Mitochondrial Ca2+ in Mouse Soleus Single Muscle Fibres in Response to Repeated Tetanic Contractions
Mitochondrial diseases form a heterogeneous group of disorders in which mutations of the mitochondrial material frequently results in muscle dysfunction. Mammalian skeletal muscle fibres are particularly rich in mitochondria, which may make up about 10 to 15 % of a fibre’s volume (Eisenberg, 1983; Chen et al., 2001). Mitochondria are differentially distributed in many rodent skeletal muscles, with a higher density found close to the sarcolemma than deep in the fibre (Eisenberg et al., 1983; Philippi & Sillau, 1994). It has long been accepted that a key function of mitochondria is to supply energy as required by the working muscle. (1990) proposed that Ca2+ plays a key role in this process by activating three key mitochondrial dehydrogenases. More recently, a rise in mitochondrial Ca2+ was suggested to directly stimulate mitochondrial oxidative phosphorylation (Kavanagh et al., 2000). While circumstantial evidence suggests that mitochondria in skeletal muscle are able to modulate their Ca2+ content, surprisingly little is know about Ca2+ movement into and out of the mitochondria in intact skeletal muscle cells during and after a bout of contractile activity. Several groups have reported that mitochondria isolated from skeletal muscle after exhaustive exercise have a higher Ca2+ content than those obtained from non-exercised muscle (Duan et al., 1990; Madsen et al., 1996). Other groups have reported that mitochondria are swollen or disrupted in skeletal muscle isolated from animals that were exercised to exhaustion, (Gollnick & King, 1969; McCutcheon et al., 1992; Sakai et al., 1999).
KeywordsSkeletal Muscle Soleus Muscle Mammalian Skeletal Muscle Skeletal Muscle Mitochondrion Soleus Fibre
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