Running exercise with end-expiratory breath holding up to the breaking point induces large and early fall in muscle oxygenation.

PURPOSE: The goal of this study was to assess the effects of repeated running bouts with end-expiratory breath holding (EEBH) up to the breaking point on muscle oxygenation. METHODS: Eight male runners participated in three randomised sessions each including two exercises on a motorised treadmill. The first exercise consisted in performing 10-12 running bouts with EEBH of maximum duration either (separate sessions) at 60% (active recovery), 80% (passive recovery) or 100% (passive recovery) of the maximal aerobic velocity (MAV). Each repetition started at the onset of EEBH and ended at its release. In the second exercise of the session, subjects replicated the same procedure but with normal breathing (NB). Arterial oxygen saturation (SpO2), heart rate (HR) and the change in vastus lateralis muscle deoxy-haemoglobin/myoglobin (Δ[HHb/Mb]) and total haemoglobin/myoglobin (Δ[THb/Mb]) were continuously monitored throughout exercises. RESULTS: On average, the EEBHs were maintained for 10.1 ± 1.1 s, 13.2 ± 1.8 s and 12.2 ± 1.7 s during exercise at 60%, 80% and 100% of MAV, respectively. In the three exercise intensities, SpO2 (mean nadir values: 76.3 ± 2.5 vs 94.5 ± 2.5%) and HR were lower with EEBH than with NB at the end of the repetitions; whereas, the mean Δ[HHb/Mb] (12.6 ± 5.2 vs 7.7 ± 4.4 µm) and Δ[THb/Mb] (- 0.6 ± 2.3 vs 3.8 ± 2.6 µm) were, respectively, higher and lower with EEBH (p < 0.05). CONCLUSION: This study showed that performing repeated bouts of running exercises with EEBH up to the breaking point induced a large and early drop in muscle oxygenation compared with the same exercise with NB. This phenomenon was probably the consequence of the strong arterial oxygen desaturation induced by the maximal EEBHs.

Swimmers can train in hypoxia at sea level through voluntary hypoventilation.

This study used an innovative technique of pulse oximetry to investigate whether swimmers can train under hypoxic conditions through voluntary hypoventilation (VH). Ten trained subjects performed a front crawl swimming series with normal breathing (NB), VH at high (VHhigh) and low pulmonary volume (VHlow). Arterial oxygen saturation was continuously measured via pulse oximetry (SpO2) with a waterproofed forehead sensor. Gas exchanges were recorded continuously and lactate concentration ([La]) was assessed at the end of each test. In VHlow, SpO2 fell down to 87% at the end of the series whereas it remained above 94% in VHhigh during most part of the series. Ventilation, oxygen uptake and end-tidal O2 pressure were lower in both VHhigh and VHlow than in NB. Compared to NB, [La] significantly increased in VHlow and decreased in VHhigh. This study demonstrated that swimmers can train under hypoxic conditions at sea level and can accentuate the glycolytic stimulus of their training if they perform VH at low but not high pulmonary volume.

Agreement between indirect calorimetry and traditional tests of lactose malabsorption.

BACKGROUND: Lactose malabsorption occurs frequently and the variable consequent intolerance may seriously impair quality of life. No reliable and convenient test method is in routine clinical practice. A recent animal study showed that the respiratory quotient changed significantly after ingestion of sucrose and lactose in naturally lactase-deficient rats. AIMS: This exploratory study evaluated the relevance of monitoring the respiratory quotient after lactose ingestion to detect malabsorption. METHODS: Healthy volunteers were identified and classified lactose absorbers and malabsorbers by a lactose tolerance test (25 g). After an overnight fast, a second lactose challenge was performed to monitor hydrogen excretion and respiratory quotient kinetics over 4h. Participants also completed questionnaires to score and localise their gastrointestinal symptoms. RESULTS: 20 subjects were enrolled (10 per group, 60% males, mean age 34 ± 4 years). Respiratory quotient kinetics were different between absorbers and malabsorbers during the first 100 min after lactose ingestion (p<0.01) and during the initial 30-50 min period. Respiratory quotient was significantly, positively correlated to peak glycaemia (R=0.74) and negatively correlated to hydrogen excretion (R=-0.51) and symptoms score (R=-0.46). CONCLUSIONS: Indirect calorimetry could improve the reliability of lactose malabsorption diagnosis. Studies on larger populations are needed to confirm the validity of this test and propose a simplified measurement.

Imaging of sarcoidosis of the airways and lung parenchyma and correlation with lung function.

Imaging has a prominent role in the assessment of sarcoidosis diagnosis and outcome, which are extremely variable. Chest radiography staging helps predict the probability of spontaneous remission, and stage IV is associated with higher mortality. However, the reproducibility of reading is poor and changes in radiography and lung function are inconsistently correlated, which may be problematic for the monitoring of disease and treatment response. Chest computed tomography (CT) makes a great diagnostic contribution in difficult cases. Bilateral hilar lymphadenopathy with peri-lymphatic micronodular pattern is highly specific for sarcoidosis. CT is important for the investigation of pulmonary complications, including aspergilloma and pulmonary hypertension. CT improves the yield of bronchoscopy for obtaining a positive endobronchial or transbronchial biopsy. CT findings may also discriminate between active inflammation and irreversible fibrosis, with occasional influence on therapeutic decisions. Three CT patterns of fibrotic sarcoidosis are identified, with different functional profiles: predominant bronchial distortion is associated with obstruction; honeycombing is associated with restriction and lower diffusing capacity of the lung for carbon monoxide; whereas functional impairment is relatively minor with linear pattern. The clinical impact of correlations between CT severity scores and functional impairment is uncertain, except for its utility elucidating the mechanisms of airflow limitation, which include bronchial distortion, peribronchovascular thickening, air-trapping and bronchial compression by lymphadenopathy.

Exercise with hypoventilation induces lower muscle oxygenation and higher blood lactate concentration: role of hypoxia and hypercapnia.

Eight men performed three series of 5-min exercise on a cycle ergometer at 65% of normoxic maximal O(2) consumption in four conditions: (1) voluntary hypoventilation (VH) in normoxia (VH(0.21)), (2) VH in hyperoxia (inducing hypercapnia) (inspired oxygen fraction [F(I)O(2)] = 0.29; VH(0.29)), (3) normal breathing (NB) in hypoxia (F(I)O(2) = 0.157; NB(0.157)), (4) NB in normoxia (NB(0.21)). Using near-infrared spectroscopy, changes in concentration of oxy-(Delta[O(2)Hb]) and deoxyhemoglobin (Delta[HHb]) were measured in the vastus lateralis muscle. Delta[O(2)Hb - HHb] and Delta[O(2)Hb + HHb] were calculated and used as oxygenation index and change in regional blood volume, respectively. Earlobe blood samples were taken throughout the exercise. Both VH(0.21) and NB(0.157) induced a severe and similar hypoxemia (arterial oxygen saturation [SaO(2)] < 88%) whereas SaO(2) remained above 94% and was not different between VH(0.29) and NB(0.21). Arterialized O(2) and CO(2) pressures as well as P50 were higher and pH lower in VH(0.21) than in NB(0.157), and in VH(0.29) than in NB(0.21). Delta[O(2)Hb] and Delta[O(2)Hb - HHb] were lower and Delta[HHb] higher at the end of each series in both VH(0.21) and NB(0.157) than in NB(0.21) and VH(0.29). There was no difference in Delta[O(2)Hb + HHb] between testing conditions. [La] in VH(0.21) was greater than both in NB(0.21) and VH(0.29) but not different from NB(0.157). This study demonstrated that exercise with VH induced a lower tissue oxygenation and a higher [La] than exercise with NB. This was caused by a severe arterial O(2) desaturation induced by both hypoxic and hypercapnic effects.

High-resolution computed tomographic imaging of airways in sarcoidosis patients with airflow obstruction.

OBJECTIVE: To investigate airway involvement in patients with pulmonary sarcoidosis and airflow obstruction (AO) using high-resolution computed tomography. METHODS: Forty-two sarcoidosis patients with AO and 42 matched sarcoidosis patients without AO were retrospectively analyzed. High-resolution computed tomographic patterns of airway involvement were bronchial distortion, peribronchovascular thickening, small airway obstruction, and bronchial compression by enlarged lymph nodes. RESULTS: Interobserver agreement was good (kappa > 0.8). High-resolution computed tomographic patterns of airway involvement were found more frequently, scored higher, and were more often multiple (P < 0.05) in patients with AO than those without. Functional improvement under treatment was observed more frequently in patients with predominant peribronchovascular thickening compared with patients with predominant bronchial distortion (P < 0.03). CONCLUSIONS: In pulmonary sarcoidosis patients with AO, high-resolution computed tomography is a reliable tool to identify underlying airways involvements, which are often multiple, and enables prediction of the therapeutic response.

Effects of a 4-week training with voluntary hypoventilation carried out at low pulmonary volumes.

This study investigated the effects of training with voluntary hypoventilation (VH) at low pulmonary volumes. Two groups of moderately trained runners, one using hypoventilation (HYPO, n=7) and one control group (CONT, n=8), were constituted. The training consisted in performing 12 sessions of 55 min within 4 weeks. In each session, HYPO ran 24 min at 70% of maximal O(2) consumption ( [V(02max)) with a breath holding at functional residual capacity whereas CONT breathed normally. A V(02max) and a time to exhaustion test (TE) were performed before (PRE) and after (POST) the training period. There was no change in V(O2max), lactate threshold or TE in both groups at POST vs. PRE. At maximal exercise, blood lactate concentration was lower in CONT after the training period and remained unchanged in HYPO. At 90% of maximal heart rate, in HYPO only, both pH (7.36+/-0.04 vs. 7.33+/-0.06; p<0.05) and bicarbonate concentration (20.4+/-2.9 mmolL(-1) vs. 19.4+/-3.5; p<0.05) were higher at POST vs. PRE. The results of this study demonstrate that VH training did not improve endurance performance but could modify the glycolytic metabolism. The reduced exercise-induced blood acidosis in HYPO could be due to an improvement in muscle buffer capacity. This phenomenon may have a significant positive impact on anaerobic performance.

Determinant factors of the decrease in aerobic performance in moderate acute hypoxia in women endurance athletes.

The purpose of this study was to evaluate the limiting factors of maximal aerobic performance in endurance trained (TW) and sedentary (UW) women. Subjects performed four incremental tests on a cycle ergometer at sea level and in normobaric hypoxia corresponding to 1000, 2500 and 4500 m. Maximal oxygen uptake decrement (Delta VO2 max) was larger in TW at each altitude. Maximal heart rate and ventilation decreased at 4500 m in TW. Maximal cardiac output remained unchanged. In both groups, arterialized oxygen saturation (Sa'O2 max) decreased at and above 2500 m and maximal O2 transport (QaO2 max) decreased from 1000 m. At 4500 m, there was no more difference in QaO2 max between TW and UW. Mixed venous O2 pressure (PvO2 max) was lower and O2 extraction (O2ERmax) greater in TW at each altitude. The primary determinant factor of VO2 max decrement in moderate acute hypoxia in trained and untrained women is a reduced maximal O2 transport that cannot be compensate by tissue O2 extraction.

Determinants of maximal oxygen uptake in moderate acute hypoxia in endurance athletes.

The factors determining maximal oxygen consumption were explored in eight endurance trained subjects (TS) and eight untrained subjects (US) exposed to moderate acute normobaric hypoxia. Subjects performed maximal incremental tests at sea level and simulated altitudes (1,000, 2,500, 4,500 m). Heart rate (HR), stroke volume (SV), cardiac output (.Q), arterialized oxygen saturation (Sa'O2), oxygen uptake (.VO2max), ventilation (.VE, expressed in normobaric conditions) were measured. At maximal exercise, ventilatory equivalent (.VE/.VO2max), O2 transport (.QaO2max) and O2 extraction (O2ERmax) were calculated. In TS, .Qmax remained unchanged despite a significant reduction in HRmax at 4,500 m. SVmax remained unchanged. .VEmax decreased in TS at 4,500 m, .VE/.VO2max was lower in TS and greater at 4,500 m vs. sea level in both groups. Sa'O2max decreased at and above 1,000 m in TS and 2,500 m in US, O2ERmax increased at 4,500 m in both groups. .QaO2max decreased with altitude and was greater in TS than US up to 2,500 m but not at 4,500 m. .VO2max decreased with altitude but the decrement (Delta.VO2max) was larger in TS at 4,500 m. In both groups Delta.VO2max in moderate hypoxia was correlated with Delta.QaO2max. Several differences between the two groups are probably responsible for the greater Delta.VO2max in TS at 4,500 m : (1) the relative hypoventilation in TS as shown by the decrement in .VEmax at 4,500 m (2) the greater.QaO2max decrement in TS due to a lower Sa'O2max and unchanged .Qmax 3) the smaller increase in O2ERmax in TS, insufficient to compensate the decrease in .QaO2max.

Prolonged expiration down to residual volume leads to severe arterial hypoxemia in athletes during submaximal exercise.

The goal of this study was to assess the effects of a prolonged expiration (PE) carried out down to the residual volume (RV) during a submaximal exercise and consider whether it would be worth including this respiratory technique in a training programme to evaluate its effects on performance. Ten male triathletes performed a 5-min exercise at 70% of maximal oxygen consumption in normal breathing (NB(70)) and in PE (PE(70)) down to RV. Cardiorespiratory parameters were measured continuously and an arterialized blood sampling at the earlobe was performed in the last 15s of exercise. Oxygen consumption, cardiac frequency, end-tidal and arterial carbon dioxide pressure, alveolar-arterial difference for O(2) (PA(O2) - Pa(O2)) and P(50) were significantly higher, and arterial oxygen saturation (87.4+/-3.4% versus 95.0+/-0.9%, p<0.001), alveolar (PA(O2)) or arterial oxygen pressure, pH and ventilatory equivalent were significantly lower in PE(70) than NB(70). There was no difference in blood lactate between exercise modalities. These results demonstrate that during submaximal exercise, a prolonged expiration down to RV can lead to a severe hypoxemia caused by a PA(O2) decrement (r=0.56; p<0.05), a widened PA(O2) - Pa(O2) (r=-0.85; p<0.001) and a right shift of the oxygen dissociation curve (r=-0.73; p<0.001).

[Pathophysiology of interstitial lung disease]. / Physiopathologie des pneumopathies interstitielles diffuses.

Chronic interstitial lung disease (ILD) groups a number of diseases with the common feature of radiological pulmonary infiltration, typical functional syndrome, and diffuse involvement of the deep pulmonary parenchyma identified histologically. Correlations between histological and radiological findings have enabled progress in both fields, leading to better interpretation of the radiological findings and optimizing the etiological diagnosis. Besides the signs themselves, their distribution in relation to the normal lung structures is highly contributive. Function tests can be used to quantify the impact on the respiratory system and assess the effect of treatment. Evidence-based criteria will progressively replace the consensual criteria enabling more effective evaluation of treatment in difficult pathological conditions such as idiopathic pulmonary fibrosis.

Effect of acute hypoxia on maximal exercise in trained and sedentary women.

PURPOSE: The purpose of this study was to determine the physiological responses of sedentary and endurance-trained female subjects during maximal exercise at different levels of acute hypoxia. METHODS: Fourteen women who were sea level residents were divided into two groups according to their level of fitness: 1) endurance-trained women (TW) (N = 7), VO(2max) = 56.3 +/- 4.7 mL.kg(-1).min(-1); and 2) sedentary women (SW) (N = 7), VO(2max) = 34.8 +/- 5.6 mL.kg(-1).min(-1). Subjects performed four maximal cycle ergometer tests in normoxia and under hypoxic conditions (F(I)O(2) = 0.187, 0.154, and 0.117, corresponding to altitudes of 1000, 2500, and 4500 m, respectively). RESULTS: VO(2max) decreased significantly by 3.6 +/- 2.1, 14 +/- 2.5, and 27.4 +/- 3.6% in TW, and by 5 +/- 4, 9.4 +/- 6.4, and 18.7 +/- 7% in SW at 1000, 2500, and 4500 m, respectively. The drop of VO(2max) (DeltaVO(2max)) was greater in TW at and above 2500 m. Arterial O2 saturation (SpO(2)) at maximal exercise was lower in TW at every altitude (1000 m: 90.9 +/- 1.9 vs 94.6 +/- 1.4%; 2500 m: 82.8 +/- 2.8 vs 90.0 +/- 2.1%; 4500 m: 65.0 +/- 4.7 vs 73.6 +/- 4.5%). Maximal heart rate decreased significantly from 1000 m in the two groups. SpO(2) was correlated to DeltaVO(2max) at 4500 m (r = -0.81, P < 0.01) and 2500 m (r = -0.81, P < 0.01), but not below. Furthermore, we noted a relationship between SpO(2) and O2 pulse (VO(2)/HR) at every F(I)O(2). CONCLUSION: These results demonstrate that endurance-trained women show a greater decrement in VO(2max) at high altitudes. This could be explained mainly by a higher arterial desaturation, which is largely caused, according to our results, by diffusion limitation.

Membrane and capillary blood components of diffusion capacity of the lung for carbon monoxide in pulmonary sarcoidosis: relation to exercise gas exchange.

BACKGROUND: Resting pulmonary diffusing capacity of the lung for carbon monoxide (DLCO) is known to be the best predictor of arterial desaturation during exercise in patients with sarcoidosis. However, the relative contribution of each of the two components of DLCO-alveolar membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc)-remains unclear. STUDY OBJECTIVES: To evaluate which component is responsible for the decrease of resting DLCO in patients with sarcoidosis, and to determine which resting pulmonary function test, including Dm and Vc, is the best predictor of gas exchange abnormalities during submaximal exercise. DESIGN: Prospective analysis of patients referred to our department of respiratory medicine. PATIENTS: Twenty four patients with pulmonary sarcoidosis were separated into two groups according to chest radiographic findings: group 1, stages 2 and 3 (n = 15); group 2, stage 4 (n = 9). All the patients completed pulmonary function tests (flows, volumes, single-breath DLCO, transfer coefficient [Ka], Dm, Vc) and submaximal exercise (two steady-state levels of mild and moderate exercise corresponding respectively to a target oxygen consumption of approximately 10 to 15 mL/min/kg). RESULTS: DLCO was reduced in the two groups (group 1, 63 +/- 16% of predicted; group 2, 64 +/- 16% of predicted). Dm was severely decreased (group 1, 58 +/- 24% of predicted; group 2, 51 +/- 15% of predicted), whereas Vc was unchanged or only mildly decreased (group 1, 81 +/- 18% of predicted; group 2, 85 +/- 28% of predicted). Whatever the group of patients and the exercise level, Dm and DLCO were the strongest predictors (p < 0.001) of gas exchange abnormalities. Ka or volumes were weak predictors, and Vc or flows were not related with exercise gas exchange. CONCLUSIONS: This study demonstrates that a decrease in Dm mostly accounts for resting DLCO reduction, and that Dm as well as DLCO are highly predictive of gas exchange abnormalities at exercise in patients with sarcoidosis.