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      Whole‐body heat stress and exercise stimulate the appearance of platelet microvesicles in plasma with limited influence of vascular shear stress

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          Abstract

          Intense, large muscle mass exercise increases circulating microvesicles, but our understanding of microvesicle dynamics and mechanisms inducing their release remains limited. However, increased vascular shear stress is generally thought to be involved. Here, we manipulated exercise‐independent and exercise‐dependent shear stress using systemic heat stress with localized single‐leg cooling (low shear) followed by single‐leg knee extensor exercise with the cooled or heated leg (Study 1, n = 8) and whole‐body passive heat stress followed by cycling (Study 2, n = 8). We quantified femoral artery shear rates ( SRs) and arterial and venous platelet microvesicles ( PMVCD41 +) and endothelial microvesicles ( EMVCD62E +). In Study 1, mild passive heat stress while one leg remained cooled did not affect [microvesicle] ( P ≥ 0.05). Single‐leg knee extensor exercise increased active leg SRs by ~12‐fold and increased arterial and venous [ PMVs] by two‐ to threefold, even in the nonexercising contralateral leg ( P < 0.05). In Study 2, moderate whole‐body passive heat stress increased arterial [ PMV] compared with baseline (mean± SE, from 19.9 ± 1.5 to 35.5 ± 5.4 PMV . μL −1.10 3, P < 0.05), and cycling with heat stress increased [ PMV] further in the venous circulation (from 27.5 ± 2.2 at baseline to 57.5 ± 7.2 PMV . μL −1.10 3 during cycling with heat stress, P < 0.05), with a tendency for increased appearance of PMV across exercising limbs. Taken together, these findings demonstrate that whole‐body heat stress may increase arterial [ PMV], and intense exercise engaging either large or small muscle mass promote PMV formation locally and systemically, with no influence upon [ EMV]. Local shear stress, however, does not appear to be the major stimulus modulating PMV formation in healthy humans.

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          Most cited references50

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          Endothelial cells release phenotypically and quantitatively distinct microparticles in activation and apoptosis.

          Endothelial cells (EC) shed endothelial microparticles (EMP) in activation and apoptosis. We compared the antigenic expression of EMP species released during activation as compared to apoptosis, in three cell lines. EC from renal and brain microvascular (MiVEC) and coronary macrovascular (MaVEC) origin were incubated with TNF-alpha to induce activation, or deprived of growth factors to induce apoptosis. Antigens expressed on EMP and EC were assayed flow cytometrically and included constitutive markers (CD31, CD51/61, CD105), inducible markers (CD54, CD62E and CD106), and annexin V binding. It was found that in apoptosis, constitutive markers in EMP were markedly increased (CD31>CD105), with a concomitant decrease in expression in EC. Annexin V EC surface binding and annexin V+ EMP were more sharply increased in apoptosis than in activation. In contrast, in activation, inducible markers in EMP were markedly increased in both EMP and EC (CD62E>CD54>CD106). Coronary MaVEC released significantly less EMP than MiVEC. EC release qualitatively and quantitatively distinct EMP during activation compared to apoptosis. Analysis of EMP phenotypic signatures may provide clinically useful information on the status of the endothelium.
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            High shear stress can initiate both platelet aggregation and shedding of procoagulant containing microparticles.

            Previous studies have demonstrated that a high level of shear stress can produce platelet aggregation without the addition of any agonist. We investigated whether high shear stress could cause both platelet aggregation and shedding of microparticles from the platelet plasma membrane. A coneplate viscometer was used to apply shear stress and microparticle formation was measured by flow cytometry. It was found that microparticle formation increased as the duration of shear stress increased. Both microparticles and the remnant platelets showed the exposure of procoagulant activity on their surfaces. Investigation of the mechanisms involved in shear-dependent microparticle generation showed that binding of von Willebrand factor (vWF) to platelet glycoprotein lb, influx of extracellular calcium, and activation of platelet calpain were required to generate microparticles under high shear stress conditions. Activation of protein kinase C (PKC) promoted shear-dependent microparticle formation. Epinephrine did not influence microparticle formation, although it enhanced platelet aggregation by high shear stress. These findings suggest the possibility that local generation of microparticles in atherosclerotic arteries, the site that pathologically high shear stress could occur, may contribute to arterial thrombosis by providing and expanding a catalytic surface for the coagulation cascade.
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              Maximal perfusion of skeletal muscle in man.

              Five subjects exercised with the knee extensor of one limb at work loads ranging from 10 to 60 W. Measurements of pulmonary oxygen uptake, heart rate, leg blood flow, blood pressure and femoral arterial-venous differences for oxygen and lactate were made between 5 and 10 min of the exercise. Flow in the femoral vein was measured using constant infusion of saline near 0 degrees C. Since a cuff was inflated just below the knee during the measurements and because the hamstrings were inactive, the measured flow represented primarily the perfusion of the knee extensors. Blood flow increased linearly with work load right up to an average value of 5.7 l min-1. Mean arterial pressure was unchanged up to a work load of 30 W, but increased thereafter from 100 to 130 mmHg. The femoral arterial-venous oxygen difference at maximum work averaged 14.6% (v/v), resulting in an oxygen uptake of 0.80 l min-1. With a mean estimated weight of the knee extensors of 2.30 kg the perfusion of maximally exercising skeletal muscle of man is thus in the order of 2.5 l kg-1 min-1, and the oxygen uptake 0.35 l kg-1 min-1. Limitations in the methods used previously to determine flow and/or the characteristics of the exercise model used may explain why earlier studies in man have failed to demonstrate the high perfusion of muscle reported here. It is concluded that muscle blood flow is closely related to the oxygen demand of the exercising muscles. The hyperaemia at low work intensities is due to vasodilatation, and an elevated mean arterial blood pressure only contributes to the linear increase in flow at high work rates. The magnitude of perfusion observed during intense exercise indicates that the vascular bed of skeletal muscle is not a limiting factor for oxygen transport.
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                Author and article information

                Contributors
                mrakobowchuk@tru.ca
                Journal
                Physiol Rep
                Physiol Rep
                10.1002/(ISSN)2051-817X
                PHY2
                physreports
                Physiological Reports
                John Wiley and Sons Inc. (Hoboken )
                2051-817X
                09 November 2017
                November 2017
                : 5
                : 21 ( doiID: 10.1002/phy2.2017.5.issue-21 )
                : e13496
                Affiliations
                [ 1 ] Centre for Human Performance, Exercise, and Rehabilitation College of Health and Life Sciences Brunel University London Uxbridge United Kingdom
                [ 2 ] Division of Sport, Health and Exercise Sciences Department of Life Sciences Brunel University London Uxbridge United Kingdom
                [ 3 ] Faculty of Science Department of Biological Sciences Thompson Rivers University Kamloops British Columbia Canada
                [ 4 ]Present address: Departamento de Desportos Universidade Federal de Pelotas Pelotas Brazil
                [ 5 ]Present address: Institute of Cardiovascular Science UCL London United Kingdom
                [ 6 ]Present address: Department of Life Sciences University of Roehampton London United Kingdom
                Author notes
                [*] [* ] Correspondence

                Mark Rakobowchuk, Faculty of Science, Department of Biological Sciences, Thompson Rivers University, 900 McGill Road, Kamloops, BC, Canada, V2C 0C3.

                Tel/Fax: +1 250 371‐5544

                E‐mail: mrakobowchuk@ 123456tru.ca

                Author information
                http://orcid.org/0000-0003-2679-0744
                http://orcid.org/0000-0002-1965-3277
                Article
                PHY213496
                10.14814/phy2.13496
                5688785
                29122961
                b0f86868-46c5-4923-b885-7420d841c949
                © 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 09 October 2017
                : 13 October 2017
                Page count
                Figures: 6, Tables: 2, Pages: 14, Words: 8529
                Funding
                Funded by: Science without Borders program (CAPES Foundation, Ministry of Education of Brazil, Brasília, DF 70040‐020, Brazil)
                Funded by: Physiological Society Research Grant
                Categories
                Thermoregulation
                Endurance and Performance
                Cellular Physiology
                Circulation
                Skeletal Muscle
                Original Research
                Original Research
                Custom metadata
                2.0
                phy213496
                November 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.2.5 mode:remove_FC converted:15.11.2017

                cycling,dynamic knee extensor exercise,microparticles,passive heating,shear stress

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