Interaction between the muscle metaboreflex and the arterial baroreflex in control of arterial pressure and skeletal muscle blood flow

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 311; no. 5; pp. H1268 - H1276
• Main Authors: Kaur, Jasdeep, Alvarez, Alberto, Hanna, Hanna W, Krishnan, Abhinav C, Senador, Danielle, Machado, Tiago M, Altamimi, Yasir H, Lovelace, Abe T, Dombrowski, Maryetta D, Spranger, Marty D, O'Leary, Donal S
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.11.2016
• Subjects: Animals; Arterial Pressure - physiology; Baroreflex - physiology; Blood pressure; Cardiac Output - physiology; Carotid Arteries; Dogs; Exercise; Female; Heart Rate; Hindlimb - blood supply; Integrative Cardiovascular Physiology and Pathophysiology; Ischemia; Ischemia - physiopathology; Male; Muscle, Skeletal - blood supply; Muscular system; Myocardial Contraction - physiology; Pressoreceptors; Reflex; Regional Blood Flow - physiology; Vasoconstriction - physiology; ischemic active skeletal muscle; sympathetic vasoconstriction; mild dynamic exercise; carotid baroreceptor unloading; exercise pressor reflex
• DOI: 10.1152/ajpheart.00501.2016
• ISSN: 0363-6135

The muscle metaboreflex and arterial baroreflex regulate arterial pressure through distinct mechanisms. During submaximal exercise muscle metaboreflex activation (MMA) elicits a pressor response virtually solely by increasing cardiac output (CO) while baroreceptor unloading increases mean arterial pressure (MAP) primarily through peripheral vasoconstriction. The interaction between the two reflexes when activated simultaneously has not been well established. We activated the muscle metaboreflex in chronically instrumented canines during dynamic exercise (via graded reductions in hindlimb blood flow; HLBF) followed by simultaneous baroreceptor unloading (via bilateral carotid occlusion; BCO). We hypothesized that simultaneous activation of both reflexes would result in an exacerbated pressor response owing to both an increase in CO and vasoconstriction. We observed that coactivation of muscle metaboreflex and arterial baroreflex resulted in additive interaction although the mechanisms for the pressor response were different. MMA increased MAP via increases in CO, heart rate (HR), and ventricular contractility whereas baroreflex unloading during MMA caused further increases in MAP via a large decrease in nonischemic vascular conductance (NIVC; conductance of all vascular beds except the hindlimb vasculature), indicating substantial peripheral vasoconstriction. Moreover, there was significant vasoconstriction within the ischemic muscle itself during coactivation of the two reflexes but the remaining vasculature vasoconstricted to a greater extent, thereby redirecting blood flow to the ischemic muscle. We conclude that baroreceptor unloading during MMA induces preferential peripheral vasoconstriction to improve blood flow to the ischemic active skeletal muscle.