PULSE DURING MENTAL AND PHYSICAL WORK. 239 



mean variation of the pulse-cycles after alcohol must consequently 

 be regarded as a real effect of alcohol. 



The bearing of this fact on the evidence for alcoholic partial paralysis 

 of the heart inhibitory mechanism depends on the previously discussed 

 difference between the latency of inhibitor and accelerator. Let us 

 repeat: Accelerator latency is 10" and over; inhibitor latency is less 

 than I". Consequently the first response of the heart to increased 

 muscular activity with a latency of less than one pulse-cycle is not an 

 accelerator impulse, but a release of the heart from the inhibitory 

 influence of the vasomotor centers. Similarly, normal respiratory 

 pulse-rhythms follow expiration and inspiration within one pulse-cycle. 

 Inspiration, the active phase of respiration, accelerates the heart with 

 a latent time of less than 1". Expiration retards the pulse with a 

 similar latent time. Such latency corresponds with the known latency 

 characteristic of the vagus, and fixes the respiratory rhythm as a 

 function of the inhibitory mechanism. The accelerator latency of 10" 

 absolutely precludes its participation in the pulse-changes correspond- 

 ing to our experimental processes, or to the respiratory rhythms of rest. 

 The flattening out of the respiratory and experimental rhythms after 

 alcohol is consequently due to a partial paralysis of the inhibitor. 



It might be objected that some other influences could produce the 

 same effect, as, for example, decreased depth of respiration. Such a 

 change in the respiration would be the exact opposite of that found by 

 Wilmanns 1 and Weissenfeld. 2 Unfortunately, our respiratory data 

 are too few to give us any clue to the situation. But even if it were 

 proved to exist, such a far-reaching flattening-out of respiration would 

 be as significant as the changes in the pulse. Instead of one being 

 referred to the other, doubtless both would have to be referred to a 

 common cause. Moreover, the pulse-changes after experimental move- 

 ments and other definite amounts of physical activity give us a clear 

 guarantee that we are not dealing with a mere accident of modified 

 respiration. The pulse-changes at the beginning of physical work have 

 a latency that shows them to be due to changes in the vagus tone. And 

 these work accelerations suffer even greater loss after the ingestion of 

 alcohol than the respiratory rhythm of rest. 



It should be noted that the inhibitor paralysis as affected by 30 and 

 45 c.c. of alcohol is not complete, but only partial. Even after 45 c.c. 

 of alcohol, increased activity still produced a faster pulse. This is in 

 line with other experimental facts. Gutnikow 3 showed that the vagus 

 could be stimulated by electricity in alcoholic narcosis; but in our 

 experiments the accelerating effect of muscular action is less after 

 alcohol, and the decreased mean variation indicates that its beginning- 

 is more sluggish. The whole picture of the effect of alcohol on the 



'Wilmanns, Archiv f. d. ges. Physiol., 1897, 66, p. 167. 

 2 Weissenfeld, Archiv f. d. ges. Physiol., 1898, 71, p. 60. 

 'Gutnikow, Zeitschr. f. klin. Med., 1892, 21, p. 168. 



