Acclimatization to 4100 m does not change capillary density or mRNA expression of potential angiogenesis regulatory factors in human skeletal muscle

Lundby, Carsten; Pilegaard, Henriette; Andersen, Jesper L.; Hall, Gerrit van; Sander, Mikael; Calbet, José A. L.

doi:10.1242/jeb.01225

Cited by 66 publications

(61 citation statements)

References 49 publications

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“…3) (Dempsey et al, 2006). Finally, Lundby et al (2004) have demonstrated no increase in the expression of either hypoxia inducible factor 1a or vascular endothelial growth factor mRNA in muscle after 2 week at a similar altitude to our investigation, and no increase in capillary-to-muscle fibre ratio after 8 week.…”

Section: Decreased Critical Powersupporting

confidence: 68%

Exercise intolerance at high altitude (5050m): Critical power and W′

Valli¹,

Cogo²,

Passino³

et al. 2011

Respiratory Physiology & Neurobiology

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a b s t r a c tThe relationship between work rate (WR) and its tolerable duration (t LIM ) has not been investigated at high altitude (HA). At HA (5050 m) and at sea level (SL), six subjects therefore performed symptomlimited cycle-ergometry: an incremental test (IET) and three constant-WR tests (% of IET WR max , HA and SL respectively: WR 1 70 ± 8%, 74 ± 7%; WR 2 86 ± 14%, 88 ± 10%; WR 3 105 ± 13%, 104 ± 9%). The power asymptote (CP) and curvature constant (W ) of the hyperbolic WR-t LIM relationship were reduced at HA compared to SL (CP: 81 ± 21 vs. 123 ± 38 W; W : 7.2 ± 2.9 vs. 13.1 ± 4.3 kJ). HA breathing reserve (estimated maximum voluntary ventilation minus end-exercise ventilation) was also compromised (WR 1 : 25 ± 25 vs. 50 ± 18 l min −1 ; WR 2 : 4 ± 23 vs. 38 ± 23 l min −1 ; WR 3 : −3 ± 18 vs. 32 ± 24 l min −1 ) with nearmaximal dyspnea levels (Borg) (WR 1 : 7.2 ± 1.2 vs. 4.8 ± 1.3; WR 2 : 8.8 ± 0.8 vs. 5.3 ± 1.2; WR 3 : 9.3 ± 1.0 vs. 5.3 ± 1.5). The CP reduction is consistent with a reduced O 2 availability; that of W with reduced muscle-venous O 2 storage, exacerbated by ventilatory limitation and dyspnea.

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Section: Decreased Critical Powersupporting

confidence: 68%

Exercise intolerance at high altitude (5050m): Critical power and W′

Valli¹,

Cogo²,

Passino³

et al. 2011

Respiratory Physiology & Neurobiology

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“…In contrast, it has also been reported that systemic hypoxia does not cause changes in the capillary bed in rodents (11% O 2 for 2 weeks and 13% O 2 for 5 months) [46, 47]. In humans exposed to 4,100 m altitude (corresponding to approximately 13% O 2 ) for 2 and 8 weeks, there were no change in VEGF levels and no evidence of angiogenesis [48]. The oxygen saturation in humans during exposure to 14% O 2 will only cause a decrease from 95 to 89% of oxygen saturation [49].…”

Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Morphology and Aerobic Capacity in Patients with Obstructive Sleep Apnoea Syndrome

Larsson

Kadi²,

Ulfberg³

et al. 2008

Respiration

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Background: Despite the fact that patients with obstructive sleep apnoea syndrome (OSAS) often have symptoms at the level of skeletal muscle such as fatigue, the question of whether the structural, cellular and functional properties of limb skeletal muscles are affected has not been fully examined. Objective: The aim was to examine physiological and muscular parameters in patients with OSAS and to assess the relationship between these parameters and the clinical symptoms. Method: Eighteen patients with OSAS and 16 controls participated. Aerobic capacity was assessed using a submaximal test. Fibre type distribution and fibre area were analyzed on muscle biopsies taken from the tibialis anterior. The microvascularization was assessed using the following parameters: (1) the number of capillaries per fibre (CAF), (2) CAF per fibre area (CAFA), (3) capillary to fibre perimeter exchange (CFPE) index, which represents the interface between muscle fibre and capillaries, and (4) length of capillary/perimeter of the fibre (LC/PF) index or capillary tortuosity, which represents the percent of muscle fibre perimeter in contact with the wall of the microvessel. Results: The OSAS group had significantly lower predicted relative maximal oxygen uptake (p = 0.0047) which was inversely correlated to the apnoea/hypopnoea index (AHI; r = –0.6, p = 0.017). There was a significantly higher CFPE index for slow type I fibres (p = 0.007) and fast type II fibres (p = 0.0126) and a significantly higher LC/PF index for type I fibres (p = 0.0003) and type II fibres (p = 0.0285) in OSAS patients compared to controls. Conclusion: OSAS patients have a higher muscle microvascularization and a lower aerobic capacity than controls. Furthermore the aerobic capacity was inversely correlated to AHI.

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“…However, peak exercise leg O 2 extraction in the natives was 7 percentage units lower than in the lowlanders, despite the fact that Vo 2max in normoxia was comparable between both groups. The only structural difference that could explain this reduced O 2 extraction capacity in the altitude natives was that they had less capillaries per muscle fiber than the lowlanders (Lundby et al, 2004b;Lundby et al, 2006).…”

Section: Calbet and Lundbymentioning

confidence: 98%

Air to Muscle O₂Delivery during Exercise at Altitude

Calbet

Lundby

2009

High Altitude Medicine & Biology

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100

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Calbet, José, and Carsten Lundby. High Alt. Med. & Biol. 10.123-134, 2009.-Hypoxia-induced hyperventilation is critical to improve blood oxygenation, particularly when the arterial Po 2 lies in the steep region of the O 2 dissociation curve of the hemoglobin (ODC). Hyperventilation increases alveolar Po 2 and, by increasing pH, left shifts the ODC, increasing arterial saturation (Sao 2 ) 6 to 12 percentage units. Pulmonary gas exchange (PGE) is efficient at rest and, hence, the alveolar-arterial Po 2 difference (Pao 2 ÀPao 2 ) remains close to 0 to 5 mm Hg. The (Pao 2 ÀPao 2 ) increases with exercise duration and intensity and the level of hypoxia. During exercise in hypoxia, diffusion limitation explains most of the additional Pao 2 ÀPao 2 . With altitude, acclimatization exercise (Pao 2 ÀPao 2 ) is reduced, but does not reach the low values observed in high altitude natives, who possess an exceptionally high DLo 2 . Convective O 2 transport depends on arterial O 2 content (Cao 2 ), cardiac output (Q), and muscle blood flow (LBF). During whole-body exercise in severe acute hypoxia and in chronic hypoxia, peak Q and LBF are blunted, contributing to the limitation of maximal oxygen uptake (Vo 2max ). During small-muscle exercise in hypoxia, PGE is less perturbed, Cao 2 is higher, and peak Q and LBF achieve values similar to normoxia. Although the Po 2 gradient driving O 2 diffusion into the muscles is reduced in hypoxia, similar levels of muscle O 2 diffusion are observed during small-mass exercise in chronic hypoxia and in normoxia, indicating that humans have a functional reserve in muscle O 2 diffusing capacity, which is likely utilized during exercise in hypoxia. In summary, hypoxia reduces Vo 2max because it limits O 2 diffusion in the lung.

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Acclimatization to 4100 m does not change capillary density or mRNA expression of potential angiogenesis regulatory factors in human skeletal muscle

Cited by 66 publications

References 49 publications

Exercise intolerance at high altitude (5050m): Critical power and W′

Exercise intolerance at high altitude (5050m): Critical power and W′

Skeletal Muscle Morphology and Aerobic Capacity in Patients with Obstructive Sleep Apnoea Syndrome

Air to Muscle O₂Delivery during Exercise at Altitude

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Acclimatization to 4100 m does not change capillary density or mRNA expression of potential angiogenesis regulatory factors in human skeletal muscle

Cited by 66 publications

References 49 publications

Exercise intolerance at high altitude (5050m): Critical power and W′

Exercise intolerance at high altitude (5050m): Critical power and W′

Skeletal Muscle Morphology and Aerobic Capacity in Patients with Obstructive Sleep Apnoea Syndrome

Air to Muscle O2Delivery during Exercise at Altitude

Contact Info

Product

Resources

About

Air to Muscle O₂Delivery during Exercise at Altitude