Key result
Cardiovascular diseases, including heart failure, hypertension, and diabetes, alter hemodynamics during the muscle metaboreflex by recruiting different cardiovascular reserves.
Why the study?
How do cardiovascular diseases impact cardiovascular regulation and hemodynamics during metaboreflex activation elicited by post-exercise muscle ischemia in humans?
How do cardiovascular diseases impact cardiovascular regulation and hemodynamics during metaboreflex activation elicited by post-exercise muscle ischemia in humans?
This review highlights the plasticity of cardiovascular regulation during exercise in patients with cardiovascular diseases, showing how different hemodynamic reserves are recruited when others are exhausted.
Alerts clinicians to modified exercise responses in HF, hypertension, and diabetes; leaves open whether metaboreflex-targeted therapies improve outcomes.
BACKGROUND: Hemodynamics during dynamic exercise is finely regulated by some neural mechanisms. One of these mechanisms is the metabolic part of the exercise pressor reflex, i.e. the muscle metaboreflex. Hemodynamic response during the metaboreflex is characterised by the recruitment of the reserves in cardiac inotropism, pre-load, after-load and chronotropism. If one of these reserves is exhausted, then the cardiovascular response is achieved by recruiting one of the other reserves, thereby indicating a remarkable plasticity of the control of circulation. CONCLUSION: In this review, the effects of a number of cardiovascular diseases - such as heart failure, heart failure with preserved ejection fraction, hypertension, type 1 and type 2 diabetes mellitus, obesity and metabolic syndrome - on hemodynamics during the metaboreflex are reviewed.
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Antonio Crisafulli (2017) conducted a review in Cardiovascular diseases. Cardiovascular diseases was evaluated. Cardiovascular diseases, including heart failure, hypertension, and diabetes, alter hemodynamics during the muscle metaboreflex by recruiting different cardiovascular reserves.
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