Effects of a 6-Week Repeated-Sprint Training With Voluntary Hypoventilation at Low and High Lung Volume on Repeated-Sprint Ability in Female Soccer Players.

PURPOSE: To investigate the effects of repeated-sprint training with voluntary hypoventilation at low (RSH-VHL) and high (RS-VHH) lung volume on repeated-sprint ability (RSA) in female athletes. METHODS: Over a 6-week period, 24 female soccer players completed 12 sessions of repeated 30-m running sprints with end-expiratory breath holding (RSH-VHL, n = 8), end-inspiratory breath holding (RS-VHH, n = 8), or unrestricted breathing (RS-URB, n = 8). Before and after training, a running RSA test consisting of performing 30-m all-out sprints until exhaustion was implemented. RESULTS: From before to after training, the number of sprints completed during the RSA test was increased in both RSH-VHL (19.3 [0.9] vs 22.6 [0.9]; P < .01) and RS-VHH (19.3 [1.5] vs 20.5 [1.7]; P < .01) but not in RS-URB (19.4 [1.3] vs 19.5 [1.7]; P = .67). The mean velocity and the percentage decrement score calculated over sprints 1 to 17 were, respectively, higher (82.2% [1.8%] vs 84.6% [2.1%] of maximal velocity) and lower (23.7% [3.1%] vs 19.4% [3.2%]) in RSH-VHL (P < .01), whereas they remained unchanged in RS-VHH and RS-URB. The mean arterial oxygen saturation recorded during training at the end of the sprints was lower in RSH-VHL (92.1% [0.4%]) than in RS-VHH (97.3% [0.1%]) and RS-URB (97.8% [0.1%]). CONCLUSIONS: This study shows that female athletes can benefit from the RSH-VHL intervention to improve RSA. The performance gains may have been limited by the short sprinting distance with end-expiratory breath holding, which provoked only moderate hypoxemia. The increase in the number of sprints in RS-VHH seems to show that factors other than hypoxia may have played a role in RSA improvement.

Physiological Responses to Supramaximal Running Exercise with End-Expiratory Breath Holding up to the Breaking Point.

This study aimed to assess the physiological responses to repeated running exercise performed at supramaximal intensity and with end-expiratory breath holding (EEBH) up to the breaking point. Eight male runners participated in two running testing sessions on a motorized treadmill. In the first session, participants performed two sets of 8 repetitions at 125% of maximal aerobic velocity and with maximum EEBH. Each repetition started at the onset of EEBH and ended at its release. In the second session, participants replicated the same procedure, but with unrestricted breathing (URB). The change in cerebral and muscle oxygenation (Δ[Hbdiff]), total haemoglobin concentration (Δ[THb]) and muscle reoxygenation were continuously assessed. End-tidal oxygen (PETO2) and carbon dioxide pressure (PETCO2), arterial oxygen saturation (SpO2) and heart rate (HR) were also measured throughout exercise.On average, EEBH was maintained for 10.1 ± 1 s. At the breaking point of EEBH, PETO2 decreased to 54.1 ± 8 mmHg, whereas PETCO2 increased to 74.8 ± 3.1 mmHg. At the end of repetitions, SpO2 (nadir values 74.9 ± 5.0 vs. 95.7 ± 0.8%) and HR were lower with EEBH than with URB. Cerebral and muscle Δ[Hbdiff] were also lower with EEBH, whereas this condition induced higher cerebral and muscle Δ[THb] and greater muscle reoxygenation. This study showed that performing repeated bouts of supramaximal running exercises with EEBH up to the breaking point induced a fall in arterial, cerebral and muscle oxygenation compared with the URB condition. These phenomena were accompanied by increases in regional blood volume likely resulting from compensatory vasodilation to preserve oxygen delivery to the brain and muscles.

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.

Modelling the relationships between arterial oxygen saturation, exercise intensity and the level of aerobic performance in acute hypoxia.

PURPOSE: The aim of this study was to establish a model to estimate the level of arterial oxygen saturation (SpO2) and help determine the appropriate hypoxic dose in humans exercising in acute hypoxia. METHODS: SpO2 values were collected in seven untrained (UTS) and seven endurance-trained male subjects (ETS) who performed six cycle incremental and maximal tests at sea level and at simulated altitudes of 1000, 1500, 2500, 3500 and 4500 m. Oxygen uptake was continuously measured and maximal oxygen uptake ([Formula: see text]) was determined in each subject and at each altitude. Intensity was expressed as percentage of [Formula: see text]. RESULTS: There were strong non-linear relationships between altitude and SpO2 at low, moderate and high intensity both in ETS and UTS (r = 0.97, p < 0.001). SpO2 was significantly correlated to exercise intensity at sea level and at all simulated altitudes in ETS but only from 2500 m in UTS. There were inverse correlations between SpO2 and sea-level [Formula: see text] at all altitudes, which were stronger from 2500 m and with the increase in exercise intensity. The three-variable model we established predicts (p < 0.001) the SpO2 level of individuals exercising in acute hypoxia based on their sea-level [Formula: see text], the intensity of exercise and the altitude level. CONCLUSION: The model demonstrates that the drop of SpO2 during exercise in acute hypoxia is larger with the increase in both sea-level [Formula: see text] and exercise intensity. The model also highlights that the pivotal altitude from which the fall in SpO2 is exacerbated is between 2000 and 2500 m, depending on both sea-level [Formula: see text] and exercise intensity.

Exercise with End-expiratory Breath Holding Induces Large Increase in Stroke Volume.

Eight well-trained male cyclists participated in two testing sessions each including two sets of 10 cycle exercise bouts at 150% of maximal aerobic power. In the first session, subjects performed the exercise bouts with end-expiratory breath holding (EEBH) of maximal duration. Each exercise bout started at the onset of EEBH and ended at its release (mean duration: 9.6±0.9 s; range: 8.6-11.1 s). At the second testing session, subjects performed the exercise bouts (same duration as in the first session) with normal breathing. Heart rate, left ventricular stroke volume (LVSV), and cardiac output were continuously measured through bio-impedancemetry. Data were analysed for the 4 s preceding and following the end of each exercise bout. LVSV (peak values: 163±33 vs. 124±17 mL, p<0.01) was higher and heart rate lower both in the end phase and in the early recovery of the exercise bouts with EEBH as compared with exercise with normal breathing. Cardiac output was generally not different between exercise conditions. This study showed that performing maximal EEBH during high-intensity exercise led to a large increase in LVSV. This phenomenon is likely explained by greater left ventricular filling as a result of an augmented filling time and decreased right ventricular volume at peak EEBH.

Impact of Hypoventilation Training on Muscle Oxygenation, Myoelectrical Changes, Systemic [K+], and Repeated-Sprint Ability in Basketball Players.

This study investigated the impact of repeated-sprint (RS) training with voluntary hypoventilation at low lung volume (VHL) on RS ability (RSA) and on performance in a 30-15 intermittent fitness test (30-15IFT). Over 4 weeks, 17 basketball players included eight sessions of straight-line running RS and RS with changes of direction into their usual training, performed either with normal breathing (CTL, n = 8) or with VHL (n = 9). Before and after the training, athletes completed a RSA test (12 × 30-m, 25-s rest) and a 30-15IFT. During the RSA test, the fastest sprint (RSAbest), time-based percentage decrement score (RSASdec), total electromyographic intensity (RMS), and spectrum frequency (MPF) of the biceps femoris and gastrocnemius muscles, and biceps femoris NIRS-derived oxygenation were assessed for every sprint. A capillary blood sample was also taken after the last sprint to analyse metabolic and ionic markers. Cohen's effect sizes (ES) were used to compare group differences. Compared with CTL, VHL did not clearly modify RSAbest, but likely lowered RSASdec (VHL: -24.5% vs. CTL: -5.9%, group difference: -19.8%, ES -0.44). VHL also lowered the maximal deoxygenation induced by sprints ([HHb]max; group difference: -2.9%, ES -0.72) and enhanced the reoxygenation during recovery periods ([HHb]min; group difference: -3.6%, ES -1.00). VHL increased RMS (group difference: 18.2%, ES 1.28) and maintained MPF toward higher frequencies (group difference: 9.8 ± 5.0%, ES 1.40). These changes were concomitant with a lower potassium (K+) concentration (group difference: -17.5%, ES -0.67), and the lowering in [K+] was largely correlated with RSASdec post-training in VHL only (r = 0.66, p < 0.05). However, VHL did not clearly alter PO2, hemoglobin, lactate and bicarbonate concentration and base excess. There was no difference between group velocity gains for the 30-15IFT (CTL: 6.9% vs. VHL: 7.5%, ES 0.07). These results indicate that RS training combined with VHL may improve RSA, which could be relevant to basketball player success. This gain may be attributed to greater muscle reoxygenation, enhanced muscle recruitment strategies, and improved K+ regulation to attenuate the development of muscle fatigue, especially in type-II muscle fibers.

Transferable Benefits of Cycle Hypoventilation Training for Run-Based Performance in Team-Sport Athletes.

PURPOSE: To determine whether high-intensity training with voluntary hypoventilation at low lung volume (VHL) in cycling could improve running performance in team-sport athletes. METHODS: Twenty well-fit subjects competing in different team sports completed, over a 3-week period, 6 high-intensity training sessions in cycling (repeated 8-s exercise bouts at 150% of maximal aerobic power) either with VHL or with normal breathing conditions. Before (Pre) and after (Post) training, the subjects performed a repeated-sprint-ability test (RSA) in running (12 × 20-m all-out sprints), a 200-m maximal run, and the Yo-Yo Intermittent Recovery Level 1 test (YYIR1). RESULTS: There was no difference between Pre and Post in the mean and best velocities reached in the RSA test, as well as in performance and maximal blood lactate concentration in the 200-m-run trial in both groups. On the other hand, performance was greater in the second part of the RSA test, and the fatigue index of this test was lower (5.18% [1.3%] vs 7.72% [1.6%]; P < .01) after the VHL intervention only. Performance was also greater in the YYIR1 in the VHL group (1468 [313] vs 1111 [248] m; P < .01), whereas no change occurred in the normal-breathing-condition group. CONCLUSION: This study showed that performing high-intensity cycle training with VHL could improve RSA and possibly endurance performance in running. On the other hand, this kind of approach does not seem to induce transferable benefits for anaerobic performance.

Physiological adaptations to repeated sprint training in hypoxia induced by voluntary hypoventilation at low lung volume.

PURPOSE: This study investigated the effects of repeated-sprint (RS) training in hypoxia induced by voluntary hypoventilation at low lung volume (RSH-VHL) on physiological adaptations, RS ability (RSA) and anaerobic performance. METHODS: Over a 3-week period, eighteen well-trained cyclists completed six RS sessions in cycling either with RSH-VHL or with normal conditions (RSN). Before (Pre) and after (Post) the training period, the subjects performed an RSA test (10 × 6-s all-out cycling sprints) during which oxygen uptake [Formula: see text] and the change in both muscle deoxyhaemoglobin (Δ[HHb]) and total haemoglobin (Δ[THb]) were measured. A 30-s Wingate test was also performed and maximal blood lactate concentration ([La]max) was assessed. RESULTS: At Post compared to Pre, the mean power output during both the RSA and the Wingate tests was improved in RSH-VHL (846 ± 98 vs 911 ± 117 W and 723 ± 112 vs 768 ± 123 W, p < 0.05) but not in RSN (834 ± 52 vs 852 ± 69 W, p = 0.2; 710 ± 63 vs 713 ± 72 W, p = 0.68). The average [Formula: see text] recorded during the RSA test was significantly higher in RSH-VHL at Post but did not change in RSN. No change occurred for Δ[THb] whereas Δ[HHb] increased to the same extent in both groups. [Lamax] after the Wingate test was higher in RSH-VHL at Post (13.9 ± 2.8 vs 16.1 ± 3.2 mmol L-1, p < 0.01) and tended to decrease in RSN (p = 0.1). CONCLUSIONS: This study showed that RSH-VHL could bring benefits to both RSA and anaerobic performance through increases in oxygen delivery and glycolytic contribution. On the other hand, no additional effect was observed for the indices of muscle blood volume and O2 extraction.

Cerebral and Muscle Oxygenation during Repeated Shuttle Run Sprints with Hypoventilation.

Ten highly-trained Jiu-Jitsu fighters performed 2 repeated-sprint sessions, each including 2 sets of 8 x ~6 s back-and-forth running sprints on a tatami. One session was carried out with normal breathing (RSN) and the other with voluntary hypoventilation at low lung volume (RSH-VHL). Prefrontal and vastus lateralis muscle oxyhemoglobin ([O2Hb]) and deoxyhemoglobin ([HHb]) were monitored by near-infrared spectroscopy. Arterial oxygen saturation (SpO2), heart rate (HR), gas exchange and maximal blood lactate concentration ([La]max) were also assessed. SpO2 was significantly lower in RSH-VHL than in RSN whereas there was no difference in HR. Muscle oxygenation was not different between conditions during the entire exercise. On the other hand, in RSH-VHL, cerebral oxygenation was significantly lower than in RSN (-6.1±5.4 vs-1.5±6.6 µm). Oxygen uptake was also higher during the recovery periods whereas [La]max tended to be lower in RSH-VHL. The time of the sprints was not different between conditions. This study shows that repeated shuttle-run sprints with VHL has a limited impact on muscle deoxygenation but induces a greater fall in cerebral oxygenation compared with normal breathing conditions. Despite this phenomenon, performance is not impaired, probably because of a higher oxygen uptake during the recovery periods following sprints.

Repeated-sprint training in hypoxia induced by voluntary hypoventilation improves running repeated-sprint ability in rugby players.

PURPOSE: The goal of this study was to determine the effects of repeated-sprint training in hypoxia induced by voluntary hypoventilation at low lung volume (VHL) on running repeated-sprint ability (RSA) in team-sport players. METHODS: Twenty-one highly trained rugby players performed, over a 4-week period, seven sessions of repeated 40-m sprints either with VHL (RSH-VHL, n = 11) or with normal breathing (RSN, n = 10). Before (Pre-) and after training (Post-), performance was assessed with an RSA test (40-m all-out sprints with a departure every 30 s) until task failure (85% of the reference velocity assessed in an isolated sprint). RESULTS: The number of sprints completed during the RSA test was significantly increased after the training period in RSH-VHL (9.1 ± 2.8 vs. 14.9 ± 5.3; +64%; p < .01) but not in RSN (9.8 ± 2.8 vs. 10.4 ± 4.7; +6%; p = .74). Maximal velocity was not different between Pre- and Post- in both groups whereas the mean velocity decreased in RSN and remained unchanged in RSH-VHL. The mean SpO2 recorded over an entire training session was lower in RSH-VHL than in RSN (90.1 ± 1.4 vs. 95.5 ± 0.5%, p < .01). CONCLUSION: RSH-VHL appears to be an effective strategy to produce a hypoxic stress and to improve running RSA in team-sport players.

Acute effects of repeated cycling sprints in hypoxia induced by voluntary hypoventilation.

PURPOSE: This study aimed to investigate the acute responses to repeated-sprint exercise (RSE) in hypoxia induced by voluntary hypoventilation at low lung volume (VHL). METHODS: Nine well-trained subjects performed two sets of eight 6-s sprints on a cycle ergometer followed by 24 s of inactive recovery. RSE was randomly carried out either with normal breathing (RSN) or with VHL (RSH-VHL). Peak (PPO) and mean power output (MPO) of each sprint were measured. Arterial oxygen saturation, heart rate (HR), gas exchange and muscle concentrations of oxy-([O2Hb]) and deoxyhaemoglobin/myoglobin ([HHb]) were continuously recorded throughout exercise. Blood lactate concentration ([La]) was measured at the end of the first (S1) and second set (S2). RESULTS: There was no difference in PPO and MPO between conditions in all sprints. Arterial oxygen saturation (87.7 ± 3.6 vs 96.9 ± 1.8% at the last sprint) and HR were lower in RSH-VHL than in RSN during most part of exercise. The changes in [O2Hb] and [HHb] were greater in RSH-VHL at S2. Oxygen uptake was significantly higher in RSH-VHL than in RSN during the recovery periods following sprints at S2 (3.02 ± 0.4 vs 2.67 ± 0.5 L min-1 on average) whereas [La] was lower in RSH-VHL at the end of exercise (10.3 ± 2.9 vs 13.8 ± 3.5 mmol.L-1; p < 0.01). CONCLUSIONS: This study shows that performing RSE with VHL led to larger arterial and muscle deoxygenation than with normal breathing while maintaining similar power output. This kind of exercise may be worth using for performing repeated sprint training in hypoxia.

Repeated-Sprint Training in Hypoxia Induced by Voluntary Hypoventilation in Swimming.

PURPOSE: Repeated-sprint training in hypoxia (RSH) has been shown as an efficient method for improving repeated-sprint ability (RSA) in team-sport players but has not been investigated in swimming. We assessed whether RSH with arterial desaturation induced by voluntary hypoventilation at low lung volume (VHL) could improve RSA to a greater extent than the same training performed under normal breathing (NB) conditions. METHODS: Sixteen competitive swimmers completed 6 sessions of repeated sprints (2 sets of 16 × 15 m with 30 s send-off) either with VHL (RSH-VHL, n = 8) or with NB (RSN, n = 8). Before and after training, performance was evaluated through an RSA test (25-m all-out sprints with 35 s send-off) until exhaustion. RESULTS: From before to after training, the number of sprints was significantly increased in RSH-VHL (7.1 ± 2.1 vs 9.6 ± 2.5; P < .01) but not in RSN (8.0 ± 3.1 vs 8.7 ± 3.7; P = .38). Maximal blood lactate concentration ([La]max) was higher after than before in RSH-VHL (11.5 ± 3.9 vs 7.9 ± 3.7 mmol/L; P = .04) but was unchanged in RSN (10.2 ± 2.0 vs 9.0 ± 3.5 mmol/L; P = .34). There was a strong correlation between the increases in the number of sprints and in [La]max in RSH-VHL only (R = .93, P < .01). CONCLUSIONS: RSH-VHL improved RSA in swimming, probably through enhanced anaerobic glycolysis. This innovative method allows inducing benefits normally associated with hypoxia during swim training in normoxia.

Hypoventilation Training at Supramaximal Intensity Improves Swimming Performance.

PURPOSE: This study aimed to determine whether hypoventilation training at supramaximal intensity could improve swimming performance more than the same training conducted under normal breathing conditions. METHODS: For a 5-wk period, 16 triathletes (12 men and 4 women) were asked to include one supramaximal set of 12 to 20 × 25-m front crawl swimming twice a week into their usual swimming session, performed either with hypoventilation at low lung volume (VHL group) or with normal breathing (CONT group). Before (Pre) and after (Post) training, all triathletes performed all-out front crawl trials for 100, 200, and 400 m. RESULTS: Time performance was significantly improved in VHL in all trials (100 m: -3.7 ± 3.7 s [-4.4% ± 4.0%]; 200 m: -6.9 ± 5.0 s [-3.6% ± 2.3%]; 400 m: -13.6 ± 6.1 s [-3.5% ± 1.5%]) but did not change in CONT. In VHL, the maximal lactate concentration (+2.35 ± 1.3 mmol·L on average) and the rate of lactate accumulation in blood (+41.7% ± 39.4%) were higher at Post than at Pre in the three trials, whereas they remained unchanged in CONT. Arterial oxygen saturation, heart rate, breathing frequency, and stroke length were not altered in both groups at the end of the training period. On the other hand, stroke rate was higher at Post compared with Pre in VHL but not different in CONT. The measurements of gas exchange for the 400-m trial revealed no change in peak oxygen consumption as well as in any pulmonary variable in both groups. CONCLUSION: This study demonstrated that VHL training, when performed at supramaximal intensity, represents an effective method for improving swimming performance, partly through an increase in the anaerobic glycolysis activity.

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.

Validity of arterialized earlobe blood gases at rest and exercise in normoxia and hypoxia.

The purpose of this study was to compare arterial and arterialized blood gases during normoxic and hypoxic exercise. In the same conditions, earlobe pulse oximetry O(2) saturation (Sp(O2)) was compared to arterial oxygen saturation (Sa(O2)). Ten men performed incremental cycle ergometer tests, in normoxia and hypoxia (FI(O2) = 0.127). Blood samples were drawn simultaneously from the radial artery and pre-warmed earlobe capillary blood of subjects at rest, submaximal and near maximal exercise. R(2) between the two samples were 0.99 for P(O2) and S(O2), 0.86 for P(CO2) and 0.97 between Sp(O2) and Sa(O2). Earlobe P(O2) mean was 4.4+/-3.6 mmHg lower than Pa(O2) in normoxia but in hypoxia only 1.1+/-2.2 mmHg low. The mean difference were low in normoxia between Sa(O2) and Sp(O2) and increased in hypoxia, were acceptable for P(CO2), S(O2), pH in all conditions. In conclusion, except for P(O2) in normoxia, pre-warmed earlobe capillary blood is a good substitute to arterial blood to allow measurement of blood gas values in normoxia and hypoxia at rest and exercise.

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.

'Oxygen uptake efficiency slope' in trained and untrained subjects exposed to hypoxia.

We assessed the ability of the oxygen uptake efficiency slope, whether calculated on 100 and 80% of maximal exercise test duration (OUES(100) and OUES(80)), to identify the change in cardiorespiratory capacities in response to hypoxia in subjects with a broad range of V(O2 peak). Four maximal exercise tests were performed in trained (T) and untrained subjects (UT) in normoxia and at 1000, 2500 and 4500 m. The mean reductions in maximal exercise capacities at 4500 m were the same in T subjects for V(O2 peak) (-30%), OUES(80) (-26%) and OUES(100) (-26%) whereas in UT subjects only OUES(100) (-14%), but not OUES(80) (-20%), was lower compared with V(O2 peak) (-21%, p<0.05). OUES(100) and OUES(80) were correlated with V(O2 peak) and the ventilatory anaerobic threshold in both groups. Multiple regression analyses showed that V(O2 peak), OUES(100) and OUES(80) were significantly linked to O(2) arterial-venous difference. The OUES(80) could be considered as an interesting sub-maximal index of cardiorespiratory fitness in normal or hypoxemic subjects unable to reach V(O2 peak).

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.