title: Physiological and biochemical effects of iron deficiency on rat skeletal muscle.
abstract: Young rats were made iron deficient by feeding them a low-iron diet for 8 wk. Iron deficiency resulted in a 50% decrease in cytochrome c and cytochrome oxidase and a 26% decrease in mitochondrial glycerol-3-phosphate dehydrogenase activity in skeletal muscle. Respiratory capacity of muscle homogenates was reduced 55%. After 8 days of iron treatment, respiratory capacity, cytochrome c, cytochrome oxidase, and glycerol-3-phosphate dehydrogenase had returned 50% toward normal. Maximum O2 uptake of contracting hindlimb muscles averaged 8.5 mumol O2.min-1.g-1 in control, 4.3 mumol O2.min-1.g-1 in iron-deficient, and 6.2 mumol O2.min-1.g-1 in the 8-day-iron-repleted rats. Muscle fatigue during 10 min of stimulation was greater in the iron-deficient group. Lactate concentration in red muscle was higher in iron-deficient than in control rats after stimulation. The muscle fatigue and lactate responses returned 50% toward normal during 8 days of iron treatment. We conclude that iron deficiency results in a decrease in skeletal muscle capacity for aerobic metabolism and, by this mechanism, increases susceptibility to fatigue.
mesh_terms: D000818:Animals; D003574:Cytochrome c Group / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005993:Glycerolphosphate Dehydrogenase / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D006614:Hindlimb; D007501:Iron / Q000097:blood / Q000494:pharmacology; D000090463:Iron Deficiencies; D008297:Male; D009119:Muscle Contraction; D009132:Muscles / Q000378:metabolism / Q000503:physiopathology*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats
chemical_list: D003574:Cytochrome c Group; D006454:Hemoglobins; D007501:Iron; D005993:Glycerolphosphate Dehydrogenase; D003576:Electron Transport Complex IV