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Aims: We asked whether acclimatization to chronic hypoxia (CH) attenuates the level of supraspinal fatigue that is observed after locomotor exercise in acute hypoxia (AH)., Methods: Seven recreationally active participants performed identical bouts of constant-load cycling (131 ± 39 W, 10.1 ± 1.4 min) on three occasions: (i) in normoxia (N, PI O2 , 147.1 mmHg); (ii) in AH (FI O2 , 0.105; PI O2 , 73.8 mmHg); and (iii) after 14 days in CH (5260 m; PI O2 , 75.7 mmHg). Throughout trials, prefrontal-cortex tissue oxygenation and middle cerebral artery blood velocity (MCAV) were assessed using near-infrared-spectroscopy and transcranial Doppler sonography. Pre- and post-exercise twitch responses to femoral nerve stimulation and transcranial magnetic stimulation were obtained to assess neuromuscular and corticospinal function., Results: In AH, prefrontal oxygenation declined at rest (Δ7 ± 5%) and end-exercise (Δ26 ± 13%) (P < 0.01); the degree of deoxygenation in AH was greater than N and CH (P < 0.05). The cerebral O2 delivery index (MCAV × Ca O2 ) was 19 ± 14% lower during the final minute of exercise in AH compared to N (P = 0.013) and 20 ± 12% lower compared to CH (P = 0.040). Maximum voluntary and potentiated twitch force were decreased below baseline after exercise in AH and CH, but not N. Cortical voluntary activation decreased below baseline after exercise in AH (Δ11%, P = 0.014), but not CH (Δ6%, P = 0.174) or N (Δ4%, P = 0.298). A twofold greater increase in motor-evoked potential amplitude was evident after exercise in CH compared to AH and N., Conclusion: These data indicate that exacerbated supraspinal fatigue after exercise in AH is attenuated after 14 days of acclimatization to altitude. The reduced development of supraspinal fatigue in CH may have been attributable to increased corticospinal excitability, consequent to an increased cerebral O2 delivery., (© 2014 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)

Challenging environmental conditions, including heat and humidity, cold, and altitude, pose particular risks to the health of Olympic and other high-level athletes. As a further commitment to athlete safety, the International Olympic Committee (IOC) Medical Commission convened a panel of experts to review the scientific evidence base, reach consensus, and underscore practical safety guidelines and new research priorities regarding the unique environmental challenges Olympic and other international-level athletes face. For non-aquatic events, external thermal load is dependent on ambient temperature, humidity, wind speed and solar radiation, while clothing and protective gear can measurably increase thermal strain and prompt premature fatigue. In swimmers, body heat loss is the direct result of convection at a rate that is proportional to the effective water velocity around the swimmer and the temperature difference between the skin and the water. Other cold exposure and conditions, such as during Alpine skiing, biathlon and other sliding sports, facilitate body heat transfer to the environment, potentially leading to hypothermia and/or frostbite; although metabolic heat production during these activities usually increases well above the rate of body heat loss, and protective clothing and limited exposure time in certain events reduces these clinical risks as well. Most athletic events are held at altitudes that pose little to no health risks; and training exposures are typically brief and well-tolerated. While these and other environment-related threats to performance and safety can be lessened or averted by implementing a variety of individual and event preventative measures, more research and evidence-based guidelines and recommendations are needed. In the mean time, the IOC Medical Commission and International Sport Federations have implemented new guidelines and taken additional steps to mitigate risk even further.

Introduction: Baroreflex sensitivity (BRS) is essential to ensure rapid adjustment to variations in blood pressure (BP). Spontaneous baroreflex function can be assessed using continuous recordings of blood pressure. The goal of this study was to compare four methods for BRS quantification [the sequence, Bernardi's (BER), frequency and transfer function methods] to identify the most consistent method across an extreme range of conditions: rest and exercise, in normoxia, hypoxia, hypocapnia, and hypercapnia. Methods: Using intra-radial artery BP in young healthy participants, BRS was calculated and compared using the four methods in normoxia, acute and chronic hypoxia (terrestrial altitude of 5,260 m) in hypocapnia (hyperventilation), hypercapnia (rebreathing) and during ramp exercise to exhaustion. Results: The sequence and BER methods for BRS estimation showed good agreement during the resting and exercise protocols, whilst the ultra- and very-low frequency bands of the frequency and transfer function methods were more discrepant. Removing respiratory frequency from the blood pressure traces affected primarily the sequence and BER methods and occasionally the frequency and transfer function methods. Discussion/Conclusion: The sequence and BER methods contained more respiratory related information than the frequency and transfer function methods, indicating that the former two methods predominantly rely on respiratory effects of BRS. BER method is recommended because it is the easiest to compute and even though it tends to overestimate BRS compared to the sequence method, it is consistent with the other methods, whilst its interquartile range is the smallest. [ABSTRACT FROM AUTHOR]

The purpose of this study was to assess the effects of purified oxygenated water on exercise performance under hypoxic conditions. Nine recreational male cyclists (age = 26.6 ± 5.2 y, weight = 87.6 ± 19.5 kg, VO2peak = 46.5 ± 5.9 mL · kg-1 · min-1) completed two 600 kJ cycling time trials under hypoxic conditions (FIO2 = 13.6% O2, Pbar = 641 mmHg) separated by 2 wk. Trials were completed following 3 d ingestion of 35 mL · kg-1 · d-1 of control (CON) or experimental (EXP) water. Time to completion, heart rate (HR), rate of perceived exertion (RPE), pulse oximetry (SaO2), blood gases (PcO2 and PcCO2), and lactate were measured during the trials. Hydration was assessed with pre- and post-exercise body weight and 24-h urine specific gravity. Performance, hydration, and blood oxygenation were unaffected by EXP water. Results of this study suggest that purified oxygenated water does not improve exercise performance in moderately active males. [ABSTRACT FROM AUTHOR]

The development of muscle fatigue is oxygen (O2)-delivery sensitive [arterial O2 content (CaO2) × limb blood flow (QL)]. Locomotor exercise in acute hypoxia (AH) is, compared with sea level (SL), associated with reduced CaO2 and exaggerated inspiratory muscle work (Winsp), which impairs QL, both of which exacerbate fatigue individually by compromising O2 delivery. Since chronic hypoxia (CH) normalizes CaO2 but exacerbates Winsp, we investigated the consequences of a 14-day exposure to high altitude on exercise-induced locomotor muscle fatigue. Eight subjects performed the identical constant-load cycling exercise (138 ± 14 W; 11 ± 1 min) at SL (partial pressure of inspired O2, 147.1 ± 0.5 Torr), in AH (73.8 ± 0.2 Torr), and in CH (75.7 ± 0.1 Torr). Peripheral fatigue was expressed as pre- to postexercise percent reduction in electrically evoked potentiated quadriceps twitch force (ΔQtw,pot). Central fatigue was expressed as the exercise-induced percent decrease in voluntary muscle activation (ΔVA). Resting CaO2 at SL and CH was similar, but CaO2 in AH was lower compared with SL and CH (17.3 ± 0.5, 19.3 ± 0.7, 20.3 ± 1.3 ml O2/dl, respectively). Winsp during exercise increased with acclimatization (SL: 387 ± 36, AH: 503 ± 53, CH: 608 ± 67 cmH2O·s -1; P < 0.01). Exercise at SL did not induce central or peripheral fatigue. ΔQtw,pot was significant but similar in AH and CH (21 ± 2% and 19 ± 3%; P < 0.24). ΔVA was significant in both hypoxic conditions but smaller in CH vs. AH (4 ± 1% vs. 8 ± 2%; P < 0.05). In conclusion, acclimatization to severe altitude does not attenuate the substantial impact of hypoxia on the development of peripheral fatigue. In contrast, acclimatization attenuates, but does not eliminate, the exacerbation of central fatigue associated with exercise in severe AH. [ABSTRACT FROM AUTHOR]-1; P < 0.01). Exercise at SL did not induce central or peripheral fatigue. ΔQtw,pot was significant but similar in AH and CH (21 ± 2% and 19 ± 3%; P < 0.24). ΔVA was significant in both hypoxic conditions but smaller in CH vs. AH (4 ± 1% vs. 8 ± 2%; P < 0.05). In conclusion, acclimatization to severe altitude does not attenuate the substantial impact of hypoxia on the development of peripheral fatigue. In contrast, acclimatization attenuates, but does not eliminate, the exacerbation of central fatigue associated with exercise in severe AH. [ABSTRACT FROM AUTHOR]

Previous studies have suggested that a reduction in cerebral oxygen delivery may limit motor drive, particularly in hypoxic conditions, where oxygen transport is impaired. We hypothesized that raising end-tidal Pco2 (Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. during incremental exercise would increase cerebral blood flow (CBF) and oxygen delivery, thereby improving peak power output (Wpeak). Amateur cyclists performed two ramped exercise tests (25 W/min) in a counterbalanced order to compare the normal, poikilocapnic response against a clamped condition, in which Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. was held at Tort throughout exercise. Tests were performed in normoxia (barometric pressure = 630 mmHg, 1,650 m) and hypoxia (barometric pressure = 425 mmHg, 4,875 m) in a hypobaric chamber. An additional trial in hypoxia investigated effects of clamping at a lower Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. 40 Torr) from ~75 to 100% Wpeak to reduce potential influences of respiratory acidosis and muscle fatigue imposed by clamping Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. at 50 Torr. Metabolic gases, ventilation, middle cerebral artery CBF velocity (transcranial Doppler), forehead pulse oximetry, and cerebral (prefrontal) and muscle (vastus lateralis) hemoglobin oxygenation (near infrared spectroscopy) were monitored across trials. Clamping Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. at 50 Torr in both normoxia (n = 9) and hypoxia (n = 11) elevated CBF velocity (~40%) and improved cerebral hemoglobin oxygenation (~15%), but decreased Wpeak (6%) and peak oxygen consumption (11%). Clamping at 40 Ton. near maximal effort in hypoxia (n = 6) also improved cerebral oxygenation (~15%), but again limited Wpeak (5%). These findings demonstrate that increasing mass cerebral oxygen delivery via CO2-mediated vasodilation does not improve incremental exercise performance, at least when accompanied by respiratory acidosis. [ABSTRACT FROM AUTHOR]

Previous attempts to detect global cerebral hemodynamic differences between those who develop headache, nausea, and fatigue following rapid exposure to hypoxia [acute mountain sickness (AMS)] and those who remain healthy have been inconclusive. In this study, we investigated the effects of two drugs known to reduce symptoms of AMS to determine if a common cerebral hemodynamic mechanism could explain the prophylactic effect within individuals. With the use of randomized, placebo-controlled, double-blind, crossover design, 20 healthy volunteers were given oral acetazolamide (250 mg), dexamethasone (4 mg), or placebo every 8 h for 24 h prior to and during a 10-h exposure to a simulated altitude of 4,875 m in a hypobaric chamber, which included 2 h of exercise at 50% of altitude-specific V̇o2max. Cerebral hemodynamic parameters derived from ultrasound assessments of dynamic cerebral autoregulation and vasomotor reactivity were recorded 15 h prior to and after 9 h of hypoxia. AMS symptoms were scored using the Lake Louise Questionnaire (LLQ). It was found that both drugs prevented AMS in those who became ill on placebo (~70% decrease in LLQ), yet a common cerebral hemodynamic mechanism was not identified. Compared with placebo, acetazolamide reduced middle cerebral artery blood flow velocity (11%) and improved dynamic cerebral autoregulation after 9 h of hypoxia, but these effects appeared independent of AMS. Dexamethasone had no measureable cerebral hemodynamic effects in hypoxia. In conclusion, global cerebral hemodynamic changes resulting from hypoxia may not explain the development of AMS. [ABSTRACT FROM AUTHOR]

We investigated the effect of acute hypoxia (AH) on dynamic cerebral autoregulation (CA) using two independent assessment techniques to clarify previous, conflicting reports. Twelve healthy volunteers (6 men, 6 women) performed six classic leg cuff tests, three breathing normoxic (FlO2 = 0.21) and three breathing hypoxic (Fl02 = 0.12) gas, using a single blinded, Latin squares design with 5-mm washout between trials. Continuous measurements of middle cerebral artery blood flow velocity (CBFv; DWL MultiDop X2) and radial artery blood pressure (ABP; Cohn 7000) were recorded in the supine position during a single experimental session. Autoregulation index (ARI) scores were calculated using the model of Tiecks et al. (Tiecks FP, Lam AM, Aashid R, Newell DW. Stroke 26: 1014-1019, 1995) from ABP and CBFv changes following rapid cuff deflation (cuff ARI) and from ABP to CBFv transfer function, impulse, and step responses (TFA ARI) obtained during a 4-mm period prior to cuff inflation. A new measure of %CBFv recovery 4 s after peak impulse was also derived from TFA. AH reduced cuff ARI (5.65 ± 0.70 to 5.01 ± 0.96, P = 0.04), TFA ARI (4.37 ± 0.76 to 3.73 ± 0.71, P 0.04), and %Recovery (62.2 ± 10.9% to 50.8 ± 9.9%, P = 0.03). Slight differences between TFA and cuff ARI values may be attributed to heightened sympathetic activity during cuff tests as well as differential sensitivity to lowand high-frequency components of CA. Together, results provide consistent evidence that CA is impaired with AH. In addition, these findings demonstrate the potential utility of TFA ARI and %Recovery scores for future CA investigations. [ABSTRACT FROM AUTHOR]

Reductions in prefrontal oxygenation near maximal exertion may limit exercise performance by impairing executive functions that influence the decision to stop exercising; however, whether deoxygenation also occurs in motor regions that more directly affect central motor drive is unknown. Multichannel near-infrared spectroscopy was used to compare changes in prefrontal, premotor, and motor cortices during exhaustive exercise. Twenty-three subjects performed two sequential, incremental cycle tests (25 W/min ramp) during acute hypoxia [79 Torr inspired Po2 (PIO2)] and normoxia (117 Torr PIO2) in an environmental chamber. Test order was balanced, and subjects were blinded to chamber pressure. In normoxia, bilateral prefrontal oxygenation was maintained during low- and moderate-intensity exercise but dropped 9.0 ± 10.7% (mean ± SD, P < 0.05) before exhaustion (maximal power = 305 ± 52 W). The pattern and magnitude of deoxygenation were similar in prefrontal, premotor, and motor regions (R² > 0.94). In hypoxia, prefrontal oxygenation was reduced 11.1 ± 14.3% at rest (P < 0.01) and fell another 26.5 ± 19.5% (P < 0.01) at exhaustion (maximal power = 256 ± 38 W, P < 0.01). Correlations between regions were high (R² > 0.61), but deoxygenation was greater in prefrontal than premotor and motor regions (P < 0.05). Prefrontal, premotor, and motor cortex deoxygenation during high-intensity exercise may contribute to an integrative decision to stop exercise. The accelerated rate of cortical deoxygenation in hypoxia may hasten this effect. [ABSTRACT FROM AUTHOR]

We sought to describe cerebrovascular responses to incremental exercise and test the hypothesis that changes in cerebral oxygenation influence maximal performance. Eleven men cycled in three conditions: 1) sea level (SL); 2) acute hypoxia [AH; hypobaric chamber, inspired Po2 (PIO2) 86 Torr]; and 3) chronic hypoxia [CH; 4,300 m, PIO2 86 Torr]. At maximal work rate (Wmax), fraction of inspired oxygen (FIo2) was surreptitiously increased to 0.60, while subjects were encouraged to continue pedaling. Changes in cerebral (frontal lobe) (Cox) and muscle (vastus lateralis) oxygenation (Mox) (near infrared spectroscopy), middle cerebral artery blood flow velocity (MCA Vmean; transcranial Doppler), and end-tidal Pco2 (PETco2) were analyzed across %Wmax (significance at P < 0.05). At SL, PETco2, MCA Vmean, and Cox fell as work rate rose from 75 to 100% Wmax. During AH, PETco2 and MCA Vmean declined from 50 to 100% Wmax, while Cox fell from rest. With CH, PETCO2 and Cox dropped throughout exercise, while MCA Vmean fell only from 75 to 100% Wmax. Mox fell from rest to 75% Wmax at SL and AH and throughout exercise in CH. The magnitude of fall in Cox, but not Mox, was different between conditions (CH > AH > SL). FIo2 0.60 at Wmax did not prolong exercise at SL, yet allowed subjects to continue for 96 ± 61 s in AH and 162 ± 90 s in CH. During Fio2 0.60, Cox rose and Mox remained constant as work rate increased. Thus cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia (PIo2 86 Torn), since its reversal was associated with improved performance. [ABSTRACT FROM AUTHOR]

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% FIO2) and acute hypoxic (Hypox: 12% FIO2) conditions. Near-infrared spectroscopy (NIRS) was used to monitor concentration (μM) changes of oxy- and deoxyhemoglobin (Δ[O2Hb], Δ[HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated (Δ[THb] = Δ[O2Hb] + Δ[HHb]) and used as an index of change in regional blood volume. Repeated-measures ANOVA were performed across treatments and work rates (α = 0.05). During Norm, cerebral oxygenation rose between 25 and 75% peak power output {Powerpeak; increased (inc) Δ[O2Hb], inc. Δ[HHb], inc. Δ[THb]}, but fell from 75 to 100% Powerpeak {decreased (dec) Δ[O2Hb], inc. Δ[HHb], no change Δ[THb]}. In contrast, during Hypox, cerebral oxygenation dropped progressively across all work rates (dec. Δ[O2Hb], inc. Δ[HHb]), whereas Δ[THb] again rose up to 75% Powerpeak 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. Δ[O2Hb], inc. Δ [HHbJ, inc. Δ[THb]), although Δ[O2Hb] was unchanged between 75 and 100% Powerpeak. 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. [ABSTRACT FROM AUTHOR]

Background: High altitude is a challenging condition caused by insufficient oxygen supply. Inability to adjust to hypoxia may lead to pulmonary edema, stroke, cardiovascular dysfunction, and even death. Thus, understanding the molecular basis of adaptation to high altitude may reveal novel therapeutics to counteract the detrimental consequences of hypoxia.Methods: Using high-throughput, unbiased metabolomic profiling, we report that the metabolic pathway responsible for production of erythrocyte 2,3-bisphosphoglycerate (2,3-BPG), a negative allosteric regulator of hemoglobin-O2 binding affinity, was significantly induced in 21 healthy humans within 2 hours of arrival at 5260 m and further increased after 16 days at 5260 m.Results: This finding led us to discover that plasma adenosine concentrations and soluble CD73 activity rapidly increased at high altitude and were associated with elevated erythrocyte 2,3-BPG levels and O2 releasing capacity. Mouse genetic studies demonstrated that elevated CD73 contributed to hypoxia-induced adenosine accumulation and that elevated adenosine-mediated erythrocyte A2B adenosine receptor activation was beneficial by inducing 2,3-BPG production and triggering O2 release to prevent multiple tissue hypoxia, inflammation, and pulmonary vascular leakage. Mechanistically, we demonstrated that erythrocyte AMP-activated protein kinase was activated in humans at high altitude and that AMP-activated protein kinase is a key protein functioning downstream of the A2B adenosine receptor, phosphorylating and activating BPG mutase and thus inducing 2,3-BPG production and O2 release from erythrocytes. Significantly, preclinical studies demonstrated that activation of AMP-activated protein kinase enhanced BPG mutase activation, 2,3-BPG production, and O2 release capacity in CD73-deficient mice, in erythrocyte-specific A2B adenosine receptor knockouts, and in wild-type mice and in turn reduced tissue hypoxia and inflammation.Conclusions: Together, human and mouse studies reveal novel mechanisms of hypoxia adaptation and potential therapeutic approaches for counteracting hypoxia-induced tissue damage. [ABSTRACT FROM AUTHOR]