Increased ergoreflex sensitivity in heart failure and neuromuscular disorders contributes to dyspnea and fatigue, which can be blunted by exercise training to restore sympatho-vagal balance.
The review highlights the role of the ergoreflex in heart failure and neuromuscular disorders, suggesting exercise training as a therapeutic option to modulate its sensitivity.
The control of ventilation and cardiovascular function during physical activity is partially regulated by the ergoreflex, a cardiorespiratory reflex activated by physical activity. Two components of the ergoreflex have been identified: the mechanoreflex, which is activated early by muscle contraction and tendon stretch, and the metaboreflex, which responds to the accumulation of metabolites in the exercising muscles. Patients with heart failure (HF) often develop a skeletal myopathy with varying degrees of severity, from a subclinical disease to cardiac cachexia. HF-related myopathy has been associated with increased ergoreflex sensitivity, which is believed to contribute to dyspnoea on effort, fatigue and sympatho-vagal imbalance, which are hallmarks of HF. Ergoreflex sensitivity increases significantly also in patients with neuromuscular disorders. Exercise training is a valuable therapeutic option for both HF and neuromuscular disorders to blunt ergoreflex sensitivity, restore the sympatho-vagal balance, and increase tolerance to physical exercise. A deeper knowledge of the mechanisms mediating ergoreflex sensitivity might enable a drug or device modulation of this reflex when patients cannot exercise because of advanced skeletal myopathy.
Aimo et al. (Fri,) conducted a review in Heart failure and neuromuscular disorders. Exercise training was evaluated. Increased ergoreflex sensitivity in heart failure and neuromuscular disorders contributes to dyspnea and fatigue, which can be blunted by exercise training to restore sympatho-vagal balance.