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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.

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.

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.)

This study aimed to determine the cardiovascular responses during a prolonged exercise with voluntary hypoventilation (VH). 7 men performed 3 series of 5-min exercise at 65% of normoxic maximal O (2) uptake under 3 conditions: (1) normal breathing (NB) in normoxia (NB (0.21)), (2) VH in normoxia (VH (0.21)), (3) NB in hypoxia (NB (0.157), inspired oxygen fraction=0.157). In both VH (0.21) and NB (0.157), there was a similar drop in arterial oxygen saturation and arterial O (2) content (CaO (2)) which were lower than in NB (0.21). Heart rate (HR), stroke volume, and cardiac output (-) were higher in VH (0.21) than in NB (0.21) during most parts of exercise whereas there was no difference between NB (0.157) and VH (0.21) or NB (0.21). HR variability analysis suggested an increased sympathetic modulation in VH (0.21) only. O (2) transport and oxygen uptake were generally not different between interventions. Mixed venous O (2) content (C-O (2)) was lower in NB (0.157) than in both VH (0.21) and NB (0.21) and not different between the latter. CaO (2)-C-O (2) was not different between NB (0.157) and NB (0.21) but lower in VH (0.21). This study shows that a prolonged exercise with VH leads to a greater cardiac activity, independent from the hypoxic effect. The greater - in VH compared to normal breathing seems to be the main factor for compensating the drop of arterial oxygen content., (© Georg Thieme Verlag KG Stuttgart · New York.)

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.

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.