Exercise-induced Arterial Hypoxemia Research Articles

Effects of three weeks base training at moderate simulated altitude with or without hypoxic residence on exercise capacity and physiological adaptations in well-trained male runners.

To test the hypothesis that 'live high-base train high-interval train low' (HiHiLo) altitude training, compared to 'live low-train high' (LoHi), yields greater benefits on performance and physiological adaptations. Sixteen young male middle-distance runners (age, 17.0 ± 1.5 y; body mass, 58.8 ± 4.9 kg; body height, 176.3 ± 4.3 cm; training years, 3-5 y; training distance per week, 30-60 km.wk-1) with a peak oxygen uptake averaging ~65 ml.min-1.kg-1 trained in a normobaric hypoxia chamber (simulated altitude of ~2,500 m, monitored by heart rate ~170 bpm; thrice weekly) for 3 weeks. During this period, the HiHiLo group (n = 8) stayed in normobaric hypoxia (at ~2,800 m; 10 h.day-1), while the LoHi group (n = 8) resided near sea level. Before and immediately after the intervention, peak oxygen uptake and exercise-induced arterial hypoxemia responses (incremental cycle test) as well as running performance and time-domain heart rate variability (5-km time trial) were assessed. Hematological variables were monitored at baseline and on days 1, 7, 14 and 21 during the intervention. Peak oxygen uptake and running performance did not differ before and after the intervention in either group (all P > 0.05). Exercise-induced arterial hypoxemia responses, measured both at submaximal (240 W) and maximal loads during the incremental test, and log-transformed root mean square of successive R-R intervals during the 4-min post-run recovery period, did not change (all P > 0.05). Hematocrit, mean reticulocyte absolute count and reticulocyte percentage increased above baseline levels on day 21 of the intervention (all P < 0.001), irrespective of group. Well-trained runners undertaking base training at moderate simulated altitude for 3 weeks, with or without hypoxic residence, showed no performance improvement, also with unchanged time-domain heart rate variability and exercise-induced arterial hypoxemia responses.

A revision of maximal oxygen consumption and exercise capacity at altitude 70 years after the first climb of Mount Everest.

On the 70th anniversary of the first climb of Mount Everest by Edmund Hillary and Tensing Norgay, we discuss the physiological bases of climbing Everest with or without supplementary oxygen. After summarizing the data of the 1953 expedition and the effects of oxygen administration, we analyse the reasons why Reinhold Messner and Peter Habeler succeeded without supplementary oxygen in 1978. The consequences of this climb for physiology are briefly discussed. An overall analysis of maximal oxygen consumption ( ) at altitude follows. In this section, we discuss the reasons for the non-linear fall of at altitude, we support the statement that it is a mirror image of the oxygen equilibrium curve, and we propose an analogue of Hill's model of the oxygen equilibrium curve to analyse the fall. In the following section, we discuss the role of the ventilatory and pulmonary resistances to oxygen flow in limiting , which becomes progressively greater while moving toward higher altitudes. On top of Everest, these resistances provide most of the limitation, and the oxygen equilibrium curve and the respiratory system provide linear responses. This phenomenon is more accentuated in athletes with elevated , due to exercise-induced arterial hypoxaemia. The large differences in that we observe at sea level disappear at altitude. There is no need for a very high at sea level to climb the highest peaks on Earth.

Exercise-induced arterial hypoxemia in female masters athletes

The purpose of the study was to characterize exercise induced arterial hypoxemia (EIAH) in female masters athletes (FMA). We hypothesized that FMA would experience EIAH during treadmill running. Eight FMA (48–57 years) completed pulmonary function testing and an incremental exercise test until exhaustion (V̇O2max⁡ = 45.7 ± 6.5, range:35–54 ml/kg/min). On a separate day, the participants were instrumented with a radial arterial catheter and an esophageal temperature probe. Participants performed three to four constant load exercise tests at 60–70 %, 75 %, 90 %, 95 %, and 100 % of maximal oxygen uptake while sampling arterial blood and recording esophageal temperature. We found that FMA decrease their partial pressure of oxygen (86.0 ± 7.6, range:73–108 mmHg), arterial saturation (96.2 ± 1.2, range:93–98 %), and widen their alveolar to arterial oxygen difference (23.2 ± 8.8, range:5–42 mmHg) during all exercise intensities however, with variability in terms of severity and pattern. Our findings suggest that FMA experience EIAH however aerobic fitness appears unrelated to occurrence or severity (r = 0.13, p = 0.756).

Exercise-induced Arterial Hypoxemia In Female Masters Athletes

Exercise-induced Arterial Hypoxemia In Female Masters Athletes

Nedocromil sodium and diphenhydramine HCl ameliorate exercise-induced arterial hypoxemia in highly trained athletes.

IntroductionExercise‐induced arterial hypoxemia (EIAH) has been observed in highly trained endurance athletes during near maximal exercise, which may be influenced by a histamine‐mediated inflammatory response at the pulmonary capillary‐alveolar membrane. In order to test this hypothesis, we examined whether the mast cell stabilizer nedocromil sodium (NS) and H1‐receptor antagonist diphenhydramine HCL (DH) would ameliorate EIAH and mitigate the drop in arterial oxyhemoglobin saturation (SaO2) during intensive exercise.MethodsSeven highly trained male cross country runners (age, 21 ± 2 years; V̇O2max, 74.7 ± 3.5 ml·kg−1·min−1) participated in the study. All subjects completed a maximal exercise treadmill test to exhaustion, followed by three 5‐min constant‐load exercise bouts at 70%, 80%, and 90% V̇O2max. Prior to testing, subjects received either placebo (PL), NS, or DH.ResultsCompared to PL, there was a significant treatment effect on SaO2 (p < 0.001) for both NS and DH during both constant‐load exercise and at V̇O2max. Post hoc tests revealed SaO2 values, compared to PL, were significantly higher at V̇O2max and during DH trials and higher with NS at constant‐load intensities except at 70% (p = 0.13).ConclusionThe findings provide further evidence that histamine contributes directly or indirectly to the development of EIAH during intense exercise in highly trained athletes.

Cardiopulmonary Exercise Testing in Athletes: Expect the Unexpected.

Cardiopulmonary exercise testing (CPET) is a tool designed to assess the integrated function of the cardiac, pulmonary, vascular and musculoskeletal systems to produce an exercise effort. CPET may be performed for performance purposes as part of optimizing a training program or for clinical purposes in athletes with established cardiovascular disease or in those with symptoms suggestive of cardiopulmonary pathology. Most normative values used for CPET parameters have been derived in the general population, in whom there will be expected differences in exercise physiology as compared to a trained athlete. In this review, our goal is to examine current available data on expected findings on CPET in athletes, highlight how these differ from the general population-derived normative values, and identify areas in need of further research to optimize the application of CPET in athletes. Athletes demonstrate differences in exercise hemodynamic and gas exchange profiles as compared to non-athletes including: higher cardiac output, faster heart rate recovery, higher peak V̇O2, higher prevalence of exercise-induced arterial hypoxemia, and lower breathing reserve. CPET is an important tool to optimize performance and assess for underlying pathology in an athletic population. The impact of routine, vigorous physical activity on exercise physiology should be integrated into determination of what constitutes a normal CPET result in an athletic individual.

Effect of training on the development of exercise-induced arterial hypoxemia in volleyball players

Background and Study Aim. The purpose of this study was to examine the effect of volleyball training on the development of exercise-induced arterial hypoxemia during incremental exercise in male competitive volleyball players.&#x0D; Material and Methods. Eight male amateur volleyball players (age 21±1.3 years) participated in a 6-week volleyball training program three times a week in the pre-season preparatory period. Before and after the training period, all players performed an incremental treadmill test to determine maximal oxygen uptake (VO2max), and oxyhemoglobin saturation (SaO2) was continuously measured using a pulse oximeter during the test. Maximal values of minute ventilation (VEmax), respiratory exchange ratio (RERmax), ventilatory equivalent for oxygen (VE/VO2) and carbon dioxide (VE/VCO2) were determined. Exercise-induced arterial hypoxemia (EIAH) was defined as a SaO2 decreased by at least 4% (ΔSaO2≤ −4%) from resting level.&#x0D; Results. All the players exhibited exercise-induced arterial hypoxemia before (ΔSaO2= –8.8±3.3%) and after (ΔSaO2= –8.31.5%) the training period. SaO2 was significantly decreased from 97.6±1% at rest to 88.7±2.7% at exhaustion before the training period, and from 97.2±1.1% at rest to 88.8±2.1% at exhaustion after training period (p &lt; 0.001). There was no significant difference in resting and lowest SaO2 values by comparison between the before and after training (p &gt; 0.05). There were no significant changes in VO2max, VEmax, RERmax, VE/VO2 and VE/VCO2 after training period (p &gt; 0.05).&#x0D; Conclusions. The results of this study showed that volleyball players with a history of anaerobic training may exhibit EIAH, but that 6-week volleyball training has no effect on the degree of exercise-induced arterial hypoxemia.

Alveolar to arterial gas exchange during constant-load exercise in healthy active men and women

ABSTRACT Inadequate hyperventilation and inefficient alveolar to arterial gas exchange are gas exchange challenges that can limit capacity and cause exercise-induced arterial hypoxaemia (EIAH). This work evaluated if the prevalence of gas exchange inefficiencies, defined as AaDO2>25 mmHg, PaCO2>38 mmHg, and/or ΔPaO2>-10 mmHg at any point during constant-load exercise in healthy, active, but not highly trained, individuals suggested an innate sex difference that would make females more susceptible to EIAH. Sixty-four healthy, active males and females completed 18-min of cycling exercise (moderate and vigorous intensity, 9 min/stage). Arterial blood gases were measured at rest and every 3-min during exercise, while constantly assessing gas exchange. Both sexes demonstrated similar levels of AaDO2 widening until the final 3 min of vigorous exercise, where females demonstrated a trend for greater widening than males (16.3±6.2 mmHg vs. 19.1±6.0 mmHg, p=0.07). Males demonstrated a blunted ventilatory response to moderate exercise with higher PaCO2 (38.5±2.6 vs. 36.5±2.4, p=0.002) and a lower ventilation when corrected for workload (0.42±0.1 vs. 0.48±0.1, p=0.002). No significant arterial hypoxaemia occurred, but in 6 M and 5 F SaO2 dropped by ≥2%. There was no difference in prevalence of pulmonary gas exchange inefficiencies between sexes, but the type of inefficiency was influenced by sex. Abbreviations: AaDO2: alveolar-arterial oxygen difference; BP: blood pressure; EIAH: exercise-induced arterial hypoxaemia; F: females; HR: heart rate; M: males; Q: cardiac output; PaCO2: arterial partial pressure of carbon dioxide; PaO2: arterial partial pressure of oxygen; ΔPaO2: change in arterial partial pressure of oxygen; PAO2: alveolar partial pressure of oxygen; RPE: rating of perceived exertion; SaO2: arterial oxygen saturation; VE: ventilation; VE/VCO2: ventilatory equivalent for carbon dioxide; VO2PEAK: peak oxygen consumption; WMAX: workload maximum

Peripheral chemoresponsiveness during exercise in male athletes with exercise‐induced arterial hypoxaemia

What is the central question of this study? Do highly trained male endurance athletes who develop exercise-induced arterial hypoxaemia (EIAH) demonstrate reduced peripheral chemoresponsiveness during exercise? What is the main finding and its importance? Those with the lowest arterial saturation during exercise have a smaller ventilatory response to hypercapnia during exercise. There was no significant relationship between the hyperoxic ventilatory response and EIAH. The findings suggest that peripheral chemoresponsiveness to hypercapnia during exercise could play a role in the development of EIAH. The findings improve our understanding of the mechanisms that contribute to EIAH. Exercise-induced arterial hypoxaemia (EIAH) is characterized by a decrease in arterial oxygen tension and/or saturation during whole-body exercise, which may in part result from inadequate alveolar ventilation. However, the role of peripheral chemoresponsiveness in the development of EIAH is not well established. We hypothesized that those with the most severe EIAH would have an attenuated ventilatory response to hyperoxia and hypercapnia during exercise. To evaluate this, on separate days, we measured ventilatory sensitivity to hyperoxia and separately hypercapnia at rest and during three different exercise intensities (25, 50% of and ventilatory threshold (∼67% of )) in 12 males cyclists ( =66.6±4.7mlkg-1 min-1 ). Subjects were divided into two groups based on their end-exercise arterial oxygen saturation (ear oximetry, ): a normal oxyhaemoglobin saturation group (NOS, =93.4±0.4%,n=5) and a low oxyhaemoglobin saturation group (LOS, =89.9±0.9%, n=7). There was no difference in (66.4±2.9vs.66.8±6.0mlkg-1 min-1 , respectively, P=0.9), peak ventilation during maximal exercise (182±15vs.197±32lmin-1 , respectively, P=0.36) or ventilatory response to hyperoxia (P=0.98) at any exercise intensity between NOS and LOS groups. However, those in the LOS group had a significantly lower ventilatory response to hypercapnia (P=0.004, (η2 =0.18). There was also a significant relationship between the mean hypercapnic response and end-exercise (r=0.75, P=0.009) but not between the mean hyperoxic response and end-exercise (r=0.21, P=0.51). A blunted hypercapnic ventilatory response may contribute to EIAH in highly trained men due to a failure to increase ventilation sufficiently to offset exercise-induced gas exchange impairments.

Cardiopulmonary Exercise Testing in Patients With Interstitial Lung Disease.

Interstitial lung disease (ILD) is a heterogeneous group of conditions characterized by fibrosis and/or inflammation of the lung parenchyma. The pathogenesis of ILD consistently results in exertional dyspnea and exercise intolerance. Cardiopulmonary exercise testing (CPET) provides important information concerning the pathophysiology of ILD that can help inform patient management. Despite the purported benefits of CPET, its clinical utility in ILD is not well defined; however, there is a growing body of evidence that provides insight into the potential value of CPET in ILD. Characteristic responses to CPET in patients with ILD include exercise-induced arterial hypoxemia, an exaggerated ventilatory response, a rapid and shallow breathing pattern, critically low inspiratory reserve volume, and elevated sensations of dyspnea and leg discomfort. CPET is used in ILD to determine cause(s) of symptoms such as exertional dyspnea, evaluate functional capacity, inform exercise prescription, and determine the effects of pharmacological and non-pharmacological interventions on exercise capacity and exertional symptoms. However, preliminary evidence suggests that CPET in ILD may also provide valuable prognostic information and can be used to ascertain the degree of exercise-induced pulmonary hypertension. Despite these recent advances, additional research is required to confirm the utility of CPET in patients with ILD. This brief review outlines the clinical utility of CPET in patients with ILD. Typical patterns of response are described and practical issues concerning CPET interpretation in ILD are addressed. Additionally, important unanswered questions relating to the clinical utility of CPET in the assessment, prognostication, and management of patients with ILD are identified.

Lung function and oxygen saturation after participation in Norseman Xtreme Triathlon.

To examine evidence of exercise-induced bronchoconstriction (EIB) defined as ≥10% reduction in forced expiratory volume in one second (FEV1 ) and exercise-induced arterial hypoxemia (EIAH) defined as ≥4% reduction in oxygen saturation (SpO2 ) from before to after participation in the Norseman Xtreme Triathlon. Secondarily, to assess whether changes in FEV1 and SpO2 are related to respiratory symptoms, training volume, and race time. In this quasi-experimental non-controlled study, we included 63 triathletes (50♂/13♀) aged 40.3 (±9.0) years (mean±SD). Fifty-seven (46♂/11♀) measured lung function and 54 (44♂/10♀) measured SpO2 before the race, 8-10minutes after the race (post-test 1) and the day after the race (post-test 2). Respiratory symptoms and training volume were recorded with modified AQUA questionnaire. ANOVA for repeated measures was used to detect differences in lung function and SpO2 . Statistical significance was accepted at 0.05 level. Twenty-six participants (46%) presented with EIB at post-test 1 and 16 (28%) at post-test 2. Lung function variables were significantly reduced from baseline to post-test 1 and 2. Thirty-five participants (65%) showed evidence of mild to moderate EIAH. No significant correlations were observed except a weak correlation between maximal reduction in FEV1 and respiratory symptoms (r=0.35, P=.016). Our results demonstrated that 46% of the participants presented with EIB and 65% showed evidence of EIAH after the Norseman Xtreme Triathlon. Changes in FEV1 and SpO2 were not correlated to weekly training hours or race time. We observed a weak correlation between maximal reduction in FEV1 and respiratory symptoms.

Hypoxic Training Is Beneficial in Elite Athletes.

There is no doubt that many hypoxic conditions or prolonged exposures to altitude result in “biological costs of hypoxic adaptations that outweigh their benefits” (1), particularly in endurance athletes exposed to a) exercise-induced arterial hypoxemia leading to a larger decrease in VO2max and aerobic endurance; b) increased sympathetic activity and decreased baroreflex sensitivity; and c) increased pulmonary arterial pressure. There is also no doubt that sleeping in moderate altitude (2000-3000 m) as performed by the athletes using either live high-train high (LHTH) or live high-train low (LHTL) methods leads to periodic breathing, intermittent hypoxia (IH) and increase in desaturation periods; e.g. 3% oxygen desaturation index, but to a larger extent in hypobaric hypoxia (HH, real altitude) than in normobaric hypoxia (NH, simulated altitude), as shown at 2250 m (2). The three main questions debated in the present contrasting perspective are however different: 1. Are there any evidences showing if the “counteracting maladaptation” (reported above) outweigh the benefits of the different hypoxic methods at short- or long-term in elite athletes? ; 2. Are there any robust data supporting that hypoxic training is beneficial in elite athletes? ; 3. Contradictory, are there robust data showing that hypoxic training is not beneficial in elite athletes?

Inspiratory muscle training effects on oxygen saturation and performance in hypoxemic rowers: Effect of sex

ABSTRACTExercise-induced arterial hypoxemia (EIAH) has been consistently reported in elite endurance athletes. This study examined the effects of an inspiratory muscle training protocol (IMT) on resting pulmonary function, end-exercise arterial oxygen saturation and performance in hypoxemic rowers. Twenty male and sixteen female well-trained hypoxemic rowers were divided into four groups: IMT-male, control-male, IMT-female and control-female. The IMT groups, additionally to the regular training, performed IMT (30 min/day, 5 times/week, 6 weeks). Before and after training, groups underwent an incremental rowing test, a 2000-m time trial and a 5-min “all-out” race. IMT increased respiratory strength in the IMT-male (135 ± 31 vs. 180 ± 22 cmH2O) and IMT-female (93 ± 19 vs. 142 ± 22 cmH2O) (P < 0.05). The IMT-female group exhibited lower EIAH and improved rowing performance in the 2000-m time trial (487 ± 32 vs. 461 ± 34 sec) and in the 5-min “all-out” test (1,285 ± 28 vs. 1,310 ± 36m) (P < 0.05). IMT protocol improved performance in IMT-male only in the 5-min test (1,651 ± 31 vs. 1,746 ± 37m) (P < 0.05). IMT may be a useful tool for increasing respiratory strength and enhancing performance in hypoxemic rowers, especially for women.Abbreviations: EIAH: Exercise-induced arterial hypoxemia; IMT: inspiratory muscle training protocol; PaO2: partial pressure of arterial oxygen; SaO2: arterial oxyhemoglobin saturation; VO2max: maximal oxygen consumption; [(A-a)DO2]: alveolar-to-arterial oxygen difference; VA/Q: ventilation-perfusion inequality/mismatching; PImax: maximal inspiratory pressure; BMI: body mass index; BSA: body surface area; FVC: vital capacity; FEV1: forced expiratory volume in 1 sec; VCin: vital capacity; MVV12: maximal voluntary ventilation in 12 sec

Sex Differences In Respiratory And Circulatory Cost And Arterial Oxygen Saturation During Hypoxic Walking

PURPOSE: Since women have smaller lungs and a decreased capacity for lung diffusion compared to men, these differences may increase the work required for women to maintain a given rate of pulmonary ventilation (VE), resulting in greater exercise-induced arterial hypoxemia (EIAH). Previous studies have ignored the energy expenditure (EE) on circulation (i.e., heart rate; HR) and ventilation during exercise. METHODS: We sought to investigate sex differences in EE, VE and HR in response to changes in SpO2. We hypothesized that women would experience greater EIAH, and that the contribution rate of EE, VE, and HR in response to changes in SpO2 would be different between the sexes. We measured EE during walking on a level gradient under normoxia (room air, 21% O2), and moderate hypoxia (13% O2). Ten healthy young men and ten healthy young women walked on a treadmill at seven speeds (0.67-1.67 m s-1). Each walking speed lasted for four minutes. EE was calculated using pulmonary oxygen uptake and carbon dioxide output. RESULTS: During walking, reductions in SpO2 trended slightly greater in women under hypoxia (71.5 ± 4.5 % for men and 67.7 ± 6.1 % for women at the fastest gait speed, P > 0.05). Hypoxia-induced elevation in EE, HR, and VE were calculated by the difference between values in hypoxia and normoxia. Using a multivariate model that combined EE, VE, and HR to predict ΔSpO2 (hypoxia-induced reduction), we obtained a very strong fit model both for men (r2 = 0.900, P < 0.001) and for women (r2 = 0.957, P < 0.001). We also tried to estimate the relative contributions of ΔEE, ΔVE, and ΔHR to predict ΔSpO2 by using standard partial regression coefficients. The contribution rate to predict ΔSpO2 was markedly different between men and women. In women, the effect of ΔEE and ΔVE were greater (EE: 28.1% in women vs. 15.8% in men; VE: 4.1% in women vs. 1.7% in men). Conversely, in men the contribution of ΔHR was greater (82.5 % in men and 67.9 % in women). Moreover, significant sex differences in breathing frequency and tidal volume were observed (P < 0.05, respectively). CONCLUSIONS: These findings suggested that high-altitude adaptation in response to hypoxemia has different underlying mechanisms between men and women. Our results can help to explain how men and women adapt high-altitude environments.

Exercise-induced arterial hypoxemia; some answers, more questions.

Exercise-induced arterial hypoxemia (EIAH) is characterized by the decrease in arterial oxygen tension and oxyhemoglobin saturation during dynamic aerobic exercise. Since the time of the initial observations, our knowledge and understanding of EIAH has grown, but many unknowns remain. The purpose of this review is to provide an update on recent findings, highlight areas of disagreement, and identify where information is lacking. Specifically, this review will place emphasis on (i) the occurrence of EIAH during submaximal exercise, (ii) whether there are sex differences in the development and severity of EIAH, and (iii) unresolved questions and future directions.

Exercise-induced arterial hypoxemia in aerobic and anaerobic trained athletes during incremental exercise

Purpose: The purpose of this study was to examine and compare the occurrence of exercise-induced arterial hypoxemia (EIAH) in aerobic and anaerobic trained athletes during an incremental treadmill exercise test. Material: International level male junior skiers including ten cross-country skiers and ten alpine skiers took part in the study. All participants performed an incremental treadmill exercise test to determine maximal oxygen uptake (VO2max), and oxyhemoglobin saturation (SaO2) was continuously measured using a pulse oximetry. Maximal minute ventilation (VEmax), maximal heart rate (HRmax), ventilatory equivalent for oxygen (VE/VO2) and carbon dioxide (VE/VCO2) were determined during the last stage of the incremental exercise test. EIAH was assumed to have developed when SaO2 decreased by at least 4% (ΔSaO2 ≤ −4%) from the baseline values. Results: VO2max, VE, maximal running speed and test time were higher in the cross-country skiers than in the alpine skiers (p &lt; 0.01), whereas HRmax, VE/VO2 and VE/VCO2 showed similar values in both group (p &gt; 0.05). All the athletes in both groups exhibited EIAH. SaO2 was significantly decreased from 97.5 ± 0.9% at rest to 89 ± 2% at exhaustion in alpine skiers and from 97.8 ± 0.7% at rest to 88.1 ± 2.4% at exhaustion in cross-country skiers (p &lt; 0.001). There were no differences in resting and lowest %SaO2 values between two groups (p &gt; 0.05). Conclusions: EIAH may occur in endurance athletes as well as anaerobic trained athletes. Well-trained athletes who have different aerobic fitness levels may exhibit similar EIAH during the incremental maximal exercise.

Exercise-induced quadriceps muscle fatigue in men and women: effects of arterial oxygen content and respiratory muscle work.

High work of breathing and exercise-induced arterial hypoxaemia (EIAH) can decrease O2 delivery and exacerbate exercise-induced quadriceps fatigue in healthy men. Women have a higher work of breathing during exercise, dedicate a greater fraction of whole-body V̇O2 towards their respiratory muscles and develop EIAH. Despite a greater reduction in men's work of breathing, the attenuation of quadriceps fatigue was similar between the sexes. The degree of EIAH was similar between sexes, and regardless of sex, those who developed the greatest hypoxaemia during exercise demonstrated the most attenuation of quadriceps fatigue. Based on our previous finding that women have a greater relative oxygen cost of breathing, women appear to be especially susceptible to work of breathing-related changes in quadriceps muscle fatigue. Reducing the work of breathing or eliminating exercise-induced arterial hypoxaemia (EIAH) during exercise decreases the severity of quadriceps fatigue in men. Women have a greater work of breathing during exercise, dedicate a greater fraction of whole-body V̇O2 towards their respiratory muscles, and demonstrate EIAH, suggesting women may be especially susceptible to quadriceps fatigue. Healthy subjects (8 male, 8 female) completed three constant load exercise tests over 4days. During the first (control) test, subjects exercised at ∼85% of maximum while arterial blood gases and work of breathing were assessed. Subsequent constant load exercise tests were iso-time and iso-work rate, but with EIAH prevented by inspiring hyperoxic gas or work of breathing reduced via a proportional assist ventilator (PAV). Quadriceps fatigue was assessed by measuring force in response to femoral nerve stimulation. For both sexes, quadriceps force was equally reduced after the control trial (-27±2% baseline) and was attenuated with hyperoxia and PAV (-18±1 and -17±2% baseline, P<0.01, respectively), with no sex difference. EIAH was similar between the sexes, and regardless of sex, subjects with the lowest oxyhaemoglobin saturation during the control test had the greatest quadriceps fatigue attenuation with hyperoxia (r2 =0.79, P<0.0001). For the PAV trial, despite reducing the work of breathing to a greater degree in men (men: 60±5, women: 75±6% control, P<0.05), the attenuation of quadriceps fatigue was similar between the sexes (36±4vs. 37±7%). Owing to a greater relative V̇O2 of the respiratory muscles in women, less of a change in work of breathing is needed to reduce quadriceps fatigue.

Prevalence of Exercise-Induced Arterial Hypoxemia in Distance Runners at Sea Level.

It has been reported that ~50% of endurance-trained men demonstrate exercise-induced arterial hypoxemia (EIAH) during heavy exercise. However, this often-cited prevalence rate comes from a single study using a cohort of 25 highly trained men who completed maximal cycle ergometry. As arterial oxyhemoglobin saturation (SpO2) during maximal exercise is reported to be significantly lower during treadmill versus cycle ergometry in the same subjects, we hypothesized that the prevalence of EIAH would be greater than previously reported (and commonly referenced) in a larger cohort of highly endurance-trained men during maximal treadmill running. Data from 124 highly trained male distance runners (V˙O2max range = 60.3-84.7 mL·kg·min) were retrospectively examined from previously published studies completed in the Indiana University Human Performance Laboratory. Subjects completed a constant speed, progressive-grade treadmill exercise test to volitional exhaustion, and arterial oxyhemoglobin saturation (SaO2ear) in all subjects was estimated using the same oximeter (Hewlett Packard 47201A). Using similar inclusion criteria as previously published for highly trained (V˙O2max > 68 mL·kg·min) and for EIAH (SaO2ear ≤ 91%), 55 of 79 subjects (70%) exhibited exercise-induced arterial desaturation. Across all 124 subjects, 104 (84%) demonstrated at least moderate EIAH (SaO2ear ≤ 93%) during maximal treadmill exercise. SaO2ear was significantly yet weakly correlated with V˙E/V˙O2 (P < 0.01, r = 0.28) and V˙E/V˙CO2 (P < 0.001, r = 0.33) but not with V˙O2max. These results indicate that the prevalence of EIAH in highly trained men during maximal treadmill exercise at sea level is greater compared with previously suggested data, with exercise mode perhaps playing a factor in the number of athletes who experience EIAH.

Exercise-Induced Hypoxemia in Juvenile Thyroid Carcinoma With Lung Metastases.

Exercise-induced arterial hypoxemia (EIAH) has been reported in patients with juvenile thyroid cancer treated with radioiodine for lung metastases. This retrospective study tested the hypothesis that EIAH is due to ventilation-perfusion-mismatch in this rare pulmonary condition. 50 patients (age 13-23 years) treated for juvenile thyroid carcinoma and lung metastasis with 131I and 24 controls with thyroid cancer but without lung metastases and prior 131I-treatment were assessed in a state of acute hypothyroidism by com-puted tomography of the lungs, pulmonary function testing, cardiopulmonary exercise test with measurements of gas exchange, oxygen saturation, alveolar-arterial difference in pO2 (p(A-a)O2) and pCO2 (p(ET-a)CO2). 10 of the 50 patients with lung metastases showed EIAH. They had more pronounced pulmonary fibrosis on computed tomography, a widened p(A-a)O2, and p(ET-a)CO2, a lower DVE/DVCO2-slope, a lower respiratory rate and no increased dead space ventilation. A more pronounced EIAH was associated with male gender, younger age, lower diffusion capacity, higher p(ET-a)CO2 during exercise and a higher peak exercise tidal volume over vital capacity ratio. EIAH in patients with thyroid carcinoma and pulmonary metastases is not related to ventilation-perfusion mismatch but to alveolar hypoventilation, possibly related to an increased work of breathing with pulmonary fibrosis.

Hyperoxia Extends Time to Exhaustion During High-Intensity Intermittent Exercise: a Randomized, Crossover Study in Male Cyclists.

BackgroundSome endurance athletes exhibit exercise-induced arterial hypoxemia during high-intensity exercise. Inhalation of hyperoxic gas during exercise has been shown to counteract this exercise-associated reduction in hemoglobin oxygen saturation (SaO2), but the effects of hyperoxic gas inhalation on performance and SaO2 during high-intensity intermittent exercise remain unclear. This study investigated the effects of hyperoxic gas inhalation on performance and SaO2 during high-intensity intermittent cycling exercise.MethodsEight male cyclists performed identical intermittent exercise tests (five sets of 3-min high-intensity cycling alternated with 3-min active recovery periods) under two different inspired air conditions, hyperoxia (HO; FiO2 = 0.36) and normoxia (NO; FiO2 = 0.21). The fifth set of each test was terminated at exhaustion, and the exercise time to exhaustion was recorded. Variables associated with arterial oxygen saturation (SpO2) were measured using an ear pulse oximeter.ResultsTime to exhaustion under HO conditions was significantly longer than under NO conditions (34.9 ± 4.6 vs. 30.0 ± 2.5 min, P = 0.004, ES = 1.32). SpO2 was maintained under HO conditions but decreased under NO conditions.ConclusionsHyperoxic gas inhalation during the entire high-intensity intermittent exercise enhanced exercise performance in male cyclists.