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Exercise intolerance is the primary chronic symptom in heart failure with preserved ejection fraction (HFpEF), the most common form of heart failure in older patients; however its pathophysiology is not well understood. Recent data suggest that peripheral factors such as skeletal muscle (SM) dysfunction may be important contributors. Therefore, 38 participants, 23 patients with HFpEF (69 ± 7 years) and 15 age-matched healthy controls (HCs), underwent magnetic resonance imaging and cardiopulmonary exercise testing to assess for SM, intermuscular fat (IMF), subcutaneous fat, total thigh, and thigh compartment (TC) areas and peak exercise oxygen consumption (peak VO2). There were no significant intergroup differences in total thigh area, TC, subcutaneous fat, or SM. However, in the HFpEF versus HC group, IMF area (35.6 ± 11.5 vs 22.3 ± 7.6 cm2, p = 0.01), percent IMF/TC (26 ± 5 vs 20 ± 5%, p = 0.005), and the ratio of IMF/SM (0.38 ± 0.10 vs 0.28 ± 0.09, p = 0.007) were significantly increased, whereas percent SM/TC was significantly reduced (70 ± 5 vs 75 ± 5, p = 0.009). In multivariate analyses, IMF area (partial r = −0.51, p = 0.002) and IMF/SM ratio (partial r = −0.45, p = 0.006) were independent predictors of peak VO2 whereas SM area was not (partial r = −0.14, p = 0.43). Thus, older patients with HFpEF have greater thigh IMF and IMF/SM ratio compared with HCs, and these are significantly related to their severely reduced peak VO2. These data suggest that abnormalities in SM composition may contribute to the severely reduced exercise capacity in older patients with HFpEF. This implicates potential targets for novel therapeutic strategies in this common debilitating disorder of older persons.

Cirrhosis patients have reduced peak aerobic power (peak VO 2 ) that is associated with reduced survival. Supervised exercise training increases exercise tolerance. The effect of home-based exercise training (HET) in cirrhosis is unknown. The objective was to evaluate the safety and efficacy of 8 weeks of HET on peak VO 2 , 6-minute walk distance (6MWD), muscle mass, and quality of life in cirrhosis. Random assignment to 8 weeks of HET (moderate to high intensity cycling exercise, 3 days/week) or usual care. Exercise adherence defined as completing ≥80% training sessions. Paired t-tests and analysis of covariance used for comparisons. Forty patients enrolled: 58% male, mean age 57 y, 70% Child Pugh-A. Between group increases in peak VO 2 (1.7, 95% CI: −0.33 to 3.7 ml/kg/min, p = 0.09) and 6MWD (33.7, 95% CI: 5.1 to 62.4 m, p = 0.02) were greater after HET versus usual care. Improvements even more marked in adherent subjects for peak VO 2 (2.8, 95% CI: 0.5–5.2 mL/kg/min, p = 0.02) and 6MWD (46.4, 95% CI: 12.4–80.5 m, p = 0.009). No adverse events occurred during testing or HET. Eight weeks of HET is a safe and effective intervention to improve exercise capacity in cirrhosis, with maximal benefits occurring in those who complete ≥80% of the program.

This study aimed to characterize peak exercise cardiac function and thigh muscle fatty infiltration and their relationships with VO 2 peak among anthracycline-treated breast cancer survivors (BCS). BCS who received anthracycline chemotherapy ~ 1 year earlier (n = 16) and matched controls (matched-CON, n = 16) were enrolled. Resting and peak exercise cardiac function, myocardial T 1 mapping (marker of fibrosis), and thigh muscle fat infiltration were assessed by magnetic resonance imaging, and VO 2 peak by cycle test. Compared to matched-CON, BCS had lower peak SV (64 ± 9 vs 57 ± 10 mL/m 2 , p = 0.038), GLS (− 30.4 ± 2.2 vs − 28.0 ± 2.5%, p = 0.008), and arteriovenous oxygen difference (16.4 ± 3.6 vs 15.2 ± 3.9 mL/100 mL, p = 0.054). Mediation analysis showed: (1) greater myocardial T 1 time (fibrosis) is inversely related to cardiac output and end-systolic volume exercise reserve; (2) greater thigh muscle fatty infiltration is inversely related to arteriovenous oxygen difference; both of which negatively influence VO 2 peak. Peak SV (R 2  = 65%) and thigh muscle fat fraction (R 2  = 68%) were similarly strong independent predictors of VO 2 peak in BCS and matched-CON combined. Post-anthracyclines, myocardial fibrosis is associated with impaired cardiac reserve, and thigh muscle fatty infiltration is associated with impaired oxygen extraction, which both contribute to VO 2 peak.

Almost half of all heart failure (HF) disease burden is due to HF with preserved ejection fraction (HFpEF). The primary symptom in patients with HFpEF, even when well compensated, is severe exercise intolerance and is associated with their reduced quality of life. Recently, studies showed that HFpEF patients have multiple skeletal muscle (SM) abnormalities, and these are associated with decreased exercise intolerance. The SM abnormalities are likely intrinsic to the HFpEF syndrome, not a secondary consequence of an epiphenomenon. These abnormalities are decreased muscle mass, reduced type I (oxidative) muscle fibers, and reduced type I-to-type II fiber ratio as well as a reduced capillary-to-fiber ratio, abnormal fat infiltration into the thigh SM, increased levels of atrophy genes and proteins, reduction in mitochondrial content, and rapid depletion of high-energy phosphate during exercise with markedly delayed repletion of high-energy phosphate during recovery in mitochondria. In addition, patients with HFpEF have impaired nitric oxide bioavailability, particularly in the microvasculature. These SM abnormalities may be responsible for impaired diffusive oxygen transport and/or impaired SM oxygen extraction. To date, exercise training (ET) and caloric restriction are some of the interventions shown to improve outcomes in HFpEF patients. Improvements in exercise tolerance following aerobic ET are largely mediated through peripheral SM adaptations with minimal change in central hemodynamics and highlight the importance of targeting SM to improve exercise intolerance in HFpEF. Focusing on the abnormalities mentioned above may improve the clinical condition of patients with HFpEF.

It is unknown if vigorous to maximal aerobic interval training (INT) is more effective than traditionally prescribed moderate-intensity continuous aerobic training (MCT) for improving peak oxygen uptake (Vo2) and the left ventricular ejection fraction (LVEF) in patients with heart failure with reduced ejection fraction. MEDLINE, PubMed, Scopus, and the Web of Science were searched using the following keywords: “heart failure,” high-intensity interval exercise,” “high-intensity interval training,” “aerobic interval training,” and “high-intensity aerobic interval training.” Seven randomized trials were identified comparing the effects of INT and MCT on peak Vo2, 5 of which measured the LVEF at rest. The trials included clinically stable patients with heart failure with reduced ejection fraction with impaired left ventricular systolic function (mean LVEF 32%) who were relatively young (mean age 61 years) and predominantly men (82%). Weighted mean differences were calculated using a random-effects model. INT led to significantly higher increases in peak Vo2 compared with MCT (INT vs MCT, weighted mean difference 2.14 ml O2/kg/min, 95% confidence interval 0.66 to 3.63). Comparison of the effects of INT and MCT on the LVEF at rest was inconclusive (INT vs MCT, weighted mean difference 3.29%, 95% confidence interval −0.7% to 7.28%). In conclusion, in clinically stable patients with heart failure with reduced ejection fraction, INT is more effective than MCT for improving peak Vo2 but not the LVEF at rest.

Purpose of Review To discuss the impact of deleterious changes in skeletal muscle morphology and function on exercise intolerance in patients with heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF), as well as the utility of exercise training and the potential of novel treatment strategies to preserve or improve skeletal muscle morphology and function. Recent Findings Both HFrEF and HFpEF patients exhibit a reduction in percent of type I (oxidative) muscle fibers and oxidative enzymes coupled with abnormal mitochondrial respiration. These skeletal muscle abnormalities contribute to impaired oxidative metabolism with an earlier shift towards glycolytic metabolism during exercise that is strongly associated with exercise intolerance. In both HFrEF and HFpEF patients, peripheral “non-cardiac” factors are important determinants of the improvement in exercise tolerance following aerobic exercise training. Adjunctive strategies that include nutritional supplementation with amino acids and/or anabolic drugs to stimulate anabolic molecular pathways in skeletal muscle show great promise for improving exercise tolerance and treating heart failure-associated sarcopenia, but these efforts remain early in their evolution, with no immediate clinical applications. Summary There is consistent evidence that heart failure is associated with multiple skeletal muscle abnormalities which impair oxygen uptake and utilization and contribute greatly to exercise intolerance. Exercise training induces favorable adaptations in skeletal muscle morphology and function that contribute to improvements in exercise tolerance in patients with HFrEF. The contribution of skeletal muscle adaptations to improved exercise tolerance following exercise training in HFpEF remains unknown and warrants further investigation.

Background 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. Methods 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, V̇O2peak), global longitudinal strain (GLS) via echocardiography and haemoglobin concentrations in the haematological cancer cohort. Hierarchical multiple regression analysis was performed to identify predictors of V̇O2peak. Results 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). V̇O2peak was significantly lower than predicted values for the haematological cancer cohort (mean difference; 9.61 ± 8.30 mL.kg−1.min−1, p < 0.001). The multiple regression analysis accounted for 35% of the variance in V̇O2peak with both SMFF (β = −0.40, ΔR2 = 0.14, p = 0.002) and haemoglobin concentrations (β = 0.50, ΔR2 = 0.23, p < 0.001) being significant independent predictors of V̇O2peak, while skeletal muscle volume (β = 0.00, ΔR2 = 0.00, p = 0.767), GLS (β = 0.06, ΔR2 = 0.00, p = 0.509), prior anthracycline treatment (β = 0.00, ΔR2 = 0.00, p = 0.962) and clinical diagnosis (β = 0.00, ΔR2 = 0.00, p = 0.555) were not. Conclusions SMFF is increased in haematological cancer patients and contributes to reduced V̇O2peak. Consequently, increased SMFF may be an important target to improve cardiovascular health and cardiorespiratory fitness in this population.

The conventional approach to cardiac magnetic resonance (CMR) involving breath holds, electrocardiography-gating, and acquisition of a short-axis (SAX) image stack, introduces technical and logistical challenges for assessing exercise left ventricular (LV) function. Real-time, free-breathing CMR acquisition of long-axis (LAX) images overcomes these issues and also enables assessment of global longitudinal strain (GLS). We evaluated the reliability of a free-breathing LAX approach compared to the standard SAX approach and the reproducibility of free-breathing LAX. LV SAX (contiguous stack) and LAX (two-chamber and four-chamber) 3T CMR cine images were acquired four times within one scan in 32 women with cardiovascular risk factors (56±10 years, 28±4 kg/m 2 ) as follows: 1) resting, gated-segmented, end-expiration breath-hold; 2) resting, real-time, free-breathing; 3) test-retest set of resting, real-time, free-breathing; 4) peak exercise (incremental-to-maximum, in-magnet, stepper test), real-time, free-breathing. A second scan was performed within one week in a subset (n = 5) to determine reproducibility of peak exercise measures. Reliability and agreement of the free-breathing LAX approach with the conventional SAX approach were assessed by intraclass correlation coefficient (ICC) and Bland-Altman plots, respectively. Normal control GLS reserve was also acquired in a separate set of 12 young, healthy control women (25±4 years, 22±2 kg/m 2 ) for comparison. Comparisons of LV volumes and function among all techniques at rest had good-to-excellent reliability (ICC = 0.80–0.96), and excellent reliability between peak exercise free-breathing LAX and SAX evaluations (ICC = 0.92–0.96). Higher resting heart rates with free-breathing acquisitions compared to breath-hold (mean difference, limits of agreement: 5, 1–12 beats per minute) reduced reliability for cardiac output (ICC = 0.67–0.79). Reproducibility of the free-breathing LAX approach was good-to-excellent at rest and peak exercise (ICC = 0.74–0.99). GLS exercise reserve was impaired in older women at cardiovascular risk compared to young healthy women (-4.7±2.3% vs -7.4±2.1%, p = 0.001). Real-time, free-breathing CMR with LAX evaluation provides a reliable and reproducible method to assess rest and peak exercise cardiac function, including GLS.

During standard cardiovascular magnetic resonance (CMR) the horizontal long‐axis cine image (i.e., 4‐chamber) is captured which includes a cross‐section of the descending aorta. The aortic cross‐section can be used to assess aortic stiffness (distensibility; ∆area/pressure) or circumferential strain (percentage vascular deformation). We examined whether descending aortic strain from traditional CMR is sensitive to age‐ and disease‐related (heart failure with preserved ejection fraction; HFpEF) arteriosclerosis. We recruited 83 participants into three groups: (1) 34 young individuals (age: 22 ± 3 years; body mass index (BMI): 24.3 ± 2.8 kg/m2); (2) 19 older individuals (age: 69 ± 5 years; BMI: 26.9 ± 4.7 kg/m2) and (3) 26 patients with HFpEF (age: 69 ± 6 years; BMI: 35.8 ± 6.1 kg/m2). All participants were studied in the same 3 T scanner (Phillips, Achieva). Descending aortic cross‐sectional area and circumferential strain were measured using cvi42 software. Blood pressure was measured via a brachial oscillometric cuff. Data were compared via ANOVA. All data are reported as means ± standard deviation. Compared to the young group (71 ± 5 mmHg), mean arterial pressure was higher in the older (83 ± 9 mmHg, P < 0.001) and HFpEF groups (86 ± 10 mmHg, P < 0.001). Minimum and maximum aortic areas were greater in the older and HFpEF groups (both, P < 0.01). Peak descending aortic strain (young: 11.4% ± 2.2%; older: 4.8% ± 1.6%; HFpEF 3.8% ± 1.6%) and absolute distension were lower (all, P < 0.02) in the older and HFpEF groups compared to the young. Peak descending aortic strain and strain rates are sensitive to age and may provide a novel assessment of arterial stiffness for longitudinal studies that utilize or have utilized CMR. What is the central question of this study? Assessing aortic stiffness requires prospective planning when done by magnetic resonance imaging (MRI), but is it possible to assess aortic stiffness from standard cardiac MRI? What is the main finding and its importance? Peak strain and systolic and diastolic strain rates of the descending aorta are sensitive to age‐related aortic stiffening, with less variability than conventional measures. The descending aorta captured in the standard four‐chamber view with cardiac MRI can be used to assess aortic stiffness and wall mechanics. These variables represent novel metrics available from every cardiac MRI ever taken.

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.