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.

Effect of altered arterial perfusion pressure on vascular conductance and muscle blood flow dynamic response during exercise in humans

2013 ◽  
Vol 114 (5) ◽  
pp. 620-627 ◽  
Author(s):  
Rodrigo Villar ◽  
Richard L. Hughson
Keyword(s):  
Blood Flow ◽  
Power Output ◽  
Perfusion Pressure ◽  
Body Position ◽  
Muscle Blood Flow ◽  
Plantar Flexion ◽  
Voluntary Contraction ◽  
Vascular Conductance ◽  
Arterial Perfusion ◽  
Three Body

Changes in vascular conductance (VC) are required to counter changes in muscle perfusion pressure (MPP) to maintain muscle blood flow (MBF) during exercise. We investigated the recruitment of VC as a function of peak VC measured in three body positions at two different work rates to test the hypothesis that adaptations in VC compensated changes in MPP at low-power output (LPO), but not at high-power output (HPO). Eleven healthy volunteers exercised at LPO and HPO (repeated plantar flexion contractions at 20–30% maximal voluntary contraction, respectively) in horizontal (HOR), 35° head-down tilt (HDT), and 45° head-up tilt (HUT). Muscle blood flow velocity and popliteal diameter were measured by ultrasound to determine MBF, and VC was estimated by dividing MBF flow by MPP. Peak VC was unaffected by body position. The rates of increase in MBF and VC were significantly faster in HUT and slower in HDT than HOR, and rates were faster in LPO than HPO. During LPO exercise, the increase in, and steady-state values of, MBF were less for HUT and HDT than HOR; the increase in VC was less in HUT than HOR and HDT. During HPO exercise, MBF in the HDT was reduced compared with HOR and HUT, even though VC reached 92% VC peak, which was greater than HOR, which was, in turn, greater than HUT. Reduced MBF during HPO HDT exercise had the functional consequence of a significant increase in muscle electromyographic index, revealing the effects of MPP on O2 delivery during exercise.

scholarly journals Individual susceptibility to hypoperfusion and reductions in exercise performance when perfusion pressure is reduced: evidence for vasodilator phenotypes

2014 ◽  
Vol 117 (4) ◽  
pp. 392-405 ◽  
Author(s):  
Robert F. Bentley ◽  
J. Mikhail Kellawan ◽  
Jackie S. Moynes ◽  
Veronica J. Poitras ◽  
Jeremy J. Walsh ◽  
...  
Keyword(s):  
Exercise Performance ◽  
Perfusion Pressure ◽  
Cardiovascular Response ◽  
Primary Objective ◽  
Isometric Handgrip ◽  
Compensatory Response ◽  
Arterial Perfusion ◽  
Muscle Oxygen ◽  
Individual Susceptibility ◽  
Arterial Blood

The primary objective of this study was to determine whether cardiovascular compensatory response phenotypes exist in the face of a reduced perfusion pressure challenge to exercising muscle oxygen delivery (O2D), and whether these responses might be exercise intensity (EI) dependent. Ten healthy men (19.5 ± 0.4 yr) completed two trials of progressive forearm isometric handgrip exercise to exhaustion (24.5 N increments every 3.5 min) in each of forearm above and below heart level [forearm arterial perfusion pressure (FAPP) difference of 29.5 ± 0.97 mmHg]. At the end of each EI, measurements of forearm blood flow (FBF; ml/min) via brachial artery Doppler and echo ultrasound, mean arterial blood pressure (MAP; mmHg) via finger photoplethysmography, and exercising forearm venous effluent via antecubital vein catheter revealed distinct cardiovascular response groups: n = 6 with compensatory vasodilation vs. n = 4 without compensatory vasodilation. Compensatory vasodilators were able to blunt the perfusion pressure-evoked reduction in submaximal O2D in the arm-above-heart condition, whereas nonvasodilators did not (−22.5 ± 13.6 vs. −65.4 ± 14.1 ml O2/min; P < 0.05), and in combination with being able to increase O2 extraction, nonvasodilators defended submaximal V̇o2 and experienced less of an accumulated submaximal O2D deficit (−80.7 ± 24.7 vs. −219.1 ± 36.0 ml O2/min; P < 0.05). As a result, the compensatory vasodilators experienced less of a compromise to peak EI than nonvasodilators (−24.5 ± 3.5 N vs. −52.1 ± 8.9 N; P < 0.05). In conclusion, in the forearm exercise model studied, vasodilatory response phenotypes exist that determine individual susceptibility to hypoperfusion and the degree to which aerobic metabolism and exercise performance are compromised.

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.

Muscle blood flow responses to dynamic exercise in young obese humans

2010 ◽  
Vol 108 (2) ◽  
pp. 349-355 ◽  
Author(s):  
Jacqueline K Limberg ◽  
Michael D. De Vita ◽  
Gregory M. Blain ◽  
William G. Schrage
Keyword(s):  
Skeletal Muscle ◽  
Body Mass Index ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Leg Exercise ◽  
Obese Subjects ◽  
Forearm Exercise

Exercise is a common nonpharmacological way to combat obesity; however, no studies have systematically tested whether obese humans exhibit reduced skeletal muscle blood flow during dynamic exercise. We hypothesized that exercise-induced blood flow to skeletal muscle would be lower in young healthy obese subjects (body mass index of >30 kg/m2) compared with lean subjects (body mass index of <25 kg/m2). We measured blood flow (Doppler Ultrasound of the brachial and femoral arteries), blood pressure (auscultation, Finapress), and heart rate (ECG) during rest and two forms of single-limb, steady-state dynamic exercise: forearm exercise (20 contractions/min at 4, 8, and 12 kg) and leg exercise (40 kicks/min at 7 and 14 W). Forearm exercise increased forearm blood flow (FBF) similarly in both groups ( P > 0.05; obese subjects n = 9, lean subjects n = 9). When FBF was normalized for perfusion pressure, forearm vascular conductance was not different between groups at increasing workloads ( P > 0.05). Leg exercise increased leg blood flow (LBF) similarly in both groups ( P > 0.05; obese subjects n = 10, lean subjects n = 12). When LBF was normalized for perfusion pressure, leg vascular conductance was not different between groups at increasing workloads ( P > 0.05). These results were confirmed when relative blood flow was expressed at average relative workloads. In conclusion, our results show that obese subjects exhibited preserved FBF and LBF during dynamic exercise.

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.

scholarly journals Cerebral blood flow, frontal lobe oxygenation and intra-arterial blood pressure during sprint exercise in normoxia and severe acute hypoxia in humans

2017 ◽  
Vol 38 (1) ◽  
pp. 136-150 ◽  
Author(s):  
David Curtelin ◽  
David Morales-Alamo ◽  
Rafael Torres-Peralta ◽  
Peter Rasmussen ◽  
Marcos Martin-Rincon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Frontal Lobe ◽  
Perfusion Pressure ◽  
Acute Hypoxia ◽  
Vascular Conductance ◽  
Sprint Exercise ◽  
Arterial Blood ◽  
Potential Damage

Cerebral blood flow (CBF) is regulated to secure brain O2 delivery while simultaneously avoiding hyperperfusion; however, both requisites may conflict during sprint exercise. To determine whether brain O2 delivery or CBF is prioritized, young men performed sprint exercise in normoxia and hypoxia (PIO2 = 73 mmHg). During the sprints, cardiac output increased to ∼22 L min−1, mean arterial pressure to ∼131 mmHg and peak systolic blood pressure ranged between 200 and 304 mmHg. Middle-cerebral artery velocity (MCAv) increased to peak values (∼16%) after 7.5 s and decreased to pre-exercise values towards the end of the sprint. When the sprints in normoxia were preceded by a reduced PETCO2, CBF and frontal lobe oxygenation decreased in parallel ( r = 0.93, P < 0.01). In hypoxia, MCAv was increased by 25%, due to a 26% greater vascular conductance, despite 4–6 mmHg lower PaCO2 in hypoxia than normoxia. This vasodilation fully accounted for the 22 % lower CaO2 in hypoxia, leading to a similar brain O2 delivery during the sprints regardless of PIO2. In conclusion, when a conflict exists between preserving brain O2 delivery or restraining CBF to avoid potential damage by an elevated perfusion pressure, the priority is given to brain O2 delivery.

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.

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