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Aerobic performance improvment and mitochondrial adaptations after endurance training in hypoxia

Malgoyre, A (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
Sanchez, H (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
Tonini, J (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
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Serrurier, B (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
Prola, A (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
Chaillou, Thomas, 1985- (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
Simler, N (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
Bigard, X (författare)
Institut de Recherche Biomdicale de Armes, La Tronche, France
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 (creator_code:org_t)
John Wiley & Sons, 2011
2011
Engelska.
Ingår i: Acta Physiologica. - : John Wiley & Sons. - 1748-1708 .- 1748-1716. ; 202:Suppl. 685
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • Aim: The aim of the present study was to examine the effects of hypoxic endurance training on both aerobic performance and mitochondrial changes within plantaris muscle, independently of hematopoietic modifications.Methods: Four groups of female rats were constituted either sedentary (S) or trained (T), in either hypoxia (H) or normoxia (N). H conditions corresponded to 14% O2 and the training program to 5 running sessions/week for 5 weeks. Duration and intensity reached progressively 75Õ up to 80% of individual maximal aerobic running velocity (MAV) in either H or N. Performances of each rat were analysed through MAV values and time to exhaustion at 65% MAV (T65). Mitochondrial oxidative capacities (Vmax) for pyruvate (pyr), palmitoyl-carnitine (PC) and palmitoyl-CoA (PCoA) were measured in plantaris skinned fibers. Citrate synthase (CS) and HAD activities were also measured.Results: MAV increased in both TN and TH rats (respectively +52%, +39%, P<0.001) without difference between H and N, whereas hypoxia specifically increased T65 (+ 39%, P<0.05) independently of training effect. The training-induced increase in CS activity (P<0.001) was more marked in TN than in TH group (+39% vs +26%, P<0.001) whereas HAD activity rose similarly in TN and TH (respectively +83%, +64%, P<0.05). Physical training increased Vmaxpyr only in N rats (+30%, P<0.001), while VmaxPCoA decreased in hypoxia (P<0.05) without change in VmaxPC. This suggests that LCFA transport by CPT-1 was limiting in hypoxia. As expected, training improved creatine kinase efficiency in N rats (+80%, P<0.005), but no change was shown in H rats.Conclusion: Regarding the modest changes in mitochondrial function, it is likely that other factors contribute to explain the improvement of physical performance after an endurance training in hypoxia.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)

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