Autonomic blockade and cardiovascular responses to static exercise in partially curarized man.

Abstract

SUMMARY1. The cardiovascular responses, heart rate and mean arterial pressure, were followed in seventeen human subjects who performed static handgrip contractions for 2 min at the same absolute force (15% of the initial maximal voluntary contraction strength) before and during partial curarization. In control contractions the rate of perceived exertion was 10 exertion units, 16 units in contractions with tubocurarine which could be maintained and 20 units in contractions that could not be maintained. Control contractions increased mean arterial pressure by 6 mmHg from 89 mmHg while heart rate was unchanged from the resting value of 68 beats min-'. With tubocurarine, larger increases in mean arterial pressure of 11 mmHg and for heart rate of 8 beats min-1 were obtained during maintained contractions, and 15 mmHg and 16 beats min1. respectively, during non-maintained contractions.2. Atropine increased resting heart rate and blood pressure with tubocurarine to 107 beats min-' and 98 mmHg, respectively, in seven subjects. The blood pressure response to exercise with tubocurarine was unaffected by atropine, but the heart rate increase was reduced from 15 to 4 beats min-'.3. Propranolol reduced resting heart rate with tubocurarine to 56 beats min-1 with no effect on blood pressure in seven subjects. The cardiovascular responses to exercise with tubocurarine were unaffected by propranolol. In contrast, phentolamine reduced resting blood pressure with tubocurarine to 80 mmHg without affecting heart rate in seven subjects. Exercise responses with tubocurarine were unaffected by phentolamine. Combinations of atropine and propranolol in fourteen subjects or atropine and phentolamine in five subjects showed similar results during exercise with tubocurarine as with the sole use of the agents used to block autonomic receptors.4. The results suggest that when partial curarization induces a disproportion between the signal from central command and that from exercising muscles, the larger signal arising from central command determines the magnitude of the cardiovascular responses. The centrally generated heart rate response is in part caused by vagal withdrawal. However, the blood pressure response cannot be * Present address: Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, TX 75235-9034, USA. J. H. MITCHELL AND OTHERSattenuated by the sole use of a-or fl-receptor adrenergic blockade or combinations of these with atropine. This suggests that there may be greater redundancy in the autonomic control of blood pressure than in the vagal control of heart rate associated with central command during static exercise in man.

Autonomic Adjustments to Exercise in Humans

“…Freychuss (97) reported that an unsuccessful attempt to isometrically contract the forearm muscles, following complete neuromuscular blockade, was still accompanied by an increase in HR and BP, albeit approximately 50% of the normal response. In line with this, partial neuromuscular blockade to augment the level of central command has generally resulted in an exaggerated cardiovascular response during static and dynamic exercise (13,106,187,224,250,261,351) (Fig. 8).…”

Muscle Metaboreflex Contribution to Sinus Node Regulation During Static Exercise

“…2 This general view came from the observation that during postexercise circulatory occlusion, a maneuver that maintains muscle metaboreflex activation while removing the central command, the increases in AP, vascular resistance, and sympathetic nerve activity to resting muscles are kept elevated above resting levels, whereas HR fully recovers. [3][4][5] However, Maciel et al 6 and Martin et al 7 reported a reduced HR response to static exercise after administration of ␤-adrenergic blocking drugs, suggesting an involvement of the sympathetic nervous system in HR regulation, although the mechanism underlying the sympathetic contribution (ie, central versus reflex) has not been determined. More recently, O'Leary 8 provided evidence that sympathetic activation originating from the muscle metaboreflex contributes substantially to the HR increase during exercise in the conscious dog, inasmuch as parasympathetic blockade with atropine did not affect the increase in AP and HR that occurred during exercise but did prevent the fall in HR during postexercise circulatory occlusion.…”

The Cardioinhibitory Responses of the Right Posterior Insular Cortex in an Epileptic Patient

“…30 s) isometric handgrip contractions of moderate intensity, such as 30% maximum voluntary contraction (MVC), produce marked tachycardia that is unaffected by ␤ -adrenoceptor blockade. Also, this rapid and early HR response to volitional handgrip exercise precedes peripheral sympathetic activation by approximately 30 s and can be severely attenuated or eliminated by vagal blockade [18,[20][21][22][23] . Thus, this HR response is linked directly to vagal withdrawal.…”