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- Jacobs, Robert A., et al.
(författare)
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Twenty-eight days of exposure to 3,454 m increases mitochondrial volume density in human skeletal muscle
- 2015
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Ingår i: Journal of Physiology. - : Blackwell Publishing. - 0022-3751 .- 1469-7793. ; 594:5, s. 1151-1166
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Tidskriftsartikel (refereegranskat)abstract
- The role of hypoxia on skeletal muscle mitochondria is controversial. Studies superimposing exercise training with hypoxic exposure demonstrate an increase in skeletal muscle mitochondrial volume density (MitoVD ) over equivalent normoxic training. In contrast, a reduction in both skeletal muscle mass and MitoVD have been reported following mountaineering expeditions. These observations may however be confounded by negative energy balance, which may obscure the results. Accordingly we sought to examine the effects of high altitude hypoxic exposure on mitochondrial characteristics, with emphasis on MitoVD , while minimizing changes in energy balance. For this purpose, skeletal muscle biopsies were obtained from 9 lowlanders at sea level (Pre) and following 7 (7 Days) and 28 (28 Days) days of exposure to 3454 m. Maximal ergometer power output, whole-body weight and composition, leg lean mass, and skeletal muscle fibre area all remained unchanged following the altitude exposure. Transmission electron microscopy determined intermyofibrillar (IMF) MitoVD was augmented (P = 0.028) by 11.5 ± 9.2% from Pre (5.05 ± 0.9%) to Day 28 (5.61 ± 0.04%). On the contrary, there was no change in subsarcolemmal (SS) MitoVD . As a result total MitoVD (IMF + SS) was increased (P = 0.031) from 6.20 ± 1.5% at Pre to 6.62 ± 1.4% on Day 28 (7.8 ± 9.3%). At the same time no changes in mass-specific respiratory capacities, mitochondrial protein or antioxidant content were found. This study demonstrates that skeletal muscle MitoVD may increase with 28 days acclimation to 3454 m.
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| 2. |
- Siebenmann, Christoph, et al.
(författare)
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Parasympathetic withdrawal increases heart rate after 2 weeks at 3454 m altitude
- 2017
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Ingår i: Journal of Physiology. - : Wiley-VCH Verlagsgesellschaft. - 0022-3751 .- 1469-7793. ; 595:5, s. 1619-1626
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Tidskriftsartikel (refereegranskat)abstract
- Chronic hypoxia increases resting heart rate (HR), but the underlying mechanism remains incompletely understood. We investigated the relative contributions of the sympathetic and parasympathetic nervous systems, along with potential non-autonomic mechanisms, by individual and combined pharmacological inhibition of muscarinic and/or beta-adrenergic receptors. In seven healthy lowlanders, resting HR was determined at sea level (SL) and after 15-18 days of exposure to 3454 m high altitude (HA) without drug intervention (control, CONT) as well as after intravenous administration of either propranolol (PROP), or glycopyrrolate (GLYC), or PROP and GLYC in combination (PROP+GLYC). Circulating noradrenaline concentration increased from 0.9 +/- 0.4 nmol l(-1) at SL to 2.7 +/- 1.5 nmol l(-1) at HA (P = 0.03). The effect of HA on HR depended on the type of autonomic inhibition (P = 0.006). Specifically, HR was increased at HA from 64 +/- 10 to 74 +/- 12 beats min-(1) during the CONT treatment (P = 0.007) and from 52 +/- 4 to 59 +/- 5 beats min(-1) during the PROP treatment (P < 0.001). In contrast, HR was similar between SL and HA during the GLYC treatment (110 +/- 7 and 112 +/- 5 beats min(-1), P = 0.28) and PROP+ GLYC treatment (83 +/- 5 and 85 +/- 5 beats min(-1), P = 0.25). Our results identify a reduction in cardiac parasympathetic activity as the primary mechanism underlying the elevated HR associated with 2 weeks of exposure to hypoxia. Unexpectedly, the sympathoactivation atHA that was evidenced by increased circulating noradrenaline concentration had little effect on HR, potentially reflecting down-regulation of cardiac beta-adrenergic receptor function in chronic hypoxia. These effects of chronic hypoxia on autonomic control of the heart may concern not only HA dwellers, but also patients with disorders that are associated with hypoxaemia.
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