Abstract
Muscle fatigue and muscle weakness: what we know and what we wish we did
Highlights
Fatigue and weakness may stem from changes within myocytes that affect cross-bridge function or Ca2+ activation, to changes within the circulation or function of the nervous system
Metabolic products of ATP hydrolysis in the cytoplasm such as inorganic phosphate (Pi), protons (H+ or pH), and ADP have often been considered as agents that could disrupt force generation at the sarcomere level (Fabiato and Fabiato, 1978; Cooke and Pate, 1985; Metzger and Moss, 1987; Nosek et al, 1987, 1990; Chase and Kushmerick, 1988, 1995; Cooke et al, 1988; Godt and Nosek, 1989; Pate and Cooke, 1989; Metzger and Moss, 1990a,b; Pate et al, 1995, 1998; Wiseman et al, 1996; Karatzaferi et al, 2003, 2008). These effects may be due to direct binding to proteins, or due to a more global alteration of cellular energetics ( GATP) in the myocyte (Karatzaferi et al, 2004)
Allen and Trajanovska (2012) provide a synthesis on the multiple roles of Pi in fatigue, including novel results from their group, showing that Pi is even more detrimental when its effects on Ca2+ release are combined with inhibition of actomyosin force generation and Ca2+ activation
Summary
Fatigue and weakness may stem from changes within myocytes that affect cross-bridge function or Ca2+ activation, to changes within the circulation or function of the nervous system. These effects may be due to direct binding to proteins, or due to a more global alteration of cellular energetics ( GATP) in the myocyte (Karatzaferi et al, 2004).
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