Background/Objective.—We examined the changes in ventilation during sleep at high altitude using the LifeShirt monitoring system on 2 climbers who were attempting to summit Mount Aconcagua (6956 m).

Methods.—Prior to the summit attempt, we measured cardiovascular and pulmonary function at 401 m (Rochester, MN) and gathered respiratory and cardiovascular data during sleep using the LifeShirt monitoring system with exposure to normobaric normoxia and normobaric hypoxia (simulated 4300 m). We then monitored the ventilatory response during sleep at 3 altitudes (4100 m, 4900 m, and 5900 m).

Results.—During normoxic sleep, subjects had normal oxygen saturation (O_2sat), heart rate (HR), respiratory rate (RR), tidal volume (V_T) and minute ventilation (V_E), and exhibited no periodic breathing (O_2sat = 100 ± 2%, HR = 67 ± 1 beats/min, RR = 16 ± 3 breaths/min, V_T = 516 ± 49 mL, and V_E = 9 ± 1 L/min, mean ± SD). Sleep during simulated 4300 m caused a reduction in O_2sat, an increase in HR, RR, V_T, and V_E, and induced periodic breathing in both climbers (O_2sat = 79 ± 4%, HR = 72 ± 14 beats/min, RR = 20 ± 3 breaths/min, V_T = 701 ± 180 mL, and V_E = 14 ± 3 L/min). All 3 levels of altitude had profound effects on O_2sat, HR, and the ventilatory strategy during sleep (O_2sat = 79 ± 2, 70 ± 8, 60 ± 2%; HR = 70 ± 12, 76 ± 6, 80 ± 3 beats/min; RR = 17 ± 6, 18 ± 4, 20 ± 6 breaths/min; V_T = 763 ± 300, 771 ± 152, 1145 ± 123 mL; and V_E = 13 ± 1, 14 ± 0, 22 ± 4 L/min; for 4100 m, 4900 m, and 5900 m, respectively). There were strong negative correlations between O_2sat and V_E and ventilatory drive (V_T/T_i, where T_i is the inspiratory time) throughout the study.

Conclusions.—Interestingly, the changes in ventilatory response during simulated altitude and at comparable altitude on Aconcagua during the summit attempt were similar, suggesting reductions in FiO₂, rather than in pressure, alter this response.