Exercise training in patients with systolic heart failure (HF) is an accepted adjunct to an evidence-based management program. This review describes the pathophysiologic features that are thought to be responsible for the exercise intolerance experienced in the HF patient. Significant research has expanded our appreciation of the interplay of hemodynamic, ventilatory, and skeletal myopathic processes in this common, chronic condition. Randomized, controlled exercise trials designed to measure endothelial function, inflammatory markers, sympathetic neural activation, and skeletal muscle metabolism and structure have further defined the pathophysiology, documented the impact of exercise training on these processes, and confirmed the benefit of this therapy. Consistent with prior clinical research and patient experience are the recently published results of the HF-ACTION (Heart Failure-A Controlled Trial Investigating Outcomes of exercise TraiNing), which demonstrated a modest improvement in exercise capacity, reduction of symptoms, and improved self-reported measures of quality of life without adverse events. Consideration is given in this review to the benefits of variable intensity programs and the addition of resistance exercise to a standard aerobic prescription. Despite increasing validation of the role exercise training plays in the modification of exercise intolerance, challenges remain in its routine therapeutic application, including acceptance and use as an adjunctive intervention in the management of the patient with HF, limited insurance coverage for HF patients in cardiac rehabilitation, tailoring of exercise programs to best address the needs of subgroups of patients, and improved short- and long-term adherence to exercise training and a physically active lifestyle.

Background Despite the substantial overlap of obesity and metabolic disease, there is hetereogeneity with respect to cardiovascular risk. We sought to investigate preclinical differences in systolic and diastolic function in obesity, and specifically compare obese individuals with and without metabolic syndrome (MS). Methods and Results Obese individuals without cardiac disease with (OB/MS+, n=124) and without MS (OB/MS−, n=37) were compared to non-obese controls (n=29). Diastolic function was assessed by transmitral and tissue Doppler. Global longitudinal strain (LS) and time-based dyssynchrony were assessed by speckle tracking. Both Ob/MS− and OB/MS+ groups had similar ejection fraction but worse systolic mechanics as assessed by LS and dyssynchrony compared with non-obese controls. Specifically, OB/MS− had 2.5% lower LS (s.e. 0.7%, P=0.001 in multivariable-adjusted analyses) and 10.8 ms greater dyssynchrony (s.e. 3.3, P=0.002), and OB/MS+ had 1.0% lower LS (s.e. 0.3%, P<0.001) and 7.8 ms greater dyssynchrony (s.e. 1.5, P<0.001) compared with controls. Obesity was associated with impaired diastolic function regardless of MS status, as evidenced by greater left atrial diameter and left ventricular mass, though diastolic dysfunction was more pronounced in OB/MS+ compared with OB/MS− individuals. Conclusions Obesity is associated with subclinical differences in both systolic and diastolic function regardless of the presence or absence of MS, although MS appears to be associated with worse diastolic dysfunction. Compared to controls, ‘metabolically healthy’ obese had lower LS, greater dyssynchrony, and early diastolic dysfunction, supporting the notion that obesity per se may have adverse cardiovascular effects regardless of metabolic disease.