Congenital vertical talus: surgical correction by a one-stage medial approach.

A single stage procedure for correction of congenital vertical talus using a medial approach is described. The operation was performed on 14 feet with good initial anatomical results in all cases. No wound healing complications were observed.

Exercise capacity and cardiac function of rats with drug-induced cardiac enlargement.

A study was undertaken to determine if sustained administration of isoproterenol (ISO) alters biochemical and functional properties of hearts and the submaximal and maximal exercise capacity of rodents. Compared with sham-treated controls of the same age, sex, and body weight, 4 wk of ISO (0.2--0.4 mg/kg sc) produced an approximate 30% increase in combined ventricle wet weight (P less than 0.001). Respiratory capacity of homogenates, total muscle protein concentration, and actomyosin and myofibril ATPase of heart muscle of the ISO-treated group were the same as in the control group. Various cardiac function parameters in situ, obtained under control conditions and in response to tyramine-induced norepinephrine release, were similar for the two groups. ISO-treated rats had slightly greater endurance for running submaximally on a treadmill than the control rats (P less than 0.10), but their maximal capacity to utilize oxygen (VO2max) was not different from controls. These findings suggest that rodent hearts moderately enlarged by relatively low doses of isoproterenol possess normal metabolic and functional capacity. However, this cardiac enlargement had no apparent effect on maximal exercise performance of the whole animal.

Effect of functional overload on substrate oxidation capacity of skeletal muscle.

We determined the effects of surgically induced functional overload (O) on rodent fast-twitch plantaris (P) and slow-twitch soleus (S) skeletal muscle substrate oxidative capacity. Compared with normal control muscles of weight-matched rats, bilateral overload produced 68 and 23% increases in the wet weight of OP and OS muscles, respectively (p less than 0.05). Total protein concentrations of the O muscles remained unchanged relative to controls. The enzymatic capacity to oxidize pyruvate, palmitate, and alpha-glycerophosphate was unchanged in OP muscles relative to controls. Certain ketone oxidative enzyme markers were increased in the whole as well as in the inner "red" and outer "white" regions of OP muscle. Citrate synthase activity (a marker for tricarboxylic acid cycle oxidative capacity) was decreased in the whole and in the red region but unchanged in the white region of OP muscles. In contrast, the above measurements were significantly decreased in the OS muscles compared with controls (p less than 0.05). These findings suggest that there is both an expansion and a change in composition of the mitochondrial pool of enlarged P muscle. The effects on OS muscle, however, suggest the possibility that the oxidative capacity is not altered parallel with the enlargement, although fibre-typing (fast-twitch to slow-twitch) changes and altered mitochondrial composition could also contribute in part to the change.

Respiratory capacity and glycogen depletion in thyroid-deficient muscle.

This study was undertaken to determine the effects of propylthiouracil-induced thyroid deficiency on a) the capacity of muscle homogenates to oxidize [2-14C]pyruvate and [U-14C]palmitate and b) glycogen depletion during exercise in liver and in fast-oxidative-glycogenolytic (FOG), fast-glycogenolytic (FG), and slow-oxidative (SO) muscle. Relative to the rates for normal rats, oxidation with pyruvate was reduced by 53, 68, and 58%, and palmitate by 40, 50, and 48% in FOG, FG, and SO muscle, respectively (P less than 0.05). Normal rats ran longer than thyroid-deficient rats at 26.7 m/min (87 +/- 8 vs. 37 +/- 5 min). After 40 min of running (22 m/min), the amount of glycogen consumed in normal FOG, FG, and SO muscle and in liver amounted to only 23, 12, 66, and 52%, respectively, of that for their thyroid-deficient counterparts. Also, normal rats maintained higher plasma free fatty acid levels than thyroid-deficient rats during both rest and exercise (P less than 0.05). These findings suggest that thyroid deficiency causes a reduced potential for FFA utilization in skeletal muscle that enhances its consumption of glycogen, thereby limiting endurance capacity.