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Correspondence to Erin J Howden; Erin.Howden@baker.edu.au Regular physical activity combined with structured exercise training has well described benefits for quality of life and mortality in a range of cardiovascular conditions. For individuals with underlying genetic cardiac myopathies there has been concern that exercise training could trigger a potentially fatal event. [...]there has been caution with recommending exercise training broadly, especially with respect to vigorous intensity exercise and participation in competitive sports. [...]our group has shown that vigorous exercise training including high intensity interval training beneficially impacts ventricular remodelling and can be sustained over a 2-year follow-up period when participants are provided with consistent support.6 Thus, these early positive findings require confirmation in follow-up randomised controlled trials that include longer-term follow-up.

PurposeSemi-supine and supine cardiopulmonary exercise testing (CPET) with concurrent cardiac imaging has emerged as a valuable tool for evaluating patients with cardiovascular disease. Yet, it is unclear how posture effects CPET measures. We aimed to discern the effect of posture on maximal oxygen uptake (VO2max) and its determinants using three clinically relevant cycle ergometers.MethodsIn random order, 10 healthy, active males (Age 27 ± 7 years; BMI 23 ± 2 kg m2) underwent a ramp CPET and subsequent constant workload verification test performed at 105% peak ramp power to quantify VO2max on upright, semi-supine and supine cycle ergometers. Doppler echocardiography was conducted at peak exercise to measure stroke volume (SV) which was multiplied by heart rate (HR) to calculate cardiac output (CO).ResultsCompared to upright (46.8 ± 11.2 ml/kg/min), VO2max was progressively reduced in semi-supine (43.8 ± 10.6 ml/kg/min) and supine (38.2 ± 9.3 ml/kg/min; upright vs. semi-supine vs. supine; all p ≤ 0.005). Similarly, peak power was highest in upright (325 ± 80 W), followed by semi-supine (298 ± 72 W) and supine (200 ± 51 W; upright vs. semi-supine vs. supine; all p < 0.01). Peak HR decreased progressively from upright to semi-supine to supine (186 ± 11 vs. 176 ± 13 vs. 169 ± 12 bpm; all p < 0.05). Peak SV and CO were lower in supine relative to semi-supine and upright (82 ± 22 vs. 92 ± 26 vs. 91 ± 24 ml and 14 ± 3 vs. 16 ± 4 vs. 17 ± 4 l/min; all p < 0.01), but not different between semi-supine and upright.ConclusionVO2max is progressively reduced in reclined postures. Thus, posture should be considered when comparing VO2max results between different testing modalities.

Correspondence to Dr Jessica J Orchard, Sydney School of Public Health, The University of Sydney, Sydney, New South Wales, Australia; jessica.orchard@sydney.edu.au Female athletes are unduly under-represented in sports cardiology research, resulting in an inferior knowledge base to inform clinical management.1 Accurate and timely diagnosis of pathology in female athletes using electrocardiography or cardiac imaging is currently limited by our poor understanding of the ranges of normality in the female athlete’s heart.2 This editorial seeks to identify factors contributing to inequitable sex representation in sports cardiology research and proposes strategies to promote greater female athlete engagement (box 1).Box 1 The six principles for sex parity in sports cardiology research 1. To date, a complete understanding of the impact of female sex hormonal changes and reproductive status on cardiovascular physiology, cardiac outcomes and exercise-induced cardiac remodelling in athletes remains elusive.3 The challenge of researching this complexity may dissuade researchers from designing studies specific for female athletes or result in strict female-specific inclusion criteria that limit the number of eligible participants. [...]there has been a tendency to restrict investigations to male athletes, thereby perpetuating the paucity of knowledge regarding cardiac events in females.6 7 Moreover, publication and funding biases, whereby negative studies are less likely to be published and lower disease burdens are less likely to receive funding, further diminish the impetus among researchers to pursue adequate female representation. [...]we recommend journals encourage data to be disaggregated by sex, even if only for a sub-analysis.

Background Pediatric cancer survivors are at increased risk of cardiac dysfunction and heart failure. Reduced peak oxygen consumption (peak VO 2 ) is associated with impaired cardiac reserve (defined as the increase in cardiac function from rest to peak exercise) and heart failure risk, but it is unclear whether this relationship exists in pediatric cancer survivors. This study sought to investigate the presence of reduced peak VO 2 in pediatric cancer survivors with increased risk of heart failure, and to assess its relationship with resting cardiac function and cardiac haemodynamics and systolic function during exercise. Methods Twenty pediatric cancer survivors (8–24 years; 10 male) treated with anthracycline chemotherapy ± radiation underwent cardiopulmonary exercise testing to quantify peak VO 2 , with a value < 85% of predicted defined as impaired peak VO 2 . Resting cardiac function was assessed using 2- and 3-dimensional echocardiography, with cardiac reserve quantified from resting and peak exercise heart rate, stroke volume index (SVI) and cardiac index (CI) using exercise cardiovascular magnetic resonance (CMR). Results Twelve of 20 survivors (60%) had reduced peak VO 2 (70 ± 16% vs. 97 ± 14% of age and gender predicted). There were no differences in echocardiographic or CMR measurements of resting cardiac function between survivors with normal or impaired peak VO 2 . However, those with reduced peak VO 2 had diminished cardiac reserve, with a lesser increase in CI and SVI during exercise (Interaction P  < 0.01 for both), whilst the heart rate response was similar ( P  = 0.71). Conclusions Whilst exercise intolerance is common among pediatric cancer survivors, it is poorly explained by resting measures of cardiac function. In contrast, impaired exercise capacity is associated with impaired haemodynamics and systolic functional reserve measured during exercise. Consequently, measures of cardiopulmonary fitness and cardiac reserve may aid in early identification of survivors with heightened risk of long-term heart failure.

Premature cardiovascular mortality is increased in long-term allogeneic stem cell transplant (allo-SCT) survivors, but little information exists regarding subclinical cardiovascular dysfunction in this population. We compared peak oxygen uptake ( V ˙ O 2peak ), a prognostic cardiovascular marker, and its determinants between long-term allo-SCT survivors and non-cancer controls. Fourteen allo-SCT survivors (mean ± SD, 44 ± 15 years, 50% male, median time since allo-SCT: 6.5 years [range 2–20]) and 14 age- and sex-matched controls (46 ± 13 years, 50% male) underwent cardiopulmonary exercise testing to quantify V ˙ O 2peak . Resting echocardiography (left-ventricular ejection fraction and strain), exercise cardiac MRI (peak cardiac and stroke volume index [CI peak , SVI peak ]), biochemistry (hemoglobin, troponin-I, B-natriuretic peptide), dual-energy x-ray absorptiometry (lean [LM] and fat [FM] mass, percent body fat [%BF]) and Fick - principal calculation (arteriovenous oxygen difference) were also performed. Survivors exhibited impaired V ˙ O 2peak as compared with controls (25.9 ± 5.1 vs. 33.7 ± 6.5 ml kg −1  min −1 , p  = 0.002), which coincided with reduced CI peak (6.6 ± 0.8 vs. 8.6 ± 1.9 L min −1  m −2 ; p  = 0.001) secondary to reduced SVI peak (48 ± 4 vs. 61 ± 8 ml m −2 ; p  < 0.001) rather than chronotropic impairment, and higher %BF (difference, 7.9%, p  = 0.007) due to greater FM (5.8 kg; p  = 0.069) and lower LM (4.3 kg, p  = 0.25). All other measures were similar between groups. Despite comparable resting cardiac function and biomarker profiles, survivors exhibited reduced V ˙ O 2peak and exercise cardiac function and increased %BF relative to controls. These results highlight potential therapeutic avenues and the utility of exercise-based cardiovascular assessment in unmasking cardiovascular dysfunction in allo-SCT survivors.

BackgroundGrowing evidence suggests that men exposed to androgen deprivation therapy (ADT) have an increased risk of cardiovascular disease. While exercise has shown to attenuate some adverse effects of ADT, the effects on cardiometabolic health have not been systematically evaluated.ObjectiveTo evaluate the effect of exercise on cardiometabolic health in men with prostate cancer (PCa) receiving ADT.MethodsA systematic literature search of MEDLINE, EMBASE, CINHAL, SCOPUS, WEB OF SCIENCE and SPORTSDICUS from database inception to April 2020 was performed. A quantitative synthesis using Cohens d effect size and a meta-analysis using random-effects models were conducted.ResultsOverall, fourteen randomised controlled trials (RCTs) and four non-randomised studies were included. Eleven RCTs (n = 939 patients) were included in the meta-analysis. Exercise training improved the 400-m-walk test (MD −10.11 s, 95% CI [−14.34, −5.88]; p < 0·00001), diastolic blood pressure (−2.22 mmHg, [−3.82, −0.61]; p = 0.007), fasting blood glucose (−0.38 mmol/L, [−0.65, −0.11]; p = 0.006), C-reactive protein (−1.16 mg/L, [−2.11, −0.20]; p = 0.02), whole-body lean mass (0.70 kg, [0.39, 1.01]; p < 0.0001), appendicular lean mass (0.59 kg, [0.43, 0.76]; p < 0.00001), whole-body fat mass (−0.67 kg, [−1.08, −0.27]; p = 0.001), whole-body fat percentage (−0.79%, [−1.16, −0.42]; p < 0.0001), and trunk fat mass (−0.49 kg, [−0.87, −0.12]; p = 0.01), compared to usual care. No significant effects on systolic blood pressure or blood lipid metabolism were detected.ConclusionsIn a small subset of evaluated studies, exercise may favourably improve some but not all markers of cardiometabolic health. Future exercise intervention trials with cardiometabolic outcomes as primary endpoints are needed to confirm these initial findings.

Anthracyclines such as doxorubicin are widely used chemotherapy drugs. A common side effect of anthracycline therapy is cardiotoxicity, which can compromise heart function and lead to dilated cardiomyopathy and heart failure. Dexrazoxane and heart failure medications (i.e., beta blockers and drugs targeting the renin–angiotensin system) are prescribed for the primary prevention of cancer therapy-related cardiotoxicity and for the management of cardiac dysfunction and symptoms if they arise during chemotherapy. However, there is a clear need for new therapies to combat the cardiotoxic effects of cancer drugs. Exercise is a cardioprotective stimulus that has recently been shown to improve heart function and prevent functional disability in breast cancer patients undergoing anthracycline chemotherapy. Evidence from preclinical studies supports the use of exercise training to prevent or attenuate the damaging effects of anthracyclines on the cardiovascular system. In this review, we summarise findings from experimental models which provide insight into cellular mechanisms by which exercise may protect the heart from anthracycline-mediated damage, and identify knowledge gaps that require further investigation. Improved understanding of the mechanisms by which exercise protects the heart from anthracyclines may lead to the development of novel therapies to treat cancer therapy-related cardiotoxicity.

Background Allogeneic stem cell transplantation (allo-SCT) is a potentially lifesaving treatment for high-risk hematological malignancy, but survivors experience markedly elevated rates of cardiovascular disease and associated functional impairment. Mounting evidence suggests regular exercise, combined with a reduction in sedentary time through replacement with light exercise may be a useful therapeutic strategy for the prevention of cardiovascular comorbidities. However, this type of intervention has yet to be evaluated in patients undergoing allo-SCT. The ALLO-Active study will evaluate the efficacy of a ~ 4 month multi-faceted exercise intervention, commenced upon admission for allo-SCT, to preserve peak oxygen uptake (VO 2 peak) and peak cardiac output, compared with usual care. The study will also evaluate the effect of the intervention on functional independence, quality of life, and symptoms of fatigue. Methods Sixty adults with hematological malignancy scheduled for allo-SCT will be randomly assigned to usual care ( n  = 30) or the exercise and sedentary behaviour intervention ( n  = 30). Participants assigned to the intervention will complete a thrice weekly aerobic and progressive resistance training program and concomitantly aim to reduce daily sedentary time by 30 min with short, frequent, light-intensity exercise bouts. Participants will undergo testing prior to, immediately after inpatient discharge, and 12 weeks after discharge. To address aim 1, VO 2 peak and peak cardiac output (multiple primary outcomes, p  < 0.025) will be assessed via cardiopulmonary exercise testing and exercise cardiac magnetic resonance imaging, respectively. Secondary outcomes include functional independence (defined as VO 2 peak ≥ 18.mL.kg −1 .min −1 ), quality of life, and fatigue (assessed via validated questionnaire). Exploratory outcomes will include indices of resting cardiac, vascular, and skeletal muscle structure and function, cardiovascular biomarkers, anxiety and depression, transplant outcomes (e.g., engraftment, graft-versus-host disease), and habitual physical activity, sedentary time, and sleep. Discussion Multi-faceted exercise programs are a promising approach for ameliorating the cardiovascular consequences of allo-SCT. If this intervention proves to be effective, it will contribute to the development of evidence-based exercise guidelines for patients undergoing allo-SCT and assist with optimising the balance between acute cancer management and long-term health. Trial Registration Australian New Zealand Clinical Trials Registry (ANZCTR), ID: 12619000741189 . Registered 17 May 2019.

Background Anthracycline chemotherapy (AC) is an efficacious (neo) adjuvant treatment for early-stage breast cancer (BCa), but is associated with an increased risk of cardiac dysfunction and functional disability. Observations suggest that regular exercise may be a useful therapy for the prevention of cardiovascular morbidity but it is yet to be interrogated in a large randomised trial. The primary aims of this study are to: 1) determine if 12-months of ET commenced at the onset of AC can reduce the proportion of BCa patients with functional disability (peak VO 2 , < 18 ml/kg/min), and 2) compare current standard-of-care for detecting cardiac dysfunction (resting left-ventricular ejection fraction assessed from 3-dimensional echocardiography) to measures of cardiac reserve (peak exercise cardiac output assessed from exercise cardiac magnetic resonance imaging) for predicting the development of functional disability 12-months following AC. Secondary aims are to assess the effects of ET on VO2peak, left ventricular morphology, vascular stiffness, cardiac biomarkers, body composition, bone mineral density, muscle strength, physical function, habitual physical activity, cognitive function, and multidimensional quality of life. Methods One hundred women with early-stage BCa (40–75 years) scheduled for AC will be randomized to 12-months of structured exercise training ( n  = 50) or a usual care control group ( n  = 50). Participants will be assessed at baseline, 4-weeks following completion of AC (4-months) and at 12-months for all measures. Discussion Women diagnosed with early-stage BCa have increased cardiac mortality. More sensitive strategies for diagnosing and preventing AC-induced cardiovascular impairment are critical for reducing cardiovascular morbidity and improving long-term health outcomes in BCa survivors. Trial registration Australia & New Zealand Clinical Trials Registry (ANZCTR), ID: 12617001408370 . Registered on 5th of October 2017.

Patients with haematological cancer often exhibit reduced cardiorespiratory fitness and an elevated risk of cardiovascular disease. The mechanisms underlying this impairment are multifactorial, but the contribution of skeletal muscle fat infiltration has not been evaluated. This study aimed to compare thigh skeletal muscle fat fraction (SMFF) in patients with haematological cancer to healthy controls and to assess the contribution of SMFF to cardiorespiratory fitness in this cohort. We performed a cross-sectional analysis of patients with haematological cancer (n = 70, 61% male, age: 51 ± 16 years) and age- and sex-matched healthy controls (n = 70, 61% male, age: 50 ± 15 years). Thigh SMFF was assessed via magnetic resonance imaging. We also measured cardiorespiratory fitness (peak oxygen uptake, V̇O peak), global longitudinal strain (GLS) via echocardiography and haemoglobin concentrations in the haematological cancer cohort. Hierarchical multiple regression analysis was performed to identify predictors of V̇O peak. SMFF was higher in the haematological cancer cohort versus the healthy control cohort (11.0% ± 3.4% vs. 8.8% ± 3.8%, p = 0.001). V̇O peak was significantly lower than predicted values for the haematological cancer cohort (mean difference; 9.61 ± 8.30 mL kg min , p < 0.001). The multiple regression analysis accounted for 35% of the variance in V̇O peak with both SMFF (β = -0.40, ΔR  = 0.14, p = 0.002) and haemoglobin concentrations (β = 0.50, ΔR  = 0.23, p < 0.001) being significant independent predictors of V̇O peak, while skeletal muscle volume (β = 0.00, ΔR  = 0.00, p = 0.767), GLS (β = 0.06, ΔR  = 0.00, p = 0.509), prior anthracycline treatment (β = 0.00, ΔR  = 0.00, p = 0.962) and clinical diagnosis (β = 0.00, ΔR  = 0.00, p = 0.555) were not. SMFF is increased in haematological cancer patients and contributes to reduced V̇O peak. Consequently, increased SMFF may be an important target to improve cardiovascular health and cardiorespiratory fitness in this population.