EDO s. | Innervation of Antagonstic Muscles. 65 
down. On withdrawing the stimulus contraction-phase again appeared 
almost as intense as on the next previous withdrawal (fig. 8, B). By 
repeating and withdrawing the stimulus a new series was obtained. This 
declined more rapidly than the former one, and when its contraction-phases 
had died out a further strengthening of the stimulus induced a new and still 
more rapidly-declining series. It is clear, therefore, that in the first series 
the contraction-phase had been exhausted only relatively to the intensity 
of the external stimulus used in that series. A stronger stimulus was 
still able to evoke more contraction-phase. I have shown a similar relation 
to exist between fatigue of reaction and intensity of stimulus in the scratch- 
reflex of the spinal dog.* On the whole, in my experience the contraction- 
phase is relatively little resistant to fatigue. It will often disappear for 
a given stimulus in three or four severe repetitions of that stimulus. It 
seems to wear out more rapidly than does the inhibition-phase of the same 
reflex. It wears out especially rapidly when the reflex excitability of the 
preparation is low, ¢g., under shock, general exhaustion, etc. 
It was said above that the contraction-phase is easily suppressed by 
chloroform narcosis. In the bulbospinal animal exhibiting extensor rigidity, 
a very considerable depth of chloroform or ether narcosis is required to 
abolish the rigidity. A depth of narcosis less than that required to abolish 
the rigidity of the muscles abolishes the contraction-phase of the “ flexion- 
reflex’ in them. When under deepening narcosis the stimulus for the 
“ flexion-reflex” is repeated at suitable intervals, the contraction-phase 
following each inhibitory relaxation of the extensor muscle becomes less, 
and finally unobtainable before extinction of the decerebrate rigidity, and 
while the inhibitory relaxation of the muscle is still obtainable. Conversely, 
after chloroform narcosis has been pushed to the extreme of abolishing all 
reflex reaction, on lightening the narcosis the decerebrate rigidity reappears, 
and the reflex inhibitory relaxation of the extensors becomes demonstrable 
at:a time when there is still no obtaining of the contraction-phase withdrawal 
of the inhibitory stimulus, occasioning no rebound contraction of the muscle. 
Asphyxial conditions tend, as is well known, to augment some reflex 
reactions before finally paralysing them. The “ flexion-reflex” is, as I have 
frequently seen in working with the spinal mammal, one of the reactions 
thus increased by impending asphyxia. It might, therefore, be thought that 
the appearance of the contraction-phase of the extensors in this reflex was 
attributable to a super-excitability, due to insufficient aeration of the blood 
from imperfect respiratory ventilation in the paralysed animal. This is not 
so; on the contrary, defective pulmonary ventilation and experimental 
—* ‘Journ. of Physiology,’ vol. 34, p. 42, 1906. 
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