Role of cardiac output versus peripheral vasoconstriction in mediating muscle metaboreflex pressor responses: dynamic exercise versus postexercise muscle ischemia

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 304; no. 8; pp. R657 - R663
• Main Authors: Spranger, Marty D, Sala-Mercado, Javier A, Coutsos, Matthew, Kaur, Jasdeep, Stayer, Doug, Augustyniak, Robert A, O'Leary, Donal S
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 15.04.2013
• Subjects: Animals; Arterial Pressure - physiology; Baroreflex - physiology; Cardiac Output - physiology; Cardiomyocytes; Data Interpretation, Statistical; Dogs; Exercise; Female; Heart rate; Heart Rate - physiology; Hindlimb - blood supply; Ischemia; Male; Muscle, Skeletal - blood supply; Muscle, Skeletal - metabolism; Muscle, Skeletal - physiology; Neural Control; Physical Exertion - physiology; Physiology; Reflex - physiology; Regional Blood Flow - physiology; Stroke; Stroke Volume - physiology; Vasoconstriction - physiology; Ventricular Function, Left - physiology
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00601.2012

Muscle metaboreflex activation (MMA) during submaximal 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 seven chronically instrumented canines, steady-state values with MMA during mild exercise (3.2 km/h) were observed by reducing hindlimb blood flow by ~60% for 3-5 min. MMA during exercise was followed by 60 s of PEMI. Control experiments consisted of normal exercise and recovery. MMA during exercise increased MAP, HR, and CO by 55.3 ± 4.9 mmHg, 42.5 ± 6.9 beats/min, and 2.5 ± 0.4 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.