These studies were undertaken to compare dual-energy x-ray absorptiometry (DXA) and computed tomography (CT) measurements of abdominal fat and to determine whether anthropometry could be combined with DXA to predict intraabdominal (visceral) fat mass in humans. Twenty-one volunteers underwent abdominal CT scans, DXA, and anthropometry. DXA- and CT-measured total abdominal fat were similar (8448 +/- 5005 and 8066 +/- 5354 mL, respectively; NS) and were highly correlated (r = 0.985, P < 0.001). The combination of anthropometry and DXA was a suboptimal predictor of CT-measured intraabdominal fat (r = 0.61, P < 0.05); however, the combination of a single CT slice (to assess the ratio of intraabdominal to total abdominal adipose tissue) and DXA-measured abdominal fat was an excellent predictor of CT-measured intraabdominal fat (r = 0.98, P < 0.001). We conclude that a single-slice CT scan (or other imaging technique) with or without DXA is required for accurate predictions of intraabdominal fat.
The benefits of aerobic exercise (AE) training on blood pressure (BP) and arterial stiffness are well established, but the effects of resistance training are less well delineated. The purpose of this study was to determine the impact of resistance vs aerobic training on haemodynamics and arterial stiffness. Thirty pre-or stage-1 essential hypertensives (20 men and 10 women), not on any medications, were recruited (age: 48.2 ± 1.3 years) and randomly assigned to 4 weeks of either resistance (RE) or AE training. Before and after training, BP, arterial stiffness (pulse wave velocity (PWV)) and vasodilatory capacity (VC) were measured. Resting systolic BP (SBP) decreased following both training modes (SBP: RE, pre 136±2.9 vs post 132±3.4; AE, pre 141±3.8 vs post 136 ± 3.4 mm Hg, P ¼ 0.005; diastolic BP: RE, pre 78 ± 1.3 vs post 74 ± 1.6; AE, pre 80 ± 1.6 vs post 77 ± 1.7 mm Hg, P ¼ 0.001). Central PWV increased (P ¼ 0.0001) following RE (11 ± 0.9-12.7 ± 0.9 m s À1 ) but decreased after AE (12.1 ± 0.8-11.1 ± 0.8 m s À1 ). Peripheral PWV also increased (P ¼ 0.013) following RE (RE, pre 11.5±0.8 vs post 12.5 ± 0.7 m s À1 ) and decreased after AE (AE, pre 12.6 ± 0.8 vs post 11.6 ± 0.7 m s À1 ). The VC area under the curve (VC AUC ) increased more with RE than that with AE (RE, pre 76±8.0 vs post 131.1±11.6; AE, pre 82.7±8.0 vs post 110.1 ± 11.6 ml per min per s per 100 ml, P ¼ 0.001). Further, peak VC (VC peak ) increased more following resistance training compared to aerobic training (RE, pre 17±1.9 vs post 25.8±2.1; AE, pre 19.2±8.4 vs post 22.9 ± 8.4 ml per min per s per 100 ml, P ¼ 0.005). Although both RE and AE training decreased BP, the change in pressure may be due to different mechanisms.
Prolonged sitting impairs endothelial function in the leg vasculature, and this impairment is thought to be largely mediated by a sustained reduction in blood flow-induced shear stress. Indeed, preventing the marked reduction of shear stress during sitting with local heating abolishes the impairment in popliteal artery endothelial function. Herein, we tested the hypothesis that sitting-induced reductions in shear stress and ensuing endothelial dysfunction would be prevented by periodic leg movement, or "fidgeting." In 11 young, healthy subjects, bilateral measurements of popliteal artery flow-mediated dilation (FMD) were performed before and after a 3-h sitting period during which one leg was subjected to intermittent fidgeting (1 min on/4 min off) while the contralateral leg remained still throughout and served as an internal control. Fidgeting produced a pronounced increase in popliteal artery blood flow and shear rate (prefidgeting, 33.7 Ϯ 2.6 s Ϫ1 to immediately postfidgeting, 222.7 Ϯ 28.3 s Ϫ1; mean Ϯ SE; P Ͻ 0.001) that tapered off during the following 60 s. Fidgeting did not alter popliteal artery blood flow and shear rate of the contralateral leg, which was subjected to a reduction in blood flow and shear rate throughout the sitting period (presit, 71.7 Ϯ 8.0 s Ϫ1 to 3-h sit, 20.2 Ϯ 2.9 s Ϫ1
This consensus statement is an update of the 2010 American College of Sports Medicine position stand on exercise and type 2 diabetes. Since then, a substantial amount of research on select topics in exercise in individuals of various ages with type 2 diabetes has been published while diabetes prevalence has continued to expand worldwide. This consensus statement provides a brief summary of the current evidence and extends and updates the prior recommendations. The document has been expanded to include physical activity, a broader, more comprehensive definition of human movement than planned exercise, and reducing sedentary time. Various types of physical activity enhance health and glycemic management in people with type 2 diabetes, including flexibility and balance exercise, and the importance of each recommended type or mode are discussed. In general, the 2018 Physical Activity Guidelines for Americans apply to all individuals with type 2 diabetes, with a few exceptions and modifications. People with type 2 diabetes should engage in physical activity regularly and be encouraged to reduce sedentary time and break up sitting time with frequent activity breaks. Any activities undertaken with acute and chronic health complications related to diabetes may require accommodations to ensure safe and effective participation. Other topics addressed are exercise timing to maximize its glucose-lowering effects and barriers to and inequities in physical activity adoption and maintenance.
Exercise of appropriate intensity is a potent stimulus for GH and cortisol secretion. Circadian and diurnal rhythms may modulate the GH and cortisol responses to exercise, but nutrition, sleep, prior exercise patterns, and body composition are potentially confounding factors. To determine the influence of the time of day on the GH and cortisol response to acute exercise, we studied 10 moderately trained young men (24.1 +/- 1.1 yr old; maximal oxygen consumption, 47.9 +/- 1.4 mL/kg.min; percent body fat, 13.2 +/- 0.6%). After a supervised night of sleep and a standard meal 12 h before exercise, subjects exercised at a constant velocity (to elicit an initial blood lactate concentration of approximately 2.5 mmol/L) on a treadmill for 30 min on 3 separate occasions, starting at 0700, 1900, and 2400 h. Blood samples were obtained at 5-min intervals for 1 h before and 5 h after the start of exercise; subjects were not allowed to sleep during this period. Subjects were also studied on 3 control days under identical conditions without exercise. There were no significant differences with time of day in the mean blood lactate and submaximal oxygen consumption values during exercise. The differences over time in serum GH and cortisol concentrations between the exercise day and the control day were determined with 95% confidence limits for each time of day. Exercise stimulated a significant increase in serum GH concentrations over control day values for approximately 105--145 min (P < 0.05) with no significant difference in the magnitude of this response by time of day. The increase in serum GH concentrations with exercise was followed by a transient suppression of GH release (for approximately 55--90 min; P < 0.05) after exercise at 0700 and 1900 h, but not at 2400 h. Although the duration of the increase in serum cortisol concentrations after exercise was similar (approximately 150--155 min; P < 0.05) at 0700, 1900, and 2400 h, the magnitude of this increase over control day levels was greatest at 2400 h. This difference was significant for approximately 130 min and approximately 40 min compared to exercise at 1900 and 0700 h, respectively (P < 0.05). The cortisol response to exercise at 0700 h was significantly greater than that at 1900 h for about 55 min (P < 0.05). A rebound suppression of cortisol release for about 50 min (P < 0.05) was observed after exercise at 2400 h, but not 0700 or 1900 h. Both baseline (before exercise) and peak cortisol concentrations were significantly higher at 0700 h than at 1900 or 2400 h (P < 0.01). We conclude that time of day does not alter the GH response to exercise; however, the exercise-induced cortisol response is modulated by time of day.
We examined the validity of percent body fat (%Fat) estimation by two-compartment (2-Comp) hydrostatic weighing (Siri 2-Comp), 3-Comp dual-energy X-ray absorptiometry (DEXA 3-Comp), 3-Comp hydrostatic weighing corrected for the total body water (Siri 3-Comp), and anthropometric methods in young and older individuals (n = 78). A 4-Comp model of body composition served as the criterion measure of %Fat (Heymsfield 4-Comp; S. B. Heymsfield, S. Lichtman, R. N. Baumgartner, J. Wang, Y. Kamen, A. Aliprantis, and R. N. Pierson Jr., Am. J. Clin. Nutr. 52: 52-58, 1990.). Comparison of the Siri 3-Comp with the Heymsfield 4-Comp model revealed mean differences of =0.4 %Fat, r values >/= r = 0.997, total error values = 0.85 %Fat, and 95% confidence intervals (Bland-Altman analysis) of =1.7 %Fat. Comparison of Siri 2-Comp, DEXA, and anthropometric models with the Heymsfield 4-Comp revealed that total error scores ranged from +/-4. 0 to +/-10.7 %Fat, and 95% confidence intervals associated with the Bland-Altman analysis ranged from +/-5.1 to +/-15.0 %Fat. We conclude that the Siri 3-Comp model provides valid and accurate body composition data when compared with a 4-Comp criterion model. However, the individual variability associated with the Siri 2-Comp, DEXA 3-Comp, and anthropometric models may limit their use in research settings. The use of anthropometric estimation methods resulted in large mean differences and a considerable amount of interindividual variability. These data suggest that the use of these techniques should be viewed with caution.
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