Periodic breathing at high altitude and ventilatory responses to O2 and CO2.

Masuyama, Shigeru; Kohchiyama, Shiro; Shinozaki, Toshihide; Okita, Shinya; Kunitomo, Fumio; Tojima, Hirokazu; Kimura, Hiroshi; Kuriyama, Takayuki; Honda, Yoshiyuki

doi:10.2170/jjphysiol.39.523

Cited by 51 publications

(34 citation statements)

References 24 publications

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“…For some athletes in the present study, respiratory events at 2,650-m simulated altitude were profound and gave rise to nocturnal periodic breathing as previously documented at much higher levels of natural or simulated altitude (35). Although we were unable to measure hypoxic ventilatory response because of a technical limitation, it is still worth noting that three of the four periodic breathers were men, which is consistent with earlier research indicating that men tend to have a higher hypoxic ventilatory response (34) and that a high response predisposes one to periodic breathing (23). It is noteworthy that periodic breathing was seen in all stages of sleep in the two periodic breathers with high AHI but only in stage 2 and REM sleep in periodic breathers with a low AHI.…”

Section: Discussionsupporting

confidence: 89%

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Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude

Kinsman¹,

Hahn²,

Gore³

et al. 2002

Journal of Applied Physiology

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Moi Chow. Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude. J Appl Physiol 92: 2114-2118, 2002; 10.1152/japplphysiol.00737. 2001.-We examined the initial effect of sleeping at a simulated moderate altitude of 2,650 m on the frequency of apneas and hypopneas, as well as on the heart rate and blood oxygen saturation from pulse oximetry (Sp O 2 ) during rapid eye movement (REM) and non-rapid eye movement (NREM) sleep of 17 trained cyclists. Pulse oximetry revealed that sleeping at simulated altitude significantly increased heart rate (3 Ϯ 1 beats/min; means Ϯ SE) and decreased Sp O 2 (Ϫ6 Ϯ 1%) compared with baseline data collected near sea level. In response to simulated altitude, 15 of the 17 subjects increased the combined frequency of apneas plus hypopneas from baseline levels. On exposure to simulated altitude, the increase in apnea was significant from baseline for both sleep states (2.0 Ϯ 1.3 events/h for REM, 9.9 Ϯ 6.2 events/h for NREM), but the difference between the two states was not significantly different. Hypopnea frequency was significantly elevated from baseline to simulated altitude exposure in both sleep states, and under hypoxic conditions it was greater in REM than in NREM sleep (7.9 Ϯ 1.8 vs. 4.2 Ϯ 1.3 events/h, respectively). Periodic breathing episodes during sleep were identified in four subjects, making this the first study to show periodic breathing in healthy adults at a level of hypoxia equivalent to 2,650-m altitude. These results indicate that simulated moderate hypoxia of a level typically chosen by coaches and elite athletes for simulated altitude programs can cause substantial respiratory events during sleep. pulse oximetry; apnea; hypopnea RECENT STUDIES ON THE USE of altitude by athletes suggest that the best effect on subsequent physical performances may be gained by sleeping in a moderately hypoxic condition (equivalent to altitudes of ϳ2,200-3,000 m) while training close to sea level (21,22). The response to this "live high, train low" approach varies widely between individuals, with some athletes showing substantial performance gains and others showing no effect or even a negative outcome (7). Athletes spend a substantial amount of time asleep while exposed to the live high, train low stimulus (3), and the respiratory events during their sleep time increase as altitude increases (28). However, substantial differences appear to exist between individuals in both the magnitude of this effect and the altitude of onset (2,8, 39). Although sleep disturbance has been shown to decrease subsequent physical work capacity and increase the self-perception of fatigue (1), no studies have monitored the sleep physiology of athletes undergoing a live high, train low program.Hyperventilation is among the first physiological adjustments to an acute increase in altitude in an attempt to compensate for the reduced PO 2 (10, 30). Episodes of hyperventilation may be separated by intervals of hypopnea or apnea. When respiratory events are cyclic and conta...

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Section: Discussionsupporting

confidence: 89%

“…A vigorous hypoxic ventilatory response is a key element in destabilizing the control system at altitude (6,23). Hypoxic ventilatory response is highly variable between individuals (4,8,12) and is depressed during sleep (11,13,34).…”

mentioning

confidence: 99%

Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude

Kinsman¹,

Hahn²,

Gore³

et al. 2002

Journal of Applied Physiology

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“…To the best of our knowledge, our study is the first not only to support this hypothesis but also, more importantly, to correlate with altitude tolerance. Other field studies performed at very high altitude tended to confirm that the higher the AHI, the higher the oxygen saturation achieved [27,33]. This relationship may be related to hyperventilation-induced improvement in Sa,O 2 associated with enhanced hypoxic chemosensitivity allowing hyperventilation after central events and, thus, to reach a higher oxygen saturation.…”

Section: Chemical Control Of Breathingmentioning

confidence: 89%

Altitude illness is related to low hypoxic chemoresponse and low oxygenation during sleep

et al. 2012

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Altitude illness remains a major cause of mortality. Reduced chemosensitivity, irregular breathing leading to central apnoeas/hypopnoeas, and exaggerated pulmonary vasoconstriction may compromise oxygenation. All factors could enhance susceptibility to acute mountain sickness (AMS).We compared 12 AMS-susceptible individuals with recurrent and severe symptoms (AMS+) with 12 ''AMS-nonsusceptible'' subjects (AMS-), assessing sleep-breathing disorders in simulated altitude as well as chemoresponsive and pulmonary vasoconstrictive responses to hypoxia.During exposure to simulated altitude, mean blood oxygen saturation during sleep was lower in AMS+ subjects (81.6¡2. ?%; p,0.001). This represented the only significant and independent predictive factor for altitude intolerance, despite a higher increase in pulmonary artery systolic pressure in response to hypoxia, a lower lung diffusing capacity and a higher endothelin-1 level at baseline in AMS+ subjects (p,0.05). AMS+ subjects were more hypoxaemic whilst exhibiting fewer respiratory events during sleep owing to lower hypoxic (isocapnic) chemoresponsiveness.In conclusion, the reduction in peripheral hypoxic chemosensitivity appears to be a major causative factor for altitude intolerance.

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“…Therefore, adaptation mechanisms are required to improve it. It has been proposed that PB, despite determining large swings in Sa,O 2 , could sustain Sa,O 2 at an average level higher than that resulting from stable breathing [15]; however, this hypothesis has not been demonstrated.…”

mentioning

confidence: 98%

“…In this condition, owing to the highly hypoxic environment, arterial oxygen saturation (Sa,O 2 ) is low and decreases further during sleep [8,10,11,15]. Therefore, adaptation mechanisms are required to improve it.…”

mentioning

confidence: 99%

Effects of high-altitude periodic breathing on sleep and arterial oxyhaemoglobin saturation

Salvaggio

Insalaco²,

Marrone³

et al. 1998

Eur Respir J

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This study aimed to investigate the effect of periodic breathing (PB) at high altitude on sleep structure and arterial oxygen saturation (Sa,O2). Five healthy subjects underwent polysomnographic studies at sea level, and during the first and the fourth week of sojourn at 5,050 m. Their breathing pattern, sleep architecture and Sa,O2 were analysed. PB was detected in the high-altitude studies during nonrapid eye movement (NREM) sleep and tended to increase from the first to the fourth week. Stages 3-4 were absent in four subjects at the first week, but only in one at the fourth week, irrespective of the amount of PB. The arousal index was 11.6+/-3.8 at sea level, 30.1+/-15.5 at the first week at altitude and 33.0+/-18.2 at the fourth week. At altitude, arousal index in NREM sleep was higher during PB than during regular breathing. In NREM sleep, the mean highest Sa,O2 levels in NREM epochs with PB were higher than in those with regular breathing by 2.8+/-1.7% at the first week and 2.9+/-1.5% at the fourth week (p<0.025). From the first to the fourth week, mean Sa,O2 increased significantly during wakefulness (5.6%), NREM (5.2% with regular breathing and 5.3% with PB) and rapid eye movement sleep (7.6%). The data demonstrate a slight role of periodic breathing in altering sleep architecture at high altitude and also show that periodic breathing induces only a minor improvement in arterial oxygen saturation during nonrapid eye movement sleep.

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Periodic breathing at high altitude and ventilatory responses to O2 and CO2.

Cited by 51 publications

References 24 publications

Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude

Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude

Altitude illness is related to low hypoxic chemoresponse and low oxygenation during sleep

Effects of high-altitude periodic breathing on sleep and arterial oxyhaemoglobin saturation

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