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Exercise Therapy for the Failing Heart—Harmful or Helpful?
normal ejection fraction. Despite significant differences in ejection
Figure 1: Pathophysiological ‘Syndrome’ of Heart Failure
fraction, signs/symptoms at presentation can be remarkably similar in
patients with HF and a reduced ejection fraction (HF-REF) and in patients
Pulmonary
Inefficient
with HF and a preserved ejection fraction (HF-PEF). In addition to the mismatching
ventilation
and dyspnea
reduced stroke volume associated with reduced LV contraction and/or
filling, an inadequate heart rate response during exercise can also
contribute to the reduced cardiac output seen in patients with systolic
Renal
and diastolic HF. Studies from our laboratory have demonstrated that
hypoperfusion
20–25% of older HF patients have chronotropic incompetence during
exercise.
6
Furthermore, those patients with chronotropic incompetence
have a significantly lower exercise capacity compared with similar HF
Decreased Left ventricular systolic
patients with a normal heart rate response. Either form of LV dysfunction
cardiac and/or
Neurohormonal
can result in a reduction in cardiac output during exercise that
output diastolic dysfunction
activation
ultimately leads to a reduced perfusion to numerous organ systems and
a variety of complex and inter-related pathophysiological responses.
These compensatory adaptations, although initially activated to
Increased Arterial
preserve vital body functions, ultimately result in a vicious spiral that afterload vasoconstriction
produces numerous signs/symptoms, including exercise intolerance
(see Figure 1).
Exercise Skeletal muscle Muscle
Exercise-related Limitations in Heart Failure
intolerance dysfunction hypoperfusion
Numerous studies
7
over the past two decades have consistently
demonstrated that the exercise capacity of HF patients, best quantified
Table 1: Pathophysiology of Heart Failure with
by oxygen consumption at peak exercise (VO
2
peak), is 15–40% below Preserved Ejection Fraction versus Heart Failure with
that of age-matched healthy subjects. Based on the Fick equation, an
Reduced Ejection Fraction
appropriate increase in VO
2
peak is dependent on both an increase in
cardiac output (which depends on appropriate heart rate and stroke
HF-PEF HF-REF
volume responses) and a concomitant ‘widening’ of the arterial–venous
Peak cardiac output ↓↓↓ ↓↓↓
oxygen content difference (i.e. increased oxygen extraction). Numerous
Peak stroke volume ↓↓↓ ↓↓↓
Peak HR ↓↓
studies
7
over the past two decades have described the plethora of
Rest/peak LVEDP ↑↑↑ ↑↑↑
‘peripheral’ abnormalities in HF patients that limit oxygen supply and/or
Peak EDV ↓↓ ↑↑
extraction by active skeletal muscle tissue. Abnormalities in vascular
Peak ESV ↔ – ↓ ↑↑↑
structure and function, including endothelial dysfunction, elevated
Rest LVEF ↔ – ↑ ↓↓↓
neurohormonal responses, and/or pulmonary dysfunction, also clearly
Wall motion abnormalities ↔ ↑↑↑
contribute to the symptoms and exercise intolerance commonly LVH Severe/concentric Thinned/eccentric
experienced by HF patients. Other peripheral abnormalities that are LV mass/volume ratio ↑↑↑ ↓↓↓
often observed in HF that contribute to exercise intolerance include:
LA size ↑↑↑
Neuroendocrine levels ↑↑ ↑↑↑
• increased sympathetic tone and peripheral vasoconstriction;
Peak VO
2
↓↓↓ ↓↓↓
• reduced skeletal muscle blood flow;
Submax (VO
2
at VAT) ↓↓ ↓↓
Aortic distensibility ↓↓↓ ↓↓↓
• abnormal/inefficient ventilation during exercise;
• reduction in oxidative (aerobic) enzymes in skeletal muscle;
HF-PEF = heart failure with preserved ejection fraction; HF-REF = heart failure with
reduced ejection fraction; HR = heart rate; LVEDP = left ventricular diastolic end pressure;
• decreased skeletal muscle mitochondrial volume and density; EDV = end-diastolic volume; ESV = end systolic volume; LVEF = left ventricular ejection fraction;
• increased non-oxidative (anaerobic) enzymes in skeletal muscle
LVH = left ventricular hypertrophy; LA = left anterior; VO2 = oxygen consumption at peak
exercise; VAT = ventilatory anaerobic threshold.
tissue; and
• generalized skeletal muscle atrophy and reduction in type I fibers. extended our pathophysiological observations and demonstrate that
morbidity and mortality are also similar between these two disorders.
Different Hearts but Same Exercise Responses The extent of the pathophysiological similarities between HF-PEF and
Despite significant underlying differences in LV structure and function, HF-REF are presented in Table 1.
research from our laboratory
8,9
has demonstrated remarkably similar
acute responses to endurance-type exercise (i.e. cardiopulmonary Exercise Therapy for Heart Failure with
exercise test responses) in older patients with HF-REF and HF-PEF. Reduced Ejection Fraction—Harmful or Helpful?
Similarities between these two HF groups in the four pivotal HF domains Over the past quarter of a century there have been dozens of studies
(exercise capacity, health-related quality of life, neurohormonal levels, and subsequent publications reporting on the effects of endurance-
and LV structure and function) has led to the conclusion that HF-PEF can or aerobic-type exercise therapy (ET) in patients with HF (primarily in
result in the full HF syndrome. Epidemiological investigations
10
have those with HF-REF).
7
Despite several early positive studies, one study
US CARDIOLOGY 57
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