Heart failure (HF) is a major and increasingly common cardiovascular syndrome, and is the end result of many cardiovascular disorders. It has been reported that HF patients with pharmacological therapy often remain burdened by dyspnea and fatigue, diminished exercise tolerance, reduced quality of life, recurrent hospitalizations, and early mortality. HF is associated with neurohumoral changes as the body attempts to reverse the effect of reduced cardiac output and organ perfusion. Persistent neurohumoral excitation, however, actually results in deterioration of myocardial function with inflammatory response, end-organ damage, and skeletal muscle derangement, which lead to worsened exercise capacity.

Physical training can have beneficial effects on neurohumoral, inflammatory, metabolic and central hemodynamic responses, as well as on endothelial, skeletal muscle and cardiovascular function, leading to improvement in functional capacity and quality of life. All these training-induced changes can effectively counteract the progression of deleterious compensatory mechanisms of HF.

Several lines of evidence suggest greater aerobic and cardiovascular adaptations after high-intensity exercise than with moderate levels in patients with coronary artery disease or left ventricular dysfunction function and in healthy subjects. Aerobic interval training (AIT) involving periods at 90% of VO2peak has been shown to rescue impaired cardiomyocyte contractility, attenuate myocardial hypertrophy, and reduce myocardial expression of atrial natriuretic peptide in animal model of post-infarction heart failure. However, underlying mechanisms of AIT-improved regulations remain unclear.

The different effects of AIT and moderate continuous training (MCT) on hemorheology, atherothrombosis or angiogenesis modulated by erythrocyte, monocyte or EPC in patients with CHF have been not investigated yet. Accordingly, the investigators will conduct this three-year study to clarify how the two exercise trainings affect cardiovascular hemorheological characteristics and atherothrombosis/ angiogenesis-related variables in patients with chronic heart failure. The investigators expect that these results obtained from this study can aid in determining appropriate exercise intervention to improve aerobic fitness as well as simultaneously improve hemodynamic control and minimize the risk of thrombogenesis in patients with CHF.

Heart failure (HF) is a major and increasingly common cardiovascular syndrome, and is the end result of many cardiovascular disorders. It has been reported that HF patients with pharmacological therapy often remain burdened by dyspnea and fatigue, diminished exercise tolerance, reduced quality of life, recurrent hospitalizations, and early mortality. HF is associated with neurohumoral changes as the body attempts to reverse the effect of reduced cardiac output and organ perfusion. Persistent neurohumoral excitation, however, actually results in deterioration of myocardial function with inflammatory response, end-organ damage, and skeletal muscle derangement, which lead to worsened exercise capacity.

Physical training can have beneficial effects on neurohumoral, inflammatory, metabolic and central hemodynamic responses, as well as on endothelial, skeletal muscle and cardiovascular function, leading to improvement in functional capacity and quality of life. All these training-induced changes can effectively counteract the progression of deleterious compensatory mechanisms of HF. Which exercise intensity yields maximal beneficial adaptations is controversial.

Several lines of evidence suggest greater aerobic and cardiovascular adaptations after high-intensity exercise than with low and moderate levels in patients with coronary artery disease or left ventricular dysfunction function and in healthy subjects. Aerobic interval training (AIT) involving periods at 90% of VO2peak has been shown to rescue impaired cardiomyocyte contractility, attenuate myocardial hypertrophy, and reduce myocardial expression of atrial natriuretic peptide in animal model of post-infarction heart failure.

However, underlying mechanisms of AIT-improved regulations of cardiac hemodynamics and risk factors in patients with CHF remain unclear.

Pathological erythrocyte deformability and aggregation reduces capillary perfusion and oxygen transfer to tissue, resulting in tissue ischemia or infraction. Shedding of procoagulant-rich microparticles from activated monocytes can accelerate the pathogenesis of atherothrombosis. Bone marrow-derived, circulating endothelial progenitor cells (EPC) is contributes to the maintenance of endothelial function and organ perfusion by mechanisms ranging from endothelial repair to angiogenesis. However, the different effects of AIT and moderate continuous training (MCT) on hemorheology, atherothrombosis or angiogenesis modulated by erythrocyte, monocyte or EPC in patients with CHF have been not investigated yet.

Accordingly, we will conduct this three-year study that includes 1st year study: the effects of AIT and MCT on hemorheology modulated by erythrocyte in patients with CHF; 2nd year: the effects of AIT and MCT on atherothrombosis modulated by monocyte in patients with CHF; and 3rd year study: the effects of AIT and MCT on angiogenesis modulated by EPC in patients with CHF to clarify how the two exercise trainings affect cardiovascular hemorheological characteristics and atherothrombosis/ angiogenesis-related variables in patients with chronic heart failure. We expect that these results obtained from this study can aid in determining appropriate exercise intervention to improve aerobic fitness as well as simultaneously improve hemodynamic control and minimize the risk of thrombogenesis in patients with CHF.

Inclusion Criteria:

• cardiac event with optimal medial treatment within 3 months and have 4 more weeks spared from heart disease attack or major cardiac procedure.

Exclusion Criteria:

• unstable angina pectoris,
• uncompensated heart failure,
• myocardial infarction during the past 4 weeks,
• complex ventricular arrhythmias,
• orthopedic or neurological limitations to exercise