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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003924naa a2200385 4500
001oai:DiVA.org:kth-208671
003SwePub
008170611s2017 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-2086712 URI
024a https://doi.org/10.1113/EP0861672 DOI
040 a (SwePub)kth
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Keramidas, Michail E.u KTH,Omgivningsfysiologi4 aut0 (Swepub:kth)u1uu7lyn
2451 0a LunHab :b interactive effects of a 10 day sustained exposure to hypoxia and bedrest on aerobic exercise capacity in male lowlanders
264 1b John Wiley & Sons,c 2017
338 a print2 rdacarrier
500 a QC 20170613
520 a NEW FINDINGS: What is the central question of this study? What are the distinct and interactive effects of a 10 day exposure to hypoxia and horizontal bedrest on the whole-body peak oxygen uptake and on the regional cerebral and skeletal muscle tissue oxygenation during upright cycle ergometry in male lowlanders? What is the main finding and its importance? A 10 day sustained exposure to hypoxia aggravates the bedrest-induced reduction in peak oxygen uptake during dynamic exercise engaging large muscle groups, but mitigates the skeletal muscle oxidative capacity impairment elicited by bedrest. The study examined the interactive effects of a 10 day exposure to hypoxia and bedrest on the whole-body peak oxygen uptake (V̇O2 peak ) during maximal exercise and on skeletal muscle and cerebral oxygenation during submaximal exercise. Nine males underwent three 10 day confinements, in a Latin-square order, as follows: (i) a normoxic bedrest [NBR; partial pressure of inspired O2 (PI,O2) = 134.2 ± 0.7 mmHg]; (ii) a hypoxic bedrest (HBR; PI,O2 = 102.9 ± 0.1 mmHg at day 1, 91.5 ± 1.2 mmHg at days 3-10); and (iii) a hypoxic ambulation (HAMB; PI,O2 as in HBR). Before, 1 (R+1) and 3 days (R+3) after each confinement, subjects performed exhaustive, incremental-load and moderate-intensity constant-load (CLTs) cycle-ergometry trials, while breathing either room air or a hypoxic gas mixture. During the CLTs, changes in the regional oxygenation of the cerebral frontal cortex and the vastus lateralis and intercostal muscles were monitored with near-infrared spectroscopy. At R+1, the confinement-related impairment in V̇O2 peak was greater after HBR than after NBR or HAMB, regardless of whether the trial was performed in room air or hypoxia (HBR, -16.2%; NBR, -8.3%; HAMB, -4.1%; P = 0.001). During the CLTs, bedrest aggravated the exercise-induced reduction in locomotor and respiratory muscle oxygenation (P ≤ 0.05); an effect that was less after HBR than after NBR (P ≤ 0.05). The hypoxic exercise-induced cerebral vasodilatory response was blunted by HBR, probably because of the marked hyperventilation-dependent hypocapnia, attendant to the sustained hypoxic stimulus. Hence, short-term exposure to hypoxia potentiates the reduction in V̇O2 peak , but it mitigates the impairment in skeletal muscle oxidative capacity induced by bedrest.
653 a NIRS
653 a VO2peak
653 a acclimation
653 a cerebral oxygenation
653 a high altitude
653 a inactivity
653 a microgravity
653 a muscle oxygenation
700a Mekjavic, Igor B4 aut
700a Eiken, Olau KTH,Omgivningsfysiologi,Omgivningsfysiologi, Environmental Physiology, Centrum för Flyg- och Rymdfysiologi, Swedish aerspace Physiology Centre4 aut0 (Swepub:kth)u1fcwvxl
710a KTHb Omgivningsfysiologi4 org
773t Experimental Physiologyd : John Wiley & Sonsg 102:6, s. 694-710q 102:6<694-710x 0958-0670x 1469-445X
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-208671
8564 8u https://doi.org/10.1113/EP086167

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