scholarly journals Sympathetic limitation of exercise hyperemia: even hypoperfused muscle is not exempted

2012 ◽  
Vol 3 ◽  
Author(s):  
D. J. Duncker ◽  
I. H. Heinonen
Keyword(s):  
Exercise Hyperemia

Training increases muscle blood flow in rats with peripheral arterial insufficiency

1990 ◽  
Vol 69 (4) ◽  
pp. 1353-1359 ◽  
Author(s):  
H. T. Yang ◽  
R. F. Dinn ◽  
R. L. Terjung
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Treadmill Running ◽  
Distal Limb ◽  
Adult Rats ◽  
Cage Activity ◽  
Exercise Hyperemia ◽  
Two Factors ◽  
Arterial Insufficiency ◽  
Peripheral Arterial

This study investigated the effect of physical training on muscle blood flow (BF) in rats with peripheral arterial insufficiency during treadmill running. Bilateral stenosis of the femoral artery of adult rats (300-350 g) was performed to reduce exercise hyperemia in the hindlimb but not limit resting muscle BF. Rats were divided into normal sedentary, acute stenosed (stenosed 3 days before the experiment), stenosed sedentary (limited to cage activity), and stenosed trained (run on a treadmill by a progressively intense program, up to 50-60 min/day, 5 days/wk for 6-8 wk). Hindlimb BF was determined with 85Sr- and 141Ce-labeled microspheres at a low (20 m/min) and high treadmill speed (30-40 m/min depending on ability). Maximal hindlimb BF was reduced to approximately 50% normal in the acute stenosed group. Total hindlimb BF (81 +/- 5 ml.min-1.100 g-1) did not change in stenosed sedentary animals with 6-8 wk of cage activity, but a redistribution of BF occurred within the hindlimb. Two factors contributed to a higher BF to the distal limb muscle of the trained animals. A redistribution BF within the hindlimb occurred in stenosed trained animals; distal limb BF increased to approximately 80% (P less than 0.001) of the proximal tissue. In addition, an increase in total hindlimb BF with training indicates that collateral BF has been enhanced (P less than 0.025). The associated increase in oxygen delivery to the relatively ischemic muscle probably contributed to the markedly improved exercise tolerance evident in the trained animals.

The effect of purinergic P2 receptor blockade on skeletal muscle exercise hyperemia in miniature swine

2014 ◽  
Vol 114 (10) ◽  
pp. 2147-2155 ◽  
Author(s):  
S. P. Mortensen ◽  
R. M. McAllister ◽  
H. T. Yang ◽  
Y. Hellsten ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Receptor Blockade ◽  
P2 Receptor ◽  
Muscle Exercise ◽  
Miniature Swine ◽  
Exercise Hyperemia

Perivascular and tissue PO2 in contracting rat spinotrapezius muscle

1987 ◽  
Vol 252 (6) ◽  
pp. H1192-H1202 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contractions ◽  
Large Decrease ◽  
Functional Hyperemia ◽  
Biochemical Status ◽  
Tissue Po2 ◽  
Close Proximity ◽  
Exercise Hyperemia ◽  
Capillary Bed

This study evaluated the possibility that during skeletal muscle contractions tissue O2 tension (Po2) around arterioles and venules decreases substantially more than in the middle of the capillary bed and thereby influences functional hyperemia. Periarteriolar [H+] and [K+] were also measured because most large arterioles are in close proximity to venules such that the biochemical status of the periarteriolar tissue could be influenced by a large decrease in O2 availability in the annulet of tissue surrounding the venules. Stimulation frequencies in the range of 2-12 Hz were used to activate the rat spinotrapezius muscle. Periarteriolar and capillary bed Po2, [H+], and [K+] changed during the first few minutes of stimulation but were restored to near resting concentrations as the functional hyperemia developed. However, perivenular Po2 decreased rapidly to approximately 50-60% of the resting gas tension as contractions began, and only minor recovery occurred. Elevation of tissue and periarteriolar Po2 with an O2-enriched superfusion solution did not prevent dilation during contractions to the same diameter as during the response at very low superfusion Po2. Therefore, the extent to which O2 influences arteriolar dilation and exercise hyperemia in the spinotrapezius muscle of the rat may depend less on periarteriolar and capillary bed Po2 than on the release of vasoactive materials from the nearby perivenular tissues as the availability of O2 decreases.

Exercise Hyperemia for the Study of Peripheral Circulation

Angiology ◽  
1980 ◽  
Vol 31 (1) ◽  
pp. 50-57 ◽  
Author(s):  
B. Dorigo ◽  
V. Bartoli ◽  
D. Grisillo ◽  
D. Beconi ◽  
A. Zanini
Keyword(s):  
Peripheral Circulation ◽  
Exercise Hyperemia

Aminophylline and interstitial adenosine during sustained exercise hyperemia

1986 ◽  
Vol 251 (6) ◽  
pp. H1232-H1243 ◽  
Author(s):  
L. P. Thompson ◽  
M. W. Gorman ◽  
H. V. Sparks
Keyword(s):  
Interstitial Fluid ◽  
Standard Dose ◽  
Adenosine Release ◽  
Adenosine Receptor Antagonist ◽  
Adenosine Concentration ◽  
Exercise Hyperemia ◽  
Before And After ◽  
Exercise Period ◽  
Arterial Plasma ◽  
Plasma Adenosine

We tested the hypothesis that an increase in interstitial fluid (ISF) adenosine concentration contributes to vasodilation of high oxidative skeletal muscle during sustained free-flow exercise. Canine calf muscles were stimulated at 3 Hz for 10 min before and after the infusion of the adenosine receptor antagonist aminophylline (10 mg/kg). The vasodilation that occurred during aminophylline infusion was allowed to decay before the postaminophylline exercise period was begun. This dose of aminophylline shifted the response to infused adenosine 20-fold during rest and reduced the response to a standard dose by 90% during exercise. Aminophylline had no significant effect on blood flow or on O2 consumption at rest or during exercise. Adenosine release (venous minus arterial plasma concentration times plasma flow) increased during 3-Hz exercise both before and after aminophylline infusion, but venous plasma adenosine concentration did not increase in either case. We developed a mathematical model of adenosine movement between ISF and plasma to help us judge whether to use adenosine release or venous concentration as an index of ISF adenosine and decided that venous concentration should be used. We conclude that aminophylline has no effect on sustained 3-Hz exercise hyperemia because under these conditions ISF adenosine concentration does not increase.

Reactive and exercise hyperemia during high levels of adenosine infusion

1982 ◽  
Vol 243 (2) ◽  
pp. H181-H186 ◽  
Author(s):  
R. L. Hester ◽  
A. C. Guyton ◽  
B. J. Barber
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Adenosine Infusion ◽  
Endogenous Adenosine ◽  
Exercise Hyperemia ◽  
The Face ◽  
Time Periods ◽  
Level 1 ◽  
Adenosine Perfusion ◽  
Quantitative Importance

In these experiments we tested the quantitative importance of adenosine as a mediator in the regulation of muscle with blood containing adenosine at concentrations more than 1,000 times the normal resting adenosine level (1, 7) so that the effect of any endogenously released adenosine would be miniscule in comparison with the effect of this perfused adenosine. Therefore, any major blood flow responses that should occur while the muscle remained continuously under the influence of the perfused adenosine could hardly be ascribed to endogenous adenosine. At the onset of the perfusion with the adenosine the blood flow increased approximately sevenfold. However, over 1-3 h of continued perfusion, the blood flow returned to or near to control despite the extreme amounts of adenosine. Then, while the muscle was still exposed to the adenosine, both reactive hyperemia and exercise hyperemia were elicited for varying time periods and varying degrees for a total of 96 separate measurements in 12 preparations. In all instances the increases in blood flow during hyperemia were almost exactly identical to those recorded prior to adenosine perfusion. Because it would have been almost impossible for the small amounts of endogenous adenosine to cause the large hyperemia responses in the face of the extreme amounts of perfused adenosine, it is concluded that both the reactive and exercise hyperemia responses are probably caused either entirely or almost entirely by factors other than adenosine.

Flow-induced dilation of rat soleus feed arteries

1997 ◽  
Vol 273 (5) ◽  
pp. H2423-H2427 ◽  
Author(s):  
Jeffrey L. Jasperse ◽  
M. Harold Laughlin
Keyword(s):  
Shear Stress ◽  
Maximum Flow ◽  
Intraluminal Pressure ◽  
Shear Stresses ◽  
Potential Contribution ◽  
Basal Diameter ◽  
Exercise Hyperemia ◽  
Feed Arteries

Flow-induced dilation is thought to contribute to dilation of skeletal muscle arteries and arterioles during exercise hyperemia. We sought to determine whether rat soleus feed arteries (SFA) exhibit flow-induced dilation and to evaluate the potential contribution of flow-induced dilation of SFA to exercise hyperemia. Rat SFA were isolated and cannulated to allow pressure and intraluminal flow to be independently controlled. Intraluminal pressure was maintained at 90 cmH2O throughout the experiment. All SFA ( n = 13) developed spontaneous tone and dilated in response to flow. Flow of 10 and 14 μl/min produced a 34 ± 14 and 56 ± 17 μm increase above basal diameter (135 ± 12 μm), respectively. Flows >14 μl/min produced little further dilation. Maximum flow-induced dilation was 86 ± 3% of passive diameter determined in calcium-free physiological saline solution. Calculated shear stress was maintained at 4–6 dyn/cm2 at flows of 10–20 μl/min but increased at greater flows because SFA did not dilate further. To determine whether dilation in response to flows in this range may contribute to exercise hyperemia, we estimated in vivo SFA blood flows from previously published soleus blood flow data. Anesthetized rats are estimated to have flows of 10 μl/min per SFA, and conscious rats are estimated to have flows of 95 (nonexercising), 153 (walking), and 225 (running) μl/min per SFA. Corresponding shear stresses were estimated to be 26 (anesthetized), 47 (conscious, nonexercising), 75 (walking), and 111 (running) dyn/cm2. Because estimated in vivo values for both flow and wall shear stress are far greater than the flow and/or shear stresses at which maximal flow-induced dilation occurs in vitro, we conclude that flow-induced dilation contributes little to dilation of SFA during locomotory exercise.

Prostaglandins and exercise hyperemia of dog skeletal muscle

1980 ◽  
Vol 238 (2) ◽  
pp. H191-H195 ◽  
Author(s):  
E. W. Young ◽  
H. V. Sparks
Keyword(s):  
Skeletal Muscle ◽  
Free Flow ◽  
Prostaglandin E ◽  
Muscle Exercise ◽  
Vascular Response ◽  
Vascular Conductance ◽  
Exercise Hyperemia ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Stimulation Of

The possibility that prostaglandins (PG) contribute to skeletal muscle exercise hyperemia was tested by blocking PG synthesis with indomethacin and by measuring muscle prostaglandin E (PGE) release. The anterior calf muscles of anesthetized dogs were stimulated at frequencies of 1 Hz, 3 Hz, and 6 Hz under conditions of free flow both before and after indomethacin (5 mg/kg). PGE release was elevated from 14.2 +/- 2.4 to 21.8 +/- 3.4 ng . min-1 . 100 g-1 (P less than 0.01) during stimulation at 3 Hz and from 17.5 +/- 5.1 to 39.2 +/- 9.8 ng . min-1 . 100 g-1 (P less than 0.05) during stimulation of 6 Hz. During exercise at 1 Hz, PGE release was not increased. Indomethacin blocked PGE release and the vascular response to arachidonic acid, but caused essentially no changes in blood flow, oxygen consumption, and vascular conductance during exercise at each frequency. Thus, although PGE release is increased during free flow exercise, inhibiting PG synthesis does not alter exercise hyperemia. However, resting vascular conductance is significantly decreased by indomethacin.

scholarly journals Sustained exercise hyperemia during prolonged adenosine infusion in humans

2019 ◽  
Vol 7 (4) ◽  
pp. e14009
Author(s):  
Sushant M. Ranadive ◽  
John R. A. Shepherd ◽  
Timothy B. Curry ◽  
Frank A. Dinenno ◽  
Michael J. Joyner
Keyword(s):  
Adenosine Infusion ◽  
Exercise Hyperemia
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