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By Medifit Biologicals.

DOPING TEST

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DOPING INTRODUCTION

In sports the athletes and players take certain prohibited drugs. The test conducted by the sports and regulatory authorities is called Dope Test. The test is conducted by testing the urine of the individual.

Use of banned performance-enhancing drugs in sports is commonly referred to as doping.

Doping test means ie. common man’s parlance, it is a test conducted to see whether the person has consumed some prohibited drugs which is intended to boost the performance by overcoming the normal fatigue or tired. It is mostly common in the sports and people who are undergoing the sports meet or after the meet. This test is conducted by the sports conducting authority by way of testing the urines of the suspects.

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PERFORMANCE SHORTCUTS 

In search of shortcut to improve their performance in the sports events, players use certain steroid drugs which acts as a stimulant. These steroid drugs acts for a quick time to release maximum possible energy stored in the muscle. Taking these drugs is against the natural life. It was came into flashlight during 1988 when Ben johnson doubted for his natural ability. After this incident all players are brought under doping test before taking participation in their events. It can be tested either from blood or urine.

DRUG TESTING

Drug testing has become an increasingly large part of both professional and amateur sports. An athlete can be called for drug testing at any time, in or out of competition. During competition, some sports only carry out drug testing on the winning team or top three competitors. Others will test by random selection from all competitors.

Every year over 100,000 drug tests are conducted worldwide at a cost of $30 million. The drug tests are designed to detect and deter abuse of performance-enhancing drugs by competitors. The testing procedures for drug abuse in sports are strict and at times deemed unfair by athletes. They are deemed unfair because athletes are responsible for knowing what is banned despite the fact that additions are made almost daily to the list of banned substances. The best possible solution is to avoid all drugs unless listed on the allowed substance list.

YEAR ROUND TESTING OF ATHLETES

There are some athletes who will try and beat the testing. When athletes know when a drug test will occur, they can prepare for it and thereby neutralize the effects of drug testing on the use of performance enhancing drugs and/or masking agents. Year-round short-notice and no-notice testing are the most effective means to curtail the use of training drugs because they make athletes always at risk to be tested.

DRUG TESTING PROCEDURE

The drug testing procedure begins with taking a urine sample. While this sounds simple, it initiates a formal and highly regulated procedure to ensure that the urine sample that arrives at the laboratory actually comes from the athlete in question, with no opportunity to tamper with the sample. Once selected for drug testing, the athlete is notified by an official and asked to sign a form acknowledging this notification. The athlete may or may not be accompanied by an official and must attend the testing station within the designated period. The testing station is supposed to be a private, comfortable place where plenty of drinks are available. Many times it is set up inside a specially designed mobile testing unit. Independent sampling officers, whom are trained and appointed by the respective governing body, carry out the collection of urine samples. Each officer carries a time-limited identity card and a letter of authority for the event to which they are allocated.

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Before giving a urine sample, the athlete is told to select two numbered bottles. After providing the sample (about 100 ml), the athlete must voluntarily complete a form.

The athlete declares any drug treatment taken in the previous seven days and must check and sign that the sample has been taken and placed in the bottles correctly.

The urine sample is then sent for analysis to a laboratory currently accredited by the IOC. In the event of a positive test result, the laboratory will notify the governing body of the sport, who will then notify the athlete. The rules of the governing body of the particular sport determine what happens next. The rules vary across governing bodies, sports and countries. An athlete is usually suspended while a positive result is investigated, but has the right to have a second analysis of the urine sample. This analysis may be observed directly by the athlete or by the athlete’s representative. There is then a hearing, at which time the athlete’s case is presented. An appeal can be made, and there have been successful appeals both in the United States and other countries.

 

BLOOD DOPING

Blood doping is the practice of boosting the number of red blood cells in the bloodstream in order to enhance athletic performance. Because such blood cells carry oxygen from the lungs to the muscles, a higher concentration in the blood can improve an athlete’s aerobic capacity (VO2 max) and endurance. Many methods of blood doping are illegal, particularly in professional sport.

 

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Methods

Drug Treatments

Many forms of blood doping stem from the misuse of pharmaceuticals. These drug treatments have been created for clinical use to increase the oxygen delivery when the human body is not able to do so naturally.

Erythropoietin (EPO)

Erythropoietin is a glycoprotein hormone produced by the interstitial fibroblasts that signal for erythropoiesis in bone marrow. The increased activity of a Hemocytoblast (RBC stem cell) allows the blood to have a greater carrying capacity for oxygen. EPO was first developed to counteract the effects of chemotherapy and radiation therapy for cancer patients. EPO also stimulates increased wound healing. The physiological side effect of EPO, particularly increased hematocrit, has become a potential drug to abuse by professional and amateur cyclists.

 

Hypoxia Inducible Factor (HIF) Stabilizer

Hypoxia-inducible factor stabilizer (HIF stabilizer) is a pharmaceutical used to treat chronic kidney disease. Like most transcription factors, the HIF transcription factor is responsible for the expression of a protein. The HIF stabilizer activates the activity of EPO due to anemia induced hypoxia, metabolic stress, and vasculogenesis—the creation of new blood vessels. HIF stabilizers as used by cyclists in combination with cobalt chloride/desferrioxamine stimulate and de-regulate the natural production of erythropoietin hormone. At physiologically low PaO2 around 40 mmHg, EPO is released from the kidneys to increase hemoglobin transportation. The combination of drugs consistently releases EPO due to increased transcription at the cellular level. The effect wears off when the HIF stabilizers, cobalt chloride/desferrioxamine is excreted and/or decayed by the body.

Blood Transfusion

Blood transfusions can be traditionally classified as autologous, where the blood donor and transfusion recipient are the same, or as allogeneic/homologous, where the blood is transfused into someone other than the donor. Blood transfusion begins by the withdrawal of 1 to 4 units of blood (1 unit = 450 ml of blood) several weeks before competition. The blood is centrifuged, the plasma components are immediately reinfused, and the corpuscular elements, principally red blood cells (RBCs), are stored refrigerated at 4◦C or frozen at −80◦C. As blood stored by refrigeration displays a steady decline in the number of RBCs, a substantial percentage, up to 40%, of the stored RBCs may not be viable. The freezing process, conversely, limits the aging of the cells, allowing the storage of the blood for up to 10 years with a 10% to 15% loss of RBCs. Stored RBCs are then reinfused, usually 1 to 7 days before a high-endurance event. As a significant amount of iron is removed by each autologous transfusion, an adequate time for recovery of not less than 3 days from the last donation, and appropriate iron supplements, are usually required for patients undergoing autologous donations. Nearly 50% of autologous donations are not used by the donor and are discarded, as current standards do not allow transfusion of these units to another patient for safety reasons.

 

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Blood Substitutes

Biochemical and biotechnological development has allowed novel approaches to this issue, in the form of engineered O2 carriers, widely known as “blood substitutes.” The blood substitutes currently available are chiefly polymerized haemoglobin solutions or haemoglobin-based oxygen carriers (HBOCs) and perfluorocarbons (PFCs).

Haemoglobin-based oxygen carriers (HBOCs)

HBOCs are intra/ inter-molecularly engineered human or animal hemoglobins, only optimized for oxygen delivery and longer intravascular circulation. The presence of 2,3-diphosphoglycerate within erythrocytes maintains the normal affinity of hemoglobin for oxygen. HBOCs do not contain erythrocytes and lose this interaction, thus, unmodified human HBOC solutions have a very high oxygen affinity which compromises their function. Chemical methods developed to overcome this problem have resulted in carriers that effectively release oxygen at the physiological pO2 of peripheral tissues. A common feature of all HBOCs is their resistance to dissociate when dissolved in media, which contrasts hemoglobin of natural dissociation under non-physiological conditions. HBOCs may hypothetically supply greater benefits to athletes than those provided by the equivalent hemoglobin in traditional RBC infusion. Recent developments have shown that HBOCs are not only simple RBC substitutes, but highly effective O2 donors in terms of tissue oxygenation. Additional effects include increases in blood serum iron, ferritin, and Epo up to 20% increased diffusion of oxygen and improved exercise capacity; increased CO2 production; and lower lactic acid generation in anaerobic activity.

Perfluorocarbons (PFCs)

PFCs, also known as fluorocarbons, are inert, water-insoluble, synthetic compounds, consisting primarily of carbon and fluorine atoms bonded together in strong C-F bonds. PFCs are substantially clear and colorless liquid emulsions that are heterogeneous in molecular weight, surface area, electronic charge, and viscosity; their high content of electron-dense fluorine atoms results in little intramolecular interaction and low surface tension, making such substances excellent solvents for gases, especially oxygen and carbon dioxide. Some of these molecules can dissolve 100 times more oxygen than plasma. PFCs are naturally hydrophobic and need to be emulsified to be injected intravenously. Since PFCs dissolve rather than bind oxygen, their capacity to serve as a blood substitute is determined principally by the pO2 gradients in the lung and at the target tissue. Therefore, their oxygen transport properties differ substantially from those of whole blood and, especially, from those of RBCs. At a conventional ambient pO2 of 135 mm Hg, the oxygen content of 900 ml/l perfluorocarbon is less than 50 ml/l, whereas an optimal oxygen content of 160 ml/l, which is still lower than that of whole blood in normal conditions, can be achieved only by a pO2 greater than 500 mm Hg. In practice, at a conventional alveolar pO2 of 135 mm Hg, PFCs will not be able to provide sufficient oxygenation to peripheral tissues.

Due to their small size, PFCs are able to permeate circulation where erythrocytes may not flow. In tiny capillaries, PFCs produce the greatest benefit, as they increase local oxygen delivery much more efficiently than would be expected from the increase in oxygen content in larger arteries.  In addition, as gases are in the dissolved state within PFCs, it pO2 promotes efficient oxygen delivery to peripheral tissues. Since the mid-1980s, improvements in both oxygen capacity and emulsion properties of PFCs have led to the development of second-generation PFC based oxygen carriers; two PFC products are currently being tested in phase III clinical trials.

 

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Cobalt Chloride Administration

Transition metal complexes are widely known to play important roles in erythropoiesis, as such, inorganic supplementation is proving to be an emerging technique in blood doping. Particularly of note is the cobalt complex, cobalamin (Vitamin B12) commonly used as a dietary supplement. Cobalamin is an important complex used in the manufacture of red blood cells and thus was of interest for potential use in blood doping. Experimental evidence, however, has shown that cobalamin has no effect on erythropoiesis in the absence of a red blood cell/oxygen deficiency. These results seem to confirm much of what is already known about the functioning of cobalamin. The signaling pathway that induces erythropoietin secretion and subsequently red blood cell manufacture using cobalamin is O2 dependent. Erythropoietin is only secreted in the kidneys when there is an O2 deficiency, as such, RBC manufacture is independent of the amount of cobalamin administered when there is no O2 deficiency. Accordingly, cobalamin is of little to no value in blood doping.

More potent for use in blood doping is Co2+ (administered as Cobalt(II) chloride, CoCl2). Cobalt chloride has been known to be useful in treating anemic patients. Recent experimental evidence has proved the efficacy of cobalt chloride in blood doping. Studies into the action of this species have shown that Co2+ induces hypoxia like responses, the most relevant response being erythropoiesis. Co2+ induces this response by binding to the N-terminus (loop helix loop domain) of the Hypoxia inducing transcription factors HIF-1α and HIF-2α, and thus stabilizes these protein complexes. Under normal O2 conditions, HIFs are destabilized as proline and asparagine residues are hydroxylated by HIF-α hydroxylases, these unstable HIFs are subsequently degraded following a ubiquitin-proteosome pathway, as such, they cannot then bind and activate transcription of genes encoding Erythropoietin (EPO). With Co2+ stabilization, degradation is prevented and genes encoding EPO can then be activated. The mechanism for this Co2+ N terminus stabilization is not yet fully understood. In addition to N-terminus binding, it has also been hypothesized that replacement of Fe2+ by Co2+ in the hydroxylase active site could be a contributing factor to the stabilizing action of Co2+. It is understood however, is that Co2+ binding permits Ubiquitin binding but prevents proteosomal degradation.

Blood doping probably started in the 1950s, but was not outlawed until 1986. While it was still legal, it was commonly used by middle and long-distance runners. The first known case of blood doping occurred at the 1980 Summer Olympics in Moscow as Kaarlo Maaninka was transfused with two pints of blood before winning medals in the 5 and 10 kilometer track races, though this was not against the rules at the time. The American cyclist Pat McDonough admitted to blood doping at the 1984 Summer Olympics in Los Angeles. Following the 1984 Summer games it was revealed that one-third of the U.S. cycling team had received blood transfusions before the games, where they won nine medals, their first medal success since the 1912 Summer Olympics.

“Blood doping” was banned by the IOC in 1985, though no test existed for it at the time.

 

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The Swedish cyclist Niklas Axelsson tested positive for EPO in 2000. The American cyclist Tyler Hamilton failed a fluorescent-activated cell sorting test for detecting homologous blood transfusions during the 2004 Olympics. He was allowed to keep his gold medal because the processing of his sample precluded conducting a second, confirmatory test. He appealed a second positive test for homologous transfusion from the 2004 Vuelta a España to the International Court of Arbitration for Sport but his appeal was denied. Hamilton’s lawyers proposed Hamilton may be a genetic chimera or have had a ‘vanishing twin’ to explain the presence of red blood cells from more than one person. While theoretically possible, these explanations were ruled to be of “negligible probability”.

The Operación Puerto case in 2006 involved allegations of doping and blood doping of hundreds of athletes in Spain.

Tour de France rider Alexander Vinokourov, of the Astana Team, tested positive for two different blood cell populations and thus for homologous transfusion, according to various news reports on July 24, 2007. Vinokourov was tested after his victory in the 13th stage time trial of the Tour on July 21, 2007. A doping test is not considered to be positive until a second sample is tested to confirm the first. Vinokourov’s B sample has now tested positive, and he faces a possible suspension of 2 years and a fine equal to one year’s salary. He also tested positive after stage 15.

Vinokourov’s teammate Andrej Kashechkin also tested positive for homologous blood doping on August 1, 2007, just a few days after the conclusion of the 2007 Tour de France (a race that had been dominated by doping scandals). His team withdrew after the revelation that Vinokourov had doped.

According to Russian investigators, 19-year-old New York Rangers prospect and Russian hockey player Alexei Cherepanov was engaged in blood doping for several months before he died on October 13, 2008, after collapsing on the bench during a game in Russia. He also had myocarditis.

The German speed skater and five-fold Olympic gold medalist Claudia Pechstein was banned for two years in 2009 for alleged blood doping, based on irregular levels of reticulocytes in her blood and the assumption that these levels were always highest during competitions. Her mean reticulocyte count over the ten years from 2000 to 2009 was 2.1% during top events like Olympic Games and during world championships. At world cup races the mean reticulocyte was 1.9% and during training phases 2.0%.

The Court of Arbitration for Sport confirmed the ban in November 2009 in stating: “…once the possibility of a blood disease has been safely excluded…”. In September 2010, the Swiss Federal Supreme Court rejected the athlete’s appeal, stating that Ms. Pechstein’s inherited blood anomaly had been known before.

On May 20, 2011 Tyler Hamilton turned in his 2004 Olympic Gold Medal to the U.S. Anti-Doping Agency after admitting to doping in a 60 Minutes interview.

On August 23, 2012 Lance Armstrong was stripped of his seven Tour de France titles and banned for life by cycling’s governing body following a report from the U.S. Anti-Doping Agency that accused him of leading a doping program during his cycling career. He later admitted to using banned substances including blood doping with transfusions and EPO in an interview with Oprah Winfrey on January 17, 2013.

 

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In June and July 2014, two mixed martial artists in the UFC, Chael Sonnen and Ali Bagautinov tested positive for EPO in out-of-competition tests.

 

Following are the list of substances banned in list of WADA in 2013.

1. Anabolic Androgenic Steroids (AAS)

a. Exogenous* AAS, including:

1-androstenediol (5α-androst-1-ene-3β,17β-diol ); 1-androstenedione (5α-

androst-1-ene-3,17-dione); bolandiol (estr-4-ene-3β,17β-diol ); bolasterone;

boldenone; boldione (androsta-1,4-diene-3,17-dione); calusterone;

clostebol; danazol ([1,2]oxazolo[4′,5′:2,3]pregna-4-en-20-yn-17α-ol); dehydrochlormethyltestosterone (4-chloro-17β-hydroxy-17α-methylandrosta-

1,4-dien-3-one); desoxymethyltestosterone (17α-methyl-5α-androst-2-en-

17β-ol); drostanolone; ethylestrenol (19-norpregna-4-en-17α-ol);

fluoxymesterone; formebolone; furazabol (17α-

methyl[1,2,5]oxadiazolo[3′,4′:2,3]-5α-androstan-17β-ol); gestrinone; 4-

hydroxytestosterone (4,17β-dihydroxyandrost-4-en-3-one); mestanolone;

mesterolone; metenolone; methandienone (17β-hydroxy-17α-

methylandrosta-1,4-dien-3-one); methandriol; methasterone (17β-hydroxy-

2α,17α-dimethyl-5α-androstan-3-one); methyldienolone (17β-hydroxy-17α-

methylestra-4,9-dien-3-one); methyl-1-testosterone (17β-hydroxy-17α-methyl-

5α-androst-1-en-3-one); methylnortestosterone (17β-hydroxy-17α-methylestr-

4-en-3-one); methyltestosterone; metribolone (methyltrienolone, 17β-

hydroxy-17α-methylestra-4,9,11-trien-3-one); mibolerone; nandrolone; 19-

norandrostenedione (estr-4-ene-3,17-dione); norboletone; norclostebol;

norethandrolone; oxabolone; oxandrolone; oxymesterone; oxymetholone;

prostanozol (17β-[(tetrahydropyran-2-yl)oxy]-1’H-pyrazolo[3,4:2,3]-5α-

androstane); quinbolone; stanozolol; stenbolone; 1-testosterone (17βdehydrochlormethyltestosterone (4-chloro-17β-hydroxy-17α-methylandrosta-

1,4-dien-3-one); desoxymethyltestosterone (17α-methyl-5α-androst-2-en-

17β-ol); drostanolone; ethylestrenol (19-norpregna-4-en-17α-ol);

fluoxymesterone; formebolone; furazabol (17α-

methyl[1,2,5]oxadiazolo[3′,4′:2,3]-5α-androstan-17β-ol); gestrinone; 4-

hydroxytestosterone (4,17β-dihydroxyandrost-4-en-3-one); mestanolone;

mesterolone; metenolone; methandienone (17β-hydroxy-17α-

methylandrosta-1,4-dien-3-one); methandriol; methasterone (17β-hydroxy-

2α,17α-dimethyl-5α-androstan-3-one); methyldienolone (17β-hydroxy-17α-

methylestra-4,9-dien-3-one); methyl-1-testosterone (17β-hydroxy-17α-methyl-

5α-androst-1-en-3-one); methylnortestosterone (17β-hydroxy-17α-methylestr-

4-en-3-one); methyltestosterone; metribolone (methyltrienolone, 17β-

hydroxy-17α-methylestra-4,9,11-trien-3-one); mibolerone; nandrolone; 19-

norandrostenedione (estr-4-ene-3,17-dione); norboletone; norclostebol;

norethandrolone; oxabolone; oxandrolone; oxymesterone; oxymetholone;

prostanozol (17β-[(tetrahydropyran-2-yl)oxy]-1’H-pyrazolo[3,4:2,3]-5α-

androstane); quinbolone; stanozolol; stenbolone; 1-testosterone (17β5α-androstane-3α,17α-diol; 5α-androstane-3α,17β-diol; 5α-androstane-

3β,17α-diol; 5α-androstane-3β,17β-diol; androst-4-ene-3α,17α-diol;

androst-4-ene-3α,17β-diol; androst-4-ene-3β,17α-diol; androst-5-ene-

3α,17α-diol; androst-5-ene-3α,17β-diol; androst-5-ene-3β,17α-diol;

4-androstenediol (androst-4-ene-3β,17β-diol); 5-androstenedione (androst-5-

ene-3,17-dione); epi-dihydrotestosterone; epitestosterone;

etiocholanolone; 3α-hydroxy-5α-androstan-17-one; 3β-hydroxy-5α-

androstan-17-one; 7α-hydroxy-DHEA ; 7β-hydroxy-DHEA ; 7-keto-DHEA;

19-norandrosterone; 19-noretiocholanolone.

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2. Other Anabolic Agents, including but not limited to:

Clenbuterol, selective androgen receptor modulators (SARMs), tibolone,

zeranol, zilpaterol.

 

S2. PEPTIDE HORMONES, GROWTH FACTORS AND RELATED

SUBSTANCES

The following substances and their releasing factors are prohibited:

1. Erythropoiesis-Stimulating Agents [e.g. erythropoietin (EPO),

darbepoetin (dEPO), hypoxia-inducible factor (HIF) stabilizers,

methoxy polyethylene glycol-epoetin beta (CERA), peginesatide

(Hematide)];

2. Chorionic Gonadotrophin (CG) and Luteinizing Hormone (LH) in

males;

3. Corticotrophins;

4. Growth Hormone (GH), Insulin-like Growth Factor-1 (IGF-1),

Fibroblast Growth Factors (FGFs), Hepatocyte Growth Factor (HGF),

Mechano Growth Factors (MGFs), Platelet-Derived Growth Factor

(PDGF), Vascular-Endothelial Growth Factor (VEGF) as well as any

other growth factor affecting muscle, tendon or ligament protein

synthesis/degradation, vascularisation, energy utilization, regenerative

capacity or fibre type switching;

and other substances with similar chemical structure or similar biological effect(s).

By Medifit Biologicals.

www.medifitbiologicals.com