Physiological and biochemical effects of iron deficiency on rat skeletal muscle
McLane, J.A.; Fell, R.D.; McKay, R.H.; Winder, W.W.; Brown, E.B.; Holloszy, J.O.
American Journal of Physiology 241(1): C47-C54
1981
ISSN/ISBN: 0002-9513 PMID: 6264804 Document Number: 172312
Young rats were made Fe-deficient by feeding them a low-Fe diet for 8 wk. Fe 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 Fe 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 .mu.mol O2 .cntdot. min-1 .cntdot. g-1 in control, 4.3 .mu.mol O2 .cntdot. min-1 .cntdot. g-1 in Fe-deficient, and 6.2 .mu.mol O2 .cntdot. min-1 .cntdot. g-1 in the 8 day Fe-repleted rats. Muscle fatigue during 10 min of stimulation was greater in the Fe-deficient group. Lactate concentration in red muscle was higher in Fe-deficient than in control rats after stimulation. The muscle fatigue and lactate responses returned 50% toward normal during 8 days of Fe treatment. Fe deficiency apparently results in a decrease in skeletal muscle capacity for aerobic metabolism and, by this mechanism, increases susceptibility to fatigue.