Effects of the Turbine™ on Ventilatory and Sensory Responses to Incremental Cycling.

INTRODUCTION: The Turbine™ is a nasal dilator marketed to athletes to increase airflow, which may serve to reduce dyspnea and improve exercise performance, presumably via reductions in the work of breathing (WOB). However, the unpublished data supporting these claims were collected in individuals at rest that were exclusively nasal breathing. These data are not indicative of how the device influences breathing during exercise at higher ventilations when a larger proportion of breathing is through the mouth. Accordingly, the purpose of this study was to empirically test the efficacy of the Turbine™ during exercise. We hypothesized that the Turbine™ would modestly reduce the WOB at rest and very low exercise intensities but would have no effect on the WOB at moderate to high exercise intensities. METHODS: We conducted a randomized crossover study in young, healthy individuals (7M:1F; age = 27 ± 5 yr) with normal lung function. Each participant performed two incremental cycle exercise tests to exhaustion with the Turbine™ device or under a sham control condition. For the sham control condition, participants were told they were breathing a low-density gas to reduce the WOB, but they were actually breathing room air. The WOB was determined through the integration of ensemble averaged esophageal pressure-volume loops. Standard cardiorespiratory measures were recorded using a commercially available metabolic cart. Dyspnea was assessed throughout exercise using the 0-10 Borg scale. RESULTS: Peak V˙O2 and work rate were not different between conditions (P = 0.70 and P = 0.35, respectively). In addition, there was no interaction or main effect of condition on dyspnea, ventilation, or WOB throughout the exercise (all P > 0.05). CONCLUSION: These findings suggest that the Turbine™ does not reduce the WOB and has no effect on dyspnea or exercise capacity.

Day-to-day variability in cardiorespiratory responses to hypoxic cycle exercise.

Repeatedly performing exercise in hypoxia could elicit an independent training response and become an unintended co-intervention. The primary purposes of this study were to determine if hypoxic exercise responses changed across repeated testing and to assess the day-to-day variability of commonly used measures of cardiorespiratory and metabolic responses to hypoxic exercise. Healthy young males (aged 23 ± 2 years) with a maximal O2 consumption of 50.7 ± 4.7 mL·kg(-1)·min(-1) performed 5 trials (H1 to H5) over a 2-week period in hypoxia (fraction of inspired oxygen = 0.13). Participants completed 3-min stages at 20%, 40%, 60%, and 10% of individual peak power. With increasing cycle exercise intensity there were increases in minute ventilation, O2 consumption, CO2 production, respiratory exchange ratio, heart rate (HR), blood lactate concentration, and ratings of perceived exertion for legs and respiratory system along with a reduction in oxyhaemoglobin saturation (%SpO2) (all p < 0.001). There were no systematic changes from H1 to H5 (p > 0.05). Most measures were highly repeatable across testing sessions with the coefficient of variation (CV) averaging ≤10% of the mean value in all variables except O2 consumption (17%), CO2 production (11%) and blood lactate concentration (17%). For HR and %SpO2 the CV was <5%. The exercise protocol did not elicit a training response when repeated 5 times during a 2-week period and the variability of exercise responses was low. We conclude that this protocol allows detection of small changes in cardiorespiratory responses to hypoxic exercise that might occur during exposure to hypoxia.

Anti-oxidant N-acetylcysteine diminishes diesel exhaust-induced increased airway responsiveness in person with airway hyper-reactivity.

BACKGROUND: Inhalation of diesel exhaust (DE) at moderate concentrations causes increased airway responsiveness in asthmatics and increased airway resistance in both healthy and asthmatic subjects, but the effect of baseline airway responsiveness and anti-oxidant supplementation on this dynamic is unknown. OBJECTIVES: We aimed to determine if changes in airway responsiveness due to DE are attenuated by thiol anti-oxidant supplementation, particularly in those with underlying airway hyper-responsiveness. METHODS: Participants took N-acetylcysteine (600 mg) or placebo capsules three times daily for 6 days. On the last of these 6 days, participants were exposed for 2 h to either filtered air (FA) or DE (300 µg/m(3) of particulate matter smaller than 2.5 microns). Twenty-six non-smokers were studied under each of three experimental conditions (filtered air with placebo, diesel exhaust with placebo, and diesel exhaust with N-acetylcysteine) using a randomized, double-blind, crossover design, with a 2-week washout between conditions. Methacholine challenge was performed pre-exposure (baseline airway responsiveness) and post-exposure (effect of exposure). RESULTS: Anti-oxidant supplementation reduced baseline airway responsiveness in hyper-responsive individuals by 20% (p = 0.001). In hyper-responsive individuals, airway responsiveness increased 42% following DE compared with FA (p = 0.03) and this increase was abrogated with anti-oxidant supplementation (diesel exhaust with N-acetylcysteine vs. filtered air with placebo, p = 0.85). CONCLUSIONS: Anti-oxidant (N-acetylcysteine) supplementation protects against increased airway responsiveness associated with DE inhalation and reduces need for supplement bronchodilators in those with baseline airway hyper-responsiveness. Individuals with variants in genes of oxidative stress metabolism when exposed to DE are protected from increases in airway responsiveness if taking anti-oxidant supplementation.

Haematological acclimation and re-acclimation to hypoxia in the mouse.

Haematological responses throughout 4 w of initial acclimation (IA) and three paradigms of re-acclimation (RA) to hypoxia (FI(O2)) were examined in female mice. We hypothesised that (i) haematological responses would be increased during re-exposure, resulting in greater O2-carrying capacity in RA compared to IA; and (ii) further improvements would occur when abbreviating the de-acclimation period to 1 w (RA↓DA) or extending the IA period to 8 w (RA↑IA). The serum [EPO] response was blunted in all RA groups compared to IA but the resulting reticulocyte response was similar in all experimental groups. The [Hb] response was the same in RA and RA↓DA as in IA but was blunted in RA↑IA due to a reduction in mean corpuscular Hb. The sensitivity of EPO-producing cells appears blunted but the sensitivity of erythroid precursors to EPO is enhanced by recent hypoxic exposure. Erythropoietic regulation is altered during RA in a manner that is dependent on the paradigm of initial exposure.

Acclimatisation in trekkers with and without recent exposure to high altitude.

In mountaineers, recent altitude exposure has been shown to improve climbing performance and clinical outcomes during re-exposure to high altitude. However, the timing of previous altitude exposure has not been clearly reported and previous findings might be driven by individuals who were still acclimatised at the time of re-exposure. Our goal was to determine whether recent altitude exposure would confer an advantage even in individuals who had de-acclimatised for ≥ 1 week before being re-exposure. Low-altitude natives kept a daily trekking log throughout 7- to 8-day trek from Lukla (2,840 m) to Gokyo Ri (5,360 m). Trekkers with recent altitude exposure (re-acclimatisers, RA; n = 20) walked 20% faster (p < 0.01), reported lower acute mountain sickness scores (9 ± 8 vs. 15 ± 13; p = 0.02), and used less medication to treat headache (p < 0.05) compared to trekkers with no recent altitude exposure (initial acclimatisers, IA; n = 30). On Gokyo Ri, S(p)O(2) was significantly higher in RA than IA trekkers (85 ± 6 vs. 78 ± 6; p = 0.01). These data indicate improved functional outcomes and physiological compensation for hypoxia in RA. However, even after de-acclimatisation for 7-30 days, it is possible that RA trekkers began the trek in a more acclimatised state than IA trekkers. RA trekkers might represent a self-selected group that has previously tolerated altitude well and has therefore opted to return. Some findings might also reflect improved psychological altitude tolerance in RA. A direct comparison of the functional and physiological responses to hypoxia throughout an initial and re-acclimatisation to high altitude is needed.

Resting and exercise ventilatory chemosensitivity across the menstrual cycle.

We hypothesized that resting and exercise ventilatory chemosensitivity would be augmented in women when estrogen and progesterone levels are highest during the luteal phase of the menstrual cycle. Healthy, young females (n = 10; age = 23 ± 5 yrs) were assessed across one complete cycle: during early follicular (EF), late follicular (LF), early luteal, and mid-luteal (ML) phases. We measured urinary conjugates of estrogen and progesterone daily. To compare values of ventilatory chemosensitivity and day-to-day variability of measures between sexes, males (n = 10; age = 26 ± 7 yrs) were assessed on 5 nonconsecutive days during a 1-mo period. Resting ventilation was measured and hypoxic chemosensitivity assessed using an isocapnic hypoxic ventilatory response (iHVR) test. The hypercapnic ventilatory response was assessed using the Read rebreathing protocol and modified rebreathing tests. Participants completed submaximal cycle exercise in normoxia and hypoxia. We observed a significant effect of menstrual-cycle phase on resting minute ventilation, which was elevated in the ML phase relative to the EF and LF phases. Compared with males, resting end-tidal CO(2) was reduced in females during the EF and ML phases but not in the LF phase. We found that iHVR was unaffected by menstrual-cycle phase and was not different between males and females. The sensitivity to chemical stimuli was unaffected by menstrual-cycle phase, meaning that any hormone-mediated effect is of insufficient magnitude to exceed the inherent variation in these chemosensitivity measures. The ventilatory recruitment threshold for CO(2) was generally lower in women, which is suggestive of a hormonally related lowering of the ventilatory recruitment threshold. We detected no effect of menstrual-cycle phase on submaximal exercise ventilation and found that the ventilatory response to normoxic and hypoxic exercise was quantitatively similar between males and females. This suggests that feed-forward and feed-back influences during exercise over-ride the effects of naturally occurring changes in sex hormones.

The pulmonary system during exercise in hypoxia and the cold.

The demands for pulmonary O(2) and CO(2) transport in the exercising human are substantial. Fortunately, the regulatory and architectural limits of the pulmonary system meet the requirements of heavy exercise in most individuals. However, in some highly trained athletes the high metabolic demand of intense exercise is in excess of the capacity of the pulmonary system. Environmental considerations, in addition to those imposed by the demands of exercise, provide further physiological challenges that must be met. Winter athletes often encounter high-altitude hypoxia and cold, either transiently during competition or repeatedly during training. In this brief review, we examine the pulmonary system during acute and chronic exercise in hypoxic and cold environmental conditions. Observations from studies conducted in humans are emphasized in order to ask questions about regulation, plasticity and the limits of human physiology. We also highlight new findings and controversial questions that would benefit from additional study.

Performance of evacuated blood collection tubes at high altitude.

Researchers and clinicians may not be aware that the performance of evacuated blood collection systems is impaired at high altitude. We tested four sizes of Vacutainer tubes at altitudes ranging from sea level to 5341 m to and determined that draw volumes are reduced by approximately 0.5 mL for every 1000 m gain in terrestrial elevation. Insufficient blood volume can limit possibilities for testing, inappropriate blood to additive ratios can skew test results and with smaller tubes at higher altitudes there is a possibility of air embolism. With foresight and proper planning, these problems can be avoided, and evacuated blood collection tubes can still be used safely and effectively at high altitude.

Lung density is not altered following intense normobaric hypoxic interval training in competitive female cyclists.

Noninvasive imaging techniques have been used to assess pulmonary edema following exercise but results remain equivocal. Most studies examining this phenomenon have used male subjects while the female response has received little attention. Some suggest that women, by virtue of their smaller lungs, airways, and diffusion surface areas may be more susceptible to pulmonary limitations during exercise. Accordingly, the purpose of this study was to determine if intense normobaric hypoxic exercise could induce pulmonary edema in women. Baseline lung density was obtained in eight highly trained female cyclists (mean +/- SD: age = 26 +/- 7 yr; height = 172.2 +/- 6.7 cm; mass = 64.1 +/- 6.7 kg; Vo(2max) = 52.2 +/- 2.2 ml.kg(-1).min(-1)) using computed tomography (CT). CT scans were obtained at the level of the aortic arch, the tracheal carina, and the superior end plate of the tenth thoracic vertebra. While breathing 15% O(2), subjects then performed five 2.5-km cycling intervals [mean power = 212 +/- 31 W; heart rate (HR) = 94.5 +/- 2.2%HRmax] separated by 5 min of recovery. Throughout the intervals, subjects desaturated to 82 +/- 4%, which was 13 +/- 2% below resting hypoxic levels. Scans were repeated 44 +/- 8 min following exercise. Mean lung density did not change from pre (0.138 +/- 0.014 g/ml)- to postexercise (0.137 +/- 0.011 g/ml). These findings suggest that pulmonary edema does not occur in highly trained females following intense normobaric hypoxic exercise.