Supplemental oxygen and hyperbaric treatment at high altitude: cardiac and respiratory response

INTRODUCTION: The most effective treatment for high altitude sickness is prompt descent. However, rapid descent is sometimes impossible and alternative solutions are desirable. Supplemental oxygen at ambient pressure and hyperbaric oxygen in a hyperbaric tent have both been demonstrated to improve symptoms and increase arterial oxygenation (SaO2) in those with high altitude sickness; however, their use in combination has not previously been described in a controlled study. METHODS AND RESULTS: In this feasibility study, the SaO2 of six healthy, well-acclimatized participants rose from 76.5 to 97.5% at 4900 m and 72.5 to 96.0% at 5700 m following the administration of oxygen via a nasal demand circuit (33 ml of oxygen per pulse) inside a hyperbaric tent (107 mmHg above ambient barometric pressure) (p < 0.05). This contrasted with an increase in SaO2 to 89.5% at 4900 m and 86.3% at 5700 m with only supplemental oxygen and an increase in SaO2 to 92.8% (4900 m) and 90.5% (5700 m) with only hyperbaric exposure. In addition, combining treatments also resulted in an increase in tidal volume (29.0 and 31.0%) and minute ventilation (12.0 and 23.0%) together with a fall in heart rate (15.0 and 17.0%) at 4900 and 5700 m, respectively. No significant differences in heart rate, tidal volume, minute ventilation, SaO2, or respiratory rate were seen when hyperbaric treatment and supplemental oxygen were directly compared. CONCLUSIONS: In healthy, well-acclimatized subjects the combination of hyperbaric exposure and supplemental oxygen has a noteworthy effect on physiological parameters at high altitude. Awareness of this knowledge may enhance the treatment of patients with life-threatening high altitude sickness.     

Characteristics of the ventilatory response in subjects susceptible to high altitude pulmonary edema during acute and prolonged hypoxia

The present study compares the changes in ventilation in response to sustained hypobaric hypoxia and acute normobaric hypoxia between subjects susceptible to high altitude pulmonary edema (HAPE-S) and control subjects (C-S). Seven HAPE-S and five C-S were exposed to simulated high altitude of 4000 m for 23 h in a hypobaric chamber. Resting minute ventilation (V(E)), tidal volume (V(T)), and respiratory frequency (f(R)), as well as the end-tidal partial pressures of oxygen (P(ET(O2))) and carbon dioxide (P(ET(CO2))) were measured in all subjects sitting in a standardized position. Six measurement periods were recorded: ZH1 at 450 m at Zurich level, HA1 on attaining 3600 m altitude, HA2 after 20 min at 4000 m, HA3 after 21 h and HA4 after 23 h at 4000 m altitude, and ZH2 immediately after recompression to Zurich level. At ZH1 and HA3, the measurements were first done in lying, then in sitting, and afterwards in standing. Peripheral arterial oxygen saturation (Sa(O2)) was continuously recorded. All respiratory parameters were also measured during exercise lasting 30 min, the work load being 50% of maximal oxygen consumption (V(O2max)) at Zurich level and 26% of the Zurich V(O2max) at 4000 m. V(E), P(ET(O2)) and P(ET(CO2)) did not significantly differ between HAPE-S and C-S at rest and during exercise periods at Zurich level and at high altitude. However, Sa(O2) was significantly lower in HAPE-S than in C-S at rest and during exercise at 4000 m. Breathing through the mouthpiece during ventilation measurements increased significantly the Sa(O2) in HAPE-S in posture tests at HA3. This effect was most pronounced in the supine posture, in which HAPE-S had the lowest Sa(O2) values. These data provide evidence that (1) gas exchange might be impaired on the level of ventilation-perfusion mismatch or due to diffusion limitation in HAPE-S during the first 23 h of exposure to a simulated altitude of 4000 m, and (2) contrary to C-S, the Sa(O2) in HAPE-S is significantly affected by body position and by mouthpiece breathing.     

Acetazolamide improves cerebral oxygenation during exercise at high altitude

Vuyk, Jaap, Jan Van Den Bos, Kees Terhell, Rene De Bos, Ad Vletter, Pierre Valk, Martie Van Beuzekom, Jack Van Kleef, and Albert Dahan. Acetazolamide improves cerebral oxygenation during exercise at high altitude. High Alt. Med. Biol. 7:290-301, 2006.--Acute mountain sickness is thought to be triggered by cerebral hypoxemia and be prevented by acetazolamide (Actz). The effect of Actz on cerebral oxygenation at altitude remains unknown. In 16 members of the 2005 Dutch Cho Oyu (8201 m, Tibet) expedition, the influence of Actz and exercise (750 mg PO daily) on heart rate, peripheral and regional cerebral oxygen saturation (Sa(O(2) ) and rS(O(2) )), the Lake Louise score (LLS), and psychomotor function were studied at 0 m 14 days prior to the expedition, after arrival at 3700 m on day 3, after arrival at 5700 m on day 29, and again at 5700 m before the end of the expedition on day 51. After arrival at 3700 m, the LLS of the climbers taking Actz (n = 8) was significantly lower compared to those who did not take Actz (n = 8): 0.75 +/- 1.0 versus 2.9 +/- 2.0, p < 0.05 (ANOVA). High LLSs were associated with low rS(O(2) ) values in rest and exercise (p < 0.01 and p < 0.001). With altitude, resting Sa(O(2) ) and resting rS(O(2) ) decreased significantly (p < 0.001), irrespective of Actz use. Exercise at 3700 m and 5700 m reduced Sa(O(2) ) and rS(O(2) ) even further compared to rest (p < 0.001), although at 3700 m the rS(O(2) ) was preserved better in those who took Actz (55.3 +/- 4.3% versus 47.9 +/- 5.7%, p < 0.05). Irrespective of Actz use, with altitude, the percentage of omissions in the vigilance and tracking test increased while the climbers' scores on vigor decreased (p < 0.05). In conclusion, at altitude, exercise-induced reduction in cerebral oxygenation is less in climbers on Actz compared to climbers not taking Actz. This effect is nullified after several weeks at altitude due to acclimatization in climbers not taking Actz.     

Supplemental oxygen effects on ventilation in acclimatized subjects exercising at 5700 m altitude

INTRODUCTION: This study examines the effect of supplemental oxygen on acclimatized mountaineers at high altitude during rest and submaximal exercise. METHODS: Three healthy, acclimatized participants undertook nine periods of data collection lasting 10 min each over 2 consecutive days at 5700 m. These occurred at rest and exercise (40 and 80 W), breathing ambient air or supplemental oxygen (2 and 4 L m min') through an open-circuit breathing system. RESULTS: As minute ventilation increased during exercise, the fraction of inspired oxygen (FIO2) fell from 0.31 at rest to 0.23 with 2 L x min(-1) of oxygen and from 0.36 to 0.26 with 4 L x min(-1). Oxygen at both flow rates resulted in a significant increase in the arterial blood saturation of oxygen (SaO2) (Rest: 79% to 96% to 97%; 40 W: 80% to 95% to 97%; 80 W: 76% to 94% to 98%) and reduction in respiratory rate (RR) (Rest: 28 to 22 to 24; 40 W: 36 to 25 to 25; 80 W: 41 to 26 to 26). Tidal volume (VT, ml x s(-1)) was found to increase with the addition of oxygen (Rest: 959 to 844 to 969; 40 W: 1393 to 1834 to 1851; 80 W: 1558 to 2105 to 2215) and resulted in a non-significant reduction in minute ventilation (VE, L) (Rest: 25 to 17 to 21; 40 W: 46 to 45 to 43; 80 W: 61 to 51 to 53). No significant changes in heart rate were observed when oxygen was used (Rest: 78 to 62 to 71; 40 W: 90 to 91 to 96; 80 W: 105 to 102 to 101). CONCLUSION: An open-circuit breathing system may increase SaO2 and reduce RR in acclimatized mountaineers during rest and sub-maximal exercise at 5700 m, though further research is needed to confirm this.     

Angiotensin-converting enzyme genotype and arterial oxygen saturation at high altitude in Peruvian Quechua

The I-allele of the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with performance benefits at high altitude (HA). In n = 142 young males and females of largely Quechua origins in Peru, we evaluated 3 specific hypotheses with regard to the HA benefits of the I-allele: (1) the I-allele is associated with higher arterial oxygen saturation (Sa(O(2))) at HA, (2) the I-allele effect depends on the acclimatization state of the subjects, and (3) the putative I-allele effect on Sa(O(2)) is mediated by the isocapnic hypoxic ventilatory response (HVR, l/min(1)/% Sa(O(2))(1)). The subject participants comprised two different study groups including BLA subjects (born at low altitude) who were lifelong sea-level residents transiently exposed to hypobaric hypoxia (<24 h) and BHA subjects (born at HA) who were lifelong residents of HA. To control for the possibility of population stratification, Native American ancestry proportion (NAAP) was estimated as a covariate for each individual using a panel of 70 ancestry-informative molecular markers (AIMS). At HA, resting and exercise Sa(O(2)) was strongly associated with the ACE genotype, p = 0.008 with approximately 4% of the total variance in Sa(O(2)) attributed to ACE genotype. Moreover, I/I individuals maintained approximately 2.3 percentage point higher Sa(O(2)) compared to I/D and D/D. This I-allele effect was evident in both BLA and BHA groups, suggesting that acclimatization state has little influence on the phenotypic expression of the ACE gene. Finally, ACE genotype was not associated with the isocapnic HVR, although HVR had a strong independent effect on Sa(O(2)) (p = 0.001). This suggests that the I-allele effect on Sa(O(2)) is not mediated by the peripheral control of breathing, but rather by some other central cardiopulmonary effect of the ACE gene on the renin-angiotensin-aldosterone system (RAAS).     

阻塞性睡眠呼吸暂停低通气综合征合并心血管疾病患者通气功能和睡眠结构的变化

 目的探讨阻塞性睡眠呼吸暂停低通气综合征(Obstructive sleep apnea/hypopnea syndrome,OSAHS)合并心血管疾病患者通气功能和睡眠结构的变化,观察经鼻持续气道正压通气的治疗效果.方法监测单纯鼾症组,鼾症合并心血管疾病组,OSAHS组,以及OSAHS合并心血管疾病组患者低通气指数、呼吸暂停指数、呼吸暂停低通气指数、最低血氧饱和度、觉醒指数及睡眠分期的变化.随机选择OSAHS合并心血管疾病患者28例实施经鼻持续气道正压通气治疗.结果 OSAHS合并心血管病组的呼吸暂停指数高于单纯OSAHS组(P＜0.05).OSAHS合并心血管疾病组的觉醒指数和3+4期睡眠时间明显小于单纯OSAHS患者(P＜0.01或P＜0.05).OSAHS合并心血管疾病患者经持续气道正压通气治疗后呼吸暂停低通气指数显著降低(P＜0.05),最低氧饱和度明显升高(P＜0.05);重度组2期睡眠明显减少(P＜0.01);重度组3+4期睡眠明显增加(P＜0.05).结论 OSAHS合并心血管疾病患者有明显的通气功能和睡眠结构紊乱,经鼻持续气道正压通气治疗后通气功能和睡眠结构紊乱明显改善.     

Proportional assist ventilation reduces the work of breathing during exercise at moderate altitude

Reducing the work of breathing (WOB) during exercise and thus the oxygen required solely for ventilation may be an option to increase the oxygen available for nonventilatory physiological tasks at altitude. This study evaluated whether pressure support ventilation (PSV) and proportional assist ventilation (PAV) may partially reduce WOB during exercise at altitude. Seven volunteers breathing with either PSV or PAV or without support (control) were examined for WOB, inspiratory pressure time product (iPTP), and (O(2)) before and during pedaling at 160 W for 4 min on an ergometer at an altitude of 2860 m, where barometric pressure and oxygen partial pressure are approximately 30% less than at sea level. PSV and PAV reduced WOB from 4.5 +/- 0.9 J/L(-1)/min(-1) during unsupported breathing to 3.7 +/- 0.4 (p < 0.05) and 3.2 +/- 0.7 (p < 0.01), respectively. iPTP was reduced during PAV (570 +/- 151 cm H(2)O/sec/min(-1), p < 0.01), but not during PSV (727 +/- 116, p = 0.58) compared with unsupported ventilation during exercise (763 +/- 90). During PSV and PAV breathing, higher arterial oxygen saturations (84 +/- 2%, p < 0.05, and 86 +/- 1%, p < 0.01, respectively) were observed compared with control (80 +/- 3%), indicating that PSV and PAV attenuated hypoxemia during exercise at altitude. Total body (O(2)), however, was not reduced during PSV or PAV. In conclusion, both PSV and PAV reduced the WOB during exercise at altitude, but only PAV reduces iPTP. Both modes reduce hypoxemia, which may be due to higher alveolar ventilation or decreased ventilation-perfusion heterogeneity compared to unsupported breathing.     

Prediction of susceptibility to acute mountain sickness by SaO2 values during short-term exposure to hypoxia

Prediction of the development of acute mountain sickness (AMS) in individuals going to high altitudes is still a matter of debate. Whereas some studies found that subjects with a blunted hypoxic ventilatory response (HVR) are predisposed to AMS, others did not. However, the HVR has often been determined under very acute (5 to 10 min) isocapnic hypoxia without consideration of the subsequent hypoxic ventilatory decline (HVD), and the assessment of AMS susceptibility was based on a single altitude exposure. Therefore, the aim of the present study was to evaluate the relationship between the individual arterial oxygen saturation (Sa(O2)) after a 20- to 30-min exposure to poikilocapnic hypoxia and the AMS susceptibility based on repeated observations. A total of 150 healthy male and female mountaineers (ages: 42 +/- 13 yr), 63 of whom had known susceptibility to AMS and 87 of whom never suffered from AMS, were exposed to various degrees of normobaric and hypobaric hypoxia. Sa(O2) values were taken by finger pulseoximetry after 20 to 30 min of hypoxic exposure. Sa(O2) values after 20 to 30 min of hypoxia were on average 4.9% lower in subjects susceptible to AMS than in those who were not. Logistic regression analysis revealed altitude-dependent Sa(O2) values to be predictive for AMS susceptibility. Based on the derived model, AMS susceptibility was correctly predicted in 86% of the selected individuals exposed to short-term hypoxia. In conclusion, Sa(O2) values after 20 to 30 min of exposure to normobaric or hypobaric hypoxia represent a useful tool to detect subjects highly susceptible to AMS.     

Effect of F(I)O(2) on physiological responses and cycling performance at moderate altitude

PURPOSE: To evaluate physiological responses and exercise performance during a "live high-train low via supplemental oxygen" (LH + TLO(2)) interval workout in trained endurance athletes. METHODS: Subjects (N = 19) were trained male cyclists who were permanent residents of moderate altitude (1800-1900 m). Testing was conducted at 1860 m (P(B) 610-612 Torr, P(I)O(2) approximately 128 Torr). Subjects completed three randomized, single-blind trials in which they performed a standardized interval workout while inspiring a medical-grade gas with F(I)O(2) 0.21 (P(I)O(2) approximately 128 Torr), F(I)O(2) 0.26 (P(I)O(2) approximately 159 Torr), and F(I)O(2) 0.60 (P(I)O(2) approximately 366 Torr). The standardized interval workout consisted of 6 x 100 kJ performed on a dynamically calibrated cycle ergometer at a self-selected workload and pedaling cadence with a work:recovery ratio of 1:1.5. RESULTS: Compared with the control trial (21% O(2)), average total time (min:s) for the 100-kJ work interval was 5% and 8% (P < 0.05) faster in the 26% O(2) and 60% O(2) trials, respectively. Consistent with the improvements in total time were increments in power output (W) equivalent to 5% (26% O(2) trial) and 9% (60% O(2) trial; P < 0.05). Whole-body [VO](2) (L.min-1) was higher by 7% and 14% (P < 0.05) in the 26% O(2) and 60% O(2) trials, respectively, and was highly correlated to the improvement in power output (r = 0.85, P < 0.05). Arterial oxyhemoglobin saturation (S(p)O(2)) was significantly higher by 5% (26% O(2)) and 8% (60% O(2)) in the supplemental oxygen trials. CONCLUSION: We concluded that a typical LH + TLO(2) training session results in significant increases in arterial oxyhemoglobin saturation, [V02] and average power output contributing to a significant improvement in exercise performance.     

Relationship between dyspnea increase and ventilatory gas exchange thresholds during exercise in children with surgically corrected heart impairment

To study the relationship between the onset of an increase in dyspnea and ventilatory threshold (VT) in children with congenital heart impairment, sixteen young subjects underwent a cardiopulmonary exercise test with dyspnea perception and ventilatory gas exchange assessments. Dyspnea score was measured from a visual analogical scale at rest and during each step of an incremental exercise test. Dyspnea score was plotted against oxygen uptake and the onset of an increase in dyspnea (DT) was determined when a brutal disruption occurs on the dyspnea score-oxygen uptake curve. VT was defined from gas exchange according to Beaver's method. The first breakdown point in the oxygen uptake-carbon dioxide production relationship locates VT. Oxygen uptake (V(.-)O (2)), pulmonary ventilation (V(.-)E), heart rate (HR), oxygen pulse (O (2) pulse = V(.-)O (2)/HR), carbon dioxide production (V(.-)CO (2)) and power output (P) were measured both at VT and DT effort level. Results pointed out that there was no significant difference between the cardiorespiratory variables measured respectively at VT and DT: V(.-)O (2) (VTV(.-)O (2) = 16.71 +/- 2.65 vs. DTV(.-)O (2) = 18.34 +/- 5.74 ml x kg (-1) x min (-1)), V(.-)E (VTV(.-)E = 24.33 +/- 6.86 vs. DTV(.-)E = 26.82 +/- 9.59 l x min (-1)), (VTV(.-)CO (2) = 789.31 +/- 165.17 vs. DTV(.-)CO (2) = 924.02 +/- 342.28 ml x min (-1)), HR (VTHR = 116 +/- 10 vs. DTHR = 123 +/- 20 beat x min (-1)), O (2) pulse (VT O (2) pulse = 7.83 +/- 2.00 vs. DT O (2) pulse = 8.01 +/- 2.13 ml x kg (-1) x beat (-1)), and P (VTP = 43 +/- 16 vs. DTP = 52 +/- 27 W). Moreover, the cardiorespiratory variables measured at DT and VT were closely related: V(.-)O (2) (r = 0.64, p < 0.01), V(.-)E (r = 0.51, p < 0.01), HR (r = 0.75, p < 0.02), O (2) pulse (r = 0.90, p < 0.001), and P (r = 0.80, p < 0.01). In addition, according to Bland and Altman's procedure, the onset of dyspnea increase and ventilatory threshold were shown in close agreement for the cardiorespiratory variables measured at these effort levels. The standard errors of the estimates were low. It was concluded that dyspnea and ventilatory gas exchange thresholds occur concomitantly and were strongly correlated in children with congenital heart impairment. The use of the onset of dyspnea increase for aerobic capacity assessment may be a good alternative to ventilatory gas exchange threshold measurement.     

Hematological and lipid profile changes in sea-level natives after exposure to 3550-m altitude for 8 months

The aim of this epidemiological study was to determinate the effects on hematological and lipid profile in a young group of newcomers to altitude after being exposed chronically for 8 months to 3550 m (n = 50), age 17.8 +/- 0.7; and not overweight, BMI 22.9 +/- 0.5). Readings taken at altitude on day 1 and on month 8 were hematocrit (Hct, %), hemoglobin (Hb, g/dL), Sa(O(2)), total leukocyte and subset count (mm(3), %), and lipid profile (mg/dL). The same measurements were taken in a comparative group (CG) at sea level (SL). At altitude, elevations of Hct (44.6 +/- 0.4; 51.2 +/- 0.4) and Hb (15.5 +/- 0.1; 17.3 +/- 0.1) were seen (p < 0.001) and none with Hb >/= 21 g/dL. No correlation was observed between Hb and Sa(O(2)), r = 0.11, p > 0.05. Total leukocyte count showed no changes (6037 +/- 74; 6002 +/- 43), but a relative neutropenia (55.2 + -1.5; 50.6 + -1.3) and lymphocytosis (34.2 + 1; 42.4 + 1, p < 0.001) between periods were found and also when compared to SL. Also, an inverse relationship between Sa(O(2)) and total leukocytes on month 8 (r = 0.46; r(2) = 0.204), suggesting a probable representation of a hypoxia effect. Total cholesterol (153.8 +/- 4.5; 157.3 +/- 5.1; p, ns) showed no changes, but a mild decrease of LDL-cholesterol (88.4 +/- 3.3; 81.0 +/- 3.9; p < 0.05), and a rise in triglycerides (121.6 +/- 10.9; 178.8 +/- 11.7; p < 0.001) was found. Changes observed in leukocytes subset count and triglycerides could suggest a contributory role of hypoxic conditions, raising some future epidemiological concerns regarding immune system and fatty acid behaviour at altitude.     

Ventilatory effects of radiographic contrast media.

Respiratory adverse reactions have been reported with the use of contrast media. This study investigates the effects of different radiographic contrast media (RCM) on ventilation and blood gases. Tidal volume and respiratory rate of male Wistar rats anaesthetised with Inactin (100 mg kg-1 intraperitoneally), were measured continuously by integration of tracheal airflow. Contrast media (diatrizoate 370, ioxaglate 320 and iopromide 300) or mannitol controls matched for volume, pH and osmolarity (4 ml kg-1) were administered via a jugular cannula (n > or = 6 per group). Carotid artery blood was sampled at 2, 7, 12, 17, 25 and 30 min post-injection for PaO2, PaCO2 and pH. Systemic blood pressure was monitored from the same cannula. No significant reduction was observed in minute ventilation (tidal volume x respiratory rate per minute) with any of the contrast media. All contrast media and control solutions produced a fall in PaO2 within 4 min; returning to basal levels at 10 min (diatrizoate 35.6% (p < 0.05), ioxaglate 15.2% (p < 0.02), iopromide 16.2% (p < 0.01); controls: 17.3% (p < 0.01), 13.5% (p < 0.02) and 12.0% (NS), respectively). The fall in PaO2 induced by diatrizoate was significantly (p < 0.05) larger in comparison to the other groups. Ioxaglate, iopromide and their mannitol controls induced a comparable fall in PaO2. There was a concurrent rise in PaCO2 and fall in pH that reached significance for diatrizoate (p < 0.01). The changes in blood gases with RCM administration cannot be explained by changes in ventilation and may be due to an effect on pulmonary perfusion.     

Prehospital supplemental oxygen in trauma patients: its efficacy and implications for military medical care

Despite its near-universal use, few data exist to support the efficacy of prehospital supplemental oxygen (PH O2) in trauma patients. Data were reviewed from 5,090 patients not requiring assisted ventilation who were transported to our level I trauma center. Of these, 2,203 (43.3%) received PH O2 and 2,887 (56.7%) did not. Patients who received PH O2 had higher mortality than those without PH O2 (2.3% vs. 1.1%, p = 0.011). When corrected for Injury Severity Score, mechanism of injury, and age, those receiving PH O2 fared worse or no better than those who did not receive it. This suggests that supplemental oxygen does not improve survival in traumatized patients who are not in respiratory distress. This has implications for the management of casualties in combat or austere environments.     

Chronic mountain sickness: recent studies of the relationship between hemoglobin concentration and oxygen transport

Although an increase in hemoglobin concentration [Hb] in high altitude residents assists oxygen transport, excessive polycythemia ([Hb] > or = 21 g/100 mL) may cause the syndrome of chronic mountain sickness (CMS). A recent theoretical analysis has suggested that increasing [Hb] above 18 g/100 mL provides no further benefit in oxygen transport at rest. To test this hypothesis, we examined oxygen transport at rest for given arterial oxygen saturations (Sa(O2), in classes at intervals of 5%) as reported in 206 residents of various altitudes. For Sa(O2) of 97% versus 87%, [Hb] and a-v oxygen content difference increased (respectively, 14.5 to 17.5 g/100 mL and 4.11 to 5.03 volume %). As Sa(O2) fell further to 66%, a-v progressively decreased to 3.77 volume %, despite an increase in [Hb] to 24.2 g/100 mL. Over the Sa(O2) range of 97% to 66%, the a-v difference changed little (-8%) compared to other subjects made acutely hypoxic (-33%), for Sa(O2) change from 97% to 75%. The results suggest that increasing [Hb] allows greater oxygen extraction (a cardiac output sparing effect), which is maximal at Sa(O2) of 87% and a [Hb] of 17.5 g/100 mL. For more severe hypoxemia, even to Sa(O2) of 66%, both increasing [Hb] and increasing output are utilized for oxygen transport.     

Effect of oxygen breathing following submaximal and maximal exercise on recovery and performance.

To determine whether supplemental oxygen following exercise hastens recovery or enhances subsequent performance we evaluated its effectiveness in 13 male athletes. The exercise periods consisted of two 5-min submaximal efforts on a treadmill ergometer followed by a single bout to exhaustion. Intervals of exercise were separated by a 4-min recovery period during which the subject breathed either 1) room air, 2) 100% oxygen, or 3) 2 min of 100% oxygen followed by 2 min of room air on three nonconsecutive days. We found that breathing 100% oxygen produced no significant difference on the recovery kinetics of minute ventilation or heart rate, or improvement in subsequent performance as measured by duration of exercise (3.33 +/- 0.04 min, air vs 3.46 +/- 0.03, oxygen) and peak VO2 (59.9 +/- 2.2 ml.kg-1.min-1, air vs 54.5 +/- 2.2, oxygen). In addition, the perceived magnitude of exertion estimated by the Borg scale was no different during oxygen breathing. These findings offer no support for the use of supplemental oxygen in athletic events requiring short intervals of submaximal or maximal exertion.     

Effect of ramp slope on ventilation thresholds and VO2peak in male cyclists.

This study investigated the effect of 10 W*min(-1) (Slow ramp, SR), 30 W*min(-1) (Medium ramp, MR) and 50 W*min(-1) (Fast ramp, FR) exercise protocols on assessments of the first (VT1) and second (VT2) ventilation thresholds and peak oxygen uptake (VO(2)peak) in 12 highly-trained male cyclists (mean +/- SD age = 26 +/- 6 yr). Expired gas sampled from a mixing chamber was analyzed on-line and VT1 and VT2 were defined as two break-points in 20-s-average plots of pulmonary ventilation (V(E)), ventilatory equivalents for O(2) (V(E)/VO(2)) and CO(2) (V(E)/VCO(2)), and fractions of expired O(2) (F(E)O(2)) and CO(2) (F(E)CO(2)). Arterialized-venous blood samples were analyzed for blood-gas and acid-base status. VO(2)peak was significantly lower (p < 0.05) for SR (4.65 +/- 0.53 l small middle dot min(-1)) compared to MR (4.89 +/- 0.56 l *min(-1)) and FR (4.88 +/- 0.57 l *min(-1)) protocols. CO(2) output and blood PCO(2) were lower (p < 0.05), and V(E)/VCO(2) was higher (p < 0.05), above VT1 for SR compared to MR and FR protocols. No significant differences were observed among the protocols for VO(2), % VO(2)peak, V(E), plasma lactate ([La(-)]) and blood hydrogen ion concentration ([H(+)]), and heart rate (HR) values at VT1 or VT2. The work rate (WR) measured at VT1, VT2 and VO(2)peak increased (p < 0.05) with steeper ramp slopes. It was concluded that, in highly-trained cyclists, assessments of VT1 and VT2 are independent of ramp rate (10, 30, 50 W*min(-1)) when expressed as VO(2), % VO(2)peak, V(E), plasma [La(-)], blood [H(+)] and HR values, whereas VO(2)peak is lower during 10 W*min(-1) compared to 30 and 50 W*min(-1) ramp protocols. In addition, the WR measured at VT1, VT2 and VO(2)peak varies with the ramp slope and should be utilized cautiously when prescribing training or evaluating performance.     

Hypoxic ventilatory response,ventilation, gas exchange,and fluid balance in acute mountain sickness

To examine whether sea-level hypoxic ventilatory responses (HVR) predict acute mountain sickness (AMS) and document temporal changes in ventilation, HVR, gas exchange, and fluid balance, we measured these parameters at low altitude (100 m) and daily during 3 days at high altitude (4559 m). At low altitude, there were no significant differences in rest or exercise isocapnic HVR, poikilocapnic HVR at rest, and hypercapnic ventilatory response between 12 subjects without significant AMS and 11 subjects who fell sick. No low altitude ventilatory responses correlated with AMS or fluid balance at high altitude. On day 1, isocapnic HVR was significantly lower in the AMS group [0.86 +/- 0.43 (SD) vs. 1.43 +/- 0.63 L/min/% Sa(O2), p < 0.05). AMS was associated with higher AaD(O2), lower Pa(O2), and Sa(O2), while Pa(CO2) was not different between subjects with and without AMS. Both groups showed equivalent reductions in urine volume, sodium output, and gain in body weight on day 1 while climbing to 4559 m, but on day 2 only subjects without AMS had diuresis, natriuresis, and weight loss. We conclude that (1) susceptibility to AMS, fluid balance, and ventilation at high altitude cannot be predicted by low altitude HVR testing and (2) that the failure to increase HVR on arrival at high altitude and impaired gas exchange, possibly due to interstitial edema, may account for the more severe hypoxemia in AMS.     

Effect of a long- and short-acting beta2-agonist on exercise-induced arterial hypoxemia

PURPOSE: determine the effect of formoterol and salbutamol on the arterial oxygen saturation (SaO(2)) of highly trained nonasthmatic athletes with exercise-induced arterial hypoxemia (EIAH). METHODS: Ten male athletes (age = 27.1 +/- 0.7, [OV0312]O(2max) = 65.2 +/- 2.5 mL.kg-1.min-1, SaO(2min) = 91.0 +/- 2.1%) with minimal bronchial reactivity to aerosols (i.e., negative methacholine challenge test) completed three identical exercise sessions differing only by the medication administered. Formoterol (F), a long-acting beta-2 agonist, was compared with salbutamol (S) and a placebo (P). F (12 microg), S (400 microg), or P was administered by a Turbuhaler, 10 min before exercise testing in a double-blind, randomized, three-way crossover design. Testing sessions included an incremental cycle ergometer test to exhaustion, while monitoring SaO(2) and ventilation, and a pre- and postexercise pulmonary function test. RESULTS: There were no significant differences between the groups in SaO(2) nadir with exercise (F = 92.0 +/- 1.0; S = 92.0 +/- 1.0; P = 91.0 +/- 0.7%). During the maximal incremental test, no differences were observed in SaO(2) or minute ventilation between the three experimental conditions. Pulmonary function tests revealed a significant increase in FEV(1) and FEV(1)/FVC after exercise in all conditions. Drug administration increased FEV(1)/FVC postexercise compared with placebo (F = 87.9 +/- 2.3, S = 87.6 +/- 1.7 > P = 85.6 +/- 2.1%; P < 0.05). CONCLUSION: An acute, inhaled, therapeutic dose of formoterol or salbutamol did not affect SaO(2) nadir or ventilation kinetics in a group of highly trained nonasthmatic athletes with EIAH.     

Oral contraceptive phase has no effect on endurance test

Thirteen female cyclists/triathletes (mean peak VO(2) = 53.0 + 5.6 ml . kg (-1) . min (-1)) using a monophasic oral contraceptive (OC) performed an endurance test (1-h cycle) at three time points of an OC cycle. Testing times were during the OC consumption phase (CONS), early in the OC withdrawal phase (WITH1) and late in the OC withdrawal phase (WITH2). Resting endogenous serum oestradiol and progesterone concentrations were measured. Power output, heart rate (HR), ventilation (V(E)), oxygen consumption (VO(2)), respiratory exchange ratio (RER), rating of perceived exertion (RPE), blood lactate and blood glucose were measured throughout the 1-h test. Serum oestradiol levels were greater during WITH2 compared to the CONS (p < 0.05). No significant differences were present between the testing times for mean power output (172 - 173 watts), HR (163 - 166 bpm), VO(2) (41.3 - 41.7 mL . kg (-1) . min (-1)), RER (0.93 - 0.94), RPE (14.5 - 14.8) and blood glucose concentration (5.3 - 5.5 mmol . L (-1)) (p > 0.05). Greater mean V. (E) (by 3.4 and 5.7 L . min (-1)) and VE/VO(2) (by 1.0 and 2.0) values were measured during CONS compared to WITH1 and WITH2 respectively and blood lactate values (by 1.2 mmol . L (-1)) compared to WITH1 only (p < 0.05). Despite variation in some physiological variables, there was no difference in endurance performance throughout an OC cycle in endurance trained female athletes.     

Oxygen uptake efficiency slope in coronary artery disease: clinical use and response to training

The Oxygen Uptake Efficiency Slope (OUES), a new parameter derived from respiratory gas analysis, has been suggested as a submaximal index of cardiopulmonary functional reserve. We evaluated the clinical application and the effect of physical training on the OUES in patients with coronary artery disease (CAD). Maximal cycle-ergometer testing with respiratory gas analysis (breath-by-breath) was performed in 590 patients with CAD and again after three months of physical training in 425 patients. OUES was determined from the linear relation of oxygen uptake (V.O (2)) vs. the logarithm of pulmonary ventilation (V (E)) during exercise, i.e. V.O (2) = a log (10) V (E) + b, where a is the OUES. The ventilatory anaerobic threshold (VAT) and the slope of the relation of V (E) nu carbon dioxide production (V.CO (2)) (V (E)-V.CO (2) slope) were also determined. Correlation coefficients of the relation from which OUES was derived in individuals averaged 0.975 +/- 0.024 (mean +/- SD) when calculated from data up to a respiratory gas exchange ratio of 1.0. Submaximal OUES was marginally lower (5.4 +/- 7.9 %, p < 0.05) than the OUES calculated from 100 % of respiratory exercise data. Of all submaximal parameters, submaximal OUES (r = 0.837, p < 0.001) and VAT (r = 0.860, p < 0.001) correlated best with peak V.O (2), followed by V (E)-V.CO (2) slope (r = - 0.469, p < 0.001). OUES was lower in patients who underwent coronary artery bypass grafting as compared with patients after coronary angioplasty (p < 0.05). Peak V.O (2) and OUES increased significantly (p < 0.001) after training with 24 +/- 19.2 % and 20.9 +/- 19.3 %, respectively. Changes in peak V.O (2) correlated better with changes in OUES and in VAT (r = 0.61 and r = 0.55, p < 0.001, respectively) than with changes in V (E)-V.CO (2) slope (r = - 0.171, p < 0.001). The submaximal OUES is clinically useful for the quantification of exercise performance and is sensitive to physical training in patients with CAD.