Does gender affect human pulmonary gas exchange during exercise?

Abstract

Womenmayexperiencegreaterpulmonarygasexchangeimpairmentduringexercisethanmen.To test this we used the multiple inert gas elimination technique to study eight women and seven men matched for age, height andV O 2 max (∼48 ml kg −1 min −1 ) during normoxic and hypoxic (inspiredP O 2 = 95 Torr) cycle exercise. Resting lung function was similar between the sexes, except for a lower carbon monoxide diffusing capacity (DL CO ) in women (P < 0.05). Arterial P O 2 ,P CO 2 and alveolar-arterial O 2 difference (A−aD O 2 ) were not significantly different in men and women. Despite a lower diffusing capacity for O 2 (DL O 2 ) in women, the ratio DL O 2 /βQ (which estimates pulmonary end-capillary diffusion equilibrium) was similar between men and women and estimates of diffusion limitation during hypoxic exercise were not different between the sexes. Ventilation-perfusion inequality (described by the second moment of the perfusion distribution, logSDQ) increased during both normoxic and hypoxic exercise. Surprisingly, logSDQ values were slightly lower for women under all conditions (P < 0.05), but this did not significantly affect gas exchange. These data indicate that these active women, despite a lower DL CO and DL O 2 , do not experience greater exercise-induced abnormalities in gas exchange than men matched for age, height, aerobic capacity and lung size. Possibly fitness level and lung size are more important in determining whether or not pulmonary gas exchange impairment occurs during exercise than sex per se.

Effects of Gas Exchange on Acid‐Base Balance

“…There do not appear to be gender differences in the age range 6 to 18 years (214). It has been suggested that women may be more susceptible to impaired pulmonary gas exchange during exercise than height-matched men, because women have smaller lung volumes, lower maximal expiratory flow rates, and smaller diffusion surface areas resulting in reduced O 2 -diffusing capacity (101,223,269). If CO 2 -diffusing capacity is similarly reduced, this may result in an increased susceptibility to respiratory acidosis under conditions of moderate-intensity exercise.…”

“…If CO 2 -diffusing capacity is similarly reduced, this may result in an increased susceptibility to respiratory acidosis under conditions of moderate-intensity exercise. The possible impairment was systematically studied using the multiple inert gas elimination technique in eight women and seven men matched for age, body fat (mean and women were lean-less than 20% body fat), height, andVo 2max during normoxic and hypoxic (inspired Po 2 = 95 mmHg) cycle exercise (223). In women, compared to men, there was a tendency for VCO 2 to be lower and respiratory exchange ratio (RER) was lower; however, there was no difference in the ventilatory equivalent for CO 2 (V E /VCO 2 ).…”

Sex matters in pulmonary arterial hypertension

“…These sex-related differences in the respiratory system persist after adjustment for body dimensions, which has been referred to as a ''dysanapsis'', or unequal growth of the lung parenchyma and bronchial tree with respect to body size. However, smaller lungs at any given body size do not affect gas exchange [6] and, if anything, would increase rather than decrease pulmonary vascular resistance. The control of breathing is also different in women, with progesterone-dependent, increased peripheral chemosensitivity [7], which results in in slightly but significantly lower arterial partial pressure of carbon dioxide [8].…”

Prior intense exercise reduces arterial carbon dioxide pressure in extreme obesity

“…The drop in PaCO2 is about 5 to 6 mmHg (from a resting value of 38 -40 mmHg to a peak exercise value of 34 mmHg). [1][2][3] In contrast, evidence suggests that subjects with extreme obesity (BMI 40 kg/m 2 ) maintain PaCO2 from rest to peak exercise. 4,5 A PaCO2 35.0 mmHg during strenuous exercise suggests poor compensatory exercise hyperventilation, and PaCO2 38.0 mmHg suggests absence of a complete hyperventilatory response.…”

“…If PaCO2 does not decrease between rest and peak exer-cise, there may still be some issues with breathing, as normal individuals do have a reduction in PaCO2 of 5 to 6 mmHg between rest and maximal exertion. [1][2][3] About 75% of individuals with extreme obesity have a PaCO2 35.0 mmHg at peak exercise despite arterial plasma lactate (a breathing stimulant) levels of 8.0 mmol/L. 4 This demonstrates that most individuals with extreme obesity have a "poor breathing response" to strenuous, near maximal exercise that is likely mechanical in nature.…”