Core temperature thresholds for hyperpnea during passive hyperthermia in humans

Abstract

Humans have higher ventilation when they are hyperthermic but it is not known whether core temperature thresholds for ventilation exist, nor has a physiological rationale been presented for this response. To examine this question, ventilation was studied in relation to core temperatures in humans rendered hyperthermic in a warm bath. Seven subjects [mean (SE), 23.3 (1.4) years] wearing only shorts and a thick felt hat with ear flaps were immersed to the neck in a bath at 41 (0.5) degrees C for 25 min. Tympanic (Tty), esophageal (Tes), thigh skin and forehead skin temperatures, heart rate, inspired minute ventilation (V1 at body temperature and pressure, saturated), ventilation frequency and oxygen consumption (VO2 at standard temperature and pressure, dry) were recorded at 30-s intervals. At immersion V1 briefly increased to 18.6 (3.0) l.min-1, returned to about the pre-immersion value, and significantly increased to 19.3 (3.0) l.min-1 by the end of immersion. VO2 increased significantly from the pre-immersion value of 0.27 l.min-1 to 0.67 l.min-1 by the first 0.5 min of immersion, but then returned to its pre-immersion value. Tty increased to 38.7 (0.2) degrees C and Tes increased to 39.0 (0.2) degrees C by the end of immersion. Core temperature thresholds for increases in V1 were evident at 38.1 degrees C when expressed against Tty and at 38.5 degrees C when expressed against Tes. The results indicated that during body warming core temperature thresholds for V1 are reached and subsequently a hyperpnea was evident, despite VO2 remaining at a resting value.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of hyperthermia and hypoxia on ventilation during low-intensity steady-state exercise

“…3) is in agreement with results from previous studies (2,25). Petersen and Vejby-Christensen (25) suggested that a core temperature threshold for ventilation existed around 38°C above which a significant hyperpnea was evident.…”

“…During the hyperthermic hypoxic exercise condition, V T increased in a relatively equal magnitude as during the normothermic hypoxic condition, yet the HVR was enhanced. This can be attributed primarily to the elevated f v as a result of the increased T es , which has been described as a thermal tachypnea (2,22). This supports the suggestion that an elevated T es influences the sensitivity of the peripheral chemoreceptors and helps explain the elevated HVR during hyperthermic exercise (Fig.…”

“…3A), and this hyperpnea remained after using ANCOVA to account for increases in V E due to V O 2 . Together, these results supported that the sensitivity of exercise ventilation to hypoxia is elevated during hyperthermia and that hyperthermia per se increases ventilation (2,37).…”

“…A neurogenic hypothesis (16) implicates core temperature as a central mediating stimulus in the control of pulmonary ventilation during both actively and passively induced hyperthermia (2,37). It suggests that increases in core temperature could increase pulmonary ventilation by several mechanisms.…”

Ventilatory changes in heat-stressed humans with spinal-cord injury

“…Since some studies have shown that thermally induced ventilatory responses are associated with increases in tidal volume, 8,31 we cannot exclude the possibility that our subjects also increased tidal volume. However, if we recalculate ventilatory heat loss using our breathing frequency data, and tidal volume changes from the existing literature (900 ml at a mean body temperature of 39.01C 8 ), we still obtain an almost identical outcome.…”