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Journal of Science and Medicine in Sport (2007) xxx, xxx—xxx
Arterial oxygen saturation during ascending to
altitude under various conditions:
Lessons from the field

Martin Burtscher
Department of Sport Science, Medical Section,University of Innsbruck, Austria Received 10 January 2007 ; received in revised form 21 June 2007; accepted 5 August 2007 KEYWORDS
When hypoxia increases during ascending in the mountains, ventilatory control and the related oxygenation may be challenged. The pre-treatment by inter- mittent hypoxia will elevate ventilation and offset hypoxemia and acetazolamide may inhibit peripheral chemosensitivity and act through central mechanisms. Tostudy these effects in the field, one well-trained male mountaineer performed four ascents from low (1300 m) to higher altitude (2600 m): (1) under control conditions, (2) after intermittent hypoxia, (3) after pre-treatment with acetazolamide, and (4) after intermittent hypoxia + acetazolamide. When ascending under control condi- tions a cascading decrease of arterial oxygen saturation (SaO2) has been observed probably because of the alternating dominance of peripheral and central mech-anisms of ventilatory control. While the pre-treatment with intermittent hypoxiaprolonged the constant SaO2 periods, the intake of acetazolamide eliminatedthis respiratory periodicity. Oxygen desaturation was best prevented by acetazo-lamide which was also associated with faster ascent times compared to controlconditions.
2007 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
exercise entilatory control, how-ever, is particularly complex during exercise in Typically, mountaineers ascend from low to higher hypoxia where the controller depends on the altitudes. In contrast to exercise at low alti- interaction among several different mechanisms.
tude they are exposed to continuously increasing Ventilatory control and the related SaO2 values hypoxia. Sufficient ventilation is important to main- might be modified, e.g. by pre-exposure to inter- tain arterial oxygen saturation (SaO2) and aerobic mittent hypoxia or the intake of acetazolamide.Short-term intermittent hypoxia has been reportedto increase ventilation and SaO2 during subse- quent exposure to hypoxia at rest and during 1440-2440/$ — see front matter 2007 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Burtscher M, Arterial oxygen saturation during ascending to altitude under variousconditions: Lessons from the field, J Sci Med Sport (2007), doi: ARTICLE IN PRESS
submaximal exercise in hypoxia probably caused by (PetCO2; Tidal Wave Sp, Novametrix, Austria) was enhanced hypoxic chemosensitivity of the periph- eral chemoreceptors.In contrast, the intakeof acetazolamide provokes metabolic acidosis andincreases the ventilatory response to the exercise mainly via central chemoreceptors and improvespulmonary gas Although often used by mountaineers, it is unknown how such inter- ascents are schematically shown in Origi- ventions would impinge on the SaO2 course during ascending to altitude. Thus, the main objec- tive of this pilot study was the monitoring of 2 values vary rhythmically. The cycle length after intermittent hypoxia seems to be pro- prolonged ascent to altitude: (1) under con- longed and after acetazolamide and intermittent trol conditions, (2) after intermittent hypoxia, hypoxia + acetazolamide cycles seems even to dis- (3) after the intake of acetazolamide, and (4) appear. In general, each cycle consists of a after combined intermittent hypoxia and acetazo- ing altitude, followed by a rather horizontalSaO2 period despite increasing altitude. Afterintermittent hypoxia the constant SaO is prolonged and starts at a lower threshold.
After acetazolamide, the initial SaO One healthy, well-trained and regularly exercis- is followed by a slowed continuous decrease of ing male mountaineer (52 years, 68 kg, 176 cm, 2. After intermittent hypoxia + acetazolamide, 2max ∼ 65 ml/(min kg)) performed four ascents this slowed decrease starts at somewhat a from low to higher altitude. He had a nor- ascent under control conditions from 98% (700 m, monly susceptible to acute mountain sickness.
rest) to 83% (2600 m, exercise); delta SaO He normally lived at low altitude (700 m) and was transported by car to an altitude of 1300 m 12%, after acetazolamide 9%, and after inter- and from there he ascended to about 2600 m.
mittent hypoxia + acetazolamide also 9%. The Ascents were performed in the winter season on average values of heart rates during the four skis carrying a light backpack (3 kg) with time ascents were very similar (136 ± 2 b/min). The intervals of 3 weeks between each ascent. The time needed for the ascent under control condi- routes and the track conditions of the four ascents tions was 132 min (590 m in altitude per hour), were very similar (solid tracks, temperature: +4 after intermittent hypoxia this time was 128 min to −4 ◦C, no wind). One month before and during (609 m/h), after acetazolamide 122 min (639 m/h), the test period no altitude sojourn above 1800 mwas allowed. The first ascent represents controlconditions. The second was carried out after inter-mittent hypoxic exposures consisting of five timesof 1 h normobaric hypoxia (14% FiO2, equivalentto about 3700 m) on five consecutive days withthe intent to enhance the sensitivity of peripheralchemoreceptors.third was performed aftertwo times 125 mg intake of acetazolamide within atime interval of 9 h with the intent to enhance thesensitivity mainly of the central chemoreceptoreffectiveness of such low dosages havebeen demonstrated and is also indicated becausediuresis increased. The fourth ascent was per-formed after intermittent hypoxia + acetazolamidepre-treatment.
Figure 1 Schematically presented SaO2 courses during
SaO2, barometric pressure, and heart rates were the ascents from about 1300 m (arrow) to about 2600 m monitored continuously using the Physiolog device under various conditions. IH = intermittent hypoxia; (Driesen + Kern GmbH, Germany). End-tidal CO2 Please cite this article in press as: Burtscher M, Arterial oxygen saturation during ascending to altitude under variousconditions: Lessons from the field, J Sci Med Sport (2007), ARTICLE IN PRESS
Arterial oxygen saturation under various conditions and after intermittent hypoxia + acetazolamide In conclusion, intermittent hypoxia and aceta- zolamide modify the cascading decrease of SaO2when ascending to altitude under control condi-tions probably because of their selective effects Discussion
on peripheral and central mechanisms of ventila-tory control. These interventions tend to improve The most interesting observations of the presented pilot study are (1) that the SaO2 course duringascending to altitude follows a biphasic patternand (2) that intermittent hypoxia, acetazolamide, Appendix A. Supplementary data
and intermittent hypoxia + acetazolamide clearlychanged the rhythmic variation of the SaO2 course Supplementary data associated with this arti- seen during the control ascent to altitude.
cle can be found, in the online version, at (1) Under control conditions, constant SaO2 peri- ods with rather decreasing PetCO2 may reflectincreasing ventilatory equivalents for CO2(VE/VCO References
sure decreased during the ascent. In contrast, 1. Burtscher M, Faulhaber M, Flatz M, Likar R, Nachbauer W.
the periods of decreasing SaO2 with relatively Effects of short-term acclimatization to altitude (3200 m) on constant PetCO2 may indicate steady state aerobic and anaerobic exercise performance. Int J Sports VE/VCO2 despite decreasing inspiratory oxygen Med 2006;27:629—35.
2. Ursino M, Magosso E, Avanzolini G. An integrated model of (2) The pre-treatment with intermittent hypoxia the human ventilatory control system: the response to hyper-
capnia. Clin Physiol 2001;21:447—64.
and/or azetazolamide clearly modified the 3. Katayama K, Sato Y, Morotome Y, Shima N, Ispida K, Mori S, SaO2 pattern observed under control condi- et al. Intermittent hypoxia increases ventilation and SaO2 tions. Intermittent hypoxia is known to enhance during hypoxic exercise and hypoxic chemosenitivity. J Appl Physiol 2001;90:1431—40.
ated with an augmented sensory response of 4. Ainslie PN, Barach A, Cummings KJ, Murrell C, Ham- lin M, Hellemans J. Cardiorespiratory and cerebrovascular responses to acute poikilocapnic hypoxia following intermit- Therefore, this likely explains the prolonged tent and continuous exposure to hypoxia in humans. J Appl constant SaO2 periods after pre-treatment with Physiol 2007;102:1953—61.
intermittent hypoxia. On the other hand, the 5. Swenson ER. Carbonic anhydrase inhibitors and ventilation: a metabolic acidosis produced by acetazolamide complex interplay of stimulation and suppression. Eur Respir
administration stimulates breathing at least 6. Jonk AM, van den Berg IP, Olfert IM, Wray DW, Arai T, Hop- partly by increasing the tonic output of the cen- kins SR, et al. Effect of acetazolamide on pulmonary and muscle gas exchange during normoxic and hypoxic exercise.
the flattening of the decreasing SaO2 periods.
J Physiol 2007;579:909—21.
7. Peng Y, Kline DD, Dick TE, Prabhakar NR. Chronic intermittent But it cannot entirely be excluded that small hypoxia enhances carotid body chemoreceptor response to changes in the ascent rate may have influenced low oxygen. Adv Exp Med Biol 2001;499:33—8.
Available online at www.sciencedirect.com Please cite this article in press as: Burtscher M, Arterial oxygen saturation during ascending to altitude under variousconditions: Lessons from the field, J Sci Med Sport (2007), doi:

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