Basal and exercise-induced skeletal muscle blood flow is augmented in type I diabetes mellitus

1999 ◽  
Vol 98 (1) ◽  
pp. 111-120 ◽  
Author(s):  
R. Andrew P. SKYRME-JONES ◽  
Karen L. BERRY ◽  
Richard C. O'BRIEN ◽  
Ian T. MEREDITH
Keyword(s):  
Diabetes Mellitus ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Type I Diabetes ◽  
Muscle Blood Flow ◽  
Young Patients ◽  
Type I ◽  
Skeletal Muscle Blood Flow ◽  
Insulin Levels ◽  
Exercise Induced

Hyperaemia occurs early in the renal and retinal microcirculation of patients with type I (insulin-dependent) diabetes mellitus, and may be critical in the development of nephropathy and retinopathy. We therefore sought to determine whether resting and exercise-induced hyperaemia was also apparent in the skeletal muscle circulation of young subjects with type I diabetes. Blood flow was assessed by venous occlusion plethysmography in 18 diabetic (DM) subjects and 20 matched controls. Exercise entailed 2 min of isotonic exercise against no load. Endothelium-dependent and -independent vasodilator function was assessed following intra-arterial infusion of acetylcholine and sodium nitroprusside respectively. Forearm blood flow (FBF) was higher in DM subjects than in controls (3.3±0.3 and 2.2±0.2 ml·min-1·100 ml-1 forearm respectively; P < 0.005). This was not due to differences in forearm or body size, blood pressure, heart rate, lipid status or glycaemic control. Peripheral insulin levels were higher in DM subjects than in controls (48.5±8 and 15.5±1.5 μ-units/ml respectively; P < 0.005). Resting FBF was closely correlated with insulin levels (r2 = 0.4; P < 0.005). Parameters of exercise-induced hyperaemia [including peak flow (16.4±1.4 and 12.0±0.7 ml·min-1·100 ml-1 forearm in DM and control subjects respectively; P < 0.01) and the volume repaid to the forearm at 5 min post-exercise (32.1±3.1 and 23.1±1.4 ml·100 ml-1 forearm respectively; P < 0.05)] were also significantly greater in DM subjects, even when differences in resting FBF were taken into account. Peak hyperaemic blood flow and the volume repaid at 5 min were also related to insulin levels (r2 = 0.16; P < 0.05 and r2 = 0.27; P < 0.005 respectively). The vasodilator response to acetylcholine was reduced in DM subjects (P < 0.05; analysis of variance), and the slope of this dose–flow relationship was inversely related to insulin levels (r2 = 0.2; P < 0.05). These data show that both resting and exercise-induced skeletal muscle blood flow are augmented in young patients with type I diabetes, possibly due to the vasodilatory effect of increased insulin levels. Diminished vasodilator responses to acetylcholine may also, in part, be a consequence of insulin-augmented resting muscle blood flow.

Basal and exercise-induced skeletal muscle blood flow is augmented in type I diabetes mellitus

2000 ◽  
Vol 98 (1) ◽  
pp. 111 ◽  
Author(s):  
R. Andrew P. SKYRME-JONES ◽  
Karen L. BERRY ◽  
Richard C. O’BRIEN ◽  
Ian T. MEREDITH
Keyword(s):  
Diabetes Mellitus ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Type I Diabetes ◽  
Muscle Blood Flow ◽  
Type I Diabetes Mellitus ◽  
Type I ◽  
Skeletal Muscle Blood Flow ◽  
Exercise Induced

Vasodilator prostanoids, but not nitric oxide, may account for skeletal muscle hyperaemia in Type I diabetes mellitus

2000 ◽  
Vol 99 (5) ◽  
pp. 383-392 ◽  
Author(s):  
R. Andrew P. SKYRME-JONES ◽  
Richard C. O'BRIEN ◽  
Ian T. MEREDITH
Keyword(s):  
Diabetes Mellitus ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Type I Diabetes ◽  
Muscle Blood Flow ◽  
Type I Diabetes Mellitus ◽  
Type I ◽  
Skeletal Muscle Blood Flow ◽  
Control Subjects ◽  
And Control

We and others have previously documented increased resting and exercise-induced skeletal muscle blood flow in young subjects with Type I (insulin-dependent) diabetes mellitus compared with healthy controls. Both NO and prostanoids are important regulators of vascular tone and may therefore contribute to this hyperaemia. The aim of the present study was to determine the contribution of NO and vasodilator prostanoids to this skeletal muscle hyperaemia in diabetes. We assessed the effects of infusion into the intrabrachial artery of the cyclo-oxygenase inhibitor acetylsalicylic acid (ASA; aspirin) and of the L-arginine analogue NG-monomethyl-L-arginine (L-NMMA) on skeletal muscle blood flow in subjects with Type I diabetes mellitus (DM subjects) and control subjects. Blood flow was measured by venous occlusion plethysmography. Isotonic forearm exercise involved 2 min of wrist flexion and extension. Resting flow (forearm blood flow; FBF) was augmented in DM subjects, as was peak exercise-related blood flow (PFBF) and the volume repaid to the forearm 5 min after exercise (AUC 5, where AUC is area under the flow–time curve) (P < 0.05), even when accounting for differences in basal flow. Infusion of L-NMMA reduced resting flow by 48% in controls (P < 0.005) and by 12% in DM subjects (not significant). L-NMMA reduced PFBF and AUC 5 by 29% (P < 0.05) and 39% (P < 0.0005) respectively in controls, but had no significant effect on these parameters in DM subjects. Infusion of ASA reduced FBF, PFBF and AUC 5 in both DM (P < 0.05) and control (P < 0.05) subjects, but the magnitude of this reduction was greater in DM than in control subjects (ANOVA, P < 0.05), even when differences in resting FBF were accounted for. Indeed, ASA eliminated the differences in FBF, PFBF and AUC 5 between DM and control subjects. Thus increased release of vasodilator prostanoids, rather than of NO, appears to account for skeletal muscle hyperaemia in Type I diabetes.

scholarly journals Elevated Skeletal Muscle Blood Flow in Noncomplicated Type 1 Diabetes Mellitus

Hypertension ◽  
1999 ◽  
Vol 34 (5) ◽  
pp. 1080-1085 ◽  
Author(s):  
Gerald Vervoort ◽  
Jack F. Wetzels ◽  
Jos A. Lutterman ◽  
Laurus G. van Doorn ◽  
Jo H. Berden ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow

Effects of Dietary Omega-3 Polyunsaturated Fatty Acids on the Skeletal-Muscle Blood-Flow Response to Exercise in Rats

2010 ◽  
Vol 20 (6) ◽  
pp. 475-486 ◽  
Author(s):  
Charles L. Stebbins ◽  
Lauren E. Hammel ◽  
Benjamin J. Marshal ◽  
Espen E. Spangenberg ◽  
Timothy I. Musch
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Blood Flow ◽  
Polyunsaturated Fatty Acids ◽  
Hind Limb ◽  
Muscle Blood Flow ◽  
Treadmill Running ◽  
Type I ◽  
Skeletal Muscle Blood Flow ◽  
Pufa Group

The polyunsaturated fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) affect vascular relaxation and involve factors (e.g., nitric oxide) that contribute to exercise-induced increases in skeletal-muscle blood flow (Q). The authors investigated whether DHA and EPA supplementation augments skeletal-muscle Q and vascular conductance (VC) and attenuates renal and splanchnic Q and VC in exercising rats. Rats were fed a diet of 5% lipids by weight, of which 20% was DHA and 30% EPA (PUFA group, n = 9), or 5% safflower oil (SO group, n = 8) for 6 wk. Heart rate (HR), blood pressure (MAP), and hind-limb, renal, and splanchnic Q were measured at rest and during moderate treadmill running. MAP, HR, and renal and splanchnic Q and VC were similar between the 2 groups at rest and during exercise. In the PUFA group, Q (158 ± 27 vs. 128 ± 28 ml · min−1 · 100 g−1) and VC (1.16 ± 0.21 vs. 0.92 ± 0.23 ml · min−1 · 100 g−1 · mm Hg−1) were greater in the exercising hind-limb muscle. Q and VC were also higher in 8 of 28 and 11 of 28 muscles and muscle parts, respectively. These increases were positively correlated to the percent sum of Types I and IIa fibers. Results suggest that DHA+EPA (a) enhances Q and VC in active skeletal muscle (especially Type I and IIa fibers) and that the increase in Q is due to an increase in cardiac output secondary to increases in VC and (b) has no apparent influence on vasoconstriction in renal and splanchnic tissue.

Increased Collagen-Linked Fluorescence in Skin of Young Patients With Type I Diabetes Mellitus

Diabetes Care ◽  
1990 ◽  
Vol 13 (5) ◽  
pp. 468-472 ◽  
Author(s):  
M. H. Dominiczak ◽  
J. Bell ◽  
N. H. Cox ◽  
D. C. McCruden ◽  
S. K. Jones ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type I Diabetes ◽  
Young Patients ◽  
Type I Diabetes Mellitus ◽  
Type I

Biphasic effect of hydrogen peroxide on skeletal muscle arteriolar tone via activation of endothelial and smooth muscle signaling pathways

2004 ◽  
Vol 97 (3) ◽  
pp. 1130-1137 ◽  
Author(s):  
Csongor Csekő ◽  
Zsolt Bagi ◽  
Akos Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Hydrogen Peroxide ◽  
Blood Flow ◽  
Smooth Muscle ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Local Regulation ◽  
Prostaglandin H ◽  
Arteriolar Tone

We hypothesized that hydrogen peroxide (H2O2) has a role in the local regulation of skeletal muscle blood flow, thus significantly affecting the myogenic tone of arterioles. In our study, we investigated the effects of exogenous H2O2 on the diameter of isolated, pressurized (at 80 mmHg) rat gracilis skeletal muscle arterioles (diameter of ∼150 μm). Lower concentrations of H2O2 (10−6–3 × 10−5 M) elicited constrictions, whereas higher concentrations of H2O2 (6 × 10−5–3 × 10−4 M), after initial constrictions, caused dilations of arterioles (at 10−4 M H2O2, −19 ± 1% constriction and 66 ± 4% dilation). Endothelium removal reduced both constrictions (to −10 ± 1%) and dilations (to 33 ± 3%) due to H2O2. Constrictions due to H2O2 were completely abolished by indomethacin and the prostaglandin H2/thromboxane A2 (PGH2/TxA2) receptor antagonist SQ-29548. Dilations due to H2O2 were significantly reduced by inhibition of nitric oxide synthase (to 38 ± 7%) but were unaffected by clotrimazole or sulfaphenazole (inhibitors of cytochrome P-450 enzymes), indomethacin, or SQ-29548. In endothelium-denuded arterioles, clotrimazole had no effect, whereas H2O2-induced dilations were significantly reduced by charybdotoxin plus apamin, inhibitors of Ca2+-activated K+ channels (to 24 ± 3%), the selective blocker of ATP-sensitive K+ channels glybenclamide (to 14 ± 2%), and the nonselective K+-channel inhibitor tetrabutylammonium (to −1 ± 1%). Thus exogenous administration of H2O2 elicits 1) release of PGH2/TxA2 from both endothelium and smooth muscle, 2) release of nitric oxide from the endothelium, and 3) activation of K+ channels, such as Ca2+-activated and ATP-sensitive K+ channels in the smooth muscle resulting in biphasic changes of arteriolar diameter. Because H2O2 at low micromolar concentrations activates several intrinsic mechanisms, we suggest that H2O2 contributes to the local regulation of skeletal muscle blood flow in various physiological and pathophysiological conditions.

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