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					J. Physiol. (1974), 240, pp. 111-124                                               111
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  BLOOD FLOW IN RESTING (CONTRALATERAL) ARM AND
        LEG DURING ISOMETRIC CONTRACTION
        BY BRITA EKLUND, L. KAIJSER AND E. KNIJTSSON
          From the Department of Clinical Physiology, Karolinska
                      8jukhuset, Stockholm, Sweden
                             (Received 7 December 1973)
                                       SUMMARY
   1. Blood flow in resting forearm and calf were measured plethysmo-
graphically in healthy young men during isometric contraction performed
both as a handgrip and as a dorsiflexion of the foot. The isometric contrac-
tion was maintained for 2 min at one third maximal voluntary contraction
for the handgrip and half maximal voluntary contraction for the dorsi-
flexion of the foot. In some experiments the possible influence on blood
flow of inadvertent muscle activation in the resting limb was checked by
recording the e.m.g.
   2. Both handgrip and dorsiflexion of the foot produced substantial
increases in heart rate and mean arterial pressure, the pressure rise being
almost linear with time throughout the contraction.
   3. Isometric contraction produced a rapid increase in forearm blood
flow which reached a maximum on average two and a half times the resting
value after 1 min and then declined slightly. Similar increases in forearm
blood flow were produced by handgrip and dorsiflexion of the foot.
   4. Unlike in the resting forearm, the blood flow in the resting calf
increased only slightly during the first minute of contraction and then
decreased again to the resting level.
   5. The flow increase in the resting limbs could not be ascribed to inad-
vertent muscle activation as judged from the e.m.g. recordings.
   6. It is concluded that isometric muscle contraction produces a rapid
increase in blood flow in the resting forearm, but only a very slight flow
increase in the calf. Since the flow increased faster than the arterial pres-
sure it must to a certain extent be induced by active neurogenic vasodila-
tation. Similarly, the relative flow decrease during the latter half of the
contraction concomitantly with a progressively rising arterial pressure
suggests that the neurogenic effect on the resistance vessels changes
character, becoming more vasoconstrictive, and this might be related to
increased effort in sustaining the contraction.


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112     BRITA EKLUND, L. KAIJSER AND E. KNUTSSON
                                   INTRODUCTION
   During heavy dynamic exercise, such as that performed on a cycle
ergometer, the forearm blood flow has been shown to decrease despite the
simultaneous increase in arterial pressure (Blair, Glover & Roddie, 1961;
BevegArd & Shepherd, 1966). BevegArd & Shepherd, however, invariably
found this decrease to be preceded by a transient increase in flow. Iso-
metric contraction, on the other hand, is accompanied by a more pro-
nounced increase in arterial pressure (Tuttle & Horvath, 1957; Lind, Taylor,
Humphreys, Kennelly & Donald, 1964). Despite the increased arterial
pressure, Lind et al. observed that during a sustained handgrip contraction
the blood flow in the resting contralateral forearm usually remained
unchanged, thus indicating an increased vascular resistance. In some of the
subjects, however, an increase in blood flow in the resting forearm was
recorded, but it was suggested that this was the consequence of inadvertent
muscle activation which could be detected from the electromyogram. The
increased vascular resistance in the resting forearm has been ascribed to
a generalized increase in vasomotor sympathetic outflow (Blair et al. 1961;
BevegArd & Shepherd, 1966). Delius, Hagbarth, Hongell & Wallin (1972)
were able to record an increased activity in sympathetic nerves in the
resting forearm and a concomitant reduction in its blood flow during
isometric contraction of leg muscles.
   Comparing the results obtained by Blair et al. (1961) and BevegArd &
Shepherd (1966) during dynamic work to those obtained by Lind et al.
(1964) during isometric contraction, there still remains a divergence of
opinion concerning the blood flow pattern in a resting limb during muscle
activity. Furthermore, Lind et al. found that although the resting forearm
blood flow usually remained unchanged during handgrip contraction, the
cardiac output increased substantially. This increase was not accounted
for by the increased blood flow in the contracting forearm or in the renal,
splanchnic and cutaneous vascular beds. Thus assuming that the blood
flow in the resting forearm is representative of the blood flow in resting
muscles generally, it still remains to be ascertained which tissues receive the
increased cardiac output. The aims of our investigations were threefold:
first, to investigate further the blood flow pattern in resting limbs during
isometric contraction, secondly, to determine whether the flow in resting
upper and lower limbs was influenced in the same manner by contraction,
and thirdly, to establish whether or not there were any differences in
resting limb flow between a contraction with the upper and lower limb,
which might indicate a segmental discrimination in vasomotor outflow
related to the activated muscles.


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       RESTING LIMB FLOW IN MUSCLE CONTRACTION 113

                                      METHODS
                                       Subjects
  Fourteen healthy men of average physical fitness aged 25-31 yr and whose informed
consent had been obtained took part in this study. Most of them had volunteered for
several previous studies in which limb blood flow had been measured in varying kinds
of work and could thus be considered as familiar with the procedures used.

                                       Procedures
  All subjects were studied in the supine position with the limbs at heart level. The
blood flow in the resting limb during isometric contraction was recorded in four sets
of experiments: (1) resting forearm flow during isometric handgrip, (2) resting leg
flow during isometric handgrip (3) resting forearm flow during isometric dorsi-
flexion of the foot, and (4) resting leg flow during isometric dorsiflexion of the foot.
All fourteen subjects took part in the first set of experiments, ten in the second,
and six of the subjects took part in all four sets. In a fifth series of experiments
electromyographic recordings were taken in two subjects to determine the degree of
inadvertent activation of the resting arm. Here, the relation between forearm blood
flow and average electromyographic activity in the same arm during voluntary
forearm muscle activity was also studied. The object of this set of experiments was
to estimate to what extent inadvertent muscle activity could have contributed to
changes in blood flow in the resting arm.
   I8ometric handgrip was performed on a strain-gauge hand-dynamometer with
immovable handles (Flygtekniska Forsoksanstalten, Stockholm). The force deve-
loped was shown to the subject on an oscilloscope. The handgrip was held for 2 min
at one third of maximal voluntary contraction (MVC) which had been determined
beforehand. With the dynamometer used, healthy young male subjects generally
sustain this force for about 2 min before fatigue ensues (our observations, cf.
Clarke, Hellon & Lind, 1958). MVC ranged between 45 and 75 kp.
   Isometric contraction with the lower limb was performed as a dorsiflexion of the
foot, the foot being at right angles to the leg, and the forefoot connected to a strain-
gauge by a non-compliant strap (Bofors BK-1). It was possible to perform this type
of leg muscle contraction without a noticeable simultaneous contraction of trunk
muscles. Previous tests showed that in this type of contraction one third MVC did not
result in the same increase in heart rate or in a similar perception of exertion as the
handgrip. Therefore one-half MVC was used and, as in the handgrip experiments,
sustained for 2 min. MVC for the dorsiflexion ranged between 16 and 24 kp.
   Each type of contraction was repeated 2-3 times with resting intervals of 10-15
min. Heart rate and intra-arterial pressure were recorded continuously before, during,
and for 2 min after the contraction. Plethysmographic inflow curves in the resting
limb under study were recorded at the shortest possible intervals for 2 min before,
during and for 2 min after the contraction. Heart rate was obtained from an e.c.g.
recording. Intra-arterial pressure was measured with a capacitance transducer
(EMT 35) through a Teflon catheter percutaneously introduced into the brachial
artery and recorded with a Mingograf 81 (Siemens-Elema, Stockholm, Sweden).
Mean pressure was obtained by electrical integration (time constant 1 sec). Blood
flow in the resting arm or leg was measured by venous occlusion plethysmography
with an air-filled plethysmograph placed around the forearm or calf, according to
Dohn (1956) and Graf & Westersten (1959). The circulation in the hand or the foot
was occluded by a cuff inflated to 240 mmHg. Forearm and calf vascular resistance


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114      BRITA EKLUND, L. KAIJSER AND E. KNUTSSON
was calculated as brachial artery mean pressure (mmHg) divided by the plethysmo-
graphically recorded flow (ml. x min- x 100 ml.-1).
   The electromyographic activity was picked up by three concentric bipolar needle
electrodes positioned in different parts of the forearm musculature. The potentials
were amplified in differential a.c. amplifiers (Grass TP 3) with a linear frequency
response between 4 and 10,000 Hz. The myosignals were displayed on an oscilloscope,
and during some of the contractions were fed into a loudspeaker thus providing the
subject with a rough indication of muscular activity. The potentials were also
rectified and time averaged (time constant 0 05 see), the integrated e.m.g. being
displayed on an ink-writer. E.m.g. recordings from the resting forearms were taken
simultaneously with plethysmographic flow measurements during contralateral
handgrip contraction of one third MVC for 2 min in order to study to what extent
involuntary activation took place. The studies were made both with the loudspeaker
switched on and off so as to check to what extent inadvertent activation could be
avoided by making the subject aware of this. In addition, forearm blood was
measured in the previously resting arm at low degrees of voluntary activity when the
subject, helped by the loudspeaker signal, maintained for 2 min a reasonably con-
stant degree of forearm muscle activity. This ranged in different experiments from
the largest inadvertent activity observed at any time during contralateral handgrip
to an activity giving 10 times larger amplitude of the integrated e.m.g.


                                        RESULTS
   Values in the text are given as mean + S.D. unless otherwise stated.
   1. Handgrip - resting forearm flow (Table 1). Handgrip quite rapidly
increased the heart rate by about 30 beats/min during the first minute of
contraction. During the remainder of the contraction only a small further
increase occurred. The mean arterial pressure increased almost linearly
with time throughout the contraction, and was terminally about 40 mmHg
higher than at rest.
   The blood flow in the resting forearm increased in all subjects, reaching
a mean maximal value of about 2-5 times higher than at rest, at about
70 sec after the start of contraction. The magnitude of the increase ranged
from 50-450% in the different subjects. In many subjects, a marked
increase in flow occurred already during the first 30 see, before the arterial
pressure was substantially increased. In eleven of the fourteen subjects the
flow again decreased towards the end of the contraction, when, however,
the mean flow for the group still remained twice the resting value. Immedi-
ately at the end of the contraction the flow fell, stabilizing at the pre-
contraction level within about 30 sec. Base-line artifacts, due to involuntary
muscle contraction or Valsalva manoeuvre, were only rarely observed.
Fig. 1 is an example of the cardiovascular changes in one subject.
  The calculated vascular resistance in the resting forearm decreased
significantly during the first minute of contraction to about half of the
resting value at the time of maximal flow. Then it again increased slightly
but at the end of the contraction it was still about 25 % lower than at rest.

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       RESTING LIMB PLOW IN MUSCLE CONTRACTION 115
   2. Handgrip - resting calf flow. Blood flow in the resting calf increased
slightly but significantly (P < 0.01) by about 50% during the first minute
of contraction (range 15-90%). In all subjects the increase was far smaller

        I 100
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                               I       1       '3       MVC I        J    I
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                                            Time (min)
    Fig. 1. Heart rate (H.R.), arterial mean pressure (Pbr.,J) and blood flow
    (B.F.) in the resting (contralateral) forearm in one subject during two
    successive isometric handgrip contractions with one third of MVC. Filled
    symbols denote the first contraction, unfilled symbols the second.

than that in the resting forearm. Taken as a percentage, it was not signi-
ficantly greater than the increase in mean arterial pressure, and hence the
calculated calf vascular resistance was not significantly changed. During the
second minute of contraction, however, when the arterial pressure con-
tinued to increase, calf flow again decreased to the resting level, thus


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116 BRITA EKLUND, L. KAIJSER AND E. KNUTSSON
signifying an increase in vascular resistance which was then about 30%
above the resting value (P < 0 05; Fig. 2).
   3. Upper limb - lower limb contraction. The heart rate increase during
dorsiflexion of the foot was of the same magnitude and followed the same
course as that during handgrip. However, the increase in arterial pressure
was slightly less marked during dorsiflexion than handgrip (Fig. 3), and
                            110   _
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                            10
                                      Rest   Max        End
                                               Contraction
   Fig. 2. Heart rate (n.R.), arterial mean pressure (Pbr.Y4), blood flow (B.F.)
   in the resting forearm and calf and calculated forearm and calf vascular
   resistances at rest and during isometric handgrip contraction. Values at rest,
   at the time ofmaximal flow increase and at the end ofthe contraction period.
   Filled symbols: handgrip contraction and forearm blood flow, open
   symbols: handgrip contraction and leg blood flow. Mean + S.D. R, units of
   resistance.


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      RESTING LIMB FLOW IN MUSCLE CONTRACTION 117
hence for a given increase in heart rate handgrip increased arterial pressure
more than dorsiflexion (Fig. 4).
  Handgrip caused the same change in forearm blood flow as dorsiflexion
of the foot; the changes in calf blood flow were the same no matter whether
the exercise was done with the upper or the lower limb (Fig. 3). However the
                  110

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              Contraction: Hand Leg          Hand Leg         Hand Leg
                   70

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              1430L j l 1
                             Rest              Max                 End
                                                     Contraction
    Fig. 3. Heart rate (n.R.), arterial mean pressure (Pbr a), blood flow (B.F.)
    in the resting forearm and the resting calf and the calculated forearm and
    calf vascular resistances at rest and during isometric handgrip and isometric
    leg contraction. Values at rest, at the time of maximum flow increase and at
    the end of the contraction period. Filled symbols: values during forearm
    flow measurement, open symbols: values during calf flow measurement.
    The first two symbols at each time: handgrip contraction; the third and the
    fourth symbol: leg contraction. Mean + S.D.


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118 BRITA EKLUND, L. KAIJSER AND E. KNUTSSON
changes in the resting forearm and calf blood flows during the handgrip
were quantitatively a little greater than those accompanying dorsiflexion
of the foot, probably because the rise in arterial blood pressure was greater.
                    50

                         40~~~~~~~~


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                    30
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                                                          0
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                             I       I
                             10      20        30         40       50
                                       A H.R. (beats/min)
    Fig. 4. Increase in mean arterial pressure and heart rate at the end of iso-
    metric handgrip contraction (filled symbols) and isometric leg contraction
    (open symbols) in six subjects. Each dot represents the mean of 4-6 deter-
    minations in one subject.

   4. E.m.g. When the subjects performed a handgrip with the loudspeaker
switched off, no electromyographic activity, or occasionally short bursts of
low degree activity, were recorded during the first minute of contraction.
However, during the second minute often an almost continuous motor unit
discharge was observed. The degree of muscle activity was low judging
from the e.m.g. showing discharges of low frequencies in one or a few motor
units. No changes in forearm blood flow were observed to accompany the
short bursts of e.m.g. activity. When the attention of the subjects was
drawn to involuntary activation in the resting arm by loudspeaker, it was
often possible to lessen the length of time during which activity occurred.
However, the magnitude or pattern of flow increase during contralateral
handgrip remained unchanged. When the subjects, guided by the loud-
speaker, maintained a constant degree of e.m.g. activity in the forearm for
2 min, it was then possible to increase muscle activity so that the amplitude
of the integrated e.m.g. was 4-S times the highest amplitude produced in-
voluntarily during contraction of the contralateral arm, without any effect
on the forearm blood flow. Not until the integrated e.m.g. activity had


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      RESTING LIMB FLOW IN MUSCLE CONTRACTION 119
increased to 8-10 times that value did a significant increase in forearm
blood flow occur. This degree of electromyographic activity invariably
produced base-line movement artifacts in the plethysmographic recordings.
This information made it possible to ascertain that no muscle activation
influencing blood flow occurred in the resting limb also when e.m.g. was not
recorded.
TABLE 1. Heart rate, mean arterial pressure, forearm blood flow and forearm
vascular resistance changes in the resting arm during contralateral isometric
handgrip contraction in fourteen subjects. Values are given as mean+S.D. at
rest, at the time for the maximum flow increase and at the end of the contraction
period. *** (P < 0*001) and ** (P < 0*01) in superscript denotes the significance
of the difference from the resting value, ** in subscript denotes the difference from
the time of maximal flow increase
                                           Rest            Max              End
Heart rate   (beats/min)                  61+ 7         88 i 9***        95 + 10*
                                                                                *
PbrA.mean (mmnHg)                         85± 7        112 ± 15***      125 ± 19
Forearm blood flow                       3-8 ± 1.3    10-6 ± 3-8***     7-8 ± 2-5 *
 (ml. x min-' x 100 ml.-l)
Resistance                               26+ 8          13 ± 5***        19 + 7*
 (mmHg/[ml. X mi.-' x 100 ml.-L])

                                     DISCUSSION
   Isometric contraction, both handgrip and dorsiflexion of the foot,
resulted in a substantial heart-rate increase and an increase in arterial
pressure which, in relation to the heart-rate increase, was far more pro-
nounced than that during dynamic work (cf. Holmgren, 1956). These
findings are in agreement with earlier studies of the cardiovascular effects
of isometric contractions (Tuttle & Horvath, 1957; Lind et al. 1964).
Associated with these changes was an increase in the blood flow in the
resting forearm. Although the increase in flow was variable the average
rise far exceeded that in arterial mean pressure, thus signifying a substan-
tial decrease in forearm vascular resistance. This finding does not fully
agree with that of Lind et al. (1964). Although they occasionally found
a flow increase under similar circumstances, they regarded it as an
exception rather than the rule, and attributed it to inadvertent activation
in the resting arm, which could also be detected electromyographically.
The flow increase in the resting forearm found in the present study was not
due to inadvertent muscle activation, since (i) the maximal flow was
recorded in the early contraction phase when electromyographic activity
was only rarely recorded, (ii) when bursts of e.m.g. activity were recorded
in this phase of a contraction no concomitant increases in flow were seen,
(iii) in order to produce a detectable blood flow increase in the previously


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120 BRITA EKLUND, L. KAIJSER AND E. KNUTSSON
resting forearm a degree of voluntary muscle activation was needed to
increase the amplitude of the integrated e.m.g. 5-10 times above the
highest spontaneous amplitude appearing in the resting arm during con-
tralateral handgrip contraction. Thus, at the present time, it appears
difficult to account for the difference between our data and those of Lind
et al., although the great inter-individual variation which we found,
together with the fact that Lind et al. presents data from only four subjects,
might, at least in part, be the explanation.
   The decreased vascular resistance in the forearm might result either from
passive distension produced by the increased intravascular pressure, or
from a decrease in neurogenic vasoconstrictor activity, or from an increase
in neurogenic vasodilator activity. Although the present experiments were
not designed to differentiate between these possibilities, the extent to
which they might affect blood flow under the experimental conditions
studied will be briefly discussed. Passive distension probably contributes
to the decrease in resistance (cf. Folkow & L6fving, 1956), although
the fact that blood flow increases early during the contraction when arterial
pressure is still moderate, suggests the contribution of other factors.
Sympathetic vasoconstrictor activity is believed to be only moderate but
a decrease in vasoconstrictor activity can, nevertheless, produce a sub-
stantial decrease in vascular resistance. Thus, a total withdrawal of
sympathetic vasoconstrictor activity in the cat (Folkow, 1952; Celander &
Folkow, 1953) or dog (Gerova & Gero, 1968) hind limb was shown to nearly
double the blood flow. In man, blocking the brachial plexus increased
forearm blood flow about three times (Barcroft, Bonnar, Edholm &
Effron, 1943; Barcroft, Edholm, Forster, Fox & McPherson, 1956; Blair
et al. 1961). However, most data in the literature suggest that physical
activity is accompanied by an increase in sympathetic activity. Thus,
blocking the deep nerves above the elbow doubled forearm blood flow
during leg exercise (Blair et al. 1961), and Delius et at. (1972) have even
been able to record an increased sympathetic activity in the resting fore-
arm during isometric leg contraction. Sympathetic vasodilator fibres
might then be considered. The existence of such fibres has been suggested
by several authors (for review, see Roddie & Shepherd, 1963) although
their nature is not clear. Cholinergic sympathetic vasodilator fibres
described in e.g. the cat seem to be lacking in man (Bolme & Fuxe, 1970;
Bolme, Novotn', Uvnis & Wright, 1970). Vasodilatation might then be
induced by ,-adrenergic effects. The magnitude of dilatation which might
be produced by such effects is at the present time uncertain. Animal
experiments suggest that it is rather small. Thus in the dog hind limb
under a-receptor blockade supramaximal sympathetic stimulation reduces
vascular resistance at the most by about 35 per cent (Gerova & Gero, 1968).

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       RESTING LIMB FLOW IN MUSCLE CONTRACTION 121
Furthermore, there is reason to believe that x- and fl-receptors at least
to a certain extent are activated by the same fibres (Viveros, Garlick &
Renkin, 1968).
   An increased secretion of adrenaline accompanies a strong isometric
contraction (Kozlowski, Brzezinska, Nazar, Kowalski & Franczyk, 1973),
but the rapid onset of blood flow increase and the rapid return to pre-
contraction level seems to exclude any mayor importance of a circulating
vasodilating substance. Thus the rapid onset of flow increase suggests
neurogenic vasodilatation and effects mediated by fl-receptors seems to be
important for the early flow increase in the resting forearm during iso-
metric contraction.
   The blood flow increase in the resting forearm did not in most subjects
reach a steady level during contraction, but tended to decrease slightly
after about 1 min. Since at the same time the arterial pressure continued
to increase, the vascular resistance must have increased. Although this
relative increase in vascular resistance developed slowly, an increase in
myogenic tone, as described by Bayliss (1902), Folkow (1949) and others
might well have contributed to it. Such a reaction is namely rather sluggish
and the increase in myogenic tone might take a minute to develop
(Bilbring, 1955; Folkow & Lbfving, 1956).
   Sympathetic vasoconstrictor activity might also contribute to the
increase in vascular resistance. Thus, a contraction with the relative force
used leads to fatigue within about 2-5 min (our observations). This means
that single muscle fibres gradually weaken, and the effort needed to main-
tain the contraction gradually increases. This is also reflected in an increased
amplitude of the integrated rectified electromyogram (Clarke et al. 1958).
There is probably an increase in sympathetic outflow from the vasomotor
centre concomitantly with this increase in motor output (Johansson, 1893;
Freyschuss, 1970) as also suggested by the increases in heart rate and
arterial pressure. This might well lead to an increased adrenergic effect
which, perhaps together with an increase in myogenic tone, attenuates the
distending effect of the increased intravascular pressure.
   In contrast to the pronounced decrease in vascular resistance and increase
in blood flow in the resting forearm, the vascular resistance in the resting
calf remains initially unchanged, and the flow increases only slightly.
This may be due to a lower distensibility of the resistance vessels of the
lower limbs either for anatomical reasons, i.e. greater wall thickness, or
because of a higher myogenic tone. Alternatively, there might be differences
in neurogenic vasomotor effects between the upper and lower limbs
(Kellerova & Delius, 1969). Of these possibilities, to the authors' best
knowledge, anatomical differences between the upper and lower limb
vessels are not described, but smooth-muscle hypertrophy in the arteriolar


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122 BRITA EKLUND, L. KAIJSER AND E. KNUTSSON
walls has been described by Kernohan, Anderson & Keith (1929) and
Furuyama (1962) as a consequence of arterial hypertension. Similarly, the
higher hydrostatic pressure in the leg might in normal subjects produce
thicker smooth-muscle layer in the leg vascular bed. A higher myogenic
tone in the leg might explain the difference found, but the lack of any
decrease in vascular resistance induced by the increased pressure suggests
the probability of an active neurogenic vasoconstrictor activity.
   Although isometric contraction affects the blood flow in resting forearm
or resting calf quite differently, whether the contraction is of arm or leg
makes very little difference. Thus, no segmental discrimination to the
effect that arm contraction affects arm blood flow more than leg flow and
vice versa could be detected. The only difference found was a slightly
smaller increase in arterial pressure for a given increase in heart rate during
foot dorsiflexion than handgrip. It has previously been pointed out that
dynamic work with the arms produces a higher heart rate and arterial
pressure than does leg work at corresponding oxygen uptake levels
(Bevegard et al. 1966). This difference has been explained by the smaller
muscle mass and a probably higher sympathetic tone during arm work.
The present study shows that arterial pressure increase is more pronounced
in relation to heart rate increase for arm than leg muscle contraction, also
when both contractions are performed with small muscle masses.
   Lind et al. (1964), when comparing the increase in cardiac output
produced by handgrip contraction with the concomitant changes in flow in
resting and contracting forearm, as well as using their own unpublished
data on renal, splanchnic and cutaneous circulation, found it difficult to
account for the cardiac output increase. Assuming that the increase in
cardiac output in our subjects was of a magnitude between that reported
by Lind et al. for handgrip contractions of 20 and 50% MVC, respectively,
the average maximal cardiac output increase in our subjects would have
been slightly below 2 I./min. Forearm and calf blood flow mainly represent
muscle + skin flow, and assuming that the average change in blood flow in
the total mass of muscle and skin of the body during contraction lies
between that found in resting forearm and calf, this increase would then
amount approximately to a doubling of the resting flow. The increase in
flow in these tissues would thus be of the order 1-5-2 I./min (for reference
see Wade & Bishop, 1962). In addition, as a result of the increased cardiac
work during contraction the coronary flow must have increased by 200-
300 ml. (Holmberg, Serzysko & Varnauskas, 1971). Thus, the calculated
increase in cardiac output may well be explained.




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       RESTING LIMB FLOW IN MUSCLE CONTRACTION                                      123

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