OBJECTIVEObservational studies show breaking up prolonged sitting has beneficial associations with cardiometabolic risk markers, but intervention studies are required to investigate causality. We examined the acute effects on postprandial glucose and insulin levels of uninterrupted sitting compared with sitting interrupted by brief bouts of light- or moderate-intensity walking.RESEARCH DESIGN AND METHODSOverweight/obese adults (n = 19), aged 45–65 years, were recruited for a randomized three-period, three-treatment acute crossover trial: 1) uninterrupted sitting; 2) seated with 2-min bouts of light-intensity walking every 20 min; and 3) seated with 2-min bouts of moderate-intensity walking every 20 min. A standardized test drink was provided after an initial 2-h period of uninterrupted sitting. The positive incremental area under curves (iAUC) for glucose and insulin (mean [95% CI]) for the 5 h after the test drink (75 g glucose, 50 g fat) were calculated for the respective treatments.RESULTSThe glucose iAUC (mmol/L) ⋅ h after both activity-break conditions was reduced (light: 5.2 [4.1–6.6]; moderate: 4.9 [3.8–6.1]; both P < 0.01) compared with uninterrupted sitting (6.9 [5.5–8.7]). Insulin iAUC (pmol/L) ⋅ h was also reduced with both activity-break conditions (light: 633.6 [552.4–727.1]; moderate: 637.6 [555.5–731.9], P < 0.0001) compared with uninterrupted sitting (828.6 [722.0–950.9]).CONCLUSIONSInterrupting sitting time with short bouts of light- or moderate-intensity walking lowers postprandial glucose and insulin levels in overweight/obese adults. This may improve glucose metabolism and potentially be an important public health and clinical intervention strategy for reducing cardiovascular risk.

Abstract-Aerobic exercise training increases arterial compliance and reduces systolic blood pressure, but the effects of muscular strength training on arterial mechanical properties are unknown. We compared blood pressure, whole body arterial compliance, aortic impedance, aortic stiffness (measured by ␤-index and carotid pulse pressure divided by normalized systolic expansion Femoral-dorsalis pedis pulse wave velocity was also higher in the athletes, but carotid-femoral pulse wave velocity was not different. Furthermore, both carotid (56Ϯ3 versus 44Ϯ2 mm Hg; PϽ0.001) and brachial (60Ϯ3 versus 50Ϯ2 mm Hg; PϽ0.01) pulse pressures were higher in the athletes, but mean arterial pressure and resting heart rate did not differ between groups. These data indicate that both the proximal aorta and the leg arteries are stiffer in strength-trained individuals and contribute to a higher cardiac afterload. (Hypertension. 1999;33:1385-1391.) Key Words: mechanical properties, arterial Ⅲ stiffness Ⅲ compliance Ⅲ exercise A rterial compliance plays a role in determining both arterial systolic and diastolic pressure and therefore, in a clinical context, influences left ventricular size and function, coronary blood flow, and the risk of cerebrovascular accidents. [1][2][3] In the past, measures of arterial compliance in humans have been invasive, and therefore surrogate measures such as peripheral pulse pressure have been applied to investigate potential relationships with clinical outcomes. Pulse pressure correlates closely with serious cardiovascular outcomes such as myocardial infarction, 4 thus highlighting arterial compliance as a potential target for risk reduction therapy.Arterial compliance decreases with increasing age, 5-8 in atherosclerosis and coronary artery disease, 5,9 -12 and in hypertensive individuals. [13][14][15] Aerobic exercise has welldocumented efficacy for cardiovascular risk reduction, and it appears that at least part of its benefit derives from modification of arterial properties. In cross-sectional studies, aerobically trained athletes have a higher arterial compliance than sedentary individuals. 6,16,17 Furthermore, arterial compliance is elevated independently of blood pressure reduction in previously sedentary males after a 4-week program of moderate-intensity aerobic exercise training. 18 These data suggest that aerobic exercise structurally modifies the large arteries, a postulate supported by studies of ex vivo aortic properties in rats, after 16 weeks of spontaneous running. 19,20 While aerobic exercise is widely recommended as a preventative and therapeutic strategy, resistance-style training is becoming more popular, although it is less well studied with respect to its effects on blood pressure, and no previous study has examined arterial mechanical properties in this context. High-level resistance training is associated with abrupt and large pressor responses 21 and in the long term leads to a concentric ventricular hypertrophy. [22][23][24][25] We hypothesize that arterial mechanical modifica...

Aims/hypothesis Brown adipose tissue (BAT) activation increases energy consumption and may help in the treatment of obesity. Cold exposure is the main physiological stimulus for BAT thermogenesis and the sympathetic nervous system, which innervates BAT, is essential in this process. However, cold-induced BAT activation is impaired in obese humans. To explore the therapeutic potential of BAT, it is essential to determine whether pharmacological agents can activate BAT. Methods We aimed to determine whether BAT can be activated in lean and obese humans after acute administration of an orally bioavailable sympathomimetic. In a randomised, double-blinded, crossover trial, we administered 2.5 mg/kg of oral ephedrine to nine lean (BMI 22±1 kg/m 2 ) and nine obese (BMI 36±1 kg/m 2 ) young men. On a separate day, a placebo was administered to the same participants. BAT activity was assessed by measuring glucose uptake with [ 18 F]fluorodeoxyglucose and positron emission tomography-computed tomography imaging.

Breaking up prolonged sitting has been beneficially associated with cardiometabolic risk markers in both observational and intervention studies. We aimed to define the acute transcriptional events induced in skeletal muscle by breaks in sedentary time. Overweight/obese adults participated in a randomized three-period, three-treatment crossover trial in an acute setting. The three 5-h interventions were performed in the postprandial state after a standardized test drink and included seated position with no activity and seated with 2-min bouts of light- or moderate-intensity treadmill walking every 20 min. Vastus lateralis biopsies were obtained in eight participants after each treatment, and gene expression was examined using microarrays validated with real-time quantitative PCR. There were 75 differentially expressed genes between the three conditions. Pathway analysis indicated the main biological functions affected were related to small-molecule biochemistry, cellular development, growth and proliferation, and carbohydrate metabolism. Interestingly, differentially expressed genes were also linked to cardiovascular disease. For example, relative to prolonged sitting, activity bouts increased expression of nicotamide N-methyltransferase, which modulates anti-inflammatory and anti-oxidative pathways and triglyceride metabolism. Activity bouts also altered expression of 10 genes involved in carbohydrate metabolism, including increased expression of dynein light chain, which may regulate translocation of the GLUT-4 glucose transporter. In addition, breaking up sedentary time reversed the effects of chronic inactivity on expression of some specific genes. This study provides insight into the muscle regulatory systems and molecular processes underlying the physiological benefits induced by interrupting prolonged sitting.