Mechanoreflex mediates the exaggerated exercise pressor reflex in heart failure

Area of Science:

• Cardiovascular Physiology
• Exercise Physiology
• Heart Failure Research

Background:

• Heart failure is characterized by exaggerated increases in mean arterial pressure (MAP) and heart rate (HR) during exercise.
• This exaggerated cardiovascular response is mediated by an overactive exercise pressor reflex (EPR).
• While group IV afferent neurons initiate the exaggerated EPR, they do not mediate the enhanced circulatory responses.

Purpose of the Study:

• To investigate the hypothesis that the mechanically sensitive component of the EPR, primarily involving group III afferent fibers, mediates the augmented EPR in heart failure.

Main Methods:

• Utilized a rat model with dilated cardiomyopathy (DCM) and a control (sham) group.
• Group IV afferent fibers were ablated in neonatal capsaicin-treated (NNCAP) animals.
• EPR was activated by electrically induced static muscle contraction, with and without gadolinium (a mechanoreceptor blocker).

Main Results:

• DCM and NNCAP rats exhibited larger increases in MAP and HR during EPR activation compared to sham rats.
• Gadolinium administration attenuated MAP and HR responses to contraction in all groups.
• The reduction in response was significantly greater in DCM and NNCAP rats, indicating a greater reliance on mechanoreceptors.

Conclusions:

• The muscle mechanoreflex is the primary mediator of the exaggerated exercise pressor reflex in heart failure.
• Mechanoreflex overactivity may be a compensatory mechanism for altered group IV fiber function.
• The muscle mechanoreflex presents a potential novel therapeutic target for managing abnormal exercise-induced circulatory responses in heart failure.