Archive for the ‘Sports Medicine’ Category


Abraham Lincoln once famously said that prohibition “makes a crime out of things that are not crimes.” WADA has done exactly that’

– Sally Jenkins, Columnist, Washington Post

‘Do we want to see the highest possible achievements by men and women who do not use performance-enhancing drugs? If so, what counts as performance-enhancing? If sports fans really want to see achievement that they can relate to, perhaps athletes should be restricted to diets of pizza and beer, and be required to have 40-hour-a-week desk jobs’ 

–  David Epstein, author, Sports Illustrated

At the London Olympics 2012, more samples were collected and analysed for ‘doping’ than any other previous games. With more than 150 scientists and 1000 lab technicians working around the clock, the (World Anti-Doping Agency) WADA-approved lab at Essex did everything to ‘uphold the fairness and integrity of the games’. Well, really?!


Athletes, coaches, team doctors, physical therapists and sports federations. all know that everyone’s ‘doing it’. Research too supports the general notion that use of performance-enhancing substances and methods is quite rampant in competitive sports.

Back in 1992, a lady named Vicky Rabinowicz went around conducting interviews of Olympic athletes; most candidly agreed that almost all medal winning athletes were ‘on drugs’ 1.

  • In 2004, Bents et al. reported in their study that almost half of college hockey players were using/ or have previously used stimulants like ephedrine, pseudoephedrine and amphetamines 2
  • Sottas and his fellow researchers reported 48% prevalence rate for ‘blood doping’ in endurance athletes 3
  • Scarpino et al. reported that of the Italian athletes they studies, 10% reported having used anabolics or amphetamines at the national or international stage; other drugs commonly used were bronchodilators and doping methods like blood doping 4
  • Thevis and co-workers found that 10% of young athletes aspiring to reach elite levels used tetrahydrocannabinol (cannabis) and other stimulants  5
  • Mottram, David and George, somewhat surprisingly, report a low level of positive samples for anabolics in athletes. However, the authors argue that athletes – more often than not – tend to use anabolics in training. Furthermore, to conducts surprise ‘out of competition’ tests is not only costly but isn’t always easy either, especially in some countries. Consequently, therefore, a study of the prevalence of anabolic usage will rarely, if ever, return a true picture 6

From these observations, it should become clear that despite the existent ban – imposed by WADA – on the use performance-enhancing drugs (PEDs), the tests conducted, and the much-publicized, ‘alleged’ detrimental health effects of PEDs, their widespread abuse by athletes still remains very much rampant!


Also, here’s an interesting aspect of drug testing. According to the International Amateur Athletic Federation’s own admittance, in any major competition only 10-15% of athletes are tested for doping. In such a scenario, the actual samples that turn out positive could be higher if all athletes were to be tested.


According to WADA’s anti-doping code, the ‘spirit of the game’ is defined as under:

‘Celebration of human spirit, body and mind’ characterized by the following values:

  • Ethics, fair play and honesty
  • Health
  • Excellence in performance
  • Character and education
  • Fun and joy
  • Teamwork
  • Dedication and commitment
  • Respect for rules and laws
  • Respect for self and other participants
  • Courage
  • Community and solidarity

The code further states that ‘doping is contrary to the spirit of the game’.


There are vast differences of opinion between everyone concerned with elite sports (let alone, sports medicine researchers) about the validity of the anti-doping measures in place. There are those who advocate ‘ban them all and hand out lifetime bans, even for first time offenders’. Others, however, (get braced for this) recommend ‘legalizing them all so that some sort of sanity could return to the use of PEDs’ and it is a more ‘level playing field’.

Legalising will ensure that research is conducted to study the drugs in detail with institution of proper dosage regimen. This will ensure that side effects are kept to the minimum and athletes can be effectively stopped from ‘abusing’ them. Legalising PEDs will, more importantly, ‘even out the playing field’.


An increasing number of people are beginning to think that banning PEDs does not solve the problem; it in fact, compounds the problem. As opposed to WADA’s aim of making the games ‘fair’, anti-doping measures make it unfair in the sense that the athletes that have used PEDs but aren’t caught (due to vested interests or otherwise!) get a massive unfair advantage.

Also, if you ever thought banning PEDs will make the contest even, think again. Genetics and some other factors like access to better training and support facilities may have, in my opinion, a bigger impact on the results of the contest.


  • Natural levels of erythropoietin (EPO, increases red cell count, improves delivery of oxygen to muscles, helps endurance sports) and growth hormone (builds muscle, strength and power) vary widely in different individuals. There are those unlucky one in whom the levels are very low. On the other hand, natives of high altitude areas have much higher physiological levels of EPO. Isn’t that unfair?!
  • Athletes of Jamaican descent have more % of fast twitch muscle making them awesome sprinters. Isn’t that unfair on the ones that don’t have that genetic gift?!
  • Athletes born at higher altitudes are blessed with huge chest cavities, more EPO production, more packed cell volume (PCV) and thus better delivery of oxygen to exercising muscles. All these physiological adaptations are in place to deal with the rarefied atmosphere at higher altitudes. This gives athletes born at higher altitudes an edge in endurance sports over other athletes. Isn’t’ that unfair?
  • Athletes from cash rich federations and with more endorsements can afford to have access to better training facilities, coaches, physios and other support staff. Isn’t that unfair?
  • Athletes with access to more money can travel to higher altitudes to train and acquire an edge over the ones that can’t. Isn’t that unfair?

Add to the list personal attributes of athletes like 7 feet tall basketball players and the massive feet of Ian Thorpe and you will realise that with genetics favouring some, it will never a level playing field out there. So, the argument that use of PEDs makes the games unfair doesn’t hold much water. The games are already stacked in favour of the genetically gifted!

And, what happens when gene doping becomes a full-fledged reality? There will no stopping the unfair advantage that the genetically engineered ‘super-athletes’ will receive! There are some indications that these super-athletes are already roaming freely amongst us! Click here to read more.

It all very well to say that WADA is making an effort to make sports a fair contest for all participants. But to say that we have been successful in preventing use of PEDs by conducting tests and banning ‘cheats’ is far from the truth. The use of PEDs continues to be widespread amongst athletes. If you’ve ever handled an elite athlete, you will know that most times clocked on the sprints, distances achieved on the javelin throws, or the poundage lifted on snatches can never be a product of just genetics, brilliant training regimens and diet alone.


There is a school of thought which suggests that legalizing PEDs will ensure a level playing field. With some vested interest not testing athletes from cash rich federations, you can bet your bottom dollar that not everything that’s going on is in ‘the spirit of the game’.

An acquaintance of mine says the other day, ‘there shouldn’t be any drug tests and everyone should be allowed to do whatever it takes to enhance their performance… Maybe, the Olympics would then be really worth watching….I’d pay a million quid to go watch the 100 metres dash then’.

And I say, ‘well, you’ve already been watching drug-loaded 100 metres sprints for quite some time now…, just that they never told you’!

Guess my friend’s remark sums up the way everyone is sceptical of the alleged success of WADA’s ‘anti-doping policy’!



(1) Raboniwicz V. Athletes and Drugs: A separate pace? Pyschol Today 1992; 25:52-53. Link

(2) Bents RT, Tokish JM, Goldberg L. Ephedrine, pseudoephedrine, and amphetamine prevalence in college hockey players: most report performance-enhancing use. Phys Sportsmed 2004; 32(9):30-34.

(3) Sottas PE, Robinson N, Fischetto G, Dolle G, Alonso JM, Saugy M. Prevalence of blood doping in samples collected from elite track and field athletes. Clin Chem 2011; 57(5):762-769.

(4) Scarpino V, Arrigo A, Benzi G, Garattini S, La VC, Bernardi LR et al. Evaluation of prevalence of “doping” among Italian athletes. Lancet 1990; 336(8722):1048-1050.

(5) Thevis M, Sauer M, Geyer H, Sigmund G, Mareck U, Schanzer W. Determination of the prevalence of anabolic steroids, stimulants, and selected drugs subject to doping controls among elite sport students using analytical chemistry. J Sports Sci 2008; 26(10):1059-1065.

(6) Mottram DR, George AJ. Anabolic steroids. Bailliere’s Best Practice & Research Clinical Endocrinology & Metabolism 2000; 14(1):55-69.

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cafe_neroGet off the Tube – straight into the nearest Cafe Nero  – pick up your favorite coffee and then off to work – isn’t that what most of us do?! Don’t we all love having our coffees, especially first thing in the morning? Yes, we do! – The reason being?! Well, for sure one of the reasons has got to be that coffee really ‘gets you going’ first thing in the morning. But, have you ever wondered how your innocuous looking cup of coffee manages to do that? Read on to find out more.


Let’s face it, we have to drink coffee every single morning coz somewhere along the line, we’ve got addicted to caffeine present in our coffee. It is this caffeine that is responsible for the ‘gets me going’ phenomenon!

It shouldn’t come as a surprise then that caffeine is the most ingested psychoactive drug (stimulant) in the world. It is a of major contents of almost all ‘stimulant’ beverages like tea, coffee, cola and energy drinks (not to mention thermogenic fat loss supplements).

According to Starbucks information on beverages, a tall latte’ contains 150mg of caffeine (filter coffee ‘venti’ – meaning twenty in Italian – is low in calories but contain a whopping 400mg per serving). Taking in that amount of the drug can have profound effects on your physiology.

What exactly are these effects and how does caffeine in your tall, skinny latte’ help you to get ‘switched on’, you might want to ask? Well, read on to find out more.


But before we get into the intricacies of what makes caffeine tick, let us have a closer look at what caffeine really is. Chemically, caffeine is 1,3,7-trimethylxanthine.

Derived from the purine xanthine, methylxanthines have numerous medicinal applications, especially in lung disease. Apart from caffeine, other methylxanthines of note are theophylline, aminophylline (both of which are used as bronchodilators – in asthma), paraxanthine and theobromine. As you may have guessed, methylxanthines are  cardiac and CNS stimulants and bronchodilators (with individual variations, of course).

On ingestion, caffeine is expeditiously absorbed through the lining of the gastrointestinal tract. Within 15 minutes of consumption of coffee, trace levels of caffeine appear in blood; peak concentrations are reached within an hour 1.

Caffeine is highly lipid soluble (dissolves rapidly and completely in fat). Thus, it can cross cell membranes (of muscle and nerve cells), especially, the blood-brain barrier (a partition which allows only certain chemicals to enter the brain matter).

Caffeine exerts its action (as given below) on various systems through a number of proposed mechanisms.

After exerting its action, caffeine is broken down by the liver and kidneys – metabolites (break down products) that are formed are paraxanthine, theobromin and theophylline1. Incidentally, these metabolites have actions similar to caffeine as well – theophylline is considered even more potent!


As mentioned previously, caffeine is the most often used stimulant in the world with prominent actions on the central nervous system as well as metabolism. As opposed to caffeine present in drinks, anhydrous form of caffeine (in the form of capsule/tablet/powder) is more potent.

Pharmacologically, caffeine is a competitive adenosine-receptor agonist, i.e. it serves as a competition for adenosine at its receptor. This receptor is responsible for suppressing neurotransmitters like adrenaline, nor-adrenaline, acetylcholine, dopamine and serotonin. Thus, ingestion of caffeine increases the production of these neurotransmitters.

However, since these neurotransmitters have complex and sometimes conflicting actions, effects of caffeine in endurance, strength and explosive sports (enhancement of performance, recovery and hydration) can be conflicting as well.

However, the main actions of caffeine can be described as under:


Caffeine improves wakefulness and vigilance. It may be also responsible for improved skill levels, especially those acquired through repeated training 2.

Foskett et. al. demonstrated in their study, improved cognitive parameters in athletes due to caffeine ingestion with enhanced sprint abilities as well as ball passing, ball control and accuracy associated with acute ingestion of caffeine3.

Because caffeine in low to moderate doses (3-6 mg/kg of body weight) has been shown to cause improved concentration during sleep-deprived spells, it may find application in services like the Special Forces 2.


Consumption of caffeine causes stimulation of metabolism and a significant increase in the production of energy 4 – thermogenic action of caffeine has been shown to last for almost 3 hours after ingestion 4. Caffeine causes mobilization of free fatty acids and fat oxidation to produce energy during exercise 5-7. Additionally, it causes extra-muscular fat oxidation as well. Thus, caffeine seems to be definitely associated with causing fat loss 7.

These metabolic-stimulatory and fat-burning effects make caffeine a crucial ingredient of most fat-loss supplements (thermogenics).


It is believed that caffeine enhances exercise performance. This is owing to its ‘glycogen-sparing effect’ – decreased utilization of muscle glycogen for energy during exercise – fats are used instead. Thus, owing to muscles glycogen lasting longer, the setting in of fatigue is prolonged.

Also, caffeine supports formation of new glycogen (glycogenesis) and thus aids in recovery after an intense exercise session.

Enhanced secretion of endorphins induced by caffeine is also a presumed mechanism in enhancing exercise performance 8 – the resultant decrease in pain perception leading to ‘feel good factor’ of beta-endorphins is well-documented 9.

In addition to the above findings, research also suggests that caffeine can improve neuromuscular transmission and muscle contraction 10;11 – both isometric and muscle endurance components are improved 10.

 To conclude, research overwhelmingly supports the view that caffeine enhances performance in endurance events 5;12, sports involving muscle power-strength components 13;14 as well as high intensity team sports 14;15.


So, the next time you are sipping that favourite coffee of yours, you know exactly what it is doing to you!

To sum up, caffeine has the following effects:

  • is more potent when ingested in the anhydrous state (as a tab/capsule/powder supplement rather than as coffee)
  • aids in sports performance
  • improves skills acquisition in sports – like ball control and passing
  • supports new glycogen formation (glycogenesis) and thus helps quicker recovery from an exercise session
  • prolongs exercise induced fatigue – by their ‘glycogen-sparing’ effect so you can keep going for a longer
  • improves neuromuscular transmission and muscle contraction
  • has thermogenic effects – stimulates metabolism causing burning of calories
  • induces fat loss – mobilizes fatty acids from fat stores and uses these as substrate (instead of glycogen) for producing energy
  • improves concentration – especially during sleep-deprived states
  • secretes beta-endorphins – makes you feel good


  1.  Harland BF. Caffeine and nutrition. Nutrition 2000; 16(7-8):522-526.
  2. Lieberman HR, Tharion WJ, Shukitt-Hale B, Speckman KL, Tulley R. Effects of caffeine, sleep loss, and stress on cognitive performance and mood during U.S. Navy SEAL training. Sea-Air-Land. Psychopharmacology (Berl) 2002; 164(3):250-261.
  3. Foskett A, Ali A, Gant N. Caffeine enhances cognitive function and skill performance during simulated soccer activity. Int J Sport Nutr Exerc Metab 2009; 19(4):410-423.
  4. Astrup A, Toubro S, Cannon S, Hein P, Breum L, Madsen J. Caffeine: a double-blind, placebo-controlled study of its thermogenic, metabolic, and cardiovascular effects in healthy volunteers. Am J Clin Nutr 1990; 51(5):759-767.
  5. Ivy JL, Costill DL, Fink WJ, Lower RW. Influence of caffeine and carbohydrate feedings on endurance performance. Med Sci Sports 1979; 11(1):6-11.
  6. Erickson MA, Schwarzkopf RJ, McKenzie RD. Effects of caffeine, fructose, and glucose ingestion on muscle glycogen utilization during exercise. Med Sci Sports Exerc 1987; 19(6):579-583.
  7. Spriet LL, MacLean DA, Dyck DJ, Hultman E, Cederblad G, Graham TE. Caffeine ingestion and muscle metabolism during prolonged exercise in humans. Am J Physiol 1992; 262(6 Pt 1):E891-E898.
  8. Laurent D, Schneider KE, Prusaczyk WK, Franklin C, Vogel SM, Krssak M et al. Effects of caffeine on muscle glycogen utilization and the neuroendocrine axis during exercise. J Clin Endocrinol Metab 2000; 85(6):2170-2175.
  9. Grossman A, Sutton JR. Endorphins: what are they? How are they measured? What is their role in exercise? Med Sci Sports Exerc 1985; 17(1):74-81.
  10. Kalmar JM, Cafarelli E. Effects of caffeine on neuromuscular function. J Appl Physiol 1999; 87(2):801-808.
  11. Lopes JM, Aubier M, Jardim J, Aranda JV, Macklem PT. Effect of caffeine on skeletal muscle function before and after fatigue. J Appl Physiol 1983; 54(5):1303-1305.
  12. Hogervorst E, Bandelow S, Schmitt J, Jentjens R, Oliveira M, Allgrove J et al. Caffeine improves physical and cognitive performance during exhaustive exercise. Med Sci Sports Exerc 2008; 40(10):1841-1851.
  13. Woolf K, Bidwell WK, Carlson AG. The effect of caffeine as an ergogenic aid in anaerobic exercise. Int J Sport Nutr Exerc Metab 2008; 18(4):412-429.
  14. Beck TW, Housh TJ, Schmidt RJ, Johnson GO, Housh DJ, Coburn JW et al. The acute effects of a caffeine-containing supplement on strength, muscular endurance, and anaerobic capabilities. J Strength Cond Res 2006; 20(3):506-510.
  15. Schneiker KT, Bishop D, Dawson B, Hackett LP. Effects of caffeine on prolonged intermittent-sprint ability in team-sport athletes. Med Sci Sports Exerc 2006; 38(3):578-585.

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00000SusThe worldwide prevalence of obesity has reached epic proportions. So much so, that calling obesity a pandemic wouldn’t amount to exaggeration! In addition to putting individual lives on the line, obesity has the ability to severely increase health care costs, negatively impacting on most economies of the world 1;2.

So, what is it that causes obesity – you might want to ask!

What causes obesity?

Well. traditionally, we have been told that ‘excess intake of calories coupled with decreased expenditure’ is the immediate cause of obesity. Excess calories are treated as reserve food material (read: fats) and deposited as triglycerides (TGs) inside adipose tissue (fat stores). However, having said that,it does not seem to be as simple as that.

Recently, it is increasingly being suggested (and, I am one of those who believes in this) that obesity may be a metabolic disorder where your nutrient metabolism goes for a toss. Also, rather than how many calories you consume, what kind of food you eat (and where the calories are coming from) will define if you stay lean or pack on weight; ingestion of nutrient-dense food is likely to make you leaner and healthier than foods that are only rich in calorie and poor in nutrients.

Also, a number of (as yet poorly understood) factors play a causative role: hormones, metabolic enzymes, metabolic rate, nutrient partitioning and calorie partitioning abilities of the individual. It must be emphasized here that the kind of food you eat will have a massive influence all of the aforementioned factors.

Anthropometric tell-tale signs of obesity are:

  • Increased waist circumference
  • Increased waist-hip ratio
  • Increased body mass index (BMI)

Adverse-effects of being Obese?

In addition to the much publicized ill-effects of obesity (given below), not many people are aware that obesity causes testosterone deficiency (TD) as well. Testosterone has a prominent effect on metabolism; deficiency can add to the problems. In addition, low levels of T can have a detrimental effect on a person’s psyche, making it hard to stick to a prescribed regimen of healthy food and exercise to counter obesity. Thus a ‘vicious cycle’ connection exists between obesity and low testosterone levels.

Well-known adverse-effects of obesity are:

  • Metabolic syndrome
  • Cardiovascular disease (CVD)
  • Diabetes Mellitus (Type 2 DM)
  • Hypertension (rise in blood pressure)

Testosterone deficiency and Obesity in Men

Testosterone (as the major male sexual hormone) is responsible for the male sexual and reproductive functions. However, not many people are aware that it plays a significant role in calorie utilization and metabolism as well. The exact mechanisms by which testosterone levels are affected in / contribute to obesity remain a mystery 3.

However, here are some interesting facts connecting testosterone to obesity are: testosterone:

  • causes nitrogen retention (read: increasing muscle mass, as part of the anabolic process) 3;4, low levels in obesity therefore cause loss of lean muscle
  • affects body composition in a positive way by reducing fat mass and increasing lean muscle mass 5, low levels therefore, reverse these effects
  • stimulates hormone sensitive lipase (enzyme responsible for fat breakdown), inhibits triglyceride uptake and mobilises fat from fat stores 6, low levels in obesity therefore, lead to increased fat deposition
  • an inverse relationship exists between parameters of obesity (WC, WHR and BMI) and plasma testosterone levels in an individual 3
  • an inverse relationship also exists between the ill-effects of obesity like metabolic syndrome, hypertension, type 2 diabetes and plasma levels of testosterone 7
  • number of studies report the irrefutable proof that low testosterone levels are connected with diabetes and cardiovascular disease 8;9
  • low levels of testosterone definitely connected with all-cause mortality 10

Thus, it can safely be said that testosterone is responsible for maintaining and increasing muscle while burning fat; low levels are responsible for fat deposition resulting in obesity, diabetes, cardiovascular disease, metabolic syndrome and increased mortality 3-5;7-10.

How can obesity be treated?

A number of strategies have been proposed by researchers, physicians and fitness professional to fight obesity. Some of these are:

  1. Calorie Deficit: This involves ‘dieting’, using liquid diets, etc. However, this causes loss of lean mass in addition to fat loss
  2. Calorie Deficit combined with Exercise: This maintains lean mass whilst causing weight loss, however a number of people have found this pretty hard to stick to
  3. Surgery (gastric binding or bariatric): effective but reserved only for the morbidly obese

A novel, effective method proposed for treating obesity is combining exercise and healthy diet with testosterone replacement therapy (TRT) – especially if accompanying signs and symptoms suggestive of hypogonadism are present. Additionally, as opposed to other modes of treatment, testosterone has the potential to elevate mood and energy and reduce fatigue 11.

Future research

Although TRT sounds like an exciting treatment option for tackling obesity, the plasma levels of testosterone at which therapy should be initiated remain undefined. Currently, it is recommended only in individuals diagnosed with testosterone deficiency (hypogonadism / erectile dysfunction).

A sad fact is that most doctors treating obese patients with diabetes or cardiovascular disease are not aware of the connection of testosterone with obesity and the potential benefits of testosterone therapy. Furthermore, the misconception that testosterone increases cardiovascular risk 12 and chances of pancreatic cancer prevents clinicians from prescribing testosterone 13.

There is a definite and realistic need to further explore this option for treating obesity in men. Also, an effort should be initiated to educate both doctors as well as members of the general population (who are struggling with obesity and its ill-effects) regarding the benefits of testosterone replacement therapy.


(1) Kypreos KE. Mechanisms of obesity and related pathologies. FEBS J 2009; 276(20):5719.

(2) Freedman DH. How to fix the obesity crisis. Sci Am 2011; 304(2):40-47.

(3) Traish AM, Feeley RJ, Guay A. Mechanisms of obesity and related pathologies: androgen deficiency and endothelial dysfunction may be the link between obesity and erectile dysfunction. FEBS J 2009; 276(20):5755-5767.

(4) Singh R, Artaza JN, Taylor WE, Braga M, Yuan X, Gonzalez-Cadavid NF et al. Testosterone inhibits adipogenic differentiation in 3T3-L1 cells: nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors. Endocrinology 2006; 147(1):141-154.

(5) Emmelot-Vonk MH, Verhaar HJ, Nakhai Pour HR, Aleman A, Lock TM, Bosch JL et al. Effect of testosterone supplementation on functional mobility, cognition, and other parameters in older men: a randomized controlled trial. JAMA 2008; 299(1):39-52.

(6) Traish AM, Abdou R, Kypreos KE. Androgen deficiency and atherosclerosis: The lipid link. Vascul Pharmacol 2009; 51(5-6):303-313.

(7) Dhindsa S, Miller MG, McWhirter CL, Mager DE, Ghanim H, Chaudhuri A et al. Testosterone concentrations in diabetic and nondiabetic obese men. Diabetes Care 2010; 33(6):1186-1192.

(8) Aversa A. Drugs targeted to improve endothelial function: clinical correlates between sexual and internal medicine. Curr Pharm Des 2008; 14(35):3698-3699.

(9) Cattabiani C, Basaria S, Ceda GP, Luci M, Vignali A, Lauretani F et al. Relationship between testosterone deficiency and cardiovascular risk and mortality in adult men. J Endocrinol Invest 2012; 35(1):104-120.

(10) Araujo AB, Dixon JM, Suarez EA, Murad MH, Guey LT, Wittert GA. Clinical review: Endogenous testosterone and mortality in men: a systematic review and meta-analysis. J Clin Endocrinol Metab 2011; 96(10):3007-3019.

(11) Saad F, Aversa A, Isidori AM, Gooren LJ. Testosterone as potential effective therapy in treatment of obesity in men with testosterone deficiency: a review. Curr Diabetes Rev 2012; 8(2):131-143.

(12) Traish AM, Kypreos KE. Testosterone and cardiovascular disease: an old idea with modern clinical implications. Atherosclerosis 2011; 214(2):244-248.

(13) Morgentaler A. Testosterone replacement therapy and prostate cancer. Urol Clin North Am 2007; 34(4):555-63, vii.

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Podcast for this blog post:

“Cocaine is a hell of a drug”- Rick James on the Chapelle Show

Cocaine, also known as coke, crack, rock and by numerous other names, is a drug used for ‘recreational purposes’. Allegedly, it causes an ‘euphoriant high’. No wonder then, that its regular use is fraught with the risks of developing a dependence. This propensity to cause cravings and the severe adverse effects associated with its regular use has resulted in a ban imposed on its use – either for medical or recreational purposes.

Recently, however, it is being increasingly suggested that cocaine has a profound effect on human metabolism and the way our bodies store fats. Thus, it is being touted as a potential drug in the fight against obesity.

Also, in sporting circles, there is a school of thought that cocaine – on account of  its stimulant effects – may help enhance performance. Athletes have tended to use cocaine both during competition and in training (to improve intensity). However, owing to severe adverse effects – even sudden death – associated with its use (in a sport setting) and the fact that cocaine use is banned by both the IOC and WADA Anti-doping code, athletes need to be wary of its use under any pretext whatsoever!

Here’s a bit more about cocaine and why you should avoid it – in competition and outside of it!

What is cocaine?

That question is probably as dumb as it can get! Most definitely, almost everyone knows a bit about cocaine. However, here’s some more info – especially relevant if you are an athlete.

Cocaine is the most powerful natural stimulant of the human central nervous system (Avois et al., 2006; Kloner & Rezkalla, 2003; Welder & Melchert, 1993) (in case, you are wondering – amphetamines aren’t natural; they are man-made). And, not to mention, cocaine also happens to be the most addictive of all drugs known to mankind (Avois et al., 2006).

Historically, humans have used cocaine as a psychoactive drug for thousands of years – dating as far back as the times of the Incas (aptly enough, one of the many street names for cocaine is Inca Message! – bet you didn’t know that…)

Pharmacologically speaking, cocaine is a triple-re-uptake-inhibitor; it inhibits the re-uptake of three chemicals (with potent neuroendocrinal actions): adrenaline, serotonin and dopamine. So, what does that mean in plain English?

Well, it means that cocaine inhibits the normal, rapid re-uptake of these neurologically active chemicals back from where they were secreted (vesicle present in the neurons or nerve endings of the central nervous system) – effectively prolonging the time duration of action of these potent neuroactive chemicals significantly. This leads to prolonged and potent physiological actions on the target cells, either in the human brain or peripheral organs like the heart – see below.

A point to be noted – the pharmacological actions of cocaine can be quite complex and may vary depending on the amount of dosage used.

What does cocaine do to your brain and body?

Normally, cocaine is administered using one of the following ways – snorting, smoking or injecting. Of these, snorting is the most popular. Owing to rapid absorption through the linings of the nasal cavities and almost immediate entry into the blood stream, this route of administration produces peak effects within 5 minutes.

Cocaine causes an ‘initial rush’ or a ‘feeling of well-being’ which is characterized by:

    • euphoria,
    • alertness,
    • clarity of thought process,
    • a decreased feeling of fatigue,
    • talkativeness, and
    • increased social interaction

This initial rush is, however, followed by depression! This is what makes cocaine a top candidate for repeated use and subsequent development of dependence (cocaine is more addictive than amphetamines).

Adverse effects that cocaine can cause are:

    • depression,
    • anxiety,
    • paranoid events,
    • arrhythmia,
    • respiratory disturbances,
    • epileptic seizures, and
    • strokes

Why are athletes tempted to use cocaine?

Contrary to popular belief, cocaine does precious little to help enhance sports, study, sexual or work-place performance! However, athlete still continue to use cocaine; believing that it may help them run that much quicker or lift that much more weight.

Cocaine may improve cognitive processes and therefore, the level of motivation (during competition) and skill-learning (during training sessions) may be affected favorably – some believe that this may be a prominent reason for athletes to get attracted to cocaine, especially since very little evidence suggests that cocaine enhances other aspects of metabolism sufficiently to affect sport performance.

Anecdotal evidence suggests that cocaine does precious little to enhance performance in ‘endurance sports’. However, an animal study conducted by Braiden et al., suggests that the opposite may be true and cocaine by accelerating glycogen degradation and accumulation of lactate during exercise, may, in fact, help endurance events (Braiden, Fellingham, & Conlee, 1994). In ‘power sports’ like weightlifting, there is evidence that some amount of benefit may be achieved through the use of cocaine (Bohn, Khodaee, & Schwenk, 2003).

Having said that, enough conflicting evidence exists for the effectiveness of cocaine use in either power or endurance sports. Additionally, some believe that cocaine may not affect sporting performance at all – favorably or otherwise. And that the sense of euphoria and clarity of thought process associated with cocaine use, creates a false sense of improved performance rather than actually improving it!

Why should athletes be discouraged from using cocaine?

Cocaine use is fraught with risks – some fatal! Cocaine (similar to amphetamines) increases risk of sudden death due to cardiac arrest during intense exercise sessions – such as an on-field sport performance, especially those involving short bursts of sprints!

Researchers believe that pathophysiological processes induced by cocaine that may be responsible (Avois et al., 2006), either singly or in combination for such fatal incidences as sudden cardiovascular death are:

    • enhanced heat production
    • increased lactic acid synthesis
    • intense constriction of blood vessels

Also, cocaine is an adrenergic drug. Regular use with resultant chronic stimulation of cardiac β1 receptors may cause death of heart cells. This may lead to fatal cardiac arrhythmia and cardiac arrest (Davis, Loiacono, & Summers, 2008).

If, however, you are not worried about the adverse effects and driven by the ‘win-at-all-costs’ attitude, another reason why you should refrain from using cocaine is because cocaine is not used in any over-the-counter drugs. Slightest traces of either cocaine or its metabolites (benzoylecgonine and methylecgonine) in urine, therefore,  constitutes a serious doping offence and ground enough for immediate suspension under the WADA (World Anti-Doping Agency) Code. Contrast that with ephedrine alkaloids which are present in some over-the-counter cough/cold medications; there can therefore be enough grounds for defending your case – whether you’ve unknowingly (or ‘otherwise’) used ephedrine/ephedra alkaloids.

Just to let you know, the World Anti-Doping Code’s Doping List classifies cocaine as an ‘indirectly acting sympathomimetic agent and a noradrenaline reuptake inhibitor and hence a performance enhancing drug (Davis et al., 2008). It is mentioned in the S6-a (stimulants) class of prohibited substances (on page 8 of the 2015 list).


To conclude, notwithstanding the anecdotal evidence, cocaine seems to do precious little to improve sports performance. It may, on the other hand, be detrimental and may also increase the risk of fatal adverse effects. In short, using cocaine – for sports persons – is a ‘lose-lose situation’.

Therefore, if you’re an athlete and looking for an ergogenic aid, cocaine is the last thing on earth that you should look to get in your system!


Avois, L., Robinson, N., Saudan, C., Baume, N., Mangin, P., & Saugy, M. (2006). Central nervous system stimulants and sport practice. Br.J Sports Med, 40 Suppl 1, i16-i20.

Bohn, A. M., Khodaee, M., & Schwenk, T. L. (2003). Ephedrine and other stimulants as ergogenic aids. Curr.Sports Med Rep., 2, 220-225.

Braiden, R. W., Fellingham, G. W., & Conlee, R. K. (1994). Effects of cocaine on glycogen metabolism and endurance during high intensity exercise. Med Sci.Sports Exerc., 26, 695-700.

Davis, E., Loiacono, R., & Summers, R. J. (2008). The rush to adrenaline: drugs in sport acting on the beta-adrenergic system. Br.J Pharmacol., 154, 584-597.

Kloner, R. A. & Rezkalla, S. H. (2003). Cocaine and the heart. N Engl J Med, 348, 487-488.

Welder, A. A. & Melchert, R. B. (1993). Cardiotoxic effects of cocaine and anabolic-androgenic steroids in the athlete. J Pharmacol. Toxicol. Methods, 29, 61-68.

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Really?! I can hear you say! And, you’re not alone! Most people associate testosterone use (and, that of other androgenic-anabolic steroids) with aggression and anti-social behaviour. Which isn’t very surprising, given the amount of rap that these ‘illegal’ substances have had from the mainstream media.

It is indeed sad that testosterone – especially when used as a steroidal supplement – has been maligned beyond belief. So much so, that we tend to associate testosterone (T) supplementation with ‘aggression’ and ‘doping’ or ‘cheating’ more readily than ‘truthfulness’ or ‘pro-social’ behavior. The truth of the matter is that T can, in fact, have positive social influence on the behaviour of men and even produces truthfulness.

Before we get into how the process of lying that is positively affected by supplementation with T, let us try to have a cursory look at what the basis of lying is.

Basis of Lying

Why do we lie? Well, even before someone starts to answer that question, you’ll know the answer will be quite complex. And, no matter how impressive the answer is, you can be rest assured that no one will ever know the complete truth. To date, no researchers, doctors or rational thinking scholars have been able to solve the riddle! Despite immense research in this direction, the psycho-physiological basis of lying is yet to be unearthed.

Some researchers believe that the internal chemistry in our bodies may have a lot to do with our tendency to lie (or be truthful). Of the numerous physiologically active chemicals and substances in our bodies that carry out (almost a million!) physiologically important roles, T has been recognised as one such chemical that influences truthfulness and social behaviour, especially so in men.

Several scientific studies – in the recent past – have demonstrated this positive association between T (supplementation) in men and truthfulness!

The Act of Lying

One of the most accepted of all social rules is the need to be truthful; don’t know how much of a religious person you are, but almost all religious scriptures advocate being truthful for the good of society.

The basis of such a rule is that truthfulness helps build trust amongst concerned parties facilitating mutual social or economic growth (Wibral, Dohmen, Klingmuller, Weber, & Falk, 2012). However, it is an undeniable fact, that no matter what part of the globe you live in, you will always come across deceitful, lying people.

Scientists for long have been studying the reasons – social, psychological and physiological – that make people susceptible to lying (Bok, 1978; DePaulo, Kashy, Kirkendol, Wyer, & Epstein, 1996; Vrij, 2001). However, no one has been quite able to crack it (the reasons).

Recently, however, a connection between T and truthfulness – not to mention, a more socially acceptable behaviour – has been suggested. And, that low testosterone levels may have something to do with lying! Scientific studies have been consistently reporting that men supplemented with steroidal injections of testosterone are more likely to be

    • truthful, and
    • to put on a more ‘pro-social behavior’

Let us get to know why!

Testosterone and the Connection with a ‘Pro-social Behavior’

Let’s have a quick look at what T is before moving on to how it influences truthfulness and a pro-social behaviour.

As we all know, testosterone is the main androgenic hormone of the human male; it is responsible for:

    • development of primary male sexual characteristics – growth of testes and penis during uterine life and again, near puberty
    • development of secondary male sexual characteristics – male pattern of distribution of bodily hair including a beard and moustache, a base voice and increase in lean mass – muscles and bones – imparting more vigor to the male

However, there seems to be more to T that just its influence on the male reproductive physiology. As mentioned earlier, T seems to affect psycho-social human behavior as well.

While research has tended to focus on the connection between aggression and testosterone, recently it is being reported that testosterone may, in fact, (at least under certain conditions) positively influence a man’s social interactions – making him more selfless (Eisenegger, Naef, Snozzi, Heinrichs, & Fehr, 2010; van, Montoya, Bos, van, & Terburg, 2012). One of the reasons cited for such unusual findings (unusual, going by current logic) is the fact that testosterone is principally a reproductive hormone; and, gaining a higher social status is a part of what is called the ‘dominance behaviour’ or the ‘alpha-male behaviour’ (seen so typically in animals) (Eisenegger et al., 2010; Eisenegger, Haushofer, & Fehr, 2011; Mazur & Booth, 1998). Therefore, being socially amicable with a selfless behaviour and reduced lying may be a part of this ‘dominance behaviour’ with the ultimate aim of dominating over other males and securing a female mate!

It is also suggested that pride may also contribute to such pro-social behavior (Wibral et al., 2012).

The acts of – sometimes unwarranted – heroism that men tend to indulge in are also blamed on T combined with such inherent characteristics as pride and the tendency to dominate.

Evidence in Favour of ‘Testosterone Truthfulness’

In a study published in 2012, Wibral and his colleagues reported that T administration may reduce the incidence of ‘self-serving’ lies (Wibral et al., 2012). The authors go on to the suggest how T may positively influence the human male psyche.

    • positively affecting social preferences and choice making
    • improving self-esteem and, therefore, the concern for social standing
    • improving concerns for the belief of others

There is also some evidence that T administration may positively affect social behavior in women too (Eisenegger et al., 2010; Wibral et al., 2012).


Testosterone may not be just a ‘male sexual hormone’; it has a lot to do with the way men interact socially as well. In a nutshell, there seems to be – in all truthfulness (!) – far more to testosterone than meets the eye!


Bok, S. (1978). Moral choice in public and private life. In Lying (pp. 326). New York: Vintage Books.

DePaulo, B. M., Kashy, D. A., Kirkendol, S. E., Wyer, M. M., & Epstein, J. A. (1996). Lying in everyday life. J Pers.Soc Psychol., 70, 979-995.

Eisenegger, C., Haushofer, J., & Fehr, E. (2011). The role of testosterone in social interaction. Trends Cogn Sci., 15, 263-271.

Eisenegger, C., Naef, M., Snozzi, R., Heinrichs, M., & Fehr, E. (2010). Prejudice and truth about the effect of testosterone on human bargaining behaviour. Nature, 463, 356-359.

Mazur, A. & Booth, A. (1998). Testosterone and dominance in men. Behav.Brain Sci., 21, 353-363.

van, H. J., Montoya, E. R., Bos, P. A., van, V. M., & Terburg, D. (2012). New evidence on testosterone and cooperation. Nature, 485, E4-E5.

Vrij, A. (2001). The pyschology of lying and the implications for professional practice. In Detecting lies and deciet (pp. 254). John Wiley & Sons.

Wibral, M., Dohmen, T., Klingmuller, D., Weber, B., & Falk, A. (2012). Testosterone administration reduces lying in men. PLoS One, 7, e46774.

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Ana_Ivanovic_Qatar_OpenAll forms of exercise, to a lesser or greater degree – involve bodily movements. These movements are nothing but changes in bone alignments – with respect to each other – brought about by rhythmical contraction-relaxation of agonistic-antagonistic (opposing) muscles. These are more often than  not, accompanied by an intense contraction (isometric) of (stability) muscles in other parts of the body.

These isometric contractions occur without much apparent changes in the angle of joints involved or lengthening or shortening of the muscle fibers (such as occurs in the muscles of the abdominals and back, not to mention, arms when we are carrying heavy grocery bags). All this, whilst active movement in the legs is going on.

As you may have guessed, the more complex (and quicker or harder) the movement/s, more the benefits – stronger bones, joints / joint structures and muscles – not to mention numerous other physiological benefits as in improved cardiovascular-respiratory and metabolic parameters, amongst others.

So, how do we create these movements and where does the energy that drives these movements comes from?

Where do we derive the energy for movements from?

The answer is – as you most likely have heard – from a high energy molecule called the ATP (for the scientifically inclined, ATP stands for ‘adenosine triphosphate’). As the name suggests, ATP contains three (tri) phosphate radicals attached to the nucleotide adenine.

The breakdown of this ATP molecule into ADP (adenosine diphosphate) – by splitting of the bond with the third phosphate radical – will release large amounts of energy. This energy is utilised to cause muscle contraction (Glaister, 2005). Bear in mind though that muscle contraction is just one of the thousand of physiological reactions where-in energy released by ATP breakdown is utilized (Baker, McCormick, & Robergs, 2010).

ATP in Muscles

During short bursts of intense exercise, there is a 1000-fold increase in ATP demand in muscles. Despite this, the muscle tissue has the ability to maintain a relatively stable concentration of ATP molecules. This imparts muscle tissue the ability to greatly vary its metabolic rate as compared to other tissue (Glaister, 2005). Thus, taxing muscles to bump up metabolic rate and burn more calories does seem to make total sense.

Shelly Ann Fraser PryceDespite the high demand of ATP in muscles, especially during bouts of intense exercise, the amount of ATP stored per muscle cell is rather small – about 8 mmol/Kg of muscle. And, at all times, the level of ATP never gets below 5 mmol/Kg – at which point, muscles fail to produce the necessary power output or contraction – a phenomenon called muscle fatigue or muscle failure (Bigland-Ritchie & Woods, 1984).

As you may well have guessed, there is a very logical reason for the low concentration of ATP in muscles and the onset of fatigue. There is no denying the fact that fatigue is a protective reflex. If it weren’t for fatigue, we would continue to contract our muscles forcefully and eventually cause irreversible muscle damage or rigor (Bogdanis, Nevill, Boobis, Lakomy, & Nevill, 1995).

Low physiological levels of ATP thus ensures that fatigue sets in within a short time during intense activity; protection of muscle tissue being the sole aim.

Energy Systems for Resynthesis of ATP

Training energy system to effectively resynthesize ATP – as quickly as possible – so that muscle contraction continues without onset of fatigue – forms the basis of most exercise protocols.

There are numerous energy systems in place within the human body which cause regeneration of ATP. Depending on the substrate used and the rate at which these systems resynthesize ATP, these energy systems are:

1. Phosphagen System – is the most rapid of the systems for regeneration of ATP molecules; it utilizes phosphates from Creatine Phosphate (CrP) in the presence of enzyme Creatine Kinase (CK). It does not require oxygen hence also called the anaerobic system.

During the first 10 seconds of a high intensity exercise (100 metre sprint), the phosphagen system is responsible for ATP regeneration (Bogdanis, Nevill, Boobis, & Lakomy, 1996). In the recent past, however,it has been suggested that there is rarely a total reliance on the phosphagen system (Casey, Constantin-Teodosiu, Howell, Hultman, & Greenhaff, 1996) and that the rate of CrP degradation to regenerate ATP begins to decline within 1.3 seconds of intense exercise (Maughan et al., 1997) – meaning other systems to regenerate ATP begin to kick in as early as 1.3 seconds after initiation of intense exercise.

Sports which typically depend on this system are 100m sprints, weight lifting, shot put and jumping events.

2. Glycolytic System – Exercise of longer than a few seconds duration will utilize blood glucose and glycogen stored in the liver to regenerate ATP. This system is slower than the phosphagen system and it produces more ATP molecules.

3. Mitochondrial Respiration – As the name suggests, this occurs in the mitochondria. It utilizes fatty acids from the blood, fat depots and muscles, glucose from diet or that stored in the liver and glycogen within the muscle. Since it requires the use of oxygen, it is also called the aerobic system.

Although the overview of energy system provided here is a very simplistic one, it will help you understand the complex interplay that exists between these systems at all intensities of exercise training – especially during incremental and maximal efforts.

To conclude, although it was always traditionally thought that training the system most suited for your sporting discipline will likely benefit your performance the most – more recently, it is being recommended that improving the efficiency of all of these systems will be more beneficial – esp. in a sport like football or tennis. Also, training one energy system will likely have carryover effect to improve another.

Reference List

Baker, J. S., McCormick, M. C., & Robergs, R. A. (2010). Interaction among Skeletal Muscle Metabolic Energy Systems during Intense Exercise. J Nutr.Metab, 2010, 905612.

Bigland-Ritchie, B. & Woods, J. J. (1984). Changes in muscle contractile properties and neural control during human muscular fatigue. Muscle Nerve, 7, 691-699.

Bogdanis, G. C., Nevill, M. E., Boobis, L. H., & Lakomy, H. K. (1996). Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise. J Appl.Physiol, 80, 876-884.

Bogdanis, G. C., Nevill, M. E., Boobis, L. H., Lakomy, H. K., & Nevill, A. M. (1995). Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man. J Physiol, 482 ( Pt 2), 467-480.

Casey, A., Constantin-Teodosiu, D., Howell, S., Hultman, E., & Greenhaff, P. L. (1996). Metabolic response of type I and II muscle fibers during repeated bouts of maximal exercise in humans. Am J Physiol, 271, E38-E43.

Glaister, M. (2005). Multiple sprint work : physiological responses, mechanisms of fatigue and the influence of aerobic fitness. Sports Med, 35, 757-777.

Maughan, R. J., Greenhaff, P. L., Leiper, J. B., Ball, D., Lambert, C. P., & Gleeson, M. (1997). Diet composition and the performance of high-intensity exercise. J Sports Sci., 15, 265-275.

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As runners, we’ve always been told not to use old, worn-out shoes. This, they said, will prevent foot, shin and other running injuries. However, in light of recent evidence, this so called ‘wisdom’ may not be true!

Over the years, sports medicine has lent credence to the notion that worn-out shoes are detrimental to your running biomechanics. Poor biomechanics, in turn, increase your chances of injuries. However, findings from recently published studies seem to contradict this point of view. Researchers now believe that to prevent injuries, you’ve got to avoid changing your running shoes frequently. They also recommend to ‘break-in’ your new trainers before taking them for a serious ‘spin’.

For too long, foot pain and injuries associated with distance running have been blamed on footwear (Grier, Knapik, Swedler, & Jones, 2011). Use of inappropriate (Taunton et al., 2003) and ill-fitting (Burns, Leese, & McMurdo, 2002) trainers is sure to cause foot injuries, they told us. Old and worn-out shoes have been branded top culprits – increasing age of the shoes increases incidence of injuries , we were told (van, 1992). This, supposedly, is due to loss of shock-absorbing abilities of the shoes as they age.

The standard recommendation for change of running footwear has been 500 miles (Fredericson, 1996). However, the authors of a study published in the British Medical Journal are of the opinion that changing trainers frequently may in fact be a bad idea (Rethnam & Makwana, 2011). Based on the findings of their study, they concluded that new shoes are associated with higher forces working on the small joints of your feet. Thus, newer shoes are more likely to cause injuries as compared to older ones. This may partly be due to the stiffness and lack of shock-absorbing properties of new shoes. The study goes on to suggest that new shoes should be ‘broken-into’ gradually; using them for milder physical work for a few weeks before taking them for a longer spin.


In conclusion, although for quite some time, it has been recommended that old and worn out trainers may be a sure recipe for disaster, that doesn’t seem to be the case anymore. Research now suggests that not changing your shoes frequently and sticking longer with your ‘broken-into’ trainers may be a better idea to avoid running injuries.


Tracking your mileage over weeks, months and years (to avoid overtraining) and reducing body mass index are other useful ways which can help you stay injury-free.


Burns, S. L., Leese, G. P., & McMurdo, M. E. (2002). Older people and ill fitting shoes. Postgrad.Med J, 78, 344-346.

Fredericson, M. (1996). Common injuries in runners. Diagnosis, rehabilitation and prevention. Sports Med, 21, 49-72.

Grier, T. L., Knapik, J. J., Swedler, D., & Jones, B. H. (2011). Footwear in the United States Army Band: injury incidence and risk factors associated with foot pain. Foot (Edinb.), 21, 60-65.

Rethnam, U. & Makwana, N. (2011). Are old running shoes detrimental to your feet? A pedobarographic study. BMC Res.Notes, 4, 307.

Taunton, J. E., Ryan, M. B., Clement, D. B., McKenzie, D. C., Lloyd-Smith, D. R., & Zumbo, B. D. (2003). A prospective study of running injuries: the Vancouver Sun Run “In Training” clinics. Br.J Sports Med, 37, 239-244.

van, M. W. (1992). Running injuries. A review of the epidemiological literature. Sports Med, 14, 320-335.

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