Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Abstract

DS. Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise. Am J Physiol Heart Circ Physiol 292: H2159 -H2166, 2007. First published December 22, 2006; doi:10.1152/ajpheart.01240.2006.-Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP); however, in heart failure (HF) although MAP increases, the rise in CO is virtually abolished, which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals are abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, and left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance (E max) and preload-recruitable stroke work (PRSW)] at rest and during mild and moderate exercise under free-flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing-induced HF. In control experiments, MMR activation at both workloads [mild exercise (3.2 km/h) and moderate exercise (6.4 km/h at 10% grade)] significantly increased CO, E max, and PRSW. In contrast, after HF was induced, CO, Emax, and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, E max and PRSW did not change. In addition, MMR activation caused no significant change in CO, E max, or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but that this ability is abolished in HF. pressor response; elastance; preload recruitable stroke work WHEN EXERCISING SKELETAL MUSCLE does not receive sufficient blood flow to meet the ongoing metabolic demands, by-products of metabolism such as lactic acid, H ϩ , adenosine, potassium, diprotonated phosphate, and arachidonic acid products, among others, accumulate within the muscle and stimulate group III and IV afferent neurons, which evokes a reflex response known as the muscle metaboreflex (MMR). This reflex response consists of increases in efferent sympathetic nerve activity (SNA) and mean arterial pressure (MAP) (1, 3, 11, 17, 18, 24, 31-35, 39, 40, 43, 46, 47, 52, 53). In addition, MMR activation causes increases in cardiac output (CO), heart rate (HR), and plasma levels of vasoactive hormones and produces vasoconstriction in the renal and the nonischemic active skeletal muscle vasculature to partially restore arterial O 2 delivery and blood flow to the hypoperfused muscles (25,33,36). The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (32,42,43). By this means the MMR-induced increases in ventricular performance act to slightly increase or sustain stroke volume (SV) despite decreas...

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

“…Steady-state data were recorded at rest, while the animal was standing on the treadmill, during exercise with unrestricted blood flow to the hindlimbs, and after metaboreflex activation elicited by reductions in HLBF achieved by partial inflation of the terminal aortic occluder, as previously described (49). After completion of the control experiments, modest congestive heart failure was induced via rapid ventricular pacing, as previously described by us and others (26,36). Briefly, the heart was paced at 240 -250 beats per minute (bpm) for ϳ30 days, and the experiments were repeated while in modest heart failure conditions [defined as resting tachycardia, reduced CO, SV, and left ventricular ϩ/ϪdP/dt, as described in our previous studies (8,14,36)].…”

Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

“…After all hemodynamic values had reached steady state, data were collected for ϳ 3-5 min. After completion of control experiments, modest congestive HF was induced via rapid ventricular pacing, a technique widely accepted to create a chronic model of ventricular failure (23,28). Briefly, the right ventricular pacing electrodes were connected to an external pacemaker set at 240 -250 beats/min for ϳ30 days.…”

“…Briefly, the right ventricular pacing electrodes were connected to an external pacemaker set at 240 -250 beats/min for ϳ30 days. After an induction of modest HF (defined as resting tachycardia, reduced CO, SV, and maximum and minimum first derivative of left ventricular pressure) as described in our previous studies (8,9,14,28), the experiments were repeated. The pacemaker was turned off before each experiment, and data collection began after the hemodynamic variables had reached steady state (ϳ30 min).…”

Comportamento do ergorreflexo na insuficiência cardíaca

“…Hence, the authors concluded that, in HF, the capacity of the muscle metaboreflex to increase the ventricular function through increases in contractility and filling pressure is evidently decreased 43 .…”