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1 Department of Aerospace Engineering and Mechanics, University of Minnesota, Minneapolis, Minnesota 55455; and 2 Baylor College of Medicine, Houston, Texas 77030
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The mechanical advantage (µ) of a respiratory
muscle is defined as the respiratory pressure generated per unit muscle
mass and per unit active stress. The value of µ can be obtained by measuring the change in the length of the muscle during inflation of
the passive lung and chest wall. We report values of µ for the
muscles of the canine diaphragm that were obtained by measuring the
lengths of the muscles during a passive quasistatic vital capacity
maneuver. Radiopaque markers were attached along six muscle bundles of
the costal and two muscle bundles of the crural left hemidiaphragms of
four bred-for-research beagle dogs. The three-dimensional locations of
the markers were obtained from biplane video-fluoroscopic images taken
at four volumes during a passive relaxation maneuver from total lung
capacity to functional residual capacity in the prone and supine
postures. Muscle lengths were determined as a function of lung volume,
and from these data, values of µ were obtained. Values of µ are
fairly uniform around the ventral midcostal and crural diaphragm but
significantly lower at the dorsal end of the costal diaphragm. The
average values of µ are 
0.35 ± 0.18 and 0.27 ± 0.16 cmH2O · g
1 · kg1 · cm2
in the prone and supine dog, respectively. These values are 1.5-2 times larger than the largest values of µ of the intercostal muscles in the supine dog. From these data we estimate that during spontaneous breathing the diaphragm contributes ~40% of inspiratory pressure in
the prone posture and ~30% in the supine posture. Passive
shortening, and hence µ, in the upper one-third of inspiratory
capacity is less than one-half of that at lower lung volume. The lower µ is attributed primarily to a lower abdominal compliance at high
lung volume.
respiratory muscles; mechanics; chest wall
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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IN PHYSICS, the term "mechanical advantage" is defined as the ratio of the force delivered to a load (FL) to the force applied at a remote point on a machine (F1). For a simple lever, this ratio FL/F1 equals the ratio of the lever arms. If the position of the fulcrum were unknown, the ratio of the lever arms could be determined by measuring the displacement of the lever arm (x1) per unit displacement of the load (xL). That is, FL = µF1, where µ = x1/xL. As stated by Maxwell's reciprocity theorem, the ratio of forces and the ratio of displacements for any multiple-degree-of-freedom linear elastic system are similarly related.
Wilson and De Troyer (28) defined the respiratory mechanical advantage
(µ) as respiratory pressure per unit muscle mass (m) and per unit active stress
(
). That is
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(1) |
Pao is the change in airway pressure that occurs when a muscle is
activated with the airway occluded. They modeled the chest wall as a
linear elastic system and applied Maxwell's reciprocity theorem to
obtain the following relation between µ and change in muscle length
during inflation of the relaxed chest wall
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(2) |
Pao
(cmH2O), µ (g), (kg/cm2), and
VL (liters). That is, the left
side of Eq. 1 with units of
centimeters water per gram equals the right side, with µ expressed per liter and in kilograms per square centimeter.
In a series of studies, De Troyer and colleagues have given substance
to this theory by demonstrating that the respiratory effects of a
number of respiratory muscles, the parasternal internal intercostals
(10, 17), the sternomastoids and scalenes (16), and the triangularis
sterni (9), are well described by Eqs. 1 and 2. That is, they
measured the change in length of each of these muscles during inflation
of the passive respiratory system to obtain
(dL/LodVL)rel
and, hence, µ. They then measured Pao when the muscle was
maximally activated, excised the activated muscle, and measured its
mass. They found that Pao/m is
proportional to µ, with a constant of proportionality of ~3
kg/cm2, a value at the upper end
of the range of values of maximum measured in vitro (26). In
addition, they tested the validity of the linear model of the
respiratory system by testing one of the fundamental properties of
linear systems, i.e., superpositon (18). For different combinations of
intercostal muscles in different interspaces, they found that, to
within 10%, Pao produced by simultaneous activation of two muscle
groups equals the sum of the Pao values produced by each group
activated alone.
As a result of the work of De Troyer et al., Eq. 2 can now be used with some confidence to obtain the
values of µ of muscles for which
Pao/m cannot be measured directly.
That is, for muscles that cannot be activated to produce a known in
a known m, µ can be obtained by
measuring
(dL/LodVL)rel.
The diaphragm falls in this category. To be sure, the diaphragm can be
activated by stimulating the phrenic nerves. However, the chest wall is
severely distorted when the diaphragm is maximally activated (14), and it is likely that diaphragm function and stress are altered by the
change in geometry and muscle length that occurs. Submaximal activation
is possible, but in the submaximally activated diaphragm is unknown.
We report values of diaphragm muscle shortening during passive inflation of the lung and chest wall. From these data and Eq. 2, we obtain values of µ for the diaphragm.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Four bred-for-research dogs were studied. The body mass of the dogs was
10.1 ± 0.3 kg, and the inspiratory capacity (IC) was 0.7 ± 0.1 liter. The video-fluoroscopic method for measuring diaphragm muscle
length has been described previously (1, 5, 24, 25). Briefly, in a
preparatory surgical procedure, silicone-coated lead spheres and
cylinders were stitched to the peritoneal surfaces of the left
hemidiaphragms of the four dogs. The pattern of placement in one dog is
shown in Fig. 1. Three or four markers were
placed at intervals of ~1 cm along each of six muscle bundles at
different points from the ventral to the dorsal end of the costal
diaphragm, and three or four markers were placed along each of two
muscle bundles of the crural diaphragm. The animals were allowed to
recover for 
3 wk. The animals were anesthetized with pentobarbital
sodium (30 mg/kg), intubated with a cuffed endotracheal tube, placed in
the prone or supine position in a radiolucent body plethysmograph situated in the test field of an orthogonal biplane fluoroscopic system, and mechanically ventilated. The dog was switched from the
ventilator to a supersyringe, and IC was determined by manually inflating the lungs to total lung capacity (TLC), defined as volume at
an airway pressure of 30 cmH2O.
Biplane fluoroscopic images were taken at TLC and at three equally
spaced volumes down to functional residual capacity (FRC).
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The coordinates of the markers in the two orthogonal images were determined, and the three-dimensional coordinates of the markers were calculated from their coordinates in the two orthogonal images. The lengths of the six muscle bundles in the costal diaphragm and two muscle bundles in the crural diaphragm were computed by adding the distances between adjacent markers along each bundle. This sum of the chord lengths is >95% of the length of a smooth curve through the points (25).
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Muscle lengths at FRC of the eight muscle bundles in the two postures are shown in Fig. 2.
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Lengths of costal bundle 3 in the prone and supine postures are plotted vs. VL in Fig. 3. This plot is representative of the data for most muscle bundles in both postures. That is, length decreased with increasing volume by about the same amount in the two volume steps at lower VL, but the change in length in the volume increment to TLC was smaller. In the prone posture the change in length in the step near TLC was about one-half of that at the lower volumes. In the supine posture the same was true for the more ventral bundles, but the change at the last volume step was larger for the more dorsal bundles.
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Fractional changes in muscle length per unit volume change for the
volume interval from FRC to FRC + 
IC are shown in Fig.
4.
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The radiopaque marker technique was adapted to the measurement of
diaphragm muscle length by Rodarte and colleagues (1, 3-5, 24,
25). In particular, Sprung et al. (25) report passive shortening of
three bundles in the costal diaphragm and one bundle in the crural
diaphragm each of five dogs. Their values of passive shortening from
FRC to TLC averaged ~25%, considerably smaller than the values
obtained earlier by sonomicrometry (22). Here we report values of
fractional shortening per liter rather than fractional shortening per
IC. The average IC of our dogs was 0.7 liter, and thus the values of
fractional shortening per liter shown in Fig. 4, ~0.35
liter1, are consistent with
the data of Sprung et al. The number of markers used in our study is
larger than in the study of Sprung et al., and more comprehensive data
on passive muscle shortening were obtained.
As shown in Fig. 2, muscle lengths were slightly larger in the supine than in the prone posture. The distribution of muscle lengths around the circumference of the diaphragm in vivo (Fig. 2) is similar to the distribution obtained by Boriek and Rodarte (2) from measurements in diaphragms that had been excised and laid flat. Muscle length is greater in the midcostal region and smaller and more variable near the dorsal end of the costal diaphragm.
The values of the quantity (dL/LodVL)rel shown in Fig. 4 constitute the primary results of this study, i.e., the values of µ for the diaphragm in the lower two-thirds of the IC. The implications of these data are discussed below.
Circumferential distribution of µ. The distribution of µ is fairly uniform around the diaphragm. However, at the dorsal end of the costal diaphragm, µ is lower than the mean. In the prone dog the region of low µ is confined to the most dorsal muscle bundle sampled. In the supine dog the region of lower µ includes the two or three most dorsal bundles. De Troyer et al. (8, 10, 15, 17) found that the distributions of mass and activation of the parasternals mirror the distribution of µ; muscles with smaller µ are thinner, and their activation during spontaneous breathing, as a fraction of maximum activation, is lower. Data in the literature show a similar correlation between the distributions of diaphragm m and the distribution of µ. The thickness of the muscle layer in the dorsal region of the costal diaphragm is about two-thirds of the thickness in the mid- and ventral regions (20). Also, blood flow to the dorsal region is smaller (6). This implies that the activation is lower in the dorsal region. Thus mass and activation are correlated with µ in the diaphragm as in the parasternals.
Relative µ values of the diaphragm and intercostal
muscles.
In the lower two-thirds of IC, µ of the canine diaphragm is
0.35 ± 0.18 and 0.27 ± 0.16 liter1 in the prone and
supine postures, respectively. This is considerably larger than the
values for the inspiratory muscles of the rib cage. De Troyer and
colleagues (10, 17) report that the values of µ for the parasternal
intercostals vary axially with interspace number and laterally within
each interspace. The maximum occurs near the sternum in the second or
third interspace, and the maximum value in supine animals is ~0.10
liter1. To compare the
values for the diaphragm and parasternals, the size of the animals
should be taken into account. One would expect that fractional length
change per IC would be independent of animal size, IC would be
proportional to body mass, and fractional shortening per liter would
therefore be inversely proportional to IC and body mass. If this were
true and if m were proportional to
body mass, Pao would be independent of animal size. The body mass of
the animals studied by De Troyer et al. ranged from 14 to 25 kg,
whereas the average body mass of our dogs was 10 kg. Scaling the data
on the parasternals to animals of our size yields 0.2 liter1 for the
parasternals. Therefore, the µ of the diaphragm is estimated to be
1.5-2 times the maximum µ of the parasternals.
Pao can be calculated by multiplying µ by
m and . Margulies (20) reported the
masses of the diaphragms of dogs as a function of body mass. For 10-kg
dogs, the size of our animals, diaphragm mass is ~56 g, and most of
this is m. Therefore, for a maximum of 2.2 kg/cm2 (12), the
maximum Pao for the diaphragm is approximately 43 and
33 cmH2O in the prone and
supine postures, respectively. Pao values of 30 to 40
cmH2O are indeed generated during
coordinated inspiratory efforts, but part of Pao is contributed by
muscles of the rib cage. The diaphragm is never maximally activated
during spontaneous inspiratory efforts (4, 13), and its contribution to
Pao is less than the value computed for maximum activation.
Although the computed value of maximum Pao for the diaphragm has no
functional significance, the value of µ can be used to infer the
value of a quantity with physiological interest, i.e., the fraction of
the total inspiratory pressure that is contributed by the diaphragm
during coordinated inspiratory effort. First, Pao, as described by
Eq. 1, must be distinguished from
transdiaphragmatic pressure (Pdi), which is often used to describe
diaphragm function. Pao is the change in airway pressure produced by
in the muscle. The is converted to Pao by a complicated
mechanism that involves the entire chest wall. Although this mechanism
cannot be traced in detail, its effect is summarized by the value of
µ. Pdi also depends on stress in the diaphragm, but the mechanism
that transforms muscle stress to Pdi is a local mechanism that can be
described in detail (4). In the midcostal region, where the diaphragm has the shape of a right circular cylinder, Pdi is proportional to
/r, where is membrane tension
(kg/cm) and r is the radius of
curvature of the sheet. In turn, = t, where
t is the thickness of the muscle
sheet. Thus
|
(3) |
(kg/cm2) to pressure
(cmH2O).
During a coordinated inspiratory effort, the diaphragm and the muscles
of the rib cage contribute to Pao. These two contributions are
denoted Paodi and
Paorc. The total is denoted
Paotot, and Paotot = Paodi + Paorc. Pdi is the difference
between gastric pressure and pleural pressure. During an inspiratory
effort against an occluded airway, the change in gastric pressure is
small compared with the change in pleural pressure, and the change in
pleural pressure equals Pao. Therefore, Pdi ~ Paotot, and the fraction f of Paotot that is contributed
by the diaphragm is
|
(4) |
Paodi from
Eq. 1 and Pdi from
Eq. 3 yields the following equation
for f
|
(5) |
Pao of 30
cmH2O, the contribution of the
diaphragm is 12 cmH2O. This
is ~30% of Paodi at maximum , and therefore is ~30% of maximum. It should be emphasized that some assumptions were made in deriving Eq. 5. In particular, it was assumed that the inspiratory
effort was a coordinated effort and that the change in gastric pressure
was small compared with Pao. Also, the values of the parameters
m, r, and
t that were substituted into
Eq. 5 came from a variety of sources.
As a result, the value of f should be taken as an estimate.
Volume dependence of µ.
In the upper one-third of IC, passive diaphragm muscle shortening per
unit increase in VL is less than
one-half of that in the lower two-thirds of IC. Thus the µ of the
diaphragm drops sharply at high
VL. We looked for the change in
coupling between the diaphragm and the lung that would account for this
decrease in diaphragm function at high volume. We focused on the muscle bundles of the midcostal diaphragm that we studied previously (1, 4,
5), i.e., costal bundles 2-4. The
coordinates of the markers on these bundles were transformed to a local
-
-
coordinate system that we used to describe this region. A
plane was fit to the 12 markers. A quadratic was fit to the distances of the markers from this plane, and the directions of the principal curvatures of the quadratic were determined. The -axis was chosen to
lie along the direction of minimum principal curvature, and the
-axis was chosen to lie parallel to the midplane of the dog. As we
found previously, the minimum principal curvature of the diaphragm
surface is small in this region, and the muscle bundles of the
midcostal diaphragm lie in planes that are nearly parallel to the
- plane shown in Fig. 5. The average
values of the - and -coordinates of corresponding markers in the
three bundles in the four dogs were computed (Fig.
6); i.e., each point in Fig. 6 is the
average of 12 values. For example, the point on the chest wall is the
average coordinate of 12 markers: 1 for each marker on the chest wall
of the 3 bundles in 4 dogs.
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and a given increase in Pdi,
gastric pressure would rise more and pleural pressure would fall less.
The data shown in Fig. 6 have an unexpected feature: the line of
insertion of the diaphragm on the chest wall moves caudally as
VL increases. Although we know
of no data on the displacement of the caudal ribs during passive
inflation, the more cranial ribs move cranially during passive
inflation (21), and the more caudal ribs also move cranially during
active inspiration (7). We therefore expected that the caudal ribs and
the line of insertion would move cranially as
VL increased. Perhaps the
location of the line of insertion is affected by tensions in the
diaphragm and abdominal muscles. If that were the case, the caudal
displacement with increasing VL
may be the result of decreasing tension in the diaphragm and increasing
tension in the abdominal muscles.
The geometric effect of the caudal displacement of the line of
insertion on muscle length is clear. Roughly speaking, shortening is
proportional to the relative displacement between the dome and the line
of insertion. For a given caudal displacement of the dome, the muscle
shortens less if the line of insertion moves caudally than it would if
the line of insertion moved cranially. The mechanical consequences of
this geometric relationship are described by Eq. 2. Greater passive shortening implies a greater inspiratory effect per unit . However, there are competing effects of shortening on muscle function. Greater shortening would cause a
greater displacement along the length-tension curve and a greater change in diaphragm shape. If the line of insertion moved cranially, maximum tension and diaphragm curvature would decrease more rapidly with increasing VL, and the
range of VL values over which
the diaphragm could exert an inspiratory force would be reduced. For example, if the axial displacement of the line of insertion shown in
Fig. 6 were reversed, muscle length at TLC would be ~50% of length
at FRC and the diaphragm would be flat. Maximum tension approaches zero
at that length (12), and tension is not converted to pressure if the
diaphragm is flat (4). Of course, this tradeoff between µ and volume
range is simply a result of the fact that the length-tension curve sets
a constraint on the work that the muscle can deliver.
Summary. The primary results of this study are as follows.
1) The value of µ for the canine diaphragm is0.35
liter1 in the prone posture
and somewhat smaller, i.e., 0.27
liter1, in the supine
posture. This is 1.5-2 times the µ of the intercostal muscles
with greatest µ. In addition, the value of µ is uniform around most
of the costal and crural diaphragms but lower near the dorsal end of
the costal diaphragm. The distributions of
m and activation are correlated with
the distribution of µ. Finally, we estimate that the diaphragm
contributes ~40% of inspiratory pressure in the prone posture. We
also estimate that, during a coordinated inspiratory effort that
produces an inspiratory pressure of 30 cmH2O, in the diaphragm is
~30% of maximum.
2) The value of µ decreases at higher
VL, and we attribute this to the
decrease in the height of the zone of apposition and, more importantly,
to a decrease in the volume expansion of the abdominal compartment at
high VL. In addition, the line
of insertion of the midcostal diaphragm moves caudally as
VL increases. As a result, the
value of µ is smaller, but the volume range of diaphragm function is larger.
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ACKNOWLEDGEMENTS |
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This work was supported by National Heart, Lung, and Blood Institute Grants HL-45545 and HL-46230.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: T. A. Wilson, 107 Akerman Hall, 110 Union St. SE, Minneapolis, MN 55455.
Received 2 March 1998; accepted in final form 18 August 1998.
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REFERENCES |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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1.
Boriek, A. M.,
S. Liu,
and
J. R. Rodarte.
Costal diaphragm curvature in the dog.
J. Appl. Physiol.
75:
527-533,
1993
2.
Boriek, A. M.,
and
J. R. Rodarte.
Inferences on passive diaphragm mechanics from gross anatomy.
J. Appl. Physiol.
77:
2065-2070,
1994
3.
Boriek, A. M.,
J. R. Rodarte,
and
S. S. Margulies.
Zone of apposition in the passive diaphragm of the dog.
J. Appl. Physiol.
81:
1929-1937,
1996
4.
Boriek, A. M.,
J. R. Rodarte,
and
T. A. Wilson.
Kinematics and mechanics of midcostal diaphragm of dog.
J. Appl. Physiol.
83:
1068-1075,
1997
5.
Boriek, A. M.,
T. A. Wilson,
and
J. R. Rodarte.
Displacements and strains in the costal diaphragm of the dog.
J. Appl. Physiol.
76:
223-229,
1994
6.
Brancatisano, A.,
T. C. Amis,
A. Tully,
W. T. Kelly,
and
L. A. Engle.
Regional distribution of blood flow within the diaphragm.
J. Appl. Physiol.
71:
583-589,
1991
7.
De Troyer, A.
The electro-mechanical response of canine inspiratory intercostal muscles to increased resistance: the caudal rib-cage.
J. Physiol. (Lond.)
451:
463-476,
1991
8.
De Troyer, A.,
and
A. Legrand.
Inhomogeneous activation of the parasternal intercostals during breathing.
J. Appl. Physiol.
79:
55-62,
1995
9.
De Troyer, A.,
and
A. Legrand.
Mechanical advantage of the canine triangularis sterni muscle.
J. Appl. Physiol.
84:
562-568,
1998
10.
De Troyer, A.,
A. Legrand,
and
T. A. Wilson.
Rostrocaudal gradient of mechanical advantage in the parasternal intercostal muscles of the dog.
J. Physiol. (Lond.)
495:
239-246,
1996[Medline].
11.
De Troyer, A.,
M. Sampson,
S. Sigrist,
and
P. T. Macklem.
Action of costal and crural parts of the diaphragm on the rib cage in dog.
J. Appl. Physiol.
53:
30-39,
1982
12.
Farkas, G. A.,
and
D. F. Rochester.
Functional characteristics of canine costal and crural diaphragm.
J. Appl. Physiol.
65:
2253-2260,
1988
13.
Hershenson, M. B.,
Y. Kikuchi,
and
S. H. Loring.
Relative strengths of the chest wall muscles.
J. Appl. Physiol.
65:
852-862,
1988
14.
Hubmayr, R. D.,
J. Sprung,
and
S. Nelson.
Determinants of transdiaphragmatic pressure in dogs.
J. Appl. Physiol.
69:
2050-2056,
1990
15.
Legrand, A.,
A. Brancatisano,
M. Decramer,
and
A. De Troyer.
Rostrocaudal gradient of electrical activation in the parasternal intercostal muscles of the dog.
J. Physiol. (Lond.)
495:
247-254,
1996[Medline].
16.
Legrand, A.,
V. Ninane,
and
A. De Troyer.
Mechanical advantage of sternomastoid and scalene muscles in dogs.
J. Appl. Physiol.
82:
1517-1522,
1997
17.
Legrand, A.,
T. A. Wilson,
and
A. De Troyer.
Mediolateral gradient of mechanical advantage in the canine parsternal intercostals.
J. Appl. Physiol.
80:
2097-2101,
1996
18.
Legrand, A.,
T. A. Wilson,
and
A. De Troyer.
Rib cage muscle interaction in airway pressure generation.
J. Appl. Physiol.
85:
198-203,
1998
19.
Loring, S. H.,
and
J. Mead.
Action of the diaphragm on the rib cage inferred from a force-balance analysis.
J. Appl. Physiol.
53:
756-760,
1982
20.
Margulies, S. S.
Regional variation in canine diaphragm thickness.
J. Appl. Physiol.
70:
2663-2668,
1991
21.
Margulies, S. S.,
J. R. Rodarte,
and
E. A. Hoffman.
Geometry and kinematics of dog ribs.
J. Appl. Physiol.
67:
707-712,
1989
22.
Newman, S.,
J. Road,
F. Bellemare,
J. P. Clozel,
C. M. Lavigne,
and
A. Grassino.
Respiratory muscle length measured by sonomicrometry.
J. Appl. Physiol.
56:
753-764,
1984
23.
Smith, J. C.,
and
S. H. Loring.
Passive mechanical properties of the chest wall.
In: Handbook of Physiology. The Respiratory System. Mechanics of Breathing. Bethesda, MD: Am. Physiol. Soc., 1986, sect. 3, vol. III, pt. 2, chapt. 25, p. 429-442.
24.
Sprung, J.,
C. Deschamps,
R. D. Hubmayr,
B. J. Walters,
and
J. R. Rodarte.
In vivo regional diaphragm function in dogs.
J. Appl. Physiol.
67:
655-662,
1989
25.
Sprung, J.,
C. Deschamps,
S. S. Margulies,
R. D. Hubmayr,
and
J. R. Rodarte.
Effect of body position on regional diaphragm function in dogs.
J. Appl. Physiol.
69:
2296-2302,
1990
26.
Tao, H.-Y.,
and
G. A. Farkas.
Predictability of ventilatory muscle optimal length based on excised dimensions.
J. Appl. Physiol.
72:
2024-2028,
1992
27.
Wilson, T. A.,
and
A. De Troyer.
Effect of respiratory muscle tension on lung volume.
J. Appl. Physiol.
73:
2283-2288,
1992
28.
Wilson, T. A.,
and
A. De Troyer.
Respiratory effect of the intercostal muscles in the dog.
J. Appl. Physiol.
75:
2636-2645,
1993
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R. L. Johnson Jr., C. C. W. Hsia, S.-I. Takeda, J. L. Wait, and R. W. Glenny Efficient design of the diaphragm: distribution of blood flow relative to mechanical advantage J Appl Physiol, September 1, 2002; 93(3): 925 - 930. [Abstract] [Full Text] [PDF]
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A. M. Boriek, N. G. Kelly, J. R. Rodarte, and T. A. Wilson Biaxial constitutive relations for the passive canine diaphragm J Appl Physiol, December 1, 2000; 89(6): 2187 - 2190. [Abstract] [Full Text] [PDF]
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C. C. W. Hsia, S.-I. Takeda, E. Y. Wu, R. W. Glenny, and R. L. Johnson Jr. Adaptation of respiratory muscle perfusion during exercise to chronically elevated ventilatory work J Appl Physiol, November 1, 2000; 89(5): 1725 - 1736. [Abstract] [Full Text] [PDF]
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M. Angelillo, A. M. Boriek, J. R. Rodarte, and T. A. Wilson Shape of the canine diaphragm J Appl Physiol, July 1, 2000; 89(1): 15 - 20. [Abstract] [Full Text] [PDF]
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A. M. Boriek, J. R. Rodarte, and T. A. Wilson Ratio of active to passive muscle shortening in the canine diaphragm J Appl Physiol, August 1, 1999; 87(2): 561 - 566. [Abstract] [Full Text] [PDF]
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