Gleeson M, Brackenbury J H
Q J Exp Physiol. 1984 Jan;69(1):61-72. doi: 10.1113/expphysiol.1984.sp002796.
In order to determine the influence of hyperthermia on respiratory, blood gas and acid-base changes in exercising birds, we exercised domestic fowl on a treadmill at ambient temperatures of 5, 20, 30 and 35 degrees C for 10 min at graded running speeds up to 4.3 km.h-1. Ventilation and gas exchange were measured continuously and arterial blood gases, pH and the concentration of lactic acid in arterial blood were measured in samples taken during the last minute of each run. During exercise at 5 degrees C rectal temperature did not change significantly from rest (isothermic condition) and there was no sign of thermal influence on respiratory pattern, such as was observed at higher ambient temperatures. At any given running speed, increased ambient temperature caused increased ventilation by an increase in respiratory frequency (f) together with a decrease in tidal volume (VT). Under isothermic conditions, at low running speeds, birds maintained an isocapnic hyperpnoea: arterial PCO2, PO2 and pH and oxygen extraction were unchanged. However at higher speeds (ca. greater than 2.5 km.h-1) some hyperventilation occurred with subsequent falls in arterial PCO2 and oxygen extraction. Arterial pH also fell significantly (P less than 0.01). During hyperthermic exercise, oxygen extraction, arterial PCO2 and bicarbonate concentration all fell significantly (P less than 0.01) and progressively with increasing work load, and birds hyperventilated at all running speeds. This produced a significant arterial hypocapnia and alkalosis at the lower speeds (P less than 0.05) but this was replaced by a hypocapnic metabolic acidosis at the higher running speeds. Blood lactate concentration rose steeply at speeds above ca. 2.5 km.h-1 but arterial pH fell by only 0.1 units or less partly as a result of buffering by blood bicarbonate. It is concluded that both hyperthermia and lactacidosis are causes of hyperventilation and arterial hypocapnia during heavy running exercise in birds. However, ventilatory adjustments similar to those observed in resting hyperthermic birds, viz. increased f and reduced VT prevent severe arterial hypocapnia from occurring in hyperthermic exercising birds.
为了确定高温对运动中鸟类呼吸、血气和酸碱变化的影响,我们让家禽在环境温度为5、20、30和35摄氏度的跑步机上运动10分钟,运动速度逐渐增加至4.3千米/小时。连续测量通气和气体交换情况,并在每次运动的最后一分钟采集动脉血样,测量动脉血气、pH值以及动脉血中乳酸浓度。在5摄氏度环境下运动时,直肠温度与静息时相比无显著变化(等温条件),且未观察到高温对呼吸模式的影响,而在较高环境温度下则有此现象。在任何给定的运动速度下,环境温度升高会导致通气增加,表现为呼吸频率(f)增加,同时潮气量(VT)减少。在等温条件下,低运动速度时,鸟类维持等碳酸血症性通气过度:动脉血二氧化碳分压(PCO2)、氧分压(PO2)、pH值以及氧摄取量均无变化。然而,在较高速度(约大于(2.5)千米/小时)时,会出现一些通气过度现象,随后动脉血PCO2和氧摄取量下降。动脉血pH值也显著下降(P小于0.01)。在高温运动期间,氧摄取量、动脉血PCO2和碳酸氢盐浓度均显著下降(P小于0.01),且随着工作量增加而逐渐下降,鸟类在所有运动速度下均出现通气过度。这在较低速度时导致显著的动脉低碳酸血症和碱中毒(P小于0.05),但在较高运动速度时则被低碳酸血症性代谢性酸中毒所取代。在速度高于约(2.5)千米/小时时,血乳酸浓度急剧上升,但动脉血pH值仅下降0.1个单位或更少,部分原因是血液碳酸氢盐的缓冲作用。研究得出结论,高温和乳酸性酸中毒都是鸟类剧烈运动时通气过度和动脉低碳酸血症的原因。然而,与静息高温鸟类中观察到的通气调节相似,即f增加和VT减少,可防止高温运动中的鸟类出现严重的动脉低碳酸血症。