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Changes of intracellular milieu with fatigue or hypoxia depress contraction of skinned rabbit skeletal and cardiac muscle.
Simple summation of all significant changes expected from each constituent altered by fatigue/hypoxia adequately predicted the observed changes in Fmax and Ca2+ sensitivity in both cardiac and skeletal muscle fibres with but one exception (the change in Ca2- sensitivity of skeletal muscle at pH 7 was slightly overestimated). Expand
Deficiency of MIP/MTMR14 phosphatase induces a muscle disorder by disrupting Ca2+ homeostasis
It is reported that mice deficient in the newly identified PtdInsP (phosphatidylinositol phosphate) phosphatase MIP/MTMR14 (muscle-specific inositolosphatase) show muscle weakness and fatigue, and the first evidence that finely controlled Ptd insurance levels in muscle cells are essential for maintaining Ca2+ homeostasis and muscle performance is provided. Expand
Muscle aging is associated with compromised Ca2+ spark signaling and segregated intracellular Ca2+ release
Using repetitive voltage stimulation on isolated muscle preparations, a segregated [Ca2+]i reserve is identified that uncouples from the normal excitation–contraction process in aged skeletal muscle, suggesting that MG29 expression is important in maintaining skeletal muscle Ca2+ homeostasis during aging. Expand
Truncation by Glu180 Nonsense Mutation Results in Complete Loss of Slow Skeletal Muscle Troponin T in a Lethal Nemaline Myopathy*
It is found that neither the intact nor the truncated slow TnT protein was present in the muscle of patients with ANM, consistent with the observed recessive pattern of inheritance of the disease and indicates a critical role of the COOH-terminal T2 domain in the integration of Tn T into myofibrils. Expand
Enhanced resistance to fatigue and altered calcium handling properties of sarcalumenin knockout mice.
The data suggest that systemic ablation of sarcalumenin caused enhanced resistance to muscle fatigue by compensatory changes in Ca2+ regulatory proteins that effect SOCE. Expand
Pinacidil suppresses contractility and preserves energy but glibenclamide has no effect during muscle fatigue.
The glibenclamide effects suggest that fatigue, elicited with intermittent contractions, activates few K(ATP) channels that affect resting tension and membrane potentials but not tetanic force, whereas opening the channel with pinacidil causes a faster decrease in tetanicforce, improves force recovery, and helps in preserving energy. Expand
Muscle Fatigue from the Perspective of a Single Crossbridge.
The repeated intense stimulation of skeletal muscle rapidly decreases its force- and motion-generating capacity. This type of fatigue can be temporally correlated with the accumulation of metabolicExpand
Increased superoxide production during fatigue in the perfused rat diaphragm.
O2- levels were determined minute to minute by measuring the reduction of cytochrome c in the perfusate as the diaphragms were subjected to various levels of contractile activity, indicating long-lasting effects on the contractile machinery. Expand
Hydrogen peroxide disrupts Ca2+ release from the sarcoplasmic reticulum of rat skeletal muscle fibers.
Elevated levels of H2O2 with exercise are capable of damaging one or more proteins of the excitation-contraction coupling process to produce a disruption in function that can account, at least in part, for the long-lasting effects of fatiguing stimulation. Expand
Inhibitory influence of phosphate and arsenate on contraction of skinned skeletal and cardiac muscle.
It was found that both Pi and Asi were more effective in decreasing Fmax as the pH was lowered (i.e., as the concentration of the diprotonated forms increased), while soleus and cardiac fibers did not exhibit this behavior. Expand