scholarly journals Effect of histamine-receptor antagonism on leg blood flow during exercise

2020 ◽  
Vol 128 (6) ◽  
pp. 1626-1634
Author(s):  
Matthew R. Ely ◽  
Stephen M. Ratchford ◽  
D. Taylor La Salle ◽  
Joel D. Trinity ◽  
D. Walter Wray ◽  
...  
Keyword(s):  
Blood Flow ◽  
Immune Responses ◽  
Histamine Receptor ◽  
Peak Capacity ◽  
Elevated Blood ◽  
Receptor Antagonism ◽  
Leg Blood Flow ◽  
Exercise Response ◽  
Exercise Induced

Leg blood flow during exercise was increased by taking antihistamines, which block the receptors for histamine, a molecule often associated with inflammatory and immune responses. The elevated blood flow occurred over exercise intensities ranging from 20 to 80% of peak capacity and during exercise of 60-min duration. These results suggest that exercise-induced elevations in histamine concentrations are involved in novel, poorly understood, and perhaps complex ways in the exercise response.

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.

scholarly journals Role of α1-adrenergic vasoconstriction in the regulation of skeletal muscle blood flow with advancing age

2009 ◽  
Vol 296 (2) ◽  
pp. H497-H504 ◽  
Author(s):  
D. Walter Wray ◽  
Steven K. Nishiyama ◽  
Russell S. Richardson
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
The Elderly ◽  
Work Rate ◽  
Leg Blood Flow ◽  
Vasoconstrictor Response ◽  
Leg Exercise ◽  
Exercise Induced ◽  
Induced Changes

α1-Adrenergic vasoconstriction during dynamic leg exercise is diminished in younger individuals, although the extent of this exercise-induced “sympatholysis” in the elderly remains uncertain. Thus, in nine young (25 ± 1 yr) and six older (72 ± 2 yr) healthy volunteers, we evaluated changes in leg blood flow (ultrasound Doppler) during blood flow-adjusted intra-arterial infusion of phenylephrine (PE; a selective α1-adrenergic agonist) at rest and during knee-extensor leg exercise at 20, 40, and 60% of maximal work rate (WRmax). To probe the potential contributors to exercise-induced changes in α1-adrenergic receptor sensitivity, exercising leg O2 consumption (V̇o2) and lactate efflux were also evaluated ( n = 10). At rest, the PE-induced vasoconstriction (i.e., decrease in leg blood flow) was diminished in older (−37 ± 3%) compared with young (−54 ± 4%) subjects. During exercise, the magnitude of α1-adrenergic vasoconstriction in the active leg decreased in both groups. However, compared with young, older subjects maintained a greater vasoconstrictor response to PE at 40% WRmax (−14 ± 3%, older; −7 ± 2%, young) and 60% WRmax (−11 ± 3%, older; −4 ± 3%, young). It is possible that this observation may be attributed to lower absolute work rates in the older group, because, for a similar absolute work rate (≈10 W) and leg V̇o2 (≈0.36 l/min), vasoconstriction to PE was not different between groups (−14 ± 3%; older; −17 ± 5%, young). Together, these data challenge the concept of reduced sympatholysis in the elderly, suggesting instead that the inhibition of α1-adrenergic vasoconstriction in the exercising leg is associated with work performed and, therefore, more closely related to the rate of oxidative metabolism than to age per se.

scholarly journals A single dose of histamine-receptor antagonists before downhill running alters markers of muscle damage and delayed-onset muscle soreness

2017 ◽  
Vol 122 (3) ◽  
pp. 631-641 ◽  
Author(s):  
Matthew R. Ely ◽  
Steven A. Romero ◽  
Dylan C. Sieck ◽  
Joshua E. Mangum ◽  
Meredith J. Luttrell ◽  
...  
Keyword(s):  
Blood Flow ◽  
Creatine Kinase ◽  
Muscle Strength ◽  
Muscle Damage ◽  
Muscle Soreness ◽  
Strength Loss ◽  
Histamine Receptor ◽  
Delayed Onset ◽  
Markers Of Inflammation ◽  
Exercise Induced

Histamine contributes to elevations in skeletal muscle blood flow following exercise, which raises the possibility that histamine is an important mediator of the inflammatory response to exercise. We examined the influence of antihistamines on postexercise blood flow, inflammation, muscle damage, and delayed-onset muscle soreness (DOMS) in a model of moderate exercise-induced muscle damage. Subjects consumed either a combination of fexofenadine and ranitidine (blockade, n = 12) or nothing (control, n = 12) before 45 min of downhill running (−10% grade). Blood flow to the leg was measured before and throughout 120 min of exercise recovery. Markers of inflammation, muscle damage, and DOMS were obtained before and at 0, 6, 12, 24, 48, and 72 h postexercise. At 60 min postexercise, blood flow was reduced ~29% with blockade compared with control ( P < 0.05). Markers of inflammation were elevated after exercise (TNF-ɑ, IL-6), but did not differ between control and blockade. Creatine kinase concentrations peaked 12 h after exercise, and the overall response was greater with blockade (18.3 ± 3.2 kU·l−1·h−1) compared with control (11.6 ± 2.0 kU·l−1·h−1; P < 0.05). Reductions in muscle strength in control (−19.3 ± 4.3% at 24 h) were greater than blockade (−7.8 ± 4.8%; P < 0.05) and corresponded with greater perceptions of pain/discomfort in control compared with blockade. In conclusion, histamine-receptor blockade reduced postexercise blood flow, had no effect on the pattern of inflammatory markers, increased serum creatine kinase concentrations, attenuated muscle strength loss, and reduced pain perception following muscle-damaging exercise. NEW & NOTEWORTHY Histamine appears to be intimately involved with skeletal muscle during and following exercise. Blocking histamine’s actions during muscle-damaging exercise, via common over-the-counter antihistamines, resulted in increased serum creatine kinase, an indirect marker of muscle damage. Paradoxically, blocking histamine’s actions attenuated muscle strength loss and reduced perceptions of muscle pain for 72 h following muscle-damaging exercise. These results indicate that exercise-induced histamine release may have a broad impact on protecting muscle from exercise-induced damage.

Does venous insufficiency impair the exercise-induced rise in arterial leg blood flow?

2011 ◽  
Vol 26 (8) ◽  
pp. 326-331 ◽  
Author(s):  
I H Nådland ◽  
J Wesche ◽  
D D Sheriff ◽  
K Toska
Keyword(s):  
Blood Flow ◽  
Healthy Subjects ◽  
Venous Insufficiency ◽  
Upright Position ◽  
Leg Blood Flow ◽  
Muscle Pump ◽  
Tilted Position ◽  
Transient Rise ◽  
Exercise Induced ◽  
Artery Flow

Objectives It has been shown that the leg muscle pump increases the immediate rise in arterial leg blood flow during upright exercise in healthy subjects. The present study is the first to investigate the muscle pump effect in exercise hyperaemia in patients with venous insufficiency, who should be lacking an optimally functioning muscle pump. Methods Any muscle pump effect is more pronounced in an upright position because of gravitation. The exercise-induced rise in femoral artery flow (FF) (ultrasound Doppler) was thus compared in the supine and 30° head-up tilted position in 10 patients. Results Neither the transient nor the steady-state rise in FF showed any difference between positions. This is in contrast to the previous findings in healthy subjects, where the transient rise in FF was larger in the tilted position. Conclusion The muscle pump effect in exercise hyperaemia seems to be reduced or lacking in these patients.

scholarly journals Taming the “sleeping giant”: the role of endothelin-1 in the regulation of skeletal muscle blood flow and arterial blood pressure during exercise

2013 ◽  
Vol 304 (1) ◽  
pp. H162-H169 ◽  
Author(s):  
Zachary Barrett-O'Keefe ◽  
Stephen J. Ives ◽  
Joel D. Trinity ◽  
Garrett Morgan ◽  
Matthew J. Rossman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiovascular Response ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Leg Blood Flow ◽  
Arterial Blood ◽  
Before And After ◽  
Exercise Induced ◽  
Response To Exercise

The cardiovascular response to exercise is governed by a combination of vasodilating and vasoconstricting influences that optimize exercising muscle perfusion while protecting mean arterial pressure (MAP). The degree to which endogenous endothelin (ET)-1, the body's most potent vasoconstrictor, participates in this response is unknown. Thus, in eight young (24 ± 2 yr), healthy volunteers, we examined leg blood flow, MAP, tissue oxygenation, heart rate, leg arterial-venous O2 difference, leg O2 consumption, pH, and net ET-1 and lactate release at rest and during knee extensor exercise (0, 5, 10, 15, 20, and 30 W) before and after an intra-arterial infusion of BQ-123 [ET subtype A (ETA) receptor antagonist]. At rest, BQ-123 did not evoke a change in leg blood flow or MAP. During exercise, net ET-1 release across the exercising leg increased approximately threefold. BQ-123 increased leg blood flow by ∼20% across all work rates (changes of 113 ± 76, 176 ± 83, 304 ± 108, 364 ± 130, 502 ± 117, and 570 ± 178 ml/min at 0, 5, 10, 15, 20, and 30 W, respectively) and attenuated the exercise-induced increase in MAP by ∼6%. The increase in leg blood flow was accompanied by a ∼9% increase in leg O2 consumption with an unchanged arterial-venous O2 difference and deoxyhemoglobin, suggesting a decline in intramuscular efficiency after ETA receptor blockade. Together, these findings identify a significant role of the ET-1 pathway in the cardiovascular response to exercise, implicating vasoconstriction via the ETA receptor as an important mechanism for both the restraint of blood flow in the exercising limb and maintenance of MAP in healthy, young adults.

Impaired leg vasodilation during dynamic exercise in healthy older women

2003 ◽  
Vol 95 (5) ◽  
pp. 1963-1970 ◽  
Author(s):  
David N. Proctor ◽  
Dennis W. Koch ◽  
Sean C. Newcomer ◽  
Khoi U. Le ◽  
Urs A. Leuenberger
Keyword(s):  
Blood Flow ◽  
Older Women ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Constant Load ◽  
Dynamic Exercise ◽  
Leg Blood Flow ◽  
Leg Cycle Ergometry ◽  
Leg Cycling ◽  
Exercise Induced

The purpose of the present study was to test the hypothesis that leg blood flow responses during leg cycle ergometry are reduced with age in healthy non-estrogen-replaced women. Thirteen younger (20-27 yr) and thirteen older (61-71 yr) normotensive, non-endurance-trained women performed both graded and constant-load bouts of leg cycling at the same absolute exercise intensities. Leg blood flow (femoral vein thermodilution), mean arterial pressure (MAP; radial artery), mean femoral venous pressure, cardiac output (acetylene rebreathing), and blood O2 contents were measured. Leg blood flow responses at light workloads (20-40 W) were similar in younger and older women. However, at moderate workloads (50-60 W), leg blood flow responses were significantly attenuated in older women. MAP was 20-25 mmHg higher ( P < 0.01) in the older women across all work intensities, and calculated leg vascular conductance (leg blood flow/estimated leg perfusion pressure) was lower ( P < 0.05). Exercise-induced increases in leg arteriovenous O2 difference and O2 extraction were identical between groups ( P > 0.6). Leg O2 uptake was tightly correlated with leg blood flow across all workloads in both subject groups ( r2 = 0.80). These results suggest the ability of healthy older women to undergo limb vasodilation in response to submaximal exercise is impaired and that the legs are a potentially important contributor to the augmented systemic vascular resistance seen during dynamic exercise in older women.

scholarly journals ­Heart Failure with Preserved Ejection Fraction Diminishes Peripheral Hemodynamics and Accelerates Exercise-Induced Neuromuscular Fatigue

2020 ◽  
Author(s):  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Thomas J. Hureau ◽  
Jayson R. Gifford ◽  
Philip Kithas ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Ejection Fraction ◽  
Knee Extension ◽  
Neuromuscular Fatigue ◽  
Preserved Ejection Fraction ◽  
Leg Blood Flow ◽  
Peripheral Hemodynamics ◽  
Exercise Induced ◽  
Knee Extension Exercise

This study investigated the impact of heart failure with a preserved ejection fraction (HFpEF) on neuromuscular fatigue and peripheral hemodynamics during small muscle mass exercise not limited by cardiac output. Eight HFpEF patients (ejection-fraction: 61±2%, NYHA II-III) and eight healthy-controls performed dynamic single-leg knee-extension exercise [80% peak workload] to task-failure and maximal intermittent isometric quadriceps contractions (8×15-s, 20-s rest). Controls repeated knee-extension at the same absolute workload as the HFpEF. During knee-extension, leg blood flow was quantified using Doppler ultrasound. Pre- to post-exercise changes in quadriceps twitch-torque (ΔQtw, peripheral fatigue), voluntary-activation (ΔVA, central fatigue), and corticospinal excitability were quantified. At the same relative intensity, HFpEF (24±5W) and controls (42±6W) had a similar time to task-failure (~10min), ΔQtw (~50%), and ΔVA (~6%) (P>0.3). This resulted in a greater exercise-induced change in neuromuscular function per unit work in HFpEF, which was significantly correlated with a slower leg blood flow response time (r=0.77). Knee-extension exercise at the same absolute workload resulted in a ~40% lower leg blood flow and greater ΔQtw (56±15 vs 11±10%) and ΔVA (5±3 vs 0±2%) in HFpEF than controls (P<0.05). Corticospinal excitability remained unaltered during exercise in both groups. Finally, despite a similar ΔVA, ΔQtw was larger in HFpEF compared to controls during isometric exercise (-49±9 vs -23±2%, P<0.05). In conclusion, HFpEF are characterized by a greater susceptibility to neuromuscular fatigue during exercise not limited by cardiac output. The patients' compromised peripheral hemodynamic response to exercise likely accounts, at least partly, for the attenuated fatigue resistance in this population.

Normal effect of insulin to stimulate leg blood flow in NIDDM

Diabetes ◽  
1995 ◽  
Vol 44 (2) ◽  
pp. 221-226 ◽  
Author(s):  
F. Dela ◽  
J. J. Larsen ◽  
K. J. Mikines ◽  
H. Galbo
Keyword(s):  
Blood Flow ◽  
Leg Blood Flow
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