Ureteral injuries during photoselective vaporization of the prostate.

Photoselective vaporization of the prostate is a relatively new surgical modality for male lower urinary tract symptoms. The method has a risk of tissue damage if laser pulses miss the prostatic adenoma and travel through the irrigation fluid in the bladder. Five cases of damage to the ureteral orifices are described, with hidden orifices, intravesical prostatic adenomas and prior prostatectomy as risk factors for laser-related injuries to ureteral orifices. A laser-coagulated ureteral orifice does not seem to regain patency spontaneously, so rapid nephrostomy and subsequent DJ stenting is recommended.

Effect of training on insulin sensitivity of glucose uptake and lipolysis in human adipose tissue.

Training increases insulin sensitivity of both whole body and muscle in humans. To investigate whether training also increases insulin sensitivity of adipose tissue, we performed a three-step hyperinsulinemic, euglycemic clamp in eight endurance-trained (T) and eight sedentary (S) young men [insulin infusion rates: 10,000 (step I), 20,000 (step II), and 150,000 (step III) microU x min(-1) x m(-2)]. Glucose and glycerol concentrations were measured in arterial blood and also by microdialysis in interstitial fluid in periumbilical, subcutaneous adipose tissue and in quadriceps femoris muscle (glucose only). Adipose tissue blood flow was measured by (133)Xe washout. In the basal state, adipose tissue blood flow tended to be higher in T compared with S subjects, and in both groups blood flow was constant during the clamp. The change from basal in arterial-interstitial glucose concentration difference was increased in T during the clamp but not in S subjects in both adipose tissue and muscle [adipose tissue: step I (n = 8), 0.48 +/- 0.18 mM (T), 0.23 +/- 0.11 mM (S); step II (n = 8), 0.19 +/- 0.09 (T), -0.09 +/- 0.24 (S); step III (n = 5), 0.47 +/- 0.24 (T), 0.06 +/- 0.28 (S); (T: P < 0.001, S: P > 0.05); muscle: step I (n = 4), 1. 40 +/- 0.46 (T), 0.31 +/- 0.21 (S); step II (n = 4), 1.14 +/- 0.54 (T), -0.08 +/- 0.14 (S); step III (n = 4), 1.23 +/- 0.34 (T), 0.24 +/- 0.09 (S); (T: P < 0.01, S: P > 0.05)]. Interstitial glycerol concentration decreased faster in T than in S subjects [half-time: T, 44 +/- 9 min (n = 7); S, 102 +/- 23 min (n = 5); P < 0.05]. In conclusion, training enhances insulin sensitivity of glucose uptake in subcutaneous adipose tissue and in skeletal muscle. Furthermore, interstitial glycerol data suggest that training also increases insulin sensitivity of lipolysis in subcutaneous adipose tissue. Insulin per se does not influence subcutaneous adipose tissue blood flow.

Glucose clearance in aged trained skeletal muscle during maximal insulin with superimposed exercise.

Insulin and muscle contractions are major stimuli for glucose uptake in skeletal muscle and have in young healthy people been shown to be additive. We studied the effect of superimposed exercise during a maximal insulin stimulus on glucose uptake and clearance in trained (T) (1-legged bicycle training, 30 min/day, 6 days/wk for 10 wk at approximately 70% of maximal O(2) uptake) and untrained (UT) legs of healthy men (H) [n = 6, age 60 +/- 2 (SE) yr] and patients with Type 2 diabetes mellitus (DM) (n = 4, age 56 +/- 3 yr) during a hyperinsulinemic ( approximately 16,000 pmol/l), isoglycemic clamp with a final 30 min of superimposed two-legged exercise at 70% of individual maximal heart rate. With superimposed exercise, leg glucose extraction decreased (P < 0.05), and leg blood flow and leg glucose clearance increased (P < 0.05), compared with hyperinsulinemia alone. During exercise, leg blood flow was similar in both groups of subjects and between T and UT legs, whereas glucose extraction was always higher (P < 0.05) in T compared with UT legs (15.8 +/- 1.2 vs. 14.6 +/- 1.8 and 11.9 +/- 0.8 vs. 8.8 +/- 1.8% for H and DM, respectively) and leg glucose clearance was higher in T (H: 73 +/- 8, DM: 70 +/- 10 ml. min(-1). kg leg(-1)) compared with UT (H: 63 +/- 8, DM: 45 +/- 7 ml. min(-1). kg leg(-1)) but not different between groups (P > 0.05). From these results it can be concluded that, in both diabetic and healthy aged muscle, exercise adds to a maximally insulin-stimulated glucose clearance and that glucose extraction and clearance are both enhanced by training.

[Munchausen syndrome]. / Münchhausens syndrom.

The case of 43 year old man who had numerous contacts with the health care system is reported. Since 1984 he had been treated 95 times for testicular problems at 45 different hospitals including 36 operations for torsion. Computer record systems had only once stopped the patient from going through another unnecessary operation. An alarm in the computer record system with reference to a contact place could make it easier to spot a patient with diagnosed Münchhausen's syndrome and give him treatment.

Training-induced enhancement of insulin action in human skeletal muscle: the influence of aging.

Age-induced reduction of whole body insulin action has been attributed to decreased insulin action in skeletal muscle. Physical training improves insulin action, but the effect has never been investigated specifically in aged human skeletal muscle. Seven young men [age: 23 +/- 1 yr (mean +/- SE; range, 21-24 yr); weight: 70 +/- 1 kg; body fat: 8 +/- 1%] and eight aged men [59 +/- 1 yr (range, 58-64 yr); 83 +/- 2 kg; 20 +/- 2%] performed one-legged bicycle training on a modified ergometer cycle for 10 weeks, 6 days/week, at 70% of VO2 peak. Glucose clearance rates in whole body and leg were measured 16 hr after training by a hyperinsulinemic (28, 88, and 480 mU.min-1.min-2), isoglycemic clamp combined with leg balance technique. Peak oxygen uptake during the bicycle test was always lower (p < .05) in aged vs. young subjects. Furthermore, VO2 peak was higher after training in trained (T) vs. untrained (UT) (p < .05) legs. Whole body glucose clearance rate was lower in aged vs. young subjects (p < .05) when expressed per kg body weight, but similar when expressed relative to fat free mass. Leg blood flow was always lower in aged vs. young men (p < .05). At basal and during insulin infusion, leg blood flow in young men did not differ significantly in T vs. UT legs (maximum insulin: 81 +/- 7 vs. 71 +/- 5 ml.min-1.kg leg-1), while in aged subjects it increased (p < .05) with training (maximum insulin: 57 +/- 5 vs. 48 +/- 5 ml.min-1.kg leg-1). Leg glucose extraction was always higher in aged vs. young men during the two last clamp steps (p < .05). Furthermore, leg glucose extraction was increased by training in young (p < .05) but not significantly in aged subjects. Leg glucose clearance rates increased (p < .05) with training and was similar in aged men (T: 1 +/- 1, 8 +/- 1, 21 +/- 2, and 24 +/- 2; UT: 1 +/- 1, 6 +/- 1, 14 +/- 2, and 20 +/- 2 ml.min-1.kg leg-1) and young men (T: 1 +/- 1, 12 +/- 3, 23 +/- 3, and 26 +/- 3; UT: 1 +/- 1, 8 +/- 2, 17 +/- 2, and 21 +/- 2 ml.min-1.kg leg-1). Therefore, insulin action in muscle is not reduced by aging. At high insulin concentrations, the leg blood flow is lower, whereas glucose extraction is higher in aged compared with young men. Training increases overall insulin action on glucose clearance in skeletal muscle identically in aged and young subjects.

Insulin-stimulated muscle glucose clearance in patients with NIDDM. Effects of one-legged physical training.

Physical training increases insulin action in skeletal muscle in healthy men. In non-insulin-dependent diabetes mellitus (NIDDM), only minor improvements in whole-body insulin action are seen. We studied the effect of training on insulin-mediated glucose clearance rates (GCRs) in the whole body and in leg muscle in seven patients with NIDDM and in eight healthy control subjects. One-legged training was performed for 10 weeks. GCR in whole body and in both legs were measured before, the day after, and 6 days after training by hyperinsulinemic (28, 88, and 480 mU x min(-1) x m(-2)), isoglycemic clamps combined with the leg balance technique. On the 5th day of detraining, one bout of exercise was performed with the nontraining leg. Muscle biopsies were obtained before and after training. Whole-body GCRs were always lower (P < 0.05) in NIDDM patients compared with control subjects and increased (P < 0.05) in response to training. In untrained muscle, GCR was lower (P < 0.05) in NIDDM patients (13 +/- 4, 91 +/- 9, and 148 +/- 12 ml/min) compared with control subjects (56 +/- 12, 126 +/- 14, and 180 +/- 14 ml/min). It Increased (P < 0.05) in both groups in response to training (43 +/- 10, 144 +/- 17, and 205 +/- 24 [NIDDM patients] and 84 +/- 10, 212 +/- 20, and 249 +/- 16 ml/min [control subjects]). Acute exercise did not increase leg GCR. In NIDDM patients, the effect of training was lost after 6 days, while the effect lasted longer in control subjects. Training increased (P < 0.05) muscle lactate production and glucose storage as well as glycogen synthase (GS) mRNA in both groups. We conclude that training increases insulin action in skeletal muscle in control subjects and NIDDM patients, and in NIDDM patients normal values may be obtained. The increase in trained muscle cannot fully account for the increase in whole-body GCR. Improvements in GCR involve enhancement of insulin-mediated increase in muscle blood flow and the ability to extract glucose. They are accompanied by enhanced nonoxidative glucose disposal and increases in GS mRNA. The improvements in insulin action are short-lived.

Paradoxical inhibition of insulin secretion by glucose in non-insulin-dependent diabetic patients.

In young healthy individuals, an i.v. glucose bolus leads to an immediate increase in plasma insulin, whereas in non-insulin-dependent diabetic patients this early response is diminished, lacking or even negative. In the present study, we sought to determine whether negative responses were also present during square-wave glucose stimulation (transition from 18 to 25 mM), whether they represented a decrease in beta-cell secretion, whether they were accompanied by an altered response to arginine (5 g L-arginine bolus), and whether they were a consequence of ageing rather than of diabetes. A group of 12 patients (aged 53 +/- 2 years, mean +/- SE) with non-insulin-dependent diabetes (D) and 12 matched healthy controls (C; aged 47 +/- 1 years) were evaluated twice at an interval of 3 months. Other baseline values were body mass index (BMI) 28 +/- 1 (D) and 26 +/- 1 (C) kg/m2, fasting C-peptide 0.85 +/- 0.12 (D) and 0.92 +/- 0.10 (C) nmol/l, and fasting P-glucose 12.3 +/- 0.9 (D) and 5.8 +/- 0.1 (C) mM, P < 0.05. Paradoxical responses (a decrease of two or more times the SD of the analysis within 15 min of increasing the glucose concentration) were seen in five diabetic patients for insulin (22 +/- 8%) and in nine diabetic patients for C-peptide (13 +/- 3%), but never in the healthy controls. Plasma glucose increased and protein decreased similarly, whether the responses were paradoxical or not. Paradoxial responses were reproduced after three months. Responses to arginine did not correlate with responses to glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Normal effect of insulin to stimulate leg blood flow in NIDDM.

In patients with non-insulin-dependent diabetes mellitus (NIDDM), a decreased effect of insulin in stimulating leg blood flow (LBF) has been reported. We reinvestigated the effect of insulin on LBF and validated our data by use of other measures. Eight healthy men (control group) and seven men with NIDDM were studied (age 59 +/- 1 and 58 +/- 3 years, weight 83 +/- 3 and 86 +/- 6 kg, fat-free mass 66 +/- 1 and 64 +/- 3 kg, respectively [mean +/- SE, all P > 0.05]; body mass index 26 +/- 1 and 29 +/- 1 kg/m2, fasting plasma insulin 72 +/- 7 and 187 +/- 22 pmol/l, fasting plasma glucose 5.8 +/- 0.2 and 10.2 +/- 1.7 mmol/l [all P < 0.05]). A three-step hyperinsulinemic glucose clamp (ambient glucose level) was performed, combined with catheterization of an artery and both femoral veins. Expiratory air was collected, LBF was measured by thermodilution, and blood was sampled and analyzed for oxygen content. Insulin concentration was increased to 416 +/- 22 and 509 +/- 43 (step I), 1,170 +/- 79 and 1,299 +/- 122 (step II), and 15,936 +/- 1,126 and 16,524 +/- 1,916 (step III) pmol/l in control and NIDDM subjects, respectively (P > 0.05). LBF increased similarly (P > 0.05) in the two groups (from 287 +/- 23 and 302 +/- 12 [basal] to 308 +/- 31 and 362 +/- 9 [I], 371 +/- 29 and 409 +/- 17 [II], and 434 +/- 32 and 472 +/- 29 [III] ml.min-1.leg-1 in control and NIDDM subjects, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of liver denervation on glucose production during running in guinea pigs.

Activity in sympathetic liver nerves has been proposed to be important for glucose production in exercising humans. However, liver denervation does not influence the exercise-induced increase in glucose production in the rat and dog. These species have a poor sympathetic liver innervation in contrast to the rich innervation in humans. The effect of liver denervation on glucose production during exercise was therefore studied in the guinea pig, a species with a rich sympathetic hepatic innervation comparable to that of humans. Guinea pigs were selectively liver denervated (n = 9) or sham operated (n = 8) and instrumented with a carotid and a jugular catheter. One week later they ran on a treadmill at 32 m/min for 20 min. Glucose turnover was evaluated by a primed constant-rate intravenous infusion of [3-3H]glucose. Arterial blood was sampled for analysis of hormones and metabolites. At rest, liver-denervated guinea pigs had lower glucose turnover and plasma concentrations of glucose, glycerol, and cortisol than control animals. During running, the increase in hepatic glucose production was similar in the two groups (4.1 +/- 0.8 vs. 3.8 +/- 0.7 mumol.min-1.100 g-1 in control animals) and so were hepatic (247 +/- 25 vs. 246 +/- 45 mmol glucose units/kg wet wt in control animals) and muscle glycogen concentrations at the end of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Physical training increases muscle GLUT4 protein and mRNA in patients with NIDDM.

Patients with non-insulin-dependent diabetes mellitus (NIDDM) exhibit insulin resistance and decreased glucose transport in skeletal muscle. Total content of muscle GLUT4 protein is not affected by NIDDM, whereas GLUT4 mRNA content is reported, variously, to be unaffected or increased. Physical training is recommended in the treatment of NIDDM, but the effect of training on muscle GLUT4 protein and mRNA content is unknown. To clarify the effect of training in NIDDM, seven men with NIDDM (58 +/- 2 years of age [mean +/- SE]) and eight healthy men (59 +/- 1 years of age) (control group) performed one-legged ergometer bicycle training for 9 weeks, 6 days/week, 30 min/day. Biopsies were obtained from the vastus lateralis leg muscle before and after training. GLUT4 protein analyses was performed along with analyses of muscle biopsies from five young (23 +/- 1 years of age) (young group), healthy subjects who participated in a previously published identical study. In response to training, maximal oxygen uptake increased (delta 3.3 +/- 1.8 in NIDDM subjects and 4.5 +/- 1.2 ml.min-1.kg-1 in control subjects [both P < 0.05]). Before training, GLUT4 protein content was similar in NIDDM, control, and young subjects (0.35 +/- 0.02, 0.34 +/- 0.03, and 0.41 +/- 0.03 arbitrary units, respectively), and it increased (P < 0.05) in all groups during training (to 0.43 +/- 0.03, 0.40 +/- 0.03, and 0.57 +/- 0.08 arbitrary units, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of training on interaction between insulin and exercise in human muscle.

Exercise adds to the effect of maximal insulin on whole body glucose uptake. Training increases contraction-induced glucose transport measured in vitro but not glucose utilization in human muscle exercising during normoinsulinemia. We studied whether exercise adds to the effect of maximal insulin in human muscle and whether trained (T) and untrained (UT) muscle differ. Six healthy men [23 +/- 0.4 (SE) yr] trained one leg for 10 wk, 6 days/wk, 30 min/day at 70% of one-legged maximal O2 uptake while keeping the other leg sedentary. At 16 h after the last training bout, both femoral veins and a radial artery were catheterized and 150-min hyperinsulinemic (480 mU.min-1.m-2) euglycemic clamp was performed. During the final 30 min, subjects performed two-legged bicycling at 76 +/- 0.3% of maximal heart rate. During exercise, blood flow (597 +/- 45 vs. 572 +/- 37 ml.min-1.kg-1), O2 uptake (74 +/- 6 vs. 68 +/- 6 ml O2.min-1.kg-1), and carbohydrate oxidation (88 +/- 10 vs. 81 +/- 7 mg.min-1.kg-1) increased similarly (P > 0.05) in T and UT legs, respectively. Arteriovenous glucose difference decreased (P < 0.05) during exercise but tended to remain higher in T (0.47 +/- 0.04) than in UT (0.41 +/- 0.05 mol/l) (P < 0.1). Glucose uptake increased with exercise, the increase being higher in T than in UT (change: 28 +/- 5 vs. 23 +/- 5 mg.min-1.kg-1; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

GLUT 4 and insulin receptor binding and kinase activity in trained human muscle.

1. Physical training enhances sensitivity and responsiveness of insulin-mediated glucose uptake in human muscle. This study examines if this effect of physical training is due to increased insulin receptor function or increased total concentration of insulin-recruitable glucose transporter protein (GLUT 4). 2. Seven healthy young subjects carried out single leg bicycle training for 10 weeks at 70% of one leg maximal oxygen uptake (VO2,max). Subsequently biopsies were taken from the vastus lateralis muscle of both legs. 3. Single leg VO2,max increased for the trained leg (46 +/- 3 to 52 +/- 2 ml min-1 kg-1 (means +/- S.E.M., P < 0.05), and cytochrome c oxidase activity was higher in this compared to the untrained leg (2.0 +/- 0.1 vs. 1.4 +/- 0.1 nmol s-1 (mg muscle)-1, P < 0.05). Insulin binding as well as basal- and insulin-stimulated receptor kinase activity did not differ between trained and untrained muscle. The concentration of GLUT 4 protein was higher in the former (14.9 +/- 1.9 vs. 11.6 +/- 1.0 arbitrary units (micrograms protein)-1 in crude membranes, P < 0.05). The training-induced increase in GLUT 4 (26 +/- 11%) matched a previously reported increase in maximum insulin-stimulated leg glucose uptake (25 +/- 7%) in the same subjects, and individual values of the two variables correlated (correlation coefficient (r) = 0.84, P < 0.05). 4. In conclusion, in human muscle training induces a local contraction-dependent increase in GLUT 4 protein, which enhances the effect of insulin on glucose uptake. On the other hand, insulin receptor function in muscle is unlikely to be affected by training.

Effect of training on insulin-mediated glucose uptake in human muscle.

During insulin stimulation whole body glucose uptake is increased in trained compared with untrained humans. However, it is not known which tissue is responsible. Seven young male subjects bicycle trained one leg for 10 wk at 70% of maximal O2 consumption (VO2max). Sixteen hours after last exercise bout, a three-step euglycemic hyperinsulinemic clamp (clamp 1) was performed (insulin levels, means +/- SE: 9 +/- 1, 53 +/- 3, 174 +/- 5, and 2,323 +/- 80 was microU/ml), with measurement of arteriovenous differences and blood flow in both legs. After 6 days of detraining subjects were restudied, having exercised the untrained leg 16 h before. VO2max for trained (T) and untrained (UT) legs was 52 +/- 2 vs. 44 +/- 2 ml.min-1.kg-1 (P < 0.05). In clamp 1 glucose uptake in T and UT legs was 1.0 +/- 0.2 vs. 0.5 +/- 0.1 mg.min-1.kg-1 (basal), 9.7 +/- 2.3 vs. 6.7 +/- 1.7 (P < 0.05) (step I), 19.2 +/- 2.8 vs. 14.3 +/- 2.0 (P < 0.05) (step II), and 22.8 +/- 2.3 vs. 18.6 +/- 2.2 (P < 0.05) (step III). During insulin infusion lactate release (P < 0.05) [8.9 +/- 1.8 vs. 2.9 +/- 0.9 mumol.min-1.kg-1 (step I), 24.6 +/- 3.1 vs. 12.5 +/- 2.6 (step III)] and glycogen storage (P < 0.1) calculated by indirect calorimetry [6.7 +/- 2.3 vs. 5.0 +/- 1.7 mg.min-1.kg-1 (step I), 16.8 +/- 2.1 vs. 14.1 +/- 1.8 (step III)] were always higher in T than in UT legs. Release of glycerol, free fatty acids, and tyrosine and clearance of insulin were not influenced by training. Insulin-mediated glucose uptake was not increased after detraining or a single bout of exercise. In conclusion, training increases sensitivity and responsiveness of insulin-mediated glucose uptake in human muscle by local mechanisms. Glycolysis and glycogen storage are equally enhanced. The training effect represents a genuine adaptation to repeated exercise but is short lived. Insulin clearance in muscle is not influenced by training.

Heart rate and plasma catecholamines during 24 h of everyday life in trained and untrained men.

Physical training decreases resting heart rate as well as heart rate and catecholamine responses to ordinary physical activity and mental stress. These effects have been speculated to diminish cardiac morbidity. However, the sparing of heartbeats and catecholamine production might be outweighed by exaggerated responses during training sessions. To elucidate this issue, heart rate was measured continuously and plasma catecholamine concentrations were measured frequently during 24 h of ordinary living conditions in seven endurance-trained athletes (T) and eight sedentary or untrained (UT) young males. T subjects had lower heart rates than UT subjects during sleep and during nontraining awake periods. However, because of the increase during training, the total 24-h heartbeat number did not differ between groups (107,737 +/- 3,819 for T vs. 113,249 +/- 6,879 for UT, P = 0.731). Neither during sleep nor during awake nontraining periods were catecholamine levels lower in T than in UT subjects. Peak catecholamine levels during exercise in T were much higher than peak levels in UT subjects, and 24-h average epinephrine and norepinephrine concentrations were twice as high. We concluded that in highly trained athletes the total number of heartbeats per day is not decreased and the catecholamine production is, in fact, increased.

Does training spare insulin secretion and diminish glucose levels in real life?

Compared with untrained subjects, in trained subjects the increased insulin sensitivity and decreased glucose induced insulin secretion will tend to promote health by decreasing glucose levels and insulin secretion, whereas the increased food intake will tend to increase these variables. To evaluate the net effect of training, we administered oral glucose loads making up identical fractions of daily carbohydrate intake (i.e., same relative glucose loads) to 8 athletes and 7 sedentary subjects (age: 25 +/- 1 vs. 24 +/- 1 yr [mean +/- SE] [NS]; body weight: 76.0 +/- 1.3 vs. 79.3 +/- 2.3 kg [NS]; maximal oxygen uptake: 76 +/- 2 vs. 48 +/- 1 ml O2.kg-1.min-1 [2P < 0.05], respectively). Furthermore, 24 h plasma concentration profiles of glucose, C-peptide, and insulin were determined during ordinary living conditions. Daily carbohydrate intake was higher (2P < 0.05) in athletes compared with sedentary subjects (678 +/- 34 vs. 294 +/- 18 g.day-1, respectively). In response to same relative oral glucose loads, glucose and C-peptide responses were similar in athletes compared to sedentary subjects. Twenty-four hour integrated glucose and C-peptide concentrations did not differ between athletes and sedentary subjects (7.4 +/- 0.2 vs. 7.3 +/- 0.6 mol.L-1.1440 min [2P > 0.05] and 923 +/- 99 vs. 1047 +/- 175 pM.ml-1.1440 min [2P > 0.05], respectively), and insulin concentrations tended to be lower in athletes compared with sedentary subjects (124 +/- 13 vs. 175 +/- 38 pM.ml-1.1440 min [2P > 0.05]).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of 5 wk of detraining on epinephrine response to insulin-induced hypoglycemia in athletes.

Long-term endurance-trained subjects are known to have an enhanced capacity to secrete epinephrine. It is, however, unknown to what extent this is a reversible phenomenon, i.e., whether the adrenal medullary secretory capacity is diminished during a period of abstinence from training. Hormonal responses to insulin-induced hypoglycemia were studied in seven endurance-trained young male athletes at the onset and the termination of a 31- to 44-day period of detraining necessitated by a sports injury that required leg casting. During insulin infusion, plasma glucose decreased to a mean range of 2.0-2.1 mM for the two conditions. The epinephrine response to hypoglycemia did not decrease significantly during the 4-6 wk of detraining (P greater than 0.05). Responses of other counterregulatory hormones, i.e., norepinephrine, glucagon, growth hormone, and cortisol, were identical in trained and detrained subjects (P greater than 0.05). Heart rate and blood pressure responses to hypoglycemia were similar in the two conditions (P greater than 0.05). In conclusion, in endurance athletes the enhanced capacity to secrete epinephrine is maintained during 5 wk of detraining.

Twenty-four-hour profile of plasma glucose and glucoregulatory hormones during normal living conditions in trained and untrained men.

Compared with untrained (UT) subjects, in trained (T) subjects the increased insulin sensitivity and decreased glucose induced insulin secretion would tend to promote health by decreasing glucose levels and insulin secretion whereas the increased food intake would tend to increase these variables. To study the net effect of training, blood was sampled from seven T and eight UT young men [VO2max: 76 +/- 2 (T) vs. 48 +/- 1 (UT) mL.kg-1.min-1] for 24 h during ordinary living conditions. Athletes exercised 204 +/- 20 min and ate 50% more calories and 130% more carbohydrate than UT subjects (P less than 0.05). However, 24-h integrated plasma concentrations of glucose, C-peptide, glucagon, free fatty acids, and glycerol as well as glycosylated hemoglobin levels were identical in T and UT subjects. Mean insulin concentration was 41% lower in T than in UT but levels differed significantly (P less than 0.05) only late during the night. Urinary excretion of pancreatic peptides paralleled plasma concentrations. In conclusion, during training adaptations in pancreas- and insulin-sensitive tissues allow the necessary increase in food intake without harmful hyperglycemia and overloading of beta-cells, but sparing of insulin secretion and reductions in glucose levels are only relative to food intake. However, training may be wholesome by increasing hepatic insulin extraction and thereby decreasing arterial insulin levels. Training-induced beta-cell adaptation is not caused by diminished average glucose levels. Finally, renal handling of insulin, C-peptide, and glucagon is not influenced by training.

Seven days of bed rest decrease insulin action on glucose uptake in leg and whole body.

Impaired glucose tolerance develops in normal humans after short-term bed rest. To elucidate the mechanism, insulin action on whole body glucose uptake rate (WBGUR) and leg glucose uptake rate (LGUR) was measured by sequential euglycemic clamp technique combined with femoral arterial and venous cannulation at insulin concentrations of 10 +/- 1, 18 +/- 1, 37 +/- 2, and 360 +/- 15 microU/ml. Studies were performed before (C) and after (BR) 7 days of strict bed rest. WBGUR was significantly lower after bed rest than before (5.5 +/- 0.4 and 7.2 +/- 0.8 mg.min-1.kg-1, respectively) when insulin was 37 microU/ml. LGUR was even more markedly depressed by bed rest, being 0.6 +/- 0.1, 0.9 +/- 0.2, and 2.8 +/- 0.4 mg.min-1.kg leg-1 (BR) compared with 0.9 +/- 0.1, 1.7 +/- 0.4, and 5.9 +/- 0.5 mg.min-1.kg leg-1 (C) (P less than 0.05) at the three lower insulin concentrations. At these insulin concentrations also, lactate release and glucose oxidation and glycogen storage estimated by indirect calorimetry were lower in the leg after bed rest. At the highest insulin dose WBGUR was similar on BR and C days, while LGUR was lower after bed rest. In conclusion, 7 days of bed rest decrease whole body insulin action, a fact that is explained by decreased insulin action in inactive muscle.

Effect of training on response to a glucose load adjusted for daily carbohydrate intake.

From responses to identical absolute glucose loads in trained (T) and untrained (UT) subjects, it has been inferred that training promotes health by reducing glucose levels and insulin secretion. To mimic daily living conditions, we studied responses to oral glucose loads making up identical fractions of daily carbohydrate intake (i.e., same relative glucose load) in seven T and eight UT males [maximal O2 uptake (VO2max) 76 +/- 2 vs. 48 +/- 1 (SE) ml.min-1.kg-1; age 24 +/- 1 vs. 25 +/- 1 yr]. Daily energy intake was higher in T than in UT subjects (18,607 +/- 835 vs. 12,493 +/- 720 kJ/day, P less than 0.05), reflecting a 2.3 times higher carbohydrate intake (678 +/- 34 vs. 294 +/- 18 g/day, P less than 0.05). After 1 g/kg body wt glucose, C-peptide and insulin responses were lower in T than in UT subjects (P less than 0.05). However, after identical relative glucose loads [high: 2.3 +/- 0.2 (T) vs. 1 (UT) g/kg; low: 1 (T) vs. 0.4 +/- 0.03 (UT) g/kg], glucose [incremental areas 300 +/- 56 (T) vs. 304 +/- 35 (UT) mM.180 min and 148 +/- 30 (T) vs. 124 +/- 22 (UT)] and C-peptide [181 +/- 18 (T) vs. 171 +/- 27 (UT) nM.180 min, and 100 +/- 13 (T) vs. 71 +/- 12 (UT)] responses did not differ between groups, while insulin responses were lower in T [at low relative load 15 +/- 4 (T) vs. 20 +/- 2 (UT) nM.180 min, P less than 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)