Journal
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
Volume 188, Issue -, Pages 74-81Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.autneu.2014.10.013
Keywords
Exercise; Chronic renal failure; Sympathetic nerve activity
Categories
Funding
- NIH [K23 HL098744]
- Satellite Healthcare, a not-for-profit renal care provider
- Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Clinical Studies Center, Decatur, GA
- Atlanta Research and Education Foundation
- PHS from the Clinical and Translational Science Award program, National Institutes of Health, National Center for Research Resources [UL1 RR025008]
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Abnormal neurocirculatory control during exercise is one important mechanism leading to exercise intolerance in patients with both end-stage renal disease (ESRD) and earlier stages of chronic kidney disease (CKD). This review will provide an overview of mechanisms underlying abnormal neurocirculatory and hemodynamic responses to exercise in patients with kidney disease. Recent studies have shown that ESRD and CKD patients have an exaggerated increase in blood pressure (BP) during both isometric and rhythmic exercise. Subsequent studies examining the role of the exercise pressor reflex in the augmented pressor response revealed that muscle sympathetic nerve activity (MSNA) was not augmented during exercise in these patients, and metaboreflex-mediated increases in MSNA were blunted, while mechanoreflex-mediated increases were preserved under basal conditions. However, normalizing the augmented BP response during exercise via infusion of nitroprusside (NTP), and thereby equalizing baroreflex-mediated suppression of MSNA, an important modulator of the final hemodynamic response to exercise, revealed that CKD patients had an exaggerated increase in MSNA during isometric and rhythmic exercise. In addition, mechanoreflex-mediated control was augmented, and metaboreceptor blunting was no longer apparent in CKD patients with baroreflex normalization. Factors leading to mechanoreceptor sensitization, and other mechanisms underlying the exaggerated exercise pressor response, such as impaired functional sympatholysis, should be investigated in future studies. Published by Elsevier B.V.
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