ECSS Paris 2023: OP-PN03
INTRODUCTION: Iron deficiency affects ~15-35% of female athletes and is associated with impaired aerobic performance [1]. However, its influence on short-duration maximal exercise, which relies on combined aerobic and anaerobic energy contributions, remains unclear, particularly under hypoxic conditions. Therefore, this study examined the effects of iron status on performance and physiological responses during all-out sprint cycling of varying durations (5-60 s) in female athletes under normoxic and hypoxic conditions. METHODS: Twenty-eight trained female athletes (iron-sufficient: n=15; iron-deficient: n=13) completed two separate experimental sessions involving four isolated maximal cycling sprints (5, 15, 30, and 60 s) performed under normoxia (FIO2=0.209) and hypoxia (FIO2=0.135). Mechanical output, vastus lateralis muscle oxygenation (near-infrared spectroscopy), and peripheral oxygen saturation (pulse oximetry) were measured during each sprint, with perceptual responses immediately afterward. Two-way repeated-measures ANOVAs (iron status and condition) were conducted separately for each sprint duration. RESULTS: When pooled across groups, total work (-6.6±16.7%) and mean power output (-6.9±16.4%) during the 60-s sprint were lower in hypoxia than normoxia (both p<.001), with no differences between iron-sufficient and iron-deficient athletes (p>.05). Peak muscle deoxygenation rate during the 15-s sprint was 10.8% greater in hypoxia than normoxia in iron-sufficient athletes only (p=.045). Peripheral oxygen saturation was not influenced by iron status (p>.05), but differed by condition, with normoxia showing greater desaturation responses during the 5-s (p<.01) and 30-s sprint (p<.05). Perceived difficulty breathing during the 60-s sprint was 20% greater in iron-deficient than iron-sufficient athletes when pooled across conditions (p=.024). No other differences were observed (p>.05). CONCLUSION: Iron status did not meaningfully impair mechanical output or physiological responses during short-duration (≤60 s) maximal sprints under normoxic or hypoxic conditions in female athletes. Although group differences were noted in muscle oxygenation and perceived breathing difficulty, these did not translate into measurable performance differences. The greater perceptual strain experienced by iron-deficient athletes nonetheless highlights the importance of monitoring and managing iron status. Comparable hypoxia-induced performance reductions between groups suggest that the performance consequences of iron deficiency may be more pronounced during repeated-sprint or endurance-type exercise, prolonged hypoxic exposure, or at greater altitude severities. [1] Sim M, et al. Iron considerations for the athletes: a narrative review. Eur J Appl Physiol. 2019;119(7):1463−78
Read CV Michelle SteinECSS Paris 2023: OP-PN03
INTRODUCTION: Females may be more susceptible to exercise-induced arterial hypoxemia (EIAH), in part due to sex differences in pulmonary structure and function which increase the likelihood of ventilatory and gas exchange limitations during exercise. These differences may be amplified at high-altitude, where changes in pulmonary diffusion capacity are known to occur. METHODS: To address this, 39 participants (16F; 26.1±4.7 years, 173.4±10.2 cm, 74.4±14.4 kg) performed an incremental maximal cycling test and 5-kilometer cycle time-trial at sea level (340m) and high-altitude (days 3-12; 3800m). Ventilation and pulmonary gas exchange were measured breath-by-breath during the incremental maximal cycling test and time-trial via metabolic cart. Arterial blood gases, corrected for changes in core-temperature, were collected at baseline and every kilometer during the time-trial via brachial artery catheter. RESULTS: Peak oxygen consumption (VO2peak) at sea level was 47.5±8.8 mL/min/kg in males and 41.3±9.1 mL/min/kg in females, which decreased by 18.0±10.4% and 19.1±5.8% at high-altitude in males and females, respectively. Throughout the time-trial, reductions in arterial oxygen saturation (SaO2) were similar between sexes at sea level (Females: -4.8±3.5% vs. Males: -4.5±2.4%; p=0.751) and high-altitude (Females: -14.4±5.7% vs. Males: -14.4±4.8%; p=0.346). A condition x altitude interaction (p<0.001) supports greater desaturation with continuing exercise at high-altitude in all participants. Considering participants’ fitness (VO2peak) as a covariate, a fitness x altitude x sex interaction (p=0.003) indicates females with higher VO2peak desaturated more at high-altitude compared to males and less fit females. The alveolar-arterial oxygen difference (A-aDO2) increased throughout the time-trial (p<0.001) and was lower at high-altitude compared to sea level throughout exercise (p=0.038) but was not different between sexes (p=0.214). However, at high-altitude, a greater widening of A-aDO2 contributed to worsened EIAH in males (p<0.001), whereas relative hypoventilation (indexed by an attenuated reduction in partial pressure of arterial carbon dioxide) contributed to EIAH in females (p<0.001 vs. males). CONCLUSION: Therefore, the aetiology of EIAH at high-altitude may differ between males and females. Relative fitness may contribute more to EIAH development at high-altitude in females than males. Further, females may experience a combination of diffusion limitation and relative hypoventilation (potentially mediated by expiratory flow limitation), compared to males who are driven mainly by diffusion limitation (i.e., a greater widening of A-aDO2). Thus, while males and females appear to experience EIAH similarly during a 5-kilometer time-trial at sea level and high-altitude, the contribution of relative fitness and underlying mechanisms may differ at high-altitude.
Read CV Lauren MaierECSS Paris 2023: OP-PN03
INTRODUCTION: Altitude training programs, particularly live high-train low (LHTL) protocols, are widely used by endurance athletes with the aim of enhancing performance through adaptations such as increases in hemoglobin mass and muscle capillary density. Recently, post-exercise ketone ester (KE) ingestion has been shown to increase serum [EPO] compared with a placebo (1). Furthermore, KE has also been shown to enhance skeletal muscle capillarization and elevate serum [EPO] in response to three weeks of excessive exercise training (2). These findings suggest that KE may induce similar effects as altitude exposure, and as such may potentially elevate the physiological and performance adaptations induced by LHTL. METHODS: Eighteen recreational cyclists (9 male, 9 female; VO2max: 52 +/- 8 mL/kg/min) performed a five-week LHTL camp involving progressive normobaric hypoxic exposure (2000-3000m simulated altitude) and 4-7 training sessions per week, followed by a one-week tapering period under normoxic conditions. Throughout this six-week period, subjects received either 25g KE (n=9) or an isocaloric placebo (CON; n=9) after each training session and 30 min pre-sleep. Experimental measurements were performed before (PRE), after (POST) LHTL, and after the taper (POST+7). Measurements included a 30-minute time trial (TT30), determination of VO2max, and hemoglobin mass. Furthermore, venous blood samples and muscle biopsies were obtained for determination of serum [EPO] and to assess skeletal muscle capillarization, as well as VEGF and HIF-1a protein content. RESULTS: In both groups, mean power output during TT30 improved by 9% alongside increases in VO2max (+8%) and absolute hemoglobin mass (+9%) from PRE to POST+7. EPO concentrations rose from ~4.2 mIU/mL at baseline to ~6.0 mIU/mL after 14 hours and remained above 5 mIU/mL during the entire intervention with significant increase at week 2 and POST. Ingestion of KE did not further improve any of these responses. Skeletal muscle capillarization, as well as vascular endothelial growth factor (VEGF) and hypoxia-inducible factor 1 alpha (HIF-1a), were neither impacted by LHTL nor by KE. CONCLUSION: These data indicate that post-exercise and pre-sleep KE ingestion does not provide beneficial effects on performance or physiological adaptations during a LHTL training program in recreational cyclists.
Read CV Wout LauriksECSS Paris 2023: OP-PN03