We examined the impact of moderate hypoxia (HYPO) on muscle activation during incremental exercise matched for both absolute and equivalent relative intensity. Fifteen active subjects (10 males, 5 females) completed two ramp incremental test and two step tests in normoxia (NORM; F i O 2 ${F_{{\mathrm{i}}{{\mathrm{O}}_2}}}$  = 0.209) and HYPO ( F i O 2 ${F_{{\mathrm{i}}{{\mathrm{O}}_2}}}$ ≈ 0.135) in counterbalanced order. The respiratory compensation point (RCP) determined from ramp testing was used to normalize relative intensity during step testing, which included a final stage to task failure (TF) above RCP. Electromyography (EMG) was recorded for rectus femoris (RF), vastus lateralis (VL) and vastus medialis (VM), and normalized to a pre-test maximal sprint effort. Linear mixed modelling was used to examine fixed effects of condition (NORM, HYPO) and intensity (absolute, relative) on EMG activity. During the ramp test, HYPO significantly reduced V ̇ O 2 peak ${\dot V_{{{\mathrm{O}}_2}{\mathrm{peak}}}}$ (∼13%), PPO (∼15%), and power at RCP (∼16%). EMG breakpoints occurred at lower absolute intensity in HYPO for RF and VL. When matched for relative intensity, muscle activity was lower in HYPO for VM and VL, but not RF. EMG activity at TF revealed a similar pattern whereby a strong association to absolute power was present regardless of test protocol or F i O 2 ${F_{{\mathrm{i}}{{\mathrm{O}}_2}}}$ . These results suggest that altered relative metabolic stress has a negligible impact on muscle activation at work rates below the RCP. For exercise in the severe domain our data aligns with the theory that muscle activation is not critically regulated to a given level at TF, but appears to be task-specific and independent of oxygen availability.

PURPOSE:Heart rate (HR) variability thresholds (HRVT) based on detrended fluctuation analysis alpha 1 (DFA a1) generally show reasonable alignment of thresholds estimations based on gas exchange responses under normoxic conditions. This study examined whether acute hypoxia would affect the agreement between HRVTs and the gas exchange equivalents during incremental cycling. METHODS:Twelve participants (five females) completed an incremental ramp test in normobaric hypoxia (FIO 2 ≈ 13.5%) and normoxia. Gas exchange and ventilatory responses alongside a high sampling rate electrocardiogram for DFA a1 computation were used to determine thresholds. Comparisons were made between the oxygen consumption (V̇O 2 ) and HR at the gas exchange threshold (GET) and respiratory compensation point (RCP) with the responses at the first and second HRVTs (HRVT 1 and HRVT 2 , respectively). RESULTS:Mean V̇O 2 and HR values were not statistically different for GET:HRVT1 (normoxia: 1.74 ± 0.41 vs 1.74 ± 0.48 L·min -1 , 133 ± 18 vs 133 ± 16 bpm; hypoxia: 1.47 ± 0.21 vs 1.45 ± 0.37 L·min -1 , 135 ± 14 vs 133 ± 15 bpm) and RCP:HRVT2 (normoxia: 2.38 ± 0.55 vs 2.37 ± 0.48 L·min -1 , 158 ± 13 vs 158 ± 14 bpm, hypoxia: 2.07 ± 0.32 vs 1.90 ± 0.43 L·min -1 and 156 ± 13 vs 152 ± 15 bpm) in any condition. All normoxic comparisons passed equivalence testing, but only GET:HRVT1 responses passed during hypoxia. Pearson's r correlation coefficients were 0.86 to 0.96 in normoxia and 0.58 to 0.79 in hypoxia. Bland-Altman analysis indicated higher degrees of bias and limit of agreements (LOA) during hypoxic testing. CONCLUSIONS:Although the V̇O 2 and HR at HRVTs retained alignment with GET/RCP in both normoxia and hypoxia, the degrees of correlation, and equivalence were weaker and the bias and LOA were larger in hypoxia. Therefore, although using HRVT alone for training boundary guidance in hypoxia is a potential option, further investigation including incorporating complementary surrogate markers is recommended.

Whilst modifications in thermoregulatory responses and plasma volume during heat acclimation (HA) are well researched, much less is known regarding hemoglobin mass. The aim of this study was to investigate the hematological adaptations associated with a long-term, progressive, work-matched controlled heart rate HA protocol. Ten males (VO2peak: 4.50 ± 0.50 L/min) completed two three-week training interventions consisting of HA (36 °C and 59

BACKGROUND:Efforts are needed to improve antidoping procedures. The widespread use of power meters among cyclists could help in this regard. However, controversy exists on whether performance monitoring through power-output data could be of help for antidoping purposes. PURPOSE:The objective of the present study was to provide insight into the feasibility and utility of implementing power-based performance monitoring in elite cycling. An expert panel of 15 applied sport scientists and professional cycling coaches were asked for their opinions and perspectives on incorporating power data into the antidoping risk-assessment process. RESULTS:Two different viewpoints were identified from the responses provided by the experts. Some believed that power monitoring could be implemented as an antidoping tool, provided that several surmountable challenges are first addressed. These authors provided suggestions related to the potential practical implementation of such measures. Others, on the contrary, believed that power meters lack sufficient reliability and suggest that the professional cycling world presents conflicts of interest that make this intervention impossible to implement nowadays. CONCLUSIONS:The debate around the utility of power-meter data in the antidoping fight has been ongoing for more than a decade. According to the opinions provided by the experts' panel, there is still no consensus on the real utility and practical implementation of this intervention.

ABSTRACT Purpose The objective of this study is to investigate the effectiveness of novel repeated-sprint training in hypoxia (RSH) protocol, likely maximizing hypoxic stimulus (higher than commonly used) while preserving training quality (interset rest in normoxia). Methods Twenty-three world-class female rugby sevens players performed four repeated-sprint training sessions (4 sets of 5 × 5-s cycle sprints—25-s intersprint recovery and 3-min interset rest) under normobaric hypoxia (RSH, exercise and interset rest at FiO2 of 10.6% and 20.9%, respectively; n = 12) or normoxia (repeated-sprint training in normoxia; exercise and interset rest at FiO2 of 20.9%; n = 11) during a 9-d training camp before international competition. Repeated-sprint ability (8 × 5-s treadmill sprints—25-s recovery), on-field aerobic capacity, and brachial endothelial function were assessed pre- and postintervention. Results Arterial oxygen saturation (pooled data: 87.0% ± 3.1% vs 96.7% ± 2.9%, P < 0.001) and peak and mean power outputs (sets 1 to 4 average decrease: −21.7% ± 7.2% vs −12.0% ± 3.8% and −24.9% ± 8.1% vs −14.9% ± 3.5%; both P < 0.001) were lower in RSH versus repeated-sprint training in normoxia. The cumulated repeated-sprint distance covered significantly increased from pre- to postintervention (+1.9% ± 3.0%, P = 0.019), irrespective of the condition (P = 0.149). On-field aerobic capacity did not change (all P > 0.45). There was no significant interaction (all P > 0.240) or condition main effect (all P > 0.074) for any brachial artery endothelial function variable. Only peak diameter increased (P = 0.026), whereas baseline and peak shear stress decreased (P = 0.014 and 0.019, respectively), from pre- to postintervention. Conclusions In world-class female rugby sevens players, only four additional repeated-sprint sessions before competition improve repeated-sprint ability and brachial endothelial function. However, adding severe hypoxic stress during sets of repeated sprints only did not provide supplementary benefits.

PURPOSE: Limb immobilization following injury can lead to detraining responses in humans, often due to reductions in mechanical loading. Adding heat stress both passively (throughout immobilization) and actively (during training when mechanical loads are compromised) can alter skeletal muscle function and may potentially enhance fitness adaptation beyond training alone. The aim of this study was to assess the impact of heat therapy during 2-weeks of lower limb immobilization and during 2 weeks of re-training in cardiorespiratory responses in recreationally active individuals. METHODS: 20 participants (mean ± SD: 34 ± 3 years, 182 ± 6 cm, 84 ± 9 kg) were tested at baseline [BASELINE] i) after 4 weeks of training [TRAINING] ii) after 2 weeks of single-leg immobilization [IMMOBILIZATION] and iii) after 2 weeks of supervised return to sport training [REHABILITATION]. Participants were separated into 2 groups (heat therapy [HEAT] vs placebo [CON]) during IMMOBILIZATION and REHABILITATION. The V̇O2 and power (watts) at VT1, VT2 and V̇O2max responses were assessed at all time points. RESULTS: TRAINING increased V̇O2 and power vs. BASELINE (p < 0.05, respectively) at VT1, VT2 and V̇O2max. IMMOBILZATION reduced V̇O2 (190 mL·min-1, p < 0.005) and power (20 ± 4 W, p < 0.001) at VT1 vs. TRAINING, with a significant interaction (p = 0.023) for V̇O2 whereby V̇O2 was reduced in HEAT (p = 0.001) but not CON (p = 0.25). REHABILITATION did not change V̇O2 at VT1 (p > 0.05) vs IMMOBILIZATION. It appeared that power was increased in HEAT (25 ± 6 W, p = 0.001), but not CON (3 ± 6 W, p = 0.999) vs. IMMOBILIZATION, however interaction was not significant (p = 0.072). IMMOBILIZATION did not affect V̇O2 at VT2 or V̇O2max (p > 0.05, respectively) vs. TRAINING in either group (p > 0.05). IMMOBILIZATION reduced power at VT2 (19 ± 5 W, p = 0.005) and V̇O2max (14 ± 4 W, p = 0.005) vs. TRAINING, with no change between groups (p > 0.05, respectively). REHABILITATION resulted in lower V̇O2 at VT2 (p = 0.004) and V̇O2max (p = 0.013) vs. TRAINING yet power at VT2 and V̇O2max increased (p < 0.05) in both groups. CONCLUSIONS: Limb immobilization induces detraining responses in both V̇O2 and power responses across intensities. Passive heating and aerobic training in the heat post-immobilisation may promote a faster return in exercise capacity at VT1 relative to a CON condition.

It is important to consider biological sex as a variable that might influence exercise adaptation in order to optimize exercise prescription for men and women. The aim of this study was to quantify the impact of biological sex on maximal oxygen uptake ( V̇ O2max) and performance outcomes after high-intensity interval training (HIIT). A systematic search and review was conducted by two independent reviewers up to 8 September 2022 using MEDLINE, SPORTDiscus, and Sports Medicine Education Index in ProQuest. Trials including healthy adults were included if they presented data for or compared male and female V̇ O2max or performance outcomes in response to HIIT. Performance outcomes included measures of exercise performance and concurrently measured physiological adaptations. Where appropriate, a random-effects, pre-post meta-analysis was undertaken. Data were sub-grouped for men and women, baseline training level, mean age, intervention type, and intervention length. Heterogeneity was assessed using Chi2, Cochran’s Q, and Higgins I2 and sensitivity analyses, where required. Study quality was assessed using the Newcastle–Ottawa Scale and publication bias was assessed through visual inspection of funnel plots. Thirty-three references from 28 trials were included in the review (n = 965; 462 women and 503 men). Meta-analyses included 19 studies for V̇ O2max, eight for peak power output from V̇ O2max testing (PPO), and five for threshold power (powerAT). Meta-analyses revealed similar increases in V̇ O2max in women (g = 0.57; 95 V̇ O2max were Δ 0.32 L·min−1 and 3.50 mL·kg−1·min−1 in men, versus Δ 0.20 L·min−1 and 3.34 mL·kg−1·min−1 for women. No significant sex differences were present for the primary analysis of any outcome. After sub-grouping, significant differences were present for PPO where the effect size was higher for well-trained women (g = 0.37) compared with well-trained men (g = 0.17), and for V̇ O2max where interventions with a duration of 4 weeks or less had significantly smaller effect sizes compared with those longer than 4 weeks (p < 0.001). Unweighted mean percentage change in V̇ O2max, PPO, and powerAT across studies was 11.16 ± 7.39 V̇ O2max and PPO (I2, range: 62.06–78.80 V̇ O2max or powerAT, but the meta-analysis of PPO could have benefitted from additional study data to strengthen results. The overlap in age categories and sensitivity of the analysis limits the accuracy of the results of the sub-grouping by age. Findings indicated no sex-specific differences for any fitness or performance outcomes. Baseline training status and intervention length accounted for most variability in outcomes. PROSPERO registration number: CRD42021272615.

This paper provides a kinetic observation of both core and skin temperatures in 108 elite athletes, during various outdoor competition events, adding to the very limited data so far available in the literature taken during elite competitions. The field skin temperature findings contrast previous laboratory findings, likely due to differences in relative air velocity and its impact on the evaporation of sweat. The rapid rise in skin temperature following cessation of exercise highlights the importance of infrared thermography measurements being taken during motion, not during breaks, when being used as a measurement of skin temperature during exercise.

PURPOSE To investigate the effects of a training camp with heat and/or hypoxia sessions on hematological and thermoregulatory adaptations. METHODS Fifty-six elite male rugby players completed a 2-week training camp with 5 endurance and 5 repeated-sprint sessions, rugby practice, and resistance training. Players were separated into 4 groups: CAMP trained in temperate conditions at sea level, HEAT performed the endurance sessions in the heat, ALTI slept and performed the repeated sprints at altitude, and H + A was a combination of the heat and altitude groups. RESULTS Blood volume across all groups increased by 140 mL (95%CI, 42-237; P = .006) and plasma volume by 97 mL (95%CI 28-167; P = .007) following the training camp. Plasma volume was 6.3% (0.3% to 12.4%) higher in HEAT than ALTI (P = .034) and slightly higher in HEAT than H + A (5.6% [-0.3% to 11.7%]; P = .076). Changes in hemoglobin mass were not significant (P = .176), despite a ∼1.2% increase in ALTI and H + A and a ∼0.7% decrease in CAMP and HEAT. Peak rectal temperature was lower during a postcamp heat-response test in HEAT (0.3 °C [0.1-0.5]; P = .010) and H + A (0.3 °C [0.1-0.6]; P = .005). Oxygen saturation upon waking was lower in ALTI (3% [2% to 5%]; P < .001) and H + A (4% [3% to 6%]; P < .001) than CAMP and HEAT. CONCLUSION Although blood and plasma volume increased following the camp, sleeping at altitude impeded the increase when training in the heat and only marginally increased hemoglobin mass. Heat training induced adaptations commensurate with partial heat acclimation; however, combining heat training and altitude training and confinement during a training camp did not confer concomitant hematological adaptations.

PurposeTo determine associations between thermal responses, medical events, performance, heat acclimation and health status during a World Athletics Championships in hot-humid conditions.MethodsFrom 305 marathon and race-walk starters, 83 completed a preparticipation questionnaire on health and acclimation. Core (Tcore; ingestible pill) and skin (Tskin; thermal camera) temperatures were measured in-competition in 56 and 107 athletes, respectively. 70 in-race medical events were analysed retrospectively. Performance (% personal best) and did not finish (DNF) were extracted from official results.ResultsPeak Tcoreduring competition reached 39.6°C±0.6°C (maximum 41.1°C). Tskindecreased from 32.2°C±1.3°C to 31.0°C±1.4°C during the races (p<0.001). Tcorewas not related to DNF (25% of starters) or medical events (p≥0.150), whereas Tskin, Tskinrate of decrease and Tcore-to-Tskingradient were (p≤0.029). A third of the athletes reported symptoms in the 10 days preceding the event, mainly insomnia, diarrhoea and stomach pain, with diarrhoea (9% of athletes) increasing the risk of in-race medical events (71% vs 17%, p<0.001). Athletes (63%) who performed 5–30 days heat acclimation before the competition: ranked better (18±13 vs 28±13, p=0.009), displayed a lower peak Tcore(39.4°C±0.4°C vs 39.8°C±0.7°C, p=0.044) and larger in-race decrease in Tskin(−1.4°C±1.0°C vs −0.9°C±1.2°C, p=0.060), than non-acclimated athletes. Although not significant, they also showed lower DNF (19% vs 30%, p=0.273) and medical events (19% vs 32%, p=0.179).ConclusionTskin, Tskinrate of decrease and Tcore-to-Tskingradient were important indicators of heat tolerance. While heat-acclimated athletes ranked better, recent diarrhoea represented a significant risk factor for DNF and in-race medical events.

To investigate the agreement between critical power (CP) and functional threshold power (FTP), 17 trained cyclists and triathletes (mean ± SD: age 31 ± 9 years, body mass 80 ± 10 kg, maximal aerobic power 350 ± 56 W, peak oxygen consumption 51 ± 10 mL⋅min –1 ⋅kg –1 ) performed a maximal incremental ramp test, a single-visit CP test and a 20-min time trial (TT) test in randomized order on three different days. CP was determined using a time-trial (TT) protocol of three durations (12, 7, and 3 min) interspersed by 30 min passive rest. FTP was calculated as 95% of 20-min mean power achieved during the TT. Differences between means were examined using magnitude-based inferences and a paired-samples t -test. Effect sizes are reported as Cohen’s d . Agreement between CP and FTP was assessed using the 95% limits of agreement (LoA) method and Pearson correlation coefficient. There was a 91.7% probability that CP (256 ± 50 W) was higher than FTP (249 ± 44 W). Indeed, CP was significantly higher compared to FTP ( P = 0.041) which was associated with a trivial effect size ( d = 0.04). The mean bias between CP and FTP was 7 ± 13 W and LoA were −19 to 33 W. Even though strong correlations exist between CP and FTP ( r = 0.969; P < 0.001), the chance of meaningful differences in terms of performance (1% smallest worthwhile change), were greater than 90%. With relatively large ranges for LoA between variables, these values generally should not be used interchangeably. Caution should consequently be exercised when choosing between FTP and CP for the purposes of performance analysis.

This pilot study examined the effect of inspiratory muscle training (IMT) on repeated-sprint ability and vastus lateralis reoxygenation. Ten recreationally trained subjects were randomly divided into two groups to complete 4 weeks of IMT or Sham (placebo) training. Pre- and post-intervention, a repeated-sprint ability (RSA) test was performed in both normoxia and hypoxia (FiO2 ≈ 14.5%). Vastus lateralis reoxygenation (VLreoxy), defined as peak to minimum amplitude deoxyhaemoglobin for each sprint/recovery cycle, was assessed during all trials using near-infrared spectroscopy. For total work performed, power analysis revealed that for small, medium and large effects (Cohen’s f ), sample sizes of n = 8, 16 and 90 respectively, are required to achieve a power of 80% at an α level of 0.05. Maximal inspiratory mouth pressure increased in IMT by 36.5%, 95% CI [20.9, 61.6] and by 2.7%, 95% CI [−4.46, 8.8] in Sham. No clear difference in the change of work completed during the sprints between groups were observed in normoxia (Sham −0.805 kJ, 95% CI [−3.92, 0.39]; IMT −2.06 kJ, 95% CI [−11.5, 4.96]; P = 0.802), or hypoxia (Sham −3.09 kJ, 95% CI [−7, 0.396]; IMT 0.354 kJ, 95% CI [−1.49, 2.1]; P = 0.802). VLreoxy in IMT increased by 9.34%, 95% CI [5.15, 13.7] in normoxia only. In conclusion, despite a large increase in IMT, this was only associated with a small effect on RSA in our pilot study cohort. Owing to a potentially relevant impact of training the inspiratory musculature, future studies should include a sample size of at least 16-20 to detect moderate to large effects on RSA.

Purpose: To investigate whether including heat and altitude exposures during an elite team-sport training camp induces similar or greater performance benefits. Methods: The study assessed 56 elite male rugby players for maximal oxygen uptake, repeated-sprint cycling, and Yo-Yo intermittent recovery level 2 (Yo-Yo) before and after a 2-week training camp, which included 5 endurance and 5 repeated-sprint cycling sessions in addition to daily rugby training. Playerswere separated into 4 groups: (1) control (all sessions in temperate conditions at sea level), (2) heat training (endurance sessions in the heat), (3) altitude (repeated-sprint sessions and sleeping in hypoxia), and (4) combined heat and altitude (endurance in the heat, repeated sprints, and sleeping in hypoxia). Results: Training increased maximal oxygen uptake (4%[10%], P =.017), maximal aerobic power (9%[8%], P <.001), and repeated-sprint peak (5%[10%], P =.004) and average power (12%[14%], P <.001) independent of training conditions. Yo-Yo distance increased (16% [17%], P <.001) but not in the altitude group (P =.562). Training in heat lowered core temperature and increased sweat rate during a heat-response test (P <.05). Conclusion: A 2-week intensified training camp improved maximal oxygen uptake, repeatedsprint ability, and aerobic performance in elite rugby players. Adding heat and/or altitude did not further enhance physical performance, and altitude appears to have been detrimental to improving Yo-Yo.

Purpose To characterise hydration, cooling, body mass loss, and core (Tcore) and skin (Tsk) temperatures during World Athletics Championships in hot-humid conditions. Methods Marathon and race-walk (20 km and 50 km) athletes (n=83, 36 women) completed a pre-race questionnaire. Pre-race and post-race body weight (n=74), Tcore (n=56) and Tsk (n=49; thermography) were measured. Results Most athletes (93%) had a pre-planned drinking strategy (electrolytes (83%), carbohydrates (81%)) while ice slurry was less common (11%; p<0.001). More men than women relied on electrolytes and carbohydrates (91%–93% vs 67%–72%, p≤0.029). Drinking strategies were based on personal experience (91%) rather than external sources (p<0.001). Most athletes (80%) planned pre-cooling (ice vests (53%), cold towels (45%), neck collars (21%) and ice slurry (21%)) and/or mid-cooling (93%; head/face dousing (65%) and cold water ingestion (52%)). Menthol usage was negligible (1%–2%). Pre-race Tcore was lower in athletes using ice vests (37.5°C±0.4°C vs 37.8°C±0.3°C, p=0.024). Tcore (pre-race 37.7°C±0.3°C, post-race 39.6°C±0.6°C) was independent of event, ranking or performance (p≥0.225). Pre-race Tsk was correlated with faster race completion (r=0.32, p=0.046) and was higher in non-finishers (did not finish (DNF); 33.8°C±0.9°C vs 32.6°C±1.4°C, p=0.017). Body mass loss was higher in men than women (−2.8±1.5% vs −1.3±1.6%, p<0.001), although not associated with performance. Conclusion Most athletes’ hydration strategies were pre-planned based on personal experience. Ice vests were the most adopted pre-cooling strategy and the only one minimising Tcore, suggesting that event organisers should be cognisant of logistics (ie, freezers). Dehydration was moderate and unrelated to performance. Pre-race Tsk was related to performance and DNF, suggesting that Tsk modulation should be incorporated into pre-race strategies.

The hematological module of the Athlete Biological Passport (ABP) is used for indirect detection of blood manipulations; however, the use of this method to detect doping, such as with microdoses of recombinant human erythropoietin (rhEPO), is problematic. For this reason, the sensitivity of ABP must be enhanced by implementing novel biomarkers. Here, we show that 5'-aminolevulinate synthase 2 (ALAS2) mRNAs are useful transcriptomic biomarkers to improve the indirect detection of rhEPO microdosing. Moreover, the sensitivity was sufficient to distinguish rhEPO administration from exposure to hypoxic conditions. Levels of mRNAs encoding carbonate anhydrase 1 (CA1) and solute carrier family 4 member 1 (SLC4A1) RNA, as well as the linear (L) and linear + circular (LC) forms of ALAS2 mRNA, were monitored for 16 days after rhEPO microdosing and during exposure to hypoxic conditions. ALAS2 mRNAs increased by 300% compared with the baseline values after rhEPO microdosing. Moreover, ALAS2 mRNAs were not significantly increased under hypoxic conditions. By contrast, CA1 mRNA was increased after both rhEPO microdosing and hypoxia, whereas SLC4A1 mRNA did not significantly increase under either condition. Furthermore, the analyses described here were performed using dried blood spots (DBSs), which provide advantages in terms of the sample collection, transport, and storage logistics. This study demonstrates that ALAS2 mRNA levels are sensitive and specific transcriptomic biomarkers for the detection of rhEPO microdosing using the hematological module of the ABP, and this method is compatible with the use of DBSs for anti-doping analyses.

Erythroferrone (ERFE) is a glycoprotein hormone secreted by erythroblasts in response to erythropoietin stimulation. ERFE suppresses the hepatic synthesis of the master iron-regulatory hormone, hepcidin. The impact of erythropoiesis stimulation on ERFE secretion in humans is poorly understood. This paucity of information is due in part to the lack of available means for ERFE quantification in serum samples. The present study tested a new sensitive sandwich immunoassay for human ERFE. This assay was used to demonstrate that injection of various erythropoiesis stimulating agents (ESAs) increased the blood ERFE levels in healthy volunteers. After exogenous stimulation of erythropoiesis, ERFE increased up to 8-fold with a detection window of 13 days. The impact of one unit of blood withdrawal on erythropoiesis stimulation of ERFE was also tested. ERFE significantly increased after blood withdrawal in subjects injected with both iron and saline solution, suggesting that iron supplementation did not mask the ERFE increase after blood withdrawal. The effects of exercise-induced muscle damage on ERFE was assessed by comparing ERFE levels with creatine kinase levels in samples from subjects with heavy exercise loads, and determined that this was not a confounder. The ERFE assay is a sensitive means to investigate the connection between iron metabolism and erythropoiesis in humans, and to detect ESA abuse in the antidoping field.

We examined the effects of increasing hypoxia severity on repeated-sprint running performance and neuromuscular fatigue. Thirteen active males completed eight sprints of 5 s (recovery = 25 s) on a motorized sprint treadmill in normoxia (sea level, SL; F-I,F- O2 = 0.21), in moderate hypoxia (MH; F-I,F- O2 = 0.17) and in severe hypoxia (SH; F-I,F- O2 = 0.13). After 6 min of passive recovery, in all conditions a second set of four sprints of 5 s was conducted in normoxia. Neuromuscular function of the knee extensors was assessed at baseline (Pre-) and 1 min after set 1 (Post-set 1) and set 2 (Post-set 2). In set 1, the mean distance covered in SL (22.9 +/- 1.2 m) was not different to MH (22.7 +/- 1.3 m; P = 0.71) but was greater than in SH (22.3 +/- 1.3 m; P = 0.04). No significant differences between conditions for mean distance occurred in set 2. There was a decrease in maximal voluntary contraction torque (Delta = -31.4 +/- 18.0 N m, P < 0.001) and voluntary activation (%VA; Delta = -7.1 +/- 5.1%, P = 0.001) from Pre- to Post-set 1, but there was no effect of hypoxia. No further change from Post-set 1 to Post-set 2 occurred for either maximal voluntary contraction or %VA. The decrease in potentiated twitch torque in SL (Delta = -13.3 +/- 5.2 N m) was not different to MH (Delta = -13.3 +/- 6.3 N m) but was lower than in SH (Delta = -16.1 +/- 4 N m) from Pre- to Post-set 1 (interaction, P < 0.003). Increasing severity of normobaric hypoxia, up to an equivalent elevation of 3600 m, can increase indices of peripheral fatigue but does not impact central fatigue after 'all-out' repeated-sprint running.

Exposure to either natural or simulated hypoxia induces hematological adaptations that may affect the parameters of the Athlete Biological Passport (ABP). The aim of the present study was to examine the effect of a novel, mixed hypoxic dose protocol on the likelihood of producing an atypical ABP finding. Ten well-trained middle-distance runners participated in a "live high, train low and high" (LHTLH) altitude training camp for 14 days. The participants spent ˜6 hr.d-1 at 3000-5400 m during waking hours and ˜10 h.d-1 overnight at 2400-3000 m simulated altitude. Venous blood samples were collected before (B0), and after 1 (D1), 4 (D4), 7 (D7), and 14 (D14) days of hypoxic exposure, and again 14 days post exposure (P14). Samples were analyzed for key parameters of the ABP including reticulocyte percentage (Ret%), hemoglobin concentration ([Hb]), and the OFF-score. The ABP adaptive model was administered at a specificity of 99% to test for atypical findings. We found significant changes in [Hb] and Ret% during the hypoxic intervention. Consequently, this led to ABP threshold deviations at 99% specificity in three participants. Only one of these was flagged as an "atypical passport finding" (ATPF) due to deviation of the OFF-score. When this sample was evaluated by ABP experts it was considered "normal". In conclusion, it is highly unlikely that the present hypoxic exposure protocol would have led to a citation for a doping violation according to WADA guidelines.

A high work of breathing can compromise limb oxygen delivery during sustained high-intensity exercise. However, it is unclear if the same is true for intermittent sprint exercise. This project examined the effect of adding an inspiratory load on locomotor muscle tissue reoxygenation during repeated-sprint exercise. Ten healthy males completed three experiment sessions of ten 10-s sprints, separated by 30-s of passive rest on a cycle ergometer. The first two sessions were "all-out' efforts performed without (CTRL) or with inspiratory loading (INSP) in a randomised and counterbalanced order. The third experiment session (MATCH) consisted of ten 10-s work-matched intervals. Tissue saturation index (TSI) and deoxy-haemoglobin (HHb) of the vastus lateralis and sixth intercostal space was monitored with near-infrared spectroscopy. Vastus lateralis reoxygenation (ΔReoxy) was calculated as the difference from peak HHb (sprint) to nadir HHb (recovery). Total mechanical work completed was similar between INSP and CTRL (effect size: -0.18, 90% confidence limit ±0.43), and differences in vastus lateralis TSI during the sprint (-0.01 ±0.33) and recovery (-0.08 ±0.50) phases were unclear. There was also no meaningful difference in ΔReoxy (0.21 ±0.37). Intercostal HHb was higher in the INSP session compared to CTRL (0.42 ±0.34), whilst the difference was unclear for TSI (-0.01 ±0.33). During MATCH exercise, differences in vastus lateralis TSI were unclear compared to INSP for both sprint (0.10 ±0.30) and recovery (-0.09 ±0.48) phases, and there was no meaningful difference in ΔReoxy (-0.25 ±0.55). Intercostal TSI was higher during MATCH compared to INSP (0.95 ±0.53), whereas HHb was lower (-1.09 ±0.33). The lack of difference in ΔReoxy between INSP and CTRL suggests that for intermittent sprint exercise, the metabolic O2 demands of both the respiratory and locomotor muscles can be met. Additionally, the similarity of the MATCH suggests that ΔReoxy was maximal in all exercise conditions.