Physiology of obesity and effects on lung function

Cheryl M. Salome, Gregory G. King and Norbert Berend

J Appl Physiol 108:206-211, 2010. First published 29 October 2009;
doi:10.1152/japplphysiol.00694.2009
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J Appl Physiol 108: 206 211, 2010.

First published October 29, 2009; doi:10.1152/japplphysiol.00694.2009.

Review

HIGHLIGHTED TOPIC

Pulmonary Physiology and Pathophysiology in Obesity

Physiology of obesity and effects on lung function

Cheryl M. Salome,1,2 Gregory G. King,1,2,3 and Norbert Berend1,2
1

Woolcock Institute of Medical Research, Glebe; 2University of Sydney, Sydney; and 3Department of Respiratory Medicine,
Royal North Shore Hospital, St. Leonards, New South Wales, Australia
Submitted 30 June 2009; accepted in final form 27 October 2009

spirometry; lung volumes lung mechanics; airway closure; ventilation distribution

risk of respiratory symptoms,

such as breathlessness, particularly during exercise, even if
they have no obvious respiratory illness (4, 45). Obesity has a
clear potential to have a direct effect on respiratory well-being,
since it increases oxygen consumption and carbon dioxide
production, while at the same time it stiffens the respiratory
system and increases the mechanical work needed for breathing. The association between obesity and asthma has also
raised new concerns about whether the mechanical effects of
obesity on the respiratory system contribute to airway dysfunction that could induce or worsen asthma. This review will
explore the effects of obesity [body mass index (BMI) 30
kg/m2] on normal pulmonary physiology. The more substantial derangements associated with the obesity-hypoventilation
syndrome are the subject of another review in this series.
OBESE PEOPLE ARE AT INCREASED

LUNG VOLUMES

The most consistently reported effect of obesity on lung

function is a reduction in the functional residual capacity
(FRC) (28, 40). This effect reflects a shift in the balance of
inflationary and deflationary pressures on the lung due to the
Address for reprint requests and other correspondence: C. Salome, Woolcock Institute of Medical Research, P.O. Box M77, Missenden Rd. NSW 2050,
Australia (e-mail: cms@woolcock.org.au).
206

mass load of adipose tissue around the rib cage and abdomen
and in the visceral cavity (52). There is an exponential relationship between BMI and FRC (28, 40), with a reduction in
FRC detectable even in overweight individuals (28). In obesity,
the reduction in FRC may become so marked that the FRC
approaches residual volume (RV).
However, the effects of obesity on the extremes of lung
volumes, at total lung capacity (TLC) and RV, are modest.
Many studies report an association between increasing body
weight and decreasing TLC (11, 28, 42); however, the changes
are small, and TLC is usually maintained above the lower limit
of normal, even in severe obesity (11, 28, 63). The RV is
usually well preserved (5, 11, 48, 63, 67), and the RV-to-TLC
ratio remains normal or slightly increased (5, 28). In the
presence of a modest reduction in TLC and a well-preserved
RV, the reduction in FRC is manifested by an increase in
inspiratory capacity and a very marked decrease in the expiratory reserve volume (ERV) (28).
The reasons for the reduction in TLC are not known, but it
is probably due to a mechanical effect of the adipose tissue,
since TLC is increased by weight loss in both mild (64) and
morbidly obese (60) subjects. A reduction in the downward
movement of the diaphragm, due to increased abdominal mass,
is likely to decrease TLC by limiting the room for lung
expansion on inflation. Alternatively, deposition of fat in sub-

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Salome CM, King GG, Berend N. Physiology of obesity and effects on lung
function. J Appl Physiol 108: 206 211, 2010. First published October 29, 2009;
doi:10.1152/japplphysiol.00694.2009.In obese people, the presence of adipose
tissue around the rib cage and abdomen and in the visceral cavity loads the chest
wall and reduces functional residual capacity (FRC). The reduction in FRC and in
expiratory reserve volume is detectable, even at a modest increase in weight.
However, obesity has little direct effect on airway caliber. Spirometric variables
decrease in proportion to lung volumes, but are rarely below the normal range, even
in the extremely obese, while reductions in expiratory flows and increases in airway
resistance are largely normalized by adjusting for lung volumes. Nevertheless, the
reduction in FRC has consequences for other aspects of lung function. A low FRC
increases the risk of both expiratory flow limitation and airway closure. Marked
reductions in expiratory reserve volume may lead to abnormalities in ventilation
distribution, with closure of airways in the dependent zones of the lung and
ventilation perfusion inequalities. Greater airway closure during tidal breathing is
associated with lower arterial oxygen saturation in some subjects, even though lung
CO-diffusing capacity is normal or increased in the obese. Bronchoconstriction has
the potential to enhance the effects of obesity on airway closure and thus on
ventilation distribution. Thus obesity has effects on lung function that can reduce
respiratory well-being, even in the absence of specific respiratory disease, and may
also exaggerate the effects of existing airway disease.

Review
PHYSIOLOGY OF OBESITY AND EFFECTS ON LUNG FUNCTION

pleural spaces (49) might directly reduce lung volume by

reducing the volume of the chest cavity, although there is no
direct evidence of any association between subpleural fat and
either body fat or lung volumes. Evidence that respiratory
muscle strength and maximum inspiratory and expiratory pressures are similar in obese and normal weight subjects (29, 48,
65) suggests that stiffening of the chest wall is probably not a
major determinant of TLC.
FAT DISTRIBUTION AND BODY COMPOSITION

obesity, as well as in studies of conscious subjects using

different measurement techniques (53, 55). Sharp et al. (52)
found that mass loading of the thorax in normal weight conscious or anesthetized/paralyzed subjects produces a parallel
rightward shift of the chest wall pressure-volume curve without
affecting compliance. The chest wall pressure-volume curve of
obese subjects resembled that of normal subjects with mass
loading of the thorax. Excess body mass in simple obesity may
act as an inspiratory threshold load, and, once the threshold is
overcome, the chest wall behaves normally.
AIRWAY FUNCTION

Spirometric variables, such as forced expiratory volume in 1

s (FEV1) and forced vital capacity (FVC), tend to decrease
with increasing BMI (51, 54, 67). However, the effect is small,
and both FEV1 and FVC are usually within the normal range in
healthy, obese adults (51, 54) and children (50). The FEV1-toFVC ratio is usually well preserved or increased (31, 44, 51,
54, 67), even in morbid obesity (5), indicating that both FEV1
and FVC are affected to the same extent. This finding implies
that the major effect of obesity is on lung volumes, with no
direct effect on airway obstruction.
Similarly, expiratory flows decrease with increasing weight
(5, 44), in proportion to the lung volumes (67). A decrease in
expiratory flows in an obese individual is unlikely to indicate
bronchial obstruction, unless the flow measurements have been
normalized for the reduction in vital capacity. Figure 1 shows
flow volume loops from a healthy obese woman with significant reduction in lung volumes, but very well preserved expiratory flows. However, the expiratory flow at 50% of the
reduced vital capacity is low compared with the predicted
value, based on the predicted vital capacity. In a large sample
of obese and normal weight nonsmokers, Rubenstein et al. (44)
found significant reductions in expiratory flows in obese men,
but not in obese women. The difference between obese and

LUNG AND RESPIRATORY SYSTEM MECHANICS

Obesity is characterized by a stiffening of the total respiratory system (35), which is presumed to be due to a combination
of effects on lung and chest wall compliance (41). Most studies
have demonstrated a reduction in lung compliance in obese
individuals (21, 40, 41, 53) that appears to be exponentially
related to BMI (40). Reductions in lung compliance may be the
result of increased pulmonary blood volume, closure of dependent airways, resulting in small areas of atelectasis (21), or
increased alveolar surface tension due to the reduction in FRC.
Evidence for an effect of obesity on chest wall compliance
varies between studies, possibly as a result of methodological
differences. Measurement of chest wall compliance is difficult,
since the respiratory muscles must be relaxed and inactive to
allow an accurate measurement. Studies of conscious, spontaneously breathing subjects have suggested that there is a
reduction in chest wall compliance in obesity (35). However,
normal chest wall compliance has been reported in studies of
anesthetized, paralyzed subjects in mild (40) or severe (21)
J Appl Physiol VOL

Fig. 1. Flow-volume loops from healthy obese female, aged 35 yr, BMI 43
kg/m2, with reduced total lung capacity (TLC), functional residual capacity
(FRC), and vital capacity, but well-preserved expiratory flows. The dashed line
shows the predicted flow-volume loop; the solid line is the actual loop. The
predicted lung volumes are shown on the bar, vertical arrow shows predicted
flow at 50% vital capacity, and horizontal arrow shows the actual value. RV,
residual volume.

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BMI is a global measure of body mass that includes both fat

and lean mass and takes no account of differences in fat
distribution. If the reduction of lung volumes in obesity is due
to a direct mechanical effect on lung volumes, then the distribution of body fat should modify the relationship between BMI
and lung volumes. Abdominal and thoracic fat are likely to
have direct effects on the downward movement of the diaphragm and on chest wall properties, while fat on the hips and
thighs would be unlikely to have any direct mechanical effect
on the lungs. Both abdominal fat, measured by waist circumference (10), waist-to-hip ratio (7), or abdominal height (37),
and thoracic or upper body fat, measured by subscapular skin
fold thickness (31) or biceps skin fold thickness (11), are
associated with reductions in lung volumes. Several studies
have used dual-energy X-ray absorptiometry (DXA) to quantify fat and lean mass in different regions of the body and relate
these findings to lung function (12, 58). Sutherland et al. (58)
used a wide range of body fat variables to determine the effect
of fat distribution on lung volumes in healthy adults. Lung
volumes were only loosely associated with BMI, but both
DXA and non-DXA-derived variables reflecting upper body fat
had highly significant negative correlations with FRC and ERV
in both men and women. There were no differences in the
strength of these associations between the markers of abdominal obesity (waist circumference, waist-to-hip ratio, DXA
waist fat, DXA abdominal fat) or thoracic fat (DXA trunk fat,
DXA thoracic fat). These findings confirm the important effect
of upper body fat on the lung, but the inability to differentiate
the effects of abdominal and thoracic fat suggests that they may
be interdependent.

207

Review
208

PHYSIOLOGY OF OBESITY AND EFFECTS ON LUNG FUNCTION

J Appl Physiol VOL

allow larger studies to determine the extent of expiratory flow

limitation in obese populations.
TIDAL VOLUMES

Tidal volumes are often reduced in severe obesity, and

breathing follows a rapid, shallow pattern (48). This pattern is
likely to be a response to the increased stiffness of the respiratory system, since a rapid, shallow breathing pattern is a
typical response to an elastic load (1), which can be induced in
normal weight subjects with elastic strapping of the chest (8).
During exercise, obese subjects preferentially increase their
breathing frequency more, and tidal volumes less, than nonobese subjects (15, 38). Similar changes occur during bronchoconstriction in association with increasing elastic loads, represented by increasing respiratory system elastance (47). However, in mild-moderate obesity, tidal volumes at rest are often
in the normal range (6, 38, 47, 62), and the frequency and
magnitude of regular sighs and deep inspirations appear similar
to those in normal weight subjects (6, 62). This suggests that
the modulation of airway smooth muscle contractility by regular tidal stretching and deep inspirations (19) may be unimpaired in mild-moderate obesity.
AIRWAY CLOSURE, VENTILATION DISTRIBUTION,
AND GAS EXCHANGE

As FRC is reduced to the extent that it approaches RV, the

obese individual is at increased risk of airway closure and
abnormalities of ventilation distribution. Indicators of gas trapping and airway closure, such as RV (48, 63) and closing
capacity (22), are not usually increased in the obese at rest.
However, there is consistent evidence that, because the FRC is
so low, closing capacity exceeds the FRC, and airway closure
can occur within the tidal breaths (17, 20, 22, 34). Closing
capacity, and particularly the extent to which closure occurs
within the range of tidal breathing, has been correlated with
arterial PO2 (17, 22), raising the possibility that airway closure
during tidal breathing is associated with underventilation of
some regions of the lung.
Physiological studies using single breath or multibreath
washout tests suggest that heterogeneity of ventilation is normal or close to normal, even in extreme obesity. Heterogeneity
of ventilation distribution, measured by slope of phase III from
single-breath washouts or by lung clearance index, is normal in
the obese (22). However, studies using imaging techniques
reveal abnormalities of regional ventilation in some obese
individuals. In an upright nonobese individual, the distribution
of regional ventilation is greatest in the lower, dependent lung
zones and decreases toward the upper zones. In obese individuals, this distribution may be reversed (14, 23, 24). Holley
et al. (23) found that, in obese subjects with marked reductions
in ERV to 20% predicted, ventilation was preferentially
distributed to the upper zones of the lung, leaving the lower,
dependent zones relatively underventilated. Demedts (14)
found reduced regional ventilation in the lower zones in obese
subjects, consistent with relative air trapping in the bases.
While the mechanism for this underventilation and air trapping
in the bases is not clear, Demedts suggests that it is unlikely,
due to intrinsic changes in the airways that cause them to close
at higher transpulmonary pressure. Instead, he suggests that
limitations in chest wall and diaphragm movements alter the

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normal weight men in expiratory flow at 50% of the reduced

vital capacity disappeared after normalization for vital capacity. However, significant differences in expiratory flow at 25%
of the reduced vital capacity persisted after normalization,
suggesting the possibility of peripheral airway obstruction in
obese men.
Mechanical properties of the airway, such as resistance and
reactance, are highly dependent on lung volume and are,
therefore, affected by any reduction in FRC. Respiratory resistance is increased in the obese (65), indicating that airway
caliber is reduced throughout the tidal breathing cycle. However, specific airway resistance, calculated by adjusting for the
lung volume at which the measurements were made, is in the
normal range (36, 44, 65, 67), so that the apparent reduction in
airway caliber in the obese is attributable to the reduction in
lung volumes rather than to airway obstruction. However,
some studies have suggested that the increase in resistance may
not be due entirely to the reduced lung volume, since differences between obese and nonobese may persist after adjustment for lung volumes (30, 63). The cause of the additional
resistance is unknown, and it is unclear whether there are any
structural changes in the airways of the obese. It is possible that
airway structures could be remodeled by exposure to proinflammatory adipokines, or damaged by the continual opening
and closing of small airways throughout the breathing cycle
(34). It is not known whether fat is present in the airways of
obese people or has any direct effect on airway structure, but
studies of diet-induced obesity in rats have reported changes in
lipid deposition in the lungs (26), which may affect surfactant
function (25). There is some evidence that peripheral airway
obstruction may be increased in the obese, since the frequency
dependence of resistance increases with increasing obesity
(67). Furthermore, frequency dependence of compliance was
increased in a group of morbidly obese subjects who had
normal lung compliance, but very low ERV (16). Longitudinal
studies of the effects of weight loss might be enlightening,
since improvements in lung volumes after weight loss that are
not accompanied by improvements in volume-adjusted airway
caliber could suggest that there is a persistent remodeling of the
airways, rather than a direct mechanical effect on airway
caliber.
Breathing at low lung volume places the tidal flow volume
loop in a region where it may encroach on the maximal flow
volume envelope (Fig. 1) and thus increase the risk of expiratory flow limitation in the obese individual. However, it is not
clear whether expiratory flow limitation is a common occurrence in the obese. Two studies (18, 39), using the negative
expiratory pressure technique, have found that expiratory flow
limitation only occurred in 20% of severely obese subjects
when upright, but both expiratory flow limitation and breathlessness increase substantially when the subjects are supine.
However, the negative expiratory pressure technique uses a
forced expiration and may not be able to detect expiratory flow
limitation that occurs during tidal breathing at low lung volumes. Ofir et al. (38) quantified expiratory flow limitation from
the flow-volume loop, as the percentage of the tidal volume
that encroached on the maximal flow envelope, and found
highly significant differences between obese and normal
weight women seated at rest. New techniques are available for
measuring expiratory flow limitation during tidal breathing,
based on the forced oscillation technique (13), that would

Review
PHYSIOLOGY OF OBESITY AND EFFECTS ON LUNG FUNCTION

configuration of the lungs and enhance basal air trapping at low

lung volumes. The distribution of perfusion is predominantly
to the lower zones, so those obese individuals with a reversal
of the normal distribution of ventilation are at risk of regional
ventilation-perfusion mismatch in the dependent zones of the
lung (23).
Mild hypoxemia and increased alveolar-arterial oxygen difference are frequently reported, even in eucapnic obese individuals (21, 22, 27, 40, 60), and have been associated with
abdominal obesity in the morbidly obese (66). However, the
effect of weight loss on gas exchange is variable, since some
studies show improvements in arterial oxygen tensions (43,
60), while others report no change (20, 64), despite a concurrent reduction in closing capacity (20). Most studies suggest
that lung CO-diffusing capacity is normal (15, 42, 53, 57), even
in morbid obesity (5). However, some studies suggest it may be
increased in extremely obese subjects (42, 44), probably as a
result of the increase in blood volume (42).
BREATHLESSNESS DURING EXERCISE AND AT REST

J Appl Physiol VOL

EFFECTS OF BRONCHOCONSTRICTION ON LUNG FUNCTION

IN THE OBESE

Recent interest in the association between obesity and

asthma raises the question of whether the physiological effects
of obesity modulate the pathophysiology of asthma. Nicolacakis et al. (36) suggest that obesity and asthma have additive,
rather than synergistic effects, on outcomes such as spirometry
and lung volumes, implying that asthma and obesity affect the
respiratory system through different processes. It remains unclear whether there is any association between obesity and
airway hyperresponsiveness, a characteristic feature of the
pathophysiology of asthma. However, the reduction in operating lung volume in the obese has the potential to modify the
effects of bronchoconstriction and increase the occurrence of
expiratory flow limitation. Bronchoconstriction in the obese is
associated with increased airway closure compared with nonobese controls (9) and thus could increase gas trapping and alter
ventilation distribution, but there are no published data about
the effect of bronchoconstriction on ventilation distribution in
the obese. Bronchoconstriction causes greater hyperinflation in
obese asthmatic (56) and nonasthmatic (47) subjects, which
may increase the severity of dyspnea (32). The occurrence of
additional elastic loads during bronchoconstriction, reflected
by greater changes in respiratory system reactance in obese
than nonobese subjects (47, 62), which are not well reflected by
spirometry, may explain why some obese asthmatic subjects
have more severe symptoms than their lean counterparts,
despite similar spirometry (61). In patients with moderate
chronic obstructive pulmonary disease, a simulated increase in
body weight of 10 kg resulted in a marked reduction in exercise
performance (59), suggesting that the combination of increased
weight and airway obstruction could have a substantial effect
on respiratory well-being.
IMPLICATIONS FOR FUTURE RESEARCH

Although the physiology of obesity and its effects on lung

function have been the subject of intense investigation over the
last 50 years, the recent observation of the association between
asthma and obesity has raised new questions about the mechanical effects of obesity on the lungs, and the mechanisms
that drive breathlessness in the obese are still not well understood.
It is still unknown whether obesity has any effect on the
structure of the airways, either by altered lipid deposition or by
remodeling. Although these questions may be best answered
by direct studies of airway pathology, physiological studies of
the effects of weight loss on volume-adjusted flow and resistance would also be useful.
Expiratory flow limitation is a potentially important determinant of breathlessness in the obese, although studies using
negative expiratory pressure suggest that flow limitation is not
a common feature of obesity. However, the negative expiratory
pressure technique may be an inappropriate method to detect
flow limitation during tidal breathing at low FRC in the obese.
Studies using a measurement based on tidal breathing (13)
would be useful to determine the prevalence of flow limitation
in obese populations and its relationship to lung volume and to
breathlessness.
Bronchoconstriction has the potential to enhance some of the
effects of obesity, such as airway closure, which may then

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Breathlessness during exercise is a common complaint

among obese individuals, but the mechanisms that drive these
symptoms are not well defined. In severely obese subjects,
Dempsey et al. (15) found that, even during maximal exercise
on a cycle ergometer, these subjects were able to increase their
ventilation sufficiently to avoid hypercapnia. Furthermore, the
ventilatory response to inhaled CO2 in these obese subjects was
not different from that in a normal weight control group (15).
Peak exercise capacity, in terms of both peak work rate and
oxygen consumption, is normal in healthy obese subjects (2, 3,
38). Ofir et al. (38) compared obese and normal weight women
during cycle exercise and found that, although oxygen consumption and minute ventilation were greater in the obese
subjects at all work rates, the relationships between breathlessness scores and both oxygen consumption and minute ventilation were no different in the obese and normal weight subjects.
The implication of this finding is that the determinants of
breathlessness were similar in obese and normal weight subjects, and that respiratory mechanical factors related to obesity
did not contribute to breathlessness in the obese subjects. Babb
et al. (3) found there was no difference in peak exercise
capacity between obese women with and without exertional
breathlessness; however, breathlessness was associated with a
greater increase in the oxygen cost of breathing during exercise.
Breathlessness at rest may also be reported by obese individuals (4, 45), but it is unclear if this is due entirely to obesity.
Sahebjami and Gartside (45, 46) found that, among 23 healthy
obese men, the 15 who reported breathing difficulties at rest
had lower maximum voluntary ventilation and lower maximal
expiratory flows at low lung volumes. The dyspneic group also
included a greater proportion of smokers, which may account
for some of the symptoms and differences in lung function.
However, the link between breathlessness and poor performance on a test of maximum voluntary ventilation may be
associated with an increase in the oxygen cost of breathing,
since the oxygen cost of breathing increases parabolically with
breathing frequency (33).

209

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PHYSIOLOGY OF OBESITY AND EFFECTS ON LUNG FUNCTION

affect ventilation distribution. A better understanding of the

extent to which obesity modifies the physiological effects of
bronchoconstriction may improve our understanding of the
relationship between asthma and obesity.

23.

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