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1967). Hypoxia aggravates the proposed threats to limb O2 delivery in two ways. First, the alveolar�Ccapillary diffusion limitation becomes more pronounced, due to a decreased at any given alveolar ventilation. Second, acute, but especially chronic, hypoxic exposures potentiate the hyperventilatory response to exercise and markedly increase Wresp (Thoden et al. 1969; Amann et al. 2007). Therefore, hypoxia exacerbates the rate of development of peripheral locomotor muscle fatigue elicited via high-intensity exercise and reduces exercise performance in two ways, namely, via reductions in and increases in Wresp (Amann et al. 2007). For example, we recently studied this website identical submaximal constant-load cycling exercise (273 W, 8.6 min) performed at sea level and simulated altitude (inspiratory O2 content = 15%). Haemoglobin saturation was substantially lower during the exercise in acute hypoxia (?95 versus?81%), whereas Wresp was about 40% higher compared with sea level (Amann et al. 2007). These drastic changes nearly doubled the rate of development of locomotor muscle fatigue during the cycling exercise and compromised the subjects�� endurance performance (Amann et al. 2006). Accumulating evidence over the past 25 years indicates a substantial Autophagy activator role of the healthy respiratory system in limiting high-intensity endurance exercise in humans. This influence is mediated via the effects of the respiratory system on locomotor muscle O2 delivery and associated consequences on the development of fatigue during exercise and an individual's aerobic capacity. Reductions in O2 delivery are caused by the failure of the pulmonary system to maintain resting arterial oxygenation during exercise and/or a respiratory muscle metaboreflex, which causes a sympathetically mediated reduction in . Furthermore, intrathoracic pressure excursions associated with the high ventilatory work during intense exercise have been suggested to limit cardiac output. Taken together, the pulmonary system is a key, although highly variable, determinant of endurance performance in healthy individuals. I thank Professor Jerry Dempsey for his comments on this manuscript. This work was supported by the US National Heart, Lung, and Blood Institute. ""Perturbed serum vitamin D levels have been shown to be associated with increased risk of cardiovascular disease. The aim of the present study was to investigate the association of Moroxydine serum 25-hydroxyvitamin D3 (25(OH)D3) levels and B ultrasonography-detected carotid plaque and carotid intima�Cmedia thickness (C-IMT) in Chinese middle-aged and elderly men. In all, 1001 men, aged 45�C78?years, were enrolled in the study. Increased C-IMT was defined as any C-IMT value in the highest quartile of the study subjects (��?0.75?mm). The study population had a median serum 25(OH)D3 level of 14.51?ng/mL (interquartile range (IQR) 10.84�C18.67?ng/mL). Subjects with carotid plaques had lower serum 25(OH)D3 levels than those without (13.