Frequency and pattern dependence of adrenergic and purinergic vasoconstriction in rat skeletal muscle arteries.

Sympathetic nerves fire in bursts followed by brief periods of quiescence. Periods of quiescence may be a valuable part of coding for different neurotransmitters. We compared adrenergic- and non-adrenergic-mediated vasoconstriction with repeating burst patterns versus constant frequency stimulation.

Alpha-Adrenergic receptor responsiveness is preserved during prolonged exercise.

Our laboratory has previously reported a decline in sympathetic nervous system restraint of skeletal muscle blood flow during prolonged mild-intensity exercise. This decline may be explained by a decrease in alpha(1)- and alpha(2)-adrenergic receptor responsiveness over time. Thus the purpose of the present study was to investigate the effect of exercise duration on alpha(1)- and alpha(2)-adrenergic receptor responsiveness during prolonged constant-load exercise.

Mechanical compression elicits vasodilatation in rat skeletal muscle feed arteries.

To date, no satisfactory explanation has been provided for the immediate increase in blood flow to skeletal muscles at the onset of exercise. We hypothesized that rapid vasodilatation is a consequence of release of a vasoactive substance from the endothelium owing to mechanical deformation of the vasculature during contraction. Rat soleus feed arteries were isolated, removed and mounted on micropipettes in a sealed chamber.

Alpha-adrenergic receptor-mediated restraint of skeletal muscle blood flow during prolonged exercise.

Sympathetic nervous system restraint of skeletal muscle blood flow during dynamic exercise has been well documented. However, whether sympathetic restraint of muscle blood flow persists and is constant throughout prolonged exercise has not been established. We hypothesized that both alpha1- and alpha2-adrenergic receptors would restrain skeletal muscle blood flow throughout prolonged constant-load exercise and that the restraint would increase as a function of exercise duration.

Neuropeptide Y1 receptor vasoconstriction in exercising canine skeletal muscles.

Existing evidence suggests that neuropeptide Y (NPY) acts as a neurotransmitter in vascular smooth muscle and is coreleased with norepinephrine from sympathetic nerves. We hypothesized that release of NPY stimulates NPY Y(1) receptors in the skeletal muscle vasculature to produce vasoconstriction during dynamic exercise. Eleven mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery.

Thermal pain perception after aerobic exercise.

Objective: To examine thermal pain perception before, 5 minutes after, and 30 minutes after 30 minutes of treadmill exercise at 75% of maximal oxygen uptake (V o 2 max).

Design: Repeated-measures.

Setting: Sports science laboratory.

Elevated temperature decreases sensitivity of P2X purinergic receptors in skeletal muscle arteries.

We hypothesized that elevated temperatures would attenuate but that reduced temperatures would potentiate the tension mediated by vascular P2X purinergic receptors. The femoral arteries of 24 rats were dissected out and placed in modified Krebs-Henseleit buffer. Arteries were cut into 2-mm sections and mounted in organ tissue baths.

Blood flow response to muscle contractions is more closely related to metabolic rate than contractile work.

The magnitude of the blood flow response to exercise has been linked to both the contractile work performed and the metabolic cost of the activity. Under certain conditions, contractile work and metabolic cost may be dissociated. This study examined the blood flow response to trains of contractions when contraction duration was manipulated under conditions of similar tension-time indexes (isometric analog of work).

Muscle blood flow response to contraction: influence of venous pressure.

The skeletal muscle pump is thought to be at least partially responsible for the immediate muscle hyperemia seen with exercise. We hypothesized that increases in venous pressure within the muscle would enhance the effectiveness of the muscle pump and yield greater postcontraction hyperemia. In nine anesthetized beagle dogs, arterial inflow and venous outflow of a single hindlimb were measured with ultrasonic transit-time flow probes in response to 1-s tetanic contractions evoked by electrical stimulation of the sciatic nerve.

Acidosis attenuates P2X purinergic vasoconstriction in skeletal muscle arteries.

Vasoconstriction via alpha(2)-receptors is known to be sensitive to acidic pH, but little is known about the pH sensitivity of P2X receptors. ATP is a cotransmitter released with norepinephrine from the sympathetic nerves and causes vasoconstriction via P2X purinergic receptors on vascular smooth muscle. We hypothesized that reductions in pH would attenuate P2X-mediated vasoconstriction in iliofemoral artery rings.

Tracheal tone and the role of ionotropic glutamate receptors in the nucleus ambiguus.

Excitatory amino acid (EAA) transmission in the rostral portion of the ventrolateral medulla (RVLM) appears to be required for reflex airway constriction. The purpose of the present study was to determine whether our prior observations of right sided dominance are also reflected at the level of the RVLM, particularly at the right nucleus ambiguus (NA). Microinjection of glutamate (109 nl, 100 mM) into the right NA of anesthetized dogs produced significant increases in tracheal smooth muscle tone as assessed by pressure changes in a saline filled cuff of the endotracheal tube (Delta15 +/- 2 mm Hg).

Intensity and duration threshold for aerobic exercise-induced analgesia to pressure pain.

Objective: To examine how exercise-induced analgesia is affected by the duration and intensity of aerobic exercise.

Design: Repeated-measures design.

Setting: Exercise science laboratory.

Vasoconstriction in exercising skeletal muscles: a potential role for neuropeptide Y?

There is evidence that neuropeptide Y (NPY) acts as a neurotransmitter in vascular smooth muscle and is released with norepinephrine from sympathetic nerves. We hypothesized that NPY Y(1) receptor stimulation would produce vasoconstriction in resting and exercising skeletal muscle. Nine mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery.

Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle.

There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis we examined the blood flow response to a brief tetanic contraction in which potassium (K(+)) was infused intra-arterially to elevate the [K(+)](o) and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed.

Role of nitric oxide in exercise sympatholysis.

The production of nitric oxide is the putative mechanism for the attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during exercise. We hypothesized that nitric oxide synthase blockade would eliminate the reduction in alpha-adrenergic-receptor responsiveness in exercising skeletal muscle. Ten mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery.

Is the blood flow response to a single contraction determined by work performed?

Nine healthy volunteers performed a series of single handgrip isometric contractions to test the hypothesis that the blood flow response to a contraction is determined solely by the tension-time index (isometric analog of work). Contractions were performed in duplicate at 15, 30, and 60% of maximal voluntary contraction (MVC) at durations of 0.5, 1, and 2 s.

Laser revascularization of ischemic skeletal muscle.

Background: Clinical trials have shown that transmyocardial laser revascularization is an effective secondary treatment for ischemic heart disease patients. Laser revascularization may also provide an alternative method for treating peripheral vascular disease.

Methods: The purpose of this study was to investigate the potential for laser revascularization in ischemic skeletal muscle.

Do P2X purinergic receptors regulate skeletal muscle blood flow during exercise?

Although there is evidence that sympathetic nerves release ATP as a neurotransmitter to produce vasoconstriction via P2X purinergic receptors, the role of these receptors in the regulation of blood flow to exercising skeletal muscle has yet to be determined. We hypothesized that there is tonic P2X receptor-mediated vasoconstriction in exercising skeletal muscle. To test this hypothesis, the effect of P2X receptor blockade on skeletal muscle blood flow was examined in six exercising mongrel dogs.

Vasoconstriction in active skeletal muscles: a potential role for P2X purinergic receptors?

There is evidence that ATP acts as a neurotransmitter in vascular smooth muscle and is coreleased with norepinephrine from sympathetic nerves. We hypothesized that P2X-receptor stimulation with the selective P2X-receptor agonist alpha,beta-methylene ATP would produce vasoconstriction in resting and exercising skeletal muscle. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery.

Endogenous vascular remodeling in ischemic skeletal muscle: a role for nitric oxide.

To test the hypothesis that nitric oxide (NO) production is essential for endogenous vascular remodeling in ischemic skeletal muscle, 22 New Zealand White rabbits were chronically instrumented with transit-time flow probes on the common iliac arteries and underwent femoral ligation to produce unilateral hindlimb ischemia. Iliac blood flow and arterial pressure were recorded at rest and during a graded exercise test. An osmotic pump connected to a femoral arterial catheter continuously delivered N-nitro-l-arginine methyl ester (a NO synthase inhibitor) or a control solution (N-nitro-d-arginine methyl ester or phenylephrine) to the ischemic limb over a 2-wk period.

Muscle pump does not enhance blood flow in exercising skeletal muscle.

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).

Elevation in resting blood flow attenuates exercise hyperemia.

These experiments tested the hypothesis that elevating muscle blood flow before exercise would wash out vasoactive substances produced by muscle contraction and reduce the magnitude of exercise hyperemia and/or delay the response. In chronically instrumented dogs (n = 7), hindlimb blood flow was measured with chronically implanted flow probes during mild treadmill exercise. In an anesthetized preparation (n = 8), arterial and venous blood flows of a single hindlimb were obtained during 1-s tetanic contractions evoked by electrical stimulation of the cut sciatic nerve.

Attenuated vascular responsiveness to noradrenaline release during dynamic exercise in dogs.

During dynamic exercise, there is reduced responsiveness to alpha(1)- and alpha(2)-adrenergic receptor agonists in skeletal muscle vasculature. However, it is desirable to examine the sympathetic responsiveness to endogenous release of neurotransmitter, since exogenous sympathomimetic agents are dependent upon their ability to reach the abluminal receptor. Therefore, to further our understanding of sympathetic control of vasomotor tone during exercise, we employed a technique that would elicit the release of endogenous noradrenaline (norepinephrine) during dynamic exercise.