Metabolic acidosis augments exercise pressor responses in chronic kidney disease

Justin D. Sprick, Doree Lynn Morison, Ida T. Fonkoue, Yunxiao Li, Dana Dacosta, Derick Rapista, Hyunkyu Choi, Jeanie Park

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Chronic kidney disease (CKD) pa-tients experience augmented blood pressure (BP) reactivity during exercise that is associated with an increased risk of cardiovascular mortality. Exaggerated exercise pressor responses in CKD are in part mediated by augmented sympathetic nerve activation due to heightened muscle mechanoreflex. One mechanism that may lead to sensi-tization of the muscle mechanoreflex in CKD is metabolic acidosis. We hypothesized that CKD patients with low serum [bicarbonate] would exhibit exaggerated increases in arterial BP, greater reductions in muscle interstitial pH, and fatigue earlier during exercise compared with CKD patients with normal serum bicarbonate concentration ([bicarbonate]). Eighteen CKD participants with normal serum [bi-carbonate] (≥24 mmol/l, normal-bicarb) and 9 CKD participants with mild metabolic acidosis ([bicarbonate] range 20–22 mmol/l, low-bicarb) performed rhythmic handgrip (RHG) exercise to volitional fatigue at 40% of maximal voluntary contraction. BP, heart rate, and muscle interstitial pH using near infrared spectroscopy were measured continuously. While mean arterial pressure (MAP) increased with exercise in both groups (P ≤ 0.002), CKD with low-bicarb had an exaggerated MAP response compared with CKD with normal-bicarb (+5.9 ± 1.3 mmHg/30 s vs. +2.6 ± 0.5 mmHg/30 s, P = 0.01). The low-bicarb group reached exhaustion earlier than the normal-bicarb group (179 ± 21 vs. 279 ± 19 s, P = 0.003). There were no differences in the change in muscle interstitial pH during exercise between groups (P = 0.31). CKD patients with metabolic acidosis have augmented exercise-induced increases in BP and poorer exercise tolerance. There was no difference in change in muscle interstitial pH between groups, however, suggesting that augmented exercise BP responses in metabolic acidosis are not due to impaired muscle-buffering capacity.

Original languageEnglish (US)
Pages (from-to)R312-R318
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume317
Issue number2
DOIs
StatePublished - Aug 2019
Externally publishedYes

Bibliographical note

Funding Information:
Research reported in this publication was supported by the National Heart Lung and Blood Institution R01 HL135183 (PI: J. Park), the National Institute of Diabetes and Digestive and Kidney Diseases (T32DK007656, PI: J. Sands); and the United States Department of Veterans Affairs Clinical Sciences Research and Development Program (I01CX001065).

Publisher Copyright:
© 2019, American Physiological Society. All rights reserved.

Keywords

  • Exercise in kidney disease
  • Exercise pressor reflex
  • Neural control of circulation
  • Serum bicarbonate

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