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ABSTRACT: 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 males, AMS symptoms were assessed during three 11-h experimental sessions: i) in Hypoxia-exercise, inspiratory O(2) fraction (FiO(2)) was 0.12 and subjects performed 4 h cycling at 45% FiO(2)-specific maximal power output from the 4(th) to the 8(th) hour; ii) in Hypoxia-rest, FiO(2) was continuously adjusted to match the same arterial oxygen saturation as in Hypoxia-exercise and subjects remained at rest; iii) in Normoxia-exercise, FiO(2) was 0.21 and subjects cycled as in Hypoxia-exercise at 45% FiO(2)-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, 2.3±1.5 and cerebral Environmental Symptom Questionnaire: 1.2±0.7, 1.0±1.0, 0.3±0.4, in Hypoxia-exercise, Hypoxia-rest and Normoxia-exercise, respectively; P<0.01). Headache scored by visual analogue scale was higher in Hypoxia-exercise and Hypoxia-rest compared to Normoxia-exercise (36±22, 35±25, 5±6, P<0.001) while the perception of fatigue was higher in Hypoxia-exercise compared to Hypoxia-rest (60±24, 32±22, 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.
Journal of Applied Physiology 11/2012; · 3.75 Impact Factor
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ABSTRACT: Contradictory results regarding the effect of hypoxia on cortex excitability have been reported in healthy subjects, possibly depending on hypoxia exposure duration. We evaluated the effects of 1- and 3-h hypoxia on motor corticospinal excitability, intracortical inhibition, and cortical voluntary activation (VA) using transcranial magnetic stimulation (TMS). TMS to the quadriceps cortex area and femoral nerve electrical stimulations were performed in 14 healthy subjects. Motor-evoked potentials (MEPs at 50-100% maximal voluntary contraction; MVC), recruitment curves (MEPs at 30-100% maximal stimulator power output at 50% MVC), cortical silent periods (CSP), and VA were measured in normoxia and after 1 (n = 12) or 3 (n = 10) h of hypoxia (Fi(O(2)) = 0.12). One-hour hypoxia did not modify any parameters of corticospinal excitability but reduced slightly VA, probably due to the repetition of contractions 1 h apart (96 ± 4% vs. 94 ± 4%; P = 0.03). Conversely, 3-h hypoxia significantly increased 1) MEPs of the quadriceps muscles at all force levels (+26 ± 14%, +24 ± 12%, and +27 ± 17% at 50, 75, and 100% MVC, respectively; P = 0.01) and stimulator power outputs (e.g., +21 ± 14% at 70% maximal power), and 2) CSP at all force levels (+20 ± 18%, +18 ± 19%, and +14 ± 22% at 50, 75, and 100% MVC, respectively; P = 0.02) and stimulator power outputs (e.g., +9 ± 8% at 70% maximal power), but did not modify VA (98 ± 1% vs. 97 ± 3%; P = 0.42). These data demonstrate a time-dependent hypoxia-induced increase in motor corticospinal excitability and intracortical inhibition, without changes in VA. The impact of these cortical changes on physical or psychomotor performances needs to be elucidated to better understand the cerebral effects of hypoxemia.
Journal of Neurophysiology 06/2012; 108(5):1270-7. · 3.32 Impact Factor
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ABSTRACT: Reduction of aerobic exercise performance observed under hypoxic conditions is mainly attributed to altered muscle metabolism due to impaired O(2) delivery. It has been recently proposed that hypoxia-induced cerebral perturbations may also contribute to exercise performance limitation. A significant reduction in cerebral oxygenation during whole body exercise has been reported in hypoxia compared with normoxia, while changes in cerebral perfusion may depend on the brain region, the level of arterial oxygenation and hyperventilation induced alterations in arterial CO(2). With the use of transcranial magnetic stimulation, inconsistent changes in cortical excitability have been reported in hypoxia, whereas a greater impairment in maximal voluntary activation following a fatiguing exercise has been suggested when arterial O(2) content is reduced. Electromyographic recordings during exercise showed an accelerated rise in central motor drive in hypoxia, probably to compensate for greater muscle contractile fatigue. This accelerated development of muscle fatigue in moderate hypoxia may be responsible for increased inhibitory afferent signals to the central nervous system leading to impaired central drive. In severe hypoxia (arterial O(2) saturation <70-75%), cerebral hypoxia per se may become an important contributor to impaired performance and reduced motor drive during prolonged exercise. This review examines the effects of acute and chronic reduction in arterial O(2) (and CO(2)) on cerebral blood flow and cerebral oxygenation, neuronal function, and central drive to the muscles. Direct and indirect influences of arterial deoxygenation on central command are separated. Methodological concerns as well as future research avenues are also considered.
AJP Regulatory Integrative and Comparative Physiology 02/2012; 302(8):R903-16. · 3.34 Impact Factor
