Conditions for dipyridamole potentiation of skeletal muscle active hyperemia

1986 ◽  
Vol 250 (1) ◽  
pp. H62-H67 ◽  
Author(s):  
R. E. Klabunde
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Recovery Time ◽  
Free Flow ◽  
Isometric Contractions ◽  
Vascular Conductance ◽  
Arterial Infusion ◽  
Maximal Tension

The effects of dipyridamole on active hyperemia were evaluated in dog gracilis muscles undergoing sustained isometric contractions. Muscles were stimulated to contract for 5, 15, 25, and 50 s at 20% maximal tension (20% Tmax) or for 10 s at 100% Tmax during intra-arterial infusion of either saline or dipyridamole (1 microM). In two separate groups of dogs, muscles were stimulated to contract under free-flow or restricted-flow (ischemic) conditions. In the later group, blood flow was reduced to 50% of precontraction level during the period of contraction. Dipyridamole increased resting vascular conductance by about 45%; however, it did not affect the change in vascular conductance resulting from muscle contraction. The recovery time for active hyperemia following free-flow contractions at 20% Tmax was not altered by dipyridamole. However, dipyridamole increased the recovery time following 50 s of restricted-flow contraction (20% Tmax) and 10 s of 100% Tmax contractions by 46 and 169%, respectively. These results suggest that adenosine contributes to active hyperemia following sustained ischemic contractions at 20% Tmax and contractions at 100% Tmax but not from contractions at 20% Tmax where blood flow is allowed to increase freely.

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.

Timed synchronization of muscle contraction to heartbeat enhances muscle hyperemia

2020 ◽  
Vol 128 (4) ◽  
pp. 805-812
Author(s):  
Gaia Giuriato ◽  
Stephen J. Ives ◽  
Cantor Tarperi ◽  
Lorenzo Bortolan ◽  
Federico Ruzzante ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Contraction ◽  
Blood Velocity ◽  
Muscle Contractions ◽  
Velocity Spectrum ◽  
Functional Hyperemia ◽  
Central Hemodynamics ◽  
Active Muscle ◽  
Vascular Conductance ◽  
Significant Difference

Blood flow (BF) to exercising muscles is susceptible to variations of intensity, and duration of skeletal muscle contractions, cardiac cycle, blood velocity, and vessel dilation. During cyclic muscle activity, these elements may change proportionally with or without direct optimal temporal alignment, likely influencing BF to active muscle. Ideally, the pulsed delivery of blood to active muscle timed with the inactive phase of muscle duty-cycle would enhance the peak and average BF. To investigate the phenomenon of muscle contraction and pulse synchronicity, electrically evoked muscle contractions (trains of 20 Hz, 200-ms duration) were synchronized with each systolic phase of the anterograde blood velocity spectrum (aBVS). Specifically, unilateral quadriceps contractions matched in-phase (IP) with the aBVS were compared with contractions matched out-of-phase (OP) with the aBVS in 10 healthy participants (26 ± 3 yr). During each trial, femoral BF of the contracting limb and central hemodynamics were recorded for 5 min with an ultrasound Doppler, a plethysmograph, and a cardioimpedance device. At steady state (5th min) IP BF (454 ± 30 mL/min) and vascular conductance (4.3 ± 0.2 mL·min−1·mmHg−1), and OP MAP (108 ± 2 mmHg) were significantly lower ( P < 0.001) in comparison to OP BF (784 ± 25 mL/min) and vascular conductance (6.7 ± 0.2 mL·min−1·mmHg−1), and IP MAP (113 ± 3 mmHg). On the contrary, no significant difference (all, P > 0.05) was observed between IP and OP central hemodynamics (HR: 79 ± 10 vs. 76 ± 11 bpm, CO: 8.0 ± 1.6 vs. 7.3 ± 1.6 L/min), and ventilatory patterns (V̇e:14 ± 2 vs. 14 ± 1 L/min, V̇o2:421 ± 70 vs. 397 ± 34 mL/min). The results suggest that muscle contractions occurring during OP that do not interfere with aBVS elicit a maximization of muscle functional hyperemia. NEW & NOTEWORTHY When muscle contraction is synchronized with the pulsed delivery of blood flow to active muscle, muscle functional hyperemia can be either maximized or minimized. This suggests a possibility to couple different strategies to enhance the acute and chronic effects of exercise on the cardiovascular system.

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.

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.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

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 Model analysis of the relationship between intracellular Po2 and energy demand in skeletal muscle

2012 ◽  
Vol 303 (11) ◽  
pp. R1110-R1126 ◽  
Author(s):  
Jessica Spires ◽  
L. Bruce Gladden ◽  
Bruno Grassi ◽  
Gerald M. Saidel ◽  
Nicola Lai
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Energy Demand ◽  
Experimental Studies ◽  
Experimental Conditions ◽  
Permeability Surface ◽  
The Relationship ◽  
And Diffusion ◽  
Main Factor

On the basis of experimental studies, the intracellular O2 (iPo2)-work rate (WR) relationship in skeletal muscle is not unique. One study found that iPo2 reached a plateau at 60% of maximal WR, while another found that iPo2 decreased linearly at higher WR, inferring capillary permeability-surface area ( PS) and blood-tissue O2 gradient, respectively, as alternative dominant factors for determining O2 diffusion changes during exercise. This relationship is affected by several factors, including O2 delivery and oxidative and glycolytic capacities of the muscle. In this study, these factors are examined using a mechanistic, mathematical model to analyze experimental data from contracting skeletal muscle and predict the effects of muscle contraction on O2 transport, glycogenolysis, and iPo2. The model describes convection, O2 diffusion, and cellular metabolism, including anaerobic glycogenolysis. Consequently, the model simulates iPo2 in response to muscle contraction under a variety of experimental conditions. The model was validated by comparison of simulations of O2 uptake with corresponding experimental responses of electrically stimulated canine muscle under different O2 content, blood flow, and contraction intensities. The model allows hypothetical variation of PS, glycogenolytic capacity, and blood flow and predictions of the distinctive effects of these factors on the iPo2-contraction intensity relationship in canine muscle. Although PS is the main factor regulating O2 diffusion rate, model simulations indicate that PS and O2 gradient have essential roles, depending on the specific conditions. Furthermore, the model predicts that different convection and diffusion patterns and metabolic factors may be responsible for different iPo2-WR relationships in humans.

Skeletal muscle blood flow and vascular conductance are enhanced in humans with high‐affinity hemoglobin during handgrip exercise in severe hypoxia

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Chad C. Wiggins ◽  
Paolo B. Dominelli ◽  
Jonathon W. Senefeld ◽  
John R.A. Shepherd ◽  
Sarah E. Baker ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Severe Hypoxia ◽  
Handgrip Exercise ◽  
Vascular Conductance ◽  
Skeletal Muscle Blood Flow ◽  
High Affinity

Energetics of isometric exercise in man

1976 ◽  
Vol 41 (2) ◽  
pp. 136-141 ◽  
Author(s):  
P. Cerretelli ◽  
A. Veicsteinas ◽  
M. Fumagalli ◽  
L. Dell'orto
Keyword(s):  
Blood Flow ◽  
Lactic Acid ◽  
Energy Demand ◽  
Muscle Blood Flow ◽  
Isometric Exercise ◽  
Isometric Contractions ◽  
Plantar Flexors ◽  
Maximal Tension ◽  
Static Contractions ◽  
O2 Debt

In isometric contractions of the plantar flexors (5–40% of maximal tension, Tmax), VO2 is linearly related to the force exerted, averaging 2 ml/min-kg of tension. At tension levels above 5% Tmax the lactic acid contribution to the overall energy demand is constant at about 20%. Therefore, up to at least 40% Tmax,-muscle blood flow is not totally occluded, though it is impaired even at low force levels. Below 5% Tmax no lactic acid (LA) accumulates in blood. The energy required for the development of the tension is linearly related to the force exerted up to 33% Tmax, thereafter increasing disproportionately. In the transition from rest to static contractions of the plantar and forearm flexors (30 and 40% Tmax, respectively) VO2 increases initially to 200% of the controls, leveling off later at 150%. During recovery, VO2 increases up to 200% of the initial resting level, due to the payment of a large O2 debt, decreasing then with a t 1/2 of about 30 s. The glycolytic component is relatively more important in isometric contractions of the forearm than of the plantar flexors. No LA accumulates in static contractions of the plantar flexors of 5–10 s duration interrupted by equal pauses.

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