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Energy metabolism in heart failure
Renée Ventura-Clapier1, Anne Garnier, Vladimir Veksler
1Cardiologie Cellulaire et Moléculaire, U-446 INSERM, Faculté de Pharmacie, Université Paris-Sud, 92296 Châtenay-Malabry, France. renee.ventura@cep.u-psud.fr
The Journal of Physiology
|December 9, 2003
Summary
Heart failure (HF) causes widespread metabolic issues in both the heart and skeletal muscles, leading to reduced energy production and utilization. These energy deficits contribute to the characteristic fatigue and exercise intolerance seen in patients with chronic heart failure.
Area of Science:
- Cardiology
- Metabolic Medicine
- Biochemistry
Background:
- Heart failure (HF) impairs the heart's ability to meet the body's energy demands.
- The precise mechanisms behind cardiac intracellular abnormalities in HF are not fully understood.
- HF is associated with peripheral symptoms like muscle fatigue and exercise intolerance.
Purpose of the Study:
- To review energy metabolism alterations in chronic heart failure (HF).
- To describe normal energy metabolism in cardiac and skeletal muscles.
- To detail the changes in energy metabolism occurring in chronic HF.
Main Methods:
- Literature review focusing on energy metabolism in chronic heart failure.
- Brief description of normal muscle energy metabolism.
- Discussion of alterations in cardiac and skeletal muscle energy metabolism in HF.
Main Results:
- Abnormalities in metabolic pathways decrease energy production, transfer, and utilization in HF.
- Skeletal muscle shows reduced mitochondrial ATP production and impaired phosphotransfer kinase activity.
- Decreased expression of mitochondrial factors and proteins contributes to energy starvation in HF.
Conclusions:
- Altered energy metabolism affects both cardiac and skeletal muscles, suggesting a generalized metabolic myopathy in HF.
- Reduced mitochondrial function and impaired energy transfer are key features of chronic HF.
- These metabolic changes underlie the reduced exercise capacity and fatigue experienced by HF patients.