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The purpose of this study was to determine the influence of 14 days of normobaric hypoxic simulated altitude exposure at 3000 m on the human plasma metabolomic profile. For 14 days, 10 well‐trained endurance runners (six men and four women; 29 ± 7 years of age) lived at 3000 m simulated altitude, accumulating 196.4 ± 25.6 h of hypoxic exposure, and trained at ∼600 m. Resting plasma samples were collected at baseline and on days 3 and 14 of altitude exposure and stored at −80°C. Plasma samples were analysed using liquid chromatography–high‐resolution mass spectrometry to construct a metabolite profile of altitude exposure. Mass spectrometry of plasma identified 36 metabolites, of which eight were statistically significant (false discovery rate probability 0.1) from baseline to either day 3 or day 14. Specifically, changes in plasma metabolites relating to amino acid metabolism (tyrosine and proline), glycolysis (adenosine) and purine metabolism (adenosine) were observed during altitude exposure. Principal component canonical variate analysis showed significant discrimination between group means (P < 0.05), with canonical variate 1 describing a non‐linear recovery trajectory from baseline to day 3 and then back to baseline by day 14. Conversely, canonical variate 2 described a weaker non‐recovery trajectory and increase from baseline to day 3, with a further increase from day 3 to 14. The present study demonstrates that metabolomics can be a useful tool to monitor metabolic changes associated with altitude exposure. Furthermore, it is apparent that altitude exposure alters multiple metabolic pathways, and the time course of these changes is different over 14 days of altitude exposure.

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Objectives: Actical® actigraphy is commonly used to monitor athlete sleep. The proprietary software, called Actiware®, processes data with three different sleep-wake thresholds (Low, Medium or High), but there is no standardisation regarding their use. The purpose of this study was to examine validity and bias of the sleep-wake thresholds for processing Actical® sleep data in team sport athletes. Design: Validation study comparing actigraph against accepted gold standard polysomnography (PSG). Methods: Sixty seven nights of sleep were recorded simultaneously with polysomnography and Actical® devices. Individual night data was compared across five sleep measures for each sleep-wake threshold using Actiware® software. Accuracy of each sleep-wake threshold compared with PSG was evaluated from mean bias with 95% confidence limits, Pearson moment-product correlation and associated standard error of estimate. Results: The Medium threshold generated the smallest mean bias compared with polysomnography for total sleep time (8.5. min), sleep efficiency (1.8%) and wake after sleep onset (-4.1. min); whereas the Low threshold had the smallest bias (7.5. min) for wake bouts. Bias in sleep onset latency was the same across thresholds (-9.5. min). The standard error of the estimate was similar across all thresholds; total sleep time ∼25. min, sleep efficiency ∼4.5%, wake after sleep onset ∼21. min, and wake bouts ∼8 counts. Conclusions: Sleep parameters measured by the Actical® device are greatly influenced by the sleep-wake threshold applied. In the present study the Medium threshold produced the smallest bias for most parameters compared with PSG. Given the magnitude of measurement variability, confidence limits should be employed when interpreting changes in sleep parameters.

This investigation examined the oxidative stress (F2-Isoprostane; F2-IsoP) and inflammatory (interleukin-6; IL-6) responses to repeat-sprint training in hypoxia (RSH). Ten trained male team sport athletes performed 3(sets)*9(repetitions)*5 s cycling sprints in simulated altitude (3000 m) and sea-level conditions. Mean and peak sprint power output (MPO and PPO) were recorded, and blood samples were collected pre-exercise, and again at 8 and 60 min post-exercise. Both MPO and PPO were significantly reduced in hypoxia (compared to sea-level) in the second (MPO: 855 ± 89 vs. 739 ± 95 W, p = .006; PPO: 1024 ± 114 vs. 895 ± 112 W, p = .010) and third (MPO: 819 ± 105 vs. 686 ± 83 W, p = .008; PPO: 985 ± 125 vs. 834 ± 99 W, p = .008) sets, respectively. IL-6 was significantly increased from pre- to 1 h post-exercise in both hypoxia (0.7 ± 0.2 vs. 2.4 ± 1.4 pg/mL, p = .004) and sea-level conditions (0.7 ± 0.2 vs. 1.6 ± 0.3 pg/mL, p < .001), with a large effect (d = 0.80) suggesting higher IL-6 levels of post-hypoxia. F2-IsoP was significantly lower 1 h post-exercise in both the hypoxic (p = .005) and sea-level (p = .002) conditions, with no differences between trials. While hypoxia can impact on exercise intensity and may result in greater post-exercise inflammation, it appears to have little effect on oxidative stress. These results indicate that team sport organisations with ready access to hypoxic training facilities could confidently administer RSH without significantly increasing the post-exercise inflammatory or oxidative stress response.

To assess the impact of ‘top-up’ normoxic or hypoxic repeat-sprint training on sea-level repeat-sprint ability, thirty team sport athletes were randomly split into three groups, which were matched in running repeat-sprint ability (RSA), cycling RSA and 20 m shuttle run performance. Two groups then performed 15 maximal cycling repeat-sprint training sessions over 5 weeks, in either normoxia (NORM) or hypoxia (HYP), while a third group acted as a control (CON). In the post-training cycling RSA test, both NORM (13.6%; p = 0.0001, and 8.6%; p = 0.001) and HYP (10.3%; p = 0.007, and 4.7%; p = 0.046) significantly improved overall mean and peak power output, respectively, whereas CON did not change (1.4%; p = 0.528, and -1.1%; p = 0.571, respectively); with only NORM demonstrating a moderate effect for improved mean and peak power output compared to CON. Running RSA demonstrated no significant between group differences; however, the mean sprint times improved significantly from pre- to post-training for CON (1.1%), NORM (1.8%), and HYP (2.3%). Finally, there were no group differences in 20 m shuttle run performance. In conclusion, ‘top-up’ training improved performance in a task-specific activity (i.e. cycling); however, there was no additional benefit of conducting this ‘top-up’ training in hypoxia, since cycle RSA improved similarly in both HYP and NORM conditions. Regardless, the ‘top-up’ training had no significant impact on running RSA, therefore the use of cycle repeat-sprint training should be discouraged for team sport athletes due to limitations in specificity.

Item does not contain fulltext, PURPOSE: This study measured the influence of acute hypoxic exercise on Interleukin-6 (IL-6), hepcidin, and iron biomarkers in athletes. METHODS: In a repeated measures design, 13 moderately trained endurance athletes performed 5 x 4 min intervals at 90 % of their peak oxygen consumption velocity (vVO2peak) in both normoxic [NORM, fraction of inspired oxygen (F IO2) = 0.2093, 15.3 +/- 1.7 km h(-1)] and simulated hypoxic (HYP, F IO2 = 0.1450, 13.2 +/- 1.5 km h(-1)) conditions. Venous blood samples were obtained pre-, post-, and 3 h post-exercise, and analysed for serum hepcidin, IL-6, ferritin, iron, soluble transferrin receptor (sTfR), and transferrin saturation. RESULTS: Peak heart rate was significantly lower in HYP compared with NORM (p = 0.01); however, the rating of perceived exertion was similar between trials (p = 0.24). Ferritin (p = 0.02), transferrin (p = 0.03), and IL-6 (p = 0.01) significantly increased immediately post-exercise in both conditions, but returned to baseline 3 h later. Hepcidin levels significantly increased in both conditions 3 h post-exercise (p = 0.05), with no significant differences between trials. A significant treatment effect was observed between trials for sTfR (p = 0.01), but not iron and transferrin saturation. CONCLUSION: Acute exercise in hypoxia did not influence post-exercise IL-6 production, hepcidin activity or iron metabolism compared with exercise at the same relative intensity in normoxia. Hence, acute exercise performed at the same relative intensity in hypoxia poses no further risk to an athlete's iron status, as compared with exercise in normoxia.

Item does not contain fulltext, PURPOSE: To assess the influence of a simulated altitude exposure (~2,900 m above sea level) for a 3 h recovery period following intense interval running on post-exercise inflammation, serum iron, ferritin, erythropoietin, and hepcidin response. METHODS: In a cross-over design, ten well-trained male endurance athletes completed two 8 x 3 min interval running sessions at 85 % of their maximal aerobic velocity on a motorized treadmill, before being randomly assigned to either a hypoxic (HYP: F IO2 ~0.1513) or a normoxic (NORM: F IO2 0.2093) 3 h recovery period. Venous blood was collected pre- and immediately post-exercise, and after 3 and 24 h of recovery. Blood was analyzed for interleukin-6, serum iron, ferritin, erythropoietin, and hepcidin. RESULTS: Interleukin-6 was significantly elevated (p < 0.01) immediately post-exercise compared to baseline (NORM: 1.08 +/- 0.061 to 3.12 +/- 1.80) (HYP: 1.32 +/- 0.86 to 2.99 +/- 2.02), but was not different between conditions. Hepcidin levels were significantly elevated (p < 0.01) at 3 h post-exercise for both conditions when compared to baseline (NORM: 3.25 +/- 1.23 to 7.40 +/- 4.00) (HYP: 3.24 +/- 1.94 to 5.42 +/- 3.20), but were significantly lower (p < 0.05) in the HYP trial compared to NORM. No significant differences existed between HYP and NORM for erythropoietin, serum iron, or ferritin. CONCLUSION: Simulated altitude exposure (~2,900 m) for 3 h following intense interval running attenuates the peak hepcidin levels recorded at 3 h post-exercise. Consequently, a hypoxic recovery after exercise may be useful for athletes with compromised iron status to potentially increase acute dietary iron absorption.

Purpose: This study aimed to assess the impact of 3 heights of simulated altitude exposure on repeat-sprint performance in teamsport athletes. Methods: Ten trained male team-sport athletes completed 3 sets of repeated sprints (9 × 4 s) on a nonmotorized treadmill at sea level and at simulated altitudes of 2000, 3000, and 4000 m. Participants completed 4 trials in a random order over 4 wk, with mean power output (MPO), peak power output (PPO), blood lactate concentration (Bla), and oxygen saturation (SaO2) recorded after each set. Results: 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 < .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 < .05; 2000 m < 3000 m < 4000 m). PPO was maintained in all sets except for set 3 at 4000 m (P < .05; vs sea level and 2000 m). BLa levels were highest at 4000 m and significantly greater (P < .05) than at sea level after all sets. Conclusions: 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.

Despite the limited research on the effects of altitude (or hypoxic) training interventions on team-sport performance, players from all around the world engaged in these sports are now using altitude training more than ever before. In March 2013, an Altitude Training and Team Sports conference was held in Doha, Qatar, to establish a forum of research and practical insights into this rapidly growing field. A round-table meeting in which the panellists engaged in focused discussions concluded this conference. This has resulted in the present position statement, designed to highlight some key issues raised during the debates and to integrate the ideas into a shared conceptual framework. The present signposting document has been developed for use by support teams (coaches, performance scientists, physicians, strength and conditioning staff) and other professionals who have an interest in the practical application of altitude training for team sports. After more than four decades of research, there is still no consensus on the optimal strategies to elicit the best results from altitude training in a team-sport population. However, there are some recommended strategies discussed in this position statement to adopt for improving the acclimatisation process when training/competing at altitude and for potentially enhancing sea-level performance. It is our hope that this information will be intriguing, balanced and, more importantly, stimulating to the point that it promotes constructive discussion and serves as a guide for future research aimed at advancing the bourgeoning body of knowledge in the area of altitude training for team sports.