Effects of five nights of normobaric hypoxia on the ventilatory responses to acute hypoxia and hypercapnia

Ainslie, Philip N.; Kolb, Jon C.; Ide, Kojiro; Poulin, Marc J.

doi:10.1016/s1569-9048(03)00190-3

Cited by 28 publications

(32 citation statements)

References 33 publications

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“…The increased AHVR (via an increase in breathing frequency) within the placebo condition is similar to previous reports [7][8][9][10][11][12]. Although the mechanism is incompletely understood, oxidative stress has been proposed to be a primary mediator, as antioxidant treatment before [20] and during [18] IH exposure prevents carotid body sensory long-term facilitation and the enhanced chemosensory response to hypoxia [20] as well as augmentation of the AHVR [3,18].…”

Section: Ahvr and Ahcvrsupporting

confidence: 84%

“…An increased AHCVR following IH has been reported previously [11][12][13], but is not a consistent observation, with shorter duration IH studies reporting no change [8,15]. Thus, the unchanged AHCVR within the placebo and nonselective COX inhibition conditions following the 6-h IH exposure are consistent with previous studies using more acute IH exposures [8,15].…”

Section: Ahvr and Ahcvrsupporting

confidence: 61%

“…Greater ventilatory instability is associated with increasing OSA severity [5] and occurs in humans following IH exposure via enhanced ventilatory responses to hypoxia [7][8][9][10][11][12] and hypercapnia [11][12][13][14]. Animal models implicate increased inflammation in promoting the IH-induced AHVR augmentation, suggesting that anti-inflammatory medications may offer a therapeutic pathway to decrease ventilatory instability and, therefore, OSA severity [18,25].…”

Section: Discussionmentioning

confidence: 99%

“…IH exposure is thought to contribute to increased ventilatory instability in OSA as both acute (minutes to hours) and chronic (days to years) exposure increase the AHVR [7][8][9][10][11] and the AHCVR [11][12][13][14], although these are not consistent findings [8,15]. The progressive increase in the AHVR and AHCVR following IH may be considered as forms of respiratory plasticity (defined as a continuing alteration in the neural system controlling breathing based on prior experience [16]).…”

Section: Introductionmentioning

confidence: 99%

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Human intermittent hypoxia-induced respiratory plasticity is not caused by inflammation

et al. 2015

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Ventilatory instability, reflected by enhanced acute hypoxic (AHVR) and hypercapnic (AHCVR) ventilatory responses is a fundamental component of obstructive sleep apnoea (OSA) pathogenesis. Intermittent hypoxia-induced inflammation is postulated to promote AHVR enhancement in OSA, although the role of inflammation in intermittent hypoxia-induced respiratory changes in humans has not been examined. Thus, this study assessed the role of inflammation in intermittent hypoxiainduced respiratory plasticity in healthy humans.In a double-blind, placebo-controlled, randomised crossover study design, 12 males were exposed to 6 h of intermittent hypoxia on three occasions. Prior to intermittent hypoxia exposures, participants ingested (for 4 days) either placebo or the nonsteroidal anti-inflammatory drugs indomethacin (nonselective cyclooxygenase (COX) inhibitor) and celecoxib (selective COX-2 inhibitor). Pre-and post-intermittent hypoxia resting ventilation, AHVR, AHCVR and serum concentration of the pro-inflammatory cytokine tumour necrosis factor (TNF)-α were assessed.Pre-intermittent hypoxia resting ventilation, AHVR, AHCVR and TNF-α concentrations were similar across all three conditions ( p⩾0.093). Intermittent hypoxia increased resting ventilation and the AHVR similarly across all conditions ( p=0.827), while the AHCVR was increased ( p=0.003) and TNF-α was decreased ( p=0.006) with only selective COX-2 inhibition.These findings indicate that inflammation does not contribute to human intermittent hypoxia-induced respiratory plasticity. Moreover, selective COX-2 inhibition augmented the AHCVR following intermittent hypoxia exposure, suggesting that selective COX-2 inhibition could exacerbate OSA severity by increasing ventilatory instability. @ERSpublications Nonsteroidal anti-inflammatory drugs do not prevent intermittent hypoxia-induced respiratory plasticity in humans http://ow.ly/MDiCk

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Section: Ahvr and Ahcvrsupporting

confidence: 84%

Section: Ahvr and Ahcvrsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Human intermittent hypoxia-induced respiratory plasticity is not caused by inflammation

et al. 2015

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“…Others have suggested that individual difference in the tolerance to hypoxia may be explained by an increased Acute Mountain Sickness (AMS) incidence [12], which subsequently affects training and adaptation and ultimately performance. In short, the differentiation between responders and non-responders is probably based on many factors including genetic predisposition [13], automatic nervous system adaptation [14], hypoxia-induced ventilator drive [15], underlying individual fitness levels, fatigue recovery and motivation [16]. It is clear that there is considerable individual variation in the physiological responses of athletes using altitude training, which makes the prediction of responders and non-responders very difficult.…”

Section: Introductionmentioning

confidence: 99%

Live High-Train Low Altitude Training: Responders and Non- Responders

Hamlin¹,

Manimmanakorn²,

Creasy³

et al. 2015

J Athl Enhancement

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Objective: Investigate differences between athletes that responded (improved performance) compared to those that did not, after a 20-day "live high-train low" (LHTL) altitude training camp. Methods:Ten elite triathletes completed 20 days of live high (1545-1650 m), train low (300 m) training. The athletes underwent (i), two 800-m swimming time trials at sea-level (1 week prior to and 1 week after the altitude camp) and (ii) two 10-min standardised submaximal cycling tests at altitude on day 1 and day 20 of the altitude camp. Acute mountain sickness (AMS) was also measured during the camp. Based on their 800-m swimming time trial performances, athletes were divided into responders (improved by 3.2 ± 2.2%, mean ± SD, n=6) and non-responders (decreased by 1.8 ± 1.2%, n=4).Results: Compared to non-responders, the responders had lower exercise heart rates (-6.3 ± 7.8%, mean ± 90% CL, and higher oxygen saturations (1.2 ± 1.3%) at the end of the 10-min submaximal test after the camp. Compared to the responders, the non-responders had substantially higher VE and VE/VO 2 during the submaximal test on day 1 of the altitude training camp, and a substantially higher RER during the submaximal test on day 20 of the camp. As a result of the altitude training, exercise economy of the non-responders compared to the responders deteriorated (i.e., non-responders required more oxygen per watt). Non-responders were 3.0 times (90% CL=0.5-16.6) more likely to suffer symptoms of acute mountain sickness during first 5 days of altitude compared to responders. Conclusion:Changes in SpO 2 , heart rate and some respiratory variables during exercise and resting AMS scores may help determine athletes that respond to LHTL altitude training camps from athletes that fail to respond to such training.

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Dose-Response of Altitude Training: How Much Altitude is Enough?

Levine

Stray-Gundersen

2006

Advances in Experimental Medicine and Biology

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Effects of five nights of normobaric hypoxia on the ventilatory responses to acute hypoxia and hypercapnia

Cited by 28 publications

References 33 publications

Human intermittent hypoxia-induced respiratory plasticity is not caused by inflammation

Human intermittent hypoxia-induced respiratory plasticity is not caused by inflammation

Live High-Train Low Altitude Training: Responders and Non- Responders

Dose-Response of Altitude Training: How Much Altitude is Enough?

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