Return to Table of Contents

Increased energy requirements for humans residing in Antarctica: A proposed model

H. LESTER REED, Department of Medicine, Madigan Army Medical Center, Tacoma, Washington 98431

HOMER LEMAR, Endocrinology Service, Madigan Army Medical Center, Tacoma, Washington 98431

Studies currently in progress are designed to identify the mechanism of the presumed 40 percent increase in energy requirement, which occurs in humans living and working at McMurdo Station, Antarctica, for as little as 4 months. Additionally, these studies will attempt to determine the relationship between increased energy requirements and increased thyroid hormone requirements, which are described for this same time period in McMurdo, Antarctica. We have studied members of the 1996-1997 winter-over party before and then monthly during their period of antarctic residence. By using measurements of both the resting oxygen consumption and submaximal exercise capacity, we are able to determine differences in oxygen use and, therefore, energy requirements, which may change during antarctic residence. We have also contrasted these subjects with similar measures in patients suffering from clinical excess thyroid hormone conditions as previously reported by our group (Gibson et al. 1993). By making this clinical comparison, we hope to understand better the relationship between increased physiological energy requirements and increased thyroid hormone tissue content common to both situations.

We have recently reported preliminary observations confirming the presence and suggesting possible mechanisms for the increased energy requirements observed in humans during antarctic residence (Do et al. 1997). Resting oxygen use increases at a rate of nearly 2.5 percent per month during the first 4 months of antarctic residence or approximately 10 percent over the 4-month study. Additionally, we have reported that in this same period the resting metabolic rate derived from a submaximal exercise calculation also increases by about 2.1 percent per month or approximately 8.0 percent over the study. The amount of energy needed to perform a predetermined level of a low workload also increases during this period by approximately 3.8 percent per month or approximately 15 percent over the study (Do et al. 1997).

Patients who are known to have excess thyroid hormone concentrations in serum and tissue also show increases in energy requirements. Interestingly, these patients show similar, although greater, increases in resting oxygen use and declines in submaximal exercise performance compared to those subjects residing for 4 months in Antarctica (Gibson et al. 1993). The energy requirements in the patients decrease with improving thyroid status following therapy, and they seem to reflect circulating thyroid hormone concentrations in that condition. The fall in work carried out at a given level of oxygen use suggests a fall in whole body efficiency and increase in heat production associated with thyroid hormone excess (Martin et al. 1991). We support the hypothesis that the major mechanisms for this change occur in the skeletal muscles and not in the cardiovascular system and, thus, the large skeletal muscle mass provides a ready source of heat generation (Zurol et al. 1990; Martin et al. 1991; Olson et al. 1991). The heterogeneous tissue-specific nature of the thyroid hormone distribution has recently been proposed (Everts et al. 1996), and we feel it may apply directly to this syndrome. For example, with extended polar residence the brain seems to have a fall in thyroid hormone while peripheral tissues, such as skeletal muscle, seem to have an augmented amount of hormone. Symptoms and findings specific to each of these two conditions are being investigated by our group.

If thyroid excess is a physiological model, we propose that the 15 percent fall in work produced for each 400 milliliters per minute per square meter (ml/min/m2) is a source for increased daily energy use and increased peripheral heat production. With the reported lower body temperature in McMurdo (Reed, Brice, et al. 1990), it is possible that some energy is conserved to maintain this lower body temperature. Then, with acute cold exposure, humans may initiate voluntary muscle contraction at low work levels and, thus, generate substantial heat to avoid further body cooling. Resting energy expenditure also appears to increase, but to a lesser degree, than exercise energy use. Perhaps resting thermogenesis is required to replace the loss of shivering thermogenesis, which occurs with hypothermic-cold adaptation found in McMurdo (Reed, Brice, et al. 1990; Do, LeMar, and Reed 1996).

Whatever the mechanism, these data support the observation of increased energy requirements for both indoor and outdoor workers in a sedentary polar camp. Additionally, the nature and direction of the increase, although reduced in magnitude, are similar to previously reported conditions of excess thyroid hormone. Future studies must address the metabolic and cognitive cost of this form of endocrine adaptation, with specific regard to the apparent shunt or shift of thyroid hormones toward skeletal tissue and away from brain or central nervous system tissues.

This research is supported by National Science Foundation grant OPP 89-22832.

References

Do, N., H. LeMar, and H. Reed. 1996. Thyroid hormone responses to environmental cold exposure and seasonal change: A proposed model. Endrocrinology and Metabolism, 3, 7-16.

Do, N., M. Staudaucher, S. Case, K. Reedy, H. LeMar, N. Finney, P. Newbauer, C. McLain, and H. Reed. 1997. Changes in skeletal muscle efficiency and resting oxygen use after four months of antarctic residence: Physiological significance of the Polar T3Syndrome. 1997 Thyroid, 7(suppl. 1), S36. [Abstract]

Everts, M., M. De Jong, C. Lim, R. Docter, E. Krenning, T. Visser, and G. Heneman. 1996. Different regulation of thyroid hormone transport in liver and pituitary: Its possible role in maintenance of low T3 production during nonthyroidal illness and fasting in man. Thyroid, 6, 359-368.

Gibson, C., R. Jones, D. Bunner, J. Lance, and H. Reed. 1993. Submaximal cycloergometry to determine changing metabolic parameters following 131I therapy for thyrotoxicosis. Endocrine Society 75th Meeting. [Abstract]

Martin, W., R. Spina, E. Korte, D. Yarasheski, T. Angelopulos, P. Nemeth, and J. Saffitz. 1991. Mechanism of impaired exercise capacity in short duration experimental hyperthyroidism. Journal of Clinical Investigation, 88, 2047-2053.

Olson, B., I. Klein, R. Benner, R. Burdett, P. Trzepacz, and G. Levey. 1991. Hyperthyroid myopathy and the response to treatment. Thyroid, 2, 137-141.

Reed, H., D. Brice, K. Shakir, K. Burman, M. D'Alesandro, and J. O'Brian. 1990. Decreased free fraction of thyroid hormones after prolonged antarctic residence. Journal of Applied Physiology, 69, 1467-1472.

Zurol, F., K. Larson, C. Bogardus, and E. Ravussin. 1990. Skeletal muscle metabolism is a major determinant of resting energy expenditure. Journal of Clinical Investigation, 86, 1423-1427.