Carl L. Keen1
Introduction
During the last decade there has been increasing interest in the idea that individuals engaged in strenuous exercise may have an increased need for several of the essential minerals. This idea has resulted in the widespread perception that mineral supplements may be advantageous for this subpopulation. The concept is based on two basic perceptions: (a) that individuals engaged in strenuous exercise have a higher requirement for some minerals compared to sedentary individuals due to increased rates of urinary and sweat losses of select minerals and (b) that the perceived inadequate intake of some minerals results in a lowering of endurance capacity and ultimately may lead to the development of some disease states. Although a significant number of athletes, coaches, and professionals in the sports medicine field believe in the salutary effects of mineral supplements, there are remarkably few data supporting a positive effect of dietary mineral supplementation on athletic performance. However, as discussed below, strenuous exercise does influence the metabolism of several minerals, and the amount of minerals lost via sweat (due to either intense heat or exercise) can be significant.
This chapter examines the current understanding of the effects of exercise on mineral metabolism and the potential consequences of these effects. The metabolism of at least eight minerals—copper, chromium, iodine, iron, magnesium, potassium, sodium, and zinc—has been suggested to be influenced by exercise. Due to space constraints, this chapter will focus on four elements—iron, magnesium, zinc, and copper—to exemplify concepts involved in exercise-and heat-induced alterations in mineral metabolism and nutrition. However, prior to this discussion a few comments will be made concerning iodine, selenium, and chromium. The reader is directed to Chapters 12 and 13 for information on exercise-and heat-induced changes in sodium and potassium metabolism.
Effects of Exercise and Heat on Iodine, Chromium, and Selenium Metabolism
Consolazio (1966) reported that a considerable amount of iodine can be lost via sweat. In that study, 12 adult males were maintained at a temperature of 38.5°C during the day and 33.1°C during the night. During the 24-hour period, the men exercised at a moderate rate on a bicycle ergometer for 1 hour. The average total sweat loss of the men over the 24-hour period was 5576 g, which resulted in an average loss of 146 µg of iodine. Given that the 1989 U.S. recommended dietary allowance (RDA) (NRC, 1989) for iodine for adult men and women is 150 µg per day, and the observation that typical iodine intakes exclusive of iodized salt range from 250 to 170 µg per day for men and women, respectively (Pennington et al., 1989), it is evident that sweat-associated iodine loss can be significant. The above findings suggest that it is critical that iodized salt (which provides >70 µg of iodine per g of salt) be consumed when an individual is in an exceptionally hot area and/or engaged in strenuous activity. Studies examining the influence of combined heat exposure and endurance exercise on iodine metabolism are needed.
As with iodine, there is limited literature on the influence of exercise and heat on selenium metabolism, although it has been suggested that athletes may benefit from selenium supplements due to its role in glutathione peroxidase synthesis. Singh et al. (1991) reported that plasma selenium concentrations decreased in men exposed to a 5-day rigorous training program conducted by the U.S. Navy, despite an increase in dietary selenium intake during the program. Singh and colleagues suggested that the decrease in plasma selenium might have reflected a shift in selenium from the plasma pool to tissues requiring increased antioxidant protection. This hypothesis would be consistent with the observation that exercise can result in increased rates of tissue lipid peroxidation (Davies et al., 1982). Although the above observations suggest that selenium metabolism may be influenced by exercise, to date there is no compelling evidence that selenium supplementation is necessary for individuals engaged in endurance activities (Lane, 1989; Lang et al., 1987).
Consolazio et al. (1964) reported an average loss of 340 µg of selenium in sweat over an 8-hour period in men maintained at a temperature of 37.8°C. However, given the observation that typical selenium intakes are only on the order of 100 µg per day (Pennington et al., 1984), the loss reported by Consolazio seems excessive, and may reflect the technical difficulties involved in measuring this element. With the exception of the data by Consolazio, there are no current reports suggesting that selenium requirements are higher in hot environments compared to temperate regions.
Although the metabolic functions of chromium have not been clearly defined, chromium is known to be involved in the regulation of carbohydrate and lipid metabolism, presumably via a role in insulin action. Although not clearly defined in humans, signs associated with marginal chromium status in experimental animals include impaired glucose tolerance, elevated circulating insulin, elevated cholesterol and triglycerides, and increased incidence of aortic plaques (Campbell and Anderson, 1987). The dietary intake of chromium has been reported to be suboptimal for the general population based on dietary survey studies (Anderson and Kozlovsky, 1985). Recent research has indicated that chromium requirements may be influenced by strenuous exercise. Anderson et al. (1984) reported that serum chromium concentrations were increased in adult males immediately after a 6-mile run at near-maximal running capacity. This increase in serum chromium was still evident 2 hours after the completion of the run, and urinary chromium loss was elevated twofold on the run day compared to non-run days. Basal urinary chromium excretions have been shown to be lower in individuals routinely engaged in strenuous activity compared to sedentary controls (Anderson et al., 1988), which suggests either that chronic exercise results in a partial depletion of body chromium stores or that it induces metabolic changes that result in a reduction in urinary chromium excretion. Consistent with the latter idea, Vallerand et al. (1984) reported that, in rats, exercise training is associated with an increase in soft tissue chromium concentrations. In addition to exercise-induced increases in urinary chromium excretion, it would be expected that chromium losses would also be increased with excessive sweating. However, due to analytical difficulties in measuring this element, accurate data on sweat-associated losses of chromium are not currently available. Consolazio et al. (1964) reported that chromium loss in sweat over an 8-hour period averaged 60 µg in men maintained at 37.8°C, a value that would be double that of the typical dietary intake of the element. Studies aimed at better defining the amount of chromium lost in sweat at different amounts of sweat loss are clearly needed.
Chromium deficiency per se has not been accepted as a health problem in endurance athletes. However, it seems prudent, given the above findings, to monitor chromium status of individuals engaged in strenuous activity for prolonged periods of time, particularly if the activity is performed in a hot environment where chromium losses in sweat would be predicted to be high. Studies on the functional consequences of activity-induced changes in chromium metabolism are needed.
Effects of Exercise and Heat on Iron Metabolism
It is well recognized that iron-deficiency anemia can be associated with a diminished performance in maximal and submaximal physical exercise (Andersen and Barkve, 1970; Edgerton et al., 1981; Gardner et al., 1977; McDonald and Keen, 1988 and references cited therein). However, there is considerable controversy about the extent to which exercise contributes to the development of iron deficiency. Although there is a common perception that athletes as a group tend to have a high incidence of anemia compared to sedentary populations, hematological surveys of elite athletes have typically not supported this idea (Brotherhood et al., 1975; de Wijn et al., 1971; Stewart et al., 1972). Thus, overt iron-deficiency anemia does not appear to be a common complication of chronic intense exercise.
High levels of physical activity have been suggested to cause ''sports anemia'' (typically defined as a drop in hemoglobin concentration, hematocrit, and red blood cell count; Balaban et al., 1989; Yoshimura, 1970). The phenomenon of sports anemia has been associated with increased erythrocyte destruction, depressed iron absorption, increased sweat loss of iron, and gastrointestinal blood loss (Dressendorfer et al., 1991; Ehn et al., 1980; Frederickson et al., 1983; Paulev et al., 1983; Puhl et al., 1981; Stewart et al., 1984). Although most investigators agree that sports anemia is common in athletes who initiate rigorous training programs, this "anemia" is typically transitory in nature with hematological values often returning to pretraining values within 3 weeks despite continued training (Frederickson et al., 1983). Based on these findings, it has been suggested by some that sports anemia may be in part a consequence of plasma volume expansion and a functional dilution of the red blood cell count because blood volume can increase by as much as 20 percent during training (Brotherhood et al., 1975; Hegenauer et al., 1983).
In recent years there has been interest in the idea that exercise training can result in reduced tissue iron stores. Ehn at al. (1980) reported low bone marrow iron stores and evidence of increased iron absorption in elite distance runners who were characterized by normal hemoglobin and serum iron levels. Low serum ferritin concentrations have been reported by numerous investigators to be a consequence of prolonged, strenuous exercise (primarily when the subject is involved in weight-bearing sports) (Magazanik et al., 1988; Nickerson et al., 1985; Parr et al., 1984; Roberts and Smith, 1990; Snyder et al., 1989). Although there is considerable debate about the extent to which iron supplements may prevent exercise-induced reductions in tissue iron stores, Snyder et al. (1989) and Nickerson et al. (1985) have reported that providing highly bioavailable iron (heme iron in meat) or iron supplements (105 mg per day) can retard the development of low serum ferritin concentrations.
Given the observation that endurance athletes are typically not characterized by a higher than normal frequency of iron-deficiency anemia (see above), many investigators have questioned the significance of the finding of low serum ferritin concentrations in these individuals. However, it is important to note that the occurrence of low tissue iron stores in these individuals could present a problem with regard to recovery from injuries that result in extensive tissue damage or blood loss. It should be noted that marginal iron deficiency resulting in impaired thermoregulation has recently been observed (Beard et al., 1990); thus exercise-induced alterations in iron status may pose particular risks for individuals exposed to extreme temperatures.
As discussed above, an increased rate of sweat loss of iron is thought to contribute to the depletion of iron stores with chronic endurance exercise. Although the loss of iron via sweat is not normally considered to be a major explanation for the iron depletion, sweat iron concentrations can range from 0.1 to 0.3 mg per liter for men and up to 0.4 mg per liter for women (Aruoma et al., 1988; Brune et al., 1986; Lamanca et al., 1988; Paulev et al., 1983). Given these concentrations, sweat can be an appreciable route of iron loss particularly when sweat rates exceed 5 liters per day. The potential interaction between prolonged exposure to high temperatures and vigorous activity with regard to iron status, and an individual's ability to thermoregulate and recover from injury is an area that needs further clarification.
In sum, dietary iron supplementation may in some instances be justified to ensure good health of the individual. However, caution must be used in advocating excessive iron supplementation, given the potential negative side effects that can be associated with its use, including possible gastrointestinal discomfort, and interactions with other metals that have similar physiochemical properties. For example, it has been suggested that high levels of supplemental iron can inhibit the absorption of zinc (Keen and Hackman, 1986; Solomons, 1986). Given that prolonged exposure to a regimen of strenuous exercise and/or exposure to conditions resulting in high rates of sweat loss is associated with marked changes in zinc metabolism (see below), the potential negative effects of excess iron supplementation are clear.
Effects of Exercise and Heat on Zinc Metabolism
Lichti et al. (1970) first demonstrated that strenuous exercise can result in marked changes in zinc metabolism. They reported a marked increase in plasma zinc concentrations in dogs following short bouts of intense exercise. This observation was extended by Hetland et al. (1975) who found that plasma zinc concentrations in men participating in a 5-hour, 70-km cross-country ski race were 19 percent higher immediately postrace compared to prerace values. However, by day 1 postrace, zinc concentrations were back to control levels. The observation that plasma zinc concentrations can increase significantly during strenuous exercise has since been verified by numerous investigators (Dressendorfer et al., 1982; Lukaski et al., 1984; Ohno et al., 1985; Van Rij et al., 1986). The magnitude of the increase in plasma zinc concentration with exercise is such that it cannot be due to hemoconcentration (Hetland et al., 1975; Lukaski et al., 1984); rather it is thought to reflect the result of muscle leakage of zinc into the extracellular fluid following muscle breakdown (Karlson et al., 1968). Following the cessation of exercise, there is normally a rapid drop in plasma zinc levels back to preexercise concentrations within a short period. It is thought that this rapid postexercise drop in plasma zinc is due to a high urinary excretion of the element coupled with a shift in the distribution of the element from the plasma fraction into the liver (Anderson et al., 1984; Campbell and Anderson, 1987; McDonald and Keen, 1988). The shift of zinc from the plasma into the liver is thought to be in part a consequence of the so-called acute-phase response, which occurs as a consequence of stressors such as infection, inflammation, and trauma. These stressors can result in the elaboration of cytokines, which result in the stimulation of the synthesis of several liver proteins (Cannon and Kluger, 1983; Cousins, 1985; Dinarello, 1989; Keen and Hackman, 1986; Singh et al., 1991). With regard to zinc, one component of the acute-phase response is an increase in liver metallothionein concentration, which can result in a sequestering of zinc in the liver (Cousins, 1985; Whanger and Oh, 1978). (Serum ferritin concentrations can increase as a result of the acute-phase response, a fact that must be considered when collecting samples for assessment of iron status; Singh et al., 1991; Taylor et al., 1987.)
Reductions in plasma zinc concentrations were also observed in men who participated in a 5-day intensive training course conducted by the U.S. Navy (Singh et al., 1991). This reduction in plasma zinc occurred despite an increase in dietary zinc intake during the training period. The authors attributed the reduction in plasma zinc primarily to a redistribution of plasma zinc into liver as a consequence of metallothionein synthesis stimulated by interleukin-6 (IL-6). (The observed increase in plasma IL-6 concentrations was associated with tissue trauma.) Consistent with the above finding, Lichton et al. (1988) observed a reduction in plasma zinc concentrations in male soldiers engaged in a 34-day field exercise at an elevation of 1800 m. The field exercise was simulated combat in which the men performed combat-support activities during both day and night and during which time they lost sleep. Activities included digging foxholes, building lava-stone walls, and walking. During the study, subjects were given a military operational ration, the meal, ready-to-eat (MRE), as their only food. Although the average zinc intake during the field exercise was lower than zinc intakes in a sedentary control group of soldiers who were fed the same food, intakes by both groups were considered adequate. Urinary zinc concentrations in the active soldiers increased from an average basal level of 400 µg per day to about 700 µg per day during the study. Sweat mineral losses were not assessed.
This finding shows that there are short-term effects of exercise on zinc metabolism; however, the immediate physiological consequences of these effects are not known. Dressendorfer and Sockolov (1980) have suggested that a high level of constant exercise can have long-lasting effects on zinc metabolism. This suggestion was based on the observation that a significant number of endurance runners were characterized by low serum zinc concentrations even when tested prior to an exercise bout. This hypozincemia in endurance runners has since been reported by other laboratories (Couzy et al., 1990; Deuster et al., 1986; Dressendorfer et al., 1982; Hackman and Keen, 1986; Haralambie, 1981).
The mechanisms underlying the development of exercise-induced hypozincemia are presumably multifactorial and may include impaired absorption of zinc, excessive sweat and urinary loss of the element, and an altered metabolism of zinc (Anderson et al., 1984; Deuster et al., 1989; Miyamura et al., 1987). Although there is considerable debate about the value of plasma zinc in diagnosing zinc deficiency, most investigators agree that prolonged low plasma zinc concentrations are indicative of suboptimal zinc status. Given that the consequences of a suboptimal zinc status can include behavioral abnormalities, impaired immunocompetence, and reduced rate of recovery from injury (Hambidge, 1989; Keen and Gershwin 1990), it is evident that the functional significance of exercise-induced hypozincemia needs to be defined in future studies. In addition, the interactive effect of prolonged exposure to high temperatures and intense exercise needs to be defined. Exposure to extremes in temperature by itself can result in a stimulation of the acute-phase response with subsequent changes in zinc metabolism (Sugawara et al., 1983; Uhari et al., 1983); sweat losses of zinc can range from 0.5 to 1 mg per liter (Aruoma et al., 1988; Van Rij et al., 1986). Thus a strong synergistic effect of prolonged exposure to exercise and heat would be predicted. To illustrate the above scenario, the following calculations can be made. First, assume a dietary zinc intake of 15 mg, with a typical absorption of 20 percent (King and Turnlund, 1989), resulting in an uptake of 3 mg of zinc. By assuming a sweat zinc concentration of 0.5 mg per liter, it is evident that sweat losses in excess of 8 liters can present a significant problem. In addition, typical urinary zinc losses under conditions of stress will average 0.5 to 0.8 mg per day. Zinc absorption may also be reduced under conditions of stress. Given the above calculations, sustained exercise in a hot environment would be predicted to have a negative impact on an individual's zinc balance. Note that an intermediate value for zinc absorption was used for these calculations. Zinc absorption from typical foods ranges from 10 to 40 percent (King and Turnlund, 1989); thus the type of meal fed will have a significant effect on the zinc balance of individuals exposed to the above conditions.
Given the frequent observation of exercise-induced hypozincemia and the potentially high amounts of the element that can be lost via sweat, there may be a need for zinc supplementation in situations where prolonged exposure to exercise and heat is anticipated. However, as discussed for iron, caution must be used when advocating zinc supplements because this element at high levels can interfere with copper absorption due to the similar physiochemical properties of zinc and copper (Keen and Hackman, 1986). Chronic (more than 6 weeks) consumption of zinc supplements in excess of 50 mg per day has been linked to the induction of copper deficiency in humans (Fischer et al., 1984; Fosmire, 1990; Prasad et al., 1978; Samman and Roberts, 1988). Lower levels of zinc supplementation have not been reported to result in copper deficiency.
Influence of Exercise and Heat on Magnesium Metabolism
There are considerable data demonstrating an effect of exercise on magnesium metabolism. Rose et al. (1970) reported that serum magnesium concentrations in marathon runners immediately following a race were significantly lower than prerace values, a phenomenon that was attributed to sweat losses of the element during the run. The idea that excessive sweating could result in a high loss of magnesium from the body is consistent with the work of Consolazio et al. (1963) who found that, under normal conditions, sweat loss accounted for over 12 percent of the total daily excretion of magnesium in men working in temperatures of 49° to 50°C. (Typical magnesium losses via sweat are on the order of 3 to 4 mg per liter [Beller et al., 1975; Consolazio et al., 1963].) The observed lowering of plasma magnesium with intense exercise has since been verified by numerous investigators (Beller et al., 1975; Deuster et al., 1987; Franz et al., 1985; Haralambie et al., 1981; Laires et al., 1988; Lijnen et al., 1988; Refsum et al., 1973; Stendig-Lindberg et al., 1987, 1989). The typical reduction in plasma magnesium following intense exercise is on the order of 10 percent. Stendig-Lindberg et al. (1989) reported that low plasma magnesium concentrations can be demonstrated in young men for up to 18 days after strenuous exertion (a 70-km march). In addition to an increased loss of magnesium via sweat, urinary magnesium loss can increase by up to 30 percent following a bout of intense exercise (Deuster et al., 1987; Lijnen et al., 1988). Although the reduction in plasma magnesium may be due in part to an increased rate of magnesium loss from the body, redistribution of magnesium from the plasma pool into other sites may also contribute to exercise-induced decreases in plasma magnesium. For example, Costill et al. (1976) reported an increased magnesium content in exercising muscle during prolonged work that paralleled the decline in plasma magnesium. Redistribution of serum magnesium into red blood cells (Abbasciano et al., 1988; Deuster et al., 1987; Lukaski et al., 1983) and into adipocytes (Franz et al., 1985) with exercise has also been reported. Researchers generally agree that prolonged exercise can result in lower than normal plasma magnesium concentrations; however, they have not agreed on the functional consequences of this reduction. Jooste et al. (1979) reported that in some cases the reduction can be severe enough to trigger epileptic-type convulsions in runners. Similarly, Liu et al. (1983) reported a case in which an exercise-induced reduction in plasma magnesium was associated with the induction of carpopedal spasms in a 24-year-old woman. Marginal magnesium deficiency has been associated with the etiology of some cardiac diseases (Rayssiguier, 1984), hypertension (Altura and Altura, 1984), and reduced work capacity (Conn et al., 1986; Keen et al., 1987; Lowney et al., 1990; Lukaski et al., 1983). Marginal magnesium status has also been implicated in a number of human psychiatric disturbances and in chronic fatigue syndrome (Cox et al., 1991).
Given the above reports, it is clear that prolonged strenuous exertion can result in reductions in plasma magnesium concentrations. These reductions can be attributed in part to an increased rate of magnesium loss via sweat, which could be significantly amplified in hot environments. Given the recognition that marginal magnesium deficiency can present a significant health risk to an individual, studies are needed that define the functional consequences of exercise-and heat-induced reductions in plasma magnesium concentrations.
Effects of Exercise and Heat on Copper Metabolism
Acute, strenuous exercise has been reported by several investigators to result in a marked increase in plasma copper concentrations, which has been attributed to an increase in plasma ceruloplasmin concentrations (Haralambie, 1975; Ohno et al., 1984; Olha et al., 1982). An increase in ceruloplasmin concentrations is consistent with the induction of an acute-phase response as discussed above. The effects of intense exercise on increasing plasma copper levels can continue for prolonged time periods. Dressendorfer et al. (1982) reported that men engaged in a 20-day, 500-km road race were characterized by plasma copper levels that increased constantly during the first week, after which they remained fairly constant. This increased copper output into the plasma as a result of exercise may have long-lasting effects, as suggested by the observation that plasma copper levels at rest tend to be higher in athletes than in untrained individuals (Haralambie, 1975; Lukaski et al., 1983; Olha et al., 1982).
Given the putative antioxidant properties of ceruloplasmin (Goldstein et al., 1979; Gutteridge, 1986), one explanation for the exercise-induced increase in the concentration of this plasma protein is as a response to tissue injury associated with oxidative damage or to the presence of an increased concentration of free radicals (Alessio et al., 1988; Davies et al., 1982; Jenkins, 1988; Kanter et al., 1986). An additional possibility is that the increased ceruloplasmin output from the liver, and hence increased levels in the plasma, is an adaptive response by the body to an increased requirement for extrahepatic copper. It is known that the higher values of maximal oxygen uptake in trained individuals are correlated to an increase in oxidative enzymes within the cell. One of the enzymes increased is the copper-containing protein, cytochrome oxidase (Terjung et al., 1973). It has been shown that ceruloplasmin copper can be incorporated into cytochrome oxidase, and cell receptor sites for ceruloplasmin have been identified (Stevens et al., 1984). Ceruloplasmin copper has also been demonstrated to be transferred to apo-copper, zinc superoxide dismutase (Percival and Harris, 1991). An increase in cellular copper, zinc superoxide dismutase activity could represent an adaptive response to exercise-induced intracellular oxidative stress (Jenkins, 1988; Lukaski et al., 1990).
In contrast to reports of increased plasma copper concentrations, Anderson et al. (1984) reported that plasma copper concentrations were similar in men prior to and after completing a 6-mile run; Lukaski et al. (1990) reported no influence of training on plasma copper concentrations in elite swimmers, and Singh et al. (1991) observed no change in plasma copper concentrations in men engaged in intense physical activity over a 5-day period. Resina et al. (1990) reported that plasma copper concentrations were lower in long-distance runners than in sedentary controls, and Dowdy and Burt (1980) reported that plasma copper concentrations and ceruloplasmin activity decreased in competitive swimmers over a 6-month period. Uhari et al. (1983) reported that plasma copper concentrations decreased in male and female subjects following exposure to hot temperatures in a sauna bath.
Reasons for the above differences in reported effects of exercise on plasma copper concentrations are various, including differences in copper status of the subjects; type, intensity, and duration of the exercise; physical condition of the individual; and extent of exercise-induced tissue trauma. Presumably, increases in plasma copper occur primarily when there is tissue damage that triggers an acute-phase response. However, note that in the study by Singh et al. (1991), despite evidence of significant tissue damage (see zinc section above), plasma copper concentrations were not elevated.
Additional studies are needed that define the mechanisms underlying exercise-induced increases in plasma copper concentrations.
It is important to point out that the occurrence of high plasma copper concentrations does not necessarily translate into high tissue copper concentrations; indeed, high plasma copper concentrations in some disease states have been correlated to low soft tissue copper concentrations (Clegg et al., 1987; Dubick et al., 1987). Although the interpretation of normal to high plasma copper concentrations with regard to assessing an individual's copper status can be difficult, there is general agreement that low plasma copper concentrations typically reflect a compromised copper status. Thus the report of low plasma copper concentrations in some endurance athletes (see above) is of concern. Although loss of basal copper via sweat is typically considered negligible (Gutteridge et al., 1985; Jacob et al., 1981), Consolazio et al. (1964) reported that the amount of copper lost via sweat can be considerable; men who were maintained at 37.8°C and 50 percent relative humidity lost as much as 1 mg per day in sweat. This value should be contrasted to typical dietary copper intakes, which are on the order of 1 to 2 mg (Pennington et al., 1989). Thus prolonged, excessive loss of copper via sweat during strenuous exercise could result in a marginal copper status. The simultaneous exposure to hot temperatures would be expected to accelerate the development of a marginal copper condition.
Conclusions
Prolonged strenuous exercise can result in marked changes in chromium, copper, iron, magnesium, and zinc metabolism. Evidence of these changes can persist for several days after the exercise is discontinued. Some of the observed changes in plasma mineral concentrations may be attributed in part to an acute-phase response, which occurs as a result of tissue trauma or stress. Reductions in plasma mineral concentrations may also in part reflect an increased loss of these minerals from the body via urine and sweat. The increased rate of mineral loss that occurs in sweat with exercise is amplified by the simultaneous exposure to hot temperatures.
Given the above observations, the following questions emerge: Do endurance-associated changes in mineral metabolism result in some or all of the following:
a compromised endurance capacity?
a compromised immune defense system?
a compromised antioxidant defense system?
a slower rate of recovery from injury?
Additional work on the influence of prolonged exposure to strenuous exercise and heat is urgently needed. The influence of diet on the above changes in mineral metabolism, or whether dietary manipulations may attenuate some of the negative consequences of these changes, is an area of research that needs to be expanded.
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Discussion
DR. NESHEIM: Thank you. We will have a few questions before we break for lunch.
PARTICIPANT: Could you elaborate some more on the magnesium uptake by lymphocytes? You mentioned in passing that there could be an increase in uptake by lymphocytes?
DR. KEEN: Yes, this has been suggested by Franz (Franz et al., 1985). And the argument is, although there is no hard data to support it, that for lipolysis, you will have an increase in a lymphocyte magnesium uptake.
While the current data for this idea are not very strong, it is in the literature that it should be considered a possibility.
An exercise-induced erythrocyte uptake of magnesium, has also been argued based on the idea that it is needed for 2, 3-diphosphoglycerate synthesis (Lukaski et al., 1983).
However, we have done a study (Lowney et al., 1990) where we looked at the influence of magnesium deficiency on erythrocyte 2, 3-diphosphoglycerate production, and it had no influence on 2, 3-diphosphoglycerate levels.
PARTICIPANT: How about the endurance study with magnesium deficiency in the animal. Why didn't that continue to go on down as you have a more severe deficiency. Here is a plateau in fact.
DR. KEEN: Yes, it is a plateau. Unfortunately, you can't get animals much more deficient and get meaningful data. We were curious if we could get a dose response using animals fed diets containing less than 50 µg of magnesium per gram, however once pronounced signs of magnesium deficiency occurred, it was difficult to get the males to run.
DR. NESHEIM: Thank you, Carl. That was very interesting and challenging and indeed reports some of the work that needs to be done.
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Carl L. Keen, Departments of Nutrition and Internal Medicine, University of California, Davis, CA 95616–8669
