Although exercise increases ventilation more than any other physiological stimulus, mechanical factors do not limit ventilation or VO2 in healthy humans. Peak inspira-tory muscle pressure developed during maximal exercise is only about 40% of the maximum capacity because inspiratory muscles operate at decreased sarcomere length (with decreased expiratory volume). However, the forces generated are sufficient to increase ventilation so PaCO2 does not increase during exercise. Also, despite tenfold increases in ventilatory flow rates with exercise, airway resistance does not increase because of active regulation of both upper and lower airways. The alae nasae flare the nostrils to decrease resistance to nose breathing and the larynx, which is important for determining resistance to mouth breathing, does not narrow as much during expiration in exercise compared to rest. Exercise also relaxes bronchial smooth muscle by sympathetic stimulation.
The pattern of breathing during exercise involves increased frequency and tidal volume, with expiratory muscles decreasing end expiratory lung volume. As exercise intensity increases, the end expiratory lung volume increases relative to lighter exercise to reduce the possibility for expiratory flow limitation (or dynamic compression; see Fig. 10 in Chapter 19). Figure 3 illustrates this with flow-volume loops measured during rest and exercise. Figure 3 also shows that there is very little flow limitation at VO2 max in healthy, young adults. In contrast, elite athletes may have significant expiratory flow limitation, with over 50% of the tidal volume hitting the maximum expiratory flow rate at the highest levels of
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