Epidural anaesthesia and cardiovascular responses to static exercise in man.

Abstract

SUMMARY1. In human subjects, sustained static contractions of the knee extensors were performed in one leg with the same absolute (10% of the initial maximal voluntary contraction) and relative (30 % of the maximal voluntary contraction immediately prior to the static exercise) intensities before and during epidural anaesthesia. Epidural anaesthesia reduced strength to 62 + 8 % of the control value and partially blocked sensory input from the working muscles. During contractions performed with the same relative force, the increases in mean arterial pressure and heart rate were greater during control contractions than during epidural anaesthesia. During contractions at the same absolute force, there was no significant difference in magnitude of cardiovascular responses between control contractions and contractions performed during epidural anaesthesia.2. The metabolic role in the exercise pressor reflex was assessed by applying an arterial leg cuff 10 s before cessation of exercise and through the following 3 min of recovery. Although mean arterial pressure and heart rate decreased immediately after cessation of exercise, application of the arterial occlusion cuff resulted in higher post-exercise mean arterial pressure and heart rate values. Control and epidural mean arterial pressures during arterial occlusion were not significantly different.3. The results of this study suggest that the reflex neural mechanism rather than the intended effort (central command) is important in determining the blood pressure and heart rate responses to static exercise in man. That is, when epidural anaesthesia diminishes sensory feedback and produces muscular weakness, central command does not determine the cardiovascular response. This conclusion, however, is opposite to that derived from experiments with partial neuromuscular blockade which demonstrated the importance of central command in determining the cardiovascular response to static exercise (Leonard, Mitchell, Mizuno, Rube, Saltin & Secher, 1985). Taken together, these two studies are complementary and support the concept that both central and reflex neural mechanisms play roles in regulating arterial blood pressure and heart rate during static exercise in man.

Limb congestion and sympathoexcitation during exercise. Implications for congestive heart failure.

“…These observations are consistent with the work ofMitchell et al (27), who demonstrated that the HR and blood pressure responses to static exercise at a given level ofrelative force were reduced by epidural anesthesia. From these results, the authors concluded that under the conditions imposed by their paradigm, sensory feedback from muscle was necessary for the full expression of central command.…”

“…These studies have suggested that HR is controlled by central command, whereas MSNA is regulated by chemically sensitive skeletal muscle afferents ( 18). We cannot entirely explain these different conclusions except to agree with Mitchell et al (27) that both central and peripheral neural mechanisms may contribute to the cardiovascular reflex response to exercise.…”

Cardiovascular and ventilatory responses to dynamic exercise during epidural anaesthesia in man.

“…In light of the above described evidence in favour of a reflex neural mechanism primarily determining the cardiovascular and ventilatory responses to dynamic exercise and the fact that epidural anaesthesia has been shown to diminish the heart rate and blood pressure responses to static exercise as compared to neuromuscular blockade (Mitchell, Reeves, Rogers & Secher, 1989;Kjoer, Secher, Reeves, Mitchell, Bach & Galbo, 1989b), it is surprising that the cardiovascular as well as ventilatory responses to dynamic exercise are not diminished in subjects studied during epidural anaesthesia (Hornbein, Sorensen & Parks, 1969;Freund et al 1979). One explanation could be the extent of the motor blockade associated with the epidural anaesthesia in those experiments.…”

“…One explanation could be the extent of the motor blockade associated with the epidural anaesthesia in those experiments. If the subjects became so weak that pedalling the cycle began to resemble intermittent 'static' exercise, then similar heart rate and blood pressure responses should be expected with and without epidural anaesthesia (Mitchell et al 1989;Kjaer et al 1989b). Consequently, we reinvestigated the influence of epidural anaesthesia on the cardiovascular and ventilatory responses to dynamic exercise attempting to obtain a minimum of motor weakness.…”

Dorsal root tetrodotoxin-resistant sodium channels do not contribute to the augmented exercise pressor reflex in rats with chronic femoral artery occlusion

“…static contraction; thin fiber muscle afferents; tetrodotoxin; sodium channel EXERCISE IS WELL KNOWN TO increase arterial pressure, heart rate (HR), and ventilation. Evidence in both animals and humans has been accumulating to demonstrate the importance of the exercise pressor reflex in evoking these effects (8,16,26,32). The afferent arm of the exercise pressor reflex arc is comprised of thinly myelinated (group III) and unmyelinated (group IV) fibers, the endings of which respond, respectively, to mechanical and metabolic stimuli arising in the contracting muscles (13,14).…”