The shortening of the R-R interval in response to voluntary and electrically induced isometric muscle contractions of short duration was investigated in 15 volunteers. In some of those experiments the effect of vagal blockade was also studied. The results show: 1) a lag time between the start of the contraction and the following decrease in R-R interval duration of 550 milliseconds; 2) a similar R-R interval response due to voluntary and electrically induced contractions of the same force; 3) no shortening of the R-R interval when the skin is stimulated without ensuing muscular contraction; 4) a complete disappearance of the response to isometric contractions during vagal blockade. A difference in lag time between the onset of arm contraction and cardiac acceleration could not be demonstrated. Most of the results give strong evidence to the existence of a muscle-heart reflex in man, involved in the instantaneous cardiac acceleration at the onset of exercise, that has its origin in the muscles and the vagal nerves as its efferent pathway.

Intrinsic properties of the human sinoatrial (SA) node have been shown to decline with age. In the present study we aimed at investigating the underlying mechanisms of age-dependent changes in intrinsic cycle length and sinoatrial conduction time. To this end, the cycle length and transmembrane potentials of the SA nodes of rabbits (2 days-5.6 years) and cats (6 weeks-18 years) were recorded and nodal conduction was reconstructed. The size of the SA nodes was measured in Sirius Red stained sections. Cycle length increases with age in both the rabbit and cat SA node, and in both species cycle length is dependent on diastolic depolarization rate and action potential duration. Nodal action potential duration increases with age in both rabbit and cat, whereas diastolic depolarization rate decreases in the cat only. The location of the primary pacemaker is not related to age. With age, sinoatrial conduction time increases in both species as a result of an enlargement of the area with low phase 0 upstroke velocities. The size of the SA node of adult animals does not increase with age.

In the isolated right atrium of the rabbit, premature beats were elicited by electrical stimulation. When the activation front of a premature beat did not reach the sinoatrial (S-A) node soon enough to discharge the pacemaker prematurely, the pause following the premature beat was compensatory. However, when the activation front forced the pacemaker to discharge prematurely, the premature beat cycle outlasted the normal spontaneous pause, although it was not completely compensatory. Moreover, several cycles after the premature beat were prolonged. The postextrasystolic pause lasted longer if the premature beat was elicited earlier in the atrial cycle. Several changes in the activity of the S-A node caused the prolonged diastole after the atrial premature beat; the most prominent change was a pacemaker shift that persisted several cycles after the premature beat. We found a progressive decrease of the conduction velocity within the S-A node when the latency between the spontaneous discharge of the pacemaker and the arrival of the premature impulse from the atrium in the S-A node was shortened. This may explain the occurrence within the S-A node of a shift of the pacemaker in the direction of the ectopic focus. The rhythm of the new pacemaker was slower than that of the original one. ADDITIONAL KEY WORDS diastolic depolarization pacemaker shift conduction velocityS-A node postextrasystolic pause automaticity compensatory pause transmembrane potentials stimulation• If an impulse originating from an atrial ectopic focus does not reach the sinoatrial (S-A) node before its spontaneous discharge, the lengthening of the interval after the premature beat is fully compensatory. The premature beat inhibits the conduction of the spontaneous impulse from the nodal pacemaker over the atrium. Only the next spontaneous impulse is conducted and activates the atrium. If, on the contrary, the impulse from the ectopic focus forces the pacemaker to discharge prematurely (1), the regularity of the pacemaker will be disturbed and the postextrasystolic pause will be too short to be compensatory, although longer than the normal interval. The postextrasystolic pause lengthens proFrom the Department of Physiology, University of Amsterdam, Amsterdam, The Netherlands.Received December 26, 1968. Accepted for publication February 15, 1969. gressively as the premature beat is elicited earlier in the atrial cycle, i.e., as the curtailed cycle is shorter. To explain this phenomenon, Wenckebach supposed that the conduction velocity of the impulse from an ectopic focus is less as the curtailed cycle is shorter. Eccles and Hoff (2) assumed that a temporary depression of rhythmicity also occurs.Since then, the factors determining the duration of the postextrasystolic pause have not been investigated. In the experiments presented here, we elicited premature beats in the atrium and in the S-A node by electrical stimulation and turned our attention to:(1) The relation between the durations of the curtailed cycle and postextrasystolic pause.(...

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