Contribution of prostaglandins to exercise-induced vasodilation in humans

1993 ◽  
Vol 265 (1) ◽  
pp. H171-H175 ◽  
Author(s):  
J. R. Wilson ◽  
S. C. Kapoor
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Catheter ◽  
Normal Subjects ◽  
Wrist Flexion ◽  
Arterial Infusion ◽  
Prostaglandin Release ◽  
Exercise Induced ◽  
Arteriolar Vasodilation

It has been postulated that endothelial release of prostaglandins contributes to exercise-induced vasodilation of skeletal muscle arterioles. To test this hypothesis, 12 normal subjects underwent brachial arterial and venous catheter insertion and instrumentation of their forearm to measure plethysmographic forearm blood flow. Forearm blood flow and arterial and venous 6-ketoprostaglandin F1 alpha (PGF1 alpha) and prostaglandin E2 (PGE2) were then measured during two levels of wrist flexion exercise (0.2 and 0.4 W). In nine of the subjects, exercise was repeated after intra-arterial infusion of indomethacin (0.3 mg/100 ml forearm vol). Exercise increased forearm blood flow (2.0 +/- 0.2 to 12.1 +/- 1.1 ml.min-1.100 ml-1) and forearm release of PGF1 alpha (162 +/- 28 to 766 +/- 193 pg.min-1.100 ml-1) and PGE2 (26 +/- 6 to 125 +/- 46 pg.min-1.100 ml-1) (all P < 0.05). Indomethacin virtually abolished forearm prostaglandin release and reduced forearm blood flow at rest (2.2 +/- 0.2 to 1.7 +/- 0.2 ml.min-1.100 ml-1), at 0.2 W (6.3 +/- 0.7 to 5.4 +/- 0.7 ml.min-1.100 ml-1), and at 0.4 W (12.2 +/- 1.5 to 10.3 +/- 1.3 ml.min-1.100 ml-1) (all P < 0.02). These data suggest that release of vasodilatory prostaglandins contributes to exercise-induced arteriolar vasodilation and hyperemia in skeletal muscle.

Contribution of endothelium-derived relaxing factor to exercise-induced vasodilation in humans

1993 ◽  
Vol 75 (6) ◽  
pp. 2740-2744 ◽  
Author(s):  
J. R. Wilson ◽  
S. Kapoor
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Endothelium ◽  
Forearm Blood Flow ◽  
Specific Inhibitor ◽  
Normal Subjects ◽  
Wrist Flexion ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Arteriolar Vasodilation

Release of endothelium-derived relaxing factor (EDRF) from the vascular endothelium may contribute to skeletal muscle arteriolar vasodilation during exercise. The present study was undertaken to test this hypothesis. Ten normal subjects underwent brachial arterial catheter insertion and instrumentation of their forearm to measure plethysmographic forearm blood flow. Forearm blood flow was then measured at rest, during two levels of wrist flexion exercise (0.2 and 0.4 W), and during 0.4-W exercise with concurrent infusion of norepinephrine (100 ng.min-1 x 100 ml forearm volume-1). Measurements were made with and without infusion of N-monomethyl-L-arginine (L-NMMA) (0.1–0.2 mg.min-1 x 100 ml forearm volume-1), a specific inhibitor of EDRF synthesis. Infusion of L-NMMA reduced resting forearm blood flow (control: 2.5 +/- 0.4 vs. L-NMMA: 1.5 +/- 0.1 ml.min-1 x 100 ml-1) and markedly reduced forearm blood flow response to acetylcholine (5 micrograms.min-1 x 100 ml forearm volume-1) (control: 20.2 +/- 2.9 vs L-NMMA: 4.0 +/- 1.0 ml.min-1 x 100 ml-1; both P < 0.01). However, L-NMMA had no significant effect on flow responses to exercise (0.2 W: 8.3 +/- 1.1 vs. 8.3 +/- 1.2; 0.4 W: 13.8 +/- 1.7 vs. 13.5 +/- 1.7; 0.4 W + norepinephrine: 10.3 +/- 2.4 vs. 9.4 +/- 2.6 ml.min-1 x 100 ml-1; all P = NS). These findings suggest that release of EDRF from the vascular endothelium contributes to skeletal muscle arteriolar vasodilation at rest but does not contribute to the arteriolar vasodilation produced by exercise.

Contribution of potassium to exercise-induced vasodilation in humans

1994 ◽  
Vol 77 (6) ◽  
pp. 2552-2557 ◽  
Author(s):  
J. R. Wilson ◽  
S. C. Kapoor ◽  
G. G. Krishna
Keyword(s):  
Skeletal Muscle ◽  
Vascular Resistance ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Bicycle Exercise ◽  
Potassium Release ◽  
Forearm Exercise ◽  
Exercise Induced ◽  
Arteriolar Vasodilation ◽  
Forearm Vascular Resistance

It has been postulated that skeletal muscle release of potassium contributes to exercise-induced vasodilation of skeletal muscle arterioles. To determine whether potassium produces muscle arteriolar vasodilation in humans, we measured plethysmographic forearm blood flow and brachial venous potassium concentrations during brachial arterial infusion of potassium (0.6, 3, 6, 15, and 30 mueq.min-1.100 ml forearm volume-1) in nine normal subjects. Infusion of potassium decreased forearm vascular resistance, with an increase in brachial venous potassium of 1 meq/l decreasing forearm vascular tone by 25–30%. We then measured plasma potassium concentrations during forearm and upright bicycle exercise in 15 normal subjects. Forearm exercise at 0.6 W decreased forearm vascular resistance by 83%, whereas brachial venous potassium increased by only 0.5 +/- 0.2 meq/l (both P < 0.05). Maximal bicycle exercise increased systemic potassium concentrations by 1.2 +/- 0.2 meq/l. These findings indicate that potassium produces muscle arteriolar vasodilation in humans and therefore supports the hypothesis that potassium release from exercising muscle contributes to exercise-induced vasodilation. The relatively small change in venous potassium noted during forearm exercise despite marked forearm vasodilation suggests that local potassium release is only a small contributor to exercise-induced vasodilation. However, potassium release during maximal exercise may have significant vasodilatory effects on arterioles both in exercising and nonexercising tissues.

Training-induced skeletal muscle adaptations are independent of systemic adaptations

1990 ◽  
Vol 68 (1) ◽  
pp. 289-294 ◽  
Author(s):  
J. R. Minotti ◽  
E. C. Johnson ◽  
T. L. Hudson ◽  
G. Zuroske ◽  
E. Fukushima ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Magnetic Resonance ◽  
Muscle Mass ◽  
Normal Subjects ◽  
Oxidative Capacity ◽  
Venous Occlusion ◽  
Resonance Spectroscopy ◽  
Wrist Flexion ◽  
Vo2 Max

To isolate the peripheral adaptations to training, five normal subjects exercised the nondominant (ND) wrist flexors for 41 +/- 11 days, maintaining an exercise intensity below the threshold required for cardiovascular adaptations. Before and after training, intracellular pH and the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) were measured by 31P magnetic resonance spectroscopy. Also maximal O2 consumption (VO2 max), muscle mass, and forearm blood flow were determined by graded systemic exercise, magnetic resonance imaging, and venous occlusion plethysmography, respectively. Blood flow, Pi/PCr, and pH were measured in both forearms at rest and during submaximal wrist flexion at 5, 23, and 46 J/min. Training did not affect VO2 max, exercise blood flow, or muscle mass. Resting pH, Pi/PCr, and blood flow were also unchanged. After training, the ND forearm demonstrated significantly lower Pi/PCr at 23 and 46 J/min. Endurance, measured as the number of contractions to exhaustion, also was increased significantly (63%) after training in the ND forearm. We conclude that 1) forearm training results in a lower Pi/PCr at identical submaximal work loads; 2) this improvement is independent of changes in VO2 max, muscle mass, or limb blood flow; and 3) these differences are associated with improved endurance and may reflect improved oxidative capacity of skeletal muscle.

Prostaglandin production contributes to exercise-induced vasodilation in heart failure

1997 ◽  
Vol 83 (6) ◽  
pp. 1933-1940 ◽  
Author(s):  
Chim C. Lang ◽  
Don B. Chomsky ◽  
Javed Butler ◽  
Shiv Kapoor ◽  
John R. Wilson
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Peak Exercise ◽  
Prostaglandin Production ◽  
Leg Blood Flow ◽  
Patients With Heart Failure ◽  
Prostaglandin F ◽  
Exercise Induced ◽  
Arteriolar Vasodilation

Lang, Chim C., Don B. Chomsky, Javed Butler, Shiv Kapoor, and John R. Wilson. Prostaglandin production contributes to exercise-induced vasodilation in heart failure. J. Appl. Physiol. 83(6): 1933–1940, 1997.—Endothelial release of prostaglandins may contribute to exercise-induced skeletal muscle arteriolar vasodilation in patients with heart failure. To test this hypothesis, we examined the effect of indomethacin on leg circulation and metabolism in eight chronic heart failure patients, aged 55 ± 4 yr. Central hemodynamics and leg blood flow, determined by thermodilution, and leg metabolic parameters were measured during maximum treadmill exercise before and 2 h after oral administration of indomethacin (75 mg). Leg release of 6-ketoprostaglandin F1α was also measured. During control exercise, leg blood flow increased from 0.34 ± 0.03 to 1.99 ± 0.19 l/min ( P < 0.001), leg O2 consumption from 13.6 ± 1.8 to 164.5 ± 16.2 ml/min ( P < 0.001), and leg prostanoid release from 54.1 ± 8.5 to 267.4 ± 35.8 pg/min ( P < 0.001). Indomethacin suppressed release of prostaglandin F1α( P < 0.001) throughout exercise and decreased leg blood flow during exercise ( P < 0.05). This was associated with a corresponding decrease in leg O2 consumption ( P < 0.05) and a higher level of femoral venous lactate at peak exercise ( P < 0.01). These data suggest that release of vasodilatory prostaglandins contributes to skeletal muscle arteriolar vasodilation in patients with heart failure.

Forearm metabolic asymmetry detected by 31P-NMR during submaximal exercise

1989 ◽  
Vol 67 (1) ◽  
pp. 324-329 ◽  
Author(s):  
J. R. Minotti ◽  
E. C. Johnson ◽  
T. L. Hudson ◽  
R. R. Sibbitt ◽  
L. E. Wise ◽  
...  
Keyword(s):  
Blood Flow ◽  
Energy Metabolism ◽  
Magnetic Resonance ◽  
Muscle Mass ◽  
Forearm Blood Flow ◽  
Training Stimulus ◽  
Normal Subjects ◽  
Submaximal Exercise ◽  
Resonance Spectroscopy ◽  
Wrist Flexion

This study evaluated the relationship of skeletal muscle energy metabolism to forearm blood flow and muscle mass in the dominant (D) and nondominant (ND) forearms of normal subjects. 31P-Magnetic resonance spectroscopy was used to determine intracellular pH and the ratio of inorganic phosphate to phosphocreatine (Pi/PCr), an index of energy metabolism. Forearm blood flow and muscle mass were measured by venous occlusion plethysmography and magnetic resonance imaging, respectively. Metabolic measurements and flow were determined at rest and during submaximal exercise in both forearms. After a warm-up period, six normal right-handed male subjects performed 7.5 min of wrist flexion exercise in the magnet (1 contraction every 5 s), first with the ND forearm and then with the D forearm, at 23, 46, and 69 J/min. At rest, there were no differences between forearms in Pi/PCr or pH. However, at each work load the D forearm demonstrated significantly lower Pi/PCr and higher pH than the ND forearm. Blood flow was not significantly different between the forearms at rest or during exercise. Because these subjects were not engaged in unilateral arm training, we conclude that 1) Pi/PCr is lower and pH is higher in the D compared with the ND forearm in normal subjects during submaximal exercise, 2) these differences are independent of muscle mass and blood flow, and 3) the cumulative effect of long-term, low-level daily activity provides an adequate training stimulus for muscular metabolic adaptations.

Forearm Blood Flow in Normal Subjects and Patients with Phobic Anxiety States

1965 ◽  
Vol 111 (477) ◽  
pp. 723-731 ◽  
Author(s):  
Max Harper ◽  
Clair Gurney ◽  
R. Douglass Savage ◽  
Martin Roth
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Emotional Stress ◽  
Forearm Blood Flow ◽  
Mental Arithmetic ◽  
Normal Subjects ◽  
Limb Blood Flow ◽  
Anxiety States ◽  
Phobic Anxiety ◽  
Fast Rates

One of the earliest studies on limb blood flow, using a volume plethysmograph to enclose the hand and forearm, was carried out by Hewlett and Van Zwaluwenburg (1909). Two of their patients were pronounced neurasthenics “with labile vasomotor systems” and these authors noted that, excluding subjects with thyrotoxicosis, “the majority of the remaining fast rates occurred in neurasthenics of the vasomotor type”. In 1938 Grant and Pearson, who developed forearm plethysmography to determine blood flow mainly in the skeletal muscle rather than the skin, noted transient increases in forearm flow with mental arithmetic in some subjects, but did not pursue this observation further. This response was studied in more detail by Abramson and Ferris (1940). Their conclusion that mental arithmetic produced an increase in forearm flow due to vasodilatation in the forearm muscles was confirmed by the work of Brod, Fencl, Hejl, and Jirka (1959), who attributed the change to emotional stress.

scholarly journals Parathyroid Hormone's Acute Effect on Vasodilatory Function

2010 ◽  
Vol 3 ◽  
pp. CMED.S4650 ◽  
Author(s):  
P. Farahnak ◽  
L. Lind ◽  
K. Mattala ◽  
I-L. Nilsson
Keyword(s):  
Cardiovascular Disease ◽  
Blood Flow ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Acute Effect ◽  
Venous Occlusion ◽  
Arterial Infusion ◽  
Resistance Vessels ◽  
Vasodilatory Function ◽  
Pth Level

Parathyroid hormone (PTH) seems to affect the risk of cardiovascular disease. The aim of the present study was to investigate PTH's acute effect on endothelial vasodilatory function in forearm resistance vessels. Ten healthy subjects underwent forearm venous occlusion plethysmography. We measured forearm blood flow at baseline and at a stable, locally increased PTH level after intra-arterial infusion of metacholine and nitroprusside. The contralateral arm served as a control. Ionized calcium (Ca++) and PTH values were normal in all subjects at baseline (1.26 ± 0.02 mM/L, 3.6 ± 1.2 pM/L). After 30 minutes of PTH infusion, the PTH level increased in the active arm (13.8 ± 4.0 pM/L P < 0.01), while the Ca++ level was unchanged (1.25 ± 0.04; mM/L). Both the PTH and the Ca++ level in the contralateral arm remained unchanged, which indicates no systemic influence. The endothelial-dependent vasodilation was inversely correlated to the Ca++ level at baseline (r = −0.75, P < 0.05) and after PTH infusion (r = −0.68, P < 0.05). The vasodilatory function was not affected during PTH-infusion.

Effect of hand heating by a warm air box on O2 consumption of the contralateral arm

1992 ◽  
Vol 72 (6) ◽  
pp. 2364-2368 ◽  
Author(s):  
E. E. Blaak ◽  
M. A. Van Baak ◽  
K. P. Kempen ◽  
W. H. Saris
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Skin Temperature ◽  
Forearm Blood Flow ◽  
Venous Blood ◽  
Oral Glucose ◽  
Glucose Load ◽  
Glucose Intake ◽  
Integrated Response

Arterialization of venous blood is often used in studying forearm metabolism. Astrup et al. [Am. J. Physiol. 255 (Endocrinol. Metab. 18): E572-E578, 1988] showed that heating of the hand by a warming blanket caused a redistribution of blood flow in the contralateral arm and thus introduced errors in forearm skeletal muscle flux calculations. The present study was undertaken to investigate how hand heating by a warm air box (60 degrees C) would affect metabolism and blood flow in the contralateral arm before and during 3 h after a glucose load. Eleven healthy volunteers (5 males, 6 females) underwent an oral glucose tolerance test (70 g) on two different occasions, one test with and one without heating of the contralateral hand, in random order. Heating the hand for 30 min before glucose intake did not affect skin temperature, rectal temperature, deep venous oxygen saturation, forearm blood flow, or oxygen consumption of forearm skeletal muscle. Although, after the glucose load, heating significantly increased forearm blood flow (P less than 0.05), the integrated response after glucose was not significantly different between control and heating experiments [67 +/- 43 and 117 +/- 41 (SE) ml/100 ml tissue]. With both conditions, there was an increase in skin temperature (P less than 0.001, integrated response control: 369 +/- 79 and heating: 416 +/- 203 degrees C) and oxygen consumption of forearm muscle (control: 290 +/- 73, P less than 0.05 and heating: 390 +/- 130 mumol/100 ml, P less than 0.05) after glucose intake. These responses did not significantly differ between the conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine contributes to hypoxia-induced forearm vasodilation in humans

1999 ◽  
Vol 87 (6) ◽  
pp. 2218-2224 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Kris Gray ◽  
Michael D. Herr
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Brachial Artery ◽  
Adenosine Receptors ◽  
Forearm Blood Flow ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Normal Subjects ◽  
Local Release ◽  
Forearm Vascular Resistance

In humans, hypoxia leads to increased sympathetic neural outflow to skeletal muscle. However, blood flow increases in the forearm. The mechanism of hypoxia-induced vasodilation is unknown. To test whether hypoxia-induced vasodilation is cholinergically mediated or is due to local release of adenosine, normal subjects were studied before and during acute hypoxia (inspired O210.5%; ∼20 min). In experiment I, aminophylline (50–200 μg ⋅ min−1 ⋅ 100 ml forearm tissue−1) was infused into the brachial artery to block adenosine receptors ( n = 9). In experiment II, cholinergic vasodilation was blocked by atropine (0.4 mg over 4 min) infused into the brachial artery ( n = 8). The responses of forearm blood flow (plethysmography) and forearm vascular resistance to hypoxia in the infused and opposite (control) forearms were compared. During hypoxia (arterial O2 saturation 77 ± 2%), minute ventilation and heart rate increased while arterial pressure remained unchanged; forearm blood flow rose by 35 ± 6% in the control forearm but only by 5 ± 8% in the aminophylline-treated forearm ( P < 0.02). Accordingly, forearm vascular resistance decreased by 29 ± 5% in the control forearm but only by 9 ± 6% in the aminophylline-treated forearm ( P < 0.02). Atropine did not attenuate forearm vasodilation during hypoxia. These data suggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role.

Muscle pump does not enhance blood flow in exercising skeletal muscle

2003 ◽  
Vol 94 (1) ◽  
pp. 6-10 ◽  
Author(s):  
Jason J. Hamann ◽  
Zoran Valic ◽  
John B. Buckwalter ◽  
Philip S. Clifford
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Tone ◽  
Venous Pressure ◽  
Adenosine Infusion ◽  
Arterial Infusion ◽  
Muscle Pump ◽  
Venous Circulation ◽  
Response To Exercise ◽  
Hyperemic Response

The muscle pump theory holds that contraction aids muscle perfusion by emptying the venous circulation, which lowers venous pressure during relaxation and increases the pressure gradient across the muscle. We reasoned that the influence of a reduction in venous pressure could be determined after maximal pharmacological vasodilation, in which the changes in vascular tone would be minimized. Mongrel dogs ( n = 7), instrumented for measurement of hindlimb blood flow, ran on a treadmill during continuous intra-arterial infusion of saline or adenosine (15–35 mg/min). Adenosine infusion was initiated at rest to achieve the highest blood flow possible. Peak hindlimb blood flow during exercise increased from baseline by 438 ± 34 ml/min under saline conditions but decreased by 27 ± 18 ml/min during adenosine infusion. The absence of an increase in blood flow in the vasodilated limb indicates that any change in venous pressure elicited by the muscle pump was not adequate to elevate hindlimb blood flow. The implication of this finding is that the hyperemic response to exercise is primarily attributable to vasodilation in the skeletal muscle vasculature.

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