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FIGURE 2 Changes in ventilation during a bout of moderate exercise and recovery afterwards. Ventilation increases immediately at the onset of exercise and then continues to increase more slowly to a plateau value during sustained exercise. Similarly, ventilation decreases immediately when exercise stops, but it takes several minutes before ventilation returns to the pre-exercise level. (Adapted from Dejours. Rev Franc Etude Clin Biol 1963; 8:439).

do not change significantly, arterial chemoreceptors are not important for hyperpnea at submaximal levels of exercise; in fact, ventilation is normal during steady-state submaximal exercise in patients without carotid bodies. However, most animals except humans actually hyperventilate during exercise, which decreases PaCo2 and arterial chemoreceptor stimulation. This limits the increase in ventilation and minimizes the work of breathing.

Near maximal levels of exercise, lactic acid starts to appear in the blood which stimulates arterial chemore-ceptors. This explains the larger increase in ventilation above the lactate threshold (Fig. 1). Ventilation increases in excess of Co2 production, decreasing PaCo2 and increasing Pao2 near maximum levels of exercise in normal subjects. The respiratory alkalosis helps compensate the metabolic acidosis from lactic acid.

other afferent signals that may fine tune ventilation during exercise originate from mechanoreceptors in the heart and nonmyelinated sensory nerves in skeletal muscle. Mechanoreceptors from the lung and chest wall can adjust the pattern of breathing during exercise to minimize the work of breathing. Even arterial chemoreceptors can be stimulated by K+ released from muscle, norepinephrine released from the sympathetic nervous system, and larger oscillations of PaCo2 during the ventilatory cycle in exercise. However, the ventilatory response to moderate, steady-state exercise is normal without any of these afferent signals, so they are not necessary for exercise hyperpnea.

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