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1 Department of Physiotherapy, Hodges, Paul W., Simon C. Gandevia, and Carolyn A. Richardson. Contractions of specific abdominal
muscles in postural tasks are affected by respiratory maneuvers.
J. Appl. Physiol. 83(3): 753-760, 1997.
postural reaction; abdominal muscles; trunk; motor control; respiratory loading; motoneuron pool
CONTRACTION OF THE MUSCLES of the anterior abdominal
wall occurs as part of the postural adjustments before the movement of the upper limb (15) and voluntary loading of the trunk (6). Rapid
flexion of the upper limb produces a brief challenge to postural
stability of the trunk as a result of reactive forces acting equal and
opposite to those producing the movement (4, 16). Movement of this type
is associated with contraction of transversus abdominis (TrA) preceding
the activation of deltoid, whereas contraction of internal oblique
(IO), external oblique (EO), and rectus abdominis (RA) occurs shortly
after the muscle responsible for initiation of the movement (i.e.,
deltoid) (15). These contractions are considered to contribute to the
maintenance of postural equilibrium and stabilization of the trunk (3, 6, 11, 15). However, the contribution of the abdominal muscles to
postural control is likely to be complicated by their role in
respiration.
Although electromyographic (EMG) activity of the abdominal muscles is
rarely recorded during quiet breathing, abdominal muscles are activated
toward the end of expiration once ventilation is increased (12).
Contraction of the abdominal muscles contributes to the regulation of
the length of the diaphragm (7), end-expiratory lung volume (14), and
expiratory airflow (1). When ventilation is increased voluntarily,
contraction of TrA, IO, EO, and RA produces expiration below functional
residual capacity (FRC) with a subsequent increase in inspiratory
volume (8, 12). In contrast, involuntary increases in ventilation due
to hyperoxic hypercapnia or loaded inspiration provoke contraction
of TrA and IO at a lower minute volume than the other abdominal muscles
(8, 25). The influence of respiratory contraction of the abdominal
muscles on their contribution to postural control has not been
considered. Abdominal expiratory muscles are depolarized in expiration
and thought to be hyperpolarized in inspiration (20). These changes
could mean that the latency to onset of postural contraction of
abdominal muscles changes with the phase of respiration and is shorter
when the motoneuron pool is already recruited.
Therefore, this study was designed to determine whether
1) timing of activation of specific
abdominal muscles would be altered in postural tasks according to the
phase of quiet respiration; 2)
timing of activation of specific abdominal muscles would be altered in
postural tasks when respiratory drives to motoneurons were increased;
and 3) timing of activation of
abdominal muscles changed during tonic activation of their motoneurons
in an expulsive effort.
Subjects. Five volunteer subjects (4 men and 1 woman) 26.6 ± 1.4 yr old and of average height
(176.4 ± 5.0 cm) and weight (69.0 ± 3.6 kg) were
studied. Subjects were excluded if they had any major neurological or
respiratory condition. The study was approved by the Medical Research
Ethics Committee of the University of Queensland. Subjects were unaware
of the experimental hypotheses and were not trained in respiratory
maneuvers.
Recordings. Fine-wire bipolar EMG
electrodes [75 µm, insulated stainless steel (A-M Systems),
1-mm insulation removed] were inserted into the left TrA, IO, and
EO under the guidance of real-time ultrasound imaging (Advanced
Technology Laboratory, Australia). The technique has been described in
detail elsewhere (5, 8). The locations for electrode insertion are
identified in Fig. 1. The electrodes were
placed 2 cm medial to the proximal end of a line drawn from the
anterior superior iliac spine to the inferior border of the rib cage
for TrA; 2 cm medial and superior to the anterior superior iliac spine
for OI; and midway between the iliac crest and inferior border to the
rib cage in the midaxillary line for EO. Surface electrodes (Ag/AgCl)
were placed over RA on either side of a line drawn between the right
and left anterior superior iliac spine 2 cm lateral to the midline and
over the muscle belly of deltoid in parallel with the muscle fibers.
Skin impedance was reduced to <5 k
The respiratory cycle was monitored by using an air-filled tube
strapped to the chest at the level of the nipples. Movement of the rib
cage was measured by changes in pressure within the device throughout
the respiratory cycle.
Experimental conditions. The subjects
stood on a force platform (SMS Healthcare, UK) that provided auditory
feedback of equality of weight bearing between the two legs. This was
necessary, since variation in weight bearing has been suggested to
influence the activation of postural muscles in limb movement tasks
(18). The sensitivity of the device was set to alarm if the imbalance between the legs exceeded 4% of total body weight. Subjects performed 40 trials of unilateral shoulder flexion to 60° from the resting position by the trunk. Movement was performed as fast as possible in
response to a visual stimulus in each of four different conditions presented in random order. Each set of limb movements was completed in
15 min for each condition. The conditions were as follows.
1) Quiet breathing: subjects
breathed at a self-selected volume and rate.
2) Inspiratory loading: in an
attempt to activate TrA preferentially during expiration (8), subjects
inspired through a narrow tube (ID 5.5 mm, length 190 mm). Expiration
was performed without resistance. After a loaded inspiration, the EMG
activity of TrA and IO increased during the expiratory phase. Subjects were unaware of possible respiratory responses to loading.
3) Expiration below FRC: to evaluate
the influence of respiratory activation of the abdominal muscles on
their reaction time latency during the postural limb movement task, the
activity of each of the abdominal muscles was increased during
expiration by voluntary forceful expiration below FRC. It was necessary
for this technique to be voluntary, since involuntary methods to
increase expiratory airflow differentially influence the abdominal
muscles (8). Subjects were instructed to maintain a normal respiratory rate throughout the procedure.
4) Static expulsive maneuvers:
subjects were asked to stop breathing and made a submaximal forced
expiration against a closed glottis to evaluate the effect of a static
contraction of the abdominal muscles.
Throughout the trials, the subjects maintained a relaxed standing
position. The visual stimulus to move was provided by a green light
placed 1.5 m in front of the subject at eye level and was preceded by a
warning stimulus by a random period of between 0.5 and 3 s. Five
practice movements were performed in each condition, with feedback from
the experimenters, to ensure consistency of response. In all
conditions, except the static expulsive maneuver, the timing of the
movement stimuli was presented at random during the respiratory cycle
so that the phase in which the limb movement occurred would vary. This
resulted in ~10 stimuli occurring at end expiration, midinspiration,
end inspiration, and midexpiration (Fig.
2A). In
each static expulsive maneuver, the subject performed two repetitions
of shoulder movement in response to the visual stimulus, and 10 trials
were recorded.
Data collection and analysis. EMG data
were sampled at 2,000 Hz by using 12 bit analog-to-digital conversion,
band-pass filtered at 20-1,000 Hz, and stored on computer for
later analysis. The time to onset of the increase in EMG activity
formed the basis of the analysis. The onset of increased EMG of each
muscle was determined automatically by using an algorithm following
full-wave rectification of the trace. The algorithm identified onset as the point where the mean of 50 consecutive samples deviated by >3 SDs
from the mean baseline activity recorded for the 100 ms before the
warning stimulus. The trials were separated into four groups based on
the phase of respiration, as assessed by the motion of the rib cage.
The phases of respiration were arbitrarily defined as (Fig.
2A): end expiration (300 ms before
the onset of rib cage expansion), midinspiration (300 ms either side of
the point halfway between end expiration and end inspiration), end
inspiration (300 ms before the cessation of rib cage expansion), and
midexpiration (300 ms either side of the point halfway between end
inspiration and end expiration). The allocation of each trial to one of
the four groups was determined by the time of onset of the increase in
deltoid EMG. Recordings were discarded if the onset of the increase in
deltoid EMG occurred outside the defined the respiratory phases.
The absolute reaction time from the stimulus to move to the onset of
increased EMG was measured for deltoid and each abdominal muscle. In
addition, the onset of increased EMG of each of the abdominal muscles
was measured relative to the onset of the increased deltoid EMG.
Negative values indicated the onset of increased abdominal muscle EMG
before the onset of the increase in deltoid EMG. The absolute reaction
time for deltoid and the abdominal muscles varied between trials within
each condition, and this may obscure any changes in timing of the
abdominal muscles relative to the arm movements in the different
respiratory phases and different experimental conditions (Fig.
2B). In contrast, the difference in
latency between the activation of the abdominal muscles and deltoid was
relatively constant within conditions (Fig.
2B; see also Ref. 15). Hence, the main
analyses were performed on the reaction times expressed as the latency
difference between the onset of activity in the deltoid and the various
abdominal muscles.
The main analysis relied on pooled measurements from each single trial
within each respiratory phase (i.e., one value per condition per
subject). However, the general conclusions were unaltered if
measurements were made when all trials in a particular condition were
averaged after rectification of the EMG signals (within or across
subjects). Rectification and averaging have been used for illustrative
purposes (see Fig. 5). An analysis of variance and Duncan's
multiple-range test were used to evaluate changes in the relative time
of onset of the increase in EMG of each muscle between the respiratory
phases for each condition. For the expulsive maneuver, the reaction
time latency of each muscle was compared with that averaged over the
four respiratory phases in the quiet-breathing condition. Throughout
the text results are expressed as means ± SE. Statistical
significance was set at the 5% level.
As judged by the absence of single and multiunit discharges in the EMG
records, all of the abdominal muscles were "silent" during quiet
breathing in the relaxed standing position (Fig. 3A).
This contrasts with earlier studies reporting activity of the abdominal
muscles in standing (7, 10, 23). This can be explained by our
instruction to relax in the standing position: when tonic activity was
occasionally observed, it ceased when subjects were reminded to relax.
In the loaded-inspiration condition, the activity of TrA and also IO,
but not EO and RA, occurred throughout expiration (Fig.
3B). This is consistent with
previous findings (8). In contrast, the activity of all abdominal
muscles increased during voluntary expiration below FRC (Fig.
3C). In each subject, a similar
pattern of muscle activation occurred during the different experimental
conditions.
Quiet breathing. When subjects
breathing quietly received a visual signal to flex their shoulder
rapidly, an increase in TrA EMG occurred before contraction of deltoid
(Figs. 4A
and 5). This "anticipatory" activity
of TrA occurred 20 ± 14 ms before the increase in deltoid EMG. The
onset of increased EMG of IO, EO, and RA followed that of deltoid
(Figs. 4A and 5). The absolute latencies for each muscle are presented in Table
1, and the relative latency between the
onset of deltoid EMG and that of each of the abdominal muscles is
presented in Table 2. There were no
significant differences in the absolute latencies across the
respiratory phases for any of the muscles. Given that the variation in
the absolute latencies was larger than the variation in the relative
latency between the abdominal muscles and deltoid, the onset of EMG in the abdominal muscles is subsequently reported relative to the onset of
deltoid (Fig. 2B; see
MATERIALS AND METHODS). When the subjects were breathing quietly, no significant difference in the
latency between the onset of increased EMG of the abdominal muscles and
deltoid occurred between the respiratory phases (Table 2).
Inspiratory loading. When subjects
breathed with an inspiratory load, the onset of the increase in TrA EMG
preceded that in deltoid EMG only when the movement occurred during the
mid-expiratory phase of the respiratory cycle (Figs.
4B and 5 and Table 2). However, some
individual subjects (including those whose data are presented in Figs.
4 and 5) also showed activation of TrA before deltoid in end
expiration. The onset of the increase in EMG of TrA relative to that of
the deltoid EMG occurred earlier in both midexpiration and end
expiration than in midinspiration and end inspiration (Figs.
4B and 5 and Table 2), although, for the group, there was no significant difference between end expiration and midinspiration. The onset of increased EMG of TrA preceded the
onset of the increase in deltoid EMG by The onset of the increase in EMG of IO preceded the onset of the
increased deltoid EMG by Voluntary expiration below FRC. When
subjects breathed voluntarily and deliberately expired below FRC, the
onset of the increased TrA EMG occurred before the increase in deltoid
EMG when movement occurred during both the mid- and end-expiratory
phases of the respiratory cycle. In midexpiration, the increase in EMG
of IO also occurred before deltoid EMG (Figs.
4C and 5 and Table 2). The onset of
the increase in TrA EMG in response to limb movement was significantly
earlier when deltoid EMG was initiated during end expiration compared
with midinspiration and for midexpiration compared with end
inspiration, end expiration, and midinspiration (Figs.
4C and 5 and Table 2). Across
subjects, the mean difference in latency of onset of the increased TrA
EMG between midexpiration and midinspiration was 107 ± 23 ms. The
onset of the increase in IO EMG was significantly earlier during
midexpiration compared with midinspiration (Table 2). The onset of the
increase in EMG of EO and RA occurred after that of deltoid and was not
significantly different between movements initiated in each of the
respiratory phases.
Static expulsive maneuver. Subjects
stopped breathing, and all of the abdominal muscles contracted during a
static expulsive maneuver. In contrast to the three earlier conditions,
the onset of increased TrA EMG followed that of deltoid by 22 ± 8 ms (Fig. 6) when the upper limb was moved.
When compared with the mean onset latency for the four phases of quiet
breathing, the onset of the increase in TrA EMG occurred significantly
later when the movement was initiated during a static expulsive
maneuver than during quiet respiration by a mean of 41 ± 13 ms
(Fig. 6).
During the expulsive maneuver, the onset of the increase in EMG of IO,
EO, and RA followed the onset of the increase in deltoid EMG. Although
the onset of increased EMG of IO relative to that of deltoid was only
of borderline significance when compared with quiet respiration, the
relative onset of EO and RA occurred significantly later when movement
was initiated during the static expulsive maneuvers. The mean delay in
onset of EMG of EO and RA, compared with quiet breathing, was 42 ± 18 and 45 ± 29 ms, respectively.
The present study has evaluated the influence of
respiratory activation of the abdominal muscles on their timing of
onset of contraction in a brief postural task. The results provide
evidence that the preparatory activation of TrA and IO occurs earlier
relative to the contraction of the arm muscle when added respiratory
activity is present in these muscles, as a result of inspiratory
loading or voluntary expiration below FRC. Respiratory modulation of
the preparatory contractions is not evident for quiet breathing. In contrast, the onset of TrA activation was delayed relative to deltoid
when motoneurons of the abdominal muscles were activated by a static
expulsive maneuver. This contradictory influence of activation of
specific abdominal muscles on their timing of EMG onset with limb
movement cannot be explained simply by reduced time needed to discharge
the abdominal motoneurons due to their concurrent activity. Additional,
presumably supraspinal, factors must be involved.
The study confirms that one or more of the abdominal muscles contract
before the agonist limb muscles when movement of the arm is performed
while standing. This "preparatory" activation of TrA and IO is
likely to be preprogrammed as their onsets occur before any relevant
afferent activity can initiate them. A recent study documented the
preparatory contractions of TrA in reaction-time movements of the arm
but did not assess the influence of respiration on them (15).
The earlier contraction of TrA and IO during expiration (when the
neural drive to these muscles is increased) compared with inspiration
in the inspiratory-loading and expiration-below-FRC conditions is
consistent with the influence of changes in membrane potential
associated with the respiratory cycle. Thus the depolarization of the
abdominal motoneurons that occurs during expiration (22) should
decrease the time needed to discharge them in a postural task, leading
to earlier activation of TrA and IO. Whereas these changes in membrane
potential (i.e., central respiratory drive potentials) have been
identified in the cat (22), their existence cannot be confirmed
directly in human studies. Consistent with the proposed relationship
between postural activity and the respiratory neural drive, Rimmer and
colleagues (21) considered that changes in intercostal muscle activity
during respiration combined with trunk rotation in humans may reflect
the sum of the central respiratory drive potentials and voluntary drive
to the muscles. Rimmer et al. (21) showed decreased postural
contraction of the internal intercostal muscles during inspiration and
increased inspiratory contraction of the external intercostal muscles
when the trunk was rotated.
However, the results of the present study cannot be explained simply by
changes in background neural drive to the abdominal motoneurons. This
is because the activation of the same muscles was relatively delayed
during a static maneuver where the activation of the abdominal
motoneurons was increased. Second, the change in timing of activation
is specific to particular muscles: being prominent for the TrA and IO
but not for RA and EO, despite the respiratory activity of all muscle
being increased in the expiration-below-FRC condition. In the previous
study of Rimmer and colleagues (21), it was hypothesized that afferent
input from muscle spindles and tendon organs may also contribute to the
variation in intercostal muscle activity. However, it is difficult to
delineate the role of muscle and other afferents in the later
modulation of the output to the various abdominal muscles associated
with arm movements. Although they are unlikely to determine the onset
times for the responses in TrA and IO, they may well contribute to the
later modulation of the EMG. Such an integration of afferent and
descending input is likely to involve spinal (2, 17) and supraspinal sites, including the respiratory centers (9, 20). However, because of
the task dependence of the responses and because they may sometimes
involve coactivation of the diaphragm (see below) and abdominal muscles
(TrA and IO), it is unlikely that the anticipatory response of the
abdominal muscles is mediated purely via output from classic
pontomedullary respiratory centers.
An alternate way to analyze the results is to consider the mechanism by
which the abdominal muscles act on the trunk. One function attributed
to the preparatory contraction of the abdominal muscles is the
production of intra-abdominal pressure to assist in the stabilization
of the trunk and to control postural equilibrium disturbed by the
movement of the arm (6, 15). The potential mechanisms for this include
an increase in tension of the thoracolumbar fascia through which TrA
attaches to the spine (24) as well as the increase in intra-abdominal
pressure itself (5, 19). To be effective, these mechanisms require
contraction of the diaphragm to prevent its passive lengthening and the
displacement of the abdominal contents. Preliminary recordings from the
diaphragm with intramuscular electrodes are consistent with its
activation together with TrA in similar tasks to those used here (P. W. Hodges and S. C. Gandevia, unpublished observations). The results
obtained during the static expulsive maneuvers support the view that
the preparatory contractions are involved in the mechanical
stabilization of the trunk. Here there is already an elevation of
intra-abdominal pressure due to the co-contraction of the diaphragm and
abdominal muscles. Hence, when the arm is required to move, there may
be less need to provide a more stable platform as this has already been
ensured by the contraction of the abdominal muscles. In this situation,
the preparatory contraction of TrA and IO was delayed until after the
onset of the movement. TrA and IO are likely to be the more important
abdominal muscles in any mechanical stabilization produced via an
increase in abdominal pressure as they are more effective in this task
than RA or EO (5, 6).
This analysis is also consistent with the observations during the
phases of respiration when the activity of some of the abdominal muscles was increased. The preparatory contractions of TrA and IO
occurred earlier when the arm movement began during expiration rather
than during inspiration. During quiet inspiration, the abdominal pressure may have already been elevated sufficiently as a
result of diaphragmatic contraction (see Ref. 13) so that there was
less need for an anticipatory contraction of the abdominal muscles.
In summary, the reported changes in timing of contraction of the
abdominal muscles in a brief postural task between phases of
respiration cannot be simply explained by the influence of conventional
respiratory drive or ongoing voluntary drive to abdominal motoneurons.
The findings are consistent with the complex interaction of respiratory
and postural demands on the abdominal muscles to optimize trunk control
during rapid movement of the upper limb. It seems that supraspinal
structures are able to select the appropriate output to abdominal and
other truncal muscles before limb movement based on the biomechanical
need for an increase in abdominal pressure.
We thank Dr. B. Richardson for supervision of the fine-wire
electrode insertion, B. Bui for technical assistance, and I. Horton for
statistical advice.
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
The influence of respiratory activity of the abdominal muscles
on their reaction time in a postural task was evaluated. The
electromyographic (EMG) onsets of the abdominal muscles and deltoid
were evaluated in response to shoulder flexion initiated by a visual
stimulus occurring at random throughout the respiratory cycle.
Increased activity of the abdominal muscles was produced by inspiratory
loading, forced expiration below functional residual capacity, and a
static glottis-closed expulsive maneuver. During quiet breathing, the
latency between activation of the abdominal muscles and deltoid was not
influenced by the respiratory cycle. When respiratory activity of the
abdominal muscles increased, the EMG onset of transversus abdominis and
internal oblique, relative to deltoid, was significantly earlier for
movements beginning in expiration, compared with inspiration [by
97-107 ms (P < 0.01) and
64-90 ms (P < 0.01),
respectively]. However, the onset of transversus abdominis EMG
was delayed by 31-54 ms (P < 0.01) when movement was performed during a static expulsive effort,
compared with quiet respiration. Thus changes occur in early
anticipatory contraction of transversus abdominis during respiratory
tasks but they cannot be explained simply by existing activation of the
motoneuron pool.
before attachment. Control
studies revealed that the onset of EMG for deltoid and RA could be
measured accurately with surface electrodes.
Fig. 1.
Location for insertion of fine-wire electrodes into transversus
abdominis (TrA), internal oblique (IO), and external oblique (EO) and
placement of surface electrodes for rectus abdominis (RA) and deltoid.
Dashed lines indicate line drawn vertically from anterior superior
iliac spine (ASIS) and horizontally between right and left ASIS for
identification of electrode sites.
[View Larger Version of this Image (18K GIF file)]
Fig. 2.
A: identification of
phases of respiration. I, inspiration; E, expiration; i, midexpiration;
ii, end expiration; iii, midinspiration; iv, end
inspiration. B: 2 trials from 1 set of rapid arm movements for a single subject,
demonstrating variation in time from stimulus to move to EMG onset
(arrows). Onset of deltoid EMG is denoted by unbroken line and onset of
TrA EMG by broken line. Note difference in absolute latency of
responses but relatively consistent period between onset of EMG of each
muscle.
[View Larger Version of this Image (24K GIF file)]
Fig. 5.
Mean of rectified EMG for 5 repetitions in 1 subject for TrA and
deltoid for trials during each phase of respiration during quiet
breathing (A), breathing with an
inspiratory load (B), and breathing
with voluntary expiration below FRC
(C). Trials were aligned to onset of
deltoid EMG before averaging. Onset of deltoid EMG is denoted by
unbroken line and that of TrA is noted by broken line. Note consistent
relationship between mean onset of EMG of deltoid and TrA between
respiratory phases with quiet breathing and variation in relationship
between phases when breathing with an an inspiratory load and breathing
with voluntary expiration below FRC.
[View Larger Version of this Image (29K GIF file)]
Fig. 3.
Representative raw EMG traces for each muscle from a
typical subject during quiet breathing
(A), breathing with an inspiratory load (B), and breathing with
voluntary expiration below functional residual capacity (FRC)
(C). Note absence of overt
muscle activity during quiet breathing, phasic increase
in TrA and IO EMG during expiration with inspiratory loading, and
phasic EMG increase in all abdominal muscles during voluntary
expiration below FRC. Resp, respiration. Dashed lines indicate end of
inspiration.
[View Larger Version of this Image (18K GIF file)]
Fig. 4.
Representative raw EMG traces for all muscles for a typical subject for
trials during 4 respiratory phases with each respiratory condition.
A: quiet breating; note increase in
TrA EMG before onset of increased deltoid EMG and constant relationship
between onset of increased EMG of each of abdominal muscles for each
respiratory phase. B: breathing with
an inspiratory load; note change in relationship between onset of
increased EMG of TrA and IO relative to deltoid with TrA, preceding
deltoid by greatest amount during midexpiration and following deltoid
during inspiration. C: breathing with
voluntary expiration below FRC; note change in relationship between
onset of increased EMG of TrA and IO relative to that of deltoid. TrA precedes deltoid during midexpiration and follows deltoid during inspiration. EMG scales are consistent between each group of trials.
[View Larger Version of this Image (50K GIF file)]
Table 1.
Absolute reaction times of abdominal and deltoid muscles with each
respiratory phase in the quiet-breathing condition
Respiratory Phase
Deltoid, ms
TrA, ms
IO, ms
EO, ms
RA, ms
End expiration
163 ± 17
145 ± 17
208 ± 17
240 ± 10
284 ± 28
Midinspiration
178 ± 16
160 ± 17
208 ± 25
239 ± 27
274 ± 39
End inspiration
149 ± 13
140 ± 20
185 ± 29
210 ± 19
260 ± 34
Midexpiration
148 ± 16
116 ± 12
169 ± 21
237 ± 25
278 ± 40
Values are means ± SE; times are in ms from the visual stimulus
to move. TrA, transversus abdominis; IO, internal oblique; EO, external
oblique; RA, rectus abdominis.
Table 2.
Relative latency between onset of EMG of deltoid and each of abdominal
muscles, with each respiratory phase and in each of the respiratory
conditions
Respiratory Condition
Phase
TrA
IO
EO
RA
Quiet respiration
EE
18 ± 12 49 ± 30
77 ± 12
119 ± 26
MI
20 ± 15 33 ± 19
65 ± 31
96 ± 37
EI
9 ± 17 38 ± 26
63 ± 21
112 ± 38
ME
32 ± 13 23 ± 19
89 ± 19
129 ± 34
F(4,3)
0.58
0.56
0.44
0.89
Inspiratory
load
EE
6 ± 26
13 ± 13
122 ± 15
168 ± 25
MI
53 ± 18
36 ± 14
92 ± 17
144 ± 57
EI
59 ± 21
62 ± 26
108 ± 21
140 ± 51
ME
38 ± 13
2 ± 32 123 ± 26
187 ± 83
F(4,3)
8.62
2.57*
0.52
0.57
Expiration
below FRC
EE
18 ± 10 13 ± 27
118 ± 32
129 ± 32
MI
44 ± 18
61 ± 24
30 ± 98
123 ± 38
EI
22 ± 11
18 ± 22
115 ± 27
129 ± 45
ME
63 ± 22
29 ± 29 97 ± 19
110 ± 38
F(4,3)
12.74
2.15*
0.43
0.53
Voluntary
expiration below FRC
22 ± 8
70 ± 11
116 ± 19
158 ± 31
F(4,1)
8.80
3.97
4.55*
4.91*
Values are means ± SE. Times are in ms from onset of deltoid
EMG. Negative values indicate onset of abdominal muscle EMG before that
of deltoid. F values for comparison between each respiratory phase for conditions of quiet respiration, inspiratory loading, and
expiration below FRC are presented along with the F values for
comparison between static expulsive maneuver and mean onset in
quiet-breathing condition. EE, end expiration; MI, midinspiration; EI,
end inspiration; ME, midexpiration.
*
P < 0.05,
P < 0.01.
38 ± 13 ms in
midexpiration but followed the onset of deltoid by 59 ± 21 ms at
end inspiration. This resulted in a mean difference of 97 ± 23 ms
in the activation times of TrA between these two respiratory phases.
There was no significant change in the absolute reaction time of
deltoid between respiratory phases
[F(4,3) = 1.13, P = 0.38].
2 ± 32 ms in midexpiration but followed it by 62 ± 26 ms at end expiration. No significant
difference was noted between the respiratory phases for EO or RA.
Fig. 6.
Representative raw EMG from abdominal muscles for a single trial of
rapid shoulder flexion occurring during performance of an expulsive
maneuver with glottis closed. Onset of deltoid EMG is denoted by an
unbroken line and that of TrA by broken line. Note delayed onset of TrA
EMG following that of deltoid.
[View Larger Version of this Image (31K GIF file)]
Financial support was gratefully received from the Menzies Foundation,
Physiotherapy Research Foundation, Dorothy Hopkins Research Award, and
the National Health and Medical Research Council of Australia.
Address for reprint requests: S. C. Gandevia, Prince of Wales Medical Research Institute, High St., Randwick, Sydney, NSW 2031, Australia.
Received 29 July 1996; accepted in final form 5 May 1997.
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