Carbohydrate ingestion, with transient endogenous insulinaemia, produces both sympathetic activation and vasodilatation in normal humans

2002 ◽  
Vol 102 (5) ◽  
pp. 523-529 ◽  
Author(s):  
Eleanor M. SCOTT ◽  
John P. GREENWOOD ◽  
Giovanni VACCA ◽  
John B. STOKER ◽  
Stephen G. GILBEY ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Sympathetic Activity ◽  
Healthy Subjects ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Carbohydrate Ingestion ◽  
Vascular Bed ◽  
Carbohydrate Meal

It has been shown that sustained insulin infusion causes an increase in sympathetic vasoconstrictor discharge but, despite this, also causes peripheral vasodilatation. The present study was designed to determine in healthy subjects the effect of ingestion of a carbohydrate meal, with its attendant physiological insulinaemia, on vascular resistance in and sympathetic vasoconstrictor discharge to the same vascular bed, and the relationship between these parameters. Fifteen healthy subjects were studied for 2h following ingestion of a carbohydrate meal. Calf vascular resistance was measured by venous occlusion plethysmography, and muscle sympathetic nerve activity was assessed by peroneal microneurography. Five of the subjects also ingested water on a separate occasion, as a control. Following the carbohydrate meal, the serum insulin concentration increased to 588±72pmol/l. This was associated with a 47% increase in skeletal muscle blood flow (P < 0.001), a 39% fall in vascular resistance (P < 0.001) and a 57% increase in sympathetic activity (P < 0.001). There was a significant correlation between the increase in insulin and the changes in blood flow, vascular resistance and sympathetic activity. In conclusion, we have shown that ingestion of a carbohydrate meal, with its attendant physiological insulinaemia, was associated with overriding skeletal muscle vasodilatation, despite an increase in sympathetic vasoconstrictor discharge to the same vascular bed. These mechanisms may be important in ensuring optimal glucose uptake and maintenance of blood pressure postprandially.

Regulation of canine skeletal muscle and hindlimb blood flow in acute anemia

1988 ◽  
Vol 66 (1) ◽  
pp. 101-105 ◽  
Author(s):  
P. Kubes ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Sympathetic Stimulation ◽  
Arterial Blood ◽  
Measured Resistance ◽  
Muscle Groups

Redistribution of blood flow away from resting skeletal muscle does not occur during anemic hypoxia even when whole body oxygen uptake is not maintained. In the present study, the effects of sympathetic nerve stimulation on both skeletal muscle and hindlimb blood flow were studied prior to and during anemia in anesthetized, paralyzed, and ventilated dogs. In one series (skeletal muscle group, n = 8) paw blood flow was excluded by placing a tourniquet around the ankle; in a second series (hindlimb group, n = 8) no tourniquet was placed at the ankle. The distal end of the transected left sciatic nerve was stimulated to produce a maximal vasoconstrictor response for 4-min intervals at normal hematocrit (Hct.) and at 30 min of anemia (Hct. = 14%). Arterial blood pressure and hindlimb or muscle blood flow were measured; resistance and vascular hindrance were calculated. Nerve stimulation decreased blood flow (p < 0.05) in the hindlimb and muscle groups at normal Hct. Blood flow rose (p < 0.05) during anemia and was decreased (p < 0.05) in both groups during nerve stimulation. However, the blood flow values in both groups during nerve stimulation in anemic animals were greater (p < 0.05) than those at normal Hct. Hindlimb and muscle vascular resistance fell significantly during anemia and nerve stimulation produced a greater increase in vascular resistance at normal Hct. Vascular hindrance in muscle, but not hindlimb, was less during nerve stimulation in anemia than at normal Hct. The data indicate that (i) maximal sympathetic stimulation produced a significant decrease in both skeletal muscle and hindlimb blood flow during anemia, (ii) the reduction in blood flow in these areas was less with sympathetic stimulation during anemia than at normal Hct., and (iii) the anemic stimulus (Hct. = 14%) does not activate maximal sympathetic vasoconstrictor tone in the skeletal muscle.

Lipolysis and Lactate Production in Human Skeletal Muscle and Adipose Tissue following Glucose Ingestion

1998 ◽  
Vol 94 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Daniëlle A. J. M. Kerckhoffs ◽  
Peter Arner ◽  
Jan Bolinder
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Muscle Blood Flow ◽  
Lactate Production ◽  
Tissue Blood Flow ◽  
Oral Glucose ◽  
Glucose Load ◽  
Carbohydrate Ingestion ◽  
Glucose Ingestion

1. Using microdialysis, we compared lipolysis, as well as the production of lactate, in human adipose tissue and muscle after the ingestion of carbohydrate. 2. The absolute concentrations of glycerol and lactate were measured in subcutaneous adipose tissue, skeletal muscle and arterialized venous blood in eight normal subjects during basal conditions and 4 h after a 75 g oral glucose load. Nutritive blood flow in muscle and adipose tissue was monitored simultaneously with the microdialysis ethanol clearance technique. 3. At baseline, the concentrations of glycerol in adipose tissue and in muscle were about 7 times and about 2.5 times higher respectively than those in plasma. After glucose ingestion, the changes in glycerol concentrations differed significantly between the three compartments (P < 0.0001). In plasma and adipose tissue, the concentrations decreased rapidly and markedly, but returned to baseline levels after 4 h. In muscle, the decrease in glycerol was less pronounced and more protracted. 4. At baseline, the concentrations of lactate in muscle and in adipose tissue were about 3 times and about 1.5 times higher respectively than those in plasma. After the ingestion of glucose, the levels increased transiently in similar ways in muscle, adipose tissue and plasma. The differences in absolute lactate concentrations between the three compartments were maintained after the glucose load (P < 0.001). 5. Adipose tissue blood flow increased transiently after glucose ingestion, whereas muscle blood flow remained unchanged. 6. Both muscle and adipose tissue are a source of glycerol and lactate release during basal conditions and after glucose ingestion. The regulation of lactate production, but not of lipolysis, after carbohydrate ingestion is similar in the two tissues.

Dissociation between volume blood flow and laser-Doppler signal from rat muscle during changes in vascular tone

1998 ◽  
Vol 274 (4) ◽  
pp. H1248-H1254 ◽  
Author(s):  
Larisa V. Kuznetsova ◽  
Nicole Tomasek ◽  
Gisli H. Sigurdsson ◽  
Andrej Banic ◽  
Dominique Erni ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Vascular Tone ◽  
Muscle Blood Flow ◽  
Laser Doppler ◽  
Ang Ii ◽  
Ganglionic Blockade ◽  
Vasoactive Substances ◽  
Total Muscle

Although the laser-Doppler flowmetry (LDF) signal from skeletal muscle has been shown to provide a good measure of blood flow under some conditions, its behavior during administration of vasoactive substances has never been addressed. The aims of this study were to compare 1) changes in LDF signal with those in total muscle blood flow measured with radioactive microspheres after ganglionic blockade (chlorisondamine) and during administration of angiotensin II (ANG II), phenylephrine (PE), and isoproterenol (Iso) and 2) changes in vascular resistance estimated by the two techniques. The LDF signal from the biceps femoris muscle was investigated in anesthetized male Wistar rats. Ganglionic blockade led to a significant ( P < 0.05) fall in mean arterial pressure (MAP) [medians (lower, upper quartiles): 78 (72, 83) vs. 127 (114, 138) mmHg under basal conditions], muscle blood flow (MBF, microsphere technique; 61%), and the LDF signal (29%). Muscle vascular resistance (MVR = MAP/MBF) was increased (64%, P < 0.05), but vascular resistance estimated as MAP/LDF signal (MVRLDF) was unchanged. During ANG II and PE infusions, MAP rose ( P< 0.05) to 178 (155, 194) and 127 (124, 142) mmHg, respectively; MBF did not change compared with the preinfusion (postganglionic blockade) level and remained significantly ( P< 0.05) lower than baseline, whereas the LDF signal increased up to a level not different from baseline. MVR rose and was significantly ( P < 0.05) higher than baseline, whereas MVRLDF did not differ significantly from baseline. During Iso infusion, MAP fell [58 (56, 60) vs. 94 (92, 102) mmHg, P < 0.05], the LDF signal was reduced (49%, P < 0.05) despite a large increase in MBF (139%, P < 0.05), and MVR fell (74%, P < 0.05), whereas MVRLDF did not change vs. preinfusion level. Our results suggest that 1) changes in the LDF signal from muscle may not correlate with changes in total muscle blood flow measured by the microsphere technique during infusion of vasoactive substances and 2) the use of LDF data for estimation of MVR during changes in vascular tone in rat skeletal muscle is probably not appropriate.

Hindlimb vascular responses to sympathetic augmentation during acute anemia

1985 ◽  
Vol 63 (7) ◽  
pp. 782-786 ◽  
Author(s):  
Stephen M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Sympathetic Activity ◽  
Carotid Arteries ◽  
Muscle Blood Flow ◽  
Recovery Period ◽  
Control Period ◽  
Whole Body ◽  
Block Group ◽  
Limb Blood Flow

The effect of increased sympathetic activity on skeletal muscle blood flow during acute anemic hypoxia was studied in 16 anesthetized dogs. Sympathetic activity was altered by clamping the carotid arteries bilaterally below the carotid sinus. One group (n = 8) was beta blocked by administration of propranolol (1 mg/kg); a second group (n = 8) was untreated. Venous outflow from the left hindlimb was isolated for measurement of blood flow and O2 uptake [Formula: see text]. After a 20-min control period, both carotid arteries were clamped (CC) for 20 min followed by a 20-min recovery period. The sequence was repeated after hematocrit was lowered to about 15% by dextran exchange for blood. Prior to anemia, CC did not alter cardiac output or limb blood flow in either group. After induction of anemia, hindlimb resistance was higher with CC in the beta block than in the no block group. Both limb blood flow and [Formula: see text] fell in the β-block group with CC during anemia. Beta block also prevented the additive increases in whole body [Formula: see text] seen with CC and induction of anemia. The data showed that the increased vasoconstrictor tone that was obtained with beta block during anemia was successful in redistributing the lower viscosity blood away from resting skeletal muscle, even to the point that muscle [Formula: see text] was decreased.

scholarly journals Sympathetic vasoconstriction in skeletal muscle: Modulatory effects of aging, exercise training, and sex

2021 ◽  
Author(s):  
Darren S DeLorey
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Vascular Resistance ◽  
Vascular Function ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Sympathetic Vasoconstriction ◽  
Effects Of Aging

The sympathetic nervous system (SNS) is a critically important regulator of the cardiovascular system. The SNS controls cardiac output and its distribution, as well as peripheral vascular resistance and blood pressure at rest and during exercise. Aging is associated with increased blood pressure and decreased skeletal muscle blood flow at rest and in response to exercise. The mechanisms responsible for the blunted skeletal muscle blood flow response to dynamic exercise with aging have not been fully elucidated; however, increased muscle sympathetic nerve activity (MSNA), elevated vascular resistance and a decline in endothelium-dependent vasodilation are commonly reported in older adults. In contrast to aging, exercise training has been shown to reduce blood pressure and enhance skeletal muscle vascular function. Exercise training has been shown to enhance nitric oxide-dependent vascular function and may improve the vasodilatory capacity of the skeletal muscle vasculature; however, surprisingly little is known about the effect of exercise training on the neural control of circulation. The control of blood pressure and skeletal muscle blood flow also differs between males and females. Blood pressure and MSNA appear to be lower in young females compared to males. However, females experience a larger increase in MSNA with aging compared to males. The mechanism(s) for the altered SNS control of vascular function in females remain to be determined. Novelty: • This review will summarize our current understanding of the effects of aging, exercise training and sex on sympathetic vasoconstriction at rest and during exercise. • Areas where additional research is needed are also identified.

Vascular Actions of Insulin in Health and Disease

1995 ◽  
Vol 20 (2) ◽  
pp. 127-154 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Arend Bonen
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Resistance ◽  
Prolonged Exposure ◽  
Muscle Blood Flow ◽  
Metabolic Effects ◽  
Smooth Muscle Tissue

Insulin has well known metabolic effects. However, depending on the magnitude and duration of the insulin stimulus, this hormone can also produce vasodilation and vascular smooth muscle growth. The association of hyperinsulinemia with the metabolic disorders of obesity and non-insulin-dependent diabetes, as well as with the cardiovascular pathologies of hypertension and atherosclerosis, has led to suggestions that perhaps elevated insulin levels are causally related to these diseases. Alternatively, insulin resistance may develop following an increase in skeletal muscle vascular resistance, with or without hypertension, such that a reduction in skeletal muscle blood flow leads to an attenuated glucose delivery and uptake. These hypotheses are explored in this review by examining the effects of insulin on vascular smooth muscle tissue during both acute and prolonged exposure. An interaction among hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with the insulin resistant state is described whereby insulin resistance can be both a cause and a result of elevated vascular resistance. The association between blood flow and insulin stimulated glucose uptake suggests that therapeutic intervention against the development of skeletal muscle vascular resistance should occur early in individuals genetically predisposed to cardiovascular pathology in order to attenuate, or avoid, insulin resistance and its sequelae. Key words: hyperinsulinemia, hyperglycemia, vascular smooth muscle, obesity, hypertension, atherosclerosis

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

scholarly journals Sequential alterations in the diameters of capillaries in rabbit skeletal muscle following deep transverse friction - a morphometric study

2005 ◽  
Vol 61 (2) ◽  
Author(s):  
M. A. Gregory ◽  
M. N. Deane ◽  
M. Marsh
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Biceps Femoris ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Cross Sectional ◽  
Biceps Femoris Muscle ◽  
Beneficial Effects ◽  
The Cross

Objective: The precise mechanisms by which massage promotes repair in injured soft tissue are unknown. Various authorshave attributed the beneficial effects of massage to vasodilation and increased skin and muscle blood flow. The aim of this study was to determine whether deep transverse friction massage (DTF) causes capillary vasodilation in untraumatised skeletal muscle. Setting: Academic institution.Interventions: Twelve New Zealand white rabbits were anaesthetised and the left biceps femoris muscle received 10 minutes of DTF. Following treatment, wedge biopsies were taken from the musclewithin 10 minutes of treatment (R1 - 4), 24 hours (R5 - 8) and 6 days(R9 - 12) after treatment. To serve as controls, similar biopsies weretaken from the right biceps femoris of animals. The samples were fixed, dehydrated and embedded in epoxy resin.Transverse sections (1µm) of muscle were cut, stained with 1% aqueous alkaline toluidine blue and examined with a light microscope using a 40X objective. Images containing capillaries were captured using an image analyser with SIS software and the cross sectional diameters of at least 60 capillaries were measured from each specimen. Main Outcome Measures: Changes in capillary diameter. Results: The mean capillary diameters in control muscle averaged 4.76 µm. DTF caused a significant immediate increase of 17.3% in cross sectional area (p<0.001), which was not significantly increased by 10.0% after 24 hours (p>0.05). Six days after treatment the cross-sectional area of the treated muscle was 7.6% smaller than the controls. Conclusions: This confirms the contention that DTF stimulates muscle blood flow immediately after treatment and this may account for its beneficial effects in certain conditions. 

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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