Jere H. Mitchell

Cardiovascular control during exercise: Central and reflex neural mechanisms

Both reflex neural and central command mechanisms have been postulated to explain the cardiovascular responses that occur during exercise. The 2 mechanisms appear to affect the same neural circuits and to be capable of working either in conjunction with one another or independently.

Regional blood flow responses to stimulation of the subthalamic locomotor region

Recent studies have suggested that descending central command from an area in the diencephalon (subthalamic locomotor region - STLR) is involved in the control of ventilation, arterial pressure and heart rate during exercise. The purpose of this study was to determine if electrical activation of the STLR in anesthetized cats elicits changes in regional blood flow and vascular resistances similar to those evoked by exercise. Therefore, organ blood flows (radioactive microsphere technique), arterial pressure (AP), heart rate (HR), and respiratory output (quantified from phrenic nerve activity) were recorded during resting conditions and during STLR stimulation. Stimulation of the subthalamic locomotor region produced increases in AP, HR and respiratory output similar to those reported previously. These changes were accompanied by increased blood flow to the heart, diaphragm and limb skeletal muscles. A concomitant decrease occurred in blood flow to the kidneys. In addition, the vascular resistances of the intestines, gallbladder and stomach increased. These vascular and respiratory responses are similar to those occurring during static exercise in conscious cats.

Static exercise in anesthetized dogs, a cause of reflex alpha-adrenergic coronary vasoconstriction

SummaryThe coronary blood flow and vascular resistance responses to static hindlimb exercise were studied in 11 anesthetized dogs after β- and combined α- and β-adrenergic blockade to determine if this stress causes coronary vasoconstriction. After β-blockade static exercise increased the blood pressure and double product, but decreased the right and left ventricular (LV) coronary blood flow and increased the coronary vascular resistance. These vascular changes primarily occurred in the epicardial and mid-myocardial but not the endocardial layers of the LV. Following combined α- and β-adrenergic blockade, the systemic hemodynamic and coronary flow and resistance changes were abolished. These data suggest that α-adrenergic mediated coronary vasoconstriction occurs during static hindlimb exercise in dogs.

Cardiac changes to signalled shock avoidance in dogs.

Abstract Alterations in heart rate (HR), left ventricular pressure (LVP), and maximum left ventricular dp/dt (LVdp/dt max) during a signalled avoidance task were studied in eight chronically prepared dogs. Four of these animals comprised a non-shock control group. In experimental animals, HR increased during the first two days of the avoidance task but did not change significantly during the last two days, while LVP remained at the supranormal post-training levels and LVdp/dt max increased over the course of the experiment. Control animals showed no change in HR or LVP, but LVdp/dt max decreased over the four experimental days. Changes in LVdp/dt max in experimentals reflect a consistent increase in cardiac sympathetic activation. However, HR changes indicate an initial increase and a subsequent decrease in sympathetic activity. It was therefore postulated that either differential activation of sympathetic cardiac fibers occurred such that during non-stress periods and subsequent exposure to stress, sympathetic influences predominate which are reflected only in LVdp/dt max changes, or sympathetic and parasympathetic fibers differentially control cardiac function during stress and non-stress conditions.