Muscle metaboreflex control of cardiac output and peripheral vasoconstriction exhibit different latencies

Experiments were designed to determine 1) the mechanisms mediating metabore flex-induced increases in systemic arterial pressure (SAP) in response to t otal vascular occlusion of hindlimb blood flow [e.g., increases in cardiac output (CO) vs. peripheral vasoconstriction] and 2) whether the individual mechanisms display differential latencies for the onset of the responses. R esponses were observed in seven dogs performing steady-state treadmill exer cise of mild and moderate workloads (3.2 km/h at; 0% grade and 6.4 km/h at 10% grade). Differential latencies were exhibited among CO, nonischemic vas cular conductance (NIVC; conductance to all nonischemic vascular beds), and renal vascular conductance (RVC), with peripheral vasoconstriction signifi cantly preceding metaboreflex-mediated increases in CO. In addition, the la tencies for SAP were not different from those for NIVC or RVC at either wor kload. During the lower workload there were small increases and then subseq uent decreases in CO before the metaboreflex-induced increase in CO, which did contribute somewhat to the initial increases in SAP. However, the incre ases in CO mediated by the metaboreflex occurred significantly later than t he initial increases in SAP. Therefore, we conclude that the substantial me taboreflex-mediated pressor responses that occur during the initial phase o f total vascular occlusion during mild and moderate exercise are primarily caused by peripheral vasoconstriction.