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The site of exercise-induced muscle fatigue is suggested to be the muscle membrane, which includes the sarcolemma and T-tubule membrane; the excitability of the membrane is dependent on the membrane potential. Significant potassium flux from the intracellular space of contracting muscle may decrease
Chronic fatigue syndrome (CFS) in human patients remain a controversial and perplexing condition with emerging zoonotic aspects. Recent advances in human medicine seem to indicate a bacterial etiology and the condition has already been described in horses, dogs, cats and birds of prey in association
Muscle activity is associated with potassium displacements, which may cause fatigue. It was reported previously that the density of the large-conductance Ca2+-dependent K+ (BK(Ca)) channel is higher in the T tubule membrane than in the sarcolemmal membrane and that the opposite is the case for the
Although previous experiments with a partially similar objective have been described in dogs, cats and rabbits, the purpose of this study was to identify and characterize mechanosensitive and chemosensitive muscle afferents in the anaesthetized rat since it is a widely used laboratory animal. The
OBJECTIVE
Skeletal muscle fatigue has been associated with potassium efflux from the myocytes, resulting in endogenous increases in blood potassium concentration ([K+]). Conversely, exogenous increases in extracellular [K+] potentiates contraction in isolated muscle preparations. The mechanisms
Local muscle fatigue may be related to potassium efflux from the muscle cell and/or lactate accumulation within the muscle. Local fatigue causes a decrease in median frequency (MPF) of the electromyogram's power spectrum during isometric contractions but its relationship to changes in potassium and
A general finding is that muscle activity leads to potassium fluxes across the muscle membrane as well as to muscle fatigue, defined as a reduction in the force-generating capacity of the muscle. However, much controversy exists regarding the causal role of potassium in fatigue development. The
The relationships between extracellular potassium elevation and EMG variables in relation to muscle fatigue were investigated during handgrip exercise in humans. Acid-base state, lactate, potassium ([K+](v)) and sodium in venous plasma, as well as variables of surface voluntary and evoked (M-wave)
The activity of ATP-sensitive potassium channels of skeletal muscle is controlled by changes in the bioenergetic state of the cell. These channels are inactive in unfatigued muscle and become activated during fatigue. It has been postulated that ATP-sensitive potassium channels shorten the action
Accumulation of K+ in skeletal muscle interstitium during intense exercise has been suggested to cause fatigue in humans. The present study examined interstitial K+ kinetics and fatigue during repeated, intense, exhaustive exercise in human skeletal muscle. Ten subjects performed three repeated,
Environment-friendly lead-free piezoelectric materials with high piezoelectric response and high stability in a wide temperature range are urgently needed for various applications. In this work, grain orientation-controlled (with a 90% ⟨001⟩c-oriented texture) (K,Na)NbO3-based ceramics with a large
An in vivo porcine model of endotoxaemia was used to study the effects of glibenclamide, a K+ ATP-sensitive potassium channel blocker. Escherichia coli lipopolysaccharides (LPS, 70 micrograms/kg, i.v., as a bolus) were infused into anaesthetized, mechanically ventilated, indomethacin-treated pigs.
The role of mitochondrial K(ATP) (mitoK(ATP)) channels on muscle fatigue was assessed in adult mouse skeletal muscle bundles. Muscle fatigue was produced by eliciting short repetitive tetani. Isometric tension and the rate of production of reactive oxygen species (ROS) were measured at room
During contractile activity, skeletal muscles undergo a net loss of cytoplasmic K(+) to the interstitial space. During intense exercise, plasma K(+) in human arterial blood may reach 8 mm, and interstitial K(+) 10-12 mm. This leads to depolarization, loss of excitability and contractile force.
The main aim was to investigate the effects of raised [K+](o) on contraction of isolated non-fatigued skeletal muscle at 37°C and 25°C to assess the physiological significance of K+ in fatigue. Mouse soleus muscles equilibrated at 25°C had good mechanical stability when temperature was elevated to