THE EFFECTS ON CONTRACTION OF FATIGUED MUSCLE OF
VARYING THE ARTERIAL BLOOD PRESSURE
That great excitement is accompanied by sympathetic innervations
which increase the contraction of the small arteries, render
unusually forcible the heart beat, and consequently raise arterial
pressure, has already been pointed out ( see p. 26). Indeed, the
counsel to avoid circumstances likely to lead to such excitement,
which is given to persons with hardened arteries or with weak
hearts, is based on the liability of serious consequences, either
in the heart or in the vessels, that might arise from an emotional
increase of pressure in these pathological conditions. That great
muscular effort also is accompanied by heightened arterial pressure
is equally well known, and is avoided by persons likely to be
injured by it. Both in excitement and in strong exertion the blood
is forced in large degree from the capacious vessels of the abdomen
into other parts of the body. In excitement the abdominal arteries
and veins are contracted by impulses from the splanchnic nerves.
In violent effort the diaphragm and the muscles of the belly wall
are voluntarily and antagonistically contracted in order to stiffen
the trunk as a support for the arms; and the increased abdominal
pressure which results forces blood out of that region and does not
permit reaccumulation. The general arterial pressure in man, as
McCurdy[80] has shown, may suddenly rise during extreme physical
effort, from approximately 110 millimeters to 180 millimeters of
mercury.
The Effect of Increasing Arterial Pressure
What effect the increase of arterial pressure, resulting from
excitement or physical strain, may have on muscular efficiency, has
received only slight consideration. Nice and I found there was need
of careful study of the relations between arterial pressure and
muscular ability, and, in 1913, one of my students, C. M. Gruber,
undertook to make clearer these relations.
The methods of anesthesia and stimulation used by Gruber were
similar to those described in the last chapter. The arterial blood
pressure was registered from the right carotid or the femoral
artery by means of a mercury manometer. A time marker indicating
half-minute intervals was placed at the atmospheric pressure level
of the manometer. And since the blood-pressure style, the writing
point of the muscle lever, and the time signal were all set in a
vertical line on the surface of the recording drum, at any given
muscular contraction the height of blood pressure was simultaneously
registered.
To increase general arterial pressure two methods were used: the
spinal cord was stimulated in the cervical region through platinum
electrodes, or the left splanchnic nerves were stimulated after the
left adrenal gland had been excluded from the circulation. This was
done in order to avoid any influence which adrenal secretion might
exert. It is assumed in these experiments that vessels supplying
active muscles would be actively dilated, as Kaufmann[81] has
shown, and would, therefore, in case of a general increase of blood
pressure, deliver a larger volume of blood to the area they supply.
The effects of increased arterial pressure are illustrated in Figs.
13, 14 and 15. In the experiment represented in Fig. 13, the rise
of blood pressure was produced by stimulation of the cervical cord,
and in Figs. 14 and 15 by stimulation of the left splanchnic nerves
after the left adrenal gland had been tied off.
The original blood pressure in Fig. 13 was 120 millimeters of
mercury. This was increased by 62 millimeters, with a rise of only
8.4 per cent in the height of contraction of the fatigued muscle.
[Illustration: Figure 13.--In this and the following records, the
upper curve indicates the blood pressure, the middle line muscular
contraction, and the lower line the time in 30 seconds (also zero
blood pressure.) Between the arrows the exposed cervical spinal
cord was stimulated.]
In Fig. 14 the original blood pressure was 100 millimeters of
mercury. By increasing this pressure 32 millimeters there resulted
simultaneous betterment of 9.8 per cent in the height of muscular
contraction. In Fig. 14 B the arterial pressure was raised 26
millimeters and the height of contraction increased correspondingly
7 per cent. In Fig. 14 C no appreciable betterment can be seen
although the blood pressure rose 18 millimeters.
[Illustration: Figure 14.--Stimulation of the left splanchnic
nerves (left adrenal gland tied off) during the periods indicated
by the arrows.]
In Fig. 15 the original blood pressure was low--68 millimeters of
mercury. This was increased in Fig. 15 A by 18 millimeters (the same
as in Fig. 14 C without effect), and there resulted an increase of
20 per cent in the height of contraction. In Fig. 15 B the pressure
was raised 24 millimeters with a corresponding increase of 90 per
cent in the muscular contraction; and in Fig. 15 C 30 millimeters
with a betterment of 125 per cent.
[Illustration: Figure 15.--During the periods indicated in the
time line the left splanchnic nerves were stimulated. The vessels
of the left adrenal gland were tied off.]
Comparison of Figs. 13, 14 and 15 reveals that the improvement
of contraction of fatigued muscle is much greater when the blood
pressure is raised, even slightly, from a low level, than when it
is raised, perhaps to a very marked degree, from a high level. In
one of the experiments performed by Nice and myself the arterial
pressure was increased by splanchnic stimulation from the low level
of 48 millimeters of mercury to 110 millimeters, and the height of
the muscular contractions was increased about sixfold (see Fig.
16).
[Illustration: Figure 16.--The bottom record (zero of blood
pressure) shows stimulation of left splanchnics; between the arrows
the pressure was kept from rising by compression of heart.]
Results confirming those described above were obtained by Gruber in a
study of the effects of splanchnic stimulation on the irritability of
muscle when fatigued. In a series of eleven observations the average
value of the barely effective stimulus (the “threshold” stimulus)
had to be increased as the condition of fatigue developed. It was
increased for the nerve-muscle by 25 per cent and for the muscle by
75 per cent. The left splanchnic nerves, disconnected from the left
adrenal gland, were now stimulated. The arterial pressure, which
had varied between 90 and 100 millimeters of mercury, was raised at
least 40 millimeters. As a result of splanchnic stimulation there
was an average recovery of 42 per cent in the nerve-muscle and of
46 per cent in the muscle. The increased general blood pressure
was effective, therefore, quite apart from any possible action of
adrenal secretion, in largely restoring to the fatigued structures
their normal irritability.
The Effect of Decreasing Arterial Pressure
Inasmuch as an increase in arterial pressure produces an increase
in the height of contraction of fatigued muscle, it is readily
supposable that a decrease in the pressure would have the opposite
effect. Such is the case only when the blood pressure falls below
the region of 90 to 100 millimeters of mercury. Thus if the arterial
pressure stands at 150 millimeters of mercury, it has to fall
approximately 55 to 65 millimeters before causing a decrease in
the height of contraction. Fig. 17 is the record of an experiment
in which the blood pressure was lowered by lessening the output of
blood from the heart by compressing the thorax. The record shows
that when the pressure was lowered from 120 to 100 millimeters of
mercury (A), there was no appreciable decrease in the height of
contraction; when lowered to 90 millimeters (B), there resulted a
decrease of 2.4 per cent; when to 80 millimeters of mercury (C), a
decrease of 7 per cent; and when to 70 millimeters (D), a decrease
of 17.3 per cent. Results similar to those represented in Fig. 17
were obtained by pulling on a string looped about the aorta just
above its iliac branches, thus lessening the flow to the hind limbs.
[Illustration: Figure 17.--The arrows indicate the points at which
the thorax began to be compressed in order to lessen the output of
blood from the heart.]
The region of 90 to 100 millimeters of mercury may therefore be
regarded as the _critical region_ at which a falling blood pressure
begins to be accompanied by a concurrent lessening of the efficiency
of muscular contraction, when the muscle is kept in continued
activity. It is at that region that the blood flow is dangerously
near to being inadequate.
An Explanation of the Effects of Varying the
Arterial Pressure
How are these effects of increasing and decreasing the arterial
blood pressure most reasonably explained? There is abundant evidence
that fatigue products accumulate in a muscle which is doing
work, and also that these metabolites interfere with efficient
contraction. As Ranke[82] long ago demonstrated, if a muscle,
deprived of circulating blood, is fatigued to a standstill, and
then the circulation is restored, the muscle again responds for a
short time to stimulation, because the waste has been neutralized
or swept away by the fresh blood. When the blood pressure is at
its normal height for warm-blooded animals (about 120 millimeters
of mercury, see Fig. 13), the flow appears to be adequate to wash
out the depressive metabolites, at least in the single muscle used
in these experiments, because a large rise of pressure produces
but little change in the fatigue level. On the other hand, when
the pressure is abnormally low, the flow is inadequate, and the
waste products are permitted to accumulate and clog the action of
the muscle. Under such circumstances a rise of pressure has a very
striking beneficial effect.
It is noteworthy that the best results of adrenin on fatigued
muscle reported by previous observers were obtained from studies on
cold-blooded animals. In these animals the circulation is maintained
normally by an arterial pressure about one-third that of warm-blooded
animals. Injection of adrenin in an amount which would not shut off
the blood supply would, by greatly raising the arterial pressure,
markedly increase the circulation of blood in the active muscle.
In short, the conditions in cold-blooded animals are quite like
those in the pithed mammal with an arterial pressure of about 50
millimeters of mercury (see Fig. 16). Under these conditions the
improved circulation causes a remarkable recovery from fatigue. That
notable results of adrenin on fatigue are observed in warm-blooded
animals only when they are deeply anesthetized or are deprived of
the medulla was claimed by Panella.[83] He apparently believed that
in normal mammalian conditions adrenin has little effect because
quickly destroyed, whereas in the cold-blooded animals, and in
mammals whose respiratory, circulatory, and thermogenic states are
made similar to the cold-blooded by anesthesia or pithing, the
contrary is true. In accordance with our observations of the effects
of blood pressure on fatigued muscle, we would explain Panella’s
results not as he has done but as due to two factors. First, the
efficiency of the muscle, when blood pressure is low, follows the
ups and downs of pressure much more directly than when the pressure
is high. And second, a given dose of adrenin always raises a low
blood pressure in atonic vessels. The improvement of circulation
is capable of explaining, therefore, the main results obtained in
cold-blooded animals and in pithed mammals.
Oliver and Schäfer reported unusually effective contractions in
muscles removed from the body after adrenal extract had been
injected. As shown in Fig. 16, however, the fact that the circulation
_had been_ improved results in continued greater efficiency of the
contracting muscle. Oliver and Schäfer’s observation may reasonably
be accounted for on this basis.
The Value of Increased Arterial Pressure in
Pain and Strong Emotion
As stated in a previous paragraph, there is evidence that the
vessels supplying a muscle dilate when the muscle becomes active.
And although the normal blood pressure (about 120 millimeters of
mercury) may be able to keep adequately supplied with blood the
single muscle used in our investigation, a higher pressure might
be required when more muscles are involved in activity, for a more
widely spread dilation might then reduce the pressure to the point
at which there would be insufficient circulation in active organs.
Furthermore, with many muscles active, the amount of waste would
be greatly augmented, and the need for abundant blood supply would
thereby to a like degree be increased. For both reasons a rise
of general arterial pressure would prove advantageous. The high
pressure developed in excitement and pain, therefore, might be
specially serviceable in the muscular activities which are likely
to accompany excitement and pain.
In connection with the foregoing considerations, the action
of adrenin on the distribution of blood in the body is highly
interesting. By measuring alterations in the volume of various
viscera and the limbs, Oliver and Schäfer[84] proved that the
viscera of the splanchnic area--e. g., the spleen, the kidneys,
and the intestines--suffer a considerable decrease of volume when
adrenin is administered, whereas the limbs into which the blood is
forced from the splanchnic region actually increase in size. The
action of adrenin indicates the relative degrees of sympathetic
innervations. In other words, at times of pain and excitement
sympathetic discharges, probably aided by the adrenal secretion
simultaneously liberated, will drive the blood out of the vegetative
organs of the interior, which serve the routine needs of the body,
into the skeletal muscles which have to meet by extra action the
urgent demands of struggle or escape.
But there are exceptions to the general statement that by adrenin
the viscera are emptied of their blood. It is well known that
adrenin has a vasodilator, not a vasoconstrictor, action on the
arteries of the heart; it is well known also that adrenin affects
the vessels of the brain and the lungs only slightly if at all.
From this evidence we may infer that sympathetic impulses, though
causing constriction of the arteries of the abdominal viscera, have
no effective influence on those of the pulmonary and intracranial
areas and actually increase the blood supply to the heart. Thus the
absolutely and immediately essential organs--those the ancients
called the “tripod of life”--the heart, the lungs, the brain (as
well as its instruments, the skeletal muscles)--are in times of
excitement abundantly supplied with blood taken from organs of less
importance in critical moments. This shifting of the blood so that
there is an assured adequate supply to structures essential for the
preservation of the individual may reasonably be interpreted as
a fact of prime biological significance. It will be placed in its
proper setting when the other evidence of bodily changes in pain
and excitement have been presented.
REFERENCES
[Footnote 80: McCurdy: American Journal of Physiology, 1901, v, p.
98.]
[Footnote 81: Kaufmann: Archives de Physiologie, 1892, xxiv, p.
283.]
[Footnote 82: Ranke: Archiv für Anatomie, 1863, p. 446.]
[Footnote 83: Panella: Archives Italiennes de Biologie, 1907,
xlviii, p. 462.]
[Footnote 84: Oliver and Schäfer: Journal of Physiology, 1895,
xviii, p. 240.]