Heinonen I, Brothers RM, Kemppainen J, Knuuti J, Kalliokoski KK, Crandall CG. Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow. J Appl Physiol 111: 818-824, 2011. First published June 16, 2011 doi:10.1152 doi:10. /japplphysiol.00269.2011cades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positronemission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 Ϯ 1.0°C to 37.4 Ϯ 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 Ϯ 0.5 to 2.3 Ϯ 1.2 ml·100 g Ϫ1 ·min Ϫ1 (P Ͻ 0.05), whereas skin blood flow under the heating source increased from 0.7 Ϯ 0.3 to 5.5 Ϯ 1.5 ml·100 g Ϫ1 ·min Ϫ1 (P Ͻ 0.01). While whole body heat stress increased intestinal temperature by ϳ1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 Ϯ 0.5 ml·100 g Ϫ1 ·min Ϫ1 ; heat stress: 1.7 Ϯ 0.3 ml·100 g Ϫ1 ·min Ϫ1 ; P ϭ 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 Ϯ 1.5 ml·100 g Ϫ1 ·min Ϫ1 ) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress. positron-emission tomography; skin blood flow; bone blood flow; heat stress WHEN HUMANS ARE EXPOSED to acute heat stress several cardiovascular adjustments occur primarily directed toward increasing skin blood flow, which are necessary to adequately dissipate an internal heat load. These responses are accomplished through a combination of local and neurally mediated cutaneous vasodilation, coupled with elevated cardiac output and redistribution of blood flow and volume away from central vascular beds, such as the splanchnic and renal circulations, to the cutaneous circulation (4, 9, 21, 29 -31). In addition, skin and muscle sympathetic nerve activities (SNA) increase during heat stress (3,5,6,17,23,34), with increases in skin SNA being responsible for sweating and cutaneous vasodilation, while increases in muscle SNA have a less clear end result.Earlier studies p...

AimsMore than 50% of patients with heart failure have preserved ejection fraction characterized by diastolic dysfunction. The prevalance of diastolic dysfunction is higher in females and associates with multiple comorbidities such as hypertension (HT), obesity, hypercholesterolemia (HC), and diabetes mellitus (DM). Although its pathophysiology remains incompletely understood, it has been proposed that these comorbidities induce systemic inflammation, coronary microvascular dysfunction, and oxidative stress, leading to myocardial fibrosis, myocyte stiffening and, ultimately, diastolic dysfunction. Here, we tested this hypothesis in a swine model chronically exposed to three common comorbidities.Methods and resultsDM (induced by streptozotocin), HC (produced by high fat diet), and HT (resulting from renal artery embolization), were produced in 10 female swine, which were followed for 6 months. Eight female healthy swine on normal pig-chow served as controls. The DM + HC + HT group showed hyperglycemia, HC, hypertriglyceridemia, renal dysfunction and HT, which were associated with systemic inflammation. Myocardial superoxide production was markedly increased, due to increased NOX activity and eNOS uncoupling, and associated with reduced NO production, and impaired coronary small artery endothelium-dependent vasodilation. These abnormalities were accompanied by increased myocardial collagen content, reduced capillary/fiber ratio, and elevated passive cardiomyocyte stiffness, resulting in an increased left ventricular end-diastolic stiffness (measured by pressure–volume catheter) and a trend towards a reduced E/A ratio (measured by cardiac MRI), while ejection fraction was maintained.ConclusionsThe combination of three common comorbidities leads to systemic inflammation, myocardial oxidative stress, and coronary microvascular dysfunction, which associate with myocardial stiffening and LV diastolic dysfunction with preserved ejection fraction.