Effects of dietary iron deficiency on lactate metabolism were studied in weanling female rats. Following an iron-deficient diet for 5 weeks, mean hemoglobin concentration was lowered to 6.4 g/dl relative to 12.2 in the control group. Mean plasma iron levels were 58 and 162 #lgldl, respectively. Significantly elevated resting lactate levels were observed in whole blood and plasma from iron-deficient anemic (relative to control) rats. Total activity of lactate dehydrogenase (LDH) was elevated in soleus and gastrocnemius muscles in response to iron deficiency from 269 ± 51 to 364 ± 60 (Mean ± SO) and from 265 ± 65 to 372 ± 61 IUllO-3.g-l , respectively. The LDH activity in heart was lowered from 700 ± 61 to 593 ± 45 IU· 10-3 • g-I. The M 3H and M 2H2 isozymes in soleus were increased from 12.7 ± 2.8 to 20.4 ± 5.8% and from 19.4 ± 6.1 to 28.2 ± 3.6%, respectively. Similar increase was observed in M 2H2 and MH 3 in gastrocnemius from 9.8 ± 0.9 to 14.8 ± 2.0% and from 17.4 ± 2.0 to 20.5 ± 2.3%, respectively.The H4 isozyme was significantly reduced in soleus, gastrocnemius, and plantaris muscles from 27.7 ± 4.7 to 12.4 ± 4.4, from 15.8 ± 1.9 to 7.2 ± 2.9, and from 10.5 ± 2.9 to 3.9 ± 2.1%, respectively. It was suggested that iron-deficiency anemia induces an elevation of lactate production following an increase in total LOH activity and change in LOH isozyme patterns.

Iron may affect both respiratory O2 transport and mitochondrial electron transport in the performance of muscle work. This study was designed to elucidate the molecular defect of iron-deficient work performance by identifying heretofore unmeasurable mitochondrial enzymes that are diminished by iron deficiency and may be restored by iron repletion. Female rats were made iron-deficient by dietary control and were repleted by oral iron. Iron deficiency reduced physical work capacity (treadmill running time), haemoglobin (Hb), and mitochondrial iron-sulphur (Fe-S) centres in heart and skeletal muscles; mitochondrial number was unaffected. Oral iron supplementation restored work capacity and Hb within 4 d to normal or near-normal levels, but in general Fe-S centres of mitochondria due to NADH dehydrogenase remained at iron-deficient levels. Subnormal concentrations of mitochondrial iron-dependent NADH dehydrogenase in muscle are not by themselves rate-limiting in work performance.

Effect of Creatine depletion by fl-guanidinopropionic acid (/3-GPA) feeding on mitochondrial morphology was studied in rats. Following /3-GPA feeding for 9 weeks, intramitochondrial inclusions running parallel to the long axis of mitochondrion were observed in skeletal muscles. A bundle of inclusions consisted of four parallel arrays containing electron-dense materials. Two outer arrays were continuous with cristal membranes and two inner arrays were chains of fine particles. Mitochondria with such inclusions were elongated probably in only a certain direction even though it was suggested that the layers of cristae were straightened two-dimensionally. Longer mitochondria ran parallel to the muscle fibers. It was also suggested that chronic stimulation of mitochondria) biogenesis by depletion of high energy phosphates may induce such inclusions within mitochondria. inclusions, rat skeletal muscle, j3-It is reported that cold acclimation enlarged the mitochondrial size in rat skeletal muscles (YAHATA and KUROSHIMA, 1977). In these muscles, the mitochondrial cristae and sarcoplasmic reticuli developed better than in the control muscles. Cold acclimation of rats also increased the activity of succinate dehydrogenase in soleus muscle fibers (MATOBA and MURAKAMI, 1981), although the mechanism of morphological and metabolic changes in mitochondria is still unclear. However, our previous study showed that the activity of gastrocnemius oxidative enzymes were elevated when the contents of adenosine triphosphate (ATP) were decreased following the chronic exposure to cold (4°C) In frogs (OHIRA and OHIRA, 1988).