The purpose of this study was to examine the effects of ginseng extract ingestion on physiological responses to intense exercise. Subjects performed a control ride (CN) on a cycle ergometer, followed by placebo (PL) and ginseng (GS) treatments. Ginseng was ingested as 8 or 16 mg/kg body weight daily for 7 days prior to trial GS. Venous blood was sampled for FFA, lactate, and glucose analyses. Due to similar findings for both dose groups, the subjects were considered as one group. Lactate, FFA, V O~, vE, and RPE increased significantly from 10 through 40 min. RER increased during the first 10 rnin of exercise and then remained stable, with no intertrial differences. Glucose did not vary significantly from 0 to 40 min or among treatments. RPE was significantly greater and time to exhaustion was significantly less during trial CN than PL or GS, while PL and GS trials were similar. The data indicated that with 1 weekof pretreatment there is no ergogenic effect of ingesting the ginseng saponin extract.
The X-linked hypophosphatemic (Hyp) mouse is a model for human X-linked hypophosphatemia. Surgical joining of normal to Hyp mice by parabiosis results in the normal mice developing low renal retention of phosphate and hypophosphatemia. These results suggest a humoral component to the renal defect. To test whether this component could be parathyroid hormone, surgical parathyroidectomy (PTX) or sham surgery was performed in mice 3 weeks after parabiotic union (n greater than 20 per group). After an overnight fast, PTX mice were hypocalcemic and hyperphosphatemic relative to sham-operated control mice. PTX normal mice joined to PTX Hyp mice were significantly lower in plasma phosphate and higher in fractional excretion of phosphate [U/P phosphate/(U/P creatinine)] when compared with PTX normal mice joined to other PTX normals. To test for more specific evidence of altered renal transport function, renal brush-border membrane vesicles (BBMV) were prepared from these mice, and phosphate and glucose uptakes were measured. The phosphate/glucose transport ratio was lower in BBMV from Hyp mice, joined to either normal mice or to Hyp mice, when compared with that from normal-normal pairs. Moreover, BBMV from normal mice joined to Hyp mice had a significantly lower phosphate/glucose uptake ratio than BBMV from normal mice joined to other normal mice, and their activity approached that of BBMV derived from Hyp mice. Glucose uptake in BBMV was unaffected by parabiosis or genotype. In summary, parabiosis of normal mice to Hyp mice resulted in the development of phosphaturia and decreased BBMV phosphate transport in the normal mice. The persistence of the phosphate transport defect in parathyroidectomized mice suggests that parathyroid hormone is not the humoral factor contributing to these results.
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