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Clinical Trial Summary

Exercise intolerance is a major limiting symptom in patients with CHF. However the poor correlation between the hemodynamic parameters of left ventricular performance at rest and exercise performance has led to the concept that peripheral factors such as muscle perfusion and muscle metabolism play a role as determinants of exercise capacity.


Clinical Trial Description

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. ;


Study Design

Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Single Blind (Subject), Primary Purpose: Health Services Research


Related Conditions & MeSH terms


NCT number NCT02732990
Study type Interventional
Source Rigshospitalet, Denmark
Contact Gregers W Munch, MSc PhD
Phone +45 35459574
Email gregers.munch@regionh.dk
Status Recruiting
Phase N/A
Start date February 2014
Completion date August 2016

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