Zinc status in athletes: Relation to diet and exercise

Abstract

Zinc is involved in the biochemical processes supporting life, such as cellular respiration, DNA reproduction, maintenance of cell membrane integrity and free radical scavenging. Zinc is required for the activity of more than 300 enzymes, covering all 6 classes of enzyme activity. Zinc binding sites in proteins are often of distorted tetrahedral or trigonal bipyramidal geometry, made up of the sulphur of cysteine, the nitrogen of histidine or the oxygen of aspartate and glutamate, or a combination. Zinc in proteins can either participate directly in chemical catalysis or be important for maintaining protein structure and stability. The nutritional habits of elite athletes during training and competition are quite different from the recommended diet in the majority of the population. Endurance athletes often adopt an unusual diet in an attempt to enhance performance: an excessive increase in carbohydrates and low intake of proteins and fat may lead to suboptimal zinc intake in 90% of athletes. Mild zinc deficiency is difficult to detect because of the lack of definitive indicators of zinc status. In athletes, zinc deficiency can lead to anorexia, significant loss in bodyweight, latent fatigue with decreased endurance and a risk of osteoporosis.

Full text

Zinc Status in Athletes
Relation to Diet and Exercise
Alessandra Micheletti, Ruggero Rossi and Stefano Rufini
School of Sports Medicine, University of Perugia, Perugia, Italy
Abstract
Zinc is involved in the biochemical processes supporting life, such as cellular
respiration, DNAreproduction, maintenance of cell membrane integrity and free
radical scavenging. Zinc is required for the activity of more than 300 enzymes,
covering all 6 classes of enzyme activity.
Zinc binding sites in proteins are often of distorted tetrahedral or trigonal
bipyramidal geometry, made up of the sulphur of cysteine, the nitrogen of histi-
dine or the oxygen of aspartate and glutamate, or a combination. Zinc in proteins
can either participate directly in chemical catalysis or be important for maintain-
ing protein structure and stability.
Thenutritionalhabitsofeliteathletesduringtrainingandcompetitionarequite
differentfrom therecommendeddietinthemajorityofthepopulation. Endurance
athletes often adopt an unusual diet in an attempt to enhance performance: an
excessive increase in carbohydrates and low intake of proteins and fat may lead
to suboptimal zinc intake in 90% of athletes. Mild zinc deficiency is difficult to
detect because of the lack of definitive indicators of zinc status. In athletes, zinc
deficiencycanlead toanorexia,significantlossinbodyweight, latentfatigue with
decreased endurance and a risk of osteoporosis.
LEADING ARTICLE
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Zinc is one of the essential trace elements and,
as such, a member of one of the major subgroups
of the micronutrientsthat have attained suchprom-
inence in human nutrition and health.
The exceptional ability of the zinc atom to par-
ticipate in strong but readily exchangeable ligand
binding, together with the notable flexibility of the
coordination geometry of this metal, has proved to
beextraordinarilyusefulinbiologicalsystems.The
incorporationofthistraceelementintomammalian
biological systems has been further facilitated by
the lack of redox properties of zinc atom, which, in
contrast to iron and copper, allows its utilisation
without the risk of oxidant damage.
Zinc is ubiquitous in subcellular metabolism,
and is an essential component of the catalytic site
or sites of at least one enzyme in all classes of
enzymatic activity. Several hundred zinc metallo-
enzymes have been identified in the plant and ani-
mal kingdoms.
[1]
Since the recognition in 1934 of zinc as an
essential trace element in humans, there has been
continuous progress in our knowledge of the role
of zinc in biochemistry and medicine. Dietary zinc
deficiency in humans was recognised in 1961, and
the first study
[2]
identifying acrodermatitis entero-
pathica as a definite disease of zinc absorption was
published in 1973. Today it is recognised that a

marginal deficiency of zinc is common throughout
the world, not only among low income people but
everywhere an unbalanced diet is consumed.
[3]
During the past decade, more than 200 zinc-
dependent transcription factors involved in the
gene expression of various proteins have beenrec-
ognised.
[4]
Also, studies on the mechanisms of low
zinc absorption in acrodermatitis enteropathica
have been carried out to identify physiological
and pathological aspects in the absorption mecha-
nism and distribution of zinc.
[5]
1. Absorption and Homeostasis
Proteins, especially of animal origin, and fat are
the most important sources of absorbable zinc. The
relatively high amounts of phytates (inositol pen-
takis and hexakisphosphates) in cereal products,
legumes and nuts can significantly decrease blood
levels of zinc in vegetarians because intestinal ab-
sorption of zinc occurs through a specific process
thatisdiminishedbyconcomitantingestionofphy-
tates, phosphates, iron and copper.
[6]
Calcium can be a potentiating factor because
it reacts with phytates, forming a precipitating com-
plex salt. Zinc can easily bind to the precipitate. The
molar ratio of phytic acid to zinc in cereal products
ranges from 18 to 37. Because of this high phytate
content, the bioavailability of zinc in wholemeal
cereal products is low compared with foods of an-
imal origin.
[7]
Protein intake is important in this
respect since proteins provide amino acids, some
which are able to desorb zinc from the precipitate
and improve bioavailability.
Cellular zinc transport is mediated by an anion
carrier, probably from the family of cytochrome
oxidase II, the protein involved in the genesis of
acrodermatitis enteropathica.
Thebody maintainszinchomeostasis bychanges
in absorption and excretion. In good nutritional
status, body loss of zinc correlates proportionally
with total dietary intake. After periodsof low zinc
intake, daily zinc losses are substantially lower
than at higher intakes. The fractional absorption
does not differ between people consuming mar-
ginal or adequate quantities of zinc, but endoge-
nous zinc is effectively conserved by the intestine
inpeoplewhosehabitualdietaryzincintakeismar-
ginal. Diminishedintake of zinc leads toincreased
efficiency of absorption and decreased faecal ex-
cretion.
[8]
Nutritional habits in elite athletes during train-
ing and competition can be quite differentfrom the
recommended diet for the general population. En-
durance athletes often adopt unusual diets in an
attempt to enhance performance: an excessive in-
crease in carbohydrates and low intake of proteins
and fat may lead to suboptimal zinc intake in 90%
of athletes.
[9]
A low fat diet could compromise health and
performance because essential fatty acids and zinc
may be too low, and zincis an important determinant
of the intestinal absorption of lipid-soluble vitamins.
Even marginal zinc deficiency causes a marked de-
crease in the intestinal absorption of lipids in general
and lowers significantly the lymphatic absorption
of vitamin A and vitamin E.
[10]
2. Requirements
Kineticstudieshave shown that in humans there
are multiple pools of zinc that fluctuate from min-
utesto years.Zinccanbindtodifferent compounds
in different concentrations. By comparing kinetics
in healthy and various disease states, the role of
zinc in disease may be elucidatedthrough the iden-
tification of differences in metabolic processes.
[11]
Absorption and excretion are regulated by genet-
ics, diet,environmentand disease.
[11]
It may be that
the maintenance of homeostasis is guaranteed by
special adaptation mechanisms developed during
ontogenesis.
It is not easy to establish a minimum zinc
requirement because the human organism seems
highly tolerant towards partial deficiencies over a
period of time, and laboratory diagnosis of marginal
zinc deficiency can be problematic because there
is no reliable single measure that can demonstrate
suboptimal zinc status.
[12]
Assessment of dietary zinc status requires sev-
eral steps, consisting of the measurement of zinc
content in foods after different preparation methods
578 Micheletti et al.
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and considering inhibition of absorption by other
compounds in the diet,and seasonal variation in con-
tent and in intake. The apparent zinc intake shows
large day-to-day variations within individual eat-
ing patterns, suggesting that a reliable estimation of
overall zincintakecan only be madeaftera long term
follow-up.
3. Zinc Deficiency and
Its Consequences
During infancy, even a moderate zinc deficiency
can seriously impair human health, performance,
reproductive systems and mental and physical de-
velopment. In particular, zinc deficiency has been
shown to adversely affect brain growth, learning
and activity.
[13]
The pathological signs of zinc
deficiency are related to impaired functioning of
plasma membrane proteins, lowered plasma mem-
brane level of thiols and reduced production of en-
zymes necessary for RNA and DNA synthesis.
[14]
Temporary zinc deficiency is not a rare event:
high physical activity, stress and dietary habits may
be involved in a complex of factors which creates
suboptimal zincuptake.If not corrected,thisshort-
age can remain for a long time or worsen without
any apparent reasonor act as a sustainingfactorfor
abnormal eating behaviour.
Zinc is a determinant at several levels for the
correct integration of the taste system. It is impor-
tant for the synthesis of gustin, a parotid metallo-
protein secreted into saliva and identified as an
isoenzymeof carbonic anhydraseconsideredrespon-
sible for the maintenance of taste acuity.
[15]
Gustin
is also a trophic factor that promotes the growth
and development of taste buds through its action
on taste bud stem cells. A consequence of zinc de-
ficiency is decrease in taste intensity (hypogeusia)
and selectivity (dysgeusia), sincezincis involved
in the neurotransmission of the electrical stimulus
generatedinthebudcellsandendinginthecentral
nervous system.
[16]
Generally, hypozincaemic individuals have
a poor appetite, do not enjoy eating and com-
plain of food, particularly protein, as being dis-
agreeable. Reduced food consumption is a major
consequence of these alterations in taste, but sub-
chronic low protein intake worsens zinc availabil-
ity. Furthermore,carbohydrate-rich foods have lower
zinc content and reduced absorption capacity because
of their phytate content. A diet particularly rich in
starchcouldbethebestwaytoincurzincdeficiency.
[17]
Hypogeusia and loss of appetite exacerbate zinc de-
ficiency and in the exercising female can result
inmenstrual cycle irregularities, amenorrhoeaand
osteoporosis. Anorexia nervosa, frequently found
in young females, especially in athletes, has a num-
ber of symptoms in common with zinc deficiency:
bodyweight loss, depression and amenorrhoea.
[18]
This aspect could be a normal biological response
to stressors: when stressful stimuli are excessive, a
large number of animal species reduce food intake
and express a progressive wasting syndrome asso-
ciatedwith hypozincaemiaand susceptibilityto in-
fections.
[19]
4. Effects of Zinc on Physical Activity
There are limited data available on the rela-
tionship between performance and zinc status,
but physical activity seems to correlate positively
with blood zinc level, perhaps through regula-
tion of taste acuity and protein intake.
[20]
Zinc
and energy could also be connected via leptin,
an adipocyte-derived hormone that reflects the
amount of energy stored in adipose tissue.
[21]
Leptintravels through the bloodstream,is trans-
ported across the blood-brain barrier and produces
effects in the brain after binding to specific leptin
receptors located in the hypothalamus. Leptin was
found to change neuropeptide Y (NPY) levels in
the hypothalamus. High levels of leptin, reflecting
high or adequate levels of body fat, were found to
downregulatehypothalamicNPYmRNAandNPY
levels,which in turnsuggestsa decreasein appetite
in response to the signal of adequate body energy
reserves.
[22]
Dysregulation of leptin during zinc deficiency
has the potential to affect both central and peripheral
physiology, in that leptin receptors have been identi-
fied within reproductive tissues of thebody. Leptin
regulatesenergyintake and expenditureand its cir-
Zinc Status in Athletes 579
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culating levels are influenced in equal measure by
caloric imbalance and plasma zinc levels.
[21]
Some data on the relationship between zinc de-
ficiency and fatigue were obtained from patients 3
to 45 days after surgery. Post-operative fatigue, a
well documented syndrome, appears to correlate
with decreased serumzinclevelin patients.
[23]
Zinc
values returned to pre-operative values around 45
days and so did muscular efficiency.
The reason is perhaps a derangement in electro-
lytes. When healthy young volunteers had their
energy intake reduced to less than 1600 kcal per
day for 6 months, they experienced soreness, mus-
cle cramps and fatigue.
[24]
In muscle, and in most
other organs, when protein content is markedly
reduced, so are the levels of potassium, magne-
sium and zinc.
[25]
Acute zinc depletion, tested in
males, did not affect peak muscular force but al-
tered the total work capacity of skeletal muscle.
[26]
Performance of strenuous physical activity in-
creases oxygen demand by 10- to 15-fold compared
with resting conditions. The resulting elevated mito-
chondrial oxygen consumption and electron trans-
port flux produces an ‘oxidative stress’ that leads
to the generation of reactive oxygen species (ROS)
and lipid peroxidation. Free radicals are mediators
of muscle inflammation and damage. Zinc has an im-
portant role in antioxidant cellular defences, being
a structural element of the non-mitochondrial form
of the enzyme superoxide dismutase (SOD). Many
stresses (ultraviolet radiation, physical exercise, hy-
poxia) can rapidly redistributezinc-containingSOD
to damaged tissues, temporarily decreasing its plasma
levels.
[27]
The antioxidant propertiesof zinc have been linked
partly to its role as an integral component of SOD, as a
stabiliser of cell membranes, as a protector of the thiol
groups of proteins against oxidation and as a competi-
tor with copperand iron for binding to oxygen ligands,
reducing the potential for hydroxyl radical (OH
•
)pro-
duction from membrane phospholipids. In particular,
training appears to upregulate the mRNAabundance
of SOD in aerobic tissues such as liver, heart and
the deep portion of vastus lateralis muscle.
[28]
Unbalanced diet could be the main reason for
the zinc deficiencies frequently found in athletes,
although in certain cases strenuous exercise could
contribute to the deficiency by increasing sweat
loss and zinc redistribution between plasma and
erythrocytes.
[29]
Significant decreases in the eryth-
rocyte content of zinc represent the acute effects of
prolonged exercise, whereas hepatic zinc increases
after daily physical training and the changeis more
elevated at the end of a competitive season. These
differences suggest that long term exercise may in-
duceredistributionofzinc.Inathletesstudiedatthe
beginning of the season there were no deficiencies of
zinc, and plasma levels in sportsmen involved in an-
aerobic training were significantly higher compared
to those undertaking aerobic activity.
[30]
Urinary zinc excretion decreased during the first
month of resistance training and then returned to
baseline values in the next 4 weeks, suggesting an
adaptation in mineral excretion in response to heavy
training.
[29]
In general, hypozincaemic athletes have a higher
viscometricerythrocyterigidityindex.
[31]
Their power
output during performance is lower and they have a
higher increase in blood lactate during exercise, re-
sulting in a lower lactate threshold.
[32]
Strenuous exercise can also have an adverse ef-
fect on bone tissue [bodyweight, bone mineral con-
tent and bone mineral density (BMD)] and a consis-
tent negative association can be observed between
changes in BMD and urinary zinc excretion.
[33]
Sazawaletal.
[34]
suggested that zinc deficiency
may be an important cause of the lower motor ac-
tivity levels associated with hyponutrition. There
was a causal relationship between delayed linear
growthand reducedmotoractivityin malnourished
pre-school children. In this population, zinc sup-
plementation can positively affect growth and motor
activity,probablybecausezinc,particularly abundant
in the brain, is important for both brain function and
development.
5. Therapy
There is a minimal daily zinc intake that cannot
be disregarded over a long period. When protein
580 Micheletti et al.
 Adis International Limited. All rights reserved. Sports Med 2001; 31 (8)

and energy intakes meet the dietary reference val-
ues for sex and age, there is no zinc deficiency and
differences observed in different physical condi-
tions depend on modified distribution of intra- and
extracellular pools.
Zinc is used in pharmacological doses to treat
diseasessuch as acrodermatitisenteropathica,Wil-
son’s disease and in cases of overt nutritional defi-
ciency. Exogenous oral zinc treatment is also
effective in patients with decreased levels of car-
bonic anhydrase and in cancer patients with taste
alterations caused by head or neck irradiation.
[35]
Zinc supplementation can be a therapeutic op-
tion in addition to nutritional approaches in many
other conditions in which a pathological or iatro-
genic condition can modify zinc disposability, such
as gastrointestinal malabsorption, acute or chronic
blood losses and in dialysed patients.
Developmentofmethodstoinvestigatezincsta-
tus and identify people at risk of zinc deficiency and
to determine the need for initiation of zinc forti-
fication of the food supply or zinc supplemen-
tation is needed. Before considering the appropri-
ateness of zinc supplementation, it is important
toassessthetypeof thedeficiency(acute, subacute
or chronic) and the degree (subclinical, mild or
severe).
There is a widespread idea that mineral supple-
ments can help athletes. This assumption originates
from the belief that the athlete has a higher than nor-
mal requirement for minerals and that even a mar-
ginal deficiencycan havea negative effecton perfor-
mance. Similar to iron, dietary zinc supplements can
improveathleticperformanceinindividualsdeficient
in this element
[36]
and possibly in athletes who do
not consume well-planned and varied diets. The
quality of physical performance per se is not asso-
ciated with the nature of the foods consumed, ex-
cept in case of diets exclusively vegetarian, with a
low protein and elevated phytate content.
[37]
Reduction in dietary zinc beyond the capacity
to maintain homeostasis leads to utilisation of zinc
fromrapidlyturningover poolslocated in the bone
and liver. Even partial depletion of theseimportant
zinc stores can lead to the rapid onset of both bio-
chemical and clinical signs of zinc deficiency. In
this case it can be useful to give athletes zinc sup-
plements, preferably in form of a single soluble
salt. Zinc acetate or zinc gluconate are better than
zincsulphate becausethey arelessacidicandcause
lessgastric mucosal injury. If zincsupplementsare
used, it is important that they are not excessive, as
excess zinc in the diet can result in a secondary
copper deficiency.
[38]
6. Conclusion
Zinc is a transition metal essential for plant and
animal nutrition. It is contained to some extent in all
vegetable material but it is not necessarily abun-
dant in edible components. When Prasad
[4]
docu-
mented for the firsttime that the Iranianand Egyp-
tian dwarfs were zinc deficient, it was commonly
believed that zinc deficiency could never occur in
humans. Today, there is a growing interest in micro-
nutrientmalnutrition,and enduranceathletesare at
risk of zinc deficiency if they have an unbalanced
diet. Given the reality of nutrient-nutrient inter-
actions, it seems to be time to give up the ancient
concepts of deficiency and excess to a global per-
spective of ‘balanced diet’.
Acknowledgements
This work was supported in part by an educational
grant from MURST(Ministerodell’UniversitàdellaRicerca
Scientificae Technologica;UniversityMinistryof Scientific
and Technology Research) 1998.
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Correspondence and offprints: Dr Alessandra Micheletti,
Department of Clinical and Experimental Medicine, Sec.
Pharmacology, Toxicology and Chemotherapy, University
of Perugia, Via del Giochetto, Perugia 06100, Italy.
E-mail: alessandramicheletti@hotmail.com
582 Micheletti et al.
 Adis International Limited. All rights reserved. Sports Med 2001; 31 (8)