Related Experiment Video
Updated: May 14, 2026
09:04
Skeletal Muscle Neurovascular Coupling, Oxidative Capacity, and Microvascular Function with 'One Stop Shop' Near-infrared Spectroscopy
Published on: February 20, 2018
Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in
Matthew Coutsos1, Javier A Sala-Mercado, Masashi Ichinose
1Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|January 29, 2013
Summary
Muscle metaboreflex activation (MMA) causes coronary vasoconstriction, particularly in heart failure. Blocking this response improves cardiac function during exercise, suggesting it limits contractility in heart failure patients.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Heart Failure Pathophysiology
Background:
- Muscle metaboreflex activation (MMA) during exercise increases cardiac workload and oxygen demand.
- Normally, increased cardiac work should induce vasodilation, but MMA leads to coronary vasoconstriction, indicating sympathetic nervous system influence.
- In heart failure, impaired contractility limits cardiac output response to MMA, with observed coronary vasoconstriction.
Purpose of the Study:
- To investigate if MMA-induced coronary vasoconstriction contributes to reduced cardiac performance in heart failure.
- To determine the role of alpha-1 adrenergic receptors in mediating this vasoconstriction.
Main Methods:
- Utilized conscious, chronically instrumented dogs.
- Induced heart failure via pacing.
- Measured MMA responses during mild exercise before and after alpha-1 adrenergic blockade (prazosin).
Main Results:
- Alpha-1 adrenergic blockade significantly enhanced increases in coronary vascular conductance, coronary blood flow, and cardiac output during MMA in dogs with heart failure.
- Maximal rate of left ventricular pressure change also improved after blockade.
Conclusions:
- Coronary vasoconstriction during MMA, mediated by alpha-1 adrenergic receptors, limits the heart's ability to increase contractility in heart failure.
- Targeting this vasoconstriction may improve cardiac performance in heart failure patients during exercise.
Related Concept Videos
01:29Heart 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...
01:22Heart 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...
01:29Pathophysiology of Cardiac Performance
Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...
01:20Exercise 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...
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...
01:26Imbalances in Cardiac Output
The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
01:26Heart 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...