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      Differences in Left Ventricular Global Function and Mechanics in Paralympic Athletes with Cervical and Thoracic Spinal Cord Injuries

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          Abstract

          Following a spinal cord injury, there are changes in resting stroke volume (SV) and its response to exercise. The purpose of the following study was to characterize resting left ventricular structure, function, and mechanics in Paralympic athletes with tetraplegia (TETRA) and paraplegia (PARA) in an attempt to understand whether the alterations in SV are attributable to inherent dysfunction in the left ventricle. This retrospective study compared Paralympic athletes with a traumatic, chronic (>1 year post-injury), motor-complete spinal cord injury (American Spinal Injury Association Impairment Scale A-B). Eight male TETRA wheelchair rugby players (34 ± 5 years, C5-C7) and eight male PARA alpine skiers (35 ± 5 years, T4-L3) were included in the study. Echocardiography was performed in the left lateral decubitus position and indices of left ventricular structure, global diastolic and systolic function, and mechanics were derived from the average across three cardiac cycles. Blood pressure was measured in the supine and seated positions. All results are presented as TETRA vs. PARA. There was no difference in left ventricular dimensions between TETRA and PARA. Additionally, indices of global diastolic function were similar between groups including isovolumetric relaxation time, early (E) and late (A) transmitral filling velocities and their ratio (E/A). While ejection fraction was similar between TETRA and PARA (59 ± 4 % vs. 61 ± 7 %, p = 0.394), there was evidence of reduced global systolic function in TETRA including lower SV (62 ± 9 ml vs. 71 ± 6 ml, p = 0.016) and cardiac output (3.5 ± 0.6 L/min vs. 5.0 ± 0.9 L/min, p = 0.002). Despite this observation, several indices of systolic and diastolic mechanics were maintained in TETRA but attenuted in PARA including circumferential strain at the level of the papillary muscle (−23 ± 4% vs. −15 ± 6%, p = 0.010) and apex (−36 ± 10% vs. −23 ± 5%, p = 0.010) and their corresponding diastolic strain rates (papillary: 1.90 ± 0.63 s −1 vs. 1.20 ± 0.51 s −1, p = 0.028; apex: 3.03 ± 0.71 s −1 vs. 1.99 ± 0.69 s −1, p = 0.009). All blood pressures were lower in TETRA. The absence of an association between reduced global systolic function and mechanical dysfunction in either TETRA or PARA suggests any reductions in SV are likely attributed to impaired loading rather than inherent left ventricular dysfunction.

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          Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings.

          To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)
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            Left ventricular strain and strain rate: characterization of the effect of load in human subjects.

            Left ventricular (LV) strain and strain rate have been proposed as novel indices of systolic function; however, there are limited data about the effect of acute changes on these parameters. Simultaneous Millar micromanometer LV pressure and echocardiographic assessment were performed on 18 patients. Loading was altered sequentially by the administration of glyceryl trinitrate (GTN) and saline fluid loading. Echocardiographic speckle tracking imaging was used to quantify the peak systolic strain (S) and peak systolic strain rate (SR S) and dp/dt max was recorded from the micromanometer data. GTN administration decreased preload (LV end diastolic pressure [LVEDP]: 15.7 vs. 8.4 mmHg, P < 0.001) and afterload (end systolic wall stress: 74 vs. 43 x 10(3)dyn/cm(2), P < 0.001). Administration of fluid increased preload (LVEDP: 11.3 vs. 18.1 mmHg, P < 0.001) and increased wall stress (53 vs. 62 x 10(3)dyn/cm(2), P < 0.003). Administration of GTN resulted in increased circumferential SR S (-1.2 vs. -1.7s(-1), P < 0.01) and longitudinal SR S (-0.9 vs. -1.0 s(-1), P < 0.001). The administration of fluid resulted in decreased circumferential SR S (-1.5 vs. -1.3s(-1), P < 0.01) and longitudinal SR S (-1.0 vs. -0.9s(-1), P < 0.01). As preload and afterload increased, decrease in circumferential SR S (r = 0.63, P < 0.001; r = 0.56, P<0.001) and longitudinal SR S were observed (r = 0.42, P < 0.003; r = 0.49 P < 0.001). Circumferential and longitudinal peak strain and systolic strain rate are sensitive to acute changes in load, an important factor that needs to be considered in their application as indices of systolic function.
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              A prospective randomised longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise training in humans.

              The principle that 'concentric' cardiac hypertrophy occurs in response to strength training, whilst 'eccentric' hypertrophy results from endurance exercise has been a fundamental tenet of exercise science. This notion is largely based on cross-sectional comparisons of athletes using echocardiography. In this study, young (27.4 ± 1.1 years) untrained subjects were randomly assigned to supervised, intensive, endurance (END, n = 10) or resistance (RES, n = 13) exercise and cardiac MRI scans and myocardial speckle tracking echocardiography were performed at baseline, after 6 months of training and after a subsequent 6 weeks of detraining. Aerobic fitness increased significantly in END (3.5 to 3.8 l min(-1), P < 0.05) but was unchanged in RES. Muscular strength significantly improved compared to baseline in both RES and END ( = 53.0 ± 1.1 versus 36.4 ± 4.5 kg, both P < 0.001) as did lean body mass (2.3 ± 0.4 kg, P < 0.001 versus 1.4 ± 0.6 kg P < 0.05). MRI derived left ventricular (LV) mass increased significantly following END (112.5 ± 7.3 to 121.8 ± 6.6 g, P < 0.01) but not RES, whilst training increased end-diastolic volume (LVEDV, END: +9.0 ± 5.0 versus RES +3.1 ± 3.6 ml, P = 0.05). Interventricular wall thickness significantly increased with training in END (1.06 ± 0.0 to 1.14 ± 0.06, P < 0.05) but not RES. Longitudinal strain and strain rates did not change following exercise training. Detraining reduced aerobic fitness, LV mass and wall thickness in END (P < 0.05), whereas LVEDV remained elevated. This study is the first to use MRI to compare LV adaptation in response to intensive supervised endurance and resistance training. Our findings provide some support for the 'Morganroth hypothesis', as it pertains to LV remodelling in response to endurance training, but cast some doubt over the proposal that remodelling occurs in response to resistance training.
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                29 March 2016
                2016
                : 7
                : 110
                Affiliations
                [1] 1Autonomic Research Laboratory, International Collaboration on Repair Discoveries, Faculty of Medicine, University of British Columbia Vancouver, BC, Canada
                [2] 2Translational Integrative Physiology Laboratory, Faculty of Education, School of Kinesiology, University of British Columbia Vancouver, BC, Canada
                [3] 3Division of Physical Medicine and Rehabilitation, Faculty of Medicine, University of British Columbia Vancouver, BC, Canada
                [4] 4GF Strong Rehabilitation Centre, Vancouver Coastal Health Vancouver, BC, Canada
                Author notes

                Edited by: Gregoire P. Millet, University of Lausanne, Switzerland

                Reviewed by: Pierre-Marie Leprêtre, Université de Picardie Jules Verne, France; Stefanos Volianitis, Aalborg University, Denmark

                *Correspondence: Andrei V. Krassioukov krassioukov@ 123456icord.org

                This article was submitted to Exercise Physiology, a section of the journal Frontiers in Physiology

                Article
                10.3389/fphys.2016.00110
                4809896
                27065879
                6990812f-1657-498e-81cc-a0ffbf674eaf
                Copyright © 2016 Currie, West and Krassioukov.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 11 September 2015
                : 07 March 2016
                Page count
                Figures: 2, Tables: 3, Equations: 0, References: 52, Pages: 8, Words: 6692
                Funding
                Funded by: International Collaboration on Repair Discoveries
                Funded by: Coloplast 10.13039/501100002907
                Funded by: Wellspect HealthCare
                Funded by: Shkreli Foundation
                Funded by: Craig H. Neilsen Foundation 10.13039/100005191
                Award ID: 281863
                Categories
                Physiology
                Original Research

                Anatomy & Physiology
                athletes,echocardiography,paraplegia,strain,stroke volume,tetraplegia
                Anatomy & Physiology
                athletes, echocardiography, paraplegia, strain, stroke volume, tetraplegia

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