Muscle oxygen transport and utilization in heart failure: implications for exercise (in)tolerance

Area of Science:

• Cardiovascular Physiology
• Skeletal Muscle Metabolism
• Exercise Science

Background:

• Chronic heart failure (CHF) is characterized by exercise intolerance, linked to oxygen (O2) transport pathway dysfunction.
• CHF alters O2 supply and demand, impacting skeletal muscle function and overall patient morbidity and mortality.
• Cardiovascular regulation shifts to prevent blood pressure instability, affecting circulation and organ function.

Purpose of the Study:

• To review the mechanistic basis of reduced maximal O2 uptake and exercise intolerance in CHF.
• To examine the role of skeletal muscle O2 supply/demand imbalance in CHF.
• To discuss therapeutic strategies targeting muscle microvascular and oxidative function.

Main Methods:

• Review of experimental evidence from human and animal models of CHF.
• Analysis of O2 transport pathway aberrations, including microvascular dysfunction.
• Focus on skeletal muscle O2 uptake kinetics and exercise capacity.

Main Results:

• CHF leads to decreased O2 supply and increased O2 demand in skeletal muscle.
• Microvascular dysfunction is a key factor in the O2 supply/demand imbalance.
• Altered reflex and humoral control, inflammation, and oxidative stress contribute to muscle dysfunction.

Conclusions:

• Skeletal muscle microvascular and oxidative dysfunction are central to exercise intolerance in CHF.
• Therapeutic strategies like exercise training and anti-inflammatory/antioxidant treatments can improve muscle function and exercise tolerance.
• Targeting the O2 transport pathway offers potential for enhancing quality of life in CHF patients.