Does gender affect pulmonary function and exercise capacity?

https://doi.org/10.1016/j.resp.2005.10.010Get rights and content

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.

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 various 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 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 system's 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.

Section snippets

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.

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

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 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)

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 70–80 l/min range (Johnson et al., 1991). Furthermore, longitudinal studies shows that habitual physical activity does not alleviate the normal age related

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)

References (52)

  • S.J. England et al.

    Fluctuations in alveolar CO2 and in base excess during the menstrual cycle

    Resp. Physiol.

    (1976)
  • B.D. Johnson et al.

    Impact of the aging pulmonary system on the response to exercise

    Clin. Chest Med.

    (1994)
  • M.L. Aitken et al.

    Influence of body size and gender on control of ventilation

    J. Appl. Physiol.

    (1986)
  • M.A. Babcock et al.

    Contribution of diaphragmatic power output to exercise-induced diaphragm fatigue

    J. Appl. Physiol.

    (1995)
  • D.A. Bayliss et al.

    Central neural mechanisms of progesterone action: application to the respiratory system

    J. Appl. Physiol.

    (1992)
  • Brown, K.R., Murphy, J.D., Ferguson, C.S., Harms, C.A. Unpublished. The effect of menstrual cycle phase on ventilation...
  • E. Byrne-Quinn et al.

    Ventilatory control in the athlete

    J. Appl. Physiol.

    (1971)
  • K.A. Carlberg et al.

    Effects of chronic estrogen treatment on water exchange in rats

    Am. J. Physiol.

    (1984)
  • R.O. Crapo et al.

    Reference values for pulmonary tissue volume, membrane diffusing capacity, and pulmonary capillary blood volume

    Bull. Eur. Physiolopathol. Respir.

    (1982)
  • J.A. Dempsey et al.

    Exercised-induced arterial hypoxaemia in healthy human subjects at sea level

    J. Physiol.

    (1984)
  • J.A. Dempsey

    Is the lung built for exercise?

    Med. Sci. Sports Exerc.

    (1986)
  • J.A. Dempsey et al.

    Exercise-induced arterial hypoxemia

    J. Appl. Physiol.

    (1999)
  • M.J. De Souza et al.

    Effects of menstrual phase and amenorrhea on exercise performance in runners

    Med. Sci. Sports. Exerc.

    (1990)
  • M.L. Dombovy et al.

    Exercise performance and ventilatory response in the menstrual cycle

    Med. Sci. Sports Exerc.

    (1987)
  • M.W. Eldridge et al.

    Exercise-induced intrapulmonary arteriovenous shunting in healthy humans

    J. Appl. Physiol.

    (2004)
  • R. Grucza et al.

    Influence of the menstrual cycle and oral contraceptives on thermoregulatory responses to exercise in young women

    Eur. J. Appl. Physiol. Occup. Physiol.

    (1993)
  • C.A. Harms et al.

    Low chemoresponsiveness and inadequate hyperventilation contribute to exercise-induced hypoxemia

    J. Appl. Physiol.

    (1995)
  • C.A. Harms et al.

    Respiratory muscle work compromises leg blood flow during maximal exercise

    J. Appl. Physiol.

    (1997)
  • C.A. Harms et al.

    Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise

    J. Appl. Physiol.

    (1998)
  • C.A. Harms et al.

    Exercise-induced arterial hypoxaemia in healthy young women

    J. Physiol. (Lond.)

    (1998)
  • C.A. Harms et al.

    Effects of respiratory muscle work on exercise performance

    J. Appl. Physiol.

    (2000)
  • C.A. Harms et al.

    Effect of exercise-induced arterial O2 desaturation on VO2max in women

    Med. Sci. Sports. Exerc.

    (2000)
  • S.R. Hopkins et al.

    Pulmonary gas exchange during exercise in athletes. I. Ventilation-perfusion mismatch and diffusion limitation

    J. Appl. Physiol.

    (1994)
  • S.R. Hopkins et al.

    Pulmonary gas exchange during exercise in women: effects of exercise type and work increment

    J. Appl. Physiol.

    (2000)
  • S.R. Hopkins et al.

    Gender and pulmonary gas exchange during exercise

    Exerc. Sport Sci. Rev.

    (2004)
  • T.J. Horton et al.

    Fuel metabolism in men and women during and after long-duration exercise

    J. Appl. Physiol.

    (1998)
  • Cited by (124)

    • Evacuation speed of human beings in road tunnels at different altitudes

      2022, Tunnelling and Underground Space Technology
    • Association of obesity-related inflammatory pathways with lung function and exercise capacity

      2021, Respiratory Medicine
      Citation Excerpt :

      These findings are in agreement with a prior study demonstrating women with higher CRP regardless of body fat composition demonstrated a greater degree of restrictive lung disease in comparison to men, and are also in keeping with female-predominant prevalence of PAH [38,39]. Women may also be more susceptible to exercise induced arterial hypertension in comparison to men placing a larger strain on the pulmonary vasculature[40]. Our study has several limitations.

    View all citing articles on Scopus

    This paper is part of the Special Issue entitled “New Directions in Exercise Physiology”, guest-edited by Susan Hopkins and Peter D. Wagner.

    View full text