Intracellular acidosis is a putative agent of skeletal muscle fatigue, in part, because it
depresses the calcium (Ca2+) sensitivity of the myofilaments. However, the molecular …

Repeated, intense contractile activity compromises the ability of skeletal muscle to generate
force and velocity, resulting in fatigue. The decrease in velocity is thought to be due, in part …

Acidosis (low pH) is the oldest putative agent of muscular fatigue, but the molecular
mechanism underlying its depressive effect on muscular performance remains unresolved …

The loss of muscle force and power during fatigue from intense contractile activity is
associated with, and likely caused by, elevated levels of phosphate (P _ i P i) and hydrogen …

In striated muscle, calcium binding to the thin filament (TF) regulatory complex activates
actin–myosin ATPase activity, and actin–myosin kinetics in turn regulates TF activation …

Muscle fatigue from intense contractile activity is thought to result, in large part, from the
accumulation of inorganic phosphate (Pi) and hydrogen ions (H+) acting to directly inhibit …

Elevated levels of the metabolic by-products, including acidosis (ie, high [H+]) and
phosphate (Pi) are putative agents of muscle fatigue; however, the mechanism through …

Intense contractile activity of skeletal muscle lasting even a few minutes results in a rapid
decline in its ability to generate force, velocity, and power—a phenomenon that …

ATP provides the energy in our muscles to generate force, through its use by myosin
ATPases, and helps to terminate contraction by pumping Ca2+ back into the sarcoplasmic …

The current study was undertaken to investigate the relative contribution of calcium and
myosin binding to thin filament activation. Using the in vitro motility assay, myosin strong …