The pathophysiology behind the breathlessness and fatigue experienced by CHF patients during exercise remains unclear. Recent evidence suggests that the peripheral skeletal muscle, which becomes abnormal in heart failure, is the source of afferent signals which disrupt normal patterns of cardiorespiratory control. When CHF patients exercise, an inappropriately strong sympathetic response further limits exercise tolerance by evoking larger than normal increases in peripheral sympathetic activation at a faster rate than in healthy individuals. A consequence of this exacerbated sympathetic response may be the further sympathetic restraint of blood flow to the active skeletal muscles resulting in hypoperfusion of the muscle vascular bed and fatigue. Small muscle mass exercise training increases muscle oxidative capacity and improves aerobic work capacity in CHF patients. A range of studies is proposed here that will provide an integrative view of the mechanistic basis behind exercise intolerance in CHF and relate the intramuscular metabolic status to the autonomic control of hemodynamics during exercise. An understanding of the mechanistic basis of the improved exercise tolerance with training, independent of improved resting cardiac function, will yield important information regarding the integrated control of blood flow and metabolic demand in CHF and highlight the importance of maintaining the integrity of the peripheral musculature in CHF.