Ventilatory chemoreflexes at rest following a brief period of heavy exercise in man.

Abstract

1. Ventilatory chemoreflex responses have been studied at rest during the recovery from a brief period of heavy exercise. 2. Six young, healthy male subjects each undertook four experimental studies. In each study measurements were made at rest during recovery from an exhaustive 1-2 min sprint on a bicycle ergometer with a workload of 400 W. Three levels of end-tidal 02 pressure (PO) were employed. Continuous ventilatory measurements were made during euoxia (end-tidal PO2, 100 Torr), hypoxia (end-tidal Po2, 50 Torr) and hyperoxia (end-tidal Po2, 300 Torr).Arterialized venous blood samples were drawn during each of the measurement periods for the estimation of arterial pH. In two of the studies, end-tidal CO2 pressure (Pco,) was maintained throughout at 1-2 Torr above the eucapnic level that existed prior to exercise (isocapnic post-exercise protocol, IPE). In the other two studies, end-tidal Pco2 was allowed to vary (poikilocapnic post-exercise protocol, PPE). Data from a previously published study on the same subjects involving an infusion of hydrochloric acid were used to provide control data with a varying level of metabolic acidosis, but with no prior exercise. 3. Ventilation-pH slopes in the IPE protocol were no different from control. Ventilation-pH slopes in the PPE protocol were significantly lower than in the IPE and control protocols (P < 0 05, ANOVA). This difference may be due to the progressive change in end-tidal PCO, in the PPE protocol compared with the constant end-tidal PCO2 in the IPE and control protocols.4. An arterial pH value of 7.35 was attained 30'4 + 2'7 min (mean+ S.E.M.) after the end of exercise in the IPE protocol and 17 1 + 1X4 min after the end of exercise in the PPE protocol. 5. Hypoxic sensitivities at an arterial pH of 7-35 were not significantly different between the IPE, PPE and control protocols (ANOVA). 6. Euoxic ventilation at an arterial pH of 7 35 was significantly greater than control for the IPE protocol (P < 0-001, Student's paired t test) and no different from control for the PPE protocol. 7. The results suggest that 30 min after heavy exercise, ventilation remains stimulated by processes other than the post-exercise metabolic acidosis, and that changes in peripheral chemoreflex sensitivity to hypoxia and acid are not implicated in this.

Effects of sodium bicarbonate ingestion on EMG, effort sense and ventilatory response during intense exercise and subsequent active recovery

“…Later, Meah and Gardner (1994) showed that an initial period of increased _ VE after active voluntary HV lasted about one minute, thus supporting the possibility that _ VE after active voluntary HV is associated with a central neural mechanism (Tawadrous and Eldridge 1974). Furthermore, Clement et al (1996) showed the possibility that ventilation during recovery after intense exercise is also related to a central influence. In that study (Clement et al 1996), they compared isocapnic _ VE at matched arterial pH (pHa) between two metabolic acidosis conditions after intense exercise and hydrochloric acid infusion, and they showed that _ VE in the exercise condition was much higher than that in the acid infusion condition.…”

“…In that study (Clement et al 1996), they compared isocapnic _ VE at matched arterial pH (pHa) between two metabolic acidosis conditions after intense exercise and hydrochloric acid infusion, and they showed that _ VE in the exercise condition was much higher than that in the acid infusion condition. Based on this finding, it was concluded that ventilation during recovery remains stimulated by processes other than post-exercise acidosis (Clement et al 1996). However, in their study, a correlation between _ VE and pHa was observed, and the slope of the _ VE-pHa relationship ( _ VE sensitivity to pHa) was not different in the two conditions, suggesting that exercise-induced acidosis (combined effect of exercise and acidosis) could be involved in post-exercise ventilation.…”

“…Furthermore, Clement et al (1996) showed the possibility that ventilation during recovery after intense exercise is also related to a central influence. In that study (Clement et al 1996), they compared isocapnic _ VE at matched arterial pH (pHa) between two metabolic acidosis conditions after intense exercise and hydrochloric acid infusion, and they showed that _ VE in the exercise condition was much higher than that in the acid infusion condition. Based on this finding, it was concluded that ventilation during recovery remains stimulated by processes other than post-exercise acidosis (Clement et al 1996).…”

“…During recovery from exercise, increase in ventilation ( _ VE) exceeding the pre-exercise level lasts for several more minutes (Clement et al 1996;Fukuba et al 2007;Haouzi et al 1993). In the case of intense exercise, although this post-exercise ventilation seems to serve as a significant means of recovery from acidosis through elimination of CO 2 (Kowaluchuk et al 1988;Yunoki et al 1999), the role of pH in ventilatory regulation after intense exercise is uncertain.…”

Mental processes and breathing during exercise

“…In contrast, Marcora et al 47) demonstrated that muscle fatigue per se enhances ventilatory response during heavy exercise, independent of metabolic stress, and they 47,48) argued that ventilatory response during exercise is mediated by the perception of effort, which is derived from corollary discharge [49][50][51] of central motor command, independent of peripheral signals. Likewise, it has been reported that ventilatory response to heavy exercise does not depend on acid-base conditions [52][53][54] and Yamanaka et al 54) have shown a strong link between effort sense and ventilatory response. In addition, Yamanaka et al 55) have demonstrated that during repeated heavy exercise performed after glycogen depletion, hyperventilation was increased in accordance with the augmentation of effort sense despite attenuation of blood pH (Fig.…”