Elsevier

Heart Failure Clinics

Volume 4, Issue 1, January 2008, Pages 99-115
Heart Failure Clinics

Exercise Intolerance

https://doi.org/10.1016/j.hfc.2007.12.002Get rights and content

Exercise intolerance is the primary symptom of chronic diastolic heart failure. It is part of the definition of heart failure and is intimately linked to its pathophysiology. Further, exercise intolerance affects the diagnosis and prognosis of heart failure. In addition, understanding the mechanisms of exercise intolerance can lead to developing and testing rational treatments for heart failure. This article focuses on the fundamental principles of exercise physiology and on the assessment, pathophysiology, and potential treatment of exercise intolerance in diastolic heart failure.

Section snippets

Importance of exercise intolerance

Heart failure is defined as a syndrome in which cardiac output is insufficient to meet metabolic demands. This definition implies that insufficient cardiac output will be expressed symptomatically. Heart failure often may manifest by occasional episodes of acute decompensation with overt systemic volume overload and pulmonary edema [1], [2]. Exertional fatigue and dyspnea, however, are the primary chronic symptoms in outpatients, even when well compensated and non-edematous, and whether

Pathophysiology of exercise intolerance

To understand the pathophysiology of exercise intolerance in DHF, the authors performed a comparative study of maximal exercise testing with expired gas in 119 older subjects in three distinct, well-defined groups: persons who had heart failure with severe left ventricular (LV) systolic dysfunction (mean EF, 30%); persons who had isolated DHF (EF ≥ 50% and no significant coronary, valvular, pericardial, or pulmonary disease and no anemia); and age-matched controls [3]. In comparison with the

Interventions to improve exercise tolerance

During exercise in normal subjects, systolic and pulse pressure increase substantially, and this response is magnified by increased arterial stiffness. Data from animal models suggest that the exercise-related increase in systolic blood pressure is mediated, in part, by exercise-induced increases in circulating angiotensin II. Indeed, in a randomized, double-blind, placebo-controlled cross-over trial, angiotensin receptor blockade reduced the exaggerated exercise increase in systolic and pulse

Summary

Even when stable and non-edematous, patients who have heart failure and normal EF have severe, chronic exercise intolerance. The pathophysiology of exercise intolerance in this syndrome is incompletely understood but probably is multifactorial. Presently available data suggest that important contributors include decreased LV diastolic compliance, decreased aortic distensibility, exaggerated exercise systolic blood pressure, relative chronotropic incompetence, and possibly anemia and skeletal

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    This work was supported in part by National Institute on Aging Grants, R37-AG18915 (MERIT), Dennis Jahnigen Career Development and Paul Beeson Award (K08-AG026764) and Claude D. Pepper Older Americans Independence Center (P30 AG21332).

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