Bibliographies thématiques / Hypoxic exercise

Littérature scientifique sur le sujet « Hypoxic exercise »

Auteur : Grafiati
Publié le 11 mars 2023

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Articles de revues sur le sujet "Hypoxic exercise"

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Ray, A. D., A. J. Roberts, S. D. Lee, G. A. Farkas, C. Michlin, D. I. Rifkin, P. T. Ostrow et J. A. Krasney. « Exercise delays the hypoxic thermal response in rats ». Journal of Applied Physiology 95, no 1 (juillet 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 et Miharu Miyamura. « Intermittent hypoxia increases ventilation and SaO2 during hypoxic exercise and hypoxic chemosensitivity ». Journal of Applied Physiology 90, no 4 (1 avril 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 et Ufuk Çakatay. « Hypoxia and Hypoxic Exercise Induced Systemic Ros Disrupts the Redox Homeostasis in the Brain ». Pakistan Journal of Medical and Health Sciences 16, no 1 (30 janvier 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 et Michael J. Joyner. « Systemic hypoxia and vasoconstrictor responsiveness in exercising human muscle ». Journal of Applied Physiology 101, no 5 (novembre 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 et 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, no 2 (février 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 et Federico Schena. « Effects of acute hypoxia on the oxygen uptake kinetics of older adults during cycling exercise ». Applied Physiology, Nutrition, and Metabolism 37, no 4 (août 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., et D. R. Seals. « Hypoxic potentiation of the ventilatory response to dynamic forearm exercise ». Journal of Applied Physiology 74, no 5 (1 mai 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 et Samuel Verges. « The effect of hypoxemia and exercise on acute mountain sickness symptoms ». Journal of Applied Physiology 114, no 2 (15 janvier 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, no 6 (décembre 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 et 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, no 1 (juillet 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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Thèses sur le sujet "Hypoxic exercise"

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Henslin, Kayla B. « Rapidity of response to hypoxic conditions during exercise / ». Connect to online version, 2009. http://minds.wisconsin.edu/handle/1793/45116.

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Seo, Yongsuk. « THE EFFECTS OF ACUTE EXERCISE ON COGNITIVE PERFORMANCE IN HYPOXIC CONDITIONS ». Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1424093235.

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De, Cort Susan Caroline. « Measurement of hypoxic ventilatory drive at rest and during exercise in normal man ». Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/18823.

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Falgin, Hultgren Jonas. « The Acute Metabolic Response of Intermittent Hypoxic Resistance Exercise : A Cross-Over RCT ». Thesis, Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:gih:diva-5791.

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Aim The aim for this present study was to investigate the acute metabolic response from intermittent resistance exercise during hypoxia, with the following research questions: (1) Are blood levels of lactate and glucose different between hypoxia and normoxia? (2) Does hypoxia induce higher lactate accumulation and pH reduction in the human skeletal muscle? (3) Is there a relationship between plasma-, blood- and muscle lactate? Method Eight healthy males (30 ± 2 years) performed 6 sets of unilateral leg extension on each leg (75% of 1RM) with randomized normoxic (20,9% inspired 𝑂2) and normobaric hypoxic (12% inspired 𝑂2) conditions. A total of 5 muscle biopsies was extracted from m. Vastus Lateralis (pre-, post exercise, 90-, 180min and 24h post exercise) during both normoxia and hypoxia trials, separated by one week for all participants. Blood samples were repeatedly taken with 20 min intervals. Heart Rate (HR) and saturation (𝑆𝑝𝑂2) were measured by a pulsoximeter during resistance exercise. Results No significant main effect was observed for blood lactate and glucose levels as well as the muscle lactate accumulation and pH between normoxia and hypoxia. However, pH in muscle showed a trend between the conditions post exercise where hypoxia reached lower levels in total (P=0.08). Significant correlations were observed for blood- and plasma lactate, where hypoxia showed a stronger relationship than normoxia (r=0.98 compared to r=0.87). Equal findings for the correlation of muscle- and plasma lactate showed an even greater coefficient value for hypoxia compared to normoxia (r=0.860 compared to r=0.59). Conclusion Summarized data indicated that no significant difference between hypoxia and normoxia was evident. Nonetheless, tendencies illustrate that hypoxia may alter the metabolic response slightly. However, further research is needed to draw a conclusion between the conditions.
Syftet med denna studie är att undersöka kroppens akuta metabola svar från intermittent styrketräning under hypoxi, med följande frågeställningar: (1) Skiljer sig nivåerna av laktat och glukos i blodet mellan hypoxi och normoxi? (2) Skapar hypoxi större laktatansamling och pH reduktion i människoskelettmuskeln? (3) Finns det en relation mellan plasma-, blod- och muskellaktat? Metod Åtta friska män (30 ± 2 år) deltog där deltagarna utförde 6 set unilateral benextension för varje ben (75% 1RM). Intermittent styrketräning randomiserades med hypoxi som utfördes med 12% syrgas och normoxi som bibehöll normal syrgasnivå (20,9% syrgas). Under två testdagar togs 5 muskelbiopsier från m. Vastus Lateralis (före-, efter träning, 90-, 180min och 24h efter träning) på vartannat ben per testdag. Hjärtfrekvensen och 𝑆𝑝𝑂2 mättes via pulsoximeter under träningen. Resultat Ingen signifikant huvudeffekt påvisades mellan hypoxi och normoxi för blodlaktat samt glukos, såväl som laktatackumulationen och pH värdet i muskeln. Muskel pH visade en trend där hypoxi efter styrketräning nådde lägre totalnivå än normoxi (P=0,08). Vidare observerades hypoxi att ha starka relationer mellan blod- och plasmalaktat jämfört med normoxi (r=0,98 vs. r=0,87). Större skillnad framgick för korrelationen mellan muskel- och plasmalaktat där hypoxi-försöket utgav starkare koefficient jämfört med normoxi (r=0,86 vs. r=0,59). Konklusion Sammanfattad data visar att hypoxi inte skapar större metabolisk respons vid intermittent styrketräning. Trots detta framkom tendenser som illustrerar att hypoxi kan påverka den metabola stressen under styrketräning. Däremot krävs vidare forskning för att kunna säkerställa effekten av hypoxi på kroppens metabola svar.
Ingår i Marcus Mobergs projekt: ”Resistance exercise under hypoxia and the acute molecular effects in human skeletal muscle
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Ernst, Melissa H. « The effects of hypobaric hypoxia on aspects of oxygen transport and utilization in mice with an inherited tolerance for hypoxic exercise / ». Electronic version (PDF), 2003. http://dl.uncw.edu/etd/2003/ernstm/melissaernst.pdf.

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Feeback, Matthew Ray. « Physiological differences before, during and after hypoxic exercise between African-American and Caucasian males ». Thesis, Kent State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3618897.

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INTRODUCTION: Hypoxia is a potent stimulus that induces neuropsychological and physical impairments in humans. It is documented that ethnic differences exists across various physiological parameters. There appears to be a varying metabolic response across ethnicities, specifically African-Americans and Caucasians. Purpose: To further elucidate physiological and cognitive performance differences between African-American (AA) and Caucasian individuals (CAU) before, during or after hypoxic and normoxic exercise. Methods: Twelve college aged (18-25) apparently healthy African-American (six volunteers) and Caucasian (six subjects) males took part in two trials consisting of normobaric normoxia and normobaric hypoxia (12% oxygen). Each subject cycled at 50% of their altitude adjusted VO2max (-26% of normoxia VO2max) for one hour after a two-hour baseline. Subjects were monitored for cerebral and arterial O2 saturation, as well as the Trail Making Test A and B (TMT) psychomotor performance. Results: Arterial saturation proved to be significantly higher in AA (86.0±4.7) compared to CAU (79.5±4.8) during the first 60 minutes of exposure to hypoxia at rest (p=0.039), but not during exercise. Cerebral oxygenation to the left frontal lobe was decreased near the conclusion and 30 minutes after normoxic exercise. TMT B data revealed that CAU (79±12.7) had faster scores than the AA subjects (98±25.1) at all time points and was significantly different at the 115 minute time point of the hypoxic trial (p=0.024). Conclusion: Data suggests that before, during and after normobaric normoxia and hypoxia trial there is a differential response between AA and CAU in regards to arterial and cerebral oxygenation and psychomotor tests.

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Feeback, Matthew R. « Physiological Differences Before, During and After Hypoxic Exercise Between African-American and Caucasian Males ». Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1385043374.

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Hopkins, Susan Roberta. « The relationship between the hypoxic ventilatory response and arterial desaturation during heavy work ». Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28535.

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Arterial desaturation in fit athletes, during exercise at an intensity greater than or equal to 90% of VO₂ max has been reported by a number of authors yet the etiology of these changes remain obscure. Inadequate pulmonary ventilation due to a blunted respiratory drive, or lung mechanics has been implicated as a factor in the etiology of this phenomenon. It was the purpose of this experiment to investigate the relationship between arterial desaturation and ventilatory response to hypoxia (HVR). Twelve healthy male subjects ( age = 23.8 ± 3.6 yrs., height = 181.6 ±₋₁ 5.6 cms., Weight = 73.7 ± 6.2 kg., VO₂ max = 63.2 ± 2.2 ml .kg . -1 2 .min⁻¹) performed a five minute exercise test on a treadmill at 100% of VO₂ max. Arterial samples for pH, PCO₂, PO₂, and SaO₂ were withdrawn via an indwelling arterial cannula at rest and every 15s throughout the exercise test. The blood gas samples were analyzed with an Instrument Laboratories 1306 blood gas analyzer. Ventilation and VO₂ were measured by a Beckman metabolic measurement cart. On a separate occasion the ventilatory response to hypoxia (HVR) was determined by recording VE as progressive hypoxia was induced by adding N₂ to a mixing chamber. SaO₂ was measured using a Hewlett-Packard ear oximeter; to maintain isocapnia small ammounts of CO₂ were added to the open circuit system. ANOVA for repeated measured was used to evaluate changes in blood gases, ventilation, and VO₂. Simple linear regression and multiple linear regression was used to evaluate the relationship between the changes in SaO₂ and HVR and the descriptive variables. Subjects showed a significant decline in arterial saturation and PO₂ over the course of the test (p < 0.01,and p < 0.01). Four subjects (Mild) exhibited modest decreases in SaO₂ to (94.6 ± 1.9%), three (Moderate) showed an intermediate response (SaO₂ 91.6 ± 0.1%) and five (Marked) demonstrated a marked decrease in arterial saturation (SaO₂ = 90.0 + 1.2%). The differences in PO₂ and SaO₂ between Mild and Marked groups were significant ( p < 0.05, and p < 0.01); there were no significant differences between groups in VE, VO₂, pH or PCO . There was no significant correlation between the lowest SaO₂ reached and HVR, or any of the descriptive variables. Nine subjects did not reach maximal VE (as determined by the VO₂ max test) on the exercise test, two subjects 2 exhibited similar ventilation, and the remaining subject exceeded maximal VE, but fell into the Mild group with respect to desaturation. Oxygen uptake exceeded that recorded for the VO₂ max determination for four of the five subjects in the Marked group; the remaining subjects demonstrated lower or similar values. It was concluded that arterial desaturation was not related to blunted hypoxic drive.
Education, Faculty of
Curriculum and Pedagogy (EDCP), Department of
Graduate
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Cheng, Hung-Yuan. « Right ventricular outflow limitation and capacity for exertion associated with age and iron status ». Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:d8621b88-c220-4ad5-bd69-ab23f9dcb9e3.

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This thesis is concerned with the role of iron in modulating right ventricular (RV) afterload during exercise in healthy people aged between 50 and 80 years. This is predicated on the requirement of the hypoxia-inducible factor (HIF) pathway for ferrous iron. A secondary objective is to examine the reactive oxygen species (ROS) hypothesis in human hypoxic pulmonary vasoconstriction (HPV) using exposure to hyperoxia. Chapters 3 and 4 describe basal relationships that may affect the HIF pathway and exercise capacity during ageing. These were explored in 113 participants using blood tests and exercise tests. Age and inflammatory factors, C-reactive protein, and ferritin were associated with impaired exercise capacity. In addition, ageing did not significantly affect haematological variables or iron status indicators. Chapters 5 and 6 describe the effect of a single intravenous iron infusion on the haematological variables in 32 participants in a randomised, placebo-controlled and double-blinded study. The effects of iron infusion on RV afterload during light exercise, and exercise capacity during heavy exercise, were examined in these participants. With iron infusion, erythropoietin production, and the increase in RV afterload during light exercise were blunted, potentially indicating involvement of the HIF pathway. However, blunting of RV afterload neither influenced the cardiac output during light exercise nor exercise capacity. Chapter 7 describes a study of 11 healthy volunteers, which investigated the ROS hypothesis in HPV using acute isocapnic hypoxia following an 8-hour exposure to hyperoxia. This sustained hyperoxic exposure did not influence the hypoxic behavior of the pulmonary vasculature. This thesis demonstrates the complex relationship between iron status and exercise capacity in older adults. It shows that the decrease in RV afterload during exercise caused by intravenous iron supplementation does not lead to an augmented cardiac output or exercise capacity. Finally, it calls into question the role of ROS in HPV.
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Heusch, Andrew I. « The effect of normobaric mormoxic and hypoxic exercise upon plasma total homocysteine and blood lipid concentrations ». Thesis, University of South Wales, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289375.

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Livres sur le sujet "Hypoxic exercise"

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Roach, Robert C., Peter D. Wagner et Peter H. Hackett, dir. Hypoxia and Exercise. Boston, MA : Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-34817-9.

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1956-, Roach Robert C., Wagner P. D, Hackett Peter H et International Hypoxia Symposium (15th : 2007 : Lake Louise, Alta.), dir. Hypoxia and the circulation. New York, N.Y : Springer, 2007.

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Sandblom, Erik. The venous circulation in teleost fish : Responses to exercise, temperature and hypoxia. Göteborg : Dept. of Zoology/Zoophysiology, Göteborg University, 2007.

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Hypoxia and Exercise. Springer, 2010.

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Hackett, Peter, Peter D. Wagner et Robert Roach. Hypoxia and Exercise. Springer, 2007.

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Hackett, Peter, Peter D. Wagner et Robert Roach. Hypoxia and the Circulation. Springer London, Limited, 2008.

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Hackett, Peter, Peter D. Wagner et Robert Roach. Hypoxia and the Circulation. Springer, 2010.

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Bailey, Damian Miles. Chronic hypobaric hypoxia : Physiological implications for exercise performance. 1997.

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(Editor), Robert Roach, Peter D. Wagner (Editor) et Peter Hackett (Editor), dir. Hypoxia and Exercise (Advances in Experimental Medicine and Biology). Springer, 2006.

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Girard, Olivier, Donald R. McCrimmon et Gregoire P. Millet, dir. High-Intensity Exercise in Hypoxia - Beneficial Aspects and Potential Drawbacks. Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-406-8.

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Chapitres de livres sur le sujet "Hypoxic exercise"

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Sainburg, Robert L., Andrew L. Clark, George E. Billman, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble et al. « Hypoxia, Focus Hypoxic Hypoxia ». Dans Encyclopedia of Exercise Medicine in Health and Disease, 431–34. Berlin, Heidelberg : Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_107.

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Sainburg, Robert L., Andrew L. Clark, George E. Billman, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble et al. « Hypoxic Training ». Dans Encyclopedia of Exercise Medicine in Health and Disease, 440. Berlin, Heidelberg : Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4285.

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Grimm, Christian, A. Wenzel, N. Acar, S. Keller, M. Seeliger et Max Gassmann. « Hypoxic Preconditioning and Erythropoietin Protect Retinal Neurons from Degeneration ». Dans Hypoxia and Exercise, 119–31. Boston, MA : Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-34817-9_11.

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Turner, Duncan L., Patricia A. Martin et Gordon S. Mitchell. « Hypoxic Exercise does not Elicit Longterm Modulation of the Normoxic Exercise Ventilatory Response in Goats ». Dans Advances in Experimental Medicine and Biology, 245–48. Boston, MA : Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1933-1_46.

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Burtscher, Martin. « Effects of Intermittent Hypoxic Training on Exercise Tolerance in Patients with Chronic Obstructive Pulmonary Disease ». Dans Intermittent Hypoxia and Human Diseases, 127–34. London : Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2906-6_10.

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Ohyabu, Yoshio, Ihoko Ohyabu, Akio Usami et Yoshiyuki Honda. « Studies on Exercise Hyperpnea in Relation with Hypoxic Ventilatory Chemosensitivity Measured at Rest ». Dans Respiratory Control, 225–34. Boston, MA : Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0529-3_25.

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Walsh, M. L., et E. W. Banister. « Acute Ventilatory Response to Ramp Exercise while Breathing Hypoxic, Normoxic, or Hyperoxic Air ». Dans Advances in Experimental Medicine and Biology, 143–46. Boston, MA : Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1933-1_29.

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Levine, Benjamin D., et James Stray-Gundersen. « The effects of altitude training are mediated primarily by acclimatization, rather than by hypoxic exercise ». Dans Advances in Experimental Medicine and Biology, 75–88. Boston, MA : Springer US, 2001. http://dx.doi.org/10.1007/978-1-4757-3401-0_7.

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Bonny, Christophe. « Blocking Stress Signaling Pathways with Cell Permeable Peptides ». Dans Hypoxia and Exercise, 133–43. Boston, MA : Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-34817-9_12.

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Levine, Benjamin D., et James Stray-Gundersen. « Dose-Response of Altitude Training : How Much Altitude is Enough ? » Dans Hypoxia and Exercise, 233–47. Boston, MA : Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-34817-9_20.

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Actes de conférences sur le sujet "Hypoxic exercise"

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Syahrastani, Argantos, Dwi Hilda Putri, Dezi Handayani et Siska Alicia Farma Alisirsyah. « Comparison of Serum HIF-1α Levels in Swimming Athletes Before and After Hypoxic Non-Hypoxic Exercise ». Dans 1st International Conference of Physical Education (ICPE 2019). Paris, France : Atlantis Press, 2020. http://dx.doi.org/10.2991/assehr.k.200805.060.

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Isaac, Ashvin, William Noffsinger, Christopher Kosky et Bhajan Singh. « Light exercise during a Hypoxic Challenge Test alters recommendations for air travel ». Dans ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3911.

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Verges, Samuel, Samarmar Chacaroun, Anna Borowik, Ignacio Vega-Escamilla Y Gonzalez, Stéphane Doutreleau, Bernard Wuyam, Elise Belaidi, Renaud Tamisier, Jean-Louis Pépin et Patrice Flore. « Hypoxic training to improve exercise capacity in obesity : a randomized controlled trial ». Dans ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1929.

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Talbot, Nick, Hung-Yuan Cheng, Thomas Smith, Keith Dorrington et Peter Robbins. « Effects of intravenous iron on hypoxic pulmonary vasoconstriction and maximal exercise capacity during sustained (8 h) hypoxia in healthy volunteers. » Dans ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2477.

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Geraskin, Dmitri, Petra Platen, Julia Franke, Christiane Andre, Wilhelm Bloch et Matthias Kohl-Bareis. « Muscle Oxygenation during Exercise under Hypoxic Conditions Assessed by Spatial-Resolved Broadband NIR Spectroscopy ». Dans European Conference on Biomedical Optics. Washington, D.C. : OSA, 2005. http://dx.doi.org/10.1364/ecbo.2005.we4.

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Geraskin, Dmitri, Petra Platen, Julia Franke, Christiane Andre, Wilhelm Bloch et Matthias Kohl-Bareis. « Muscle oxygenation during exercise under hypoxic conditions assessed by spatially resolved broadband NIR spectroscopy ». Dans European Conference on Biomedical Optics 2005, sous la direction de Kai Licha et Rinaldo Cubeddu. SPIE, 2005. http://dx.doi.org/10.1117/12.632841.

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Lee, W., B. Lee, H. Seo, H. Park, J. Park, S. Lee, S. Lee et al. « The Effects of Exercise with Intermittent Hypoxic Normobaric Environment on Change of Cytokines in Mice Lung Tissue. » Dans American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2103.

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Cao, Zhengtao, Yuanyuan Liu, Chengyu Liu, Jun Yang, Chenyu Luo, Binhua Wang, Haitao Wang, Yanyan Wang et Mengsun Yu. « Analysis of Heart Rate Variability between Rest and Exercise States in Hypoxic Environment Using Fuzzy Measure Entropy ». Dans 2016 8th International Conference on Information Technology in Medicine and Education (ITME). IEEE, 2016. http://dx.doi.org/10.1109/itme.2016.0028.

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Askari, Shahbaz, Zoya Bastany, Liisa Holsti, Ali Gorji et Guy D. Dumont. « Combined low-frequency EEG and NIRS during hypoxia ». Dans Biophotonics in Exercise Science, Sports Medicine, Health Monitoring Technologies, and Wearables, sous la direction de Babak Shadgan et Amir H. Gandjbakhche. SPIE, 2020. http://dx.doi.org/10.1117/12.2550234.

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Teckchandani, Taylor A., David Mac Quarrie, Jyotpal Singh et J. Patrick Neary. « Effects of normobaric hypoxia on cardiac mechanical function using seismocardiography ». Dans Biophotonics in Exercise Science, Sports Medicine, Health Monitoring Technologies, and Wearables, sous la direction de Babak Shadgan et Amir H. Gandjbakhche. SPIE, 2020. http://dx.doi.org/10.1117/12.2546378.

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