The Effects of Hypoxia and Core Temperature on Ventilation During Low Intensity Exercise

The independent and combined effects of hypoxia and elevated esophageal temperature (T,,) were investigated for their effects on the level and lunetics of exercise ventilation (VE). In either a 'hyperthermic' T,, or a 'normothermic' Tes session, 11 college-aged, healthy males were immersed to the shoulders and pedalled on an underwater cycle ergometer at a steady-state oxygen consumption (V02) of 0.87 ~.min-' (SD 0.07). Following a 30-min rest and 20-min warm-up, a 30-min steady-state cycling period was divided into three 10 min gas phases when participants inhaled: air (Euoxia 1 (El)), hypoxic gas (12 % 0 2 and 88 % N2 (HI)), and air (Euoxia 2 (E2)). End-tidal C02 (PETC02) was maintained at an isocapnic level of 5.19 kPa (SD 0.71) throughout the exercise. Venous blood samples were drawn at rest and 5 min into all gas phases. Results showed a significant increase in \jE during all hyperthermia conditions (0.0kP c 0.048), however, during hyperthermic hypoxia there was a disproportionate and significant (P = 0.017) increase in VE relative to normothermic hypoxia. This was the main explanation for a significant core temperature and gas type interaction (P = 0.012) for VE. A main effect of core temperature (P = 0.007) was evident on ventilation frequency (f,) with an increased rate of breathing in hyperthennic relative to the normothermic exercise. This gave evidence of a thermally-induced tachypnea which corresponded to significant decreases in inspiratory time (TI) (P = 0.035) and expiratory time (P = 0.014) and was independent of any changes in tidal volume (VT) (P = 0.801). As such inspiratory flow ( v T . ~ f l ) was significantly increased in hyperthermic- relative to normothermic (P = 0.003) exercise, an increase that was pronounced (P = 0.013) during hyperthermic hypoxia. A significant reduction of the time constants (z) for vE was evident (P = 0.032) during the onset of exercise under the hyperthermic as compared to the normothermic condition. This reduction in z was associated with an increase in T,, (R' =0.829, P = 0.01 1) but not in skin temperature. Between core temperature levels there were no significant changes in z for the VE response from euoxic to hypoxic steady-state exercise. From normothermic to hyperthermic exercise increases of VE in El were 9.4 % (SD 9.7) and not significantly different than the 6.9 % (SD 10.7) increase in V02. However in HI, vE and V O ~ increased by 29.2 % (SD 25.5) and 13.5 % (SD 10. I), respectively, which bordered a significant difference (P = 0.056). No changes in lactate or potassium (K') levels were evident across all gas type and core temperature conditions. In conclusion, these results suggest the following: 1) During low intensity, steady-state exercise an elevated Tes caused an increased vE, which was mediated by an increased f,. 2) The addition of hypoxia during hyperthermic exercise caused a multiplicative increase in VE which corresponded with a multiplicative increase in V~.T~-'. This would suggest the possibility of a core temperature mediated stimulation of the peripheral chemoreceptors. 3) An increased Tes during the onset of exercise but not during the transition from low intensity euoxic to hypoxic exercise shortened the time course of the VE response. 4) Oxygen consumption, K+ and lactate did not appear to be significant mediators of the augmented hyperthermic hypoxic VE response. Overall the results support the hypothesis that temperature plays a significant role in the control of ventilation, particularly during hypoxic exercise.