Physical training has been shown to improve glucose tolerance and insulin sensitivity. In the present study, insulin action was determined using the euglycemic clamp technique in six untrained nonobese subjects before, during, and after long-term mild regular jogging. After 1 yr of jogging, steady-state plasma insulin levels (I) decreased significantly, and the metabolic clearance rate of insulin was increased by 87%, although insulin infusion rate during the clamp was constant for each individual. The amount of glucose infused (glucose metabolism, M) tended to increase from 6.16 +/- 0.94 to 8.15 +/- 1.94 mg.kg-1.min-1 after regular jogging for 1 yr, although that was not statistically significant. However, M/I increases significantly from 0.060 +/- 0.012 to 0.184 +/- 0.056 (P less than 0.05) after 1 yr. The concentrations of plasma free fatty acids during the hyperinsulinemic clamp decreased more significantly after 1 yr of jogging (P less than 0.05). The concentrations of plasma glycerol decreased gradually before and after long-term regular jogging, showing only a 50–60% reduction in 120 min. Therefore, long-term mild regular jogging, which did not influence either body mass index or maximal O2 uptake, appears to improve insulin action in both carbohydrate and lipid metabolism and to increase the metabolic clearance rate of insulin.

To clarify the difference in immunity between untrained subjects and well-trained athletes, the number of total leukocytes (WBC), lymphocytes, and neutrophils, percentages of various lymphocyte subpopulations (OKT3, OKT4, OKT8, Leu7, OKla1), and the levels of lymphocyte transformation response to phytohemagglutinin (PHA) were determined in five untrained male subjects and six male athletes before, immediately after, and 24 and 72 h after acute physical exercise at 60% of VO2max for 2 h. Exercise produced a significant rise in the number of WBC, lymphocytes, and neutrophils in both groups. Immediately after exercise, the percentage of OKT3 or OKT4 positive cells had significantly decreased in both groups, whereas that of OKT8 positive cells had markedly increased only in the athletes. Neither group showed any change in the percentage of OKla1 positive cells. In both groups, the response of lymphocytes to PHA immediately after exercise was significantly lower than before, 24 h and 72 h after exercise. The level of Leu7 positive cells rose remarkably immediately after exercise in the athletes, but not significantly in the untrained subjects. These results suggest that an increase in Leu7 positive cells provides added host defense capacity in trained athletes during periods of stress which impair T-lymphocyte function.

Physical training has been shown to improve glucose tolerance and insulin action. In the present study, insulin action was determined using the euglycemic clamp technique in six trained male athletes compared with six untrained controls matched by age, sex, and weight at 14, 38, and 86 hours and at 6 days after cessation of exercise. The rate of insulin-mediated glucose uptake (glucose disposal) was 9.40 +/- 0.46 mg.kg-1.min-1 (mean +/- SEM) for the athletes at 14 h after the last exercise bout, compared with 6.80 +/- 0.86 mg.kg-1.min-1 obtained for the untrained controls (p less than 0.01). Glucose disposal was gradually decreased to 7.78 +/- 0.87 mg.kg-1.min-1 at 38 h, 6.82 +/- 0.49 mg.kg-1.min-1 at 86 h and to 7.11 +/- 1.00 mg.kg-1.min-1 at 6 days after cessation of physical training. At 38 h, 86 h, and 6 days of detraining, glucose disposal exhibited by training athletes did not differ significantly from untrained controls. These results suggest that physical training increases insulin action, and that this effect could be reversed to the control levels within 38 h after detraining.

To estimate physical training effects quantitatively, the relationship between tissue sensitivity to exogenous insulin (glucose metabolism determined by euglycemic insulin-clamp technique) and maximal oxygen uptake (VO2 max) was defined in 9 well-trained athletes and 14 untrained subjects with normal glucose tolerance. Tissue sensitivity to exogenous insulin in the athletes was significantly higher than in the controls (P less than 0.001). Seven untrained subjects continued the physical exercise program. After physical training for 1 month, glucose metabolism increased from 40.3 +/- 3.9 mumol/kg/min to 42.2 +/- 4.4 mumol/kg/min (P less than 0.05) and VO2 max also increased significantly (P less than 0.05). During euglycemic hyperinsulinemia, both plasma FFA (P less than 0.001) and glycerol (P less than 0.05) decreased rapidly after physical training. Glucose metabolism directly correlated with VO2 max (P less than 0.001). These results suggest that the euglycemic insulin-clamp technique provides a reliable estimate of training effects, tissue sensitivity to physiologic hyperinsulinemia is 46% higher in trained athletes, and physical training improves insulin sensitivity not only in glucose metabolism but also in lipid metabolism.

Adrenal insufficiency in human and rat is associated with an impairment of the diuretic response to water load, and only glucorticoids (GCs) restore this deficit. Our observation that GCs potentiate atrial natriuretic polypeptide (ANP)-stimulated cGMP production in cultured renal cells prompted us to examine the possibility that GCs may restore the diuretic response through the potentiation of ANP action. Initially, changes in urine volume and ANP levels were studied in adrenalectomized (Adx) and sham-operated intact rats after an oral water load of 5 ml/100 g BW. Urine volume after water load was 4.5 +/- 0.5 ml/30 min in the intact rats, whereas it was 0.8 +/- 0.2 ml/30 min in the Adx rats. In the intact rats, a significant increase in plasma ANP level was observed 30 min after the water load, whereas no increase was observed in Adx rats. This defective ANP response may be involved in the impairment of the diuretic response in Adx rats. Indeed, pretreatment of Adx rats with dexamethasone (Dex, 20 micrograms/100 g BW) increased plasma ANP levels even before water load and improved diuretic response. Subsequently, effect of iv administration of human or rat ANP at a pharmacological dose (2.5 micrograms/100 g BW) on urine volume, osmolarity, and urinary excretion of cGMP, and sodium was studied in Adx rats that received an oral water load 30 min before ANP. Dex treatment was achieved by per os administration 3 h before the ANP injection. In Adx rats, the urine volume after ANP administration was 1.2 +/- 0.1 ml/30 min, and pretreatment with Dex markedly increased the urine volume to 6.3 +/- 0.4 ml/30 min. Dex also increased ANP-induced osmolar and sodium excretion by 2.6- and 2.9-fold, respectively. Although urinary excretion of cGMP was increased in Adx rats by ANP administration, a further significant increase was observed by the pretreatment with Dex. Injection of (Bu)2cGMP to Adx rats pretreated with Dex resulted in a significant increase in urine volume and osmolar and sodium excretion. However, no significant increase in urine volume was observed in Adx rats not pretreated with Dex. The present study suggests that GCs restore the diuretic response to acute water load not only by increasing the secretion of ANP but also by potentiating ANP-stimulated cGMP production. Furthermore, GCs may augment ANP action at one or more steps other than cGMP formation because administration of (Bu)2cGMP to Adx rats did not correct the diuretic response to water load.