Ventilatory responses to hypoxia and high altitude during sleep in aconcagua climbers

Eric M. Snyder, Jan Stepanek, Sheryl L. Bishop, Bruce D. Johnson

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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 (O2sat), heart rate (HR), respiratory rate (RR), tidal volume (VT) and minute ventilation (VE), and exhibited no periodic breathing (O2sat = 100 ± 2%, HR = 67 ± 1 beats/min, RR = 16 ± 3 breaths/min, VT = 516 ± 49 mL, and VE = 9 ± 1 L/min, mean ± SD). Sleep during simulated 4300 m caused a reduction in O 2sat, an increase in HR, RR, VT, and VE, and induced periodic breathing in both climbers (O2sat, = 79 ± 4%, HR = 72 ± 14 beats/min, RR = 20 ± 3 breaths/min, VT = 701 ± 180 mL, and VE = 14 ± 3 L/min). All 3 levels of altitude had profound effects on O2sat, HR, and the ventilatory strategy during sleep (O2sat, = 79 ± 2, 70 ± 8, 60 ± 2%; HR = 70 ± 12, 76 ± 6, 80 ± 3 beats/min: RR = 17 ± 6, 18 ± 4, 20 ± 6 breaths/min; VT = 763 ± 300, 771 ± 152, 1145 ± 123 mL; and VE = 13 ± 1, 14 ± 0, 22 ± 4 L/min; for 4100 m, 4900 m, and 5900 m, respectively). There were strong negative correlations between O2sat and VE and ventilatory drive (VT/Ti. where Ti 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.

Original languageEnglish (US)
Pages (from-to)138-145
Number of pages8
JournalWilderness and Environmental Medicine
Volume18
Issue number2
DOIs
StatePublished - 2007

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Altitude Sickness
Ventilation
Sleep
Respiratory Rate
Heart Rate
Respiration
Tidal Volume
Oxygen
Pressure
Lung

Keywords

  • High altitude
  • Hypoxia
  • Low-oxygen
  • Periodic breathing
  • Respiration
  • Sleep
  • Ventilatory response

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation
  • Orthopedics and Sports Medicine

Cite this

Ventilatory responses to hypoxia and high altitude during sleep in aconcagua climbers. / Snyder, Eric M.; Stepanek, Jan; Bishop, Sheryl L.; Johnson, Bruce D.

In: Wilderness and Environmental Medicine, Vol. 18, No. 2, 2007, p. 138-145.

Research output: Contribution to journalArticle

Snyder, Eric M. ; Stepanek, Jan ; Bishop, Sheryl L. ; Johnson, Bruce D. / Ventilatory responses to hypoxia and high altitude during sleep in aconcagua climbers. In: Wilderness and Environmental Medicine. 2007 ; Vol. 18, No. 2. pp. 138-145.
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abstract = "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 (O2sat), heart rate (HR), respiratory rate (RR), tidal volume (VT) and minute ventilation (VE), and exhibited no periodic breathing (O2sat = 100 ± 2{\%}, HR = 67 ± 1 beats/min, RR = 16 ± 3 breaths/min, VT = 516 ± 49 mL, and VE = 9 ± 1 L/min, mean ± SD). Sleep during simulated 4300 m caused a reduction in O 2sat, an increase in HR, RR, VT, and VE, and induced periodic breathing in both climbers (O2sat, = 79 ± 4{\%}, HR = 72 ± 14 beats/min, RR = 20 ± 3 breaths/min, VT = 701 ± 180 mL, and VE = 14 ± 3 L/min). All 3 levels of altitude had profound effects on O2sat, HR, and the ventilatory strategy during sleep (O2sat, = 79 ± 2, 70 ± 8, 60 ± 2{\%}; HR = 70 ± 12, 76 ± 6, 80 ± 3 beats/min: RR = 17 ± 6, 18 ± 4, 20 ± 6 breaths/min; VT = 763 ± 300, 771 ± 152, 1145 ± 123 mL; and VE = 13 ± 1, 14 ± 0, 22 ± 4 L/min; for 4100 m, 4900 m, and 5900 m, respectively). There were strong negative correlations between O2sat and VE and ventilatory drive (VT/Ti. where Ti 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.",
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N2 - 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 (O2sat), heart rate (HR), respiratory rate (RR), tidal volume (VT) and minute ventilation (VE), and exhibited no periodic breathing (O2sat = 100 ± 2%, HR = 67 ± 1 beats/min, RR = 16 ± 3 breaths/min, VT = 516 ± 49 mL, and VE = 9 ± 1 L/min, mean ± SD). Sleep during simulated 4300 m caused a reduction in O 2sat, an increase in HR, RR, VT, and VE, and induced periodic breathing in both climbers (O2sat, = 79 ± 4%, HR = 72 ± 14 beats/min, RR = 20 ± 3 breaths/min, VT = 701 ± 180 mL, and VE = 14 ± 3 L/min). All 3 levels of altitude had profound effects on O2sat, HR, and the ventilatory strategy during sleep (O2sat, = 79 ± 2, 70 ± 8, 60 ± 2%; HR = 70 ± 12, 76 ± 6, 80 ± 3 beats/min: RR = 17 ± 6, 18 ± 4, 20 ± 6 breaths/min; VT = 763 ± 300, 771 ± 152, 1145 ± 123 mL; and VE = 13 ± 1, 14 ± 0, 22 ± 4 L/min; for 4100 m, 4900 m, and 5900 m, respectively). There were strong negative correlations between O2sat and VE and ventilatory drive (VT/Ti. where Ti 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.

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KW - High altitude

KW - Hypoxia

KW - Low-oxygen

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KW - Respiration

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KW - Ventilatory response

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