Symposium: nutrition and Exercise
Nutrition at High Altitude1 Medical Department, Hermes Arzneimittel GmbH, D-8023 Grosshesselohe, Germany haustion, intestinal complaints and increased basal metabolism accompanied by hormonal changes, may be reasons for weight loss at high altitudes. Very little data are available on micronutrient me tabolism at high altitude. There are also practically no data on nutrient intake. Hannon et al. (4) showed a marked decrease of bicarbonate in serum. Most of this loss was replaced by an increase in chloride and, to a lesser extent, by protein aniónand phosphate. On the other hand, there was a decrease in sodium, potassium and magnesium, but calcium was elevated. The au thors attribute this to a reduction of plasma volume. In addition, this may also reflect insufficient nutrient intake. Some exploratory data showed that the rec ommended daily intake for most minerals and vita mins was not achieved by a "normal" diet at base camp. Another topic of interest is whether nutrients can be used prophylactically against some of the degen erative changes that occur at high altitude. During hypoxia, oxidative injury may be enhanced as a con sequence of alterations in the oxidation-reduction po tential (5). This may lead to increased oxidative stress. A correlation has recently been identified between in creased metabolic rate as a consequence of exercise and increased tissue damage due to free radical pa thology (6-9). Vitamin E reduces free radical reactions through its stabilizing effect on various components of the respiratory chain. Thus, vitamin E contributes to aerobic energy production (10-12), and vitamin E
ABSTRACT Food records confirm that there is a high risk of malnutrition at high altitudes because of the usual lack of fresh food. As to the use of pharmacologie properties of micronutrients, only some data on vitamin E are described. Two placebo-controlled studies showed that a prolonged stay at high altitude caused a decrease in physical performance and a deterioration of blood flow, most probably because of increased lipid peroxidation. Supplementation with vitamin E prevented these changes. More research is desirable to obtain valid data on nutritional requirements and to obtain the basis for special recommendations for nutrition at high altitude. J. Nutr. 122: 778-781, 1992. INDEXING KEY WORDS:
•food requirement •food intake •vitamin E •prophylaxis •free radicals
Physical activity at high altitude, such as high al titude mountaineering, has several nutritional aspects. Among these are the weight loss known to occur at high altitude, the possibility of micronutrient mal nutrition and the possibility of offsetting some of the deleterious effects of a stay at high altitude through nutritional supplementation. One problem during trekking or expeditions to high altitudes is weight loss. Normally people lose between 5 and 10% body weight and this of course is much more if people suffer from an illness such as diarrhea. Increased energy requirement as well as malabsorption may be the cause of this weight loss. In a recent study Kayser et al. (1) showed that there is no protein malabsorption until an altitude of 5,000 m, but that pro tein turnover seems to be increased. Rai et al. (2)found that there is also no fat malabsorption until 4,700 m. On the other hand, the results of Boyer and Blume (3) indicate a reduced fat absorption at 6,300 m. From these data it can be concluded that there is no malabsorption of macronutrients at altitudes where base camps are normally established. Malabsorption at higher altitudes is of less practical significance. It seems that other factors, such as reduced appetite, ex-
1Presented as part of a symposium: Nutrition and Exercise, given at the 75th Annual Meeting of the Federation of American Societies for Experimental Biology, Atlanta, GA, April 22, 1991. This sym posium was sponsored by the American Institute of Nutrition and supported in part by grants from Proctor and Gamble Company, the Coca Cola Company, the Quaker Oats Company, Ocean Spray Cranberries, Inc., Bronson Pharmaceuticals, NPH, and Hoffman LaRoche. Guest editors for this symposium were L. P. Packer, De partment of Molecular and Cell Biology, University of California, Berkeley, CA and V. N. Singh, Clinical Nutrition, Roche Vitamins and Fine Chemicals, Nutley, NJ. 1To whom correspondence should be addressed: Hermes Arz neimittel GmbH, Georg-Kalb-Strasse 5-8, D-8023 Grosshesselohe, Germany.
0022-3166/92 $3.00 ©1992 American Institute of Nutrition.
778
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
IREHE M. SIMON-SCHNASS2
SYMPOSIUM:
NUTRITION
AND EXERCISE
779
%of baseline
%of baseline
260
ISO
200
126 150
100
Baseline
tl Basecamp
L
1Treatment-froup
t2 Basecamp
Basecamp
Baseline
t3 Basecamp
1Treatment group
•Control-group
I Control group
••: no évaluation b«cku»eof too mmnj drop out«
FIGURE 1 Anaerobic threshold during a prolonged stay at high altitude (5100 m) with and without supplementation with vitamin E compared with preexpedition value, tl, t2 and t3 are measured 2, 4 and 6 wk after baseline.
deficiency leads to reduced cell respiration (6, 12). This is especially apparent when the available oxygen is also limited, as can occur because of high demand, poor local supply or lower partial pressure of oxygen at high altitude. Such impairment of metabolism is especially pronounced under conditions of increased physical load at high altitude. Investigations on the anaerobic threshold (Fig. 1) confirmed the previous observation that a prolonged stay at high altitude causes a shift to the left of the lactic acid curve during performance and a decrease of the anaerobic threshold. Both indicate reduced physical performance. Additional daily intake of 2X 200 mg of vitamin E prevented these changes (13). In experimental animals and in man, the exhalation of pentane has been demonstrated to be related to vita min E status (8, 11). In animals, exercise-induced lipid peroxidation could be prevented by vitamin E admin istration (7,9). In this experiment (Fig. I), the pentane expiration was maintained constant in the vitamin E group, indicating that no additional lipid peroxidation had occurred. However, in the control group the mean expired pentane rose by > 100%. It was concluded from this study (13) that climbing at high altitude may incur a risk of metabolically induced cell damage. One of the main tasks of blood is substance ex change (including oxygen exchange) between individ ual tissues. This is performed in the terminal vessels of the capillary system. The lack of oxygen at high altitude causes some significant changes of blood composition and rhéologieproperties. The special rheological properties of blood arise from its twophase composition of plasma and blood cells. The vis cosity of blood depends largely on the packed cell vol ume, plasma viscosity, the flexibility of the red blood cells and their tendency to aggregate (14, 15), so blood viscosity varies as a function of flow conditions.
FIGURE 2 Pentane exhalation during a prolonged stay at high altitude (5100 m) with and without supplementation with vitamin E compared with preexpedition value, tl, t2 and t3 are measured 2, 4 and 6 wk after baseline.
Erythrocyte flexibility depends, among other things, on membrane fluidity. Loss of membrane flexibility can occur due to hypo- and hyperthermia, membrane defects and aging of the cell (16). One of the important underlying phenomena is oxidative change to mem brane lipids, which may be triggered by free radicals (17). In addition to blood viscosity, the elasticity and integrity of the vascular wall plays an important role in capillary flow. Here too, oxidative damage is be lieved to be a pathogenic factor (18-20). The viscosity of blood is determined not only by hematocrit but also by plasma viscosity and the flex ibility of the erythrocytes. Data from studies of sub jects at high altitude (Fig. 3) show that a decreased filterability of the erythrocytes may be due to an in creased lipid peroxidation of membrane lipids (22).
Filtration quotient
0,65
0,45
Baseline
tl Basecamp
L_J Treatment group
12 Basecamp I Control group
FIGURE 3 Filterability of red blood cells during a pro longed stay at high altitude (4300 m) with and without sup plementation with vitamin E compared with preexpedition value, tl and t2 are measured 2 and 4 wk after baseline.
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
100
SIMON-SCHNASS
780 7, normal activity
substances (17, 20, 26, 27). Given the relationship of free radical damage to both hypoxia (causative) and cellular antioxidant defense systems (preventative), antioxidants, especially vitamin E, might play a sig nificant role in the prevention of high altitude dete riorations.
130
110
Baseline
II
tl
Basecamp
Treatment group
t2
Basecamp
H Control group
FIGURE 4 Protein C during a prolonged stay at high al titude (4300 m) with and without supplementation with vi tamin E compared with preexpedition value, tl and t2 are measured 2 and 4 wk after baseline.
Also, a disturbance was shown in the coagulation sys tem. It could be shown that the activity of protein C, a coagulation inhibitor, was significantly reduced, which may lead to increased coagulation (22). Under this condition it can be assumed that an increased granulocyte stimulation occurred (23). Proteases can then be released, which damage not only endothelial cells and proteins bound to the endothelial cells, but also hydrolyze proteins free in the plasma (23). This could explain the drop in protein C observed (Fig. 4) in the control group. Because there was no drop in protein C activity in the vitamin E group, it may be suggested that vitamin E supplementation may have stabilized both endothelial cells and leukocytes and protected protein hydrolysis. The data as a whole show that a relatively quick rise in altitude and continued presence at high altitude produces changes in a wide range of measurements (22) that point to impaired blood rheology (22). Mountain sickness is often at tributed to general disturbances of the microcircula tion. This aggravates the risk of frostbite, retinal hem orrhage and cerebral and pulmonary edema. There seems to be a combination of increased precapillary vascular resistance and microrheological and hemostatic disturbances (24). Oral administration of 2X 200 mg of vitamin E daily (25) showed that the deterioration in measurements seen in the control group was prevented. It seems of interest to study whether this positive effect can also be found in other hypoxic conditions, such as chronic obstructive pulmonary diseases, cardiac and cerebral ischemia and peripheral circulation dis turbance. Evidence is accumulating that indicates oxidative injury mediated by free radicals may be an important factor in various pathologies. Protection against these damaging free radical processes is provided by antioxidant defense systems, including vitamin E and other
1. Kayser, B. (1991) Protein digestibility at 5000 m. In: Interna tional Congress of Mountain Medicine, Crans Montana. 2. Rai, R. M., Malhotra, M. S., Dimri, G. P. & Sampathkumar, T. (1975) Utilization of different quantities of fat at high al titude. Am. J. Clin. Nutr. 28: 242-245. Î.Boyer, S. J. & Blume, F. D. (1984) Weight loss and changes in body composition at high altitude. J. Appi. Physiol. 57: 15801585. 4. Hannon, J. P., Harris, C. W. & Shields, J. L. (1970) Altera tions in the serum electrolyte levels of women during high altitude (4300 m) acclimatization. Int. J. Biometeorol. 14: 201-209. 5. Jones, D. P. (1985) The role of oxygen concentration in oxidative stress: Hypoxic and hyperoxic models. In: Oxidative Stress (Sies, H., éd.),pp. 151-195, Academic Press, London, England. 6. Demopoulos, H. B., Santomier, J. P., Seligman, M. L. & Pietronigro, D.D. (1986) Free radical pathology: Rationale and toxi cology of antioxidants and other supplements in sports medicine and exercise science. In: Sport, Health, and Nutrition; The 1984 Olympic Scientific Congress Proceedings (Katch, F. I., ed.), vol. 2, pp. 139-190, Human Kinetics, Champaign, IL. 7. Dillard, C. J., Dumelin, E. E. &.Tappel, A. L. (1977) Effect of dietary vitamin E on expiration of pentane and ethane by the rat. Lipids 12: 109-114. 8. DUlard, C. J., Litov, R. E., Savin, W. M., Dumelin, E. E. & Tappel, A. L. (1978) Effects of exercise, vitamin E, and ozone on pul monary function and lipid peroxidation. J. Appi. Physiol. 45: 927-932. 9. Packer, L. (1984) Vitamin E, physical exercise and tissue dam age in animals. Med. Biol. 62: 105-109. 10. Cormier, M. (1977) Regulatory mechanisms of energy needs: Vitamins in energy utilization. Prog. Food Nutr. Sci. 2: 347356. 11. Schwarz, K. (1962) Vitamin E, trace elements, and sulfhydryl groups in respiratory decline. Vitam. Horm. 20: 463-484. 12. Schwarz, K. (1972) The cellular mechanisms of vitamin E ac tion: Direct and indirect effects of alpha-tocopherol on mitochondrial respiration. Ann. NY Acad. Sci. 203: 42-52. 13. Simon-Schnass, I. & Pabst, H. (1988) Influence of vitamin E on physical performance. Int. J. Vitam. Nutr. Res. 58: 49-54. 14. Ernst, E., Matrai, A. & Aschenbrenner, E. (1985) Blood rheology in athletes. J. Sports Med. Phys. Fitness 25: 207-210. 15. Ernst, E., ed. (1986) Hämorheologie fürden praktiker. W. Zuckschwerdt Verlag, Munich, Germany. 16. Schmid-Schönbein, H. (1982) Blood rheology in hemoconcentration. In: High altitude physiology and medicine (Brendel, W. & Zink, R. A., eds.), pp. 109-116, Springer Verlag, New York, NY. 17. Kappus, H. (1985) Lipid peroxidation: Mechanisms, analysis, enzymology and biological relevance. In: Oxidative Stress (Sies, H., éd.), pp. 273-310, Academic Press, London, England. 18. Killer, E. & Riess, H. (1988) Erworbene plasmatische Gerinningsstörungen. In: Hamorrhagische Diathese und Thrombose (Killer, E. & Riess, H., eds.), pp. 86-109, Wissenschaftliche Verlagsgesellschaft, Stuttgart, Germany.
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
LITERATURE CITED
SYMPOSIUM: NUTRITION AND EXERCISE
24. 25.
26. 27.
reaktionen. In: Immunologie. (Beniamini, E. &. Leskowitz, S., eds.), pp. 197-2125, Schwer Verlag, Stuttgart, Germany. Hultgren, H. N. (1970) High altitude pulmonary edema. Adv. Cardiol. 5:24-31. Simon-Schnass, I., Reimann, J. & Böhlau,V. (1984) VitaminE-therapie: Zur frage der résorptionvon vitamin E. Notabene Medici 14: 793-794. Tappel, A. L. (1972) Vitamin E and free radical peroxidation of lipids. Ann. NY Acad. Sci. 203: 12-28. Chow, C. K. (1979) Nutritional influence on cellular antioxidant defense systems. Am. J. Clin. Nutr. 32: 10661081.
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
19. Thews, G., Mutschler, E. & Vaupel, P. (1982) Anatomie, Phy siologie, Pathophysiologie des Menschen, Wissenschaftliche Verlagsgesellschaft, Stuttgart, Germany. 20. Leibovitz, B. E. &. Siegel, B. V. (1980) Aspects of free rad ical reactions in biological systems: Aging. J. Gerontol. 35: 45-56. 21. Simon-Schnass, I. & Koeppe, H. W. (1983) Vitamin E und arteriosklerose. Zschr. Allgemeinmed. 59: 1474-1476. 22. Simon-Schnass, I. & Korniszewski, L. (1990) The influence of vitamin E on rheological parameters in high altitude mountain eers. Int. J. Vitam. Nutr. Res. 60: 26-34. 23. Beniamini, E. & Leskowitz, S. (1988) Ãœberempfindlichkeits-
781
Nutrition at High Altitude1 Medical Department, Hermes Arzneimittel GmbH, D-8023 Grosshesselohe, Germany haustion, intestinal complaints and increased basal metabolism accompanied by hormonal changes, may be reasons for weight loss at high altitudes. Very little data are available on micronutrient me tabolism at high altitude. There are also practically no data on nutrient intake. Hannon et al. (4) showed a marked decrease of bicarbonate in serum. Most of this loss was replaced by an increase in chloride and, to a lesser extent, by protein aniónand phosphate. On the other hand, there was a decrease in sodium, potassium and magnesium, but calcium was elevated. The au thors attribute this to a reduction of plasma volume. In addition, this may also reflect insufficient nutrient intake. Some exploratory data showed that the rec ommended daily intake for most minerals and vita mins was not achieved by a "normal" diet at base camp. Another topic of interest is whether nutrients can be used prophylactically against some of the degen erative changes that occur at high altitude. During hypoxia, oxidative injury may be enhanced as a con sequence of alterations in the oxidation-reduction po tential (5). This may lead to increased oxidative stress. A correlation has recently been identified between in creased metabolic rate as a consequence of exercise and increased tissue damage due to free radical pa thology (6-9). Vitamin E reduces free radical reactions through its stabilizing effect on various components of the respiratory chain. Thus, vitamin E contributes to aerobic energy production (10-12), and vitamin E
ABSTRACT Food records confirm that there is a high risk of malnutrition at high altitudes because of the usual lack of fresh food. As to the use of pharmacologie properties of micronutrients, only some data on vitamin E are described. Two placebo-controlled studies showed that a prolonged stay at high altitude caused a decrease in physical performance and a deterioration of blood flow, most probably because of increased lipid peroxidation. Supplementation with vitamin E prevented these changes. More research is desirable to obtain valid data on nutritional requirements and to obtain the basis for special recommendations for nutrition at high altitude. J. Nutr. 122: 778-781, 1992. INDEXING KEY WORDS:
•food requirement •food intake •vitamin E •prophylaxis •free radicals
Physical activity at high altitude, such as high al titude mountaineering, has several nutritional aspects. Among these are the weight loss known to occur at high altitude, the possibility of micronutrient mal nutrition and the possibility of offsetting some of the deleterious effects of a stay at high altitude through nutritional supplementation. One problem during trekking or expeditions to high altitudes is weight loss. Normally people lose between 5 and 10% body weight and this of course is much more if people suffer from an illness such as diarrhea. Increased energy requirement as well as malabsorption may be the cause of this weight loss. In a recent study Kayser et al. (1) showed that there is no protein malabsorption until an altitude of 5,000 m, but that pro tein turnover seems to be increased. Rai et al. (2)found that there is also no fat malabsorption until 4,700 m. On the other hand, the results of Boyer and Blume (3) indicate a reduced fat absorption at 6,300 m. From these data it can be concluded that there is no malabsorption of macronutrients at altitudes where base camps are normally established. Malabsorption at higher altitudes is of less practical significance. It seems that other factors, such as reduced appetite, ex-
1Presented as part of a symposium: Nutrition and Exercise, given at the 75th Annual Meeting of the Federation of American Societies for Experimental Biology, Atlanta, GA, April 22, 1991. This sym posium was sponsored by the American Institute of Nutrition and supported in part by grants from Proctor and Gamble Company, the Coca Cola Company, the Quaker Oats Company, Ocean Spray Cranberries, Inc., Bronson Pharmaceuticals, NPH, and Hoffman LaRoche. Guest editors for this symposium were L. P. Packer, De partment of Molecular and Cell Biology, University of California, Berkeley, CA and V. N. Singh, Clinical Nutrition, Roche Vitamins and Fine Chemicals, Nutley, NJ. 1To whom correspondence should be addressed: Hermes Arz neimittel GmbH, Georg-Kalb-Strasse 5-8, D-8023 Grosshesselohe, Germany.
0022-3166/92 $3.00 ©1992 American Institute of Nutrition.
778
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
IREHE M. SIMON-SCHNASS2
SYMPOSIUM:
NUTRITION
AND EXERCISE
779
%of baseline
%of baseline
260
ISO
200
126 150
100
Baseline
tl Basecamp
L
1Treatment-froup
t2 Basecamp
Basecamp
Baseline
t3 Basecamp
1Treatment group
•Control-group
I Control group
••: no évaluation b«cku»eof too mmnj drop out«
FIGURE 1 Anaerobic threshold during a prolonged stay at high altitude (5100 m) with and without supplementation with vitamin E compared with preexpedition value, tl, t2 and t3 are measured 2, 4 and 6 wk after baseline.
deficiency leads to reduced cell respiration (6, 12). This is especially apparent when the available oxygen is also limited, as can occur because of high demand, poor local supply or lower partial pressure of oxygen at high altitude. Such impairment of metabolism is especially pronounced under conditions of increased physical load at high altitude. Investigations on the anaerobic threshold (Fig. 1) confirmed the previous observation that a prolonged stay at high altitude causes a shift to the left of the lactic acid curve during performance and a decrease of the anaerobic threshold. Both indicate reduced physical performance. Additional daily intake of 2X 200 mg of vitamin E prevented these changes (13). In experimental animals and in man, the exhalation of pentane has been demonstrated to be related to vita min E status (8, 11). In animals, exercise-induced lipid peroxidation could be prevented by vitamin E admin istration (7,9). In this experiment (Fig. I), the pentane expiration was maintained constant in the vitamin E group, indicating that no additional lipid peroxidation had occurred. However, in the control group the mean expired pentane rose by > 100%. It was concluded from this study (13) that climbing at high altitude may incur a risk of metabolically induced cell damage. One of the main tasks of blood is substance ex change (including oxygen exchange) between individ ual tissues. This is performed in the terminal vessels of the capillary system. The lack of oxygen at high altitude causes some significant changes of blood composition and rhéologieproperties. The special rheological properties of blood arise from its twophase composition of plasma and blood cells. The vis cosity of blood depends largely on the packed cell vol ume, plasma viscosity, the flexibility of the red blood cells and their tendency to aggregate (14, 15), so blood viscosity varies as a function of flow conditions.
FIGURE 2 Pentane exhalation during a prolonged stay at high altitude (5100 m) with and without supplementation with vitamin E compared with preexpedition value, tl, t2 and t3 are measured 2, 4 and 6 wk after baseline.
Erythrocyte flexibility depends, among other things, on membrane fluidity. Loss of membrane flexibility can occur due to hypo- and hyperthermia, membrane defects and aging of the cell (16). One of the important underlying phenomena is oxidative change to mem brane lipids, which may be triggered by free radicals (17). In addition to blood viscosity, the elasticity and integrity of the vascular wall plays an important role in capillary flow. Here too, oxidative damage is be lieved to be a pathogenic factor (18-20). The viscosity of blood is determined not only by hematocrit but also by plasma viscosity and the flex ibility of the erythrocytes. Data from studies of sub jects at high altitude (Fig. 3) show that a decreased filterability of the erythrocytes may be due to an in creased lipid peroxidation of membrane lipids (22).
Filtration quotient
0,65
0,45
Baseline
tl Basecamp
L_J Treatment group
12 Basecamp I Control group
FIGURE 3 Filterability of red blood cells during a pro longed stay at high altitude (4300 m) with and without sup plementation with vitamin E compared with preexpedition value, tl and t2 are measured 2 and 4 wk after baseline.
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
100
SIMON-SCHNASS
780 7, normal activity
substances (17, 20, 26, 27). Given the relationship of free radical damage to both hypoxia (causative) and cellular antioxidant defense systems (preventative), antioxidants, especially vitamin E, might play a sig nificant role in the prevention of high altitude dete riorations.
130
110
Baseline
II
tl
Basecamp
Treatment group
t2
Basecamp
H Control group
FIGURE 4 Protein C during a prolonged stay at high al titude (4300 m) with and without supplementation with vi tamin E compared with preexpedition value, tl and t2 are measured 2 and 4 wk after baseline.
Also, a disturbance was shown in the coagulation sys tem. It could be shown that the activity of protein C, a coagulation inhibitor, was significantly reduced, which may lead to increased coagulation (22). Under this condition it can be assumed that an increased granulocyte stimulation occurred (23). Proteases can then be released, which damage not only endothelial cells and proteins bound to the endothelial cells, but also hydrolyze proteins free in the plasma (23). This could explain the drop in protein C observed (Fig. 4) in the control group. Because there was no drop in protein C activity in the vitamin E group, it may be suggested that vitamin E supplementation may have stabilized both endothelial cells and leukocytes and protected protein hydrolysis. The data as a whole show that a relatively quick rise in altitude and continued presence at high altitude produces changes in a wide range of measurements (22) that point to impaired blood rheology (22). Mountain sickness is often at tributed to general disturbances of the microcircula tion. This aggravates the risk of frostbite, retinal hem orrhage and cerebral and pulmonary edema. There seems to be a combination of increased precapillary vascular resistance and microrheological and hemostatic disturbances (24). Oral administration of 2X 200 mg of vitamin E daily (25) showed that the deterioration in measurements seen in the control group was prevented. It seems of interest to study whether this positive effect can also be found in other hypoxic conditions, such as chronic obstructive pulmonary diseases, cardiac and cerebral ischemia and peripheral circulation dis turbance. Evidence is accumulating that indicates oxidative injury mediated by free radicals may be an important factor in various pathologies. Protection against these damaging free radical processes is provided by antioxidant defense systems, including vitamin E and other
1. Kayser, B. (1991) Protein digestibility at 5000 m. In: Interna tional Congress of Mountain Medicine, Crans Montana. 2. Rai, R. M., Malhotra, M. S., Dimri, G. P. & Sampathkumar, T. (1975) Utilization of different quantities of fat at high al titude. Am. J. Clin. Nutr. 28: 242-245. Î.Boyer, S. J. & Blume, F. D. (1984) Weight loss and changes in body composition at high altitude. J. Appi. Physiol. 57: 15801585. 4. Hannon, J. P., Harris, C. W. & Shields, J. L. (1970) Altera tions in the serum electrolyte levels of women during high altitude (4300 m) acclimatization. Int. J. Biometeorol. 14: 201-209. 5. Jones, D. P. (1985) The role of oxygen concentration in oxidative stress: Hypoxic and hyperoxic models. In: Oxidative Stress (Sies, H., éd.),pp. 151-195, Academic Press, London, England. 6. Demopoulos, H. B., Santomier, J. P., Seligman, M. L. & Pietronigro, D.D. (1986) Free radical pathology: Rationale and toxi cology of antioxidants and other supplements in sports medicine and exercise science. In: Sport, Health, and Nutrition; The 1984 Olympic Scientific Congress Proceedings (Katch, F. I., ed.), vol. 2, pp. 139-190, Human Kinetics, Champaign, IL. 7. Dillard, C. J., Dumelin, E. E. &.Tappel, A. L. (1977) Effect of dietary vitamin E on expiration of pentane and ethane by the rat. Lipids 12: 109-114. 8. DUlard, C. J., Litov, R. E., Savin, W. M., Dumelin, E. E. & Tappel, A. L. (1978) Effects of exercise, vitamin E, and ozone on pul monary function and lipid peroxidation. J. Appi. Physiol. 45: 927-932. 9. Packer, L. (1984) Vitamin E, physical exercise and tissue dam age in animals. Med. Biol. 62: 105-109. 10. Cormier, M. (1977) Regulatory mechanisms of energy needs: Vitamins in energy utilization. Prog. Food Nutr. Sci. 2: 347356. 11. Schwarz, K. (1962) Vitamin E, trace elements, and sulfhydryl groups in respiratory decline. Vitam. Horm. 20: 463-484. 12. Schwarz, K. (1972) The cellular mechanisms of vitamin E ac tion: Direct and indirect effects of alpha-tocopherol on mitochondrial respiration. Ann. NY Acad. Sci. 203: 42-52. 13. Simon-Schnass, I. & Pabst, H. (1988) Influence of vitamin E on physical performance. Int. J. Vitam. Nutr. Res. 58: 49-54. 14. Ernst, E., Matrai, A. & Aschenbrenner, E. (1985) Blood rheology in athletes. J. Sports Med. Phys. Fitness 25: 207-210. 15. Ernst, E., ed. (1986) Hämorheologie fürden praktiker. W. Zuckschwerdt Verlag, Munich, Germany. 16. Schmid-Schönbein, H. (1982) Blood rheology in hemoconcentration. In: High altitude physiology and medicine (Brendel, W. & Zink, R. A., eds.), pp. 109-116, Springer Verlag, New York, NY. 17. Kappus, H. (1985) Lipid peroxidation: Mechanisms, analysis, enzymology and biological relevance. In: Oxidative Stress (Sies, H., éd.), pp. 273-310, Academic Press, London, England. 18. Killer, E. & Riess, H. (1988) Erworbene plasmatische Gerinningsstörungen. In: Hamorrhagische Diathese und Thrombose (Killer, E. & Riess, H., eds.), pp. 86-109, Wissenschaftliche Verlagsgesellschaft, Stuttgart, Germany.
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
LITERATURE CITED
SYMPOSIUM: NUTRITION AND EXERCISE
24. 25.
26. 27.
reaktionen. In: Immunologie. (Beniamini, E. &. Leskowitz, S., eds.), pp. 197-2125, Schwer Verlag, Stuttgart, Germany. Hultgren, H. N. (1970) High altitude pulmonary edema. Adv. Cardiol. 5:24-31. Simon-Schnass, I., Reimann, J. & Böhlau,V. (1984) VitaminE-therapie: Zur frage der résorptionvon vitamin E. Notabene Medici 14: 793-794. Tappel, A. L. (1972) Vitamin E and free radical peroxidation of lipids. Ann. NY Acad. Sci. 203: 12-28. Chow, C. K. (1979) Nutritional influence on cellular antioxidant defense systems. Am. J. Clin. Nutr. 32: 10661081.
Downloaded from https://academic.oup.com/jn/article-abstract/122/suppl_3/778/4755359 by University of Rhode Island user on 18 October 2018
19. Thews, G., Mutschler, E. & Vaupel, P. (1982) Anatomie, Phy siologie, Pathophysiologie des Menschen, Wissenschaftliche Verlagsgesellschaft, Stuttgart, Germany. 20. Leibovitz, B. E. &. Siegel, B. V. (1980) Aspects of free rad ical reactions in biological systems: Aging. J. Gerontol. 35: 45-56. 21. Simon-Schnass, I. & Koeppe, H. W. (1983) Vitamin E und arteriosklerose. Zschr. Allgemeinmed. 59: 1474-1476. 22. Simon-Schnass, I. & Korniszewski, L. (1990) The influence of vitamin E on rheological parameters in high altitude mountain eers. Int. J. Vitam. Nutr. Res. 60: 26-34. 23. Beniamini, E. & Leskowitz, S. (1988) Ãœberempfindlichkeits-
781
