scholarly journals Absence of compensatory vasodilation with perfusion pressure challenge in exercise: evidence for and implications of the noncompensator phenotype

2018 ◽  
Vol 124 (2) ◽  
pp. 374-387 ◽  
Author(s):  
Robert F. Bentley ◽  
Jeremy J. Walsh ◽  
Patrick J. Drouin ◽  
Aleksandra Velickovic ◽  
Sarah J. Kitner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Delivery ◽  
Exercise Tolerance ◽  
Forearm Blood Flow ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Interindividual Differences ◽  
Arterial Blood ◽  
Pressor Responses

Compromising oxygen delivery (O2D) during exercise requires compensatory vasodilatory and/or pressor responses to protect O2D:demand matching. The purpose of the study was to determine whether compensatory vasodilation is absent in some healthy young individuals in the face of a sudden reduction in exercising forearm perfusion pressure and whether this affects the exercise pressor response. Twenty-one healthy young men (21.6 ± 2.0 yr) completed rhythmic forearm exercise at a work rate equivalent to 70% of their own maximal exercise vasodilation. During steady-state exercise, the exercising arm was rapidly adjusted from below to above heart level, resulting in a reduction in forearm perfusion pressure of −30.7 ± 0.9 mmHg. Forearm blood flow (ml/min; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (mmHg; finger photoplethysmography), and exercising forearm venous effluent (antecubital vein catheter) measurements revealed distinct compensatory vasodilatory differences. Thirteen individuals responded with compensatory vasodilation (509 ± 128 vs. 632 ± 136 ml·min−1·100 mmHg−1; P < 0.001), while eight individuals did not (663 ± 165 vs. 667 ± 167 ml·min−1·100 mmHg−1; P = 0.6). Compensatory pressor responses between groups were not different (5.5 ± 5.5 and 9.7 ± 9.5 mmHg; P = 0.2). Forearm blood flow, O2D, and oxygen consumption were all protected in compensators (all P > 0.05) but not in noncompensators, who therefore suffered compromises to exercise performance (6 ± 14 vs. −36 ± 29 N; P = 0.004). Phenotypic differences were not explained by potassium or nitric oxide bioavailability. In conclusion, both compensator and noncompensator vasodilator phenotype responses to a sudden compromise to exercising muscle blood flow are evident. Interindividual differences in the mechanisms governing O2D:demand matching should be considered as factors influencing exercise tolerance. NEW & NOTEWORTHY In healthy young individuals, compromising submaximally exercising muscle perfusion appears to evoke compensatory vasodilation to defend oxygen delivery. Here we report the absence of compensatory vasodilation in 8 of 21 such individuals, despite their vasodilatory capacity and increases in perfusion with increasing exercise intensity being indistinguishable from compensators. The absence of compensation impaired exercise tolerance. These findings suggest that interindividual differences in oxygen delivery:demand matching efficacy affect exercise tolerance and depend on the nature of a delivery:demand matching challenge.

Potentiation of the exercise pressor reflex by muscle ischemia

1989 ◽  
Vol 66 (3) ◽  
pp. 1046-1053 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Flow ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Arterial Occlusion ◽  
Acid Base Balance ◽  
Active Muscle ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Static Contraction

The reflex responses to static contraction are augmented by ischemia. The metabolic “error signals” that are responsible for these observed responses are unknown. Therefore this study was designed to test the hypothesis that static contraction-induced pressor responses, which are enhanced during muscle ischemia, are the result of alterations in muscle oxygenation, acid-base balance, and K+. Thus, in 36 cats, the pressor response, active muscle blood flow, and muscle venous pH, PCO2, PO2, lactate, and K+ were compared during light and intense static contractions with and without arterial occlusion. During light contraction (15–16% of maximal), active muscle blood flow increased without and decreased with arterial occlusion (+35 +/- 12 vs. -60 +/- 11%). Arterial occlusion augmented these pressor responses by 132 +/- 25%. Without arterial occlusion, changes (P less than 0.05) were seen in PO2, O2 content, PCO2, and K+. Lactate and pH were unchanged. With arterial occlusion, changes in muscle PCO2 were augmented and significant changes were seen in pH and lactate. During intense static contraction (67–69% of maximal), muscle blood flow decreased without arterial occlusion (-39 +/- 9%) and decreased further during occlusion (-81 +/- 6%). Arterial occlusion augmented the pressor responses by 39 +/- 12%. All metabolic variables increased during contraction without arterial occlusion, but occlusion failed to augment any of these changes. These data suggest that light static ischemic contractions cause increases in muscle PCO2 and lactate and decreases in pH that may signal compensatory reflex-induced changes in arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Maintained exercise pressor response in heart failure

1998 ◽  
Vol 85 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Allen R. Kunselman ◽  
David H. Silber ◽  
Lawrence I. Sinoway
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Ambient Pressure ◽  
Muscle Blood Flow ◽  
Positive Pressure ◽  
Arterial Blood ◽  
Muscle Reflex ◽  
The Impact

The impact of forearm blood flow limitation on muscle reflex (metaboreflex) activation during exercise was examined in 10 heart failure (HF) (NYHA class III and IV) and 9 control (Ctl) subjects. Rhythmic handgrip contractions (25% maximal voluntary contraction, 30 contractions/min) were performed over 5 min under conditions of ambient pressure or with +50 mmHg positive pressure about the exercising forearm. Mean arterial blood pressure (MAP) and venous effluent hemoglobin (Hb) O2 saturation, lactate and H+ concentrations ([La] and [H+], respectively) were measured at baseline and during exercise. For ambient contractions, the increase (Δ) in MAP by end exercise (ΔMAP; i.e., the exercise pressor response) was the same in both groups (10.1 ± 1.2 vs. 7.33 ± 1.3 mmHg, HF vs. Ctl, respectively) despite larger Δ[La] and Δ[H+] for the HF group ( P < 0.05). With ischemic exercise, the ΔMAP for HF (21.7 ± 2.7 mmHg) exceeded that of Ctl subjects (12.2 ± 2.8 mmHg) ( P < 0.0001). Also, for HF, Δ[La] (2.94 ± 0.4 mmol) and Δ[H+] (24.8 ± 2.7 nmol) in the ischemic trial were greater than in Ctl (1.63 ± 0.4 mmol and 15.3 ± 2.8 nmol; [La] and [H+], respectively) ( P < 0.02). Hb O2 saturation was reduced in Ctl from ∼43% in the ambient trial to ∼27% with ischemia ( P < 0.0001). O2 extraction was maximized under ambient exercise conditions for HF but not for Ctl. Despite progressive increases in blood perfusion pressure over the course of ischemic exercise, no improvement in Hb O2saturation or muscle metabolism was observed in either group. These data suggest that muscle reflex activation of the pressor response is intact in HF subjects but the resulting improvement in perfusion pressure does not appear to enhance muscle oxidative metabolism or muscle blood flow, possibly because of associated increases in sympathetic vasoconstriction of active skeletal muscle.

Evaluation of muscle metaboreflex function through graded reduction in forearm blood flow during rhythmic handgrip exercise in humans

2011 ◽  
Vol 301 (2) ◽  
pp. H609-H616 ◽  
Author(s):  
Masashi Ichinose ◽  
Stephane Delliaux ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Takeshi Nishiyasu
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Voluntary Contraction ◽  
Open Loop ◽  
Handgrip Exercise ◽  
Hemodynamic Responses ◽  
Muscle Metaboreflex ◽  
Arterial Blood

Hypoperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Our aim was to determine the muscle metaboreflex threshold and gain in humans by creating an open-loop relationship between active muscle blood flow and hemodynamic responses during a rhythmic handgrip exercise. Eleven healthy subjects performed the exercise at 5 or 15% of maximal voluntary contraction (MVC) in random order. During the exercise, forearm blood flow (FBF), which was continuously measured using Doppler ultrasound, was reduced in five steps by manipulating the inner pressure of an occlusion cuff on the upper arm. The FBF at each level was maintained for 3 min. The initial reductions in FBF elicited no hemodynamic changes, but once FBF fell below a threshold, mean arterial blood pressure (MAP) and heart rate (HR) increased and total vascular conductance (TVC) decreased in a linear manner. The threshold FBF during the 15% MVC trial was significantly higher than during the 5% MVC trial. The gain was then estimated as the slope of the relationship between the hemodynamic responses and FBFs below the threshold. The gains for the MAP and TVC responses did not differ between workloads, but the gain for the HR response was greater in the 15% MVC trial. Our findings thus indicate that increasing the workload shifts the threshold for the muscle metaboreflex to higher blood flows without changing the gain of the reflex for the MAP and TVC responses, whereas it enhances the gain for the HR response.

Do vasoregulatory mechanisms in exercising human muscle compensate for changes in arterial perfusion pressure?

2007 ◽  
Vol 293 (5) ◽  
pp. H2928-H2936 ◽  
Author(s):  
Kathryn L. Walker ◽  
Natasha R. Saunders ◽  
Dennis Jensen ◽  
Jennifer L. Kuk ◽  
Suzi-Lai Wong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Human Muscle ◽  
Isometric Handgrip ◽  
Vascular Conductance ◽  
Arterial Perfusion ◽  
Arterial Blood ◽  
Myogenic Regulation

We tested the hypothesis that vasoregulatory mechanisms completely counteract the effects of sudden changes in arterial perfusion pressure on exercising muscle blood flow. Twelve healthy young subjects (7 female, 5 male) lay supine and performed rhythmic isometric handgrip contractions (2 s contraction/ 2 s relaxation 30% maximal voluntary contraction). Forearm blood flow (FBF; echo and Doppler ultrasound), mean arterial blood pressure (arterial tonometry), and heart rate (ECG) were measured. Moving the arm between above the heart (AH) and below the heart (BH) level during contraction in steady-state exercise achieved sudden ∼30 mmHg changes in forearm arterial perfusion pressure (FAPP). We analyzed cardiac cycles during relaxation (FBFrelax). In an AH-to-BH transition, FBFrelax increased immediately, in excess of the increase in FAPP (∼69% vs. ∼41%). This was accounted for by pressure-related distension of forearm resistance vasculature [forearm vascular conductance (FVCrelax) increased by ∼19%]. FVCrelax was restored by the second relaxation. Continued slow decreases in FVCrelax stabilized by 2 min without restoring FBFrelax. In a BH-to-AH transition, FBFrelax decreased immediately, in excess of the decrease in FAPP (∼37% vs. ∼29%). FVCrelax decreased by ∼14%, suggesting pressure-related passive recoil of resistance vessels. The pattern of FVCrelax was similar to that in the AH-to-BH transition, and FBFrelax was not restored. These data support rapid myogenic regulation of vascular conductance in exercising human muscle but incomplete flow restoration via slower-acting mechanisms. Local arterial perfusion pressure is an important determinant of steady-state blood flow in the exercising human forearm.

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

Vasodilation contributes to the rapid hyperemia with rhythmic contractions in humans

1998 ◽  
Vol 76 (4) ◽  
pp. 418-427 ◽  
Author(s):  
J K Shoemaker ◽  
M E Tschakovsky ◽  
R L Hughson
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Perfusion Pressure ◽  
Blood Velocity ◽  
Pulsed Doppler ◽  
Contraction Rate ◽  
Handgrip Exercise ◽  
Arterial Diameter ◽  
Exercise Tests ◽  
Rhythmic Contractions

The hypothesis that the rapid increases in blood flow at the exercise onsetare exclusively due to the mechanical effects of the muscle pump was tested in six volunteersduring dynamic handgrip exercise. While supine, each subject completed a series of eightdifferent exercise tests in which brachial artery blood pressure (BP) was altered by25–30 mmHg (1 mmHg = 133.3 Pa) by positioning the arm above or below the heart.Two different weights, corresponding to 4.9 and 9.7% of maximal voluntary isometriccontraction, were raised and lowered at two different contraction rate schedules (1s:1s and 2s:2swork–rest) each with a 50% duty cycle. Beat-by-beat measures of mean blood velocity (MBV)(pulsed Doppler) were obtained at rest and for 5 min following step increases in work ratewith emphasis on the first 24 s. MBV was increased 50–100% above rest following the firstcontraction in both arm positions (p < 0.05). The increase in MBV from rest was greaterin the below position compared with above, and this effect was observed following the first andsubsequent contractions (p < 0.05). However, the positional effect on the increase inMBV could not be explained entirely by the ~40% greater BP in this position. Also, the greaterworkload resulted in greater increases in MBV as early as the first contraction, compared withthe light workload (p < 0.05) despite similar reductions in forearm volume followingsingle contractions. MBV was greater with faster contraction rate tests by 8 s of exercise. Itwas concluded that microvascular vasodilation must act in concert with a reduction in venouspressure to increase forearm blood flow within the initial 2–4 s of exercise.Key words: Doppler, mean blood velocity, arterial diameter,handgrip exercise, perfusion pressure.

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

Regional circulatory responses to hypocapnia and hypercapnia in bar-headed geese

1986 ◽  
Vol 250 (3) ◽  
pp. R499-R504 ◽  
Author(s):  
F. M. Faraci ◽  
M. R. Fedde
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Pectoral Muscle ◽  
Blood Flows ◽  
Arterial Blood ◽  
Blood Flow Reduction ◽  
Extreme Altitude ◽  
Anser Indicus ◽  
O2 Delivery

To investigate mechanisms that may allow birds to tolerate extreme high altitude (hypocapnic hypoxia), we examined the effects of severe hypocapnia and moderate hypercapnia on regional blood flow in bar-headed geese (Anser indicus), a species that flies at altitudes up to 9,000 m. Cerebral, coronary, and pectoral muscle blood flows were measured using radioactive microspheres, while arterial CO2 tension (PaCO2) was varied from 7 to 62 Torr in awake normoxic birds. Arterial blood pressure was not affected by hypocapnia but increased slightly during hypercapnia. Heart rate did not change during alterations in PaCO2. Severe hypocapnia did not significantly alter cerebral, coronary, or pectoral muscle blood flow. Hypercapnia markedly increased cerebral and coronary blood flow, but pectoral muscle blood flow was unaffected. The lack of a blood flow reduction during severe hypocapnia may represent an important adaptation in these birds, enabling them to increase O2 delivery to the heart and brain at extreme altitude despite the presence of a very low PaCO2.

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