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

Walker, Kathryn; Saunders, Natasha; Jensen, Dennis; Kuk, Jennifer L.; Wong, Suzi-Lai; Pyke, Kyra E.; Dwyer, Erin M.; Tschakovsky, Michael E.

doi:10.1152/ajpheart.00576.2007

Cited by 22 publications

(52 citation statements)

References 37 publications

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“…The coefficient of variation within subjects across the five measurements ranged from 1.36% to 1.8%. A lack of change in a conduit vessel that is exposed to differences in hydrostatic pressure and in brief elevations in shear is a common finding in our laboratory and others (6,51). Subjects were then instrumented for measurement of heart rate (HR; ECG electrodes in standard CM 5 placement), beat-by-beat arterial blood pressure (finger photoplethysmograph cuff on the middle finger of the left hand supported in a sling at heart level; Finometer MIDI; Finapres Medical Systems, Amsterdam, the Netherlands), and right CFA blood velocity (pulsed Doppler ultrasound, Model 500V TCD; Multigon Industries, Mt.…”

Section: General Methodssupporting

confidence: 52%

“…Mechanisms that elevate the pressure gradient for blood flow through the CFA supplied vascular bed (37,47) could include the reduction of venous pressure by the muscle pump (25) and the restoration of arterial hydrostatic pressure in the lower limbs upon standing (37). Mechanisms that increase resistance vessel caliber could include local vasodilator substances (8), mechanical vessel compression effects on vascular tone (9), and possibly resistance vessel mechanical distension via increased local hydrostatic pressure upon standing (51).…”

Section: Mechanisms Localized To the Lower Limbs Explain Ioh On Risinmentioning

confidence: 99%

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Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Tschakovsky

Matusiak

Vipond

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Tschakovsky ME, Matusiak K, Vipond C, McVicar L. Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat. Am J Physiol Heart Circ Physiol 301: H2102-H2112, 2011. First published August 19, 2011 doi:10.1152/ajpheart.00571.2011.-The cause(s) of initial orthostatic hypotension (transient fall in blood pressure within 15 s upon active rising) have not been established. We tested the hypothesis that this hypotension is due to local vascular phenomena in contracting leg muscles from the brief effort of standing up. Seventeen young healthy subjects (2 male and 15 female, 22.5 Ϯ 1.0 years) performed an active rise from resting squat after a 10-s squat, a 1-min squat, or a 5-min squat. Beat-by-beat arterial blood pressure, cardiac output, heart rate, and stroke volume (Finometer finger photoplethysmography) and right common femoral artery blood flow (Doppler and Echo ultrasound) were recorded. Data are means Ϯ SE. Quiet standing before squat represented baseline. Peak increases in lower limb and total vascular conductance (ml·min Ϫ1 ·mmHg Ϫ1 ) upon standing were not different within squat conditions (10-s squat, 50.0 Ϯ 12.4 vs. 44.3 Ϯ 5.0; 1-min squat, 54.7 Ϯ 9.2 vs. 50.5 Ϯ 4.5; 5-min squat, 67.4 Ϯ 13.7 vs. 58.8 Ϯ 3.9; all P Ͼ 0.574). Mean arterial blood pressure (in mmHg) fell to a nadir well below standing baseline in all conditions despite increases in cardiac output. The hypotension predicted by the increase in leg vascular conductance accounted for this hypotension [observed vs. predicted (in mmHg): 10-s squat, Ϫ17.1 Ϯ 2.1 vs. Ϫ18.3 Ϯ 5.5; 1-min squat, Ϫ22.0 Ϯ 3.8 vs. Ϫ25.3 Ϯ 4.9; 5-min squat, Ϫ28.3 Ϯ 4.0 vs. Ϫ29.2 Ϯ 6.7]. We conclude that rapid contraction induced dilation in leg muscles with the effort of standing, along with a minor potential contribution of elevated lower limb arterio-venous pressure gradient, outstrips compensatory cardiac output responses and is the cause of initial orthostatic hypotension upon standing from squat. blood pressure; syncope; muscle blood flow; muscle contraction; sympathetic withdrawal; cardiopulmonary baroreflex

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Section: General Methodssupporting

confidence: 52%

Section: Mechanisms Localized To the Lower Limbs Explain Ioh On Risinmentioning

confidence: 99%

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Tschakovsky

Matusiak

Vipond

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…2). Walker et al (40), using a forearm occlusion model, found that changing arm position from the above heart to below heart position during isometric handgrip contraction rapidly increased both perfusion pressure and forearm vascular conductance. Taken together, the results of these studies and the current study indicate that changes in body position which alter perfusion pressure also alter limb vascular conductance.…”

Section: Discussionmentioning

confidence: 99%

“…Previous experiments in humans in which changes in body position were used to alter femoral artery perfusion pressure during passive leg movement (13,33) indicate that altered perfusion pressure changes both leg blood flow and vascular conductance independent of muscle contraction. Additionally, changing arm position during muscle contractions caused a change in fore-arm vascular conductance that was attributed to vascular smooth muscle myogenic responses because it was independent of changes in muscle contraction or metabolism (40). Thus, the primary goal of the current experiments was to apply a standardized vascular occlusion stimulus (to elicit reactive hyperemia) with the arm positioned above or below the heart.…”

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confidence: 99%

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Jasperse

Shoemaker

Gray

et al. 2015

Journal of Applied Physiology

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Jasperse JL, Shoemaker JK, Gray EJ, Clifford PS. Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia. J Appl Physiol 119: 569 -575, 2015. First published July 2, 2015; doi:10.1152/japplphysiol.01253.2013.-Studies have reported a greater blood flow response to muscle contractions when the limb is below the heart compared with above the heart, and these results have been interpreted as evidence for a skeletal muscle pump contribution to exercise hyperemia. If limb position affects the blood flow response to other vascular challenges such as reactive hyperemia, this interpretation may not be correct. We hypothesized that the magnitude of reactive hyperemia would be greater with the limb below the heart. Brachial artery blood flow (Doppler ultrasound) and blood pressure (finger-cuff plethysmography) were measured in 10 healthy volunteers. Subjects lay supine with one arm supported in two different positions: above or below the heart. Reactive hyperemia was produced by occlusion of arterial inflow for varying durations: 0.5 min, 1 min, 2 min, or 5 min in randomized order. Peak increases in blood flow were 77 Ϯ 11, 178 Ϯ 24, 291 Ϯ 25, and 398 Ϯ 33 ml/min above the heart and 96 Ϯ 19, 279 Ϯ 62, 550 Ϯ 60, and 711 Ϯ 69 ml/min below the heart (P Ͻ 0.05). Thus a standard stimulus (vascular occlusion) elicited different responses depending on limb position. To determine whether these differences were due to mechanisms intrinsic to the arterial wall, a second set of experiments was performed in which acute intraluminal pressure reduction for 0.5 min, 1 min, 2 min, or 5 min was performed in isolated rat soleus feed arteries (n ϭ 12). The magnitude of dilation upon pressure restoration was greater when acute pressure reduction occurred from 85 mmHg (mimicking pressure in the arm below the heart; 28.3 Ϯ 7.9, 37.5 Ϯ 5.9, 55.1 Ϯ 9.9, and 68.9 Ϯ 8.6% dilation) than from 48 mmHg (mimicking pressure in the arm above the heart; 20.8 Ϯ 4.8, 22.6 Ϯ 4.4, 31.2 Ϯ 5.8, and 49.2 Ϯ 7.1% dilation). These data support the hypothesis that arm position differences in reactive hyperemia are at least partially mediated by mechanisms intrinsic to the arterial wall. Overall, these results suggest the need to reevaluate studies employing positional changes to examine muscle pump influences on exercise hyperemia. muscle blood flow; muscle contraction; skeletal muscle pump; functional hyperemia AT THE ONSET OF DYNAMIC EXERCISE, there is a rapid increase in blood flow [30,31,41, and see Fig. 2 in Clifford and Hellsten (5)]. In fact, even a single muscle contraction produces a prompt increase in blood flow (1,7,14,26,36,39). There has been a debate over the last few decades about whether this rapid hyperemia is due to the muscle pump mechanism or to rapid vasodilation (5, 35).The muscle pump, as described by Laughlin (20), depends on an increased pressure gradient across the skeletal muscle vascular bed. Muscle contraction compresses the veins within the contracting muscle, expelling blood from the veins. ...

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“…This is surprising if we consider that the first observation of the phenomenon by Sir William Bayliss was in fact a rapid blood flow increase in the hindlimbs in response to a brief occlusion of the abdominal aorta (3). The existence of a rapid myogenic constriction (28,29,49) and dilatation (5, 38) has then been documented in different preparations.…”

Section: The Rapid Hyperemic Response To Brief Spontaneous Contractionsmentioning

confidence: 99%

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

Turturici

Mohammed

Roatta

2012

Journal of Applied Physiology

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Turturici M, Mohammed M, Roatta S. Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds. J Appl Physiol 113: 524 -531, 2012. First published June 7, 2012 doi:10.1152/japplphysiol.00237.2012.-Several mechanisms have been hypothesized to contribute to the rapid hyperemia at the onset of exercise. The aim of the present study was to investigate the role played by the mechanosensitivity of the vascular network. In 12 anesthetized rabbits blood flow was recorded from the exclusively muscular masseteric artery in response to brief spontaneous contractions (BSC) of the masseter muscle, artery occlusion (AO), muscle compression (MC), and muscle stretch (MS). Activation of masseter muscle was monitored by electromyography (EMG). Responses to AO were also recorded from the mostly cutaneous facial and the central ear arteries. Five animals were also tested in the awake condition. The hyperemic response to BSC (peak amplitude of 394 Ϯ 82%; time to peak of 1.8 Ϯ 0.8 s) developed with a latency of 300 -400 ms from the beginning of the EMG burst and 200 -300 ms from the contractioninduced transient flow reduction. This response was neither different from the response to AO (peak amplitude ϭ 426 Ϯ 158%), MC, and MS (P ϭ 0.23), nor from the BSC response in the awake condition. Compared with the masseteric artery, the response to AO was markedly smaller both in the facial (83 Ϯ 18%,) and in the central ear artery (68 Ϯ 20%) (P Ͻ 0.01). In conclusion, the rapid contractioninduced hyperemia can be replicated by a variety of stimuli affecting transmural pressure in muscle blood vessels and is thus compatible with the Bayliss effect. This prominent mechanosensitivity appears to be a characteristic of muscle and not cutaneous vascular beds. muscle stretch; myogenic response; rapid dilatation; reactive hyperemia; muscle compression SKELETAL MUSCLE BLOOD FLOW has long been known to exhibit a rapid increase at the onset of exercise (1,9,12,22,27). The mechanisms behind this phenomenon are still a matter of debate despite the many new insights provided by different research groups in recent years. In particular it has been shown that the contraction-induced compression of venous compartments (muscle pump) cannot fully account for the blood flow increase and that the additional occurrence of a rapid active dilatation is required (18,33,45,46). Other studies have shown that this rapid dilatation is mediated neither by changes in sympathetic neural drive (7, 41), nor by ACh spillover from the motor endplate (6, 33), nor by endothelium-released NO (6), although this last assertion is debated (see DISCUSSION). As early as 1974, Mohrman and Sparks (31) hypothesized that the rapid dilatation could result from the myogenic response of muscle blood vessels to decreased transmural pressure, which in turn results from the increase in intramuscular (extravascular) pressure produced by the contraction. They showed, in fact, that the rapid hypere...

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

Cited by 22 publications

References 37 publications

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

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