Cardiac rehabilitation (CR) has evolved from foundations as a postmyocardial infarction mobilization strategy for patients who were typically unstable, into a comprehensive, multidisciplinary program for most patients with cardiovascular disease aimed at optimizing cardiovascular health, reducing morbidity, and enhancing functional recovery. Although contemporary CR patients are now usually more stable from a cardiovascular perspective, needs have expanded for comprehensive approaches to exercise, lifestyle, care coordination, risk factor modification, and stress management. Furthermore, contemporary CR patients now typically include older adults who are contending with cardiovascular disease in the context of multimorbidity, frailty, sarcopenia, sensory limits, and cognitive impairment. The physiological mechanisms underlying exercise intolerance in cardiovascular disease include impairments in cardiac output, vascular function, and skeletal muscle metabolism and relate to elemental biological mechanisms that are common to all 3 as well as to noncardiovascular disease and aging. CR provides an important opportunity to address such aggregate risk. Nonetheless, CR remains underutilized, particularly by older adults, women, and those struggling with cognitive impairments, frailty, logistics, and social barriers to care. Emerging strategies, such as home-based and hybrid CR models, resistance training, and digital health technologies, are expanding the potential for access and effectiveness. Future research brings important opportunities to hone personalized CR strategies tailored to contemporary patient populations, including optimized exercise prescriptions as well as pharmacological, nutritional, and technological adjuncts. Related prospects to distinguish the biological mechanisms underlying patient-preferred clinical end points (eg, independence, quality of life) remain critical to augmenting CR’s value in the contemporary therapeutic landscape.

Heart failure with preserved ejection fraction (HFpEF) is the fastest growing form of heart failure in the United States. The cardinal feature of HFpEF is reduced exercise tolerance (peak oxygen uptake, JOURNAL/jcprh/04.03/01273116-202001000-00003/3FSM1/v/2023-09-11T232142Z/r/image-gif o _2peak) secondary to impaired cardiac, vascular, and skeletal muscle function. There are currently no evidence-based drug therapies to improve clinical outcomes in patients with HFpEF. In contrast, exercise training is a proven effective intervention for improving JOURNAL/jcprh/04.03/01273116-202001000-00003/3FSM1/v/2023-09-11T232142Z/r/image-gif o _2peak, aerobic endurance, and quality of life in HFpEF patients. This brief review discusses the pathophysiology of exercise intolerance and the role of exercise training to improve JOURNAL/jcprh/04.03/01273116-202001000-00003/3FSM1/v/2023-09-11T232142Z/r/image-gif o _2peak in clinically stable HFpEF patients. It also discusses the mechanisms responsible for the exercise training–mediated improvements in JOURNAL/jcprh/04.03/01273116-202001000-00003/3FSM1/v/2023-09-11T232142Z/r/image-gif o _2peak in HFpEF. Finally, it provides evidence-based exercise prescription guidelines for cardiac rehabilitation specialists to assist them with safely implementing exercise-based cardiac rehabilitation programs for HFpEF patients.

Heart failure with reduced ejection fraction is associated with increased exercise intolerance, morbidity, and mortality. Importantly, exercise intolerance in heart failure with reduced ejection fraction is a key factor limiting patient quality of life and survival. Exercise intolerance in heart failure with reduced ejection fraction stems from a multi-organ failure to maintain homeostasis at rest and during exercise, including the heart, skeletal muscle, and autonomic nervous system, lending itself to a system constantly trying to “catch-up”. Hemodynamic control during exercise is regulated primarily by the autonomic nervous system, whose operation, in turn, is partly regulated via reflexive information from exercise-stimulated receptors throughout the body (e.g., arterial baroreflex, central and peripheral chemoreceptors, and the muscle metabo- and mechanoreflexes). Persons with heart failure with reduced ejection fraction exhibit malfunctioning autonomic reflexes, which lead to exaggerated sympathoexcitation and attenuated parasympathetic tone. Chronic elevation of sympathetic activity is associated with increased morbidity and mortality. In this review, we provide an overview of how each main exercise-related autonomic reflex is changed in heart failure with reduced ejection fraction, and the role of exercise training in attenuating or reversing the counterproductive changes.

Children with congenital heart disease are at risk for developing increased arterial stiffness and this may be modulated by physical activity. Objective To compare arterial stiffness in high‐ and low‐physically active children with congenital heart disease and healthy age‐ and sex‐matched controls. Patients: Seventeen children with congenital heart disease (12 ± 2 years; females = 9), grouped by low‐ and high‐physical activity levels from accelerometry step count values, and 20 matched controls (11 ± 3 years; females = 9) were studied. Outcome Measures Carotid‐radial pulse wave velocity was assessed with applanation tonometry to determine arterial stiffness. Body composition and 6‐min walk test measures were performed. Data were analyzed using analysis of variance and multiple regression. Significance was P < .05. Results Arterial stiffness was increased in low‐physically active children with congenital heart disease (9.79 ± 0.97 m/s) compared to high‐physically active children with congenital heart disease (7.88 ± 0.71 m/s; P = .002) and healthy‐matched controls (8.67 ± 1.28 m/s; P = .015). There were no differences in body composition measures between groups (all P > .05), but 6‐min walk test distance was less in both congenital heart disease groups (high‐physically active: 514 ± 40 m; low‐physically active: 539 ± 49 m) versus controls (605 ± 79 m; all P < .05). Average daily step count significantly predicted arterial stiffness in children with congenital heart disease (R² = 0.358) with a negative correlation (R = −0.599, P = .011), while % fat mass (P = .519) and % lean mass (P = .290) did not predict arterial stiffness. Conclusions Low‐physically active children with congenital heart disease have increased arterial stiffness compared to high‐physically active children with congenital heart disease and healthy‐matched controls. Regular physical activity in children with congenital heart disease may modulate arterial stiffness.

Heart failure (HF) has a major impact on exercise tolerance that may (in part) be due to abnormalities in body and skeletal muscle composition. This systematic review and meta-analysis aims to assess how differences in whole-body and skeletal muscle composition between patients with HF and non-HF controls (CON) contribute to reduced peak oxygen uptake (VO₂peak). The PubMed database was searched from 1975 to May 2024 for eligible studies. Cross-sectional studies with measures of VO₂peak, body composition, or muscle biopsies in HF and CON were considered. Out of 709 articles, 27 studies were included in this analysis. Compared with CON, VO₂peak [weighted mean difference (WMD): −9.96 mL/kg/min, 95% confidence interval (CI): −11.71 to −8.21), total body lean mass (WMD: −1.63 kg, 95% CI: −3.05 to −0.21), leg lean mass (WMD: −1.38 kg, 95% CI: −2.18 to −0.59), thigh skeletal muscle area (WMD: −10.88 cm² , 95% CI: −21.40 to −0.37), Type I fibres (WMD: −7.76%, 95% CI: −14.81 to −0.71), and capillary-to-fibre ratio (WMD: −0.27, 95% CI: −0.50 to −0.03) were significantly lower in HF. Total body fat mass (WMD: 3.34 kg, 95% CI: 0.35–6.34), leg fat mass (WMD: 1.37 kg, 95% CI: 0.37–2.37), and Type IIx fibres (WMD: 7.72%, 95% CI: 1.52–13.91) were significantly higher in HF compared with CON. Absolute VO₂peak was significantly associated with total body and leg lean mass, thigh skeletal muscle area, and capillary-to-fibre ratio. Individuals with HF display abnormalities in body and skeletal muscle composition including reduced lean mass, oxidative Type I fibres, and capillary-to-fibre ratio that negatively impact VO₂peak.

Exercise intolerance is a hallmark feature in heart failure with preserved ejection fraction (HFpEF). Prior heavy exercise (“priming exercise”) speeds pulmonary oxygen uptake (V̇o_2p) kinetics in older adults through increased muscle oxygen delivery and/or alterations in mitochondrial metabolic activity. We tested the hypothesis that priming exercise would speed V̇o_2pon-kinetics in patients with HFpEF because of acute improvements in muscle oxygen delivery. Seven patients with HFpEF performed three bouts of two exercise transitions: MOD1, rest to 4-min moderate-intensity cycling and MOD2, MOD1 preceded by heavy-intensity cycling. V̇o_2p, heart rate (HR), total peripheral resistance (TPR), and vastus lateralis tissue oxygenation index (TOI; near-infrared spectroscopy) were measured, interpolated, time-aligned, and averaged. V̇o_2pand HR were monoexponentially curve-fitted. TPR and TOI levels were analyzed as repeated measures between pretransition baseline, minimum value, and steady state. Significance was P < 0.05. Time constant (τ; tau) V̇o_2p(MOD1 49 ± 16 s) was significantly faster after priming (41 ± 14 s; P = 0.002), and the effective HR τ was slower following priming (41 ± 27 vs. 51 ± 32 s; P = 0.025). TPR in both conditions decreased from baseline to minimum TPR ( P < 0.001), increased from minimum to steady state ( P = 0.041) but remained below baseline throughout ( P = 0.001). Priming increased baseline ( P = 0.003) and minimum TOI ( P = 0.002) and decreased the TOI muscle deoxygenation overshoot ( P = 0.041). Priming may speed the slow V̇o_2pon-kinetics in HFpEF and increase muscle oxygen delivery (TOI) at the onset of and throughout exercise. Microvascular muscle oxygen delivery may limit exercise tolerance in HFpEF.