Maximal dynamic exercise results in a postexercise hyperglycemia in healthy young subjects. We investigated the influence of maximal exercise on glucoregulation in non-insulin-dependent diabetic subjects (NIDDM). Seven NIDDM and seven healthy control males bicycled 7 min at 60% of their maximal O2 consumption (VO2max), 3 min at 100% VO2max, and 2 min at 110% VO2max. In both groups, glucose production (Ra) increased more with exercise than did glucose uptake (Rd) and, accordingly, plasma glucose increased. However, in NIDDM subjects the increase in Ra was hastened and Rd inhibited compared with controls, so the increase in glucose occurred earlier and was greater [147 +/- 21 to 169 +/- 19 (30 min postexercise) vs. 90 +/- 4 to 100 +/- 5 (SE) mg/dl (10 min postexercise), P less than 0.05]. Glucose levels remained elevated for greater than 60 min postexercise in both groups. Glucose clearance increased during exercise but decreased postexercise to or below (NIDDM, P less than 0.05) basal levels, despite increased insulin levels (P less than 0.05). Plasma epinephrine and glucagon responses to exercise were higher in NIDDM than in control subjects (P less than 0.05). By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. It is concluded that, because of exaggerated counter-regulatory hormonal responses, maximal dynamic exercise results in a 60-min period of postexercise hyperglycemia and hyperinsulinemia in NIDDM. However, this event is followed by a period of increased insulin effect on Rd that is present 24 h after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

The present study was designed to test the hypothesis that the exercise-induced changes in blood mononuclear cell (BMNC) subsets, BMNC proliferative responses and lymphokine activated killer (LAK) cell activity are mediated by increased epinephrine concentrations. Healthy male volunteers 1) exercised on a bicycle ergometer (75% of VO2max, 1 h) and 2) on another day were given epinephrine as an intravenous infusion to obtain plasma epinephrine concentrations comparable with those seen during exercise. Blood samples were collected in the basal state, during the last minutes of exercise or epinephrine infusion and 2 h later. During both perturbations the %CD3+ and %CD4+ T cells declined and the %CD16+ NK cells increased. Two h afterwards the CD14+ monocytes increased, while no changes were observed in %CD8+ T cells or %CD20+ B cells. The phytohemagglutinin (PHA) response declined during both epinephrine infusion and exercise experiments. The changes in interleukin-2 (IL-2) effect on proliferation and cytotoxic activity (LAK cell activity) were more pronounced in exercise experiments than during epinephrine. Exercise and epinephrine caused increase in concentrations of lymphocytes and neutrophils, but the changes were more pronounced in exercise experiments. The results indicate that, in response to physical exercise, the rise in plasma epinephrine may contribute to the changes in cellular immunity.

Pregnancy after bariatric surgery seems safe but larger studies matching or adjusting for body mass index are needed to improve the surveillance of these pregnancies and to assist in preventing adverse outcomes.

No abstract

Hypoxia and physical training alter the responses of glucoregulatory hormones to absolute work loads in opposite directions. These effects have tentatively been ascribed to changes in maximal O2 consumption (VO2 max) and ensuing changes in relative work loads. However, hypoxia as well as training may more specifically influence the hormonal response. We therefore differentiated the influence of hypoxia, training, and VO2 max, respectively, on the hormonal response to bicycle exercise. Responses to hypoxia in a low-pressure chamber (PB = 465 vs. 730 Torr) were studied at given absolute and relative (85% VO2 max) work loads in seven endurance-trained athletes (T) and 7 age and weight-matched sedentary subjects (C). Concentrations in plasma of norepinephrine, growth hormone, adrenocorticotropic hormone, and cortisol were always closely related to the relative work load. However, the epinephrine response in T, but not in C, was at the same relative work load higher during hypoxia (5.84 +/- 0.83 nmol/l) than during normoxia (4.26 +/- 0.44, P less than 0.05). These results indicate that the hormonal response is influenced by hypoxia and physical training, mainly via changes in the relative work load. However, in trained subjects both at rest and during exercise, an enhancing effect of hypoxia per se on the epinephrine response is seen, probably due to an increased adrenal medullary secretory responsiveness in long-term endurance-trained subjects.