Mechanisms of Circulatory Abnormalities and Fatigue in Patients with Cardiovascular Diseases

Graphic- Mechanisms of Circulatory Abnormalities and Fatigue in Patients with Cardiovascular Diseases
Experimental pharmacological blockade of group III/IV muscle afferents normalized the exaggerated systemic blood pressure increase and the suboptimal increase in leg blood flow during exercise in hypertensive patients to levels observed in normotensive individuals.

Premature fatigue, a hallmark of individuals with cardiovascular diseases such as heart failure or hypertension, substantially impairs the patients’ ability to effectively execute tasks of daily living. Although researchers long believed that patients’ abnormal circulatory response to physical activity contributed to this premature fatigue, they did not fully understand the mechanism(s)underlying the circulatory abnormalities. Markus Amann, PhD, and colleagues recently discovered that both heart failure and hypertension impair an important neurocirculatory control mechanism in humans—specifically, a reflex loop mediated by neural feedback from muscles to the central nervous system. This impairment results in excessive sympathetic nervous system activity, and largely accounts for the circulatory abnormalities observed during physical activities. In additional experiments, Amann’s group demonstrated that the mechanism underlying the impaired circulatory control also accounts for the premature fatigue and limited ability to execute tasks of daily living in patients with cardiovascular diseases.


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Group III/IV muscle afferents impair limb blood in patients with chronic heart failure. Amann M, Venturelli M, Ives SJ, Morgan DE, Gmelch B, Witman MA, Groot HJ, Wray WD, Stehlik J, Richardson RS. Int J Cardiol. 2015 June 15;174(2):368.

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Exercise pressor reflex contributes to the cardiovascular abnormalities characterizing hypertensive humans during exercise. Sidhu SK, Weavil JC, Rossman MJ, Jessop JE, Buys MJ, Supiano MS, Richardson RS, Bledsoe AD, Amann M. Hypertension. 2019 December;74(6):1468.