Respiratory Physiology & Neurobiology 151 (2006) 124131

Does gender affect pulmonary function

and exercise capacity?
Craig A. Harms
1A Natatorium, Department of Kinesiology, Kansas State University, Manhattan, KS 66506, USA
Accepted 21 October 2005

Abstract
It is well established that women exhibit several anatomic and physiologic characteristics that distinguish their responses to
exercise from those of men. These factors have been shown to influence the training response and contribute to lower maximal
aerobic power in women. Additionally, the reproductive hormones, estrogen and progesterone, can influence ventilation, substrate
metabolism, thermoregulation, and pulmonary function during exercise. Pulmonary structural and morphologic differences
between genders include smaller vital capacity and maximal expiratory flow rates, reduced airway diameter, and a smaller
diffusion surface than age- and height-matched men. These differences may have an effect on the integrated ventilatory response,
respiratory muscle work, and in pulmonary gas exchange during exercise. Specifically, recent evidence suggests that during heavy
exercise, women demonstrate greater expiratory flow limitation, an increased work of breathing, and perhaps greater exercise
induced arterial hypoxemia compared to men. The consequence of these pulmonary effects has the potential to adversely affect
aerobic capacity and exercise tolerance in women.
2005 Elsevier B.V. All rights reserved.
Keywords: Gender; Sex differences; Exercise; Gas exchange; Ventilatory limitations

1. Introduction
Participation in regular physical activity is well recognized as having important health benefits. As a result
of increased awareness and emphasis in physical activity, research investigating the effect of exercise on var This paper is part of the Special Issue entitled New Directions
in Exercise Physiology, guest-edited by Susan Hopkins and Peter
D. Wagner.
Tel.: +1 785 532 0706; fax: +1 785 532 6486.
E-mail address: caharms@ksu.edu.

1569-9048/$ see front matter 2005 Elsevier B.V. All rights reserved.
doi:10.1016/j.resp.2005.10.010

ious physiologic systems has dramatically increased

over the past several decades. However, the vast majority of this research has investigated the physiologic
responses in men while comparatively few articles have
focused on women or on sex differences. Consequently,
research investigating gender on various components
of physical performance and on various physiological
systems is still evolving. For example, it is known that
there are important sex differences with regard to cardiovascular function (Wiebe et al., 1998; Spina et al.,
1993), thermoregulation (Stephenson and Kolka, 1985;
Grucza et al., 1993), substrate metabolism (Horton et

C.A. Harms / Respiratory Physiology & Neurobiology 151 (2006) 124131

al., 1998; Tarnopolsky, 2000; Mittendorfer et al., 2002),

and pulmonary function (Harms et al., 1998b; Hopkins
et al., 2000; McClaran et al., 1998) during exercise
which may have implications for exercise tolerance.
Specific in regards to the pulmonary system, there has
been considerable interest in defining sex-based differences in the pulmonary systems response to exercise.
Important sex differences exist in resting pulmonary
function that might have an effect on the integrated
ventilatory response, respiratory muscle work, and on
gas exchange during exercise which may in turn affect
exercise capacity in health.

2. Basis for sex differences in pulmonary

function
The basis for sex differences in pulmonary function
and exercise tolerance is primarily from two sources;
namely hormones (especially progesterone and estrogen), and in structural/morphological differences. This
review will address the role of each of these mechanisms and how they can affect pulmonary function.
2.1. Hormones
Great strides have been made in existing knowledge about the interactions of physical activity with the
neuroendocrine reproductive hormones. Much less in
known, however, about the effects of specific female
steroid hormones on physical performance. Studies
to date suggest that there may be subtle physiological variations in vascular volume dynamics, ventilation, thermoregulation, and substrate metabolism
throughout the normal menstrual cycle (Lebrun et al.,
1995; Lebrun, 1993). With the exception of a possible luteal phase improvement in endurance exercise,
there does not appear to be any conclusive evidence
of the effects of the menstrual cycle on actual athletic performance (Lebrun et al., 1995; De Souza et al.,
1990).
The menstrual cycle can affect pulmonary function
during exercise primarily through changes in circulating levels of progesterone and estrogen. Progesterone
is found in high concentrations in the luteal phase
of the menstrual cycle (Dombovy et al., 1987) and
during pregnancy. Effects of progesterone on the pulmonary system include hyperventilation (Moore et al.,

125

1987), a partially compensated respiratory alkalosis

(England and Farhi, 1976), and an increase in both
the resting hypercapnic ventilatory response (HCVR)
and the hypoxic ventilatory response (HVR) (Moore
et al., 1987; Schoene et al., 1981). Progesterone also
increases central ventilatory drive, which may affect
breathing responsiveness during exercise (Dombovy et
al., 1987). However, no studies have been able to correlate actual progesterone levels with the alterations
in ventilatory responsiveness. An augmented ventilatory drive associated with increased progesterone levels
coupled with a reduced airway diameter in women (see
below) may contribute to an increased prevalence of
expiratory flow limitation during exercise (McClaran
et al., 1998).
Increased estrogen levels tend to increase fluid
retention and therefore increase blood volume
(Carlberg et al., 1984), which could potentially affect
gas exchange in the lung. Sansores et al. (1995)
demonstrated that resting diffusing capacity (DLCO)
is reduced during the early follicular phase of the
menstrual cycle (when progesterone and estrogen levels are low), compared to the late follicular and mid
luteal phases. The authors speculate that this difference is likely attributed to changes in pulmonary blood
volume. These effects during exercise have not been
directly investigated, although our lab has recently
shown that pulmonary capillary blood volume and lung
diffusing capacity are reduced during high intensity
exercise during the early follicular phase of the menstrual cycle compared to the late follicular and mid
luteal phases (Brown et al., unpublished).
In addition, progesterone and estrogen receptors
have recently been identified in mast cells in human
airways (Zhao et al., 2001). This discovery may help
explain and account for some of the effects of sex hormones in airway function and differences in ventilation.
Obviously, the responses of the respiratory system to
endogenous variations in the female steroid hormones
during the menstrual cycle are extremely complex and
are not yet completely understood.
2.2. Morphology
Under normal circumstances, for the standard young
healthy normally fit adult male, it is clear that structural and functional capacity of the pulmonary system,
including the lung and chest wall and the supporting

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C.A. Harms / Respiratory Physiology & Neurobiology 151 (2006) 124131

neural control system, exceeds the demands placed on

them for flow rate, volume, and O2 and CO2 exchange
(Dempsey, 1986). Women, however, may be an exception as morphological differences in lung structure
between sexes have been documented. For example,
prediction equations for lung function show a significant sex difference in adults (Crapo et al., 1982).
Specifically, height-matched men have larger diameter airways (Mead, 1980) and larger lung volumes and
diffusion surfaces (Schwartz et al., 1988; Thurlbeck,
1982) compared with postpubertal women. It has been
suggested that sex differences in lung diffusing capacity can be explained by fewer total number of alveoli
(smaller surface area) and smaller airway diameter relative to lung size in women (lower maximum flow rates),
and these differences probably become significant relatively late in the growth period of the lung (Mead,
1980; Thurlbeck, 1982). Also, adult women consistently have smaller lung volumes and lower maximal
expiratory flow rates even when corrected for sitting
height relative to men (Crapo et al., 1982). Sitting
height or differences in trunk length for the same standing height account for some, but not all, sex differences
in lung volumes and maximal expiratory flow rates in
teenagers and young adults (Crapo et al., 1982). There
does not, however, appear to be a sex difference in the
elastic properties of the lungs (Rohrbach et al., 2003)
and chest wall or pulmonary compliance (Johnson et
al., 1993). Therefore, given these pulmonary structural
differences that exist between men and women, and
recognizing that physical training sufficient to increase
maximal aerobic capacity has no measurable effect on
lung function or structure, it could be predicted that
women would be more susceptible to pulmonary limitations during exercise compared to men given similar
metabolic demands.

3. Gender and alveolar ventilation

3.1. Gender and chemosensitivity
It is currently believed that endurance athletes commonly have altered respiratory drives, with a decreased
ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) (Byrne-Quinn et al., 1971; Schoene et
al., 1981). Such changes may benefit these athletes by
allowing less ventilation during exercise (providing it

does not lead to increased arterial desaturation) and by

decreasing the subjective sensation of dyspnea that may
be a factor in limiting maximal exercise performance,
as well as allowing them to continue exercising despite
the onset of hypoxia. However, it is not known whether
this decrease is linked to prolonged training or if it is
an innate characteristic.
It is currently debatable whether or not there is a
sex difference in chemosensitivity in the ventilatory
response to hypoxia and hypercapnia. It is known that
there are sex related differences in HVR that tend to
vary with ovarian hormones (Aitken et al., 1986; White
et al., 1983). It has been suggested that the endogenous surge of progesterone during the menstrual cycle
may exert a deleterious effect on performance through
alterations in these respiratory drives. Progesterone and
estrogen raises both alveolar ventilation and HVR via
central (Bayliss and Millhorn, 1992) and peripheral
(Tatsumi et al., 1997) receptor-mediated mechanisms.
However, Regensteiner et al. (1988) have shown no sex
differences in resting HVR or HCVR, although mild
exercise did increase HVR in men but not in women.
3.2. Hyperventilation of exercise
The hyperventilation of heavy exercise leads to significant increases in both inspiratory and expiratory
muscle work and in both the resistive and elastic work
of breathing. Nevertheless, a substantial reserve exists
for increases in ventilation in the young to middle
aged normal, healthy untrained man, even at maximal exercise (Dempsey et al., 1984). However, the
endurance trained man with a higher maximal oxygen uptake (V O2 max ) and CO2 production, producing a high ventilatory demand, begins to approach the
mechanical limits for inspiratory and expiratory pressure and flow development (Johnson et al., 1992). Thus,
as the tidal loop begins to intersect the maximal flowvolume loop (MFVL), end expiratory lung volume
begins to increase in order to permit further increases in
flow rate within the MFVL. This relative hyperinflation
results in further increases in the elastic work of breathing, and inspiratory muscle work approaches 8595%
of capacity of the inspiratory muscles to produce pressure (Johnson et al., 1992). Expiratory flow limitation
in turn causes reflex inhibition of the hyperventilatory
response (Johnson et al., 1993), constrains ventilation,
and increases the work associated with breathing. A

C.A. Harms / Respiratory Physiology & Neurobiology 151 (2006) 124131

127

Fig. 1. Response to progressive exercise, showing group mean tidal flow-volume loops for less-fit (n = 15); (A) and highly fit women (n = 14);
(B) at rest and during light (55% V O2 max ), moderate (74% V O2 max ), heavy (90% V O2 max ), near-maximal (96% V O2 max ), and maximal exercise
plotted relative to group mean maximal voluntary flow-volume loop. V E max , maximal ventilation. Flow limitation is present when expiratory
tidal flow-volume loop intersects boundary of volitional maximal flow-volume loop. Data are from McClaran et al. (1998).

greater work of breathing likely leads to more rapid respiratory muscle fatigue (Babcock et al., 1995). Thus,
the effects of mechanical constraints of the lung on volumes and maximal expiratory flow rates become very
important to control of breathing during high intensity
exercise.
Because women tend to show reduced airway diameter compared to men (see above), women are more
likely to show greater mechanical limits to expiratory
flow creating a smaller maximal flow:volume envelope compared to men (McClaran et al., 1998). Fig. 1
shows ensemble averaged tidal flow:volume loops for
rest through maximal exercise in highly fit and less-fit
women. This figure demonstrates that the combination
of increased ventilatory demand with airways vulnerable to closure in women likely leads to significant
expiratory flow limitation sooner (i.e., at a lower V E
70100 l/min) and at a much lower V O2 ) than their
male contemporaries. As a result, women would probably show increased hyperinflation, marked increases
in both the elastic and flow resistive work of breathing,
and dyspnea at a given V E compared to the average
man. Also, it would be expected that women would
experience a lack of substantial hyperventilation at a
V O2 (and V CO2 ) that men would typically would not.
As a consequence of greater EFL, the active healthy
female may be especially vulnerable to high fatiguing

levels of the work of breathing during heavy exercise. During exercise at intensities >80% V O2 max of
sustained exercise, the diaphragm consistently shows
fatigue at end-exercise, as demonstrated using bilateral phrenic nerve stimulation (Johnson et al., 1993).
An important consequence of high levels of respiratory muscle work and respiratory muscle fatigue is
vasoconstriction and reduction in blood flow to the
working locomotor muscles, accompanied by changes
in vascular resistance (Harms et al., 1997, 1998a)
which can compromise exercise tolerance (Harms et
al., 2000a). Therefore, it is likely, although not yet
proven, that respiratory muscle fatigue would be more
readily incurred during heavy exercise in women versus
men and women would perhaps show a greater distribution of blood flow from the respiratory muscles to
the locomotor muscles than men.

4. Gender and gas exchange

Sufficient studies in young adult men have been
conducted to document clearly that untrained subjects
normally widen their A-aDO2 two- to three-fold from
rest to maximal exercise, and that they also hyperventilate, which raises alveolar PO2 sufficiently during
strenuous exercise to prevent PaO2 from falling below

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C.A. Harms / Respiratory Physiology & Neurobiology 151 (2006) 124131

resting levels. However, a significant reduction in the

arterial partial pressure of oxygen (PaO2 ) (<90 mmHg)
during heavy exercise, termed exercise induced arterial
hypoxemia (EIAH) has been well documented in some
fit adult men over the past several decades (Dempsey
and Wagner, 1999; Harms and Stager, 1995; Dempsey
et al., 1984). The cause of EIAH is believed to be due to
an excessive widening of the alveolar arterial oxygen
difference, an insufficient hyperventilatory response
(Dempsey and Wagner, 1999), and to a lesser extent,
intrapulmonary arteriovenous shunts (Eldridge et al.,
2004). Evidence suggests that even mild EIAH can
have a significant detrimental effect on limiting O2
transport during heavy exercise (Harms et al., 2000b;
Powers et al., 1989). Gas exchange limitations are more
common in those individuals capable of a high level of
aerobic work.
Given gender-based pulmonary structural differences that exist between men and women (see above),
it is tempting to propose that women are more susceptible to EIAH than men. To date, there are few published
temperature corrected arterial blood gas data directly
comparing pulmonary gas exchange between genders.
A recent review has discussed in detail gender and pulmonary gas exchange during exercise (Hopkins and
Harms, 2004). From this review, data in Fig. 2 compiled from previously published studies (Dempsey et
al., 1984; Harms et al., 1998b; Hopkins et al., 2000;
Hopkins et al., 1994; Olfert et al., 2004; Rice et al.,
1999) in 57 women (V O2 max 3270 ml/kg/min) and
135 men (V O2 max 3083 ml/kg/min) show that the
slope of the relationship of the A-aDO2 V O2 relationship during heavy to maximal exercise is greater
in women than men. From these data, 12% of the
women with a V O2 max of less than 50 ml/kg/min had
evidence of gas exchange impairment. For men of
the same fitness level, less than 2% have evidence
of gas exchange impairment. These differences in gas
exchange are reflected in the PaO2 data and women
have a greater negative slope of the PaO2 /V O2 relationship than do men. Approximately 10% of women
with a V O2 max less than 50 ml/kg/min had a PaO2 of
less than 90 mmHg during heavy and maximal exercise compared to less than 2% of the men. It should be
kept in mind that when lung size and fitness level are
controlled for, many of the gas exchange differences
between genders seem to be lost. These data suggest
that women may be more susceptible to gas exchange

Fig. 2. Gender differences in arterial blood gases during exercise at

90100% of V O2 max . Closed symbols are data from women, open
symbols are data from men. Circles are cycle data, squares are running data. Faint dotted line represents level at which impairment is
suggested to occur (see text for details). The A-aDO2 (A) is increased
and the PaO2 (B) is less in women compared to men at any level of
V O2 . However, alveolar ventilation is not reduced in women compared to men, as the PaCO2 if anything, is lower in women at any
given VO2 . Data from Dempsey et al. (1984); Harms et al. (1998b);
Hopkins et al. (2000); Hopkins et al. (1994); Olfert et al. (2004);
Rice et al. (1999).

C.A. Harms / Respiratory Physiology & Neurobiology 151 (2006) 124131

impairments than men, although there is a need for

more descriptive data in women to be certain. Clearly,
more testing is needed to determine: (a) the prevalence
of EIAH among the normal population of women; (b)
if women are more susceptible to EIAH than men; and
(c) the mechanisms responsible for the EIAH.

129

capacity. In particular, a greater ventilatory work associated with increased expiratory flow limitation during
exercise and gas exchange impairments seem to be of
primary concern. It should be emphasized, however,
that the amount of literature investigating these issues
is limited. Certainly, much more research is needed to
substantiate these ideas.

5. Aging
Healthy aging causes reductions in lung elastic
recoil, vital capacity, diffusion surface area, and chest
wall compliance. Accordingly, in highly fit elderly individuals, significant expiratory flow limitation with an
accompanying increase in the EELV and increased ventilatory work begins during submaximal exercise at
V E values in the 7080 l/min range (Johnson et al.,
1991). Furthermore, longitudinal studies shows that
habitual physical activity does not alleviate the normal age related reduction in the maximal flow:volume
envelope and increased lung volume at airway closure throughout the latter stages of life (McClaran et
al., 1995). Exercise induced arterial hypoxemia also
occurs in the highly fit elderly persons at V O2 max
values in the 4060 ml/kg/min range (1.52.5 times
age predicted normal V O2 max values), but the prevalence of hypoxemia is less than in younger highly fit
males at much higher V O2 max values (Johnson et al.,
1994). Apparently then in most fit, healthy subjects the
age related decline in V O2 max and in pulmonary O2
transport capacity are similar. Given the gender effects
on lung structure and function in young adults, aging
females might be even more susceptible to pulmonary
limitations in exercise performance.

6. Summary
Traditionally, the lung is not thought to limit exercise tolerance. However, increasing evidence suggests
that the pulmonary system may not always exceed the
metabolic demand of exercise. Pulmonary limitations
to exercise are found in individuals of varying fitness
levels and both genders. However, women may be more
prone to pulmonary limitations during heavy exercise
(and perhaps submaximal intensities) than men due to
the influence of the reproductive hormones (estrogen
and progesterone) combined with a reduced pulmonary

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