Effects of Aerobic Exercise and Training on the Trace Minerals Chromium, Zinc and Copper

Summary

Sports Medicine 4: 9-18 (1987) 0112-1642/87/0001-0009/$05.00/0 © ADIS Press Limited All rights reserved.

Effects of Aerobic Exercise and Training on the Trace Minerals Chromium, Zinc and Copper

Wayne W. Campbell and Richard A. Anderson us Department of Agriculture, ARS Vitamin and Mineral Nutrition Laboratory, Beltsville Human Nutrition Research Center, Beltsville

Aerobic exercise and training lead to numerous changes and/or adaptations in the normal physiological functioning of the body. The trace minerals chromium. zinc. and copper are directly involved in maintaining and regulating many of these physiological processes. especially those involved in normal carbohydrate. fat and protein metabolism and the ultimate formation of usable energy. Therefore. it is important to establish whether exercise and training alter the functions of these trace elements. and to determine the overall effects of exercise on nutritional status and physical performance.

Exercise results in a marked mobilisation of chromium into circulation. while zinc and copper levels have been shown to either remain stable or increase. Exercise also results in large increases in excretion of chromium. zinc and copper. Urinary chromium excretion has been shown to increase on an exercise day compared with a rest day. while increased zinc losses occur in urine and sweat and increased copper losses occur in urine. sweat. and faeces. When exercise-enhanced trace mineral losses are coupled with dietary intakes below the recommended levels. which are commonplace for both sedentary and exercising individuals. the nutritional status and overall health of exercising individuals may be suboptimal. Individuals who train intensively may be at special risk due to repeated in-creased losses. Trained athletes have lower resting urinary chromium losses. larger in-creases in urinary chromium losses due to exercise. lower resting serum zinc levels. and possible alterations in copper nutriture compared with sedentary controls. These changes suggest an altered metabolism and/or nutritional status of the trace minerals chromium. zinc. and copper in trained individuals and those who exercise strenuously.

Aerobic exercise such as running, biking, swim-ming and aerobic dance are becoming more and more popular. This type of exercise, if performed at high intensity and for long duration, leads to many metabolic, cardiovascular and muscular changes in the body. The trace elements chro-mium, zinc, and copper are directly involved in many of the physiological processes that may be altered by either acute exercise or long tetm train-ing. It is therefore important to determine whether strenuous exercise or endurance training alters the

status of these elements by causing changes in con-centrations of these trace minerals in tissues and blood, changes in excretion rates from the body and/or changes in factors that are influenced or controlled by these trace elements.

1. Chromium

The main metabolic functions of chromium (Cr) have not yet been clearly defined but are directly related to the regulation of carbohydrate and lipid

Effects of Exercise on Chromium, Zinc and Copper

metabolism, primarily by potentiating insulin ac-tion (Anderson 1981). A marginal chromium status may lead to signs of impaired glucose tolerance, elevated circulating insulin, elevated cholesterol and triglycerides, and increased incidence of aortic plaques (Anderson 1981). The suggested safe and adequate intake for chromium is 50 to 200 JLg/day for adults; however, up to 90% of self-selected diets may be below this level (Anderson & Kozlovsky 1985; National Research Council 1980). Diets high in simple sugars stimulate increases in urinary chromium losses up to 300% (Kozlovsky et al. 1986). These low dietary intakes and possible in-creases in urinary losses due to dietary habits may result in abnormal carbohydrate and lipid metab-olism.

Good dietary sources of chromium include mushrooms, oysters, black pepper, brewers yeast, apples with skins, wine and beer. Considerable losses of dietary chromium may occur during mill-ing and processing of foods, therefore dietary in-take of highly processed foods should be limited (Borel & Anderson 1984) The concentration of other trace minerals, including zinc and copper, also decreases during processing and refining.

1.1 Effects of Exercise on Chromium Mobilisation and Excretion

The first major work on the effects of exercise on chromium mobilisation and excretion was con-ducted on 9 healthy male runners, aged 23 to 46 years, who were subjected to a 6-mile run at or near their maximal pace (Anderson et al. 1982, 1984, 1986b). Serum chromium concentration in-creased significantly immediately after the run and remained elevated for 2 hours (Anderson et al. 1984). This increase signifies a marked mobilisa-tion of chromium from body stores in response to strenuous exercise. Mobilisation of chromium leads to increased losses since renal reabsorption of chro-mium is usually less than 5% (Donaldson et al. 1982) and thus most mobilised chromium is sub-sequently excreted in the urine. The urinary chro-mium concentration was higher for all runners 2 hours after the run, increasing an average 4.7-fold

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from pre-run values (table I). When chromium ex-cretion was expressed per mg urinary creatinine the post-run: pre-run ratio of 3.7 again indicated in-creased chromium losses due to strenuous running (table I). Expressing chromium concentration in the urine as a function of creatinine was done to min-imise changes in urine volume (Anderson et aJ. 1982). Finally, 24-hour urinary chromium excre-tion doubled on the exercise day compared to the non-exercise day (Anderson et al. 1982).

A second study was conducted to further define the influence of exercise on chromium excretion (Anderson et al. 1986a). Chromium excretion was determined for 8 trained male runners and 5 un-trained male runners on a rest day and following a controlled interval exercise period (30 seconds running, 30 seconds rest) on a treadmill at 90% V02max to exhaustion. All subjects were fed a con-stant diet throughout the study containing 9JLg chromium/1000 calories. This was done to min-imise any possible influences of dietary intake on chromium losses. Urinary chromium excretion of the trained runners significantly increased (p < 0.05) on the exercise day compared to the non-exercise day. However, there were no significant changes in urinary losses of the untrained runners due to the exercise.

The difference in chromium excretion between trained and untrained runners may be due to the duration and absolute intensity of the exercise. The untrained runners became fatigued sooner than the trained runners and thus were exposed to a shorter time of stress. The total exercise time for the un-trained runners may not have been enough to stim-ulate chromium mobilisation from stores and, therefore, chromium excretion was unchanged. The trained runners, by exercising longer, may have given their bodies more time to initiate physiolog-ical alterations resulting in chromium mobilisation and thus increased chromium losses. In a previous study, men had increased chromium losses after a 6-mile run, irrespective of training status (Ander-son et al. i 982).

To date, the possible contributions of sweat to increased chromium losses during exercise have not been established. These losses must be determined

Effects of Exercise on Chromium, Zinc and Copper II

Table I. Effect on urinary chromium of running 6 miles (mean ± SEM) [adapted from Anderson et al. 1982]

Pre-run 2 hours post-runa Post-run; pre-run

Cr concentration 0.15 ± 0.03 0.72 ± 0.21 4.7 ± 0.8 (ppb)

Urinary excretion 6.3 ± 0.8 31.3 ± 9.3 6.3 ± 2.5 (ng/hr)

Cr : creatinine ratio 0.09 ± 0.02 0.36 ± 0.10 3.7 ± 0.62 (ng Cr/mg creatinine)

a Post-run values were significantly different (p < 0.05) to pre-run values.

to more fully understand changes in chromium status due to stresses such as exercise.

1.2 Effects of Training on Chromium Losses

It is not known whether the body adapts in some way to these increased chromium losses due to ex-ercise. A study with rats has shown that training leads to enhanced tissue levels of chromium in the heart and kidney, but not the gastrocnemius muscle or liver (Vallerand et a1. 1984). These higher chro-mium levels may result from preservation of body stores due to improved gastrointestinal absorption or decreased urinary excretion of chromium. Cur-rently, no data exist to show changes in absorption in response to either exercise or training.

Differences in basal urinary chromium excre-tion have been shown between trained and un-trained men consuming a constant chromium diet (Anderson et a1. 1986a). On a non-exercise day, trained runners excreted significantly less chro-mium (p < 0.05) than sedentary control subjects (0.09 ± 0.01 ~gfday and 0.21 ± 0.03 ~gfday, re-spectively). This decrease may indicate a training adaptation whereby the athletes have increased their ability to conserve chromium, possibly through in-creased tissue storage as in the rat study (Vallerand et aL 1984). Conversely, it may indicate that the body stores of these athletes have been depleted and that chromium was being removed from plasma in an attempt to replenish these . stores. Support for this storage repletion hypothesis has

been seen during the initial stage of chromium re-pletion (3 days of CrCl3 infusion) in a total par-enteral nutrition patient suffering from chromium deficiency (Jeejeebhoy et al. 1977). Urinary excre-tion levels were lower than the infusion levels dur-ing the chromium repletion stage indicating a posi-tive balance and net uptake of chromium into the body. This net uptake continued until there was an apparent saturation of stores. If chromium stores were depleted in response to repeated periods of exercise, chromium status of the trained athletes may have been depleted, resulting in increased chromium retention. Sedentary individuals ex-posed to periodic exercise would not show these decreased excretions on rest days because their stores would still be adequate. Future research is needed to identify what compensatory mechan-ism(s), if any, the body uses to compensate for chromium losses due to exercise and/or training.

2. Zinc

A component of more than 100 enzymes, zinc (Zn) has a variety of physiological functions in the body, including helping maintain normal carbo-hydrate, lipid and protein metabolism (Under-wood 1977). The Recommended Dietary Allow-ance (RDA) for zinc is 15 mg/day for adults (National Research Council 1980), yet large seg-ments of the US popUlation are consuming levels one-half or less of this amount (Smith et a1. 1983). A deficiency of zinc impairs growth and cell rep-


lication, sexual maturation, fertility and reproduc-tion, wound healing, immune defences and taste acuity (Underwood 1977). Plasma zinc concentra-tions are the most widely used index of status, with normal values ranging from 75 to 125 ~gjdl (11.5 to 19.1 ~mo1/L) [Smith et al. 1983]. These circu-lating levels may reflect a pool of exchangeable zinc that can be mobilised during strenuous exercise and used in metabolically active tissues (Lukaski et al. 1984).

Good dietary sources of zinc include beef, liver, oysters, and dark meat from turkey and chicken (Underwood 1977). Whole grains and cereals, nuts, and legumes may also contain zinc, but these non-meat sources may be less bioavailable because of the presence of phytate and dietary fibre in foods derived from plants (Smith et al. 1983).

2.1 Effects of Exercise on Zinc Mobilisation and Excretion

Total plasma zinc levels have been shown to either remain stable (Anderson et al. 1984) or in-crease (Lukaski et al. 1984; Ohno et al. 1985) im-mediately following strenuous exercise. A study de-signed to determine the effects of varied intakes of zinc on postexercise changes in plasma zinc levels showed that cycling on a bicycle ergometer to ex-haustion significantly increased (p < 0.01) plasma zinc concentrations in 5 healthy men regardless of their zinc status (Lukaski et al. 1984). The post-exercise increases in plasma zinc levels were greater in the zinc-replete state than in the zinc-deplete state, (19 and 8%, respectively). When corrections were made for the effects of haemoconcentration (van Beaumont quotient) due to plasma volume decrease during exercise, differences in zinc status were noted. When dietary zinc intakes were ade-quate, plasma zinc levels did not change in pro-portion to plasma volume shifts, but during zinc depletion they did. The authors suggested that while plasma zinc levels were high, indicating adequate zinc stores in tissues, there was a net retention of zinc in the plasma, and that strenuous exercise re-sulted in a mobilisation of zinc from tissues such as muscle. However, during the zinc-deplete state,

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there was a net efflux of zinc from the plasma, pos-sibly into tissues. The combined stresses of low zinc intake and maximal exercise resulted in a relative reduction of circulating exchangeable zinc, reflect-ing an alteration in some body zinc pools (Lukaski et al. 1984). Exercise-induced muscle breakdown and injury could also explain the increased plasma zinc concentrations.

Similar increases in plasma zinc due to stren-uous exercise were reported in 11 sedentary healthy male students subjected to a 30-minute work pe-riod on a bicycle ergometer at 75% V02max con-sumption (Ohno et al. 1985). Immediately after ex-ercise, total plasma zinc concentrations increased significantly (p < 0.05) and then returned to pre-exercise levels following 30 minutes of rest. Cou-pled with this, there was a significant decrease (p < 0.05) in total zinc concentrations in erythrocytes immediately after exercise and a return to pre-ex-ercise levels 30 minutes after exercise. Anderson et al. (1984) reported no change in serum zinc im-mediately following a strenuous 6-mile run; how-ever, there was a significant decrease (p < 0.05) in serum zinc 2 hours after the run. This decrease may reflect a redistribution of zinc from serum into tis-sues or erythrocytes. Alternatively, leucocytic en-dogenous mediator, a polypeptide hormone re-leased by phagocytes in response to stress, may have mediated a redistribution of circulating zinc into the liver (Pekarek et al. 1972). The actual physio-logical significance of changes in plasma zinc con-centration due to exercise-induced stress is un-known at present.

Urinary losses of zinc increased significantly (p < 0.05) on a run day versus a non-run day in male runners (711 ~gjday versus 489 ~gjday, respec-tively) [Anderson et al. 1986b]. This represented a 1.6-fold increase in urinary zinc losses due to run-ning and raised the total zinc output in urine above the normal range of 300 to 600 ~g/day for adults (Underwood 1977). Assuming an average daily in-take for zinc of9 to 15 mg/day and 40% absorption (Smith et al. 1983), the urinary zinc losses on the exercise day would represent 12 to 20% ofthe total zinc absorbed; based on 10% absorption, these losses would increase to 47 to 79%.


Zinc losses in sweat must also be considered during exercise. Heavy sweating in hot and humid environments has been shown to result in major zinc losses (Consolazio et al. 1964; Jacob et al. 1981), and may contribute to zinc deficiency (Pra-sad et al. 1963). These losses have been shown to decrease in the same environment after acclima-tisation (Consolazio et al. 1964) or when the sub-jects were zinc deficient (Prasad et al. 1963). Actual measurements of losses in sweat from exercise are not presently available. However, considering the high perspiration rates in athletes, the importance of zinc lost in this way should certainly not be ne-glected (Haralambie 1981).

2.2 Effects of Training on Resting Serum Zinc Levels

Long term endurance training has been shown to significantly decrease resting serum zinc levels in both male (Dressendorfer & Sockolov 1980; Haralambie 1981) and female (Haralambie 1981) athletes compared to sedentary controls (table 11). 23% of the male runners, (average weekly training distance, 22 miles), were considered hypozin-caemic - less than 65 ~g/dl (9.9 ~mol/L) serum zinc [Dressendorfer & Sockolov 1980]. Addition-ally, those runners who trained the most tended to have the lowest zinc levels. Similar results were found in male and female athletes who trained for 90 to 120 minutes, 4 times per week; 23% of the male athletes and 43% of the female athletes pre-sented hypozincaemia - less than 75 ~gfdl (11.5 Ilmol/L) serum zinc [Haralambie 1981]. No differ-ences in plasma zinc levels were found between 44 male university athletes and 20 untrained controls (Lukaski et al. 1983). However, this finding may be due to both the athletic and non-athletic groups in the study being in good physical condition with the mean V02max for both groups above 45 ml/kgj min. Supplementation of both male runners and non-runners with 22.5mg zinc/day for 4 weeks re-sulted in a significant increase in serum zinc levels (Hackman & Keen 1986). Many of these men had presupplementation serum zinc levels below 'nor-mal' [80 p,g/dl (12.2 p,mol/L»), suggesting marginal

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status. Changes in serum zinc levels did not be-come apparent until the third and fourth week of supplementation, suggesting that during the first 2 weeks there was a net uptake of zinc into partially deplete stores.

The implications of these findings are not com-pletely understood. The very low zinc levels of many highly trained athletes suggest these people are hypozincaemic, yet no mention of signs or symptoms of zinc deficiency were noted. The cor-responding subjects may be experiencing a sub-clinical deficiency as a result of accumulating high losses and/or diminished zinc intake (Haralambie 1981). This view is supported by the observed in-creased losses of zinc in urine and sweat with ex-ercise and low dietary intakes. While a cause-and-effect relationship between level of training and zinc status has not been established, it may be that run-ners are compromised in their zinc status, or at least display a different metabolic profile for zinc (Hackman & Keen 1986).

2.3 Effects of Zinc Supplementation and Exercise on Changes in High Density Lipoprotein Cholesterol

The preceding sections on zinc may lead many to think zinc supplementation is the key to offset-ting any possible problems with zinc status due to exercise and endurance training. This belief mus) be viewed with caution. While zinc is a relatively safe trace mineral, the ingestion of pharmacologi-cal levels, more than 10 times Recommended Diet-ary Allowance (RDA), has been shown to be det-rimental to health. Firstly, excess zinc intake inhibits the absorption of copper, adversely affect-ing copper status (Klevay et al. 1979). Secondly, ingesting approximately 10 times RDA of zinc for 5 weeks by 12 healthy, non-obese men was shown to significantly decrease (p = 0.0001) serum high density lipoprotein cholesterol (HDL-C) concen-tration from 40.5 mg/dl to 30.1 mg/dl (Hooper et al. 1980). This is important because HDL-C is con-sidered to be 'antiatherogenic' and thus protective against the development of coronary artery dis-ease. A sustained fall in HDL-C concentration as-

Effects of Exercise on Chromium, Zinc and Copper 14

Table II. Resting zinc levels of athletes and sedentary controls (mean ± SEM)

Type of athlete

Runners male

Competitive athletes (age 16-30 years) male female

Col/ege athletes male

Zinc concentration (ltg/dl)

athletes

76 ± 13"

87.0 ± 10.0

controls

94 ± 12" (serum)

96.7 ± 12.6 (serum)

87.0 ± 8.0 (plasma)

References

Dressendorler & Sockolov (1980)

Haralambie (1981)

Lukaski (1983)

a Values for athletes and controls were significantly different (p < 0.05). b Median.

sociated with administration of high levels of zinc might increase the risk of coronary artery disease (Hooper et a1. 1980). A study of 270 healthy men and women over 60 years of age demonstrated sig-nificant relationships between level of exercise, ingestion of zinc supplements, and serum HDL-C (Goodwin et a1. 1985). High-density lipoprotein cholesterol levels increased with increasing activity level only in those subjects who were not taking any supplemental zinc. The subjects who con-sumed zinc supplements (median supplement in-take, 15mg) showed no increase in HDL-C with increased activity level. When zinc supplements were withdrawn for 8 weeks from 22 of the subjects who took high levels of supplemental zinc (17.5 to 52.2 mg/day), HDL-C levels significantly increased (2.0 mg/dl, p = 0.04). The highest increases were seen in the higher physical activity group. The authors cautioned that, . while statistically signifi-cant, this relationship was weak and could almost entirely be explained by 2 subjects at the low end of the physical activity scale and 1 at the upper end (Goodwin et a1. 1985). Further, another study by the same group reported that supplementing II male endurance-trained runners and 12 male se-dentary controls for 8 weeks with 28.7mg of ele-mental zinc per day (approximately twice RDA)

neither altered serum HDL-C concentrations for either group nor offset the beneficial effect of ex-ercise on lipid and lipoprotein concentrations (Crouse et a1. 1984).

These data demonstrate that it is very import-ant to overall health to take in zinc at physiological levels near the RDA. Drastically altering the rela-tive quantities of zinc consumed or supplementing with non-physiological amounts is unwise and should be avoided.

3. Copper

Copper is an essential nutrient that has a wide variety of functions including key roles in iron me-tabolism, cross-linking of connective tissues, neurotransmitter and brain function, lipid metab-olism and energy production (O'Dell 1984). The recommended safe and adequate intake of copper is 2 to 3 mg/day for adults (National Research Council 1980). The typical dietary intake of copper in the United States and other Westemised coun-tries is approximately one-half this amount (Fields 1985). While overt copper deficiency is not a prob-lem in humans (Underwood 1977), marginal cop-per intakes for extended periods may be detrimen-tal to overall health (Fields 1985). As with zinc,


copper intakes should be at or near the recom-mended safe and adequate levels. Excessive copper intakes are potentially toxic (Underwood 1977).

The richest sources of dietary copper are crus-taceans and shellfish, especially oysters, organ meats, nuts, dried legumes and potatoes (Under-wood 1977). Poor dietary sources include highly refined cereals and white sugar, honey and dairy products (Underwood 1977). Copper metabolism is impaired by the ingestion of simple sugars; high intakes of fructose and sucrose may exacerbate health problems associated with marginal copper intake (Fields 1985).

3.1 Effects of Strenuous Exercise on Copper Mobilisation and Excretion

Changes in circulating copper levels due to ex-ercise are varied. Serum copper levels increased 37.3% in trained and 21.5% in untrained men, in response to graded bicycle ergometry to exhaus-tion; during prolonged cycling the levels increased by 32.2 and 14.9%, respectively (Olha et al. 1982). Both types of exercise protocols resulted in a sig-nificantly larger (p < 0.001) increase in circulating copper levels of the trained men compared with untrained men. Plasma copper levels significantly increased (p < 0.001) immediately after exercise in 7 sedentary healthy males who cycled on a bicycle ergometer for 30 minutes at 70 to 80% V02max,

and returned to resting levels 30 minutes post-exercise (Ohno et al. 1984). Conversely, no changes in serum copper levels were found immediately following or 2 hours after a 6-mile run in males (Anderson et al. 1984).

Copper losses through sweat may be consider-able, especially for people living in warm and hu-mid climates. During 10 days of observation of 3 men fed a constant copper diet (3.5 mg/day) and housed in a controlled environment (37.8°C, 50% humidity), a significant negative copper balance was observed (Consolazio et al. 1964). The average sweat loss of copper was 1.6 mg/day, or about 45% of their daily dietary intake. Other reports have confirmed these large copper losses due to sweat (Hohnadel et al. 1973; Jacob et al. 1981).

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The combined stresses of strenuous exercise and reduced dietary intakes of copper resulted in in-creased faecal copper losses for 14 young athletes who competed in a SOkm ski race (Rusin et al. 1980b). Urinary copper losses also increased due to this exercise, but, this may be of minor signifi-cance since urinary excretion of copper is small compared with faecal excretion (Mason 1979). There was a significant drop in copper excretion on rest days compared with heavy exercise days.

3.2 Effects of Training on Resting Serum Copper Levels

Resting plasma or serum copper levels have been shown to be higher (Conn et al. 1986; Lukaski et al. 1983), unchanged (Olha et al. 1982) or lower (Dowdy & Burt 1980; Rusin et al. 1980a) in trained athletes compared with sedentary controls. 44 male university athletes who competed in a variety of sports at the university level had significantly higher (p < 0.01) mean plasma copper concentrations than 20 untrained controls (Lukaski et al. 1983). Similar increased resting plasma copper levels were re-ported for 31 male and female elite runners, aged 10 to 17 years, compared with 21 age-matched con-trols (Conn et al. 1986). Plasma copper did not cor-relate with V02max in either study (Conn et al. 1986; Lukaski et al. 1983). The higher copper levels were postulated to relate to increased levels of cerulo-plasmin (a copper-containing protein) and copper-dependent enzyme activities such as cytochrome oxidase (Dowdy & Dohm 1972; Lukaski et al. 1983; Ruckman & Sherman 1981). However, during a 6-month study involving a university swim team, serum copper levels dropped from an average of 64 ~g/dl during the first 3 months of training to a mean of 50 ~g/dl during the final 3 months of the study (Dowdy & Burt 1980). Likewise, the average serum ceruloplasmin level dropped from 36.8IU during the first month to 2S.2IU during the second month and remained depressed throughout the study period. It was suggested that the fall in cop-per and ceruloplasmin levels was due to heavy epi-dermal cell sloughing associated with prolonged water immersion during swimming (Lukaski et al.


1983), but no data or further reasoning were given to support this hypothesis. Intense ski training in adolescents resulted in a similar decreased ceru-loplasmin activity (Rusin et a1. 1980a). The com-bined stresses of training, growth, and low dietary copper intakes resulted in a 29% decrease in copper oxidase activity in the athletes, possibly indicating dietary copper deficiency. Taken together, these data indicate that copper nutriture may be altered due to intensive training, especially in people with added stresses, such as growth and low copper in-takes.

4. Conclusion

The science of exercise physiology is involved in attempting to establish the physiological changes of the body when exposed to the stresses of exer-cise and training, and to define the 'optimal' con-ditions for athletic performance. Nutrition has been long recognised as one factor which may directly relate to these changes and to determining the lim-its of maximal performance. Unfortunately, very little attention has been given to trace mineral nu-triture, namely chromium, zinc and copper, as re-lated to performance, and only in the past 5 to 10 years has research begun to investigate changes in chromium, zinc and copper mobilisation, excre-tion, and status related to exercise and training.

Strenuous exercise results in a marked mobilis-ation of chromium into serum, while zinc and cop-per levels have been shown to either remain stable or increase. The increases in circulating levels of these minerals presumably results from a release from tissue storage pools allowing these trace min-erals to be transported to where they are needed to aid in the increased physiological work associated with exercise.

Exercise also results in large increases in excre-tion levels of chromium, zinc and copper. Urinary chromium levels increase 4.7-fold following exer-cise compared with levels before exercise, and there is a doubling of urinary chromium output on an exercise day versus a non-exercise day. Increased zinc losses occur in the urine and sweat, while in-creased copper losses occur in urine, sweat and

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faeces. Losses of these trace minerals may be im-portant in determining the overall trace mineral status and requirements of individuals. When very large losses are coupled with low dietary intakes, the body may be placed in a compromised nutri-tional state. Without proper amounts of these min-erals, many body processes involving carbohy-drate, fat, and protein metabolism are altered, possibly affecting performance.

Several differences have also been shown in the status indices of chromium, zinc and copper in trained athletes. Trained athletes have: (a) lower basal urinary chromium excretion and larger in-creases in losses due to exercise; (b) lower serum zinc levels; and (c) possible alterations in copper nutriture as evidenced by changes in serum copper, ceruloplasmin and cytochrome oxidase activities compared with sedentary controls. These changes suggest that trace mineral status and metabolism are altered in trained individuals.

A cause-and-effect relationship between lower exercise performance and marginal chromium, zinc and copper status has not been established. How-ever, proper dietary management of these trace minerals, as well as all nutritional components, is a sound preventive approach to ensure that trace minerals do not become limiting factors in per-formance. An athlete's diet should contain a variety of foods, including foods rich in trace minerals such as whole grains and cereals, legumes, green leafy vegetables, meats and fish. Highly processed and refined foods should be limited: trace minerals are often lost during processing. It may be difficult to consume adequate trace minerals strictly from dietary food sources; supplementation may be nec-essary to obtain the recommended dietary levels for chromium, zinc, and copper. This may be es-pecially true for people on low calorie diets such as people on weight-reducing programmes and ath-letes who must control their weight for competi-tion. If supplementing, a multivitamin, multimi-neral supplement that contains from 1 to 2 times the Recommended Dietary Allowance for the es-sential nutrients should be used. There is no evi-dence that supplementing with large quantities of trace minerals is advantageous to health or athletic


performance; 'megadosing' with essential nutrients may be dangerous. Care should be taken to ensure that the trace minerals chromium, zinc, and copper are present in the supplement since these elements have been shown not only to be low in diets of sedentary individuals, but losses of these minerals may be increased due to strenous exercise.

More research is needed to better define how changes in trace mineral nutriture affect physio-logical functioning and performance, whether the body has any adaptive mechanisms to help offset the increased losses, and whether these losses in-crease dietary requirements.

References

Anderson RA. Nutritional role of chromium. Science ofthe Total Environment 17: 13-29, 1981

Anderson RA, Bryden NA, Polansky MM, Deuster PA. Con-trolled exercise effects on chromium excretion of trained and untrained runners consuming a constant diet. Federation Pro-ceedings 45: 971, 1986a

Anderson RA, Kozlovsky AS. Chromium intake, absorption and excretion of subjects consuming self-selected diets. American Journal of Clinical Nutrition 41: 1177-1183, 1985

Anderson RA, Polansky MM, Bryden NA. Strenuous running: acute effects on chromium, copper, zinc, and selected clinical variables in urine and serum of male runners. Biological Trace Element Research 6: 327-336, 1984

Anderson RA, Polansky MM, Bryden NA, Guttman HN. Stren-uous exercise may increase dietary needs for chromium and zinc. In Katch (Ed) Sport, Health, and Nutrition: 1984 Olym-pic Scientific Congress Proceedings, Vol. 2, Human Kinetics Publishers, Champaign, 1986b

Anderson RA, Polansky MM, Bryden NA, Roginski EE, Patter-son KY. et al. Effect of exercise (running) on serum glucose, insulin, glucagon, and chromium excretion. Diabetes 31: 212-216, 1982

Borel JS, Anderson RA. Chromium. In Frieden E. (Ed.) Bio-chemistry of the essential ultratrace elements, Plenum Pub-lishing Corporation, 1984

Conn CA, Ryder E, Schemmel RA, Ku P, Seefeldt V, et al. Re-lationship of maximal oxygen consumption to plasma and erythrocyte magnesium and to plasma copper levels in elite young runners and controls. Federation Proceedings 45: 972, 1986

Consolazio CF, Nelson RA, Matoush LO, Hughes RC, Urone P. Trace mineral losses in sweat. Report number 284 of US Army number 3A12501A283 (Military Internal Medicine) Sub-Task number 03 (Biochemistry), pp. 1-12, US Army Medical Re-search and Nutrition Laboratory, Fitzsimmons General Hos-pital, Denver, 1964

Crouse EF, Hooper PL, Atterbom HA, Papenfuss RL. Zinc inges-tion and lipoprotein values in sedentary and endurance-trained men. Journal of the American Medical Association 252: 785-787, 1984

Donaldson DL, Anderson RA, Veillon C, Mertz WE. Renal ex-cretion of orally and parenterally administered chromium-51. Federation Proceedings 41: 391, 1982

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Dowdy RP, Burt J. Effect of intensive, long-term training on cop-per and iron nutriture in man. Federation Proceedings 39: 786, 1980

Dowdy RP, Dohm GL. Effect of training and exercise on serum ceruloplasmin in rats. Proceedings of the Society of Experi-mental Biology and Medicine 139: 489-491, 1972

Dressendorfer RH, Sockolov R. Hypozincemia in runners. Phy-sician and Sportsmedicine 8: 97-100, 1980

Fields M. Newer understanding of copper metabolism. Internal Medicine 6: 91-98, 1985

Goodwin JS, Hunt WC, Hooper P, Garry PJ. Relationship be-tween zinc intake, physical activity, and blood levels of high-density lipoprotein cholesterol in a healthy elderly population. Metabolism 34: 519-523, 1985

Hackman RM, Keen CL. Changes in serum zinc and copper lev-els after zinc supplementation in running and nonrunning men. In Katch (Ed.) Sport, health, and nutrition: 1984 Olympic Sci-entific Congress Proceedings, Vol. 2, Human Kinetics Pub-lishers, Champaign, 1986

Haralambie G. Serum zinc in athletes in training. International Journal of Sports Medicine 2: 136-138, 1981

Hahnadel DC, Sunderman Jr FW, Nechay MW, McNeely MD. Atomic absorption spectrometry of nickel, copper, zinc, and lead in sweat collected from healthy subjects during sauna bathing. Clinical Chemistry 19: 1288-1292, 1973

Hooper PL, Visconti L, Garry PJ, Johnson GE. Zinc lowers high-density lipoprotein-cholesterollevels. Journal of the American Medical Association 244: 1960-1961, 1980

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Authors' address: R.A. Anderson, US Department of Agriculture, ARS Vitamin and Mineral Nutrition Laboratory, Beltsville Hu-man Nutrition Centre, Beltsville, MD 20705 (USA).

Documents

Effects of Aerobic Exercise and Training on the Trace Minerals Chromium, Zinc and Copper