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Purpose: To investigate the effects of a repeated-sprint training in hypoxia induced by voluntary hypoventilation at low lung volume (RSH-VHL) including end-expiratory breath holding (EEBH) of maximal duration. Methods: Over a 4-week period, twenty elite judo athletes (10 women and 10 men) were randomly split into two groups to perform 8 sessions of rowing repeated-sprint exercise either with RSH-VHL (each sprint with maximal EEBH) or with unrestricted breathing (RSN, 10-s sprints). Before (Pre-), 5 days after (Post-1) and 12 days after (Post-2) the last training session, participants completed a repeated-sprint ability (RSA) test on a rowing ergometer (8 × 25-s "all-out" repetitions interspersed with 25 s of passive recovery). Power output (PO), oxygen uptake, perceptual-motor capacity (turning off a traffic light with a predetermined code), cerebral (Δ[Hbdiff]) and muscle (Δ[Hb/Mb]diff) oxygenation, cerebral total haemoglobin concentration (Δ[THb]) and muscle total haemoglobin/myoglobin concentration (Δ[THb/Mb]) were measured during each RSA repetition and/or recovery period. Results: From Pre-to Post-1 and Post-2, maximal PO, mean PO (MPO) of the first half of the test (repetitions 1–4), oxygen uptake, end-repetition cerebral Δ[Hbdiff] and Δ[THb], end-repetition muscle Δ[Hb/Mb]diff and Δ[THb/Mb] and perceptual-motor capacity remained unchanged in both groups. Conversely, MPO of the second half of the test (repetitions 5–8) was higher at Post-1 than at Pre-in RSH-VHL only (p < 0.01), resulting in a lower percentage decrement score over the entire RSA test (20.4% ± 6.5% vs. 23.9% ± 7.0%, p = 0.01). Furthermore, MPO (5–8) was greater in RSH-VHL than in RSN at Post-1 (p = 0.04). These performance results were accompanied by an increase in muscle Δ[THb/Mb] (p < 0.01) and a concomitant decrease in cerebral Δ[THb] (p < 0.01) during the recovery periods of the RSA test at Post-1 in RSH-VHL. Conclusion: Four weeks of RSH-VHL including maximal EEBH improved the ability of elite judo athletes to repeat high-intensity efforts. The performance improvement, observed 5 days but not 12 days after training, may be due to enhanced muscle perfusion. The unchanged oxygen uptake and the decrease in cerebral regional blood volume observed at the same time suggest that a blood volume redistribution occurred after the RSH-VHL intervention to meet the increase in muscle perfusion. [ABSTRACT FROM AUTHOR]

The aim of this study was to determine the influence of swim intensity on acute responses to dynamic apnoea. 9 swimmers performed one 50 m front crawl trial in four different conditions: at 400 m velocity (V400) with normal breathing (NB), at V400 in complete apnoea (Ap), at maximal velocity (Vmax) with NB and at Vmax in Ap. Peak heart rate (HRpeak), blood lactate concentration after exercise (Lacpost ex) and Borg rating of perceived exertion (RPE) were measured. Arterial oxygen saturation (SpO2) was monitored with a pulse oximeter at forehead level during and after exercise. In Ap, swimming at V400 induced a significantly lower HRpeak and Lacpost ex than swimming at Vmax whilst RPE and the kinetics of SpO2 were not different at V400 and at Vmax. The minimal value of SpO2 in Ap was reached 10 to 11 s after the end of V400 and Vmax (81.7 ± 10.1% and 84.4 ± 10.6%, respectively). Swimming a 50 m front crawl in Ap resulted in a large decrease in SpO2 which occurred only after the cessation of exercise. The higher duration of apnoea during submaximal exercise could explain why SpO2 and RPE reached the same values as for maximal exercise.​ [ABSTRACT FROM AUTHOR]

We aimed to evaluate 1) the altitude where maximal heart rate (HRmax) decreases significantly in both trained and untrained subjects in moderate acute hypoxia, and 2) if the HRmax decrease could partly explain the drop of VO2max. Seventeen healthy males, nine trained endurance athletes (TS) and eight untrained individuals (US) were studied. Subjects performed incremental exercise tests at sea level and at 5 simulated altitudes (1000, 1500, 2500, 3500, 4500 meters). Power output (PO, heart rate (HR), arterial oxygen saturation (SaO2), oxygen uptake (VO2), arterialized blood pH and lactate were measured. Both groups showed a progressive reduction in VO2max. The decrement in HRmax (ΔHRmax) was significant from 1000 m for TS and 2500 m for US and more important in TS than US (at 1500 m and 3500 m). At maximal exercise, TS had a greater reduction in SaO2 (ΔSaO2) at each altitude. ΔHRmax observed in TS was correlated with ΔSaO2. When the two groups were pooled, simple regressions showed that ΔVO2max was correlated with both ΔSaO2 and ΔHRmax. However, a multiple regression analysis demonstrated that ΔSaO2 alone may account for ΔVO2max. Furthermore, in spite of a greater reduction in SaO2 and HRmax in TS, no difference was evidenced in relative ΔVO2max between groups. Thus, in moderate acute hypoxia, the reduction in SaO2 is the primary factor to explain the drop of VO2max in trained and untrained subjects. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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.

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[Hb diff ]), total haemoglobin concentration (Δ[THb]) and muscle reoxygenation were continuously assessed. End-tidal oxygen (PETO 2 ) and carbon dioxide pressure (PETCO 2 ), arterial oxygen saturation (SpO 2 ) 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, PETO 2 decreased to 54.1 ± 8 mmHg, whereas PETCO 2 increased to 74.8 ± 3.1 mmHg. At the end of repetitions, SpO 2 (nadir values 74.9 ± 5.0 vs. 95.7 ± 0.8%) and HR were lower with EEBH than with URB. Cerebral and muscle Δ[Hb diff ] 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., Competing Interests: The authors declare no conflict of interest., (Copyright: © Academy of Physical Education in Katowice.)

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 (SpO 2 ), 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, SpO 2 (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., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: The aim of this study was to establish a model to estimate the level of arterial oxygen saturation (SpO 2 ) and help determine the appropriate hypoxic dose in humans exercising in acute hypoxia., Methods: SpO 2 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 SpO 2 at low, moderate and high intensity both in ETS and UTS (r = 0.97, p < 0.001). SpO 2 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 SpO 2 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 SpO 2 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 SpO 2 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 SpO 2 is exacerbated is between 2000 and 2500 m, depending on both sea-level [Formula: see text] and exercise intensity.

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., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

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 (30-15 IFT ). 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 30-15 IFT . During the RSA test, the fastest sprint (RSA best ), time-based percentage decrement score (RSA Sdec ), 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 RSA best , but likely lowered RSA Sdec (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 RSA Sdec post-training in VHL only ( r = 0.66, p < 0.05). However, VHL did not clearly alter PO 2 , hemoglobin, lactate and bicarbonate concentration and base excess. There was no difference between group velocity gains for the 30-15 IFT (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., (Copyright © 2020 Lapointe, Paradis-Deschênes, Woorons, Lemaître and Billaut.)

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.

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. [La max ] 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 O 2 extraction.

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 ([O 2 Hb]) and deoxyhemoglobin ([HHb]) were monitored by near-infrared spectroscopy. Arterial oxygen saturation (SpO 2 ), heart rate (HR), gas exchange and maximal blood lactate concentration ([La] max ) were also assessed. SpO 2 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., Competing Interests: The authors declare that they have no conflict of interest., (© Georg Thieme Verlag KG Stuttgart · New York.)

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 SpO 2 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.

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-([O 2 Hb]) 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 [O 2 Hb] 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.

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.

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.

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., (Copyright © 2013 Elsevier B.V. All rights reserved.)

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.

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., (Copyright 2010 Elsevier B.V. All rights reserved.)

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).

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.

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.

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).

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.