Sympathetic restraint of muscle blood flow at the onset of dynamic exercise

2002 ◽  
Vol 92 (6) ◽  
pp. 2452-2456 ◽  
Author(s):  
Jason J. Hamann ◽  
John B. Buckwalter ◽  
Zoran Valic ◽  
Philip S. Clifford
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Saline Control ◽  
Adrenergic Blockade ◽  
Arterial Infusion ◽  
Blood Flows ◽  
Peak Blood ◽  
Sustained Increase

Little attention has focused on sympathetic influences on skeletal muscle blood flow at the onset of exercise. We hypothesized that 1) the sympathetic nervous system constrains muscle blood flow and 2) the decline from peak blood flow is mediated by increasing sympathetic vasoconstrictor tone. Mongrel dogs ( n = 7) ran on a treadmill after intra-arterial infusion of saline (control) or combined α1- and α2-adrenergic blockade (prazosin and rauwolscine). Immediate and rapid increases in hindlimb blood flow occurred at commencement of exercise with peak iliac blood flows averaging 933 ± 79 and 1,227 ± 90 ml/min during control and blockade conditions, respectively. At 1 min of exercise, hindlimb blood flow had decreased to 629 ± 54 and 1,057 ± 89 ml/min. In the absence of sympathetic vasoconstrictor tone, there was an enhanced peak blood flow at the onset of exercise. In addition, α-blockade attenuated the overshoot of hindlimb blood flow compared with the control condition. These data suggest that an immediate and sustained increase in sympathetic outflow restrains hindlimb blood flow at the onset of exercise and is responsible, at least in part, for an overshoot of blood flow to exercising skeletal muscle.

Skeletal muscle blood flow capacity: role of muscle pump in exercise hyperemia

1987 ◽  
Vol 253 (5) ◽  
pp. H993-H1004 ◽  
Author(s):  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Muscle Pump ◽  
Blood Flows ◽  
Flow Capacity

An appreciation for the potential of skeletal muscle vascular beds for blood flow (blood flow capacity) is required if one is to understand the limits of the cardiorespiratory system in exercise. To assess this potential, an index of blood flow capacity that can be objectively measured is required. One obvious index would be to measure maximal muscle blood flow (MBF). However, a unique value for maximal MBF cannot be measured, since once maximal vasodilation is attained MBF is a function of perfusion pressure. Another approach would be to measure maximal or peak vascular conductance. However, peak vascular conductance is different among skeletal muscles composed of different fiber types and is a function of perfusion pressure during peak vasodilation within muscle composed of a given fiber type. Also, muscle contraction can increase or decrease blood flow and/or the apparent peak vascular conductance depending on the experimental preparation and the type of muscle contraction. Blood flows and calculated values of conductance appear to be greater during rhythmic contractions (with the appropriate frequency and duration) than observed in resting muscle during what is called "maximal" vasodilation. Moreover, dynamic exercise in conscious subjects produces the greatest skeletal muscle blood flows. The purpose of this review is to consider the interaction of the determinants of muscle blood flow during locomotory exercise. Emphasis is directed toward the hypothesis that the "muscle pump" is an important determinant of perfusion of active skeletal muscle. It is concluded that, during normal dynamic exercise, MBF is determined by skeletal muscle vascular conductance, the perfusion pressure gradient, and the efficacy of the muscle pump.

Role of nitric oxide in skeletal muscle blood flow at rest and during dynamic exercise in humans

1997 ◽  
Vol 273 (1) ◽  
pp. H405-H410 ◽  
Author(s):  
R. C. Hickner ◽  
J. S. Fisher ◽  
A. A. Ehsani ◽  
W. M. Kohrt
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
And Control

The role of nitric oxide at rest and in the active hyperemic response within skeletal muscle was investigated in eight physically active men. Three microdialysis probes were inserted into the vastus lateralis of the quadriceps femoris muscle group in each subject. Microdialysis probes were perfused with a Ringer solution containing 5.0 mM ethanol, 2.5 mM glucose, and either 10 mg/ml of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) monoacetate salt, 30 mg/ml of the nitric oxide precursor L-arginine, or no additional substance (control probe). Subjects performed one-legged cycling exercise at work rates ranging from 25 to 100 W. Dialysate and perfusate ethanol concentrations were presented as the ratio of [ethanol]dialysate to [ethanol]perfusate (ethanol outflow-to-inflow ratio), an indicator that is inversely related to blood flow. The ethanol outflow-to-inflow ratios at rest were 0.614 +/- 0.032, 0.523 +/- 0.023, and 0.578 +/- 0.039 in the L-NMMA, L-arginine, and control probes, respectively. Calculated resting blood flows were therefore 8.7 +/- 4.1, 20.5 +/- 4.6, and 14.0 +/- 4.7 ml.min-1.100 g-1 around the L-NMMA, L-arginine, and control probes, respectively. The ethanol outflow-to-inflow ratios were significantly higher at all exercise intensities in the L-NMMA probe than in the control and L-arginine probes, resulting in calculated blood flows of 195 +/- 55, 407 +/- 47, and 352 +/- 60 ml.min-1.100 g-1 at 25 W and 268 +/- 65, 602 +/- 129, and 519 +/- 113 ml.min-1.100 g-1 at 100 W around the L-NMMA, L-arginine, and control probes, respectively. Skeletal muscle blood flow was therefore reduced both at rest and during continuous, dynamic exercise by the action of L-NMMA, whereas blood flow was increased only at rest by L-arginine.

Muscle blood flow during exercise in sedentary and trained hypothyroid rats

1995 ◽  
Vol 269 (6) ◽  
pp. H1949-H1954 ◽  
Author(s):  
R. M. McAllister ◽  
M. D. Delp ◽  
K. A. Thayer ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Treadmill Running ◽  
Exercise Intolerance ◽  
Vastus Lateralis Muscle ◽  
Blood Flows ◽  
Vastus Intermedius

Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.

Skeletal muscle vasodilation at the onset of exercise

1998 ◽  
Vol 85 (5) ◽  
pp. 1649-1654 ◽  
Author(s):  
John B. Buckwalter ◽  
Stephen B. Ruble ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscarinic Receptors ◽  
Treadmill Exercise ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Iliac Arteries ◽  
Blood Flows ◽  
Peak Blood

The purpose of this study was to determine whether β-adrenergic or muscarinic receptors are involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs ( n = 7) were instrumented with flow probes on both external iliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 μg), both drugs, or saline was infused intra-arterially immediately before treadmill exercise at 3 miles/h, 0% grade. Immediate and rapid increases in iliac blood flow occurred with initiation of exercise under all conditions. Peak blood flows were not significantly different among conditions (682 ± 35, 646 ± 49, 637 ± 68, and 705 ± 50 ml/min, respectively). Although the doses of antagonists employed had no effect on heart rate or systemic blood pressure, they were adequate to abolish agonist-induced increases in iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of β-adrenergic and muscarinic receptors is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs.

Effects of intra-arterial arginine-vasopressin infusions on peripheral blood flows in conscious dogs

1986 ◽  
Vol 71 (6) ◽  
pp. 713-721 ◽  
Author(s):  
Jean-Francois Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Small Intestine ◽  
Arginine Vasopressin ◽  
Muscle Blood Flow ◽  
Plasma Concentrations ◽  
Abdominal Fat ◽  
Conscious Dogs ◽  
Bone Blood Flow ◽  
Blood Flows

1. We reported in an earlier study that intravenous infusions of arginine-vasopressin (AVP), 220 pg min−1 kg−1 for 1 h, substantially reduced blood flow to the skin, skeletal muscle, pancreas, colon, small intestine, abdominal fat and myocardium [1] in conscious dogs. In the present study, we infused AVP directly into the artery supplying these organs and tissues in order to determine the relative contribution of local versus systemic mechanisms in the vascular resistance changes previously observed. 2. Regional blood flows were measured with radioactive microspheres in conscious, chronically instrumented dogs before and during intra-arterial infusions of AVP administered into the left axillary artery (n = 6), the left coronary artery (n = 6), and the cranial mesenteric artery (n = 6). The infusion rates were calculated to increase local, target organ plasma concentrations of AVP to the levels reached in our previous study while minimizing systemic changes. 3. Left axillary AVP artery infusion significantly reduced skin and compact bone blood flow, but had no effect on skeletal muscle blood flow. Intra-coronary AVP infusion had no effect on myocardial blood flow nor on cardiac output. Intramesenteric AVP infusion had no effect on blood flow to the colon, small intestine and abdominal fat, but significantly reduced blood flow to those areas of the pancreas which received blood from the cannulated artery. 4. Measurements in a limited number of dogs indicated that the local axillary and mesenteric venous levels of AVP were similar when the hormone was infused systemically at a rate of 220 pg min−1 kg−1 or intra-arterially at a lower rate. 5. These findings suggest that the increase in resistance measured in the skeletal muscle, small intestine, colon and abdominal fat after systemic administration of small amounts of AVP results in large part from indirect mechanisms. Direct vasoconstrictor effects of AVP at these plasma concentrations appear limited to the skin, the pancreas and the compact bones.

Effects of hyperthyroidism on muscle blood flow during exercise in rats

1995 ◽  
Vol 268 (1) ◽  
pp. H330-H335 ◽  
Author(s):  
R. M. McAllister ◽  
J. C. Sansone ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Citrate Synthase ◽  
Muscle Blood Flow ◽  
Left Ventricular ◽  
Submaximal Exercise ◽  
Treadmill Running ◽  
Exercise Intolerance ◽  
Blood Flows

Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6–12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25–60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1–2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50–150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.

Adrenoceptor regulation of canine skeletal muscle blood flow during carbon monoxide hypoxia

1991 ◽  
Vol 69 (10) ◽  
pp. 1399-1404 ◽  
Author(s):  
P. Kubes ◽  
K. A. Nesbitt ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Peripheral Blood Flow ◽  
Neural Activation ◽  
Adrenergic Blockade ◽  
Skeletal Muscle Blood Flow ◽  
Anesthetized Dogs ◽  
Adrenoceptor Regulation

We questioned whether carbon monoxide hypoxia (COH) would affect peripheral blood flow by neural activation of adrenoceptors to the extent we had found in other forms of hypoxia. We studied this problem in hindlimb muscles of four groups of anesthetized dogs (untreated, α1-blocked, α1 + α2-blocked, and β2-blocked). Cardiac output increased, but hindlimb blood flow [Formula: see text] and resistance (RL) remained at prehypoxic levels during COH (O2 content reduced 50%) in untreated animals. When activity in the sciatic nerve was reversibly cold blocked, [Formula: see text] doubled and RL decreased 50%. These changes with nerve block were the same during COH, suggesting that neural activity to hindlimb vasculature was not increased by COH. In animals treated with phenoxybenzamine (primarily α1-blocked), RL dropped (~50%) during COH, an indication that catecholamines played a significant role in maintaining tone to skeletal muscle. Animals with both α1 + α2-adrenergic blockade (phenoxybenzamine and yohimbine added) did not survive COH. RL was higher in β2-block than in the untreated group during COH, but nerve cooling indicated that β2-adrenoceptor vasodilation was accomplished primarily by humoral means. The above findings demonstrated that adrenergic receptors were important in the regulation of [Formula: see text] and RL during COH, but they were not activated by sympathetic nerve stimulation to the limb muscles.Key words: α1-adrenoreceptor blockade, α2-adrenoreceptor blockade, peripheral vascular resistance, skeletal muscle, blood flow.

Regional blood flows in salt loading hypertension in the dog

1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Salt Loading ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
Regional Blood Flows

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

scholarly journals Muscle metaboreflex activation during dynamic exercise vasoconstricts ischemic active skeletal muscle

2015 ◽  
Vol 309 (12) ◽  
pp. H2145-H2151 ◽  
Author(s):  
Jasdeep Kaur ◽  
Tiago M. Machado ◽  
Alberto Alvarez ◽  
Abhinav C. Krishnan ◽  
Hanna W. Hanna ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Threshold Level ◽  
Dynamic Exercise ◽  
Adrenergic Blockade ◽  
Muscle Metaboreflex ◽  
Group Iii ◽  
Arterial Blood ◽  
Sympathetic Vasoconstriction ◽  
Before And After

Metabolite accumulation due to ischemia of active skeletal muscle stimulates group III/IV chemosensitive afferents eliciting reflex increases in arterial blood pressure and sympathetic activity, termed the muscle metaboreflex. We and others have previously demonstrated sympathetically mediated vasoconstriction of coronary, renal, and forelimb vasculatures with muscle metaboreflex activation (MMA). Whether MMA elicits vasoconstriction of the ischemic muscle from which it originates is unknown. We hypothesized that the vasodilation in active skeletal muscle with imposed ischemia becomes progressively restrained by the increasing sympathetic vasoconstriction during MMA. We activated the metaboreflex during mild dynamic exercise in chronically instrumented canines via graded reductions in hindlimb blood flow (HLBF) before and after α1-adrenergic blockade [prazosin (50 μg/kg)], β-adrenergic blockade [propranolol (2 mg/kg)], and α1 + β-blockade. Hindlimb resistance was calculated as femoral arterial pressure/HLBF. During mild exercise, HLBF must be reduced below a threshold level before the reflex is activated. With initial reductions in HLBF, vasodilation occurred with the imposed ischemia. Once the muscle metaboreflex was elicited, hindlimb resistance increased. This increase in hindlimb resistance was abolished by α1-adrenergic blockade and exacerbated after β-adrenergic blockade. We conclude that metaboreflex activation during submaximal dynamic exercise causes sympathetically mediated α-adrenergic vasoconstriction in ischemic skeletal muscle. This limits the ability of the reflex to improve blood flow to the muscle.

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