Therefore, in the upper as well as in the lower limb vasculature, repetitive exposure to increased shear stress over a long-term period results in improved FMD of large conduit arteries as well as greater vasodilatory capacity during isolated exercise in the predominantly trained muscles. Long-term training involving predominantly the lower limbs also results in enhanced vascular reactivity in upper limb conduit and resistance vessels.
Mild-to-moderate obesity in prepubertal boys without insulin resistance is associated with impaired endothelial function and blunted muscle perfusion response to local dynamic exercise without alteration of vascular smooth muscle reactivity.
Objective: Although increased blood flow (BF) in exercising muscles is thought to be impaired in obese subjects and may contribute to physical inactivity, data are scarce in this regard and the involvement of endothelium dysfunction remains partly hypothetical. Methods: A total of 16 middle-aged obese men (body mass index, BMIX30 kg m À2 ) and 16 normal-weight men (BMIo25 kg m À2 ), matched for age, were recruited. We used ultrasonography to compare intima-media thickness (IMT) and distensibility of the carotid artery, flow-mediated dilation (FMD), nitrate-dependent dilation (NDD) and peak BF during postischemic hyperemia in the brachial artery (a conduit artery), and leg BF during knee-extensor exercise (indicative of resistance vessel function) in obese and in normal-weight men. In addition, 10 obese men participated in an 8 week individualized low-intensity training program. Results: Compared with normal-weight men, obese men had higher carotid IMT (0.50 ± 0.01 vs 0.62 ± 0.04 mm, Po0.05) but lower carotid distensibility (0.26±0.03 vs 0.11±0.03 mm Hg À1 10 À2 , Po0.05), FMD (5.7±0.4 vs 3.3±0.5%, Po0.05) and peak BF during post-ischemic hyperemia (398 ± 52 vs 229 ± 24%, Po0.05), despite similar maximal shear rate, without NDD differences. Lower limb BF (ml min À1 100 g À1 ) increased significantly from rest to maximal exercise in both groups with lower values in obese men (at peak power, 36.9 ± 1.6 vs 31.5 þ 2.2 ml min À1 100 g À1 , Po0.05). Exercise training normalized carotid distensibility (0.14±0.04 before vs 0.23±0.03 mm Hg À1 10 À2 after training, P ¼ 0.09) and FMD (2.7±0.4 before vs 4.8±0.5% after training, Po0.05), but did not improve brachial post-ischemic peak BF or exercising leg BF. Conclusions: In obese men, conduit and resistance vessel reactivity is depressed, but a short-term low-intensity exercise training improves distensibility and endothelium dependent vasodilation in the large conduit artery, but not post ischemic or exercise muscle BF.
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