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Zinc status in athletes: Relation to diet and exercise



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.
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
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.
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.
Sports Med 2001; 31 (8): 577-582
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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
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.
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
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.
During the past decade, more than 200 zinc-
dependent transcription factors involved in the
gene expression of various proteins have beenrec-
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.
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
tates, phosphates, iron and copper.
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.
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
ginal. Diminishedintake of zinc leads toincreased
efficiency of absorption and decreased faecal ex-
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.
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.
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.
Absorption and excretion are regulated by genet-
ics, diet,environmentand disease.
It may be that
the maintenance of homeostasis is guaranteed by
special adaptation mechanisms developed during
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.
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.
Adis International Limited. All rights reserved. Sports Med 2001; 31 (8)
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
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.
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.
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.
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
nervous system.
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
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.
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-
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.
and energy could also be connected via leptin,
an adipocyte-derived hormone that reflects the
amount of energy stored in adipose tissue.
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
levels,which in turnsuggestsa decreasein appetite
in response to the signal of adequate body energy
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
Adis International Limited. All rights reserved. Sports Med 2001; 31 (8)
culating levels are influenced in equal measure by
caloric imbalance and plasma zinc levels.
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.
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.
In muscle, and in most
other organs, when protein content is markedly
reduced, so are the levels of potassium, magne-
sium and zinc.
Acute zinc depletion, tested in
males, did not affect peak muscular force but al-
tered the total work capacity of skeletal muscle.
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
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
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.
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
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-
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.
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
In general, hypozincaemic athletes have a higher
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.
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.
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
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.
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.
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
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
in this element
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.
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.
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
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’.
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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... nimmt Zink als Cofaktor mehrerer Enzyme, wie der AP und der Kollagenase, eine Rolle in der Knochenmineralisation und der Synthese der kollagenen Strukturen des Knochens ein[70]. Ein Zinkmangel ist kein seltenes Ereignis und kann durch eine suboptimale Zinkaufnahme bei körperlichen Belastungen, Stress und einseitigen Ernährungsgewohnheiten bedingt sein und zu einer verminderten Knochendichte führen[70,71].Vitamine stellen eine Gruppe von lebensnotwendigen organischen Verbindungen unterschiedlicher Stoffklassen dar, welche vom Körper nicht selbst synthetisiert werden können und durch die Nahrung aufgenommen werden müssen.Trotz der Wichtigkeit einer adäquaten Aufnahme der Vitamine C, E und K ist die Verlässlichkeit und der Nutzen ihrer laborchemischen Bestimmung nicht vollständig nachgewiesen und wird in dieser Arbeit nicht thematisiert. Für das labordiagnostische Assessment sind vor allem die Vitamine B6, B9 und B12 geeignet. ...
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Zusammenfassung Hintergrund Die labordiagnostische Untersuchung stellt eine wichtige Möglichkeit zur Beurteilung und Optimierung der Leistungs- und Regenerationsfähigkeit professioneller Athleten dar. Ferner ist sie für die Prävention, Diagnostik und Rehabilitation von Verletzungen und Überbelastungen von Bedeutung. Fragestellung Ziel dieser Arbeit ist die Darstellung muskuloskelettaler laborchemischer Parameter, die relevante Erkenntnisse für die medizinische Betreuung von Leistungssportlern liefern. Material und Methoden Literaturrecherche und narratives Review. Ergebnisse Die Bestimmung des Vitamin-D-, Calcium- und Knochenstoffwechsels stellt die laborchemische Basisdiagnostik im Rahmen der Beurteilung des Skelettstatus mit zusätzlichem präventivem Nutzen bezüglich muskuloskelettaler Verletzungen dar. Ferner können muskuläre Serummarker, z. B. Laktatdehydrogenase (LDH), Kreatinkinase (CK), Myoglobin und Aspartat-Aminotransferase (ASAT), helfen, eine metabolische Adaptation an das physische Training festzustellen und Aussagen über die muskuläre Arbeitslast und mögliche Schädigungen zu gewinnen. Die Energieverfügbarkeit kann durch eine entsprechende Bilanzierung sowie die laborchemische Bestimmung der Makro- und Mikronährstoffe eingeschätzt und optimiert werden. Schlussfolgerungen Die labordiagnostische Untersuchung besitzt in der Betreuung von Athleten eine sportartenübergreifende klinische Relevanz. Sie dient der Erreichung einer höchstmöglichen Leistungsfähigkeit sowie optimalen Prävention von Knochen- und Muskelverletzungen, wobei sämtliche Mangelzustände (z. B. Vitamin D) ausgeglichen werden sollten. Durch eine Periodisierung der laborchemischen Untersuchungen, mit zumindest zwei Labordiagnostiken im Jahr, und Aufstellung individueller Variabilitäts- und Referenzbereiche kann ferner eine bessere Beurteilbarkeit erreicht werden.
... Micronutrients, including vitamins B 1 , B 2 , and C and the minerals potassium, calcium, iron, copper, zinc, and especially magnesium, are known to be lost in sweat or urine. 18,51,52,75 Further, studies on athletes' dietary intake demonstrate that they regularly do not meet the recommended minimum intake in several micronutrients such as vitamin E, magnesium, folate, and copper, among others. 25 As such, it may be important to monitor micronutrient deficiencies in the elite athlete population as it can affect physical performance. ...
Context Malnutrition is well-studied in various aspects of the orthopaedic literature, most commonly in relation to arthroplasty, spine surgery, and trauma. However, the management of nutritional deficiencies is commonly overlooked among orthopaedic sports medicine providers. The purpose of this article is to analyze the available sports medicine literature to review the associations between malnutrition and the management of orthopaedic sports medicine patients from a treatment and performance standpoint. Evidence Acquisition PubMed was searched for relevant articles published from 1979 to 2019. Study Design Clinical review. Level of Evidence Level 4. Results Few studies exist on the implications of macronutrient deficiencies specific to orthopaedic sports medicine procedures. Interestingly, micronutrient disorders—namely, hypovitaminosis D and iron deficiency—have been well studied and may lead to worse postoperative outcomes, injury rates, and athletic performance. Nutritional supplementation to correct such deficiencies has been shown to mitigate these effects, though further study is required. Conclusion Nutritional deficiencies are highly prevalent in orthopaedic sports medicine patients, and practitioners should be aware of their potential effects on treatment and performance outcomes. Management of such deficiencies and their effect on surgical patients remain an area of potential future research. Future studies are warranted in order to explore the potential therapeutic role of nutritional supplementation to prevent complications after common orthopaedic sports medicine procedures, improve athletic performance, and reduce injury rates.
... No support for 'preventing URI'. Regular high-dose zinc supplementation can decrease immune function and should be avoided [96,103] ...
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Respiratory and gastrointestinal infections limit an athlete’s availability to train and compete. To better understand how sick an athlete will become when they have an infection, a paradigm recently adopted from ecological immunology is presented that includes the concepts of immune resistance (the ability to destroy microbes) and immune tolerance (the ability to dampen defence yet control infection at a non-damaging level). This affords a new theoretical perspective on how nutrition may influence athlete immune health; paving the way for focused research efforts on tolerogenic nutritional supplements to reduce the infection burden in athletes. Looking through this new lens clarifies why nutritional supplements targeted at improving immune resistance in athletes show limited benefits: evidence supporting the old paradigm of immune suppression in athletes is lacking. Indeed, there is limited evidence that the dietary practices of athletes suppress immunity, e.g. low-energy availability and train- or sleep-low carbohydrate. It goes without saying, irrespective of the dietary preference (omnivorous, vegetarian), that athletes are recommended to follow a balanced diet to avoid a frank deficiency of a nutrient required for proper immune function. The new theoretical perspective provided sharpens the focus on tolerogenic nutritional supplements shown to reduce the infection burden in athletes, e.g. probiotics, vitamin C and vitamin D. Further research should demonstrate the benefits of candidate tolerogenic supplements to reduce infection in athletes; without blunting training adaptations and without side effects.
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Zinc is one of the most abundant metal ions in the central nervous system (CNS), where it plays a crucial role in both physiological and pathological brain functions. Zinc promotes antioxidant effects, neurogenesis, and immune system responses. From neonatal brain development to the preservation and control of adult brain function, zinc is a vital homeostatic component of the CNS. Molecularly, zinc regulates gene expression with transcription factors and activates dozens of enzymes involved in neuronal metabolism. During development and in adulthood, zinc acts as a regulator of synaptic activity and neuronal plasticity at the cellular level. There are several neurological diseases that may be affected by changes in zinc status, and these include stroke, neurodegenerative diseases, traumatic brain injuries, and depression. Accordingly, zinc deficiency may result in declines in cognition and learning and an increase in oxidative stress, while zinc accumulation may lead to neurotoxicity and neuronal cell death. In this review, we explore the mechanisms of brain zinc balance, the role of zinc in neurological diseases, and strategies affecting zinc for the prevention and treatment of these diseases.
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Adequate amounts of a wide range of micronutrients are needed by body tissues to maintain health. Dietary intake must be sufficient to meet these micronutrient requirements. Mineral deficiency does not seem to be the result of a physically active life or of athletic training but is more likely to arise from disturbances in the quality and quantity of ingested food. The lack of some minerals in the body appears to be symbolic of the modern era reflecting either the excessive intake of empty calories or a negative energy balance from drastic weight-loss diets. Several animal studies provide convincing evidence for an association between dietary micronutrient availability and microbial composition in the gut. However, the influence of human gut microbiota on the bioaccessibility and bioavailability of trace elements in human food has rarely been studied. Bacteria play a role by effecting mineral bioavailability and bioaccessibility, which are further increased through the fermentation of cereals and the soaking and germination of crops. Moreover, probiotics have a positive effect on iron, calcium, selenium, and zinc in relation to gut microbiome composition and metabolism. The current literature reveals the beneficial effects of bacteria on mineral bioaccessibility and bioavailability in supporting both the human gut microbiome and overall health. This review focuses on interactions between the gut microbiota and several minerals in sport nutrition, as related to a physically active lifestyle.
Currently, there is no doubt about the prevailing influence of the level of physical activity of an individual on the functional state of the body. However, the available literature data on the impact of physical stress on the body's supply of trace elements and their distribution in tissues are largely contradictory. This review of available literature data provides an insight into the relationship between physical activity and microelement homeostasis. The influence of human physical activity on the exchange of toxic (lead, cadmium, Nickel, etc.) and essential trace elements, such as iron, selenium, copper, cobalt, chromium, and zinc is reviewed. Based on the analyzed works, it is concluded that in order to correct the metabolic and microelement status of a person during physical activity, the most reasonable and necessary is the modulation of homeostasis of zinc and selenium.
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Human salivary gustin stimulated activity of brain calmodulin-dependent cyclic nucleotide phosphodiesterase (cAMP PDEase; 3',5'-cyclic-nucleotide phosphodiesterase, EC in a dose-dependent manner in the absence of calmodulin. At physiological levels found in human saliva, gustin activated cAMP PDEase 5- to 6-fold. Activation of PDEase occurred with as little as 500 ng of gustin. Comparative sensitivity of activation of PDEase by gustin was intermediate between calmodulin and lysophosphatidylcholine with maximal activation and half-maximal activation (indicated in parentheses) at 3 X 10(-8) M (4.3 X 10(-9) M), 3.4 X 10(-6) M (3.4 X 10(-7) M), and 2.5 X 10(-3) M (4.0 X 10(-5) M) for calmodulin, gustin, and lysophosphatidylcholine, respectively. No other major salivary protein activated PDEase. Anticalmodulin antibody completely inhibited calmodulin-activated cAMP PDEase activity, but the antibody had no effect on gustin-activated cAMP PDEase activity. A sensitive calmodulin RIA indicated that no calmodulin was detected in any gustin preparation that activated cAMP PDEase. Both gustin and calmodulin rendered cAMP PDEase thermally labile to a similar extent and increased Vmax without affecting the apparent Km for the substrate cAMP. Activation by gustin and calmodulin was unaffected by lubrol-PX, trypsin inhibitor, pepstatin A, or leupeptin. In the presence of 1 mM EGTA, gustin activated cAMP PDE 5- to 6-fold, but the activating ability was completely lost after gustin was heated at 100 degrees C for 5 min. In contrast, calmodulin lost all activating ability in the presence of 1 mM EGTA, whereas heating calmodulin at 100 degrees C for 5 min did not affect its activation of cAMP PDEase. Lysophosphatidylcholine-activation of cAMP PDEase, like gustin activation, was unaffected by EGTA, but lysophosphatidylcholine-activation of cAMP PDEase, like calmodulin activation, was unaffected by heating at 100 degrees C for 5 min.
The effects of oxidative stress within post mitotic cells such as neurones may be cumulative, and injury by free radical species is a major potential cause of the age-related deterioration in neuronal function seen in several neurodegenerative diseases. There is strong evidence that oxidative stress plays an important role in the pathogenesis of motor neurone disease (MND). Point mutations in the antioxidant enzyme Cu, Zn superoxide dismutase (SOD1) are found in some pedigrees with the familial form of MND. How mutations in this ubiquitous enzyme cause the relatively selective cell death of specific groups of motor neurones is not clear, although a number of hypotheses have been forwarded. These include (1) the formation of hydroxyl radicals, (2) the catalysis of reactions of the nitrogen centred oxidant species peroxynitrite, (3) toxicity of copper or zinc and (4) protein aggregation. Some experimental support for these different hypotheses has been produced by manipulating cells in culture to express the mutant SOD1 proteins and by generating transgenic mice which over-express mutant SOD1. Observations in these model systems are, in some cases at least, supported by observations made on pathological material from patients with similar SOD1 mutations. Furthermore, there are reports of evidence of free radical mediated damage to neurones in the sporadic form of MND. Several lines of evidence suggest that alterations in the glutamatergic neurotransmitter system may also play a key role in the injury to motor neurones in sporadic MND. There are several important subcellular targets, which may be preferentially impaired within motor neurones, including neurofilament proteins and mitochondria. Future research will need to identify the aspects of the molecular and physiological phenotype of human motor neurones that makes them susceptible to degeneration in MND, and to identify those genetic and environmental factors which combine to cause this disease in individuals and in familial pedigrees.
We previously described a disorder in 18 patients with decreased parotid saliva gustin/carbonic anhydrase (CA) VI secretion associated with loss of taste (hypogeusia) and smell (hyposmia) and distorted taste (dysgeusia) and smell (dysosmia). Because gustin/CAVI is a zinc-dependent enzyme we instituted a study of treatment with exogenous zinc to attempt to stimulate synthesis/secretion of gustin/CAVI and thereby attempt to correct the symptoms of this disorder. Fourteen of the 18 patients with this disorder completed the study. They were treated with 100 mg of exogenous zinc daily for 4 to 6 months, in an open clinical trial. Both before and after treatment, measurements were obtained of parotid saliva gustin/CAVI, parotid saliva, serum and urine zinc, taste and smell function, and, in some patients, examination of circumvallate taste buds by electron microscopy. Treatment success was predicated upon significant increases in parotid saliva gustin/CAVI. This occurred in 10 of the 14 patients who were labeled responders; they also exhibited improvement in taste and smell acuity, a diminution in dysgeusia and dysosmia and increased zinc concentrations in parotid saliva, serum, and urine. Taste bud morphology returned to normal in each responder in whom it was measured. No increase in gustin/CAVI occurred in 4 patients who were labeled nonresponders; they exhibited no improvement in taste or smell acuity and no increases in parotid saliva zinc. However, serum and urine zinc increased to levels similar to those measured in the 10 responders. Two of 4 nonresponders reported diminution in dysgeusia and dysosmia. Taste bud morphology did not change from the abnormal state in the 1 nonresponder in whom it was measured. Zinc treatment is effective in patients in whom this trace metal increases synthesis/secretion of gustin/CAVI and ineffective in those in whom it does not. Increased gustin/CAVI in this disorder is probably associated with zinc stimulation of the gene responsible for the synthesis/secretion of gustin/CAVI. Among nonresponders, zinc was ineffective for several possible reasons, including resistance to zinc and possible sialylation of gustin/CAVI, which may render it functionally ineffective. Results suggest the hypothesis that gustin/CAVI is a trophic factor that promotes growth and development of taste buds through its action on taste bud stem cells.
The importance of the presence of zinc in human physiology and pathology has been analysed. The disturbances in the prostaglandin synthesis in the impaired intestinal zinc absorbtion have been of special interest. It is known that the deficiency of zinc results in the inborn clinical syndrome oh he disease and both its past and present treatment methods.
Some aspects of zinc nutritive status in patients suffering from anorexia nervosa were evaluated. Basic anthropometric measurements, Zn levels in serum, urine and hair as well as serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH; Zn-dependent enzymes) and delayed dermal hypersensitivity were tested both in patients and in control subjects. The patients showed higher Zn levels in serum (123%), hair (85%) and urine (215%) than controls, whereas ALP and LDH values were 38 and 21%, respectively, lower than those from the control group. Half of the patients showed hypoergy, and less than 50% of them were able to show a normal immune response. These results suggest that Zn-dependent functions may be impaired in anorexia nervosa as a consequence of Zn unavailability.
Triceps skin fold, arm muscular performance and fatigue were quantified, haematocrit measured and haemoglobin, serum total protein, albumin, transferrin, zinc and copper concentrations determined in 60 patients (36 women, 24 men) before and 3-45 days after surgery. On days 3 and 9 after surgery, there was a significant (P less than 0.05) decrease in serum zinc concentrations but by 45 days concentrations had return to pre-operative values. In contrast, serum copper concentrations were significantly (P less than 0.05) elevated until day 45. Haematocrit and haemoglobin and albumin concentrations were decreased significantly (P less than 0.05) 3 and 9 days after surgery, whereas serum total protein concentrations remained significantly (P less than 0.05) lower for 45 days compared with concentrations prior to surgery.
Effects of physical training on fasting erythrocyte and plasma zinc distributions were studied on seven previously sedentary male students. The training consisted of running over 5 km, 6 times/week for 10 weeks. Maximum aerobic capacity (VO2max) and 12 min walk-run performance increased significantly (p less than 0.01) after training. The erythrocyte concentrations of total zinc and of zinc derived from carbonic anhydrase I (CA-I) rose significantly (p less than 0.05) after training, whereas no such effects were noted in CA-II-derived zinc, Cu2Zn2 superoxide dismutase-derived zinc, and other zinc. On the other hand, no effect of training was found in total or alpha 2-macroglobulin-bound zinc in plasma, although albumin-bound zinc concentration declined significantly (p less than 0.05). Following the training period, however, the response to a VO2max test of the van Beaumont quotient (J Appl Physiol 1973;34:102-6) for total plasma zinc had decreased significantly (p less than 0.05), suggesting a relative reduction of the circulating exchangeable zinc. In addition, there were significant (p less than 0.05) decreases in plasma iron and ferritin concentrations after training, indicating latent iron deficiency anemia. These results may suggest that the changes in CA-I-derived zinc and/or albumin-bound zinc portend zinc deficiency during running training and that sports anemia precedes hypozincemia in athletes.
Serum zinc was measured four times (October, January, March and May) in six young male athletes during a nine-month sporting season in relation to eleven other parameters. A significant decrease in serum zinc was observed after five months of intensive training (all values remaining in the normal range). This cannot be explained by changes in dietary habits, plasma protein concentrations, hormonal changes nor by the existence of minor infectious or inflammatory pathologies. The dietary intakes seemed adequate. These results support the hypothesis that zinc status may be slightly altered in the high-level athlete.
During the last decade there has been considerable interest in the idea that dietary trace element supplementation can result in an improvement in athletic performance. The current paper discusses this idea as it relates to 3 elements: iron, zinc and magnesium. Emphasis has been placed on examining the implicit assumptions underlying the idea that mineral supplements help the athlete. These assumptions include the beliefs that the athlete has a higher than normal requirement for minerals; that the athlete consumes a diet inadequate in these minerals; and that a marginal deficiency of these elements has a direct effect on athletic performance. Evidence is presented that both iron deficiency and magnesium deficiency can result in a significant reduction in exercise performance; however, the biochemical lesions under-lying the reductions in exercise performance have not been identified. There is evidence that dietary magnesium intake may be suboptimal in some individuals, thus dietary supplementation of this element may be useful in some population groups. Excessive magnesium supplementation is not thought to be a serious health problem. Similar to magnesium, dietary iron supplements can improve athletic performance in individuals severely deficient in this element. However, few studies have documented a need for iron supplements in healthy athletes. If iron supplements are used, it is important that the level of supplementation is not excessive, as excess iron in the diet can result in an induced zinc deficiency. In marked contrast to iron and magnesium, there is little evidence for the idea that zinc deficiency influences exercise performance in humans. Despite this fact, zinc supplements have been widely advocated for the athlete, as it is known that intense exercise can result in changes in zinc metabolism. If zinc supplements are used, it is important that they are not excessive, as excess zinc in the diet can result in a secondary copper deficiency.