Aerobic exercise training improves insulin sensitivity without changes in body weight, body fat, adiponectin, and inflammatory markers in overweight and obese girls

The aim of this study was to examine the effect of aerobic exercise training on insulin sensitivity in overweight and obese girls. Nineteen overweight and obese girls (mean +/- SD: age, 13.1+/-1.8 years; body mass index, 26.8+/-3.9 kg/m(2)) volunteered for this study. Body composition (dual-energy x-ray absorptiometry), insulin sensitivity (oral glucose tolerance test and homeostasis model assessment estimate of insulin resistance; n=15), adiponectin, C-reactive protein (CRP), interleukin (IL) 6, insulin-like growth factor-1, soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 serum levels, and blood lipids and lipoproteins were assessed before and after 12 weeks of aerobic training. Cardiorespiratory fitness increased by 18.8% (P<.05) as a result of training. The area under the insulin concentration curve (insulin area under the curve) decreased by 23.3% (12781.7+/-7454.2 vs 9799.0+/-4918.6 microU.min/mL before and after intervention, respectively; P=.03). Insulin sensitivity was improved without changes in body weight (pre-intervention, 67.9+/-14.5 kg; post-intervention, 68.3+/-14.0 kg) or percent body fat (pre-intervention, 41.4% +/- 4.8%; post-intervention, 40.7%+/-5.2%). The lower limb fat-free mass increased by 6.2% (P<.01) as a result of training, and changes in lower limb fat-free mass were correlated with changes in the insulin area under the curve (r= -.68; P< .01). Serum adiponectin, IL-6, and CRP concentrations did not change (pre-intervention vs post-intervention: adiponectin, 9.57+/-3.01 vs 9.08+/-2.32 microg/mL; IL-6, 1.67+/-1.29 vs 1.65+/-1.25 pg/mL, CRP, 3.21+/-2.48 vs 2.73+/-1.88 mg/L) whereas insulin-like growth factor-1 was lower after training (pre-intervention, 453.8 +/- 159.3 ng/mL; post-intervention, 403.2+/- 155.1 ng/mL; P<.05). In conclusion, 12 weeks of aerobic training improved insulin sensitivity in overweight and obese girls without change in body weight, percent body fat, and circulating concentrations of adiponectin, IL-6, CRP, and other inflammatory markers. These findings suggest that increased physical activity may ameliorate the metabolic abnormalities associated with obesity in children with a mechanism other than the parameters cited earlier.     

Effect of water ingestion on cardiovascular and thermal responses to prolonged cycling and running in humans: a comparison

The aim of this investigation was to examine the effect of water ingestion on physiological responses to prolonged cycling (CYC) and running (RUN). A group of 11 men with mean (SEM) maximal oxygen uptake (V˙O_2max) 48.5 (1.8) ml·kg^–1·min^–1 on a cycle-ergometer and 52.1 (2.2) ml·kg^–1·min^–1 on a treadmill (P<0.01) exercised for 90 min on four occasions, twice on each ergometer, at 60% of mode specific V˙O_2max. No fluid was taken (D) in one trial on each ergometer, whereas 60% of fluid losses were replaced by drinking water in the other trial (W). In CYC, water ingestion attenuated the change in cardiac output ( ) and the reduction in stroke volume (ΔSV) [ΔSV: –22.7 (3.8) in D, –10.7 (2.9) ml·beat^–1 in W, P<0.01; : –1.9 (0.5) in D, –0.2 (0.4) l·min^–1 in W at 85 min, P<0.01], but did not affect rectal temperature [T _re at 90 min: 38.8 (0.1)°C in D, 38.7 (0.1)°C in W]. In contrast, fluid replacement reduced hyperthermia in RUN [T _re at 90 min: 39.6 (0.2) in D, 39.1 (0.2)°C in W, P<0.01], and this was linked with a higher skin blood flow [RUN-W 88.9 (8.5), RUN-D 70.7 (8.4)%, P<0.05]. The and ΔSV were also attenuated with water ingestion in this mode of exercise (P<0.05). It is concluded that water ingestion improves physiological function in both cycling and running, but that the underlying mechanism is different in the two modes of exercise. Electronic Publication     

Cardiac output decline in prolonged dynamic exercise is affected by the exercise mode

The aim of this study was to compare the cardiovascular responses to prolonged submaximal cycling and running. Eleven males [maximal oxygen uptake (VO(2max)): 3.58+/-0.15 l min(-1) for running and 3.84+/-0.16 l min(-1) for cycling; mean+/-SE] either cycled (C) or ran (R) for 90 min at 60% of mode-specific VO(2max), on two randomly assigned occasions. Cardiac output declined after 85 min of exercise in C (-1.9+/-0.5 l min(-1), P<0.01) but not in R, as a result of a more pronounced decrease in stroke volume in the former exercise mode (-22.7+/-3.8 ml beat(-1) vs -14.3+/-1.9 ml beat(-1), P<0.01) since heart rate did not differ between trials. Stroke volume responses were despite a higher level of dehydration (-3.3+/-0.2% in R vs -2.8+/-0.2% in C, P<0.05) and hyperthermia in R (39.6+/-0.1 vs 38.8+/-0.1 degrees C in C at 90 min, P<0.01). Finally, mean skin blood flow was lower in R than C (72+/-8 vs 89+/-10%; P<0.05). In conclusion, stroke volume and cardiac output decline was more pronounced in cycling than in running despite lower dehydration and rectal temperature in the former exercise mode.     

Circulating levels of KL-6 in acute respiratory distress syndrome sepsis or traumatic brain injury in critically ill children

KL-6 is a high molecular weight glycoprotein that is expressed on the apical borders of normal secretary alveolar epithelial cells. The aim of our study was to elucidate the potential role of circulating levels of KL-6, related to C-reacting protein (CRP), disease severity (PRISM, TISS), length of stay (LOS) or mechanical ventilation (LOMV), and outcome, in children with acute respiratory distress syndrome (ARDS), sepsis, or traumatic brain injury (TBI). KL-6 concentrations were monitored using solid phase sandwich enzyme-linked immunosorbent assay in plasma of nine patients with ARDS and compared to nine patients with TBI, nine with sepsis, and nine ventilated patients with cancer of matched illness severity on days 1, 3, 5, 7, and 10. Initial respiratory/ventilatory parameters (oxygenation index, plateau pressures) were recorded for ARDS patients. Patients with ARDS had higher early plasma levels of KL-6 (956 +/- 400 U/ml), as compared to patients with TBI (169 +/- 9 U/ml), sepsis (282 +/- 81 U/ml), and ventilated controls (255 +/- 40 U/ml). Significant correlations were demonstrated between plasma KL-6 concentration and oxygenation index, PaO(2): FiO(2) ratio, LOS and LOMV, but not with CRP or PRISM. Only in patients with ARDS, plasma KL-6 levels were higher in non-survivors than survivors (P < 0.03). Plasma KL-6 levels have possible prognostic significance and may provide a useful marker for ARDS in critically ill children.     

Antineutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis after immunisation with bacterial proteins

OBJECTIVE: There is circumstantial evidence for a role for infections in the development of the small vessel vasculitides associated with antineutrophil cytoplasmic antibodies (ANCA). The aim of this study was to determine whether the immunisation of rats with bacterial proteins could result in circulating ANCA, T cells with specificity for ANCA antigens, and a systemic vasculitis. METHODS: Adult male Wistar rats were immunised with pasteurised sonicated S. aureus (n = 7), E. coli (n = 8), purified protein derivative (PPD, n = 5), myeloperoxidase (MPO, n = 5) or phosphate-buffered saline (PBS, n = 5), in complete and in incomplete Freund's adjuvant. ANCA were assayed by indirect immunofluorescent (IIF) examination of normal rat neutrophils, and in ELISAs using human proteinase 3 (PR3), MPO and bactericidal/permeability-inreasing protein (BPI). The T cell response to PR3, MPO and BPI was assessed by a whole blood T cell proliferative assay in vitro, and by a delayed type hypersensitivity (DTH) response in vivo. Kidney and bowel were examined histologically for evidence of vasculitis and colitis. RESULTS: One rat from each group immunised with S. aureus or E. coli developed pauciimmune segmental glomerular sclerosis. The rat immunised with E. coli had additionally an arteritis affecting renal interlobular and gut vessels. This rat had circulating C-ANCA, that produced granular cytoplasmic neutrophil fluorescence with central accentuation, but the target antigen could not be determined in ELISAs using human PR3, MPO or BPI. In animals immunised with S. aureus or E. coli, there was no significant T cell proliferative or DTH response specific for human PR3, MPO or BPI. CONCLUSION: The development of ANCA and vasculitis in a rat immunised with bacterial proteins indicates that the relationship between infections and ANCA should be investigated further.