Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training "specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia [fraction of inspired oxygen (Fi(O(2))) = 21% or 13.5%]. Biopsies were taken from the musculus vastus lateralis, and cycle-ergometric incremental maximum oxygen uptake (VO(2max)) exercise tests were performed under normoxia, before and after the 10-wk training program. The main finding was a significant increase (P < 0.05) of fatty acid oxidation capacity per muscle mass, after endurance and strength training under normoxia [2.6- and 2.4-fold for endurance training normoxia group (ET(N)) and strength training normoxia group (ST(N)); n = 8 and 3] and hypoxia [2.0-fold for the endurance training hypoxia group (ET(H)) and strength training hypoxia group (ST(H)); n = 7 and 7], and higher coupling control of oxidative phosphorylation. The enhanced lipid oxidative phosphorylation (OXPHOS) capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P < 0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in muscle mass-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, and octanoylcarnitine). No significant increase was observed in mitochondrial DNA (mtDNA) content. Physiological OXPHOS capacity increased significantly in ET(N) (P < 0.01), with the same trend in ET(H) and ST(H) (P < 0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active lifestyle induced muscular changes of mitochondrial quality representative of mitochondrial health.
Prediction of the development of acute mountain sickness (AMS) in individuals going to high altitudes is still a matter of debate. Whereas some studies found that subjects with a blunted hypoxic ventilatory response (HVR) are predisposed to AMS, others did not. However, the HVR has often been determined under very acute (5 to 10 min) isocapnic hypoxia without consideration of the subsequent hypoxic ventilatory decline (HVD), and the assessment of AMS susceptibility was based on a single altitude exposure. Therefore, the aim of the present study was to evaluate the relationship between the individual arterial oxygen saturation (Sa(O2)) after a 20- to 30-min exposure to poikilocapnic hypoxia and the AMS susceptibility based on repeated observations. A total of 150 healthy male and female mountaineers (ages: 42 +/- 13 yr), 63 of whom had known susceptibility to AMS and 87 of whom never suffered from AMS, were exposed to various degrees of normobaric and hypobaric hypoxia. Sa(O2) values were taken by finger pulseoximetry after 20 to 30 min of hypoxic exposure. Sa(O2) values after 20 to 30 min of hypoxia were on average 4.9% lower in subjects susceptible to AMS than in those who were not. Logistic regression analysis revealed altitude-dependent Sa(O2) values to be predictive for AMS susceptibility. Based on the derived model, AMS susceptibility was correctly predicted in 86% of the selected individuals exposed to short-term hypoxia. In conclusion, Sa(O2) values after 20 to 30 min of exposure to normobaric or hypobaric hypoxia represent a useful tool to detect subjects highly susceptible to AMS.
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