Evidence for a rapid vasodilatory contribution to immediate hyperemia in rest-to-mild and mild-to-moderate forearm exercise transitions in humans

2004 ◽  
Vol 97 (3) ◽  
pp. 1143-1151 ◽  
Author(s):  
Natasha R. Saunders ◽  
Michael E. Tschakovsky

Controversy exists regarding the contribution of a rapid vasodilatory mechanism(s) to immediate exercise hyperemia. Previous in vivo investigations have exclusively examined rest-to-exercise (R-E) transitions where both the muscle pump and early vasodilator mechanisms may be activated. To isolate vasodilatory onset, the present study investigated the onset of exercise hyperemia in an exercise-to-exercise (E-E) transition, where no further increase in muscle pump contribution would occur. Eleven subjects lay supine and performed a step increase from rest to 3 min of mild (10% maximal voluntary contraction), rhythmic, dynamic forearm handgrip exercise, followed by a further step to moderate exercise (20% maximal voluntary contraction) in each of arm above ( condition A) or below ( condition B) heart level. Beat-by-beat measures of brachial arterial blood flow (Doppler ultrasound) and blood pressure (arterial tonometry) were performed. We observed an immediate increase in forearm vascular conductance in E-E transitions, and the magnitude of this increase matched that of the R-E transitions within each of the arm positions ( condition A: E-E, 52.8 ± 10.7 vs. R-E, 60.3 ± 11.7 ml·min−1·100 mmHg−1, P = 0.66; condition B: E-E, 43.2 ± 12.8 vs. R-E, 33.9 ± 8.2 ml·min−1·100 mmHg−1, P = 0.52). Furthermore, changes in forearm vascular conductance were identical between R-E and E-E transitions over the first nine contraction-relaxation cycles in condition A. The immediate and identical increase in forearm vascular conductance in R-E and E-E transitions within arm positions provides strong evidence that rapid vasodilation contributes to immediate exercise hyperemia in humans. Specific vasodilatory mechanisms responsible remain to be determined.

2005 ◽  
Vol 99 (1) ◽  
pp. 376-377 ◽  
Author(s):  
A. Leroy-Willig

The following is the abstract of the article discussed in the subsequent letter: Although skeletal muscle perfusion is fundamental to proper muscle function, in vivo measurements are typically limited to those of limb or arterial blood flow, rather than flow within the muscle bed itself. We present a noninvasive functional MRI (fMRI) technique for measuring perfusion-related signal intensity (SI) changes in human skeletal muscle during and after contractions and demonstrate its application to the question of occlusion during a range of contraction intensities. Eight healthy men (aged 20–31 yr) performed a series of isometric ankle dorsiflexor contractions from 10 to 100% maximal voluntary contraction. Axial gradient-echo echo-planar images (repetition time = 500 ms, echo time = 18.6 ms) were acquired continuously before, during, and following each 10-s contraction, with 4.5-min rest between contractions. Average SI in the dorsiflexor muscles was calculated for all 240 images in each contraction series. Postcontraction hyperemia for each force level was determined as peak change in SI after contraction, which was then scaled to that obtained following a 5-min cuff occlusion of the thigh (i.e., maximal hyperemia). A subset of subjects ( n = 4) performed parallel studies using venous occlusion plethysmography to measure limb blood flow. Hyperemia measured by fMRI and plethysmography demonstrated good agreement. Postcontraction hyperemia measured by fMRI scaled with contraction intensity up to 60% maximal voluntary contraction. fMRI provides a noninvasive means of quantifying perfusion-related changes during and following skeletal muscle contractions in humans. Temporal changes in perfusion can be observed, as can the heterogeneity of perfusion across the muscle bed.


2004 ◽  
Vol 97 (6) ◽  
pp. 2385-2394 ◽  
Author(s):  
D. M. Wigmore ◽  
B. M. Damon ◽  
D. M. Pober ◽  
J. A. Kent-Braun

Although skeletal muscle perfusion is fundamental to proper muscle function, in vivo measurements are typically limited to those of limb or arterial blood flow, rather than flow within the muscle bed itself. We present a noninvasive functional MRI (fMRI) technique for measuring perfusion-related signal intensity (SI) changes in human skeletal muscle during and after contractions and demonstrate its application to the question of occlusion during a range of contraction intensities. Eight healthy men (aged 20–31 yr) performed a series of isometric ankle dorsiflexor contractions from 10 to 100% maximal voluntary contraction. Axial gradient-echo echo-planar images (repetition time = 500 ms, echo time = 18.6 ms) were acquired continuously before, during, and following each 10-s contraction, with 4.5-min rest between contractions. Average SI in the dorsiflexor muscles was calculated for all 240 images in each contraction series. Postcontraction hyperemia for each force level was determined as peak change in SI after contraction, which was then scaled to that obtained following a 5-min cuff occlusion of the thigh (i.e., maximal hyperemia). A subset of subjects ( n = 4) performed parallel studies using venous occlusion plethysmography to measure limb blood flow. Hyperemia measured by fMRI and plethysmography demonstrated good agreement. Postcontraction hyperemia measured by fMRI scaled with contraction intensity up to ∼60% maximal voluntary contraction. fMRI provides a noninvasive means of quantifying perfusion-related changes during and following skeletal muscle contractions in humans. Temporal changes in perfusion can be observed, as can the heterogeneity of perfusion across the muscle bed.


2002 ◽  
Vol 93 (2) ◽  
pp. 555-560 ◽  
Author(s):  
Darren S. DeLorey ◽  
Simon S. Wang ◽  
J. Kevin Shoemaker

The effect of augmented sympathetic outflow on forearm vascular conductance after single handgrip contractions of graded intensity was examined to determine whether sympatholysis occurs early in exercise ( n = 7). While supine, subjects performed contractions that were 1 s in duration and 15, 30, and 60% of maximal voluntary contraction (MVC) in intensity. The contractions were repeated during control and lower body negative pressure (LBNP) (−40 mmHg) sessions. Forearm blood flow (FBF; Doppler ultrasound) and mean arterial pressure were measured continuously for 30 s before and 60 s after the single contractions. Vascular conductance (VC) was calculated. Total postcontraction blood flow increased in an exercise intensity-dependent manner. Compared with control, LBNP caused a reduction in baseline and postexercise FBF ( P < 0.05), VC ( P < 0.01), as well as total excess flow ( P < 0.01). Specifically, during LBNP, baseline FBF and VC were reduced by 29 and 34% of control, respectively ( P < 0.05). After the 15% MVC contraction, peak VC during LBNP was reduced by a magnitude similar to that during baseline (i.e., ∼30%), but it was only reduced by 15% during both the 30 and 60% MVC trials ( P < 0.01). It was concluded that the stimuli for exercise hyperemia during moderate and heavy, but not mild, handgrip exercise intensities, diminish the vasoconstrictor effects of LBNP. Furthermore, these data demonstrate that this sympatholysis occurs early in exercise.


2003 ◽  
Vol 95 (2) ◽  
pp. 829-837 ◽  
Author(s):  
Taija Finni ◽  
John A. Hodgson ◽  
Alex M. Lai ◽  
V. Reggie Edgerton ◽  
Shantanu Sinha

The distribution of strain along the soleus aponeurosis tendon was examined during voluntary contractions in vivo. Eight subjects performed cyclic isometric contractions (20 and 40% of maximal voluntary contraction). Displacement and strain in the apparent Achilles tendon and in the aponeurosis were calculated from cine phase-contrast magnetic resonance images acquired with a field of view of 32 cm. The apparent Achilles tendon lengthened 2.8 and 4.7% in 20 and 40% maximal voluntary contraction, respectively. The midregion of the aponeurosis, below the gastrocnemius insertion, lengthened 1.2 and 2.2%, but the distal aponeurosis shortened 2.1 and 2.5%, respectively. There was considerable variation in the three-dimensional anatomy of the aponeurosis and muscle-tendon junction. We suggest that the nonuniformity in aponeurosis strain within an individual was due to the presence of active and passive motor units along the length of the muscle, causing variable force along the measurement site. Force transmission along intrasoleus connective tissue may also be a significant source of nonuniform strain in the aponeurosis.


2021 ◽  
Author(s):  
Felix Nolte

In this thesis, elastography is evaluated in combination with optical coherence tomography (OCT). Two approaches to OCT based elastography, Digital image correlation (DIC) and Doppler optical coherence elastography (DOCE), are evaluated for an intravascular setup using in vivo images from a porcine carotid model. DIC tracks the displacement of speckle patterns in consecutive frames, allowing the calculation of axial and lateral strain. Rapid speckle decorrelation was observed in preprocessed structural images, affecting the tracking and limiting the feasibility of this algorithm. DOCE measures axial strain based on relative tissue velocities. Rotational movement of the imaging optical fibre was the biggest source of artefacts in this imaging mode, but could be removed with a newly developed algorithm, based on the phase change induced in a surrounding catheter. The standard deviation of phase after artefact removal, measured in a stationary phantom experiment, was ~0.2 rad, corresponding to a minimum detectable velocity of 792 μm/s at a Doppler angle of 20°. The sensitivity allowed the detection of arterial blood flow velocity and pattern and the detection of adjacent veins, but did not allow direct elastography.


2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Liang Du ◽  
Jingwan Zhang ◽  
Alexander Clowes ◽  
David Dichek

Background Autogenous vein grafts are effective therapies for obstructive arterial disease. However, their long-term utility is limited by stenosis and occlusion. Genetic engineering of veins that prevents intimal hyperplasia and atherosclerosis could significantly improve the clinical utility of vein grafts. We recently reported that a helper-dependent adenoviral vector (HDAd) reduces atherosclerosis 4 wks after gene transfer in fat-fed rabbits and can express a therapeutic transgene (apo AI) in normal rabbit carotids for at least 48 wks. Use of HDAd for vein graft gene therapy will depend on achievement of similarly high and persistent transgene expression in grafted veins. Hypothesis We tested the hypothesis that Ad-mediated transgene expression in grafted veins (at an early time point) can be increased by varying the timing of gene transfer. Methods Rabbit external jugular veins were transduced by exposure to a beta galactosidase (b-gal)-expressing Ad: in situ either without (a) or with (b) immediate arterial grafting; c) ex vivo with grafting after overnight incubation with Ad; d) in vivo immediately after grafting and e) in vivo 4 wks after grafting (n = 6 - 19 veins/group). Transgene expression was measured in veins removed 3 d after Ad exposure by PCR quantitation of b-gal mRNA and by en-face planimetry of blue-stained area. Results B-gal transgene expression was higher in ungrafted veins than in veins grafted immediately after gene transfer (84 ± 17 vs 9.4 ± 2.0 arbitrary units (AU); P < 0.0001). Overnight incubation of veins with Ad increased gene expression ex vivo by 10-fold but neither this nor performing vector infusion immediately after grafting improved gene expression (11 ± 4.7 and 9.1 ± 1.8 AU; P > 0.9 for both vs immediately grafted veins). Delaying gene transfer until 4 wks after grafting significantly increased gene expression, to a level equivalent to transgene expression in ungrafted veins (61 ± 11 AU; P = 0.3 vs ungrafted veins). En face planimetry yielded similar results. Conclusions Exposure of a transduced vein to arterial blood flow is associated with significant loss of transgene expression. Transgene expression in grafted veins is significantly higher when gene transfer is performed 4 wks after exposure of the vein to arterial blood flow.


1983 ◽  
Vol 54 (2) ◽  
pp. 434-437 ◽  
Author(s):  
D. R. Seals ◽  
R. A. Washburn ◽  
P. G. Hanson ◽  
P. L. Painter ◽  
F. J. Nagle

The purpose of this study was to investigate the influence of the size of the active muscle mass on the cardiovascular response to static contraction. Twelve male subjects performed one-arm handgrip (HG), two-leg extension (LE), and a “dead-lift” maneuver (DL) in a randomly assigned order for 3 min at 30% of maximal voluntary contraction. O2 uptake (VO2), heart rate (HR), and mean intra-arterial blood pressure (MABP) were measured at rest and, in addition to absolute tension exerted, throughout contraction. There was a direct relationship between the size of the active muscle mass and the magnitude of the increases in VO2, HR, and MABP, even though all contractions were performed at the same relative intensity. Tension, VO2, HR, and MABP increased progressively from HG to LE to DL. It was concluded that at the same percentage of maximal voluntary contraction, the magnitude of the cardiovascular response to isometric exercise is directly influenced by the size of the contracting muscle mass.


2006 ◽  
Vol 100 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Shigehiko Ogoh ◽  
R. Matthew Brothers ◽  
Quinton Barnes ◽  
Wendy L. Eubank ◽  
Megan N. Hawkins ◽  
...  

The purpose of this study was to examine the hypothesis that the operating point of the cardiopulmonary baroreflex resets to the higher cardiac filling pressure of exercise associated with the increased cardiac filling volumes. Eight men (age 26 ± 1 yr; height 180 ± 3 cm; weight 86 ± 6 kg; means ± SE) participated in the present study. Lower body negative pressure (LBNP) was applied at 8 and 16 Torr to decrease central venous pressure (CVP) at rest and during steady-state leg cycling at 50% peak oxygen uptake (104 ± 20 W). Subsequently, two discrete infusions of 25% human serum albumin solution were administered until CVP was increased by 1.8 ± 0.6 and 2.4 ± 0.4 mmHg at rest and 2.9 ± 0.9 and 4.6 ± 0.9 mmHg during exercise. During all protocols, heart rate, arterial blood pressure, and CVP were recorded continuously. At each stage of LBNP or albumin infusion, forearm blood flow and cardiac output were measured. During exercise, forearm vascular conductance increased from 7.5 ± 0.5 to 8.7 ± 0.6 U ( P = 0.024) and total systemic vascular conductance from 7.2 ± 0.2 to 13.5 ± 0.9 l·min−1·mmHg−1 ( P < 0.001). However, there was no significant difference in the responses of both forearm vascular conductance and total systemic vascular conductance to LBNP and the infusion of albumin between rest and exercise. These data indicate that the cardiopulmonary baroreflex had been reset during exercise to the new operating point associated with the exercise-induced change in cardiac filling volume.


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