Exercise and arterial adaptation in humans: uncoupling localized and systemic effects

Previous studies have established effects of exercise training on arterial wall thickness, remodeling, and function in humans, but the extent to which these changes are locally or systemically mediated is unclear. We examined the brachial arteries of the dominant (D) and nondominant (ND) upper limbs of elite racquet sportsmen and compared them to those of matched healthy inactive controls. Carotid and superficial femoral artery responses were also assessed in both groups. High-resolution duplex ultrasound was used to examine resting diameter, wall thickness, peak diameter, and blood flow. We found larger resting arterial diameter in the preferred arm of the athletes (4.9 ± 0.5 mm) relative to their nonpreferred arm (4.3 ± 0.4 mm, P < 0.05) and both arms of control subjects (D: 4.1 ± 0.4 mm; ND: 4.0 ± 0.4, P < 0.05). Similar limb-specific differences were also evident in brachial artery dilator capacity (5.5 ± 0.5 vs. 4.8 ± 0.4, 4.8 ± 0.6, and 4.8 ± 0.6 mm, respectively; P < 0.05) following glyceryl trinitrate administration and peak blood flow (1,118 ± 326 vs. 732 ± 320, 737 ± 219, and 698 ± 174 ml/min, respectively; P < 0.05) following ischemic handgrip exercise. In contrast, athletes demonstrated consistently lower wall thickness in carotid (509 ± 55 μm), brachial (D: 239 ± 100 μm; ND: 234 ± 133 μm), and femoral (D: 479 ± 38 μm; ND: 479 ± 42 μm) arteries compared with control subjects (carotid: 618 ± 74 μm; brachial D: 516 ± 100 μm; ND: 539 ± 129 μm; femoral D: 634 ± 155 μm; ND: 589 ± 112 μm; all P < 0.05 vs. athletes), with no differences between the limbs of either group. These data suggest that localized effects of exercise are evident in the remodeling of arterial size, whereas arterial wall thickness appears to be affected by systemic factors.

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Gender Differences on the Effect of Non-HDL-C on Blood Pressure, Blood Flow Velocities and Arterial Wall Thickness; An Observational Analysis in Madurai Population

Annals of International medical and Dental Research ◽

10.21276/aimdr.2018.4.1.ph1 ◽

2017 ◽

Vol 4 (1) ◽

Author(s):

John Rajpathy ◽

M. Mariappan ◽

J. Vijay Anto

Keyword(s):

Blood Pressure ◽

Gender Differences ◽

Blood Flow ◽

Wall Thickness ◽

Arterial Wall ◽

Observational Analysis ◽

Arterial Wall Thickness ◽

Blood Flow Velocities ◽

Flow Velocities

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Vascular Fluid Mechanics, the Arterial Wall, and Atherosclerosis

Journal of Biomechanical Engineering ◽

10.1115/1.2891384 ◽

1992 ◽

Vol 114 (3) ◽

pp. 274-282 ◽

Cited By ~ 321

Author(s):

R. M. Nerem

Keyword(s):

Cell Culture ◽

Blood Flow ◽

Fluid Mechanics ◽

Arterial Wall ◽

Disease Process ◽

The United States ◽

Structure And Function ◽

Medium Size ◽

Important Relationship ◽

And Function

Atherosclerosis, a disease of large- and medium-size arteries, is the chief cause of death in the United States and in most of the western world. Severe atherosclerosis interferes with blood flow; however, even in the early stages of the disease, i.e. during atherogenesis, there is believed to be an important relationship between the disease processes and the characteristics of the blood flow in the arteries. Atherogenesis involves complex cascades of interactions among many factors. Included in this are fluid mechanical factors which are believed to be a cause of the highly focal nature of the disease. From in vivo studies, there is evidence of hemodynamic influences on the endothelium, on intimal thickening, and on monocyte recruitment. In addition, cell culture studies have demonstrated the important effect of a cell’s mechanical environment on structure and function. Most of this evidence is for the endothelial cell, which is believed to be a key mediator of any hemodynamic effect, and it is now well documented that cultured endothelial monolayers, in response to a fluid flow-imposed laminar shear stress, undergo a variety of changes in structure and function. In spite of the progress in recent years, there are many areas in which further work will provide important new information. One of these is in the engineering of the cell culture environment so as to make it more physiologic. Animal studies also are essential in our efforts to understand atherogenesis, and it is clear that we need better information on the pattern of the disease and its temporal development in humans and animal models, as well as the specific underlying biologic events. Complementary to this will be in vitro model studies of arterial fluid mechanics. In addition, one can foresee an increasing role for computer modelling in our efforts to understand the pathophysiology of the atherogenic process. This includes not only computational fluid mechanics, but also modelling the pathobiologic processes taking place within the arterial wall. A key to the atherogenic process may reside in understanding how hemodynamics influences not only intimal smooth muscle cell proliferation, but also the recruitment of the monocyte/macrophage and the formation of foam cells. Finally, it will be necessary to begin to integrate our knowledge of cellular phenomena into a description of the biologic processes within the arterial wall and then to integrate this into a picture of the disease process itself.

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Linked opening angle and histological and mechanical aspects of the proximal pulmonary arteries of healthy and pulmonary hypertensive rats and calves

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00025.2011 ◽

2011 ◽

Vol 301 (5) ◽

pp. H1810-H1818 ◽

Cited By ~ 11

Author(s):

Lian Tian ◽

Steven R. Lammers ◽

Philip H. Kao ◽

Mark Reusser ◽

Kurt R. Stenmark ◽

...

Keyword(s):

Mechanical Behavior ◽

Wall Thickness ◽

Arterial Wall ◽

Chronic Hypoxia ◽

Pulmonary Arteries ◽

Opening Angle ◽

Histological Structure ◽

Arterial Remodeling ◽

Stiffness Ratio ◽

Arterial Wall Thickness

Understanding how arterial remodeling changes the mechanical behavior of pulmonary arteries (PAs) is important to the evaluation of pulmonary vascular function. Early and current efforts have focused on the arteries' histological changes, their mechanical properties under in vitro mechanical testing, and their zero-stress and no-load states. However, the linkage between the histology and mechanical behavior is still not well understood. To explore this linkage, we investigated the geometry, residual stretch, and histology of proximal PAs in both adult rat and neonatal calf hypoxic models of pulmonary hypertension (PH), compared their changes due to chronic hypoxia across species, and proposed a two-layer mechanical model of artery to relate the opening angle to the stiffness ratio of the PA outer to inner layer. We found that the proximal PA remodeling in calves was quite different from that in rats. In rats, the arterial wall thickness, inner diameter, and outer layer thickness fraction all increased dramatically in PH and the opening angle decreased significantly, whereas in calves, only the arterial wall thickness increased in PH. The proposed model predicted that the stiffness ratio of the calf proximal PAs changed very little from control to hypertensive group, while the decrease of opening angle in rat proximal PAs in response to chronic hypoxia was approximately linear to the increase of the stiffness ratio. We conclude that the arterial remodeling in rat and calf proximal PAs is different and the change of opening angle can be linked to the change of the arterial histological structure and mechanics.

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