The efficiency of "living high, training low" (LHTL) remains controversial, despite its wide utilization. This study aimed to verify whether maximal and/or submaximal aerobic performance were modified by LHTL and whether these effects persist for 15 days after returning to normoxia. Last, we tried to elucidate whether the mechanisms involved were only related to changes in oxygen-carrying capacity. Eleven elite middle-distance runners were tested before (Pre), at the end (Post1), and 15 days after the end (Post2) of an 18-day LHTL session. Hypoxic group (LHTL, n = 5) spent 14 h/day in hypoxia (6 nights at 2,500 m and 12 nights at 3,000 m), whereas the control group (CON, n = 6) slept in normoxia (1,200 m). Both LHTL and CON trained at 1,200 m. Maximal oxygen uptake and maximal aerobic power were improved at Post1 and Post2 for LHTL only (+7.1 and +3.4% for maximal oxygen uptake, +8.4 and +4.7% for maximal aerobic power, respectively). Similarly oxygen uptake and ventilation at ventilatory threshold increased in LHTL only (+18.1 and +12.2% at Post1, +15.9 and +15.4% at Post2, respectively). Heart rate during a 10-min run at 19.5 km/h decreased for LHTL at Post2 (-4.4%). Despite the stimulation of erythropoiesis in LHTL shown by the 27.4% increase in serum transferrin receptor and the 10.1% increase in total hemoglobin mass, red cell volume was not significantly increased at Post1 (+9.2%, not significant). Therefore, both maximal and submaximal aerobic performance in elite runners were increased by LHTL mainly linked to an improvement in oxygen transport in early return to normoxia and probably to other process at Post2.

Increased urinary CST3 concentrations allow the accurate detection of tubular dysfunction among pure and mixed nephropathies. Because of its ability to be processed on automated clinical chemistry analyzers, this assay could easily be used as an adjunct to the standard panel used to screen kidney pathologies, even in emergency situations.

Iron is essential for oxygen transport because it is incorporated in the heme of the oxygen-binding proteins hemoglobin and myoglobin. An interaction between iron homeostasis and oxygen regulation is further suggested during hypoxia, in which hemoglobin and myoglobin syntheses have been reported to increase. This study gives new insights into the changes in iron content and iron-oxygen interactions during enhanced erythropoiesis by simultaneously analyzing blood and muscle samples in humans exposed to 7 to 9 days of high altitude hypoxia (HA). HA up-regulates iron acquisition by erythroid cells, mobilizes body iron, and increases hemoglobin concentration. However, contrary to our hypothesis that muscle iron proteins and myoglobin would also be up-regulated during HA, this study shows that HA lowers myoglobin expression by 35% and down-regulates iron-related proteins in skeletal muscle, as evidenced by decreases in L-ferritin (43%), transferrin receptor (TfR; 50%), and total iron content (37%). This parallel decrease in L-ferritin and TfR in HA occurs independently of increased hypoxia-inducible factor 1 (HIF-1) mRNA levels and unchanged binding activity of iron regulatory proteins, but concurrently with increased ferroportin mRNA levels, suggesting enhanced iron export. Thus, in HA, the elevated iron requirement associated with enhanced erythropoiesis presumably elicits iron mobilization and myoglobin down-modulation, suggesting an altered muscle oxygen homeostasis.

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