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The alterations in serum levels of T3, T4, TSH and TBG, TSH response to 100 mug iv TRH, and urinary excretion of T3 and T4 were studied in 8 healthy men at sea level (SL), on days 1, 2, 4, 8 and 16 after arrival by air at high altitude (3,700 m, HA), and during days 5 to 7 after their return to SL. No significant alterations in serum levels of TSH and TBG or TSH response to TRH were observed during exposure to HA or on return to SL. There was, however, an acute elevation in both serum total T3 and T4. Serum total T3 from a mean basal+/-SE value of 128+/-13 ng/dl increased to 320+/-18 on day 1 and remained significantly elevated at 225+/-48 up to day 8 after arrival at high altitude. Similarly serum total T4 increased from basal level of 9+/-0.92 mug/dl to 15.2+/-1.2 and remained elevated till day 16 and it was 11+/-1.19 mug/dl during days 5 to 7 after return to SL. The urinary excretion of both T3 and T4 was decreased. These changes perhaps were the result of complex physiologic adjustments on acute exposure to high altitude, like shrinkage of the T3 and T4 distribution pools, altered binding capacities of thyroid hormones binding proteins, and a reduction in clearance of thyroid hormones from the plasma compartment; and were probably not suggestive of an enhanced thyroid activity. Their actual significance in high altitude adaptation in man is not clearly understood.

In a preliminary pilot study we had reported a significant difference in urinary catecholamine excretion between symptomatic and asymptomatic individuals inducted to high altitude by air. The present study covers slower induction by road; 25 lowlanders ascended from 1,800 to 3,658 m in 50 h and 33 similar subjects covered the journey in 6 h. They were studied according to the protocal used in the initial study. None of the 58 subjects inducted by road developed symptoms of high-altitude illness. Their urinary catecholamine excretion remained normal during the 10 days' stay at high altitude. These findings lend support to our earlier contention that there might be a relationship between increased sympathoadrenal activity and high-altitude illnesses.

Resting stroke volume and cardiac output of 50 normal healthy sea-level residents (group A) were estimated by the noninvasive technique of electrical impedance plethysmography. They were then airlifted to an altitude of 3,658 m and serial estimations carried out at 0-4 h and 5-8 h and on the 2nd, 3rd, 4th, 5th, and 10th days. The subjects were brought back to sea level and studied for up to 5 days. Thirty permanent residents of high altitude (group B) and sixteen lowlanders temporarily resident at high altitude (group C) were also subjected to similar studies. It was found that resting stroke volume and cardiac output of group A started falling immediately on arrival at high altitude, reached the minimum on the 3rd day and tended to improved on the 4th and 5th day, but showed a secondary fall on the 10th day. The reduction in stroke volume in this group was not fully compensated by tachycardia. On return to sea level the cardiac output normalized immediately, the stroke volume on the 2nd day. At sea level goup A had values similar to group B and at high altitude to group C.