Article

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

Authors:
• University of Lille, Pluridisciplinary Research Unit Sport Health & Society (URePSSS)
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## 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.

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... 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). ...
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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. ...
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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. ...
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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.
... 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.
... 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. ...
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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. ...
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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). ...
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Purpose: This study investigated the effects of repeated-sprint (RS) training in hypoxia induced by voluntary hypoventilation at low lung volume (RSH-VHL) on physiological adaptations, RS ability (RSA) and anaerobic performance. Methods: Over a 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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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 [$$\dot{V}{\text{O}}_{2\hbox{max} }$$]). 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 $$\dot{V}{\text{O}}_{2\hbox{max} }$$ (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 $$\dot{V}{\text{O}}_{2\hbox{max} }$$ for RSH versus RSN was not significantly different.
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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.
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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.
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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.
Article
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.
Article
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.
Article
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.
Article
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.
Article
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)
Article
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.
Article
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.
Article
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.
Article
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.
Article
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.
Article
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.
Article
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).
Article
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.