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Muscle Metaboreflex Induced Increases in Effective Arterial Elastance
Author(s) -
Mannozzi Joseph T,
AlHassan Mohamed,
Lessanework Beruk B,
Alvarez Alberto,
O'Leary Donal S
Publication year - 2019
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.2019.33.1_supplement.540.3
Subject(s) - cardiology , contractility , stroke volume , medicine , skeletal muscle , perfusion , cardiac output , vascular resistance , hemodynamics , heart rate , treadmill , vascular smooth muscle , blood pressure , smooth muscle
Dynamic exercise elicits robust changes in sympathetic activity in part due to accumulation of metabolites within the active skeletal muscle which activates group III and IV afferents triggering the muscle metaboreflex. This reflex raises cardiac output via tachycardia, increased ventricular contractility, and central blood volume mobilization which improves perfusion to the active skeletal muscle. An important component of maintaining exercise performance is optimal ventricular ‐ vascular coupling which can change with exercise, aging, as well as pathophysiological conditions. The effect of muscle metaboreflex activation (MMA) on ventricular ‐ vascular interactions is unknown. We hypothesized that MMA increases Effective Arterial Elastance (E a ). We utilized two previously published methods of evaluating E a (End Systolic Pressure / Stroke Volume (M 1 ) and Heart Rate x Vascular Resistance (M 2 )) at rest, during mild treadmill exercise, and during MMA induced via partial reductions in hindlimb blood flow imposed during exercise. At rest E a averaged 3.0 ± 0.1 and 3.0 ± 0.2 mmHg/mL for M 1 and M 2 , respectively. With the transition from rest to mild exercise little change in E a occurred, whereas with subsequent MMA, E a increased significantly by 33.6% ± 2.7 and 20.5% ± 2.3 for M 1 and M 2 . We conclude that MMA elicits robust increases in E a which parallel the substantial increases in ventricular performance thereby optimizing ventricular ‐ vascular coupling. Support or Funding Information Supported by HL‐55473, HL‐126706, HL120822 and R25 GM058905 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .