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Modulation of cardiac output alters the mechanisms of the muscle metaboreflex during dynamic exercise
Author(s) -
Ichinose Masashi,
SalaMercado Javier A,
Coutsos Matthew,
Li ZhenHua,
Ichinose Tomoko K,
O'Leary Donal S
Publication year - 2009
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.23.1_supplement.787.4
Subject(s) - vasoconstriction , cardiac output , medicine , cardiology , peripheral , blood pressure , chemistry , endocrinology , anesthesia
Muscle metaboreflex activation (MMA) in conscious dogs during mild to moderate exercise elicits a pressor response primarily due to an increased cardiac output (CO). However, when the ability to increase CO is limited, such as in heart failure or during maximal exercise, the MMA‐induced increases in arterial pressure (AP) occur solely via peripheral vasoconstriction. However, how the mechanisms of this pressor response are altered is unknown. We tested the hypothesis that this change in metaboreflex function from increased CO to increased vasoconstriction is dependent on the level of CO. The muscle metaboreflex was activated during mild dynamic exercise (3.2 km/h) via partial reduction of hindlimb blood flow. MMA increased CO and AP while vascular conductance of all non‐ischemic areas (NIVC) did not change. CO was then reduced to the same level observed during exercise prior to MMA via partial occlusion of the inferior and superior vena cavae. AP dropped rapidly with the reduction in CO but subsequently nearly completely recovered. With the removal of the MMA‐induced rise in CO, NIVC decreased sharply. We conclude that whether vasoconstriction occurs with MMA depends on whether CO rises. NIH HL 55473