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Role of cardiac output vs. peripheral vasoconstriction in mediating the muscle metaboreflex pressor response during dynamic exercise and post‐exercise muscle ischemia
Author(s) -
Spranger Marty D.,
Sala-Mercado Javier A.,
Coutsos Matthew,
Kaur Jasdeep,
Stayer Douglas,
O'Leary Donal S.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1091.45
Subject(s) - vasoconstriction , peripheral , cardiology , cardiac output , ischemia , medicine , heart rate , reflex , mean arterial pressure , blood pressure , anesthesia
Muscle metaboreflex activation (MMA) during sub‐maximal dynamic exercise in normal individuals increases mean arterial pressure (MAP) via increases in cardiac output (CO) with little peripheral vasoconstriction. The rise in CO occurs primarily via increases in heart rate (HR) with maintained or slightly increased stroke volume. When the reflex is sustained during recovery (postexercise muscle ischemia ‐ PEMI), HR declines yet MAP remains elevated. The role of CO in mediating the pressor response during PEMI is controversial. In five chronically instrumented canines, steady state values with MMA during mild exercise (3.2 kph) were observed by reducing hindlimb blood flow by ~60% for 3–5 minutes. MMA was followed by 60 seconds of PEMI. Control experiments consisted of normal exercise and recovery. MMA during exercise increased MAP, HR and CO by 61.4 ± 4.0 mmHg, 47.1 ± 7.8 bpm, and 2.71 ± 0.43 l/min, respectively. During sustained MMA via PEMI, MAP remained elevated and CO remained well above the normal recovery levels. Neither MMA during dynamic exercise nor during PEMI significantly affected peripheral vascular conductance. We conclude that the sustained increase in MAP during PEMI is driven by a sustained increase in CO not peripheral vasoconstriction. HL‐55743 and HL‐095819