ACCLIMATIZATION TO 4,300-M ALTITUDE DECREASES RELIANCE ON FAT AS A SUBSTRATE

We tested the hypothesis that exposure to altitude decreases reliance on free fatty acids (FFA) as substrates and increases dependency on bl ood glucose. Therefore, the effects of exercise, hypobaric hypoxia, an d altitude acclimatization on FFA, glycerol and net glucose uptake and release [= 2(leg blood flow)(arteriovenous concentration)] and on fat ty acid (FA) consumption by the legs (= 3 x glycerol release + FFA upt ake) were measured. Because sympathetic responses have been implicated , we utilized nonspecific beta-blockade and observed responses to exer cise, altitude, and altitude acclimatization. We studied six healthy b eta-blocked men (beta) and five matched controls (C) during rest and c ycle ergometry exercise (88 W) at 49% of sea-level (SL) peak O-2 uptak e at the same absolute power output on acute altitude exposure (A1; ba rometric pressure = 430 Torr) and after 3 wk of chronic altitude expos ure to 4,300 m (A2). During exercise at SL, FA consumption rates incre ased (P < 0.05). On arrival at 4,300 m, resting leg FFA uptake and FA consumption rates were not significantly different from those at SL. H owever, after acclimatization to altitude, at rest leg FA consumption decreased to essentially zero in both C and beta groups. During exerci se at altitude after acclimatization, leg FA consumption increased sig nificantly, but values were less than at SL or A1 (P < 0.05), whereas glucose uptake increased relative to SL values. Furthermore, beta-bloc kade significantly increased glucose uptake relative to control. We co nclude that 1) chronic altitude exposure decreases leg FA consumption during rest and exercise; 2) relative to SL, FFA uptake decreases whil e glucose uptake increases during exercise at altitude; and 3) beta-bl ockade potentiates these effects.