SODIUM REGULATING HORMONES AT HIGH-ALTITUDE - BASAL AND POSTEXERCISE LEVELS

High altitude (HA)-induced diuresis is associated with marked changes in sodium and water regulating hormones, particularly the renin-angiot ensin-aldosterone system (RAAS) and atrial natriuretic hormone (ANH). These hormones are also strongly stimulated by physical exercise, whic h is a major component of daily activity at HA. In spite of the numero us studies in literature, a clear relationship between hormonal change s, HA diuresis, and physical exercise has not yet been established. We therefore evaluated the response of sodium regulating hormones to exh austive exercise in a group of seven males exposed to prolonged HA hyp oxia. The study was divided into four phases: sea level (SL1), after 7 (P1) and after 21 (P2) days at 5050 m (Italian National Research Coun cil Pyramid Laboratory, Nepal), and back at sea level (SL2). At each p hase plasma hematocrit (Ht), total body water (TBW), 24-hr sodium excr etion (uNa), and urinary volume (uV) were evaluated together with PRA, plasma aldosterone, and ANH, in samples drawn basally from patients i n upright position, and at the end of graded step-wise (30 W/2 min) ma ximal exercise. Levels of uNa and uV were raised at P1 and then declin ed at P2, with a parallel decrease in TBW and an increase in Ht. Basal PRA and aldosterone levels were suppressed both at P1 and P2 (from 1. 9 +/- 0.4 to 0.08 +/- 0.03 and 0.5 +/- 0.1ng/mL/3 h, and from 7.9 +/- 1.8 to 3.9 +/- 0.4 and 4.5 +/- 0.4 ng/dL, respectively; P < .05). Exha ustive exercise at HA did not induce any significant response in PRA a nd aldosterone, unlike SL1. Otherwise, at P1 ANH levels remained uncha nged both basally and during exercise, while at P2 they decreased sign ificantly vs. SL1, both basally and after exercise (from 13.3 +/- 5.7 to 3.5 +/- 1.2 and from 40.2 +/- 10.2 to 17.5 +/- 8.3, respectively; P < .05). Our data show that PRA and aldosterone levels were constantly suppressed at HA and were unresponsive to exercise, whereas the ANH r esponse was significantly stimulated during acute HA exposure, but not during chronic exposure. This suggests that hypoxia-induced chemorece ptor stimulation may cause the natriuretic phenomenon through direct s uppression of the RAAS.