaired contractile protein interaction. At the muscle level, a decrease in the force-generating capacity can result from (i) an impaired force per cross-bridge, (ii) a reduced myofibrillar Ca2+ sensitivity and (iii) a decreased Ca2+ release from the sarcoplasmic reticulum (SR). During prolonged activity, the interstitial K+ increases and concentrations of 10–12 mm have been observed. Therefore, resultant sarcolemmal excitability, leading to a reduction in the amplitude of the action potential, can result in impaired SR Ca2+ release. This last factor was the point of interest in a recent article in The Journal of Physiology by Clausen & Nielsen (2007), that investigated the effect of excitability failure on force production during fatigue of rat soleus muscle exposed to different bath K+ concentrations ([K+]o). Clausen & Nielsen showed that the rate of force decline was greater when muscle was pre-exposed for 10–40 min to a high [K+]o (10 mm) and then electrically stimulated compared with low [K+]o (4 mm). They also showed that this increased fatigability could be counteracted by applying different agents known to directly or indirectly stimulate the Na+–K+ pumps. Thus, the data obtained by Clausen & Nielsen (2007) strongly indicate that these high [K+]o values induce a reduction in sarcolemmal excitability, leading to a decrease in soleus endurance which can be prevented by the stimulation of the Na+–K+ pump. Nevertheless, it is possible that these results are confined to the experimental conditions used to induce fatigue. In their study, Clausen & Nielsen (2007) stimulated soleus muscle continuously at 60 Hz for 1 min; muscle endurance was then assessed by calculating the rate of force decline over the first 20 s of stimulation. In this letter, the possibility that a rise in [K+]o may not be a critical factor of muscle fatigue under physiological conditions is discussed.
Databáze: OpenAIRE
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