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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Exercise and Cardiac Output01:17

Exercise and Cardiac Output

Regular physical activity is essential for maintaining cardiovascular health, with aerobic exercises being particularly effective. According to the American Heart Association, 150 minutes of moderate to intense aerobic exercise per week is recommended for a healthy heart. Aerobic activities may include brisk walking, running, bicycling, cross-country skiing, and swimming, ideally performed three to five times per week.
Sustained exercise increases the muscles' oxygen demand, which can be met...
Exercise and Cardiovascular Response01:20

Exercise and Cardiovascular Response

Exercise significantly impacts cardiovascular response, which is crucial for understanding patient health and designing effective treatment plans.
Light to moderate physical activity initiates a series of interconnected responses in the body. The heart rate modestly increases in anticipation of the workout, followed by widespread vasodilation as oxygen consumption by skeletal muscles increases. This results in decreased peripheral resistance, increased capillary blood flow, and accelerated...

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A Pacing-Controlled Procedure for the Assessment of Heart Rate-Dependent Diastolic Functions in Murine Heart Failure Models
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Adaptations in autonomic function during exercise training in heart failure.

Carlos Eduardo Negrao1, Holly R Middlekauff

  • 1Heart Institute (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Sao Paulo, Brazil. cndnegrao@incor.usp.br

Heart Failure Reviews
|October 13, 2007
PubMed
Summary

Heart failure (HF) exercise intolerance stems from skeletal myopathy, not cardiac issues. Exercise training improves HF by reducing sympathetic activity and enhancing muscle function.

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Last Updated: Jul 10, 2026

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Area of Science:

  • Cardiology
  • Exercise Physiology
  • Skeletal Muscle Biology

Background:

  • Heart failure (HF) is characterized by neurohumoral excitation, but its precise mechanisms remain unclear.
  • Exercise intolerance in chronic HF patients is increasingly attributed to skeletal myopathy rather than cardiac limitations.
  • Sympathetic nervous system overactivity is implicated in the development of skeletal myopathy in HF.

Purpose of the Study:

  • To explore the mechanisms linking neurohumoral excitation and skeletal myopathy in heart failure.
  • To investigate the role of sympathetic overactivity in exercise limitation in chronic HF.
  • To evaluate the impact of exercise training on neurohumoral and skeletal muscle abnormalities in HF.

Main Methods:

  • Review of existing literature on neurohumoral regulation, baroreceptor and chemoreceptor function in HF.
  • Analysis of evidence linking sympathetic activity to skeletal muscle dysfunction, ischemia, and inflammation in HF models and patients.
  • Examination of studies investigating the effects of exercise training on central sympathetic outflow, autonomic control, and peripheral muscle characteristics in HF.

Main Results:

  • Abnormalities in baroreceptors, chemoreceptors, and the central nervous system contribute to neurohumoral excitation in HF.
  • Sympathetic overactivity in HF may lead to skeletal muscle underperfusion, ischemia, oxidative stress, and inflammation, causing exercise limitation.
  • Exercise training demonstrably reduces central sympathetic outflow, improves autonomic control, enhances peripheral blood flow, and increases muscle mass in HF patients.

Conclusions:

  • Skeletal myopathy, driven by sympathetic overactivity, is a primary cause of exercise intolerance in chronic heart failure.
  • Exercise training offers a potent non-pharmacological intervention for HF, mitigating sympathetic drive and improving skeletal muscle health.
  • Targeting neurohumoral dysregulation and skeletal muscle dysfunction through exercise is crucial for managing heart failure.