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Ray, A. D., A. J. Roberts, S. D. Lee, G. A. Farkas, C. Michlin, D. I. Rifkin, P. T. Ostrow y J. A. Krasney. "Exercise delays the hypoxic thermal response in rats". Journal of Applied Physiology 95, n.º 1 (julio de 2003): 272–78. http://dx.doi.org/10.1152/japplphysiol.00057.2003.
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Exercise exacerbates acute mountain sickness. In infants and small mammals, hypoxia elicits a decrease in body temperature (Tb) [hypoxic thermal response (HTR)], which may protect against hypoxic tissue damage. We postulated that exercise would counteract the HTR and promote hypoxic tissue damage. Tb was measured by telemetry in rats ( n = 28) exercising or sedentary in either normoxia or hypoxia (10% O2, 24 h) at 25°C ambient temperature (Ta). After 24 h of normoxia, rats walked at 10 m/min on a treadmill (30 min exercise, 30 min rest) for 6 h followed by 18 h of rest in either hypoxia or normoxia. Exercising normoxic rats increased Tb (°C) vs. baseline (39.68 ± 0.99 vs. 38.90 ± 0.95, mean ± SD, P < 0.05) and vs. sedentary normoxic rats (38.0 ± 0.09, P < 0.05). Sedentary hypoxic rats decreased Tb (36.15 ± 0.97 vs. 38.0 ± 0.36, P < 0.05) whereas Tb was maintained in the exercising hypoxic rats during the initial 6 h of exercise (37.61 ± 0.55 vs. 37.72 ± 1.25, not significant). After exercise, Tb in hypoxic rats reached a nadir similar to that in sedentary hypoxic rats (35.05 ± 1.69 vs. 35.03 ± 1.32, respectively). Tb reached its nadir significantly later in exercising hypoxic vs. sedentary hypoxic rats (10.51 ± 1.61 vs. 5.36 ± 1.83 h, respectively; P = 0.002). Significantly greater histopathological damage and water contents were observed in brain and lungs in the exercising hypoxic vs. sedentary hypoxic and normoxic rats. Thus exercise early in hypoxia delays but does not prevent the HTR. Counteracting the HTR early in hypoxia by exercise exacerbates brain and lung damage and edema in the absence of ischemia.
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Katayama, Keisho, Yasutake Sato, Yoshifumi Morotome, Norihiro Shima, Koji Ishida, Shigeo Mori y Miharu Miyamura. "Intermittent hypoxia increases ventilation and SaO2 during hypoxic exercise and hypoxic chemosensitivity". Journal of Applied Physiology 90, n.º 4 (1 de abril de 2001): 1431–40. http://dx.doi.org/10.1152/jappl.2001.90.4.1431.
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The purpose of this study was 1) to test the hypothesis that ventilation and arterial oxygen saturation (SaO2 ) during acute hypoxia may increase during intermittent hypoxia and remain elevated for a week without hypoxic exposure and 2) to clarify whether the changes in ventilation and SaO2 during hypoxic exercise are correlated with the change in hypoxic chemosensitivity. Six subjects were exposed to a simulated altitude of 4,500 m altitude for 7 days (1 h/day). Oxygen uptake (V˙o 2), expired minute ventilation (V˙e), and SaO2 were measured during maximal and submaximal exercise at 432 Torr before (Pre), after intermittent hypoxia (Post), and again after a week at sea level (De). Hypoxic ventilatory response (HVR) was also determined. At both Post and De, significant increases from Pre were found in HVR at rest and in ventilatory equivalent for O2(V˙e/V˙o 2) and SaO2 during submaximal exercise. There were significant correlations among the changes in HVR at rest and inV˙e/V˙o 2 and SaO2 during hypoxic exercise during intermittent hypoxia. We conclude that 1 wk of daily exposure to 1 h of hypoxia significantly improved oxygenation in exercise during subsequent acute hypoxic exposures up to 1 wk after the conditioning, presumably caused by the enhanced hypoxic ventilatory chemosensitivity.
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Ağaşcioğlu, Eda ,., Ridvan Çolak, Mehmet Can Atayik, Ahmet Çevik Tufan y Ufuk Çakatay. "Hypoxia and Hypoxic Exercise Induced Systemic Ros Disrupts the Redox Homeostasis in the Brain". Pakistan Journal of Medical and Health Sciences 16, n.º 1 (30 de enero de 2022): 397–402. http://dx.doi.org/10.53350/pjmhs22161397.
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Aim: We aimed to investigate the overall effects of hypoxic/normoxic exercise and hypoxia on redox status in both systemic circulation and brain, and to prove whether the variations in plasma redox status could affect the brain’s own redox homeostasis, vice versa. Methods: We designed hypoxic, normoxic exercise groups with their respective controls. We studied on redox status biomarkers i.e., hydroperoxide, low molecular weight thiols, protein thiols, total thiols, and advanced oxidation protein products in frontal cortex; total antioxidant and total oxidant status in the plasma. Results: There is no statistically significant difference observed in redox homeostasis of the brain after hypoxic and/or normoxic exercise or hypoxia itself with an increased systemic oxidant status. Conclusions: Live in hypoxia and exercise at normoxia might diminish the hazardous effect of ROS on the brain at hypoxia. From our findings, thiols, which are the indicators of the antioxidant power of the brain, are found to be protected in groups that are exposed to long-term hypoxia and exercise at normoxia. It might be possible that people who are exposed to hypoxia will be least affected by this damage with normoxic exercise, or even will not be affected at all. Keywords: Hypoxic exercise, Redox homeostasis, Brain, Plasma
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Wilkins, Brad W., William G. Schrage, Zhong Liu, Kellie C. Hancock y Michael J. Joyner. "Systemic hypoxia and vasoconstrictor responsiveness in exercising human muscle". Journal of Applied Physiology 101, n.º 5 (noviembre de 2006): 1343–50. http://dx.doi.org/10.1152/japplphysiol.00487.2006.
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Exercise blunts sympathetic α-adrenergic vasoconstriction (functional sympatholysis). We hypothesized that sympatholysis would be augmented during hypoxic exercise compared with exercise alone. Fourteen subjects were monitored with ECG and pulse oximetry. Brachial artery and antecubital vein catheters were placed in the nondominant (exercising) arm. Subjects breathed hypoxic gas to titrate arterial O2 saturation to 80% while remaining normocapnic via a rebreath system. Baseline and two 8-min bouts of rhythmic forearm exercise (10 and 20% of maximum) were performed during normoxia and hypoxia. Forearm blood flow, blood pressure, heart rate, minute ventilation, and end-tidal CO2 were measured at rest and during exercise. Vasoconstrictor responsiveness was determined by responses to intra-arterial tyramine during the final 3 min of rest and each exercise bout. Heart rate was higher during hypoxia ( P < 0.01), whereas blood pressure was similar ( P = 0.84). Hypoxic exercise potentiated minute ventilation compared with normoxic exercise ( P < 0.01). Forearm blood flow was higher during hypoxia compared with normoxia at rest (85 ± 9 vs. 66 ± 7 ml/min), at 10% exercise (276 ± 33 vs. 217 ± 27 ml/min), and at 20% exercise (464 ± 32 vs. 386 ± 28 ml/min; P < 0.01). Arterial epinephrine was higher during hypoxia ( P < 0.01); however, venoarterial norepinephrine difference was similar between hypoxia and normoxia before ( P = 0.47) and during tyramine administration ( P = 0.14). Vasoconstriction to tyramine (%decrease from pretyramine values) was blunted in a dose-dependent manner with increasing exercise intensity ( P < 0.01). Interestingly, vasoconstrictor responsiveness tended to be greater ( P = 0.06) at rest (−37 ± 6% vs. −33 ± 6%), at 10% exercise (−27 ± 5 vs. −22 ± 4%), and at 20% exercise (−22 ± 5 vs. −14 ± 4%) between hypoxia and normoxia, respectively. Thus sympatholysis is not augmented by moderate hypoxia nor does it contribute to the increased blood flow during hypoxic exercise.
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Ainslie, Philip N., Alice Barach, Carissa Murrell, Mike Hamlin, John Hellemans y Shigehiko Ogoh. "Alterations in cerebral autoregulation and cerebral blood flow velocity during acute hypoxia: rest and exercise". American Journal of Physiology-Heart and Circulatory Physiology 292, n.º 2 (febrero de 2007): H976—H983. http://dx.doi.org/10.1152/ajpheart.00639.2006.
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We examined the relationship between changes in cardiorespiratory and cerebrovascular function in 14 healthy volunteers with and without hypoxia [arterial O2 saturation (SaO2) ∼80%] at rest and during 60–70% maximal oxygen uptake steady-state cycling exercise. During all procedures, ventilation, end-tidal gases, heart rate (HR), arterial blood pressure (BP; Finometer) cardiac output (Modelflow), muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasound) were measured continuously. The effect of hypoxia on dynamic cerebral autoregulation was assessed with transfer function gain and phase shift in mean BP and MCAV. At rest, hypoxia resulted in increases in ventilation, progressive hypocapnia, and general sympathoexcitation (i.e., elevated HR and cardiac output); these responses were more marked during hypoxic exercise ( P < 0.05 vs. rest) and were also reflected in elevation of the slopes of the linear regressions of ventilation, HR, and cardiac output with SaO2 ( P < 0.05 vs. rest). MCAV was maintained during hypoxic exercise, despite marked hypocapnia (44.1 ± 2.9 to 36.3 ± 4.2 Torr; P < 0.05). Conversely, hypoxia both at rest and during exercise decreased cerebral oxygenation compared with muscle. The low-frequency phase between MCAV and mean BP was lowered during hypoxic exercise, indicating impairment in cerebral autoregulation. These data indicate that increases in cerebral neurogenic activity and/or sympathoexcitation during hypoxic exercise can potentially outbalance the hypocapnia-induced lowering of MCAV. Despite maintaining MCAV, such hypoxic exercise can potentially compromise cerebral autoregulation and oxygenation.
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Zerbini, Livio, Alfredo Brighenti, Barbara Pellegrini, Lorenzo Bortolan, Tommaso Antonetti y Federico Schena. "Effects of acute hypoxia on the oxygen uptake kinetics of older adults during cycling exercise". Applied Physiology, Nutrition, and Metabolism 37, n.º 4 (agosto de 2012): 744–52. http://dx.doi.org/10.1139/h2012-048.
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Pulmonary oxygen uptake, heart rate (HR), and deoxyhemoglobin (HHb) kinetics were studied in a group of older adults exercising in hypoxic conditions. Fourteen healthy older adults (aged 66 ± 6 years) performed 4 exercise sessions that consisted of (i) an incremental test to exhaustion on a cycloergometer while breathing normoxic room air (fractional inspired oxygen (FiO2) = 20.9% O2); (ii) an incremental test to exhaustion on a cycloergometer while breathing hypoxic room air (FiO2 = 15% O2); (iii) 3 repeated square wave cycling exercises at moderate intensity while breathing normoxic room air; and (iv) 3 repeated square wave cycling exercises at moderate intensity while breathing hypoxic room air. During all exercise sessions, pulmonary gas exchange was measured breath-by-breath; HHb was determined on the vastus lateralis muscle by near-infrared spectroscopy; and HR was collected beat-by-beat. The pulomary oxygen uptake kinetics became slower in hypoxia (31 ± 9 s) than in normoxia (27 ± 7 s) because of an increased mismatching between O2 delivery to O2 utilization at the level of the muscle. The HR and HHb kinetics did not change between hypoxia and normoxia,
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Fregosi, R. F. y D. R. Seals. "Hypoxic potentiation of the ventilatory response to dynamic forearm exercise". Journal of Applied Physiology 74, n.º 5 (1 de mayo de 1993): 2365–72. http://dx.doi.org/10.1152/jappl.1993.74.5.2365.
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The slope of the relationship between ventilation (VI) and O2 consumption, as derived in progressive-intensity exercise tests, is increased markedly by systemic hypoxia. The mechanisms underlying the hypoxic potentiation of the ventilatory response to exercise have not been established, partly because several factors that can increase respiratory drive (e.g., metabolic rate, cardiac output, circulating catecholamine levels) change significantly and simultaneously under these conditions. In an effort to avoid these confounding changes, we sought to determine whether hypoxia potentiates the ventilatory response to dynamic forearm exercise in humans. Forearm exercise increased the O2 consumption by only 80–90 ml/min; nevertheless, hypoxia resulted in a significant potentiation of VI that was mediated by a marked increase in breathing frequency. These observations led us to hypothesize that the hypoxic potentiation of VI is due to an exaggerated stimulation of chemosensitive afferent nerve endings within the exercising muscles ("muscle chemoreceptors"). We tested this hypothesis in separate experiments under conditions of forearm ischemia so that the stimulus to the muscle chemoreceptors in normoxic and hypoxic exercise would be the same. The magnitude of the change in VI evoked by hypoxic ischemic exercise was significantly greater than the sum of the separate changes evoked by normoxic ischemic exercise and hypoxic ischemic rest. We conclude that the combination of dynamic forearm exercise and hypoxia potentiates VI and that this effect is mediated by neural structures that govern respiratory frequency. Moreover the potentiated ventilatory response cannot be attributed to an exaggerated stimulation of intramuscular chemoreceptors.
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Rupp, Thomas, Marc Jubeau, Guillaume Y. Millet, Stéphane Perrey, François Esteve, Bernard Wuyam, Patrick Levy y Samuel Verges. "The effect of hypoxemia and exercise on acute mountain sickness symptoms". Journal of Applied Physiology 114, n.º 2 (15 de enero de 2013): 180–85. http://dx.doi.org/10.1152/japplphysiol.00769.2012.
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Performing exercise during the first hours of hypoxic exposure is thought to exacerbate acute mountain sickness (AMS), but whether this is due to increased hypoxemia or other mechanisms associated with exercise remains unclear. In 12 healthy men, AMS symptoms were assessed during three 11-h experimental sessions: 1) in Hypoxia-exercise, inspiratory O2 fraction (FiO2) was 0.12, and subjects performed 4-h cycling at 45% FiO2-specific maximal power output from the 4th to the 8th hour; 2) in Hypoxia-rest, FiO2 was continuously adjusted to match the same arterial oxygen saturation as in Hypoxia-exercise, and subjects remained at rest; and 3) in Normoxia-exercise, FiO2 was 0.21, and subjects cycled as in Hypoxia-exercise at 45% FiO2-specific maximal power output. AMS scores did not differ significantly between Hypoxia-exercise and Hypoxia-rest, while they were significantly lower in Normoxia-exercise (Lake Louise score: 5.5 ± 2.1, 4.4 ± 2.4, and 2.3 ± 1.5, and cerebral Environmental Symptom Questionnaire: 1.2 ± 0.7, 1.0 ± 1.0, and 0.3 ± 0.4, in Hypoxia-exercise, Hypoxia-rest, and Normoxia-exercise, respectively; P < 0.01). Headache scored by visual analog scale was higher in Hypoxia-exercise and Hypoxia-rest compared with Normoxia-exercise (36 ± 22, 35 ± 25, and 5 ± 6, P < 0.001), while the perception of fatigue was higher in Hypoxia-exercise compared with Hypoxia-rest (60 ± 24, 32 ± 22, and 46 ± 23, in Hypoxia-exercise, Hypoxia-rest, and Normoxia-exercise, respectively; P < 0.01). Despite significant physiological stress during hypoxic exercise and some AMS symptoms induced by normoxic cycling at similar relative workload, exercise does not significantly worsen AMS severity during the first hours of hypoxic exposure at a given arterial oxygen desaturation. Hypoxemia per se appears, therefore, to be the main mechanism underlying AMS, whether or not exercise is performed.
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McGinnis, Graham, Brian Kliszczewiscz, Matthew Barberio, Christopher Ballmann, Bridget Peters, Dustin Slivka, Charles Dumke et al. "Acute Hypoxia and Exercise-Induced Blood Oxidative Stress". International Journal of Sport Nutrition and Exercise Metabolism 24, n.º 6 (diciembre de 2014): 684–93. http://dx.doi.org/10.1123/ijsnem.2013-0188.
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Hypoxic exercise is characterized by workloads decrements. Because exercise and high altitude independently elicit redox perturbations, the study purpose was to examine hypoxic and normoxic steady-state exercise on blood oxidative stress. Active males (n = 11) completed graded cycle ergometry in normoxic (975 m) and hypoxic (3,000 m) simulated environments before programing subsequent matched intensity or workload steady-state trials. In a randomized counterbalanced crossover design, participants completed three 60-min exercise bouts to investigate the effects of hypoxia and exercise intensity on blood oxidative stress. Exercise conditions were paired as such; 60% normoxic VO2peak performed in a normoxic environment (normoxic intensity-normoxic environment, NI-NE), 60% hypoxic VO2peak performed in a normoxic environment (HI-NE), and 60% hypoxic VO2peak performed in a hypoxic environment (HI-HE). Blood plasma samples drawn pre (Pre), 0 (Post), 2 (2HR) and 4 (4HR) hr post exercise were analyzed for oxidative stress biomarkers including ferric reducing ability of plasma (FRAP), trolox equivalent antioxidant capacity (TEAC), lipid hydroperoxides (LOOH) and protein carbonyls (PCs). Repeated-measures ANOVA were performed, a priori significance of p ≤ .05. Oxygen saturation during the HI-HE trial was lower than NI-NE and HI-NE (p < .05). A Time × Trial interaction was present for LOOH (p = .013). In the HI-HE trial, LOOH were elevated for all time points post while PC (time; p = .001) decreased post exercise. As evidenced by the decrease in absolute workload during hypoxic VO2peak and LOOH increased during HI-HE versus normoxic exercise of equal absolute (HI-NE) and relative (NI-NE) intensities. Results suggest acute hypoxia elicits work decrements associated with post exercise oxidative stress.
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Wang, Jong-Shyan, Min-Huan Wu, Tso-Yen Mao, Tieh-cheng Fu y Chih-Chin Hsu. "Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans". Journal of Applied Physiology 109, n.º 1 (julio de 2010): 219–29. http://dx.doi.org/10.1152/japplphysiol.00138.2010.
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Hypoxic preconditioning prevents cerebrovascular/cardiovascular disorders by increasing resistance to acute ischemic stress, but severe hypoxic exposure disturbs vascular hemodynamics. This study compared how various exercise regimens with/without hypoxia affect hemodynamics and oxygenation in cardiac, muscle, and cerebral tissues during severe hypoxic exposure. Sixty sedentary males were randomly divided into five groups. Each group ( n = 12) received one of five interventions: 1) normoxic (21% O2) resting control, 2) hypoxic (15% O2) resting control, 3) normoxic exercise (50% maximum work rate under 21% O2; N-E group), 4) hypoxic-relative exercise (50% maximal heart rate reserve under 15% O2; H-RE group), or 5) hypoxic-absolute exercise (50% maximum work rate under 15% O2; H-AE group) for 30 min/day, 5 days/wk, for 4 wk. A recently developed noninvasive bioreactance device was used to measure cardiac hemodynamics, and near-infrared spectroscopy was used to assess perfusion and oxygenation in the vastus lateralis (VL)/gastrocnemius (GN) muscles and frontal cerebral lobe (FC). Our results demonstrated that the H-AE group had a larger improvement in aerobic capacity compared with the N-E group. Both H-RE and H-AE ameliorated the suppression of cardiac stroke volume and the GN hyperemic response (Δtotal Hb/min) and reoxygenation rate by acute 12% O2 exposure. Simultaneously, the two hypoxic interventions enhanced perfusion (Δtotal Hb) and O2 extraction [ΔdeoxyHb] of the VL muscle during the 12% O2 exercise. Although acute 12% O2 exercise decreased oxygenation (ΔO2Hb) of the FC, none of the 4-wk interventions influenced the cerebral perfusion and oxygenation during normoxic/hypoxic exercise tests. Therefore, we conclude that moderate hypoxic exercise training improves cardiopulmonary fitness and increases resistance to disturbance of cardiac hemodynamics by severe hypoxia, concurrence with enhancing O2 delivery/utilization in skeletal muscles but not cerebral tissues.
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Georges, Thomas, Pierre Menu, Camille Le Blanc, Sophie Ferreol, Marc Dauty y Alban Fouasson-Chailloux. "Contribution of Hypoxic Exercise Testing to Predict High-Altitude Pathology: A Systematic Review". Life 12, n.º 3 (5 de marzo de 2022): 377. http://dx.doi.org/10.3390/life12030377.
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Altitude travelers are exposed to high-altitude pathologies, which can be potentially serious. Individual susceptibility varies widely and this makes it difficult to predict who will develop these complications. The assessment of physiological adaptations to exercise performed in hypoxia has been proposed to help predict altitude sickness. The purpose of this review is to evaluate the contribution of hypoxic exercise testing, achieved in normobaric conditions, in the prediction of severe high-altitude pathology. We performed a systematic review using the databases PubMed, Science Direct and Embase in October 2021 to collect studies reporting physiological adaptations under hypoxic exercise testing and its interest in predicting high-altitude pathology. Eight studies were eligible, concerning 3558 patients with a mean age of 46.9 years old, and a simulated mean altitude reaching of 5092 m. 597 patients presented an acute mountain sickness during their altitude travels. Three different protocols of hypoxic exercise testing were used. Acute mountain sickness was defined using Hackett’s score or the Lake Louise score. Ventilatory and cardiac responses to hypoxia, desaturation in hypoxia, cerebral oxygenation, core temperature, variation in body mass index and some perceived sensations were the highlighted variables associated with acute mountain sickness. A decision algorithm based on hypoxic exercise tests was proposed by one team. Hypoxic exercise testing provides promising information to help predict altitude complications. Its interest should be confirmed by different teams.
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Montero, David y Carsten Lundby. "No Improved Performance With Repeated-Sprint Training in Hypoxia Versus Normoxia: A Double-Blind and Crossover Study". International Journal of Sports Physiology and Performance 12, n.º 2 (febrero de 2017): 161–67. http://dx.doi.org/10.1123/ijspp.2015-0691.
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Context:Few recent studies indicate that short-term repeated-sprint (RS) training in hypoxia (RSH) improves RS performance compared with identical training under normoxic conditions (RSN) in endurance-trained subjects.Purpose:To determine the effects of RSH against RSN on RS performance under normoxic and moderate hypoxic conditions, using a randomized, doubleblind, crossover experimental design.Methods:Fifteen endurance-trained male subjects (age 25 ± 4 y) performed 4 wk of RS training (3 sessions/wk) in normobaric hypoxia (RSH, FiO2 = 13.8%) and normoxia (RSN, FiO2 = 20.9%) in a crossover manner. Before and after completion of training, RS tests were performed on a cycle ergometer with no prior exercise (RSNE), after an incremental exercise test (RSIE), and after a time-trial test (RSTT) in normoxia and hypoxia.Results:Peak power outputs at the incremental exercise test and time-trial performance were unaltered by RSH in normoxia and hypoxia. RS performance was generally enhanced by RSH, as well as RSN, but there were no additional effects of RSH over RSN on peak and mean sprint power output and the number of repeated sprints performed in the RSNE, RSIE, and RSTT trials under normoxic and hypoxic conditions.Conclusions:The present double-blind crossover study indicates that RSH does not improve RS performance compared with RSN in normoxic and hypoxic conditions in endurance-trained subjects. Therefore, caution should be exercised when proposing RSH as an advantageous method to improve exercise performance.
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Kammerer, Tobias, Valentina Faihs, Nikolai Hulde, Manfred Stangl, Florian Brettner, Markus Rehm, Mareike Horstmann et al. "Hypoxic-Inflammatory Responses under Acute Hypoxia: In Vitro Experiments and Prospective Observational Expedition Trial". International Journal of Molecular Sciences 21, n.º 3 (4 de febrero de 2020): 1034. http://dx.doi.org/10.3390/ijms21031034.
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Induction of hypoxia-inducible-factor-1α (HIF-1α) pathway and HIF-target genes allow adaptation to hypoxia and are associated with reduced incidence of acute mountain sickness (AMS). Little is known about HIF-pathways in conjunction with inflammation or exercise stimuli under acute hypobaric hypoxia in non-acclimatized individuals. We therefore tested the hypotheses that (1) both hypoxic and inflammatory stimuli induce hypoxic-inflammatory signaling pathways in vitro, (2) similar results are seen in vivo under hypobaric hypoxia, and (3) induction of HIF-dependent genes is associated with AMS in 11 volunteers. In vitro, peripheral blood mononuclear cells (PBMCs) were incubated under hypoxic (10%/5% O2) or inflammatory (CD3/CD28) conditions. In vivo, Interleukin 1β (IL-1β), C-X-C Chemokine receptor type 4 (CXCR-4), and C-C Chemokine receptor type 2 (CCR-2) mRNA expression, cytokines and receptors were analyzed under normoxia (520 m above sea level (a.s.l.)), hypobaric hypoxia (3883 m a.s.l.) before/after exercise, and after 24 h under hypobaric hypoxia. In vitro, isolated hypoxic (p = 0.004) or inflammatory (p = 0.006) stimuli induced IL-1β mRNA expression. CCR-2 mRNA expression increased under hypoxia (p = 0.005); CXCR-4 mRNA expression remained unchanged. In vivo, cytokines, receptors, and IL-1β, CCR-2 and CXCR-4 mRNA expression increased under hypobaric hypoxia after 24 h (all p ≤ 0.05). Of note, proinflammatory IL-1β and CXCR-4 mRNA expression changes were associated with symptoms of AMS. Thus, hypoxic-inflammatory pathways are differentially regulated, as combined hypoxic and exercise stimulus was stronger in vivo than isolated hypoxic or inflammatory stimulation in vitro.
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Katayama, Keisho, Shin Yamashita, Koji Ishida, Erika Iwamoto, Teruhiko Koike y Mitsuru Saito. "Hypoxic effects on sympathetic vasomotor outflow and blood pressure during exercise with inspiratory resistance". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, n.º 5 (1 de marzo de 2013): R374—R382. http://dx.doi.org/10.1152/ajpregu.00489.2012.
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The purpose of the present study was to clarify the influence of inspiratory resistive breathing during exercise under hypoxic conditions on muscle sympathetic nerve activity (MSNA) and blood pressure (BP). Six healthy males completed this study. The subjects performed a submaximal exercise test using a cycle ergometer in a semirecumbent position under normoxic [inspired oxygen fraction (FiO2) = 0.21] and hypoxic (FiO2 = 0.12–0.13) conditions. The subjects carried out two 10-min exercises at 40% peak oxygen uptake [spontaneous breathing for 5 min and voluntary breathing with inspiratory resistance for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were set at 0.5 s each)]. MSNA was recorded via microneurography of the right median nerve at the elbow. A progressive increase in MSNA burst frequency (BF) during leg-cycling exercise with inspiratory resistance in normoxia and hypoxia were accompanied by an augmentation of BP. The increased MSNA BF and mean arterial BP (MBP) during exercise with inspiratory resistive breathing in hypoxia (MSNA BF, 55.7 ± 1.4 bursts/min, MBP, 134.3 ± 6.6 mmHg) were higher than those in normoxia (MSNA BF, 39.2 ± 1.8 bursts/min, MBP, 123.6 ± 4.5 mmHg). These results suggest that an enhancement of inspiratory muscle activity under hypoxic condition leads to large increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise.
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Ainslie, Philip N., Michael Hamlin, John Hellemans, Peter Rasmussen y Shigehiko Ogoh. "Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, n.º 5 (noviembre de 2008): R1613—R1622. http://dx.doi.org/10.1152/ajpregu.90420.2008.
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We examined the effects of exposure to 10–12 days intermittent hypercapnia [IHC: 5:5-min hypercapnia (inspired fraction of CO2 0.05)-to-normoxia for 90 min ( n = 10)], intermittent hypoxia [IH: 5:5-min hypoxia-to-normoxia for 90 min ( n = 11)] or 12 days of continuous hypoxia [CH: 1,560 m ( n = 7)], or both IH followed by CH on cardiorespiratory and cerebrovascular function during steady-state cycling exercise with and without hypoxia (inspired fraction of oxygen, 0.14). Cerebrovascular reactivity to CO2 was also monitored. During all procedures, ventilation, end-tidal gases, blood pressure, muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAv) were measured continuously. Dynamic cerebral autoregulation (CA) was assessed using transfer-function analysis. Hypoxic exercise resulted in increases in ventilation, hypocapnia, heart rate, and cardiac output when compared with normoxic exercise ( P < 0.05); these responses were unchanged following IHC but were elevated following the IH and CH exposure ( P < 0.05) with no between-intervention differences. Following IH and/or CH exposure, the greater hypocapnia during hypoxic exercise provoked a decrease in MCAv ( P < 0.05 vs. preexposure) that was related to lowered cerebral oxygenation ( r = 0.54; P < 0.05). Following any intervention, during hypoxic exercise, the apparent impairment in CA, reflected in lowered low-frequency phase between MCAv and BP, and MCAv-CO2 reactivity, were unaltered. Conversely, during hypoxic exercise following both IH and/or CH, there was less of a decrease in muscle oxygenation ( P < 0.05 vs. preexposure). Thus IH or CH induces some adaptation at the muscle level and lowers MCAv and cerebral oxygenation during hypoxic exercise, potentially mediated by the greater hypocapnia, rather than a compromise in CA or MCAv reactivity.
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Li, Jia, Yanchun Li, Muhammed M. Atakan, Jujiao Kuang, Yang Hu, David J. Bishop y Xu Yan. "The Molecular Adaptive Responses of Skeletal Muscle to High-Intensity Exercise/Training and Hypoxia". Antioxidants 9, n.º 8 (24 de julio de 2020): 656. http://dx.doi.org/10.3390/antiox9080656.
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High-intensity exercise/training, especially interval exercise/training, has gained popularity in recent years. Hypoxic training was introduced to elite athletes half a century ago and has recently been adopted by the general public. In the current review, we have summarised the molecular adaptive responses of skeletal muscle to high-intensity exercise/training, focusing on mitochondrial biogenesis, angiogenesis, and muscle fibre composition. The literature suggests that (peroxisome proliferator-activated receptor gamma coactivator 1-alpha) PGC-1α, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor 1-alpha (HIF1-α) might be the main mediators of skeletal muscle adaptations to high-intensity exercises in hypoxia. Exercise is known to be anti-inflammatory, while the effects of hypoxia on inflammatory signalling are more complex. The anti-inflammatory effects of a single session of exercise might result from the release of anti-inflammatory myokines and other cytokines, as well as the downregulation of Toll-like receptor signalling, while training-induced anti-inflammatory effects may be due to reductions in abdominal and visceral fat (which are main sources of pro-inflammatory cytokines). Hypoxia can lead to inflammation, and inflammation can result in tissue hypoxia. However, the hypoxic factor HIF1-α is essential for preventing excessive inflammation. Disease-induced hypoxia is related to an upregulation of inflammatory signalling, but the effects of exercise-induced hypoxia on inflammation are less conclusive. The effects of high-intensity exercise under hypoxia on skeletal muscle molecular adaptations and inflammatory signalling have not been fully explored and are worth investigating in future studies. Understanding these effects will lead to a more comprehensive scientific basis for maximising the benefits of high-intensity exercise.
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Giesbrecht, G. G., A. Puddy, M. Ahmed, M. Younes y N. R. Anthonisen. "Exercise endurance and arterial desaturation in normobaric hypoxia with increased chemosensitivity". Journal of Applied Physiology 70, n.º 4 (1 de abril de 1991): 1770–74. http://dx.doi.org/10.1152/jappl.1991.70.4.1770.
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We studied whether exercise endurance under normobaric hypoxia can be enhanced by increasing hypoxic ventilatory sensitivity with almitrine bismesylate (ALM). On both ALM and placebo (PL) days, resting subjects breathed a hypoxic gas mixture (an inspired O2 fraction of 10.4-13.2%), which lowered resting arterial O2 saturation (SaO2) to 80%. After 15 min of rest there was a 3-min warm-up period of exercise at 50 W (light) on a cycle ergometer, followed by a step increase in load to 60% of the previously determined maximum power output with room-air breathing (moderate), which was maintained until exhaustion. With PL, SaO2 decreased rapidly with the onset of exercise and continued to fall slowly during moderate exercise, averaging 71.0 +/- 1.8% (SE) at exhaustion. With ALM, saturation did not differ from PL during air breathing but significantly exceeded SaO2 with PL, by 3.4% during resting hypoxia, by 4.0% at the start of exercise, and by 5.9% at exhaustion. Ventilation was not affected by ALM during air breathing and was slightly, although not significantly, increased during hypoxic rest and exercise. ALM was associated with an increased heart rate during room air breathing but not during hypoxia. Endurance time was 20.6 +/- 1.6 min with ALM and 21.3 +/- 0.9 min with PL. During hypoxic exercise, the potential benefit of greater saturation with ALM is apparently offset by other unidentified factors.
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Wang, Jong-Shyan, Ya-Lun Chang, Yi-Ching Chen, Hsing-Hua Tsai y Tieh-Cheng Fu. "Effects of normoxic and hypoxic exercise regimens on monocyte-mediated thrombin generation in sedentary men". Clinical Science 129, n.º 4 (27 de mayo de 2015): 363–74. http://dx.doi.org/10.1042/cs20150128.
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Hypoxic exercise training (HET) is superior to normoxic exercise training (NET) for enhancing aerobic capacity. Furthermore, HET effectively suppresses procoagulant monocyte-derived microparticle formation and monocyte-mediated thrombin generation under severe hypoxic stress, compared to NET does. Therefore, HET can be considered an effective exercise strategy that improves aerobic capacity and simultaneously increases the resistance to monocyte-related thrombosis provoked by severe hypoxia.
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BAILEY, Damian M., Bruce DAVIES y Ian S. YOUNG. "Intermittent hypoxic training: implications for lipid peroxidation induced by acute normoxic exercise in active men". Clinical Science 101, n.º 5 (21 de septiembre de 2001): 465–75. http://dx.doi.org/10.1042/cs1010465.
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Oxidant generation during regular physical exercise training may influence the adaptive responses that have been shown to confer protection against oxidative stress induced by subsequent acute exercise. To examine this, we randomly assigned 32 males to either a normoxic (n = 14) or a hypoxic (n = 18) group. During the acute phase, subjects in the hypoxic group performed two maximal cycling tests in a randomized double-blind fashion: one under conditions of normoxia and the other under hypoxic conditions (inspired fraction of O2 = 0.21 and 0.16 respectively). During the intermittent phase, the normoxic and hypoxic groups each trained for 4 weeks at the same relative exercise intensity, under conditions of normoxia and hypoxia respectively. During acute exercise under hypoxic conditions, the venous concentrations of lipid hydroperoxides and malondialdehyde were increased, despite a comparatively lower maximal oxygen uptake (o2max) (P < 0.05 compared with normoxia). The increases in lipid hydroperoxides and malondialdehyde were correlated with the exercise-induced decrease in arterial haemoglobin oxygen saturation (r =-0.61 and r =-0.50 respectively; P < 0.05), but not with o2max. Intermittent hypoxic training attenuated the increases in lipid hydroperoxides and malondialdehyde induced by acute normoxic exercise more effectively than did normoxic training, due to a selective mobilization of α-tocopherol (P < 0.05). The latter was related to enhanced exercise-induced mobilization/oxidation of blood lipids due to a selective increase in o2max (P < 0.05 compared with normoxic group). We conclude that lipid peroxidation induced by acute exercise (1) increases during hypoxia; (2) is not regulated exclusively by a mass action effect of o2; and (3) is selectively attenuated by regular hypoxic training. Oxidative stress may thus be considered as a biological prerequisite for adaptation to physical stress in humans.
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Babcock, M. A., B. D. Johnson, D. F. Pegelow, O. E. Suman, D. Griffin y J. A. Dempsey. "Hypoxic effects on exercise-induced diaphragmatic fatigue in normal healthy humans". Journal of Applied Physiology 78, n.º 1 (1 de enero de 1995): 82–92. http://dx.doi.org/10.1152/jappl.1995.78.1.82.
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We examined the effects of hypoxia on exercise-induced diaphragmatic fatigue. Eleven subjects with a mean maximal O2 uptake of 52.4 +/- 0.7 ml.kg-1.min-1 completed one normoxic (arterial O2 saturation 96-94%) and one hypoxic (inspiratory O2 fraction = 0.15; arterial O2 saturation 83–77%) exercise test at 85% maximal O2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (BPNS) was used to determine the pressure generation of the diaphragm pre- and postexercise at 1, 10, and 20 Hz. There was increased flow limitation during hypoxic vs. normoxic exercise. There was a decrease in hypoxic exercise time (normoxic 24.9 +/- 0.7 min vs. hypoxic 15.8 +/- 0.8 min; P < 0.05). After exercise the BPNS transdiaphragmatic pressure (Pdi) was significantly reduced at 1 and 10 Hz after both exercise tests. The BPNS Pdi was recovered to control values by 60 min postnormoxic exercise but was still reduced 90 min posthypoxic exercise. The mean percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Experiencing the same amount of diaphragm fatigue in a shorter time period in hypoxic exercise may have been due to 1) the increased expiratory flow limitation and diaphragmatic muscle work, 2) decreased O2 transport to the diaphragm, and/or 3) increased levels of circulating metabolites.
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Horiuchi, Masahiro, Yoshiyuki Fukuoka, Katsuhiro Koyama y Samuel J. Oliver. "Five Days of Tart Cherry Supplementation Improves Exercise Performance in Normobaric Hypoxia". Nutrients 15, n.º 2 (12 de enero de 2023): 388. http://dx.doi.org/10.3390/nu15020388.
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Previous studies have shown tart cherry (TC) to improve exercise performance in normoxia. The effect of TC on hypoxic exercise performance is unknown. This study investigated the effects of 5 days of tart cherry (TC) or placebo (PL) supplementation on hypoxic exercise performance. Thirteen healthy participants completed an incremental cycle exercise test to exhaustion (TTE) under two conditions: (i) hypoxia (13% O2) with PL and (ii) hypoxia with TC (200 mg anthocyanin per day for 4 days and 100 mg on day 5). Pulmonary gas exchange variables, peripheral arterial oxygen saturation (SpO2), deoxygenated hemoglobin (HHb), and tissue oxygen saturation (StO2) assessed by near-infrared spectroscopy in the vastus lateralis muscle were measured at rest and during exercise. Urinary 8-hydro-2′ deoxyguanosine (8-OHdG) excretion was evaluated pre-exercise and 1 and 5 h post-exercise. The TTE after TC (940 ± 84 s, mean ± standard deviation) was longer than after PL (912 ± 63 s, p < 0.05). During submaximal hypoxic exercise, HHb was lower and StO2 and SpO2 were higher after TC than PL. Moreover, a significant interaction (supplements × time) in urinary 8-OHdG excretion was found (p < 0.05), whereby 1 h post-exercise increases in urinary 8-OHdG excretion tended to be attenuated after TC. These findings indicate that short-term dietary TC supplementation improved hypoxic exercise tolerance, perhaps due to lower HHb and higher StO2 in the working muscles during submaximal exercise.
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Kleinnibbelink, Geert, Arie P. J. van Dijk, Alessandro Fornasiero, Guilherme F. Speretta, Christopher Johnson, Nicholas Sculthorpe, Keith P. George, John D. Somauroo, Dick H. J. Thijssen y David L. Oxborough. "Acute exercise-induced changes in cardiac function relates to right ventricular remodeling following 12-wk hypoxic exercise training". Journal of Applied Physiology 131, n.º 2 (1 de agosto de 2021): 511–19. http://dx.doi.org/10.1152/japplphysiol.01075.2020.
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During exercise, the right ventricle is exposed to a disproportionally higher wall stress than the left ventricle, which is further exaggerated under hypoxia. In this study, we showed that 12-wk high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline cardiac increase in RV fractional area change to acute exercise. These data suggest that acute RV responses to exercise are related to subsequent right ventricular remodeling in healthy individuals upon hypoxic training.
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Casey, Darren P., David P. Treichler, Charles T. Ganger, Aaron C. Schneider y Kenichi Ueda. "Acute dietary nitrate supplementation enhances compensatory vasodilation during hypoxic exercise in older adults". Journal of Applied Physiology 118, n.º 2 (15 de enero de 2015): 178–86. http://dx.doi.org/10.1152/japplphysiol.00662.2014.
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We have previously demonstrated that aging reduces the compensatory vasodilator response during hypoxic exercise due to blunted nitric oxide (NO) signaling. Recent evidence suggests that NO bioavailability can be augmented by dietary nitrate through the nitrate-nitrite pathway. Thus we tested the hypothesis that acute dietary nitrate supplementation increases the compensatory vasodilator response to hypoxic exercise, particularly in older adults. Thirteen young (25 ± 1 yr) and 12 older (64 ± 2 yr) adults performed rhythmic forearm exercise at 20% of maximum voluntary contraction during normoxia and hypoxia (∼80% O2 saturation); both before (control) and 3 h after beetroot juice (BR) consumption. Forearm vascular conductance (FVC; ml·min−1·100 mmHg−1) was calculated from forearm blood flow (ml/min) and blood pressure (mmHg). Compensatory vasodilation was defined as the relative increase in FVC due to hypoxic exercise (i.e., % increase compared with respective normoxic exercise trial). Plasma nitrite was determined from venous blood samples obtained before the control trials and each of the exercise trials (normoxia and hypoxia) after BR. Consumption of BR increased plasma nitrite in both young and older adults ( P < 0.001). During the control condition, the compensatory vasodilator response to hypoxic exercise was attenuated in older compared with young adults (3.8 ± 1.7% vs. 14.2 ± 1.2%, P < 0.001). Following BR consumption, compensatory vasodilation did not change in young (13.7 ± 3.3%, P = 0.81) adults but was substantially augmented in older adults (11.4 ± 2.1%, P < 0.01). Our data suggest that acute dietary nitrate supplementation increases the compensatory vasodilator response to hypoxic exercise in older but not young adults.
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Park, Hun-young, Sang-seok Nam, Hirofumi Tanaka y Dong-jun Lee. "Hemodynamic, Hematological, and Hormonal Responses to Submaximal Exercise in Normobaric Hypoxia in Pubescent Girls". Pediatric Exercise Science 28, n.º 3 (agosto de 2016): 417–22. http://dx.doi.org/10.1123/pes.2015-0176.
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Purpose:The aim of this study was to investigate hemodynamic, hematological, and immunological responses to prolonged submaximal cycle ergometer exercise at a simulated altitude of 3000 m in pubescent girls.Methods:Ten girls, 12.8 ± 1.0 years old, exercised on a cycle ergometer for 60 min at a work rate corresponding to 50% maximal oxygen consumption measured at sea level, under two environmental conditions; sea level (normoxia) and a simulated 3000 m altitude (normobaric hypoxia).Results:There were no significant differences in tidal volume, ventilation, oxygen consumption, cardiac output, stroke volume, and heart rate between the two exercise conditions. However, reticulocyte, adrenocorticotropic hormone, and cortisol concentrations increased significantly from pre- to postexercise in the hypoxic environment. Leukocyte and T-cell count increased and B-cell count decreased after exercise under both conditions. There were no significant changes in natural killer cell count.Conclusion:Our simulated hypoxic environment provided a mild environmental stressor that did not impose a heavy burden on the cardiovascular, hematological, or immunological functions during submaximal exercise in pubescent girls.
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Sotiridis, Alexandros, Tadej Debevec, Adam C. McDonnell, Urša Ciuha, Ola Eiken y Igor B. Mekjavic. "Exercise cardiorespiratory and thermoregulatory responses in normoxic, hypoxic, and hot environment following 10-day continuous hypoxic exposure". Journal of Applied Physiology 125, n.º 4 (1 de octubre de 2018): 1284–95. http://dx.doi.org/10.1152/japplphysiol.01114.2017.
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We examined the effects of acclimatization to normobaric hypoxia on aerobic performance and exercise thermoregulatory responses under normoxic, hypoxic, and hot conditions. Twelve men performed tests of maximal oxygen uptake (V̇O2max) in normoxic (NOR), hypoxic [HYP; 13.5% fraction of inspired oxygen (FiO2)], and hot (HE; 35°C, 50% relative humidity) conditions in a randomized manner before and after a 10-day continuous normobaric hypoxic exposure [FiO2 = 13.65 (0.35)%, inspired partial pressure of oxygen = 87 (3) mmHg]. The acclimatization protocol included daily exercise [60 min at 50% hypoxia-specific peak power output (Wpeak)]. All maximal tests were preceded by a steady-state exercise (30 min at 40% Wpeak) to assess the sweating response. Hematological data were assessed from venous blood samples obtained before and after acclimatization. V̇o2max increased by 10.7% ( P = 0.002) and 7.9% ( P = 0.03) from pre-acclimatization to post acclimatization in NOR and HE, respectively, whereas no differences were found in HYP [pre: 39.9 (3.8) vs. post: 39.4 (5.1) ml·kg−1·min−1, P = 1.0]. However, the increase in V̇O2max did not translate into increased Wpeak in either NOR or HE. Maximal heart rate and ventilation remained unchanged following acclimatization. Νo differences were noted in the sweating gain and thresholds independent of the acclimatization or environmental conditions. Hypoxic acclimatization markedly increased hemoglobin ( P < 0.001), hematocrit ( P < 0.001), and extracellular HSP72 ( P = 0.01). These data suggest that 10 days of normobaric hypoxic acclimatization combined with moderate-intensity exercise training improves V̇o2max in NOR and HE, but does not seem to affect exercise performance or thermoregulatory responses in any of the tested environmental conditions. NEW & NOTEWORTHY The potential crossover effect of hypoxic acclimatization on performance in the heat remains unexplored. Here we show that 10-day continuous hypoxic acclimatization combined with moderate-intensity exercise training can increase maximal oxygen uptake in hot conditions.
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Tremblay, Joshua C., Philip N. Ainslie, Rachel Turner, Hannes Gatterer, Maja Schlittler, Simon Woyke, Ivo B. Regli, Giacomo Strapazzon, Simon Rauch y Christoph Siebenmann. "Endothelial function and shear stress in hypobaric hypoxia: time course and impact of plasma volume expansion in men". American Journal of Physiology-Heart and Circulatory Physiology 319, n.º 5 (1 de noviembre de 2020): H980—H994. http://dx.doi.org/10.1152/ajpheart.00597.2020.
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Using a normoxic crossover study design, we examined the impact of hypobaric hypoxia (4 days; altitude equivalent, 3,500 m) and hemoconcentration on blood viscosity, shear stress, and endothelial function. Blood viscosity increased during the hypoxic exposure and was accompanied by elevated resting and exercising arterial shear stress. Flow-mediated dilation stimulated by reactive hyperemia and handgrip exercise was preserved throughout the hypoxic exposure. Plasma volume expansion reversed the hypoxia-associated hemoconcentration and selectively increased handgrip exercise flow-mediated dilation.
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Hughson, Richard L. y John M. Kowalchuk. "Kinetics of Oxygen Uptake for Submaximal Exercise in Hyperoxia, Normoxia, and Hypoxia". Canadian Journal of Applied Physiology 20, n.º 2 (1 de junio de 1995): 198–210. http://dx.doi.org/10.1139/h95-014.
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This study evaluated the dynamic response of [Formula: see text] in 6 healthy men at the onset and end of submaximal step changes in work rate during a pseudorandom binary sequence (PRBS) exercise test and during ramp incremental exercise to exhaustion while breathing three different gas mixtures. The fractional concentrations of inspired O2 were 0.14, 0.21, and 0.70 for the hypoxic, normoxic, and hyperoxic tests, respectively. Both maximal [Formula: see text] and work rate was significantly reduced in hypoxic tests compared to normoxic and hyperoxic tests. Maximal work rate was greater in hyperoxia than in normoxia. Work rate at ventilatory threshold was lower in hypoxia than in normoxia and hyperoxia but above the upper limit of exercise for the submaximal tests. Hypoxia significantly slowed the response of [Formula: see text] both at the onset and end of exercise compared to normoxia and hyperoxia. Hypoxia also modified the response to PRBS exercise, and again there was no difference between normoxia and hyperoxia. These data support the concept that [Formula: see text] kinetics can be slowed from the normoxic response by a hypoxic gas mixture. Key words: [Formula: see text]max, ventilatory threshold, oxygen deficit, pseudorandom binary sequence
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Fornasiero, Alessandro, Spyros Skafidas, Federico Stella, Andrea Zignoli, Aldo Savoldelli, Mark Rakobowchuk, Barbara Pellegrini, Federico Schena y Laurent Mourot. "Cardiac Autonomic and Physiological Responses to Moderate- intensity Exercise in Hypoxia". International Journal of Sports Medicine 40, n.º 14 (24 de octubre de 2019): 886–96. http://dx.doi.org/10.1055/a-1015-0647.
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AbstractExercise physiological responses can be markedly affected by acute hypoxia. We investigated cardiac autonomic and physiological responses to different hypoxic training protocols. Thirteen men performed three exercise sessions (5×5-min; 1-min passive recovery): normoxic exercise at 80% of the power output (PO) at the first ventilatory threshold (N), hypoxic exercise (FiO2=14.2%) with the same PO as N (HPO) and hypoxic exercise at the same heart rate (HR) as N (HHR). PO was lower in HHR (21.1±9.3%) compared to N and HPO. Mean HR was higher in HPO (154±11 bpm, p<0.01) than N and HHR (139±10 vs. 138±9 bpm; p=0.80). SpO2 was reduced (p<0.01) to a similar extent (p>0.05) in HPO and HHR compared to N. HR recovery (HRR) and HR variability indices were similar in N and HHR (p>0.05) but reduced in HPO (p<0.05), mirroring a delayed parasympathetic reactivation. Blood lactate and ventilation were similar in N and HHR (p>0.05) and increased in HPO (p<0.001). During recovery oxygen consumption and ventilation were similar in N and HHR (p>0.05) and increased in HPO (p<0.01). Moderate HR-matched hypoxic exercise triggers similar cardiac autonomic and physiological responses to normoxic exercise with a reduced mechanical load. On the contrary, the same absolute intensity exercise in hypoxia is associated with increased exercise-induced metabolic stress and delayed cardiac autonomic recovery.
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Nordsborg, Nikolai B., José A. L. Calbet, Mikael Sander, Gerrit van Hall, Carsten Juel, Bengt Saltin y Carsten Lundby. "Human muscle net K+ release during exercise is unaffected by elevated anaerobic metabolism, but reduced after prolonged acclimatization to 4,100 m". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, n.º 1 (julio de 2010): R306—R313. http://dx.doi.org/10.1152/ajpregu.00062.2010.
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It was investigated whether skeletal muscle K+ release is linked to the degree of anaerobic energy production. Six subjects performed an incremental bicycle exercise test in normoxic and hypoxic conditions prior to and after 2 and 8 wk of acclimatization to 4,100 m. The highest workload completed by all subjects in all trials was 260 W. With acute hypoxic exposure prior to acclimatization, venous plasma [K+] was lower ( P < 0.05) in normoxia (4.9 ± 0.1 mM) than hypoxia (5.2 ± 0.2 mM) at 260 W, but similar at exhaustion, which occurred at 400 ± 9 W and 307 ± 7 W ( P < 0.05), respectively. At the same absolute exercise intensity, leg net K+ release was unaffected by hypoxic exposure independent of acclimatization. After 8 wk of acclimatization, no difference existed in venous plasma [K+] between the normoxic and hypoxic trial, either at submaximal intensities or at exhaustion (360 ± 14 W vs. 313 ± 8 W; P < 0.05). At the same absolute exercise intensity, leg net K+ release was less ( P < 0.001) than prior to acclimatization and reached negative values in both hypoxic and normoxic conditions after acclimatization. Moreover, the reduction in plasma volume during exercise relative to rest was less ( P < 0.01) in normoxic than hypoxic conditions, irrespective of the degree of acclimatization (at 260 W prior to acclimatization: −4.9 ± 0.8% in normoxia and −10.0 ± 0.4% in hypoxia). It is concluded that leg net K+ release is unrelated to anaerobic energy production and that acclimatization reduces leg net K+ release during exercise.
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Lhuissier, François J., Maxime Brumm, Didier Ramier y Jean-Paul Richalet. "Ventilatory and cardiac responses to hypoxia at submaximal exercise are independent of altitude and exercise intensity". Journal of Applied Physiology 112, n.º 4 (15 de febrero de 2012): 566–70. http://dx.doi.org/10.1152/japplphysiol.00906.2011.
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The hypoxic exercise test combining a 4,800-m simulated altitude and a cycloergometer exercise at 30% of normoxic maximal aerobic power (MAP) is used to evaluate the individual chemosensitivity to hypoxia in submaximal exercise conditions. This test allows the calculation of three main parameters: the decrease in arterial oxygen saturation induced by hypoxia at exercise (ΔSae) and the ventilatory (HVRe) and cardiac (HCRe) responses to hypoxia at exercise. The aim of this study was to determine the influence of altitude and exercise intensity on the values of ΔSae, HVRe, and HCRe. Nine subjects performed hypoxic tests at three simulated altitudes (3,000 m, 4,000 m, and 4,800 m) and three exercise intensities (20%, 30%, and 40% MAP). ΔSae increased with altitude and was higher for 40% MAP than for 20% or 30% ( P < 0.05). For a constant heart rate, the loss in power output induced by hypoxia, relative to ΔSae, was independent of altitude (4,000–4,800 m) and of exercise intensity. HVRe and HCRe were independent of altitude (3,000–4,800 m) and exercise intensity (20%-40% MAP). Moreover, the intraindividual variability of responses to hypoxia was lower during moderate exercise than at rest ( P < 0.05 to P < 0.001). Therefore, we suggest that HVRe and HCRe are invariant parameters that can be considered as intrinsic physiological characteristics of chemosensitivity to hypoxia.
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Cooper, D. M., D. H. Wasserman, M. Vranic y K. Wasserman. "Glucose turnover in response to exercise during high- and low-FIO2 breathing in man". American Journal of Physiology-Endocrinology and Metabolism 251, n.º 2 (1 de agosto de 1986): E209—E214. http://dx.doi.org/10.1152/ajpendo.1986.251.2.e209.
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The purpose of this study was to assess whether breathing high or low concentrations of O2 could affect glucose turnover during exercise in man. Ten healthy subjects performed two constant work-rate exercise tests, one when the fraction of inspired O2 (FIO2) was 0.15 and the other at the same work rate but when the FIO2 was 0.80. The work rate for each subject was chosen so that blood lactate would be elevated during hypoxia, but would be lower during hyperoxia. Glucose appearance (Ra) and disappearance (Rd) were measured using the primed, constant infusion of [3-3H]glucose. Although the work rate was the same during hypoxia and hyperoxia in each subject, hypoxic exercise was accompanied by a significantly larger rest to exercise increase in Rd (delta Rd) compared with hyperoxia by 265%. Similarly, delta Ra was greater during hypoxia than during hyperoxia by 188%. Lactate to pyruvate ratios were significantly higher during hypoxic exercise suggesting a shift in the cell redox to a more reduced state. Insulin and glucagon were not affected by the FIO2, but both epinephrine and norepinephrine were increased during hypoxic exercise, which may explain the increase in Ra. The regulation of blood glucose during exercise in vivo appears to be dependent on the availability of oxygen to the working muscle cells.
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Syahrastani, Syahrastani, Argantos Argantos y Siska Alicia Farma. "Comparison of Serum HIF-1α Levels in Swimming Athletes Before and After Hypoxic Non-Hypoxic Exercise". Eksakta : Berkala Ilmiah Bidang MIPA 21, n.º 1 (30 de abril de 2020): 36–39. http://dx.doi.org/10.24036/eksakta/vol21-iss1/223.
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The situation of lack of oxygen supply to cells and tissues is often not realized by many people (hypoxia). Hypoxia can occur in various situations in life. The main effect of hypoxia is the effect on the brain, so the body will do everything it can to restore the state of homeostasis. HIF-1α protein is a marker of hypoxic conditions. HIF-1α regulates the synthesis of many genes to maintain and restore body homeostasis from hypoxia to normoxia. This study was a descriptive study with cross-sectional design. The sample of this study were six swimming athletes with a 12-19 year age range who met the inclusion and exclusion criteria. The HIF-1α protein is measured by the ELISA method. Data were analyzed statistically. The results showed higher levels of HIF-1α after anaerobic exercise than the levels of HIF-1α before and after aerobic exercise. This is greatly influenced by the intensity of the exercise carried out. This proves that cellular adaptation to hypoxia is more stable in aerobic exercise, where the body's metabolism during aerobic exercise is more stable
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Rowell, L. B. y J. R. Blackmon. "Venomotor responses during central and local hypoxia". American Journal of Physiology-Heart and Circulatory Physiology 255, n.º 4 (1 de octubre de 1988): H760—H764. http://dx.doi.org/10.1152/ajpheart.1988.255.4.h760.
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Venomotor responses, measured as the pressure rise in occluded forearm veins, were used in a two-part experiment to test presence or absence of sympathetic neuroeffector mechanisms in 10 men made moderately to severely hypoxemic. In part I, forearm venoconstriction was induced by ice water on the contralateral forearm (a spinal reflex) in eight supine, resting men who breathed air, 10.3% oxygen or 7.7% oxygen. Large reflex venoconstrictions persisted during hypoxia. In part II (seven men), venoconstriction was centrally induced by exercise while subjects were 1) normoxic; 2) arm hypoxic, body normoxic; 3) arm hyperoxic (or normoxic), body hypoxic; or 4) both arm and body hypoxic. Arm vs. body oxygen tensions were separated by occluding the arm as one gas mixture was breathed, then switching the subject to another mixture as the arm remained occluded. Strong venoconstrictor responses to moderate exercise (100-150 W) persisted during both local and central hypoxemia. We conclude that moderate to severe hypoxemia does not block, pre- or postjunctionally, sympathetic venoconstriction that originates from spinal reflexes (cold). Venoconstriction in exercise (presumably originating in higher centers) was not blocked by moderate hypoxemia; severe hypoxemia was not studied.
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Gonzalez, Norberto C., Richard L. Clancy, Yoshihiro Moue y Jean-Paul Richalet. "Increasing maximal heart rate increases maximal O2 uptake in rats acclimatized to simulated altitude". Journal of Applied Physiology 84, n.º 1 (1 de enero de 1998): 164–68. http://dx.doi.org/10.1152/jappl.1998.84.1.164.
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Gonzalez, Norberto C., Richard L. Clancy, Yoshihiro Moue, and Jean-Paul Richalet. Increasing maximal heart rate increases maximal O2 uptake in rats acclimatized to simulated altitude. J. Appl. Physiol. 84(1): 164–168, 1998.—Maximal exercise heart rate (HRmax) is reduced after acclimatization to hypobaric hypoxia. The low HRmax contributes to reduce maximal cardiac output (Q˙max) and may limit maximal O2 uptake (V˙o 2 max). The objective of these experiments was to test the hypothesis that the reduction inQ˙max after acclimatization to hypoxia, due, in part, to the low HRmax, limitsV˙o 2 max. If this hypothesis is correct, an increase inQ˙max would result in a proportionate increase inV˙o 2 max. Rats acclimatized to hypobaric hypoxia [inspired[Formula: see text]([Formula: see text]) = 69.8 ± 3 Torr for 3 wk] exercised on a treadmill in hypoxic ([Formula: see text] = 71.7 ± 1.1 Torr) or normoxic conditions ([Formula: see text] = 142.1 ± 1.1 Torr). Each rat ran twice: in one bout the rat was allowed to reach its spontaneous HRmax, which was 505 ± 7 and 501 ± 5 beats/min in hypoxic and normoxic exercise, respectively; in the other exercise bout, HRmax was increased by 20% to the preacclimatization value of 600 beats/min by atrial pacing. This resulted in an ∼10% increase inQ˙max, since the increase in HRmax was offset by a 10% decrease in stroke volume, probably due to shortening of diastolic filling time. The increase inQ˙max was accompanied by a proportionate increase in maximal rate of convective O2 delivery (Q˙max × arterial O2 content), maximal work rate, and V˙o 2 max in hypoxic and normoxic exercise. The data show that increasing HRmax to preacclimatization levels increasesV˙o 2 max, supporting the hypothesis that the low HRmax tends to limitV˙o 2 maxafter acclimatization to hypoxia.
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Kim, Sung-Woo, Won-Sang Jung, Jeong-Weon Kim, Sang-Seok Nam y Hun-Young Park. "Aerobic Continuous and Interval Training under Hypoxia Enhances Endurance Exercise Performance with Hemodynamic and Autonomic Nervous System Function in Amateur Male Swimmers". International Journal of Environmental Research and Public Health 18, n.º 8 (9 de abril de 2021): 3944. http://dx.doi.org/10.3390/ijerph18083944.
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Hypoxic training is often performed by competitive swimmers to enhance their performance in normoxia. However, the beneficial effects of aerobic continuous and interval training under hypoxia on hemodynamic function, autonomic nervous system (ANS) function, and endurance exercise performance remain controversial. Here we investigated whether six weeks of aerobic continuous and interval training under hypoxia can improve hematological parameters, hemodynamic function, ANS function, and endurance exercise performance versus normoxia in amateur male swimmers. Twenty amateur male swimmers were equally assigned to the hypoxic training group or normoxic training group and evaluated before and after six weeks of training. Aerobic continuous and interval training in the hypoxia showed a more significantly improved hemodynamic function (heart rate, −653.4 vs. −353.7 beats/30 min; oxygen uptake, −62.45 vs. −16.22 mL/kg/30 min; stroke volume index, 197.66 vs. 52.32 mL/30 min) during submaximal exercise, ANS function (root mean square of successive differences, 10.15 vs. 3.32 ms; total power, 0.72 vs. 0.20 ms2; low-frequency/high-frequency ratio, −0.173 vs. 0.054), and endurance exercise performance (maximal oxygen uptake, 5.57 vs. 2.26 mL/kg/min; 400-m time trial record, −20.41 vs. −7.91 s) than in the normoxia. These indicate that hypoxic training composed of aerobic continuous and interval exercise improves the endurance exercise performance of amateur male swimmers with better hemodynamic function and ANS function.
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Houssiere, Anne, Boutaina Najem, Agniezka Ciarka, Sonia Velez-Roa, Robert Naeije y Philippe van de Borne. "Chemoreflex and metaboreflex control during static hypoxic exercise". American Journal of Physiology-Heart and Circulatory Physiology 288, n.º 4 (abril de 2005): H1724—H1729. http://dx.doi.org/10.1152/ajpheart.01043.2004.
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To investigate the effects of muscle metaboreceptor activation during hypoxic static exercise, we recorded muscle sympathetic nerve activity (MSNA), heart rate, blood pressure, ventilation, and blood lactate in 13 healthy subjects (22 ± 2 yr) during 3 min of three randomized interventions: isocapnic hypoxia (10% O2) (chemoreflex activation), isometric handgrip exercise in normoxia (metaboreflex activation), and isometric handgrip exercise during isocapnic hypoxia (concomitant metaboreflex and chemoreflex activation). Each intervention was followed by a forearm circulatory arrest to allow persistent metaboreflex activation in the absence of exercise and chemoreflex activation. Handgrip increased blood pressure, MSNA, heart rate, ventilation, and lactate (all P < 0.001). Hypoxia without handgrip increased MSNA, heart rate, and ventilation (all P < 0.001), but it did not change blood pressure and lactate. Handgrip enhanced blood pressure, heart rate, MSNA, and ventilation responses to hypoxia (all P < 0.05). During circulatory arrest after handgrip in hypoxia, heart rate returned promptly to baseline values, whereas ventilation decreased but remained elevated ( P < 0.05). In contrast, MSNA, blood pressure, and lactate returned to baseline values during circulatory arrest after hypoxia without exercise but remained markedly increased after handgrip in hypoxia ( P < 0.05). We conclude that metaboreceptors and chemoreceptors exert differential effects on the cardiorespiratory and sympathetic responses during exercise in hypoxia.
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Kopp, Renate, Louise Köblitz, Margit Egg y Bernd Pelster. "HIF signaling and overall gene expression changes during hypoxia and prolonged exercise differ considerably". Physiological Genomics 43, n.º 9 (mayo de 2011): 506–16. http://dx.doi.org/10.1152/physiolgenomics.00250.2010.
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Exercise as well as hypoxia cause an increase in angiogenesis, changes in mitochondrial density and alterations in metabolism, but it is still under debate whether the hypoxia inducible factor (HIF) is active during both situations. In this study gene expression analysis of zebrafish larvae that were raised under normoxic, hypoxic, or training conditions were compared, using microarray analysis, quantitative real-time PCR and protein data. Although HIF expression is posttranslationally regulated, mRNA expression levels of all three isoforms ( HIF-1α, HIF-2α, and HIF-3α) differed in each of the experimental groups, but the changes observed in hypoxic animals were much smaller than in trained larvae. Prominent changes were seen for Hif-2α expression, which significantly increased after the first day of exercise and then decreased down to values significantly below control values. HIF-3α mRNA expression in turn increased significantly, and at the end of the training period (9–15 days postfertilization) it was elevated three times. At the protein level a transient increase in HIF-1α was observed in hypoxic larvae, whereas in the exercise group the amount of HIF-1α protein even decreased below the level of control animals. The analyzed transcriptome was more affected in hypoxic zebrafish larvae, and hardly any genes were similarly altered by both treatments. These results clearly showed that HIF proteins played different roles in trained and hypoxic zebrafish larvae and that the exercise-induced transition to a more aerobic phenotype was not achieved by persistent activation of the hypoxic signaling pathway.
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Casey, Darren P., Brandon D. Madery, Tasha L. Pike, John H. Eisenach, Niki M. Dietz, Michael J. Joyner y Brad W. Wilkins. "Adenosine receptor antagonist and augmented vasodilation during hypoxic exercise". Journal of Applied Physiology 107, n.º 4 (octubre de 2009): 1128–37. http://dx.doi.org/10.1152/japplphysiol.00609.2009.
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We tested the hypothesis that adenosine contributes to augmented skeletal muscle vasodilation during hypoxic exercise. In separate protocols, subjects performed incremental rhythmic forearm exercise (10% and 20% of maximum) during normoxia and normocapnic hypoxia (80% arterial O2 saturation). In protocol 1 ( n = 8), subjects received an intra-arterial administration of saline (control) and aminophylline (adenosine receptor antagonist). In protocol 2 ( n = 10), subjects received intra-arterial phentolamine (α-adrenoceptor antagonist) and combined phentolamine and aminophylline administration. Forearm vascular conductance (FVC; in ml·min−1·100 mmHg−1) was calculated from forearm blood flow (in ml/min) and blood pressure (in mmHg). In protocol 1, the change in FVC (ΔFVC; change from normoxic baseline) during hypoxic exercise with saline was 172 ± 29 and 314 ± 34 ml·min−1·100 mmHg−1 (10% and 20%, respectively). Aminophylline administration did not affect ΔFVC during hypoxic exercise at 10% (190 ± 29 ml·min−1·100 mmHg−1, P = 0.4) or 20% (287 ± 48 ml·min−1·100 mmHg−1, P = 0.3). In protocol 2, ΔFVC due to hypoxic exercise with phentolamine infusion was 313 ± 30 and 453 ± 41 ml·min−1·100 mmHg−1 (10% and 20% respectively). ΔFVC was similar at 10% (352 ± 39 ml·min−1·100 mmHg−1, P = 0.8) and 20% (528 ± 45 ml·min−1·100 mmHg−1, P = 0.2) hypoxic exercise with combined phentolamine and aminophylline. In contrast, ΔFVC to exogenous adenosine was reduced by aminophylline administration in both protocols ( P < 0.05 for both). These observations suggest that adenosine receptor activation is not obligatory for the augmented hyperemia during hypoxic exercise in humans.
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Xu, Jing, Jinshu Zeng, Yelei Yan y Fei Xu. "Hypoxic Exercise Exacerbates Hypoxemia and Acute Mountain Sickness in Obesity: A Case Analysis". International Journal of Environmental Research and Public Health 18, n.º 17 (28 de agosto de 2021): 9078. http://dx.doi.org/10.3390/ijerph18179078.
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Acute mountain sickness (AMS) is a common syndrome characterized by headache, dizziness, loss of appetite, weakness, and nausea. As a major public health issue, obesity has increased in high altitude urban residents and intermittent commuters to high altitudes. The present study investigated acute hypoxic exposure and hypoxic exercise on hypoxemia severity and AMS symptoms in a physically active obese man. In this case analysis, peripheral oxygen saturation (SpO2) was used to evaluate hypoxemia, heart rate (HR) and blood pressure (BP) were used to reflect the function of autonomic nervous system (ANS), and Lake Louise scoring (LLS) was used to assess AMS. The results showed that acute hypoxic exposure led to severe hypoxemia (SpO2 = 72%) and tachycardia (HRrest = 97 bpm), and acute hypoxic exercise exacerbated severe hypoxemia (SpO2 = 59%) and ANS dysfunction (HRpeak = 167 bpm, SBP/DBP = 210/97 mmHg). At the end of the 6-h acute hypoxic exposure, the case developed severe AMS (LLS = 10) symptoms of headache, gastrointestinal distress, cyanosis, vomiting, poor appetite, and fatigue. The findings of the case study suggest that high physical activity level appears did not show a reliable protective effect against severe hypoxemia, ANS dysfunction, and severe AMS symptoms in acute hypoxia exposure and hypoxia exercise.
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Burleson, M., B. Shipman y N. Smatresk. "Ventilation and acid-base recovery following exhausting activity in an air-breathing fish". Journal of Experimental Biology 201, n.º 9 (1 de mayo de 1998): 1359–68. http://dx.doi.org/10.1242/jeb.201.9.1359.
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The effects of exhausting activity in normoxic (PO2=20.7 kPa) and hypoxic (PO2<2.7 kPa) water on ventilatory, metabolic and acid-base variables were examined in spotted gar (Lepisosteus oculatus) to determine the role of the air-breathing organ in supporting active metabolism and recovery. The level of aquatic hypoxia used effectively eliminated the gills as a site of O2 uptake, forcing the fish to respire as a unimodal air-breather. Swimming duration (until exhaustion) was not significantly different in normoxic and hypoxic water. Blood gas, acid-base, cardiovascular and ventilatory variables were monitored at intervals from 15 min to 24 h post-exercise. Fish survived exhaustive exercise using a combination of anaerobic metabolism and increased ventilation (aerial and aquatic), despite respiratory and metabolic acidoses. The cardiovascular effects of exercise (heart rate and dorsal aortic blood pressure) were minor. The metabolic effects of exercise were similar to those in unimodal water-breathing fish; however, even hypoxic animals recovered from exhaustive exercise by 24 h. Thus, the results of this study show that air breathing in L. oculatus allows gar to exercise to the same extent in normoxic and hypoxic water and enables them to re-establish blood gas and acid-base balance after exhaustive activity even in hypoxic water. <P>
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Favret, Fabrice, Kyle K. Henderson, Julie Allen, Jean-Paul Richalet y Norberto C. Gonzalez. "Exercise training improves lung gas exchange and attenuates acute hypoxic pulmonary hypertension but does not prevent pulmonary hypertension of prolonged hypoxia". Journal of Applied Physiology 100, n.º 1 (enero de 2006): 20–25. http://dx.doi.org/10.1152/japplphysiol.00673.2005.
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Our laboratory has previously shown an attenuation of hypoxic pulmonary hypertension by exercise training (ET) (Henderson KK, Clancy RL, and Gonzalez NC. J Appl Physiol 90: 2057–2062, 2001), although the mechanism was not determined. The present study examined the effect of ET on the pulmonary arterial pressure (Pap) response of rats to short- and long-term hypoxia. After 3 wk of treadmill training, male rats were divided into two groups: one (HT) was placed in hypobaric hypoxia (380 Torr); the second remained in normoxia (NT). Both groups continued to train in normoxia for 10 days, after which they were studied at rest and during hypoxic and normoxic exercise. Sedentary normoxic (NS) and hypoxic (HS) littermates were exposed to the same environments as their trained counterparts. Resting and exercise hypoxic arterial Po2 were higher in NT and HT than in NS and HS, respectively, although alveolar ventilation of trained rats was not higher. Lower alveolar-arterial Po2 difference and higher effective lung diffusing capacity for O2 in NT vs. NS and in HT vs. HS suggest ET improved efficacy of gas exchange. Pap and Pap/cardiac output were lower in NT than NS in hypoxia, indicating that ET attenuates the initial vasoconstriction of hypoxia. However, ET had no effect on chronic hypoxic pulmonary hypertension: Pap and Pap/cardiac output in hypoxia were similar in HS vs HT. However, right ventricular weight was lower in HT than in HS, although Pap was not different. Because ET attenuates the initial pulmonary vasoconstriction of hypoxia, development of pulmonary hypertension may be delayed in HT rats, and the time during which right ventricular afterload is elevated may be shorter in this group. ET effects may improve the response to acute hypoxia by increasing efficacy of gas exchange and lowering right ventricular work.
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Kapus, Jernej, Igor Mekjavic, Adam McDonnell, Anton Ušaj, Janez Vodičar, Peter Najdenov, Miroljub Jakovljević, Polona Jaki Mekjavić, Milan Žvan y Tadej Debevec. "Cardiorespiratory Responses of Adults and Children during Normoxic and Hypoxic Exercise". International Journal of Sports Medicine 38, n.º 08 (31 de mayo de 2017): 627–36. http://dx.doi.org/10.1055/s-0043-109376.
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AbstractWe aimed to elucidate potential differential effects of hypoxia on cardiorespiratory responses during submaximal cycling and simulated skiing exercise between adults and pre-pubertal children. Healthy, low-altitude residents (adults, N=13, Age=40±4yrs.; children, N=13, age=8±2yrs.) were tested in normoxia (Nor: PiO2=134±0.4 mmHg; 940 m) and normobaric hypoxia (Hyp: PiO2=105±0.6 mmHg; ~3 000 m) following an overnight hypoxic acclimation (≥12-hrs). On both days, the participants underwent a graded cycling test and a simulated skiing protocol. Minute ventilation (VE), oxygen uptake (VO2), heart rate (HR) and capillary-oxygen saturation (SpO2) were measured throughout both tests. The cycling data were interpolated for 2 relative workload levels (1 W·kg−1 & 2 W·kg−1). Higher resting HR in hypoxia, compared to normoxia was only noted in children (Nor:78±17; Hyp:89±17 beats·min−1; p<0.05), while SpO2 was significantly lower in hypoxia (Nor:97±1%; Hyp:91±2%; p<0.01) with no between-group differences. The VE, VO2 and HR responses were higher during hypoxic compared to normoxic cycling test in both groups (p<0.05). Except for greater HR during hypoxic compared to normoxic skiing in children (Nor:155±19; Hyp:167±13 (beats·min−1); p<0.05), no other significant between-group differences were noted during the cycling and skiing protocols. In summary, these data suggest similar cardiorespiratory responses to submaximal hypoxic cycling and simulated skiing in adults and children.
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Klokker, M., M. Kjaer, N. H. Secher, B. Hanel, L. Worm, M. Kappel y B. K. Pedersen. "Natural killer cell response to exercise in humans: effect of hypoxia and epidural anesthesia". Journal of Applied Physiology 78, n.º 2 (1 de febrero de 1995): 709–16. http://dx.doi.org/10.1152/jappl.1995.78.2.709.
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For the response of immunologically competent blood cells to exercise, the importance of afferent nerve impulses was evaluated. On separate days, seven males cycled in a recumbent position approximately 60% of maximal O2 uptake with and without sensory nerve blockade by lumbar epidural anesthesia. Blood samples were collected after 60 min of rest, 20 min of exercise, and 120 min postexercise. Subsequently, on each day, the subjects were exposed to 11.5% O2–88.5% N2 for 10 min. This was followed by 20 min of hypoxic exercise at the same work rate, and a final blood sample was obtained. The concentrations of lymphocytes expressing the cluster designation (CD) cell-surface antigens CD3, CD4, CD8, and CD14 became elevated during exercise, and these responses were enhanced by hypoxia (P < or = 0.01). The most pronounced changes were within the concentrations of CD16+ and CD56+ natural killer cells, which increased twofold during normoxic and fivefold during hypoxic exercise (P < or = 0.01). Sensory nerve blockade decreased the number of CD3+ and CD4+ cells and increased the percentage of CD16+ cells, independent of exercise and hypoxia (P < or = 0.05). Sensory nerve blockade caused minor enhancement in the increase of unstimulated natural killer cell activity during exercise (P = 0.07) and enhanced the interferon-alpha-stimulated activity at normoxia (P < or = 0.05), whereas no effect was detected at hypoxia. The results demonstrate that the responses of immunological competent cells to normoxic and hypoxic exercise are not abolished by blockade of nerve impulses from active muscle.
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Schmitt, P. M., F. L. Powell y S. R. Hopkins. "Ventilation-perfusion inequality during normoxic and hypoxic exercise in the emu". Journal of Applied Physiology 93, n.º 6 (1 de diciembre de 2002): 1980–86. http://dx.doi.org/10.1152/japplphysiol.01108.2001.
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Many avian species exhibit an extraordinary ability to exercise under hypoxic condition compared with mammals, and more efficient pulmonary O2 transport has been hypothesized to contribute to this avian advantage. We studied six emus ( Dromaius novaehollandaie, 4–6 mo old, 25–40 kg) at rest and during treadmill exercise in normoxia and hypoxia (inspired O2 fraction ≈ 0.13). The multiple inert gas elimination technique was used to measure ventilation-perfusion (V˙/Q˙) distribution of the lung and calculate cardiac output and parabronchial ventilation. In both normoxia and hypoxia, exercise increased arterial Po 2 and decreased arterial Pco 2, reflecting hyperventilation, whereas pH remained unchanged. The V˙/Q˙ distribution was unimodal, with a log standard deviation of perfusion distribution = 0.60 ± 0.06 at rest; this did not change significantly with either exercise or hypoxia. Intrapulmonary shunt was <1% of the cardiac output in all conditions. CO2 elimination was enhanced by hypoxia and exercise, but O2 exchange was not affected by exercise in normoxia or hypoxia. The stability of V˙/Q˙ matching under conditions of hypoxia and exercise may be advantageous for birds flying at altitude.
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Maciejczyk, Mateusz, Anna Zalewska, Małgorzata Gryciuk, Katarzyna Hodun, Miłosz Czuba, Kamila Płoszczyca, Małgorzata Charmas, Jerzy Sadowski y Marcin Baranowski. "Effect of Normobaric Hypoxia on Alterations in Redox Homeostasis, Nitrosative Stress, Inflammation, and Lysosomal Function following Acute Physical Exercise". Oxidative Medicine and Cellular Longevity 2022 (25 de febrero de 2022): 1–18. http://dx.doi.org/10.1155/2022/4048543.
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Hypoxia is a recognized inducer of oxidative stress during prolonged physical activity. Nevertheless, previous studies have not systematically examined the effects of normoxia and hypoxia during acute physical exercise. The study is aimed at evaluating the relationship between enzymatic and nonenzymatic antioxidant barrier, total antioxidant/oxidant status, oxidative and nitrosative damage, inflammation, and lysosomal function in different acute exercise protocols under normoxia and hypoxia. Fifteen competitive athletes were recruited for the study. They were subjected to two types of acute cycling exercise with different intensities and durations: graded exercise until exhaustion (GE) and simulated 30 km individual time trial (TT). Both exercise protocols were performed under normoxic and hypoxic ( Fi O 2 = 16.5 % ) conditions. The number of subjects was determined based on our previous experiment, assuming the test power = 0.8 and α = 0.05 . We demonstrated enhanced enzymatic antioxidant systems during hypoxic exercise (GE: ↑ catalase (CAT), ↑ superoxide dismutase; TT: ↑ CAT) with a concomitant decrease in plasma reduced glutathione. In athletes exercising in hypoxia, redox status was shifted in favor of oxidation reactions (GE: ↑ total oxidant status, ↓ redox ratio), leading to increased oxidation/nitration of proteins (GE: ↑ advanced oxidation protein products (AOPP), ↑ ischemia-modified albumin, ↑ 3-nitrotyrosine, ↑ S-nitrosothiols; TT: ↑ AOPP) and lipids (GE: ↑ malondialdehyde). Concentrations of nitric oxide and its metabolites (peroxynitrite) were significantly higher in the plasma of hypoxic exercisers with an associated increase in inflammatory mediators (GE: ↑ myeloperoxidase, ↑ tumor necrosis factor-alpha) and lysosomal exoglycosidase activity (GE: ↑ N-acetyl-β-hexosaminidase, ↑ β-glucuronidase). Our study indicates that even a single intensive exercise session disrupts the antioxidant barrier and leads to increased oxidative and nitrosative damage at the systemic level. High-intensity exercise until exhaustion (GE) alters redox homeostasis more than the less intense exercise (TT, near the anaerobic threshold) of longer duration ( 20.2 ± 1.9 min vs. 61.1 ± 5.4 min—normoxia; 18.0 ± 1.9 min vs. 63.7 ± 3.0 min—hypoxia), while hypoxia significantly exacerbates oxidative stress, inflammation, and lysosomal dysfunction in athletic subjects.
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Jung, Won-Sang, Sung-Woo Kim, Jeong-Weon Kim y Hun-Young Park. "Resistance Training in Hypoxia as a New Therapeutic Modality for Sarcopenia—A Narrative Review". Life 11, n.º 2 (30 de enero de 2021): 106. http://dx.doi.org/10.3390/life11020106.
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Hypoxic training is believed to be generally useful for improving exercise performance in various athletes. Nowadays, exercise intervention in hypoxia is recognized as a new therapeutic modality for health promotion and disease prevention or treatment based on the lower mortality and prevalence of people living in high-altitude environments than those living in low-altitude environments. Recently, resistance training in hypoxia (RTH), a new therapeutic modality combining hypoxia and resistance exercise, has been attempted to improve muscle hypertrophy and muscle function. RTH is known to induce greater muscle size, lean mass, increased muscle strength and endurance, bodily function, and angiogenesis of skeletal muscles than traditional resistance exercise. Therefore, we examined previous studies to understand the clinical and physiological aspects of sarcopenia and RTH for muscular function and hypertrophy. However, few investigations have examined the combined effects of hypoxic stress and resistance exercise, and as such, it is difficult to make recommendations for implementing universal RTH programs for sarcopenia based on current understanding. It should also be acknowledged that a number of mechanisms proposed to facilitate the augmented response to RTH remain poorly understood, particularly the role of metabolic, hormonal, and intracellular signaling pathways. Further RTH intervention studies considering various exercise parameters (e.g., load, recovery time between sets, hypoxic dose, and intervention period) are strongly recommended to reinforce knowledge about the adaptational processes and the effects of this type of resistance training for sarcopenia in older people.
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Wang, Jong-Shyan y Ya-Ting Chiu. "Systemic hypoxia enhances exercise-mediated bactericidal and subsequent apoptotic responses in human neutrophils". Journal of Applied Physiology 107, n.º 4 (octubre de 2009): 1213–22. http://dx.doi.org/10.1152/japplphysiol.00316.2009.
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Phagocytosis and oxidative burst are critical host defense mechanisms in which neutrophils clear invading pathogens. Clearing phagocytic neutrophils by triggering apoptosis is an essential process for controlling inflammation. This study elucidates how various exercise bouts with/without hypoxia affected neutrophil bactericidal activity and subsequent apoptosis in humans. Fifteen sedentary males performed six distinct experimental tests in an air-conditioned normobaric hypoxia chamber: two normoxic exercises [strenuous exercise (SE; up to maximal O2consumption) and moderate exercise (ME; 50% maximal O2consumption for 30 min) while exposed to 21% O2], two hypoxic exercises (ME for 30 min while exposed to 12% and 15% O2), and two hypoxic exposures (resting for 30 min while exposed to 12% and 15% O2). The results showed that 1) plasma complement-C3a desArg/C4a desArg/C5a concentrations were increased, 2) expressions of L-selectin/lymphocyte functin-associated antigen-1/Mac-1/C5aR on neutrophils were enhanced, 3) phagocytosis of neutrophils to Esherichia coli and release of neutrophil oxidant products by E. coli were elevated, and 4) E. coli -induced phosphotidylserine exposure or caspase-3 activation of neutrophils were promoted immediately and 2 h after both 12% O2exposure at rest and with ME as well as normoxic SE. Although neither normoxic ME nor breathing 15% O2at rest influenced these complement- and neutrophil-related immune responses, ME at both 12% and 15% O2resulted in enhanced complement activation in the blood, expressions of opsonic/complement receptors on neutrophils, or the bactericidal activity and apoptosis of neutrophils. Moreover, the increased neutrophil oxidant production and apoptosis by normoxic SE and hypoxic ME were ameliorated by treating neutrophils with diphenylene iodonium (a NADPH oxidase inhibitor). Therefore, we conclude that ME at 12–15% O2enhances bactericidal capacity and facilitates the subsequent apoptosis of neutrophils.
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Tan, Can Ozan, Yu-Chieh Tzeng, Jason W. Hamner, Renaud Tamisier y J. Andrew Taylor. "Alterations in sympathetic neurovascular transduction during acute hypoxia in humans". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, n.º 11 (1 de junio de 2013): R959—R965. http://dx.doi.org/10.1152/ajpregu.00071.2013.
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Resting vascular sympathetic outflow is significantly increased during and beyond exposure to acute hypoxia without a parallel increase in either resistance or pressure. This uncoupling may indicate a reduction in the ability of sympathetic outflow to effect vascular responses (sympathetic transduction). However, the effect of hypoxia on sympathetic transduction has not been explored. We hypothesized that transduction would either remain unchanged or be reduced by isocapnic hypoxia. In 11 young healthy individuals, we measured beat-by-beat pressure, multiunit sympathetic nerve activity, and popliteal blood flow velocity at rest and during isometric handgrip exercise to fatigue, before and during isocapnic hypoxia (∼80% SpO2), and derived sympathetic transduction for each subject via a transfer function that reflects Poiseuille's law of flow. During hypoxia, heart rate and sympathetic nerve activity increased, whereas pressure and flow remained unchanged. Both normoxic and hypoxic exercise elicited significant increases in heart rate, pressure, and sympathetic activity, although sympathetic responses to hypoxic exercise were blunted. Hypoxia slightly increased the gain relation between pressure and flow (0.062 ± 0.006 vs. 0.074 ± 0.004 cm·s−1·mmHg−1; P = 0.04), but markedly increased sympathetic transduction (−0.024 ± 0.005 vs. −0.042 ± 0.007 cm·s−1·spike−1; P < 0.01). The pressor response to isometric handgrip was similar during normoxic and hypoxic exercise due to the balance of interactions among the tachycardia, sympathoexcitation, and transduction. This indicates that the ability of sympathetic activity to affect vasoconstriction is enhanced during brief exposure to isocapnic hypoxia, and this appears to offset the potent vasodilatory stimulus of hypoxia.
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MacNutt, Meaghan J., Carli M. Peters, Catherine Chan, Jason Moore, Serena Shum y A. William Sheel. "Day-to-day variability in cardiorespiratory responses to hypoxic cycle exercise". Applied Physiology, Nutrition, and Metabolism 40, n.º 2 (febrero de 2015): 155–61. http://dx.doi.org/10.1139/apnm-2014-0297.
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Repeatedly performing exercise in hypoxia could elicit an independent training response and become an unintended co-intervention. The primary purposes of this study were to determine if hypoxic exercise responses changed across repeated testing and to assess the day-to-day variability of commonly used measures of cardiorespiratory and metabolic responses to hypoxic exercise. Healthy young males (aged 23 ± 2 years) with a maximal O2 consumption of 50.7 ± 4.7 mL·kg−1·min−1 performed 5 trials (H1 to H5) over a 2-week period in hypoxia (fraction of inspired oxygen = 0.13). Participants completed 3-min stages at 20%, 40%, 60%, and 10% of individual peak power. With increasing cycle exercise intensity there were increases in minute ventilation, O2 consumption, CO2 production, respiratory exchange ratio, heart rate (HR), blood lactate concentration, and ratings of perceived exertion for legs and respiratory system along with a reduction in oxyhaemoglobin saturation (%SpO2) (all p < 0.001). There were no systematic changes from H1 to H5 (p > 0.05). Most measures were highly repeatable across testing sessions with the coefficient of variation (CV) averaging ≤10% of the mean value in all variables except O2 consumption (17%), CO2 production (11%) and blood lactate concentration (17%). For HR and %SpO2 the CV was <5%. The exercise protocol did not elicit a training response when repeated 5 times during a 2-week period and the variability of exercise responses was low. We conclude that this protocol allows detection of small changes in cardiorespiratory responses to hypoxic exercise that might occur during exposure to hypoxia.
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Chen, Yu-Wen, Yi-Ching Chen y Jong-Shyan Wang. "Absolute hypoxic exercise training enhances in vitro thrombin generation by increasing procoagulant platelet-derived microparticles under high shear stress in sedentary men". Clinical Science 124, n.º 10 (4 de febrero de 2013): 639–49. http://dx.doi.org/10.1042/cs20120540.
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HS (high shear) stress associated with artery stenosis facilitates TG (thrombin generation) by increasing the release of procoagulant PDMPs (platelet-derived microparticles). Physical exercise and hypoxia may paradoxically modulate vascular thrombotic risks. The aim of the present study was to investigate how exercise training with/without hypoxia affected TG mediated by PDMPs under physio-pathological shear flows. A total of 75 sedentary males were randomly divided into five groups (n=15 in each group): 21% O2 [NC (normoxic control)] or 15% O2 [HC (hypoxic control)] at rest or were trained at 50% of peak work rate under 21% O2 [NT (normoxic training)] or 15% O2 [HAT (hypoxic-absolute training)], or 50% of HR (heart rate) reserve under 15% O2 [HRT (hypoxic-relative training)] for 30 min/day, 5 days/week for 4 weeks. The PDMP characteristics and dynamic TG were measured by flow cytometry and thrombinography respectively. Before the intervention, strenuous exercise markedly increased the PDMP count (14.8%) and TG rate (19.5%) in PDMP-rich plasma at 100 dynes/cm2 of shear stress (P<0.05). After the interventions, both NT and HRT significantly attenuated the enhancement of HS-induced PDMPs (4.7 and 4.9%) and TG rate (3.8 and 3.0%) (P<0.05) by severe exercise. Conversely, HAT notably promoted the PDMP count (37.3%) and TG rate (38.9%) induced by HS (P<0.05), concurrent with increasing plasma TF (tissue factor) and coagulation factor V levels at rest or following exercise. We conclude that both HRT and NT depress similarly HS-mediated TG during exercise, but HAT accelerates the prothrombotic response to vigorous exercise. These findings provide new insights into how exercise training under a hypoxic condition influences the risk of thrombosis associated with stenotic arteries.