Padilla Danielle J, McDonough Paul, Kindig Casey A, Erickson Howard H, Poole David C
Department of Anatomy and Physiology, 228 Coles Hall, Kansas State University, Manhattan, KS 66506, USA.
J Appl Physiol (1985). 2004 Jun;96(6):2187-93. doi: 10.1152/japplphysiol.00998.2003. Epub 2004 Feb 6.
Despite enormous rates of minute ventilation (Ve) in the galloping Thoroughbred (TB) horse, the energetic demands of exercise conspire to raise arterial Pco(2) (i.e., induce hypercapnia). If locomotory-respiratory coupling (LRC) is an obligatory facilitator of high Ve in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251-256, 1983), Ve should drop precipitously when LRC ceases at the galloptrot transition, thus exacerbating the hypercapnia. TB horses (n = 5) were run to volitional fatigue on a motor-driven treadmill (1 m/s increments; 14-15 m/s) to study the dynamic control of breath-by-breath Ve, O(2) uptake, and CO(2) output at the transition from maximal exercise to active recovery (i.e., trotting at 3 m/s for 800 m). At the transition from the gallop to the trot, Ve did not drop instantaneously. Rather, Ve remained at the peak exercising levels (1,391 +/- 88 l/min) for approximately 13 s via the combination of an increased tidal volume (12.6 +/- 1.2 liters at gallop; 13.9 +/- 1.6 liters over 13 s of trotting recovery; P < 0.05) and a reduced breathing frequency [113.8 +/- 5.2 breaths/min (at gallop); 97.7 +/- 5.9 breaths/min over 13 s of trotting recovery (P < 0.05)]. Subsequently, Ve declined in a biphasic fashion with a slower mean response time (85.4 +/- 9.0 s) than that of the monoexponential decline of CO(2) output (39.9 +/- 4.7 s; P < 0.05), which rapidly reversed the postexercise arterial hypercapnia (arterial Pco(2) at gallop: 52.8 +/- 3.2 Torr; at 2 min of recovery: 25.0 +/- 1.4 Torr; P < 0.05). We conclude that LRC is not a prerequisite for achievement of Ve commensurate with maximal exercise or the pronounced hyperventilation during recovery.
尽管疾驰的纯种马（TB）有着极高的分钟通气量（Ve），但运动产生的能量需求仍导致动脉血二氧化碳分压（Pco₂）升高（即引发高碳酸血症）。如果运动-呼吸耦合（LRC）是马在疾驰等运动状态下维持高Ve的必要促进因素（如Bramble和Carrier在《科学》219: 251 - 256, 1983中所述），那么当LRC在疾驰-小跑过渡阶段停止时，Ve应会急剧下降，从而加剧高碳酸血症。对5匹TB马在电动跑步机上进行运动直至自愿疲劳（速度以1 m/s递增，从14 - 15 m/s），以研究从最大运动到主动恢复阶段（即3 m/s小跑800 m）逐次呼吸的Ve、氧气摄取量和二氧化碳排出量的动态控制。从疾驰过渡到小跑时，Ve并非瞬间下降。相反，通过潮气量增加（疾驰时为12.6 ± 1.2升；小跑恢复的13秒内为13.9 ± 1.6升；P < 0.05）和呼吸频率降低[113.8 ± 5.2次/分钟（疾驰时）；小跑恢复的13秒内为97.7 ± 5.9次/分钟（P < 0.05）]的共同作用，Ve在大约13秒内维持在运动峰值水平（1,391 ± 88升/分钟）。随后，Ve以双相方式下降，其平均反应时间（85.4 ± 9.0秒）比二氧化碳排出量的单指数下降反应时间（39.9 ± 4.7秒；P < 0.05）更慢，二氧化碳排出量的快速下降迅速逆转了运动后的动脉高碳酸血症（疾驰时动脉血Pco₂：52.8 ± 3.2 Torr；恢复2分钟时：25.0 ± 1.4 Torr；P < 0.05）。我们得出结论，LRC并非实现与最大运动相称的Ve或恢复过程中明显过度通气的必要条件。
