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Cerebral and Muscle Oxygenation during Repeated Shuttle Run Sprints with Hypoventilation
Abstract
Ten highly-trained Jiu-Jitsu fighters performed two 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 oxyhaemoglobin ([O2Hb]) and deoxyhaemoglobin ([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 µa). 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.
... Until 2020, the studies that had dealt with the acute effects of VHL exercise had used EEBH of fixed duration (Kume et al., 2016;Woorons et al., 2010Woorons et al., , 2014Woorons et al., , 2017 or fixed distance (Woorons et al., 2019). Recently, a more ambitious approach consisting of performing EEBH up to the breaking point has been tested (Woorons et al., 2021a(Woorons et al., , 2021b. ...
... First, and importantly, the impact of this specific approach on cerebral oxygenation is still unknown. A study that investigated the effects of repeated back-and-forth running sprints with non-maximum EEBH reported lower cerebral oxygenation compared with the same exercise with unrestricted breathing (Woorons et al., 2019). However, no change in cerebral blood volume was observed. ...
... Yet, it has been shown that to be effective, the LLTH approach should be performed at high exercise intensities (in particular through repeated sprints in hypoxia) to induce muscle tissue adaptations that may be favourable to performance (McLean et al., 2014). Previously, studies that used non-maximum EEBH during repeated sprints found no difference in muscle oxygenation compared with the same exercise with unrestricted breathing or, if so, only towards the end of exercise (Woorons et al., 2017(Woorons et al., , 2019. From a training perspective, it may be important to assess whether larger muscle deoxygenation may be obtained with maximum EEBH. ...
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.
... Since then, the acute effects of the VHL technique have been widely investigated. The studies that dealt with this topic have reported larger levels of carbon dioxide partial pressures (Woorons et al. 2007(Woorons et al. , 2011, lower blood, muscle and cerebral oxygenation (Kume et al. 2016;Woorons et al. 2007Woorons et al. , 2010Woorons et al. , 2014Woorons et al. , 2017Woorons et al. , 2019a and greater stimulation of the anaerobic glycolysis (Kume et al. 2016;Woorons et al. 2010Woorons et al. , 2014 compared with the same exercise performed with unrestricted breathing. Changes at the cardiac level have also been found during VHL exercise (Woorons et al. 2011. ...
... So far, in most of the studies dealing with the effects of VHL exercise, the EEBHs have been performed over a fixed duration (i.e., 4-6 s) (Kume et al. 2016;Woorons et al. 2007Woorons et al. , 2010Woorons et al. , 2017, a fixed distance (Woorons et al. 2019a) or until the subjects felt a strong urge to breathe (Woorons et al. 2014). In a recent study, the subjects were required for the first time to perform the EEBHs for as long as possible (i.e., up to the breaking point) during a cycle exercise at high intensity ). ...
... Using the near-infrared spectroscopy (NIRS) technique, some studies have reported higher vastus lateralis muscle deoxygenation during low-intensity cycle exercises with VHL as compared with the same exercise with normal breathing (Kume et al. 2016;Woorons et al. 2010). On the other hand, other studies which investigated the effects of repeated sprints with VHL found no difference between conditions (Woorons et al. 2019a) or, if so, only towards the end of exercise ). These latter outcomes may explain why no improvement in muscle O 2 utilisation was reported after a period of repeated-sprint training with VHL (Lapointe et al. 2020;Woorons et al. 2019b). ...
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 randomized sessions each including two exercises on a motorized 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.
... Near-infrared spectroscopy is a non-invasive method for continuous monitoring tissue oxygen availability and utilization via changes in concentration of oxyhemoglobin (O 2 Hb, O 2 delivery), deoxyhemoglobin (HHb, O 2 extraction), total hemoglobin (THb, local blood volume), and tissue saturation index (TSI, dynamic balance between O 2 delivery and utilization) [37,38]. High-intensity interval cycling and running exercise causes decreased skeletal muscle oxygenation, as indicated by the greater concentration of HHb, with a concomitant lower concentration of O 2 Hb or/and a lower tissue saturation index [39][40][41][42][43][44]. Regarding different types of muscle contraction, greater alterations in muscle oxygenation were found during pure concentric compared to pure eccentric maximal exercise [45][46][47]. ...
... It is known that there is a significant decrease in muscle ∆[O 2 Hb] and an increase in muscle ∆[HHb] in response to acute high-intensity interval exercise when performed in a wide range of exercise durations (6-30 s), recovery periods (12 s-2 min), and exercise types (cycling and running) [39][40][41][42][43][44]. This is also the case in the present investigation, where the three different modes of muscle contraction during HIIE caused significant decreases in ∆[O 2 Hb] and significant increases in ∆[HHb], whereas this response (i.e., decreased ∆[O 2 Hb] and increased ∆[HHb]) is an indication of decreased muscle oxygenation [49]. ...
... The HIIE adopted in the present study did not cause any alteration in cerebral oxygenation (i.e., ∆ [40,43,49,50,65,66]. It seems that cerebral oxygenation is mainly affected by the level of fatigue that a HIIE bout can cause; this was not the case in the present investigation, where the eccentric and the concentric exercises did not cause significant reductions in performance. ...
The aim of the present study was to study the effects of cycling and pure concentric and pure eccentric high-intensity interval exercise (HIIE) on skeletal muscle (i.e., vastus lateralis) and cerebral oxygenation. Twelve healthy males (n = 12, age 26 ± 1 yr, body mass 78 ± 2 kg, height 176 ± 2 cm, body fat 17 ± 1% of body mass) performed, in a random order, cycling exercise and isokinetic concentric and eccentric exercise. The isokinetic exercises were performed on each randomly selected leg. The muscle and the cerebral oxygenation were assessed by measuring oxyhemoglobin, deoxyhemoglobin, total hemoglobin, and tissue saturation index. During the cycling exercise, participants performed seven sets of seven seconds maximal intensity using a load equal to 7.5% of their body mass while, during isokinetic concentric and eccentric exercise, they were performed seven sets of five maximal muscle contractions. In all conditions, a 15 s rest was adopted between sets. The cycling HIIE caused greater fatigue (i.e., greater decline in fatigue index) compared to pure concentric and pure eccentric isokinetic exercise. Muscle oxygenation was significantly reduced during HIIE in the three exercise modes, with no difference between them. Cerebral oxygenation was affected only marginally during cycling exercise, while no difference was observed between conditions. It is concluded that a greater volume of either concentric or eccentric isokinetic maximal intensity exercise is needed to cause exhaustion which, in turn, may cause greater alterations in skeletal muscle and cerebral oxygenation.
... Most investigations involving power efforts and muscle oxygenation analysis during high-intensity exercises were performed on a cycle ergometer [12][13][14][15] and in repeated sprint 13,16,17 but with measurements conducted in one muscle group 16,18 or in independent exercise to compare arm vs leg oxygen responses 13 . Rissanen et al. 19 performed simultaneous analysis in biceps brachii and vastus lateralis in incremental treadmill running, observing differences between less and more active muscle oxygenation, especially in severe-intensity exercise. ...
... Most investigations involving power efforts and muscle oxygenation analysis during high-intensity exercises were performed on a cycle ergometer [12][13][14][15] and in repeated sprint 13,16,17 but with measurements conducted in one muscle group 16,18 or in independent exercise to compare arm vs leg oxygen responses 13 . Rissanen et al. 19 performed simultaneous analysis in biceps brachii and vastus lateralis in incremental treadmill running, observing differences between less and more active muscle oxygenation, especially in severe-intensity exercise. ...
... NIRS is a non-invasive method that has been shown to be a significant tool capable of estimating the muscle oxygenation events, such as variations in oxyhemoglobin (O 2 Hb), deoxyhemoglobin (HHb), total hemoglobin (tHb) and tissue saturation index (TSI) in skeletal muscle 30,31 . This technique based on optical principles has been commonly used in clinical studies involving pathologies and exercise prescription 32,33 and recently focused on inactive participants 12 , active subjects 34,35 and athletes 16,[36][37][38] to improve the knowledge about physiological and performance responses. In a recent systematic review, Perrey and Ferrari 39 suggested that the popularity of muscle oxygenation studies in exercise increased after the commercialization of portable wireless muscle oximeters. ...
High-intensity exercises including tethered efforts are commonly used in training programs for athletes, active and even sedentary individuals. Despite this, the knowledge about the external and internal load during and after this effort is scarce. Our study aimed to characterize the kinetics of mechanical and physiological responses in all-out 30 seconds (AO30) tethered running and up to 18 minutes of passive recovery. Additionally, in an innovative way, we investigated the muscle oxygenation in more or less active muscles (vastus lateralis and biceps brachii, respectively) during and after high-intensity tethered running by near-infrared spectroscopy – NIRS. Twelve physically active young men were submitted to AO30 on a non-motorized treadmill to determine the running force, velocity and power. We used wearable technologies to monitor the muscle oxygenation and heart rate responses during rest, exercise and passive recovery. Blood lactate concentration and arterial oxygen saturation were also measured. In a synchronized analysis by high capture frequency of mechanical and physiological signals, we advance the understanding of AO30 tethered running. Muscle oxygenation responses showed rapid adjustments (both, during and after AO30) in a tissue-dependence manner, with very low tissue saturation index observed in biceps brachii during exercise when compared to vastus lateralis. Significant correlations between peak and mean blood lactate with biceps brachii oxygenation indicate an important participation of less active muscle during and after high-intensity AO30 tethered running.
... Cerebral and muscle oxygenation were assessed using the nearinfrared spectroscopy (NIRS) technique (Boushel and Piantadosi, 2000) at wavelengths between 760 and 850 nm. For cerebral oxygenation, we used the PortaLite device (Artinis Medical Systems, Einsteinweg, Netherlands) which position was standardized on the surface of the right prefrontal cortex (above the eyebrow, between the midline of the skull and the temporalis muscle) Willis et al., 2017;Woorons et al., 2019b). The probe was secured with a double-sided tape and was placed under the headband used for maintaining the forehead sensor of the pulse oximeter. ...
... In a recent (acute) study, it was shown that the repetition of supramaximal running exercises with EEBH up to the breaking point could decrease SpO 2 down to~75% and induce a large and early increase in muscle blood volume as compared to the same exercise with unrestricted breathing (Woorons et al., 2023). Conversely, the repetition of sprints with non-maximal EEBH (i.e., 6-s duration) did not yield any change in muscle Δ[THb/ Mb] Woorons et al., 2019b). As suggested (Woorons et al., 2023), the strong hypoxic effect induced by the maximal EEBH may (acutely) provoke a compensatory vasodilation, possibly mediated by the release in nitric oxide (Casey et al., 2010;Wilkins et al., 2008), to preserve muscle O 2 delivery. ...
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.
... [HHb], and was used as an index of the regional blood volume. 24 The tissue saturation index (TSI; expressed in percentages and calculated as [O 2 Hb]/([tHb]) was used as an indicator of muscle oxygenation. 10,15 Before the start of the RSH, a 1-minute stabilization period was carried out, during which participants sat on the saddle of the bicycle and kept their right-leg straight. ...
... Changes in [O 2 Hb], [HHb], [tHb], and TSI (Δ ) were calculated and normalized from this stabilization period (arbitrarily defined as 0). 24 ...
Purpose : This study aimed to investigate acute psychophysiological responses to repeated-sprint training in hypoxia (RSH) combined with whole-body cryotherapy (WBC). Method : Sixteen trained cyclists performed 3 sessions in randomized order: RSH, WBC-RSH (WBC pre-RSH), and RSH-WBC (WBC post-RSH). RSH consisted of 3 sets of 5 × 10-second sprints with 20-second recovery at a simulated altitude of 3000 m. Power output, muscle oxygenation (tissue saturation index), heart-rate variability, and recovery perception were analyzed. Sleep quality was assessed on the nights following test sessions and compared with a control night using nocturnal ActiGraphy and heart-rate variability. Results : Power output did not differ between the conditions ( P = .27), while the decrease in tissue saturation index was reduced for WBC-RSH compared to RSH-WBC in the last set. In both conditions with WBC, the recovery perception was higher compared to RSH (WBC-RSH: +15.4%, and RSH-WBC: +21.9%, P < .05). The number of movements during the RSH-WBC night was significantly lower than for the control night (−18.7%, P < .01) and WBC-RSH (−14.9%, P < .05). RSH led to a higher root mean square of the successive differences of R-R intervals and high-frequency band during the first hour of sleep compared to the control night ( P < .05) and RSH-WBC ( P < .01). Conclusions : Inclusion of WBC in an RSH session did not modify the power output but could improve prolonged performance in hypoxia by maintaining muscle oxygenation. A single RSH session did not deteriorate sleep quality. WBC, particularly when performed after RSH, positively influenced recovery perception and sleep.
... The meta-analysis for breath-holding interventions on physical sport performance showed no effect for short-term interventions, but a positive medium effect for longerterm interventions. Regarding short-term interventions, most studies showed no effects (Bouten et al., 2020;Malakhov et al., 2014;Robertson et al., 2020;Stavrou et al., 2017;Woorons, Dupuy, et al., 2019;Woorons et al., 2017), and two studies showed large negative effects on physical sport performance (Guimard et al., 2014;Malakhov et al., 2014). The first analysis (k = 10) resulted in a large heterogeneity (see I² and Tau²) but when the outliers are removed, with k = 8 results show a moderate heterogeneity almost entirely due to sampling error (see I² and Tau²). ...
... One of the main explanations put forward to explain the lack of effects of short-term breath-holding interventions is that as muscular and cerebral oxygenation is reduced during breath-holding, performing this technique before or during exercise could hinder muscle and cerebral functioning (Guimard et al., 2014;Woorons, Dupuy, et al., 2019;Woorons et al., 2017). Other disadvantages of breath-holding short-term interventions are related to decreased heart rate, peripheral vasoconstriction, and discomfort (Bouten et al., 2020). ...
Breathing techniques are predicted to affect specific physical and psychological states, such as relaxation or activation, that might benefit physical sport performance (PSP). Techniques include slow-paced breathing (SPB), fast-paced breathing (FBP), voluntary hyperventilation (VH), breath-holding (BH), and alternate- and uni-nostril breathing. A systematic literature search of six electronic databases was conducted in April 2022. Participants included were athletes and exercisers. In total, 37 studies were eligible for inclusion in the systematic review, and 36 were included in the five meta-analyses. Random effects meta-analyses for each breathing technique were computed separately for short-term and longer-term interventions. Results showed that SPB and BH were related to improved PSP, with large and small effect sizes for longer-term interventions, respectively. In short-term interventions, SPB, BH, and VH were unrelated to PSP. There was some evidence of publication bias for SPB and BH longer-term interventions, and 41% of the studies were coded as having a high risk of bias. Due to an insufficient number of studies, meta-analyses were not computed for other breathing techniques. Based on the heterogeneity observed in the findings, further research is required to investigate potential moderators and develop standardised breathing technique protocols that might help optimise PSP outcomes.
... 15 During the recovery periods following an exercise bout with VHL, stroke volume and subsequentlyVO 2 are largely augmented, probably due to a "pump effect" (ie, large venous return to the heart) that occurs at the cessation of the breath holding. 16,19,26 When this phenomenon is regularly reproduced during training, it could lead to an increase in both stroke volume andVO 2 during a regular exercise. 15 Even though gas exchange was not measured in this study, it is very likely that the same physiological adaptations occurred. ...
... 15 Even though gas exchange was not measured in this study, it is very likely that the same physiological adaptations occurred. The fact that the SpO 2 levels in the subjects of the VHL group were similar to those reported in the previous studies 19,26 allows to ascertain that the "exhale-hold" technique was correctly performed. A greater stroke volume and the consecutive enhanceḋ VO 2 may have played an important role in the improved running RSA after the high-intensity VHL training in cycling. ...
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.
... 6 For instance, previous studies have compared changes in muscle and cerebral tissue oxygenation between normoxia and hypoxia during exercise. 28,[83][84][85][86][87][88] Therefore, a systematic understanding of both central and peripheral oxygenation changes in situations where O 2 availability is limited could pave the way for further comprehensive reviews. ...
Background
Near-infrared spectroscopy (NIRS) technology has allowed for the measurement of cerebral and skeletal muscle oxygenation simultaneously during exercise. Since this technology has been growing and is now successfully used in laboratory and sports settings, this systematic review aimed to synthesize the evidence and enhance an integrative understanding of blood flow adjustments and oxygen (O2) changes (i.e., the balance between O2 delivery and O2 consumption) within the cerebral and muscle systems during exercise.
Methods
A systematic review was conducted using PubMed, Embase, Scopus, and Web of Science databases to search for relevant studies that simultaneously investigated cerebral and muscle hemodynamic changes using the near-infrared spectroscopy system during exercise. This review considered manuscripts written in English and available before February 9, 2023. Each step of screening involved evaluation by 2 independent authors, with disagreements resolved by a third author. The Joanna Briggs Institute Critical Appraisal Checklist was used to assess the methodological quality of the studies.
Results
Twenty studies were included, of which 80% had good methodological quality, and involved 290 young or middle-aged adults. Different types of exercises were used to assess cerebral and muscle hemodynamic changes, such as cycling (n = 11), treadmill (n = 1), knee extension (n = 5), isometric contraction of biceps brachii (n = 3), and duet swim routines (n = 1). The cerebral hemodynamics analysis was focused on the frontal cortex (n = 20), while in the muscle, the analysis involved vastus lateralis (n = 18), gastrocnemius (n = 3), biceps brachii (n = 5), deltoid (n = 1), and intercostal muscle (n = 1). Overall, muscle deoxygenation increases during exercise, reaching a plateau in voluntary exhaustion, while in the brain, oxyhemoglobin concentration increases with exercise intensity, reaching a plateau or declining at the exhaustion point.
Conclusion
Muscle and cerebral oxygenation respond differently to exercise, with muscle increasing O2 utilization and cerebral tissue increasing O2 delivery during exercise. However, at the exhaustion point, both muscle and cerebral oxygenation become compromised. This is characterized by a reduction in blood flow and a decrease in O2 extraction in the muscle, while in the brain, oxygenation reaches a plateau or decline, potentially resulting in motor failure during exercise.
... A permanent marker was used to replicate the position of the probe. The NIRS signals were sampled at 10 Hz, and a 10th-order, low-pass, zero-phase Butterworth filter (cutoff frequency: 0.1 Hz) was applied (Faiss et al. 2015;Woorons et al. 2019). The NIRS data were averaged for each sprint and are presented as changes from the resting baseline value evaluated for 60 s in the supine position before the warm-up (ΔO 2 Hb, ΔHHb, ΔtHb, and ΔTSI, respectively). ...
PurposeThe present study investigated the effects of adding heat stress to repeated-sprint training in hypoxia on performance and physiological adaptations in well-trained athletes.Methods
Sixteen canoe/kayak sprinters conducted 2 weeks of repeated-sprint training consisting of three sets of 5 × 10 s sprints with 20 s active recovery periods under conditions of either normobaric hypoxia (RSH, FiO2: 14.5%, ambient temperature: 18 ℃, n = 8) or combined heat and normobaric hypoxia (RSHH, FiO2: 14.5%, ambient temperature: 38 ℃, n = 8). Before and after training, the 10 × 10 s repeated-sprint ability (RSA) test and 500 m time trial were performed on a canoe/kayak ergometer.ResultsPeak and average power outputs during the RSA test were significantly improved after training in both RSH (peak power: + 21.5 ± 4.6%, P < 0.001; average power: + 12.5 ± 1.9%, P < 0.001) and RSHH groups (peak power: + 18.8 ± 6.6%, P = 0.005; average power: + 10.9 ± 6.8%, P = 0.030). Indirect variables of skeletal muscle oxygen extraction (deoxygenated hemoglobin) and blood perfusion (total hemoglobin) during the RSA test were significantly increased after training in the RSH group (P = 0.041 and P = 0.034, respectively) but not in the RSHH group. In addition, finish time during the 500 m time trial was significantly shortened after the training only in the RSH group (RSH: − 3.9 ± 0.8%, P = 0.005; RSHH: − 3.1 ± 1.4%, P = 0.078).Conclusion
Adding heat stress to RSH does not enhance performance improvement and may partially mask muscle tissue adaptation.
... Therefore, VHL during HIIE did not affect oxidative metabolism in the working muscles. Similarly, Woorons et al. 17 reported that repeated sprint exercises with VHL did not affect muscle tissue oxygenation. Therefore, VHL during repeated sprint exercises had relatively minor impact on local blood flow and oxygen utilization in working muscles. ...
Purpose:
This study aimed to determine the systemic and peripheral responses to high-intensity interval exercise (HIIE) with voluntary hypoventilation at low lung volume (VHL) or HIIE under hypoxic conditions.
Methods:
Ten male participants completed a single session of HIIE (three sets of 6 × 8-s high-intensity pedaling at 170% of maximal oxygen uptake [VO2max]) under three different conditions: normoxia with normal breathing (NOR: 23 °C, 20.9% of fraction of inspired oxygen [FiO2]), hypoxia with normal breathing (HYP: 23 °C, 14.5% FiO2), and normoxia with VHL (VHL: 23 °C, 20.9% FiO2). A randomized crossover design was used. Power output, arterial oxygen saturation (SpO2), heart rate, and muscle oxygenation were monitored during the exercise and the 16-s recovery. Muscle blood flow (mBF) of the vastus lateralis was also evaluated.
Results:
SpO2 during the exercise and the 16-s recovery in the VHL group was significantly lower than in that of the NOR group. However, this parameter in the VHL group was significantly higher than that of the HYP group (NOR: 94.9 ± 0.4%, HYP: 82.8 ± 1.2%, VHL: 90.4 ± 0.5%; p < 0.001). Muscle oxygen saturation was significantly lower in the HYP group than those in the VHL and NOR groups (NOR: 79.6 ± 17.4%, HYP: 65.5 ± 7.7%, VHL: 74.4 ± 7.8%; p = 0.024). No significant difference in this parameter was observed between the VHL and NOR groups (p > 0.05). Additionally, the exercise-induced increase in mBF did not differ significantly among three groups (p > 0.05).
Conclusion:
HIIE-induced SpO2 decrease was smaller under hypoxic conditions than during VHL. Moreover, mBF was not enhanced by the addition of VHL during HIIE.
... Different path lengths (DPF) were used for BB (3.78) and VL (3.83) 10 . The signals were smoothed using a 10 th order low-pass zero-phase Butterworth filter (cutoff frequency of 0.1 Hz) 50 There was an increase in running power in the first second until a peak power was reached at approximately 6 s and a consequent decrease after this time for all interventions, without any effects of IMW on the studied parameter. Panels B, C, D and E display the peak, mean and minimum values for power, force, velocity and FI, respectively. ...
Inspiratory muscle warm-up (IMW) has been used as a resource to enhance exercises and sports performance. However, there is a lack of studies in the literature addressing the effects of different IMW loads (especially in combination with a shorter and applicable protocol) on high-intensity running and recovery phase. Thus, this study aimed to investigate the effects of three different IMW loads using a shorter protocol on mechanical, physiological and muscle oxygenation responses during and after high-intensity running exercise. Sixteen physically active men, randomly performed four trials 30 s all-out run, preceded by the shorter IMW protocol (2 × 15 breaths with a 1-min rest interval between sets, accomplished 2 min before the 30 s all-out run). Here, three IMW load conditions were used: 15%, 40%, and 60% of maximal inspiratory pressure (MIP), plus a control session (CON) without the IMW. The force, velocity and running power were measured (1000 Hz). Two near-infrared spectroscopy (NIRS) devices measured (10 Hz) the muscle’s oxygenation responses in biceps brachii (BB) and vastus lateralis (VL). Additionally, heart rate (HR) and blood lactate ([Lac]) were also monitored. IMW loads applied with a shorter protocol promoted a significant increase in mean and minimum running power as well as in peak and minimum force compared to CON. In addition, specific IMW loads led to higher values of peak power, mean velocity (60% of MIP) and mean force (40 and 60% of MIP) in relation to CON. Physiological responses (HR and muscles oxygenation) were not modified by any IMW during exercise, as well as HR and [Lac] in the recovery phase. On the other hand, 40% of MIP presented a higher tissue saturation index (TSI) for BB during recovery phase. In conclusion, the use of different loads of IMW may improve the performance of a physically active individual in a 30 s all-out run, as verified by the increased peak, mean and minimum mechanical values, but not in performance assessed second by second. In addition, 40% of the MIP improves TSI of the BB during the recovery phase, which can indicate greater availability of O2 for lactate clearance.
... Furthermore, teamsport athletes often perform sprints with changes of direction (COD) in their training. While VHL has been successfully implemented during acute exercise with COD (Woorons et al., 2019a), the eccentric phase induced by repeated COD over weeks of training may increase muscle damages and/or neuromuscular fatigue (Chaabene et al., 2018). This approach therefore needs to be tested before recommending implementation within daily practice. ...
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.
... Considering that RSH-VHL did not increase the index of muscle blood volume and did not improve the index of muscle O 2 extraction to a greater extent than in RSN, it is likely that the higher V O 2 was due to an increased cardiac output, and subsequently a higher muscle blood flow. It is important to note that previous studies dealing with the acute effects of VHL exercise have reported a higher V O 2 during the periods of recovery (Woorons et al. 2011(Woorons et al. , 2019. This phenomenon would be mainly due to an augmented stroke volume as a consequence of the large and brief inspirations that follow the cessation of the breath holding and that create a "pump effect" (Woorons et al. 2011). ...
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 three-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 (10x6-s all-out cycling sprints) during which oxygen uptake (V ̇O_2) 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±117W and 723±112 vs 768±123W, p<0.05) but not in RSN (834±52 vs 852 ± 69W, p=0.2; 710±63 vs 713±72W, p=0.68). The average V ̇O_2 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.
Purpose
To investigate the impact of voluntary hypoventilation at low lung volumes (VHL) during upper body repeated sprints (RS) on performance, metabolic markers and muscle oxygenation in Brazilian Jiu-Jitsu (BJJ) athletes.
Methods
Eighteen male well-trained athletes performed two randomized RS sessions, one with normal breathing (RSN) and another with VHL (RS-VHL), on an arm cycle ergometer, consisting of two sets of eight all-out 6-s sprints performed every 30 s. Peak (PPO), mean power output (MPO), and RS percentage decrement score were calculated. Arterial oxygen saturation (SpO2), heart rate (HR), gas exchange, and muscle oxygenation of the long head of the triceps brachii were continuously recorded. Blood lactate concentration ([La]) was measured at the end of each set. Bench press throw peak power (BPPP) was recorded before and after the RS protocol.
Results
Although SpO2 was not different between conditions, PPO and MPO were significantly lower in RS-VHL. E, HR, [La], and RER were lower in RS-VHL, and VO2 was higher in RS-VLH than in RSN. Muscle oxygenation was not different between conditions nor was its pattern of change across the RS protocol influenced by condition. [La] was lower in RS-VHL than in RSN after both sets.
Conclusion
Performance was significantly lower in RS-VHL, even though SPO2 was not consistent with hypoxemia. However, the fatigue index was not significantly affected by VHL, nor was the neuromuscular upper body power after the RS-VHL protocol. Additionally, [La] was lower, and oxygen consumption was higher in RS-VHL, suggesting a higher aerobic contribution in this condition.
Background
In the last 5 years since our last systematic review, a significant number of articles have been published on the technical aspects of muscle near-infrared spectroscopy (NIRS), the interpretation of the signals and the benefits of using the NIRS technique to measure the physiological status of muscles and to determine the workload of working muscles.
Objectives
Considering the consistent number of studies on the application of muscle oximetry in sports science published over the last 5 years, the objectives of this updated systematic review were to highlight the applications of muscle oximetry in the assessment of skeletal muscle oxidative performance in sports activities and to emphasize how this technology has been applied to exercise and training over the last 5 years. In addition, some recent instrumental developments will be briefly summarized.
Methods
Preferred Reporting Items for Systematic Reviews guidelines were followed in a systematic fashion to search, appraise and synthesize existing literature on this topic. Electronic databases such as Scopus, MEDLINE/PubMed and SPORTDiscus were searched from March 2017 up to March 2023. Potential inclusions were screened against eligibility criteria relating to recreationally trained to elite athletes, with or without training programmes, who must have assessed physiological variables monitored by commercial oximeters or NIRS instrumentation.
Results
Of the identified records, 191 studies regrouping 3435 participants, met the eligibility criteria. This systematic review highlighted a number of key findings in 37 domains of sport activities. Overall, NIRS information can be used as a meaningful marker of skeletal muscle oxidative capacity and can become one of the primary monitoring tools in practice in conjunction with, or in comparison with, heart rate or mechanical power indices in diverse exercise contexts and across different types of training and interventions.
Conclusions
Although the feasibility and success of the use of muscle oximetry in sports science is well documented, there is still a need for further instrumental development to overcome current instrumental limitations. Longitudinal studies are urgently needed to strengthen the benefits of using muscle oximetry in sports science.
FNIRS pre-processing and processing methodologies are very important—how a researcher chooses to process their data can change the outcome of an experiment. The purpose of this review is to provide a guide on fNIRS pre-processing and processing techniques pertinent to the field of human motor control research. One hundred and twenty-three articles were selected from the motor control field and were examined on the basis of their fNIRS pre-processing and processing methodologies. Information was gathered about the most frequently used techniques in the field, which included frequency cutoff filters, wavelet filters, smoothing filters, and the general linear model (GLM). We discuss the methodologies of and considerations for these frequently used techniques, as well as those for some alternative techniques. Additionally, general considerations for processing are discussed.
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.
Near‐infrared spectroscopy (NIRS) is a common tool used to study oxygen availability and utilisation during repeated‐sprint exercise. However, there are inconsistent methods of smoothing and determining peaks and nadirs from the NIRS signal, which make interpretation and comparisons between studies difficult. To examine the effects of averaging method on deoxy‐haemoglobin concentration ([HHb]) trends, nine males performed ten 10‐s sprints, with 30 s of recovery, and six analysis methods were used for determining peaks and nadirs in the [HHb] signal. First, means were calculated over predetermined windows in the last 5 and 2 s of each sprint and recovery period. Second, moving 5‐ and 2‐s averages were also applied, and peaks/nadirs were determined for each 40‐s sprint/recovery cycle. Third, a Butterworth filter was used to smooth the signal, and the resulting signal output was used to determine peaks and nadirs from predetermined time points and a rolling approach. Correlation and residual analysis showed that the Butterworth filter attenuated the “noise” in the signal, while maintaining the integrity of the raw data (r = 0.9892; mean standardised residual ‐9.71×10³ ± 3.80). Means derived from predetermined windows, irrespective of length and data smoothing, underestimated the magnitude of peak and nadir [HHb] compared to a rolling mean approach. Consequently, sprint‐induced metabolic changes (inferred from Δ[HHb]) were underestimated. Based on these results, we suggest using a digital filter to smooth NIRS data, rather than an arithmetic mean, and a rolling approach to determine peaks and nadirs for accurate interpretation of muscle oxygenation trends.
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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, 7 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 a RSA test (40-m all-out sprints with a departure every 30 s) until task failure (85% of the peak velocity of 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 < 0.01) but not in RSN (9.8 ± 2.8 vs. 10.4 ± 4.7; + 6 %; p = 0.74). 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<0.01).
CONCLUSION: RSH-VHL appears to be an effective strategy to produce a hypoxic stress and to improve running RSA in team sport players.
This study examined the effects of Sprint Interval Cycling (SIT) on muscle oxygenation ki-netics and performance during the 30-15 intermittent fitness test (IFT). Twenty-five women hockey players of Olympic standard were randomly selected into an experimental group (EXP) and a control group (CON). The EXP group performed six additional SIT sessions over six weeks in addition to their normal training program. To explore the potential training-induced change, EXP subjects additionally completed 5 x 30s maximal intensity cycle testing before and after training. During these tests near-infrared spectroscopy (NIRS) measured parameters; oxyhaemoglobin + oxymyoglobin (HbO2+ MbO2), tissue deoxyhae-moglobin + deoxymyoglobin (HHb+HMb), total tissue haemoglobin (tHb) and tissue oxy-genation (TSI %) were taken. In the EXP group (5.34±0.14 to 5.50±0.14m.s-1) but not the CON group (pre = 5.37±0.27 to 5.39±0.30m.s-1) significant changes were seen in the 30-15 IFT performance. EXP group also displayed significant post-training increases during the sprint cycling: ΔTSI (−7.59±0.91 to −12.16±2.70%); ΔHHb+HMb (35.68±6.67 to 69.44 ±26.48μM.cm); and ΔHbO2+ MbO2 (−74.29±13.82 to −109.36±22.61μM.cm). No significant differences were seen in ΔtHb (−45.81±15.23 to −42.93±16.24). NIRS is able to detect positive peripheral muscle oxygenation changes when used during a SIT protocol which has been shown to be an effective training modality within elite athletes.
During supramaximal exercise, exacerbated at exhaustion and in hypoxia, the circulatory system is challenged to facilitate oxygen delivery to working tissues through cerebral autoregulation which influences fatigue development and muscle performance. The aim of the study was to evaluate the effects of different levels of normobaric hypoxia on the changes in peripheral and cerebral oxygenation and performance during repeated sprints to exhaustion. Eleven recreationally active participants (six men and five women; 26.7 ± 4.2 years, 68.0 ± 14.0 kg, 172 ± 12 cm, 14.1 ± 4.7% body fat) completed three randomized testing visits in conditions of simulated altitude near sea-level (~380 m, FIO2 20.9%), ~2000 m (FIO2 16.5 ± 0.4%), and ~3800 m (FIO2 13.3 ± 0.4%). Each session began with a 12-min warm-up followed by two 10-s sprints and the repeated cycling sprint (10-s sprint: 20-s recovery) test to exhaustion. Measurements included power output, vastus lateralis, and prefrontal deoxygenation [near-infrared spectroscopy, delta (Δ) corresponds to the difference between maximal and minimal values], oxygen uptake, femoral artery blood flow (Doppler ultrasound), hemodynamic variables (transthoracic impedance), blood lactate concentration, and rating of perceived exertion. Performance (total work, kJ; −27.1 ± 25.8% at 2000 m, p < 0.01 and −49.4 ± 19.3% at 3800 m, p < 0.001) and pulse oxygen saturation (−7.5 ± 6.0%, p < 0.05 and −18.4 ± 5.3%, p < 0.001, respectively) decreased with hypoxia, when compared to 400 m. Muscle Δ hemoglobin difference ([Hbdiff]) and Δ tissue saturation index (TSI) were lower (p < 0.01) at 3800 m than at 2000 and 400 m, and lower Δ deoxyhemoglobin resulted at 3800 m compared with 2000 m. There were reduced changes in peripheral [Δ[Hbdiff], ΔTSI, Δ total hemoglobin ([tHb])] and greater changes in cerebral (Δ[Hbdiff], Δ[tHb]) oxygenation throughout the test to exhaustion (p < 0.05). Changes in cerebral deoxygenation were greater at 3800 m than at 2000 and 400 m (p < 0.01). This study confirms that performance in hypoxia is limited by continually decreasing oxygen saturation, even though exercise can be sustained despite maximal peripheral deoxygenation. There may be a cerebral autoregulation of increased perfusion accounting for the decreased arterial oxygen content and allowing for task continuation, as shown by the continued cerebral deoxygenation.
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.
Many sport competitions, typically involving the completion of single- (e.g. track-and-field or track cycling events) and multiple-sprint exercises (e.g. team and racquet sports, cycling races), are staged at terrestrial altitudes ranging from 1000 to 2500 m. Our aim was to comprehensively review the current knowledge on the responses to either acute or chronic altitude exposure relevant to single and multiple sprints. Performance of a single sprint is generally not negatively affected by acute exposure to simulated altitude (i.e. normobaric hypoxia) because an enhanced anaerobic energy release compensates for the reduced aerobic adenosine triphosphate production. Conversely, the reduction in air density in terrestrial altitude (i.e. hypobaric hypoxia) leads to an improved sprinting performance when aerodynamic drag is a limiting factor. With the repetition of maximal efforts, however, repeated-sprint ability is more altered (i.e. with earlier and larger performance decrements) at high altitudes (>3000–3600 m or inspired fraction of oxygen <14.4–13.3%) compared with either normoxia or low-to-moderate altitudes (<3000 m or inspired fraction of oxygen >14.4%). Traditionally, altitude training camps involve chronic exposure to low-to-moderate terrestrial altitudes (<3000 m or inspired fraction of oxygen >14.4%) for inducing haematological adaptations. However, beneficial effects on sprint performance after such altitude interventions are still debated. Recently, innovative ‘live low-train high’ methods, in isolation or in combination with hypoxic residence, have emerged with the belief that up-regulated non-haematological peripheral adaptations may further improve performance of multiple sprints compared with similar normoxic interventions.
Background
Repeated-sprint training in hypoxia (RSH) is a recent intervention regarding which numerous studies have reported effects on sea-level physical performance outcomes that are debated. No previous study has performed a meta-analysis of the effects of RSH. Objective
We systematically reviewed the literature and meta-analyzed the effects of RSH versus repeated-sprint training in normoxia (RSN) on key components of sea-level physical performance, i.e., best and mean (all sprint) performance during repeated-sprint exercise and aerobic capacity (i.e., maximal oxygen uptake []). Methods
The PubMed/MEDLINE, SportDiscus®, ProQuest, and Web of Science online databases were searched for original articles—published up to July 2016—assessing changes in physical performance following RSH and RSN. The meta-analysis was conducted to determine the standardized mean difference (SMD) between the effects of RSH and RSN on sea-level performance outcomes. ResultsAfter systematic review, nine controlled studies were selected, including a total of 202 individuals (mean age 22.6 ± 6.1 years; 180 males). After data pooling, mean performance during repeated sprints (SMD = 0.46, 95% confidence interval [CI] −0.02 to 0.93; P = 0.05) was further enhanced with RSH when compared with RSN. Although non-significant, additional benefits were also observed for best repeated-sprint performance (SMD = 0.31, 95% CI −0.03 to 0.89; P = 0.30) and (SMD = 0.18, 95% CI −0.25 to 0.61; P = 0.41). Conclusion
Based on current scientific literature, RSH induces greater improvement for mean repeated-sprint performance during sea-level repeated sprinting than RSN. The additional benefit observed for best repeated-sprint performance and for RSH versus RSN was not significantly different.
Fan, Jui-Lin, and Bengt Kayser. Fatigue and exhaustion in hypoxia: the role of cerebral oxygenation. High Alt Med Biol. 17:72–84, 2016.—It is well established that ascent to high altitude is detrimental to one's aerobic capacity and exercise performance. However, despite more than a century of research on the effects of hypoxia on exercise performance, the underlying mechanisms remain incompletely understood. While the cessation of exercise, or the reduction of its intensity, at exhaustion, implies reduced motor recruitment by the central nervous system, the mechanisms leading up to this muscular derecruitment remain elusive. During exercise in normoxia and moderate hypoxia (∼1500–2500 m), peripheral fatigue and activation of muscle afferents probably play a major role in limiting exercise performance. Meanwhile, studies suggested that cerebral tissue deoxygenation may play a pivotal role in impairing aerobic capacity during exercise in more severe hypoxic conditions (∼4500–6000 m). However, recent studies using end-tidal CO2 clamping, to improve cerebral tissue oxygenation during exercise in hypoxia, failed to demonstrate an improvement in exercise performance. In light of these recent findings, which seem to contradict the hypothetical role of cerebral tissue deoxygenation as a performance limiting factor at high altitude, this short review aims to provide a critical reappraisal of the extant literature and ends exploring some potential avenues for further research in this field.
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 : 16 competitive swimmers completed six sessions of repeated sprints (two sets of 16×15 m with 30 s send-off) either with VHL (RSH-VHL, n=8) or with NB (RSN, n=8). Before (pre-) and after (post-) training, performance was evaluated through an RSA test (25m all-out sprints with 35 s send-off) until exhaustion. Results : From pre- to post-, the number of sprints was significantly increased in RSH-VHL (7.1 ± 2.1 vs 9.6 ± 2.5; p<0.01) but not in RSN (8.0 ± 3.1 vs 8.7 ± 3.7; p=0.38). Maximal blood lactate concentration ([La]max) was higher at post compared to pre- in RSH-VHL (11.5 ± 3.9 vs 7.9 ± 3.7 mmol.l-137 ; p=0.04) but was unchanged in RSN (10.2 ± 2.0 vs 9.0 ± 3.5 mmol.l-138 ; p=0.34). There was a strong correlation between the increases in the number of sprints and in [La]max in RSH-VHL only (R=0.93; p<0.01).
Conclusion : Repeated sprint training in hypoxia induced by voluntary hypoventilation at low lung volume improved repeated sprint ability 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 carried out under normal breathing conditions.
Methods: Over a 5-week period, sixteen triathletes (12 men, 4 women) were asked to include twice a week into their usual swimming session one supramaximal set of 12 to 20 x 25m, 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 over 100, 200 and 400m.
Results: Time performance was significantly improved in VHL in all trials [100m: - 3.7 ± 3.7s (- 4.4 ± 4.0%); 200m: - 6.9 ± 5.0s (- 3.6 ± 2.3%); 400m: - 13.6 ± 6.1s (-3.5 ± 1.5%)] but did not change in CONT. In VHL, maximal lactate concentration (+ 2.35 ± 1.3 mmol.L-1 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 to Pre- in VHL but was not different in CONT. The measurements of gas exchange over 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.
The aim of this study was to compare the training effects based on repeated sprint ability (RSA) (with one change of direction) with an intensive repeated sprint ability (IRSA) (with two changes of direction) on jump performance and aerobic fitness. Eighteen male basketball players were assigned to repeated sprint ability and intensive repeated sprint ability training groups (RSAG and IRSAG). RSA, IRSA, squat jump (SJ), countermovement jump (CMJ) and Yo-Yo intermittent recovery level 1 test were assessed before and after four training weeks. The RSA and IRSA trainings consisted of three sets of six sprints (first two weeks) and eight sprints (second two weeks) with 4-min sets recovery and 20-s of sprints recovery. Four weeks of training led to an overall improvement in most of the measures of RSA, but little evidence of any differences between the two training modes. Jump performance was enhanced: CMJ of 7.5% (P < 0.0001) and 3.1% (P = 0.016) in IRSAG and RSAG respectively. While SJ improved of 5.3% (P = 0.003) for IRSAG and 3.4% (P = 0.095) for RSAG. Conversely the Yo-Yo distance increased 21% (P = 0.301) and 34% (P = 0.017) in IRSAG and RSAG respectively. Therefore, short-term repeated sprint training with one/two changes of direction promotes improvements in both RSA and IRSA respectively but the better increase on jump performance shown a few changes on sprint and endurance performances.
In 2007, Wilber1 presented the main altitude/hypoxic training methods used by elite athletes: ‘live high—train high’ (LHTH) and ‘live high—train low’ (LHTL); sleeping at altitude to gain the haematological adaptations (increased erythrocyte volume) but training at sea level to maximise performance (maintenance of sea-level training intensity and oxygen flux). The LHTL method can be accomplished through a number of methods and devices: natural/terrestrial altitude, nitrogen dilution, oxygen filtration and supplemental oxygen. Another method is the ‘live low—train high’ (LLTH) method including intermittent hypoxic exposure at rest (IHE) or during intermittent hypoxic training sessions (IHT). Noteworthy, all supporting references were conducted with endurance elite athletes (ie, cyclists, triathletes, cross-country skiers, runners, swimmers, kayakers and rowers) and there is an extensive literature relative to LHTH as well as LHTL. However, there is a lack of evidence for the applicability of these methods in team-sport athletes.
In recent times, media reports have provided us with coverage of some high-profile clubs or national squads in various team-sport disciplines undertaking fitness programmes at altitude during the early preseason or in preparation of a major competition. Despite the evident observation that athletes from different team sports and from all around the world are using altitude training more than ever before, it is …
Over the past two decades, intermittent hypoxic training (IHT), that is, a method where athletes live at or near sea level but train under hypoxic conditions, has gained unprecedented popularity. By adding the stress of hypoxia during 'aerobic' or 'anaerobic' interval training, it is believed that IHT would potentiate greater performance improvements compared to similar training at sea level. A thorough analysis of studies including IHT, however, leads to strikingly poor benefits for sea-level performance improvement, compared to the same training method performed in normoxia. Despite the positive molecular adaptations observed after various IHT modalities, the characteristics of optimal training stimulus in hypoxia are still unclear and their functional translation in terms of whole-body performance enhancement is minimal. To overcome some of the inherent limitations of IHT (lower training stimulus due to hypoxia), recent studies have successfully investigated a new training method based on the repetition of short (<30 s) 'all-out' sprints with incomplete recoveries in hypoxia, the so-called repeated sprint training in hypoxia (RSH). The aims of the present review are therefore threefold: first, to summarise the main mechanisms for interval training and repeated sprint training in normoxia. Second, to critically analyse the results of the studies involving high-intensity exercises performed in hypoxia for sea-level performance enhancement by differentiating IHT and RSH. Third, to discuss the potential mechanisms underpinning the effectiveness of those methods, and their inherent limitations, along with the new research avenues surrounding this topic.
To investigate the interaction between the development of peripheral locomotor muscle fatigue, muscle recruitment and performance during repeated-sprint exercise (RSE).
In a single-blind, randomised and cross-over design, ten male team-sport athletes performed two RSE (fifteen 5-s cycling sprints interspersed with 25 s of rest; power self-selected) in normoxia and in acute moderate hypoxia (FIO2 0.138). Mechanical work, total electromyographic intensity (summed quadriceps electromyograms, RMSsum) and muscle (vastus lateralis) and pre-fontal cortex near-infrared spectroscopy (NIRS) parameters were calculated for every sprint. Blood lactate concentration ([Lac(-)]) was measured throughout the protocol. Peripheral quadriceps fatigue was assessed via changes in potentiated quadriceps twitch force (ΔQtw,pot) pre- versus post-exercise in response to supra-maximal magnetic femoral nerve stimulation. The central activation ratio (QCAR) was used to quantify completeness of quadriceps activation.
Compared with normoxia, hypoxia reduced arterial oxygen saturation (-13.7%, P=0.001), quadriceps RMSsum (-13.7%, P=0.022), QCAR (-3.3%, P=0.041) and total mechanical work (-8.3%, P=0.019). However, the magnitude of quadriceps fatigue induced by RSE was similar in the two conditions (ΔQtw,pot: -53.5% and -55.1%, P=0.71). The lower cycling performance in hypoxia occurred despite similar metabolic (muscle NIRS parameters and blood [Lac(-)]) and functional (twitch and M-wave) muscle states.
Results suggest that the central nervous system regulates quadriceps muscle recruitment and, thereby, performance to limit the development of muscle fatigue during intermittent, short sprints. This finding highlights the complex interaction between muscular perturbations and neural adjustments during sprint exercise, and further supports the presence of pacing during intermittent sprint exercise.
While intermittent hypoxic training (IHT) has been reported to evoke cellular responses via hypoxia inducible factors (HIFs) but without substantial performance benefits in endurance athletes, we hypothesized that repeated sprint training in hypoxia could enhance repeated sprint ability (RSA) performed in normoxia via improved glycolysis and O(2) utilization. 40 trained subjects completed 8 cycling repeated sprint sessions in hypoxia (RSH, 3000 m) or normoxia (RSN, 485 m). Before (Pre-) and after (Post-) training, muscular levels of selected mRNAs were analyzed from resting muscle biopsies and RSA tested until exhaustion (10-s sprint, work-to-rest ratio 1∶2) with muscle perfusion assessed by near-infrared spectroscopy. From Pre- to Post-, the average power output of all sprints in RSA was increased (p<0.01) to the same extent (6% vs 7%, NS) in RSH and in RSN but the number of sprints to exhaustion was increased in RSH (9.4±4.8 vs. 13.0±6.2 sprints, p<0.01) but not in RSN (9.3±4.2 vs. 8.9±3.5). mRNA concentrations of HIF-1α (+55%), carbonic anhydrase III (+35%) and monocarboxylate transporter-4 (+20%) were augmented (p<0.05) whereas mitochondrial transcription factor A (-40%), peroxisome proliferator-activated receptor gamma coactivator 1α (-23%) and monocarboxylate transporter-1 (-36%) were decreased (p<0.01) in RSH only. Besides, the changes in total hemoglobin variations (Δ[tHb]) during sprints throughout RSA test increased to a greater extent (p<0.01) in RSH. Our findings show larger improvement in repeated sprint performance in RSH than in RSN with significant molecular adaptations and larger blood perfusion variations in active muscles.
Reduction of aerobic exercise performance observed under hypoxic conditions is mainly attributed to altered muscle metabolism due to impaired O(2) delivery. It has been recently proposed that hypoxia-induced cerebral perturbations may also contribute to exercise performance limitation. A significant reduction in cerebral oxygenation during whole body exercise has been reported in hypoxia compared with normoxia, while changes in cerebral perfusion may depend on the brain region, the level of arterial oxygenation and hyperventilation induced alterations in arterial CO(2). With the use of transcranial magnetic stimulation, inconsistent changes in cortical excitability have been reported in hypoxia, whereas a greater impairment in maximal voluntary activation following a fatiguing exercise has been suggested when arterial O(2) content is reduced. Electromyographic recordings during exercise showed an accelerated rise in central motor drive in hypoxia, probably to compensate for greater muscle contractile fatigue. This accelerated development of muscle fatigue in moderate hypoxia may be responsible for increased inhibitory afferent signals to the central nervous system leading to impaired central drive. In severe hypoxia (arterial O(2) saturation <70-75%), cerebral hypoxia per se may become an important contributor to impaired performance and reduced motor drive during prolonged exercise. This review examines the effects of acute and chronic reduction in arterial O(2) (and CO(2)) on cerebral blood flow and cerebral oxygenation, neuronal function, and central drive to the muscles. Direct and indirect influences of arterial deoxygenation on central command are separated. Methodological concerns as well as future research avenues are also considered.
Short-duration sprints ( Using laboratory and field-based protocols, performance analyses have consistently shown that fatigue during RSE typically manifests as a decline in maximal/mean sprint speed (i.e. running) or a decrease in peak power or total work (i.e. cycling) over sprint repetitions. A consistent result among these studies is that performance decrements (i.e. fatigue) during successive bouts are inversely correlated to initial sprint performance. To date, there is no doubt that the details of the task (e.g. changes in the nature of the work/recovery bouts) alter the time course/magnitude of fatigue development during RSE (i.e. task dependency) and potentially the contribution of the underlying mechanisms. At the muscle level, limitations in energy supply, which include energy available from phosphocreatine hydrolysis, anaerobic glycolysis and oxidative metabolism, and the intramuscular accumulation of metabolic by-products, such as hydrogen ions, emerge as key factors responsible for fatigue. Although not as extensively studied, the use of surface electromyography techniques has revealed that failure to fully activate the contracting musculature and/or changes in inter-muscle recruitment strategies (i.e. neural factors) are also associated with fatigue outcomes. Pending confirmatory research, other factors such as stiffness regulation, hypoglycaemia, muscle damage and hostile environments (e.g. heat, hypoxia) are also likely to compromise fatigue resistance during repeated-sprint protocols.
To assess potential metabolic and microcirculatory alterations in critically ill patients, near-infrared spectroscopy (NIRS) has been used, in combination with a vascular occlusion test (VOT), for the non-invasive measurement of tissue oxygen saturation (StO2), oxygen consumption, and microvascular reperfusion and reactivity. The methodologies for assessing StO2 during a VOT, however, are very inconsistent in the literature and, consequently, results vary from study to study, making data comparison difficult and potentially inadequate. Two major aspects concerning the inconsistent methodology are measurement site and probe spacing. To address these issues, we investigated the effects of probe spacing and measurement site using 15 mm and 25 mm probe spacings on the thenar and the forearm in healthy volunteers and quantified baseline, ischemic, reperfusion, and hyperemic VOT-derived StO2 variables.
StO2 was non-invasively measured in the forearm and thenar in eight healthy volunteers during 3-minute VOTs using two InSpectra tissue spectrometers equipped with a 15 mm probe or a 25 mm probe. VOT-derived StO2 traces were analyzed for base-line, ischemic, reperfusion, and hyperemic parameters. Data were categorized into four groups: 15 mm probe on the forearm (F15 mm), 25 mm probe on the forearm (F25 mm), 15 mm probe on the thenar (T15 mm), and 25 mm probe on the thenar (T25 mm).
Although not apparent at baseline, probe spacing and measurement site significantly influenced VOT-derived StO2 variables. For F15 mm, F25 mm, T15 mm, and T25 mm, StO2 ownslope was -6.4 +/- 1.7%/minute, -10.0 +/- 3.2%/minute, -12.5 +/- 3.0%/minute, and -36.7 +/- 4.6%/minute, respectively. StO2 upslope was 105 +/- 34%/minute, 158 +/- 55%/minute, 226 +/- 41%/minute, and 713 +/- 101%/minute, and the area under the hyperemic curve was 7.4 +/- 3.8%.minute, 10.1 +/- 4.9%.minute, 12.6 +/- 4.4%.minute, and 21.2 +/- 2.7%.minute in these groups, respectively. Furthermore, the StO2 parameters of the hyperemic phase of the VOT, such as the area under the curve, significantly correlated to the minimum StO2 during ischemia.
NIRS measurements in combination with a VOT are measurement site-dependent and probe-dependent. Whether this dependence is anatomy-, physiology-, or perhaps technology-related remains to be elucidated. Our study also indicated that reactive hyperemia depends on the extent of ischemic insult.
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.
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 influence of 180 degrees changes of direction during a repeated-sprint running test on performance, cardiorespiratory variables, muscle deoxygenation and post-exercise blood lactate ([La] (b)) levels. Thirteen team-sport athletes (22+/-3 yr) performed 6 repeated maximal sprints with (RSS, 6 x[2 x 12.5 m]) or without (RS, 6 x 25 m) changes of direction. Best and mean running time, percentage speed decrement (%Dec), pulmonary oxygen uptake ( V O (2)), vastus lateralis deoxygenation (Hb (diff)) and [La] (b) were calculated for each condition. Best and mean times for both protocols were largely correlated (r =0.63 and r =0.78, respectively), and were 'ALMOST CERTAINLY' higher for RSS compared with RS (e. g., 5.30+/-0.17 vs. 4.09+/-0.17 s for mean time, with the qualitative analysis revealing a 100% chance of RSS time being greater than RS). In contrast, %Dec was 'POSSIBLY' lower for RSS (2.6+/-1.2 vs. 3.2+/-1.3%, with a 79% chance of a real difference). Compared with RS, V O (2) (40.4+/-4.2 vs. 38.9+/-3.8 mL x min (-1) x kg (-1), with a 90% chance of a real difference) and [La] (b) (10.0+/-1.7 vs. 9.3+/-2.4 mmol.L (-1), with a 70% chance of a real difference) were 'POSSIBLY' higher. Conversely, there were no differences in Hb (diff) (11.5+/-3.2 vs. 10.9+/-3.0 microM, with the comparison rated as 'UNCLEAR'). To conclude, the present results suggest that the ability to repeat sprints can be considered as a general quality. They also suggest that repeated shuttle sprints might be an effective training practice for eliciting a greater systemic physiological load, but perhaps not a greater loading of the vastus lateralis.
The study examined the influence of cerebral (prefrontal cortex) and muscle (vastus lateralis) oxygenation on the ability to perform repeated, cycling sprints. Thirteen team-sport athletes performed ten, 10-s sprints (with 30 s of rest) under normoxic (F(I)O(2) 0.21) and acute hypoxic (F(I)O(2) 0.13) conditions in a randomised, single-blind fashion and crossover design. Mechanical work was calculated and arterial O(2) saturation (S(p)O(2)) was estimated via pulse oximetry for every sprint. Cerebral and muscle oxy-(O(2)Hb), deoxy-(HHb), and total haemoglobin (THb) were monitored continuously by near-infrared spectroscopy. Compared with normoxia, hypoxia induced larger decrements in S(p)O(2) and work (11.6 and 7.6%, respectively; P < 0.05). In the muscle, we observed a fairly constant level of deoxygenation across sprints, with no effect of the condition. In normoxia, regional cerebral oxygenation increased during the first two sprints and slightly fluctuated thereafter. In contrast, this initial cerebral hyper-oxygenation was attenuated in hypoxia. Changes in [O(2)Hb] and [HHb] occurred earlier and were larger in hypoxia compared with normoxia (P < 0.05), while regional blood volume (Delta[THb]) remained unaffected by the condition. Changes in cerebral [HHb] and mechanical work were strongly correlated in normoxia and hypoxia (R(2) = 0.81 and R(2) = 0.85, respectively; P < 0.05), although the slope of this relationship differed (normoxia, -351.3 +/- 183.3 vs. hypoxia, -442.4 +/- 227.2; P < 0.05). The results of this NIRS study show that O(2) availability influences prefrontal cortex, but not muscle, oxygenation during repeated, short sprints. By using a hypoxia paradigm, the study suggests that cerebral oxygenation contributes to the impairment of repeated-sprint ability.
Aerobic exercise capacity decreases with exposure to hypoxia. This article focuses on the effects of hypoxia on nervous system function and the potential consequences for the exercising human. Emphasis is put on somatosensory muscle afferents due to their crucial role in the reflex inhibition of muscle activation and in cardiorespiratory reflex control during exercise. We review the evidence of hypoxia influences on muscle afferents and discuss important consequences for exercise performance. Efferent (motor) nerves are less affected at altitude and are thought to stay fairly functional even in severe levels of arterial hypoxemia. Altitude also alters autonomic nervous system functions, which are thought to play an important role in the regulation of cardiac output and ventilation. Finally, the consequences of hypoxia-induced cortical adaptations and dysfunctions are evaluated in terms of neurotransmitter turnover, brain electrical activity, and cortical excitability. Even though the cessation of exercise or the reduction of exercise intensity, when reaching maximum performance, implies reduced motor recruitment by the nervous system, the mechanisms that lead to the de-recruitment of active muscle are still not well understood. In moderate hypoxia, muscle afferents appear to play an important role, whereas in severe hypoxia brain oxygenation may play a more important role.
We hypothesized that near-infrared spectroscopy (NIRS) measures of hemoglobin and/or myoglobin O2 saturation (IR-SO2) in the vascular bed of exercising muscle would parallel changes in femoral venous O2 saturation (SfvO2) at the onset of leg-kicking exercise in humans. Six healthy subjects performed transitions from rest to 48 +/- 3 (SE)-W two-legged kicking exercise while breathing 14, 21, or 70% inspired O2. IR-SO2 was measured over the vastus lateralis muscle continuously during all tests, and femoral venous and radial artery blood samples were drawn simultaneously during rest and during 5 min of exercise. In all gas-breathing conditions, there was a rapid decrease in both IR-SO2 and SfvO2 at the onset of moderate-intensity leg-kicking exercise. Although SfvO2 remained at low levels throughout exercise, IR-SO2 increased significantly after the first minute of exercise in both normoxia and hyperoxia. Contrary to the hypothesis, these data show that NIRS does not provide a reliable estimate of hemoglobin and/or O2 saturation as reflected by direct femoral vein sampling.
Near-infrared spectroscopy (NIRS) was utilized to gain insights into the kinetics of oxidative metabolism during exercise transitions. Ten untrained young men were tested on a cycle ergometer during transitions from unloaded pedaling to 5 min of constant-load exercise below (<VT) or above (>VT) the ventilatory threshold. Vastus lateralis oxygenation was determined by NIRS, and pulmonary O2 uptake (Vo --> Vo2) was determined breath-by-breath. Changes in deoxygenated hemoglobin + myoglobin concentration Delta[deoxy(Hb + Mb)] were taken as a muscle oxygenation index. At the transition, [Delta[deoxy(Hb + Mb)]] was unmodified [time delay (TD)] for 8.9 +/- 0.5 s at <VT or 6.4 +/- 0.9 s at >VT (both significantly different from 0) and then increased, following a monoexponential function [time constant (tau) = 8.5 +/- 0.9 s for <VT and 7.2 +/- 0.7 s for >VT]. For >VT a slow component of Delta[deoxy(Hb + Mb)] on-kinetics was observed in 9 of 10 subjects after 75.0 +/- 14.0 s of exercise. A significant correlation was described between the mean response time (MRT = TD + tau) of the primary component of Delta[deoxy(Hb + Mb)] on-kinetics and the tau of the primary component of the pulmonary Vo2 on-kinetics. The constant muscle oxygenation during the initial phase of the on-transition indicates a tight coupling between increases in O2 delivery and O2 utilization. The lack of a drop in muscle oxygenation at the transition suggests adequacy of O2 availability in relation to needs.
To determine if fatigue at maximal aerobic power output was associated with a critical decrease in cerebral oxygenation, 13 male cyclists performed incremental maximal exercise tests (25 W/min ramp) under normoxic (Norm: 21% Fi(O2)) and acute hypoxic (Hypox: 12% Fi(O2)) conditions. Near-infrared spectroscopy (NIRS) was used to monitor concentration (microM) changes of oxy- and deoxyhemoglobin (Delta[O2Hb], Delta[HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated (Delta[THb] = Delta[O2Hb] + Delta[HHb]) and used as an index of change in regional blood volume. Repeated-measures ANOVA were performed across treatments and work rates (alpha = 0.05). During Norm, cerebral oxygenation rose between 25 and 75% peak power output {Power(peak); increased (inc) Delta[O2Hb], inc. Delta[HHb], inc. Delta[THb]}, but fell from 75 to 100% Power(peak) {decreased (dec) Delta[O2Hb], inc. Delta[HHb], no change Delta[THb]}. In contrast, during Hypox, cerebral oxygenation dropped progressively across all work rates (dec. Delta[O2Hb], inc. Delta[HHb]), whereas Delta[THb] again rose up to 75% Power(peak) and remained constant thereafter. Changes in cerebral oxygenation during Hypox were larger than Norm. In muscle, oxygenation decreased progressively throughout exercise in both Norm and Hypox (dec. Delta[O2Hb], inc. Delta [HHb], inc. Delta[THb]), although Delta[O2Hb] was unchanged between 75 and 100% Power peak. Changes in muscle oxygenation were also greater in Hypox compared with Norm. On the basis of these findings, it is unlikely that changes in cerebral oxygenation limit incremental exercise performance in normoxia, yet it is possible that such changes play a more pivotal role in hypoxia.
Purpose:
Compelling evidences suggest larger performance decrements during hypoxic vs. normoxic repeated sprinting, yet the underlying mechanical alterations have not been thoroughly investigated. Therefore, we examined the effects of different levels of normobaric hypoxia on running mechanical performance during repeated treadmill sprinting.
Methods:
Thirteen team-sport athletes performed eight, 5-s sprints with 25-s of passive recovery on an instrumented treadmill in either normoxia near sea level (SL; FiO2 = 20.9%), moderate (MH; FiO2 = 16.8%; corresponding to ~1800 m altitude) or severe normobaric hypoxia (SH; FiO2 = 13.3%; ~3600 m).
Results:
Net power output in the horizontal direction did not differ (P>0.05) between conditions for the first sprint (pooled values: 13.09±1.97 W.kg) but was lower for the eight sprints in SH, compared to SL (-7.3±5.5%, P<0.001) and MH (-7.1±5.9%, P<0.01), with no difference between SL and MH (+0.1±8.0%, P=1.00). Sprint decrement score was similar between conditions (pooled values: -11.4±7.9%, P=0.49). Mean vertical, horizontal and resultant ground reaction forces decreased (P<0.001) from the first to the last repetition in all conditions (pooled values: -2.4±1.9%, -8.6±6.5% and -2.4±1.9%). This was further accompanied by larger kinematic (mainly contact time: +4.0±2.9%, P<0.001 and +3.3±3.6%, P<0.05; respectively; and stride frequency: -2.3±2.0%, P<0.01 and -2.3±2.8%, P<0.05; respectively) and spring-mass characteristics (mainly vertical stiffness: -6.0±3.9% and -5.1±5.7%, P<0.01; respectively) fatigue-induced changes in SH compared with SL and MH.
Conclusion:
In severe normobaric hypoxia, impairments in repeated-sprint ability and in associated kinetics/kinematics and spring-mass characteristics exceed those observed near sea level and in moderate hypoxia (i.e., no or minimal difference). Specifically, severe hypoxia accentuates the RSA fatigue-related inability to effectively apply forward-oriented ground reaction force and to maintain vertical stiffness and stride frequency.
The present study compared the performance (peak speed, distance, and acceleration) of ten amateur team-sport athletes during a clustered (i.e., multiple sets) repeated-sprint protocol, (4 sets of 4, 4-s running sprints; i.e., RSR444) in normobaric normoxia (FiO2 = 0.209; i.e., RSN) with normobaric hypoxia (FiO2 = 0.140; i.e., RSH). Subjects completed two separate trials (i. RSN, ii. RSH; randomised order) between 48 h and 72 h apart on a non-motorized treadmill. In addition to performance, we examined blood lactate concentration [La-] and arterial oxygen saturation (SpO2) before, during, and after the RSR444. While there were no differences in peak speed or distance during set 1 or set 2, peak speed (p = 0.04 and 0.02, respectively) and distance (p = 0.04 and 0.02, respectively) were greater during set 3 and set 4 of RSN compared with RSH. There was no difference in the average acceleration achieved in set 1 (p = 0.45), set 2 (p = 0.26), or set 3 (p = 0.23) between RSN and RSH; however, the average acceleration was greater in RSN than RSH in set 4 (p < 0.01). Measurements of [La-] were higher during RSH than RSN immediately after Sprint 16 (10.2 ± 2.5 vs 8.6 ± 2.6 mM; p = 0.02). Estimations of SpO2 were lower during RSH than RSN, respectively, immediately prior to the commencement of the test (89.0 ± 2.0 vs 97.2 ± 1.5 %), post Sprint 8 (78.0 ± 6.3 vs 93.8 ± 3.6 %) and post Sprint 16 (75.3 ± 6.3 vs 94.5 ± 2.5 %; all p < 0.01). In summary, the RSR444 is a practical protocol for the implementation of a hypoxic repeated-sprint training intervention into the training schedules of team-sport athletes. However, given the inability of amateur team-sport athletes to maintain performance in hypoxic (FiO2 = 0.140) conditions, the potential for specific training outcomes (i.e. speed) to be achieved will be compromised, thus suggesting that the RSR444 should be used with caution.
This study aimed to assess the impact of three simulated altitude exposure heights on repeat sprint performance in team sport athletes.
Ten trained male team sport athletes completed three sets of repeated sprints (9 x 4 s) on a non-motorised treadmill at sea-level or at simulated altitudes of 2000, 3000 and 4000 m. Participants completed four trials in a random order over 4 weeks, with mean power output (MPO), peak power output (PPO), blood lactate concentration (BLa) and oxygen saturation (SaO2) recorded after each set.
Each increase in simulated altitude corresponded with a significant decrease in SaO2. Total work across all sets was highest at sea-level and correspondingly lower at each successive altitude (p<0.05; sea level < 2000 m < 3000 m < 4000 m). In the first set, MPO was reduced only at 4000 m, but for subsequent sets, decreases in MPO were observed at all altitudes (p<0.05; 2000 m < 3000 m < 4000 m). PPO was maintained in all sets except for set 3 at 4000 m (p<0.05, vs sea level and 2000 m). BLa levels were highest at 4000 m and significantly greater (p<0.05) than at sea-level after all sets.
These results suggest that 'higher may not be better', as a simulated altitude of 4000 m may potentially blunt absolute training quality. Therefore, it is recommended that a moderate simulated altitude (2000-3000 m) be employed when implementing intermittent hypoxic repeat sprint training for team sport athletes.
The ability to repeatedly produce a high-power output or sprint speed is a key fitness component of most field and court sports. The aim of this study was to evaluate the validity and reliability of eight different approaches to quantify this parameter in tests of multiple-sprint performance. Ten physically active men completed two trials of each of two multiple-sprint running protocols with contrasting recovery periods. Protocol 1 consisted of 12 x 30-m sprints repeated every 35 seconds; protocol 2 consisted of 12 x 30-m sprints repeated every 65 seconds. All testing was performed in an indoor sports facility, and sprint times were recorded using twin-beam photocells. All but one of the formulae showed good construct validity, as evidenced by similar within-protocol fatigue scores. However, the assumptions on which many of the formulae were based, combined with poor or inconsistent test-retest reliability (coefficient of variation range: 0.8-145.7%; intraclass correlation coefficient range: 0.09-0.75), suggested many problems regarding logical validity. In line with previous research, the results support the percentage decrement calculation as the most valid and reliable method of quantifying fatigue in tests of multiple-sprint performance.
The relative roles of ventilation-perfusion (VA/Q) inequality, alveolar-capillary diffusion resistance, postpulmonary shunt, and gas phase diffusion limitation in determining arterial PO2 (PaO2) were assessed in nine normal unacclimatized men at rest and during bicycle exercise at sea level and three simulated altitudes (5,000, 10,000, and 15,000 ft; barometric pressures = 632, 523, and 429 Torr). We measured mixed expired and arterial inert and respiratory gases, minute ventilation, and cardiac output. Using the multiple inert gas elimination technique, PaO2 and the arterial O2 concentration expected from VA/Q inequality alone were compared with actual values, lower measured PaO2 indicating alveolar-capillary diffusion disequilibrium for O2. At sea level, alveolar-arterial PO2 differences were approximately 10 Torr at rest, increasing to approximately 20 Torr at a metabolic consumption of O2 (VO2) of 3 l/min. There was no evidence for diffusion disequilibrium, similar results being obtained at 5,000 ft. At 10 and 15,000 ft, resting alveolar-arterial PO2 difference was less than at sea level with no diffusion disequilibrium. During exercise, alveolar-arterial PO2 difference increased considerably more than expected from VA/Q mismatch alone. For example, at VO2 of 2.5 l/min at 10,000 ft, total alveolar-arterial PO2 difference was 30 Torr and that due to VA/Q mismatch alone was 15 Torr. At 15,000 ft and VO2 of 1.5 l/min, these values were 25 and 10 Torr, respectively. Expected and actual PaO2 agreed during 100% O2 breathing at 15,000 ft, excluding postpulmonary shunt as a cause of the larger alveolar-arterial O2 difference than accountable by inert gas exchange.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of these experiments was to examine mechanisms by which hypercapnia produces vasodilatation in brain. We examined the hypothesis that dilatation of cerebral arterioles during hypercapnia is dependent on activation of ATP-sensitive potassium channels and formation of nitric oxide.
Diameters of cerebral arterioles were measured using a closed cranial window in anesthetized rabbits. Changes in diameter of arterioles were measured in response to topical application of acetylcholine and sodium nitroprusside and during two levels of systemic hypercapnia.
Increasing arterial PCO2 from 32 +/- 1 mm Hg (mean +/- SE) to 54 +/- 1 and 66 +/- 1 mm Hg dilated cerebral arterioles by 25 +/- 3% and 38 +/- 5%, respectively, from a control diameter of 93 +/- 3 microns. The response to the low level of hypercapnia was attenuated (25 +/- 3% versus 16 +/- 4%, P < .05) by glibenclamide (1 mumol/L), an inhibitor of ATP-sensitive potassium channels. Vasodilatation in response to the high level of hypercapnia was not affected by glibenclamide. Increases in arteriolar diameter in response to sodium nitroprusside were not inhibited by glibenclamide. NG-nitro-L-arginine (300 mumol/L), an inhibitor of nitric oxide synthase, completely inhibited dilatation of cerebral arterioles in response to the low level of hypercapnia and inhibited vasodilatation during the high level of hypercapnia by 66%.
Thus, activation of glibenclamide-sensitive potassium channels may contribute to dilatation of cerebral arterioles during hypercapnia. Cerebral vasodilatation during hypercapnia is dependent in large part on production of nitric oxide.
Near infrared spectroscopy (NIRS) has been used to measure concentration changes of cerebral hemoglobin and cytochrome in neonates, children, and adults, to study cerebral oxygenation and hemodynamics. To derive quantitative concentration changes from measurements of light attenuation, the optical path length must be known. This is obtained by multiplying the source/ detector separation by a laboratory measured differential path length factor (DPF) which accounts for the increased distance traveled by light due to scattering. DPF has been measured by time of flight techniques on small populations of adults and postmortem infants. The values for adults are greater than those for newborns, and it is not clear how to interpolate the present data for studies on children. Recent developments in instrumentation using phase resolved spectroscopy techniques have produced a bedside unit which can measure optical path length on any subject. We have developed an intensity modulated optical spectrometer which measures path length at four wavelengths. Two hundred and eighty three subjects from 1 d of age to 50 y were studied. Measurements were made at a fixed frequency of 200 MHz and a source detector separation of 4.5 cm. Results suggest a slowly varying age dependence of DPF, following the relation DPF690 = 5.38 + 0.049A0.877, DPF744 = 5.11 + 0.106A0.723, DPF807 = 4.99 + 0.067A0.814, and DPF832 = 4.67 + 0.062A0.819, where DPF690 is the DPF measured at 690 nm and A is age is expressed in years from full term. There was a wide scatter of values, however, implying that ideally DPF should be measured at the time of each study.
Fatigue of voluntary muscular effort is a complex phenomenon. To date, relatively little attention has been placed on the role of the central nervous system (CNS) in fatigue during exercise despite the fact that the unwillingness to generate and maintain adequate CNS drive to the working muscle is the most likely explanation of fatigue for most people during normal activities. Several biological mechanisms have been proposed to explain CNS fatigue. Hypotheses have been developed for several neurotransmitters including serotonin (5-HT; 5-hydroxytryptamine), dopamine, and acetylcholine. The most prominent one involves an increase in 5-HT activity in various brain regions. Good evidence suggests that increases and decreases in brain 5-HT activity during prolonged exercise hasten and delay fatigue, respectively, and nutritional manipulations designed to attenuate brain 5-HT synthesis during prolonged exercise improve endurance performance. Other neuromodulators that may influence fatigue during exercise include cytokines and ammonia. Increases in several cytokines have been associated with reduced exercise tolerance associated with acute viral or bacterial infection. Accumulation of ammonia in the blood and brain during exercise could also negatively effect the CNS function and fatigue. Clearly fatigue during prolonged exercise is influenced by multiple CNS and peripheral factors. Further elucidation of how CNS influences affect fatigue is relevant for achieving optimal muscular performance in athletics as well as everyday life.
Near-infrared spectroscopy (NIRS) is a non-invasive method for monitoring oxygen availability and utilization by the tissues. In intact skeletal muscle, NIRS allows semi-quantitative measurements of haemoglobin plus myoglobin oxygenation (tissue O2 stores) and the haemoglobin volume. Specialized algorithms allow assessment of the oxidation-reduction (redox) state of the copper moiety (CuA) of mitochondrial cytochrome c oxidase and, with the use of specific tracers, accurate assessment of regional blood flow. NIRS has demonstrated utility for monitoring changes in muscle oxygenation and blood flow during submaximal and maximal exercise and under pathophysiological conditions including cardiovascular disease and sepsis. During work, the extent to which skeletal muscles deoxygenate varies according to the type of muscle, type of exercise and blood flow response. In some instances, a strong concordance is demonstrated between the fall in O2 stores with incremental work and a decrease in CuA oxidation state. Under some pathological conditions, however, the changes in O2 stores and redox state may diverge substantially.
The aim of this study was to investigate the performance of in vivo quantitative near-infrared spectroscopy (NIRS) in skeletal muscle at various workloads. NIRS was used for the quantitative measurement of O2 consumption (mVO2) in the human flexor digitorum superficialis muscle at rest and during rhythmic isometric handgrip exercise in a broad range of work intensities (10-90% MVC=maximum voluntary contraction force). Six subjects were tested on three separate days. No significant differences were found in mVO2 measured over different days with the exception of the highest workload. The within-subject variability for each workload measured over the three measurements days ranged from 15.7 to 25.6% and did not increase at the high workloads. The mVO2 was 0.14 +/- 0.01 mlO2 min-1 100 g-1 at rest and increased roughly 19 times to 2.68 +/- 0.58 mlO2 min-1 100 g-1 at 72% MVC. These results show that local muscle oxygen consumption at rest as well as during exercise at a broad range of work intensities can be measured reliably by NIRS, applied to a uniform selected subject population. This is of great importance as direct local measurement of mVO2 during exercise is not possible with the conventional techniques. The method is robust enough to measure over separate days and at various workloads and can therefore contribute to a better understanding of human physiology in both the normal and pathological state of the muscle.
A new forehead noninvasive oxygen saturation sensor may improve signal quality in patients with low cardiac index.
To examine agreement between oxygen saturation values obtained by using digit-based and forehead pulse oximeters with arterial oxygen saturation in patients with low cardiac index.
A method-comparison study was used to examine the agreement between 2 different pulse oximeters and arterial oxygen saturation in patients with low cardiac index. Readings were obtained from a finger and a forehead sensor and by analysis of a blood sample. Bias, precision, and root mean square differences were calculated for the digit and forehead sensors. Differences in bias and precision between the 2 noninvasive devices were evaluated with a t test (level of significance P<.05).
Nineteen patients with low cardiac index (calculated as cardiac output in liters per minute divided by body surface area in square meters; mean 1.98, SD 0.34) were studied for a total of 54 sampling periods. Mean (SD) oxygen saturations were 97% (2.4) for blood samples, 96% (3.2) for the finger sensor, and 97% (2.8) for the forehead sensor. By Bland Altman analysis, bias +/- precision was -1.16 +/- 1.62% for the digit sensor and -0.36 +/- 1.74% for the forehead sensor; root mean square differences were 1.93% and 1.70%, respectively. Bias and precision differed significantly between the 2 devices; the forehead sensor differed less from the blood sample.
In patients with low cardiac index, the forehead sensor was better than the digit sensor for pulse oximetry.
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).
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.