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Pathophysiology of Exercise Intolerance in Chronic Diseases: the Role of Diminished Cardiac Performance in Mitochondrial and Heart Failure Patients

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Pathophysiology of Exercise Intolerance in Chronic Diseases: the Role of Diminished Cardiac Performance in Mitochondrial and Heart Failure Patients Open Access Heart failure and cardiomyopathies Open Heart: first published as 10.1136/openhrt-2017-000632 on 28 July 2017. Downloaded from Pathophysiology of exercise intolerance in chronic diseases: the role of diminished cardiac performance in mitochondrial and heart failure patients Jodi McCoy,1 Matthew Bates,1,2 Christopher Eggett,1 Mario Siervo,1 Sophie Cassidy,1 Jane Newman,1 Sarah A Moore,3 Grainne Gorman,3,4 Michael I Trenell,1,5 Lazar Velicki,6 Petar M Seferovic,7 John G F Cleland,8 Guy A MacGowan,9 Doug M Turnbull,3,4 Djordje G Jakovljevic1,10 To cite: McCoy J, Bates M, ABSTRACT KEY QUESTIONS Eggett C, et al. Pathophysiology Objective Exercise intolerance is a clinical hallmark of exercise intolerance in of chronic conditions. The present study determined chronic diseases: the role of What is already known about this subject? pathophysiological mechanisms of exercise intolerance in diminished cardiac performance Exercise intolerance is a clinical hallmark of cardiovascular, neuromuscular, and metabolic disorders. ► in mitochondrial and heart chronic conditions and strong predictor of Methods In a prospective cross-sectional observational failure patients. Open Heart morbidity and mortality. 2017;4:e000632. doi:10.1136/ study 152 patients (heart failure reduced ejection openhrt-2017-000632 fraction, n=32; stroke, n=34; mitochondrial disease, What does this study add? n=28; type two diabetes, n=28; and healthy controls, ► The study highlights that pathophysiological n=30) performed cardiopulmonary exercise testing with mechanisms of exercise intolerance differ among Received 22 March 2017 metabolic and haemodynamic measurements. Peak patients groups. Revised 22 May 2017 exercise O consumption and cardiac power output were Accepted 20 June 2017 2 measures of exercise tolerance and cardiac performance. How might this impact on clinical practice? Results Exercise tolerance was significantly diminished in ► Clinical care teams may improve management patients compared with controls (ie, by 45% stroke, 39% of patients, their stress tolerance and quality mitochondria disease, and 33% diabetes and heart failure, of life by prescribing appropriate interventions http://openheart.bmj.com/ p<0.05). Cardiac performance was only significantly specifically targeting the underlying cause of reduced in heart failure (due to reduced heart rate, stroke exercise intolerance that is, heart function and / or volume, and blood pressure) and mitochondrial patients ability of skeletal muscles to extract oxygen. (due reduced stroke volume) compared with controls (ie, by 53% and 26%, p<0.05). Ability of skeletal muscles to extract oxygen (ie, arterial-venous O difference) was 2 higher rates of mortality, and increased inci- diminished in mitochondrial, stroke, and diabetes patients dence of heart failure and coronary artery (by 24%, 22%, and 18%, p<0.05), but increased by 21% 1 2 8 disease. Similarly, patients with type two on September 30, 2021 by guest. Protected copyright. in heart failure (p<0.05) compared with controls. Cardiac diabetes, stroke, heart failure, pulmonary, output explained 65% and 51% of the variance in peak O2 consumption (p<0.01) in heart failure and mitochondrial and neuromuscular disorders presented with lower level of exercise tolerance show patients, whereas arterial-venous O2 difference explained increased rate of disease progression and 69% (p<0.01) of variance in peak O2 consumption in diabetes, and 65% and 48% in stroke and mitochondrial mortality.3–7 It is therefore not surprising that patients (p<0.01). exercise intolerance has been an important Conclusions Different mechanisms explain exercise therapeutic target in chronic conditions intolerance in patients with heart failure, mitochondrial using both pharmacological and physiolog- dysfunction, stroke and diabetes. Their better ical interventions.9–13 understanding may improve management of patients, their Exercise intolerance is a complex clinical stress tolerance and quality of life. syndrome represented with reduced oxygen For numbered affiliations see (O ) consumption during physiological stim- end of article. 2 INTRODUCTION ulation.14 Aetiology of exercise intolerance Correspondence to Exercise intolerance is a clinical hallmark of can be explained by diminished capacity of Dr Djordje G Jakovljevic, chronic diseases associated with increased the cardiovascular system to supply oxygen Institute of Cellular Medicine, morbidity and mortality, and reduced quality (heart function and cardiac output), and The Medical School, Newcastle 1–7 University, NE2 4HH. UK; d. of life for patients. Healthy individuals with inability of the skeletal muscles to utilise jakovljevic@ ncl. ac. uk diminished exercise tolerance demonstrate delivered oxygen (mitochondrial function), McCoy J, et al. Open Heart 2017;4:e000632. doi:10.1136/openhrt-2017-000632 1 Open Heart Open Heart: first published as 10.1136/openhrt-2017-000632 on 28 July 2017. Downloaded from or both.14 In healthy individuals exercise capacity seems pressure, ECG, and exercise stress testing. Participants to be limited by the ability of the cardiovascular system were excluded from the study if they had an absolute to deliver oxygen to the exercising muscles.15 In patients contraindication to cardiopulmonary exercise stress with chronic conditions, that is,. diabetes mellitus, cardio- testing previously suggested.30 All participants provided vascular, pulmonary, and neuromuscular disorders, the informed written consent according to the Declaration pathophysiology of exercise intolerance is not well under- of Helsinki. stood with evidence supporting mechanisms associated with peripheral and/or central (cardiac) limitations to Procedures exercise.16–22 Although aetiology of exercise intolerance All participants underwent graded cardiopulmonary in heart failure has been studied more extensively than exercise testing using an electromagnetically controlled any other chronic condition, the evidence so far has been semi-recumbent bicycle ergometer (Corival; Lode, equivocal.23–29 Groningen, The Netherlands) with non-invasive gas-ex- Better understanding of mechanisms of exercise intol- change (Metalyzer 3B, Cortex, Leipzig, Germany) and erance is important as it may lead to improved patient cardiac output with the bioreactance method (NICOM, management and quality of life. Therefore, the present Cheetah Medical, Delaware).31 32 The signal processing study was designed to determine underlying pathophys- unit of the NICOM determines the relative phase shift iological mechanisms of exercise intolerance in patients (Δα) between input signals relative to the output signal. with different chronic conditions. We tested the hypoth- The Δα is in response to any changes in blood flow that esis that diminished cardiac performance is the major pass through the aorta. Cardiac output is then derived cause of exercise intolerance in cardiovascular, neuro- by Cardiac output=(C×VET×Δα dtmax)×HR, where C is muscular, and metabolic disorders. the constant of proportionality and VET is ventricular ejection fraction time.31 32 The value of C has been previ- ously validated to account for patient age, gender, height METHODS and weight. Stroke volume can then be calculated from Study design cardiac output and heart rate. Prospective, single-centre, cross-sectional, observational Online expired gas was measured to determine peak O2 study evaluated mechanisms of exercise intolerance in consumption, along with electrocardiography (standard patients with cardiovascular, neuromuscular, and meta- 12-lead configuration appropriate for exercise testing), bolic disorders. Data were collected between September and non-invasive blood pressure monitoring (brachial 2012 and January 2016, and analysed between February artery cuff sphygmomanometery). Cardiovascular and and June 2016. The study was approved by the Research metabolic measurements were monitored and analysed Ethics Committee North East of England - Tyne and Wear during the 5 min rest period and throughout exercise http://openheart.bmj.com/ South. protocol. All participants performed exercise protocol until they reached volitional exhaustion, or were unable Participants to continue cycling at the required cadence of between One hundred and fifty two patients were recruited to 60–70 revolutions per minute. Peak exercise was defined participate in this study. Study participants included: 1) as the absence of any rise in oxygen consumption when 32 patients with stable chronic heart failure with reduced exercise intensity was increased, inability of the patient to left ventricular ejection fraction (LVEF, 32%±9%; New continue to pedal at the required cadence, or achieved York Heart Association functional class II and III), 2) 34 respiratory exchange ratio >1.1. Peak O2 consumption on September 30, 2021 by guest. Protected copyright. patients with a history of ischaemic stroke >6 months prior was defined as the average oxygen uptake in the last 30 s to the study (National Institutes of Health Stroke Scale of exercise. Cardiac power output (watts), as the measure average score of 3, ranging from 0 to 8) with no concom- of overall cardiac function and performance,33 was calcu- itant history of heart failure. All stroke patients were lated using the following equation: CPO = (QT x MAP) x –3 able to mobilise independently with/without a stick for 2.22×10 , where QT is cardiac output, MAP is the mean 6 min; 3) 28 patients with mitochondrial disease related arterial pressure, and 2.22×10–3 is the conversion
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