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In recent years, in comparison to conventional aerobic endurance training (AET), resistance training (RT) is being touted as a superior method of weight loss.

And most fitness experts seem to agree. But, is it really?

Delve a bit deeper into science and you realise that evidence for RT being a better weight-loss tool, is not all that strong and AET (and in some individuals, high-intensity, interval training – HIIT) may be better!

Interesting to note here that while RT may have its own set of metabolic benefits, AET may still be better than RT at reducing risks of metabolic disorders too.

WHY ARE YOU TOLD THAT RESISTANCE TRAINING WILL CAUSE WEIGHT LOSS?!

It is a common (and, somewhat dogmatic) belief amongst exercisers, exercise-fitness professionals and clinicians that resistance or strength training (ST), in addition to improving your lean body mass (LBM), is the best way to burn more calories and therefore, lose weight as well.

And, this is how – they’ll tell ya – it (apparently) works:

  • RT or ST has the potential to increase your LBM, also called fat-free mass (FFM), including muscle mass – there is enough evidence to support this 1–4
  • Skeletal muscle is the most metabolically active tissue in the body – well, no! Its more complicated than that (see below)
  • Increase in muscle mass translates into more calories burned throughout the day, even when resting – evidence equivocal (see below)
  • Therefore, more muscle you carry, more is your resting metabolic rate (RMR) and more calories you burn throughout the day (increase in total daily energy expenditure (TDEE)
  • Increase in TDEE (with or without a nutritional calorific deficit) leads to weight loss

WHAT’S WRONG WITH WHAT THEY TELL YOU?

While all that sounds good in theory, everything isn’t as cut and dry as they make it out to be:

  1. Skeletal muscle isn’t the most metabolically active of the tissues in the body – heart and the kidneys are! These organs have the highest metabolic rates, 2x those of the liver and the brain and a whopping 35x that of the skeletal muscle! 5 Having said that though, of all the tissues, skeletal muscle may indeed contribute significantly towards energy expended during the day. This is so because skeletal muscle wins on account of sheer mass – it weighs much more than all these other organs mentioned.
  2. Increased muscle mass does not bump up your metabolism to the point that it will burn additional calories which will translate into weight loss:
  • Previous studies examining the effects of RT on RMR have reported mixed results – both in men and women 2,3,6–15
  • Only older men (and not older women or younger men and women) show an elevated RMR in response to RT; most studies support this finding 2,3,6,10,11,13
  • In younger men & women and in older women, there seems to be a consistent lack of change in RMR in response to RT; the association between RT and rise in RMR all but disappears 7,8,12,14,15
  • Recent studies have shown mixed results too – with some showing an increase in RMR in response to RT; 16,17 others, a no change. 18,19 Interestingly, one study showed a fall in RMR in response to ‘dieting’, which could not be stopped by resistance training 20
  • A rare study that compared the effects of RT on RMR across various age groups, reported no changes in RMR in either young or older individuals! 12
  • A study by Lemmer et al. 17 reported some curious findings:
  1. RMR in response to RT is more affected by gender than age; men are more likely to benefit from RT than women
  2. When younger and older men were pooled together, a significant increase in RMR with RT was shown
  3. Younger and older women showed no effect on RMR in response to RT

In a nutshell, RT does not alter energy expenditure significantly outside of the exercise session and especially in younger men or in women across all age groups.

WEIGHT / FAT LOSS WITH RESISTANCE TRAINING

Misinterpretation of current ACSM and other guidelines 21–23 have led to the dogmatic belief amongst exercise-fitness professionals that RT has conclusively been proven to reduce body weight. In reality, a closer look at existing literature suggests that the evidence for RT as an effective tool for weight-loss remains equivocal, at best. 24–29

  • The ACSM guidelines on ‘strategies for weight loss and prevention of weight regain in adults’ states that, ‘research evidence does not support RT as effective for weight loss’ and points out that ‘the effects of RT for prevention of weight gain (after initial weight loss) are largely unknown’ 21
  • While few studies have observed some reduction in body fat with RT,30–32 others have found no effect on body fat % even when the intervention was continued for 12-52 weeks 33–35
  • Interestingly, one study found a gender-based differential effect of RT on body fat – reduction in body fat was observed in the group containing younger and older men pooled together but not in women. 17 This finding is not dissimilar to the findings from other studies that RT enhances RMR only in older men 7,8,12,14,15

There is, however, a need to mention here that although RT does not seem to contribute significantly to calorie expenditure outside of the exercise session or fat loss, it is associated with numerous health benefits – increased lean mass, improved work capacity and decreased chronic disease risk factors (sarcopenia), to name a few. 36,37

HIGH-INTENSITIY, INTERVAL TRAINING

HIIT, they will tell you, will not only burn calories during the workout but also increase your calorie expenditure through the rest of the day (through increased excess post-exercise oxygen consumption – EPOC – a fancy term the whole town and his wife seems to be using these days!). And, that will translate into weight loss!

EPOC or oxygen debt, as it used to be called previously, is the mechanism by which the body makes up for the oxygen deficit created during an exercise session by increasing oxygen consumption well after cessation of exercise – breathlessness you experience for a few minutes after you’ve climbed to the top of the stairs is an example.

In reality, increase in EPOC after an HIIT session is modest (only 6-15% of total energy expenditure). EPOC alone, therefore, may be insignificant for causing weight loss. 38

Having said that, a study published in 2002 in the European Journal of Applied Physiology utilising circuit type of resistance training with relatively heavy weights and short rest periods generated EPOC which increased resting metabolic rate by 21% and 19% for 24 and 48 hours post- workout. As the authors content, if these numbers are applied to a typical 180-pound individual, it would amount to 773 calories expended over 2 days after cessation of the exercise session! 39 So, HIIT does seem to have benefits.

However, whereas in overweight-obese / untrained individuals, it is difficult to achieve the high-intensity and the duration required to elicit a high enough EPOC to be of any consequence for weight loss. And, prescription of such complex methods of training – needing highly skilled movements – is likely to reduce exercise enjoyment and long-term adherence in novice and out-of-shape individuals, in seasoned exercisers, HIIT and EPOC may be an effective way to bump up calorie burning and improve body composition.

AEROBIC ENDURANCE TRAINING

Also known as ‘low-intensity, steady state’ (LISS) cardio or ‘long, slow distance’ (LSD) training, aerobic endurance training (AET) may just be the best tool out there, for most people when it comes to losing weight.

Researchers from the University of Pittsburgh, Pennsylvania, conducted a study comparing RT with AET in young women 40. The results will come as a surprise (for most)! Apparently, not only is AET better than RT at reducing body fat % but it also wins hands down when it comes to:

  • improving cardiorespiratory fitness
  • improving insulin sensitivity
  • reducing visceral adipose tissue (fat surrounding organs)
  • reducing abdominal fat, and
  • reducing inter-muscular (within muscle) fat

Other studies have also supported the idea that AET may be better at reducing visceral and abdominal fat, not to mention, the overall body fat%.

  • A study published in Dec, 2012 reported that while AET and combined AET/RT exercise programs caused more weight loss than RT alone, AET/RT and RT resulted in increased lean mass. However, although requiring a double time commitment over AET alone, a combined AET/RT exercise program did not result in ‘significantly more weight loss over AET alone’ 41
  • Another study published in the American Journal of Physiology – Endocrinology and Metabolism concluded that AET caused significant reductions in:
    1. Whole body fat including subcutaneous abdominal fat, visceral adipose tissue (VAT – fat around the organs) and liver fat content
    2. plasma liver enzymes, esp. alanine aminotransferase (enzyme reflecting the amount of liver damage), and
    3. HOMA (Homeostasis Model Assessment – a measure of the level of your steady state pancreatic beta cell function (%B) and insulin sensitivity (%S)

Resistance training, on the other hand, failed to significantly affect these variable 42

  • Owing to results like these, it shouldn’t come as a surprise that AET is recommended to be central to exercise programs for reducing VAT and its metabolic adverse effects – obesity and other metabolic disorders 43
  • Even in the absence of significant weight loss, AET may improve metabolic disease parameters, esp. in patients of type 2 diabetes 44

WOMEN AND AEROBIC ENDURANCE TRAINING

Why do women prefer conventional AET?

As if the results of the studies mentioned above didn’t come as shocking enough for you, here’s something that is even more thought-provoking – something that might answer your question of why women tend to favour treadmills over free-weights!

It appears that AET is more effective in (overweight and obese, both young and older) women than in men 40. Furthermore, there is some evidence to suggest that women enjoy AET more than RT 45; the opposite seems to be true with young men – they seem to enjoy RT more (now come on, do we even need any proof of that?!).

My hunch is that is that women find AET more enjoyable because it is more effective for them! Not surprisingly then – call it nature or subconscious minds at work – there seems to be a very valid reason why you see more women heading to the treadmill rather than the ‘free-weights section’!

RT OR AET and METABOLIC DISEASE

Abdominal obesity is a prominent risk factor for metabolic disease (type II diabetes, cardiovascular disease, etc.). 46 Results from the STRRIDE study suggest that AET was associated with significant reductions in VAT, a measure of abdominal obesity. 47,48

Although in comparison to AET, RT does not cause much difference in measures of fat tissue, it does cause a significant reduction in CRP (a parameter, high levels of which, suggests a low-grade, chronic systemic inflammation with the potential to develop into cardiovascular disease and diabetes type II). 49 Important to note here that an inverse association seems to exist between aerobic fitness and chronic systemic inflammation.50,51  Sedentariness increases inflammatory markers. 49

Conflicting data exists over the superiority of AET over RT for the reduction of metabolic disease risk parameters (HbA1c, blood lipids including triglycerides and LDL particle size). Having said, regular and long-term, moderate intensity exercise seems to increase HDL and lower triglycerides, even in the absence of weight loss. 52

Although RT has benefits of its own, a combination of AET and RT exercise regimen – although more effective at reducing the risk of metabolic disease than RT alone – were not significantly different from AET alone 53. This effectively suggests that the RT component may be contributing precious little (if at all) to the disease prevention effect of an AET-RT exercise program.

A NEAT SOLUTION TO THE PROBLEM

Of all the components of human daily energy expenditure (BMR, thermic energy of food, exercise-related activity thermogenesis (EAT) and non-exercise activity thermogenesis (NEAT)), NEAT is the most modifiable parameter and is capable of significantly pushing up your total daily energy expenditure (TDEE) than exercise sessions (!), even in intense exercisers 54.

Even very low-level physical activities like mastication (chewing) and fidgeting can increase energy expenditure by 20-40% above your resting metabolic rate!

NEAT includes energy expenditure of walking, talking, going for your job, sitting, toe-tapping, shopping, dancing, etc.

COMMENT

It is likely that AET (treadmill runs) may be more effective than RT – especially in overweight women – for reducing body fat and preventing metabolic diseases. Also,

  • RT seems to contribute very little to weight-loss
  • RT doesn’t seem to contribute towards (metabolic) disease prevention-management as much as AET does
  • Combination of RT and AET does not seem to afford any more benefits over AET alone when weight loss or metabolic disease management is the prime goal

CONCLUSION

Looking at much of the evidence, the question that begs to be answered is: ‘what if we were all wrong about our weight-loss exercise strategies and indeed, about our obsession with the fat-burning abilities of resistance training? And, what if those women on treadmills were right all along?!

I reckon, it’s time we stopped ridiculing (or even downright laughing at) those men / women who hit the treadmill every single time they’re at the gym.

TAKE HOME MESSAGE

  • Resistance training may be contributing precious little towards calorie burning outside of exercise sessions and eventual weight loss!
  • HIIT in overweight – obese and untrained individuals HIIT may not be ideal; in seasoned exercisers, may lead to significant calorie expenditure both in and outside of the exercise sessions
  • Aerobic Endurance training seems to be the best tool for total body weight and fat reduction – needs to a be an integral part of almost every weight-loss program
  • Aerobic Endurance training wins hands down for metabolic disease management
  • Women do not seem to respond as well to resistance training, aerobic endurance training and HIIT may be better options
  • NEAT can contribute significantly to total daily energy expenditure – staying active through the day can really bump your calorific expenditure (probably more so than RT or AET)

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Historical Perspective

Believe it or not, gout – previously called ‘the disease of the kings’ or arthritis of the rich as opposed to rheumatism – arthritis of the poor! – was first described by the Egyptians (when it was known as podagra) in 2640 BC. It was later recognised by Hippocrates in the 5th century BC, who referred to it as ‘the unwalkable disease’ and went on to describe its presentation and disease course in striking detail – most of his clinical perceptions of the conditions are still as relevant today as they were 2,500 years ago (Nuki & Simkin, 2006; Star & Hochberg, 1993)! Talk about being ‘ahead of time’!

Modern day Prevalence of the Disease

In more recent times, gout and hyperuricemia (raised uric acid levels in blood), have shown a steady rise in prevalence and incidence (doubled), especially in the US (Choi, Atkinson, Karlson, Willett, & Curhan, 2004; Choi & Curhan, 2008; Roubenoff et al., 1991). Population studies have reported the incidence of gout in much of the developed world to range between 1-2% (Richette & Bardin, 2010); incidence of hyperuricemia may be as high as 15-20% (Doherty, 2009; Mikuls et al., 2005). Males are more likely to be affected – 80% of cases of gout in Northern Europe tended to be men (Annemans et al., 2008; Doherty, 2009). It is the commonest inflammatory arthritis in men (Choi et al., 2004; Choi & Curhan, 2008; Richette & Bardin, 2010; Roubenoff et al., 1991) and the most common inflammatory arthritis in older women (Doherty, 2009). Prevalence increases with age, in both sexes (Doherty, 2009; Star & Hochberg, 1993). Age and gender specificity of the condition explains the rarity of the conditioning in young, pre-menopausal women (Doherty, 2009; Wallace, Riedel, Joseph-Ridge, & Wortmann, 2004).

Natural Course of the Disease

Gout / gouty arthritis refers to an acute attack of inflammatory arthritis, provoked by the release of monosodium urate (MSU) crystals into joint spaces. Natural course of the disease (Doherty, 2009; Richette & Bardin, 2010, 2012; Wallace et al., 2004) is characterised by 3 distinct phases:

  1. Asymptomatic hyperuricemia (raised serum uric acid – sUA),
  2. Episodes of acute attacks, and
  3. Asymptomatic, inflammation/pain-free intervals and progression on to chronic gouty arthritis

Characteristic presentation of an acute attack is typically an inflamed base of (usually) the big toe (the first metatarsophalangeal – MTP – joint), with warmth, redness and pain. Rarely, other joints may also be involved.

Pathogenesis: The Conventional View

There is no denying that diet does play a crucial role in prevention and treatment of gout. Traditionally, hyperuricemia – resulting from an increased production of uric acid (due to increased purine breakdown after ingestion of purine-rich, animal-based, proteinaceous foods) has been suggested to be majorly causative of gout. In humans, uric acid is the final metabolite of both dietary and endogenously produced purine metabolism (Richette & Bardin, 2012). Sometime during the Miocene period, it is believed that human beings lost the ability to produce an enzyme called ‘uricase’ , which is normally responsible for converting the insoluble uric acid into highly soluble, allantoin (Doherty, 2009). When the accumulation of uric acid (98% of which is present in ionic form) crosses a saturation point, it combines with Na+ in the extracellular spaces and forms MSU crystals and precipitates into joint spaces leading to gout (Richette & Bardin, 2010, 2012). Not surprising then, that avoiding purine-rich foods – meats, poultry, fish, soy and non-soy legumes – with the aim of reducing sUA, is the standard dietary advice given and followed. Conventional pharmaceutical approach (urate lowering therapy – ULT), through the use of drugs like allopurinol, also aims to reduce sUA (Richette & Bardin, 2012). That said, there seem to be some major problems with this hypothesis at all levels:

  1. Although, high intake of purine-containing foods does indeed increase the risk of urate deposition, and increases up to five-fold, the risk of gout attack amongst known patients, how it does so, still remains a query (Zhang et al., 2012)
  2. Meat-eaters will typically have other confounding factors as well – a diet high in sugar, sweetened beverages, refined grains, processed meats and low ingestion of fruits and veggies, not to mention cigarette smoking and ingestion of alcohol (which itself increases uric acid levels – more on this later)
  3. Purine-rich vegetarian foods do not seem to increase the risk – it has been reported that dietary intake of soy and non-soy legumes reduces the risk of gout (Teng, Pan, Yuan, & Koh, 2015)
  4. In rare cases, gouty arthritis can develop in patients with no history of hyperuricemia (McCarty, 1994; Urano et al., 2002)
  5. It is not the sUA per se but the rapid dissolution of already formed urate deposits and precipitation of MSU crystals in the joint spaces is what triggers
    an acute attack of gout (Richette & Bardin, 2012) – attacks during the first few months of initiation of a ULT supports this notion
  6. Although mechanisms vary, other factors or conditions can also lead to an acute attack through lowering of urate levels: systemic inflammation, ingestion of whiskey and post-surgery. Alcohol intake is associated with both increased endogenous urate production (Bleyer & Hart, 2006) and rapid, transient decrease in sUA through its uricosuric (increased renal excretion of uric acid) actions
  7. Release of pro-inflammatory molecules, cytokines and interleukins (IL-6), which are a hallmarks of systemic inflammation, have been shown to stimulate the hypothalamo-pituitary-adrenocortical axis leading to release of cortisol (Dunn, 2000; Wang & Dunn, 1999). It is suggested that cortisol may be secreted through the same mechanism in gouty arthritis too. Cortisol has a uricosuric effect (McCarty, 1994) and thus, may contribute to an acute attack of gout
  8. 20-25% of asymptomatic patients with sUA exhibit MSU crystal deposits in their joints – especially the knees and the first MTP joint (Pineda et al., 2011; Puig et al., 2008; Richette & Bardin, 2012) and yet do not suffer from attacks of gout – suggesting that other factors must be at play
  9. There is ample evidence to suggest that genetic factors, obesity (especially, during early adulthood) and systemic inflammation contribute significantly to gout (Bleyer & Hart, 2006; Roubenoff et al., 1991; Teng et al., 2015; Urano et al., 2002). And, a serious discussion on these factors by the research community is long overdue.
  10. Genetic and other metabolic disorders (suggestive of systemic inflammation) occur concurrently with gout: obesity, diabetes, chronic renal failure, to name a few

The Fructose Connection

Whereas fructose from natural sources seem to be benign, there is some evidence to suggest that higher intake of fructose – especially, through artificial sources (high-fructose corn syrup and excess of table sugar), may produce metabolic anomalies, including hypertriglyceridemia and sUA (Angelopoulos et al., 2009). Fructose does this through both increased endogenous production and reduced renal excretion (Nakagawa et al., 2006).

Take Home Message

  1. Not enough evidence that avoiding meats will reduce uric acid levels or likelihood of an acute attack of gout
  2. Raised uric acid levels, by themselves may not be responsible for an acute attack of gout
  3. If you already have hyperuricemia, beware of factors or conditions that cause sudden reduction in serum uric acid levels – avoid alcohol
  4. Fructose from artificial sources (including but not limited to, sweetened beverages) should be avoided
  5. Reduction of system inflammation (weight loss, paleo / keto diet) may help

References

Angelopoulos, T. J., Lowndes, J., Zukley, L., Melanson, K. J., Nguyen, V., Huffman, A., & Rippe, J. M. (2009). The effect of high-fructose corn syrup consumption on triglycerides and uric acid. The Journal of Nutrition, 139(6), 1242S–1245S. https://doi.org/10.3945/jn.108.098194

Annemans, L., Spaepen, E., Gaskin, M., Bonnemaire, M., Malier, V., Gilbert, T., & Nuki, G.(2008). Gout in the UK and Germany: prevalence, comorbidities andmanagement in general practice 2000-2005. Annals of the Rheumatic Diseases,67(7), 960–6. https://doi.org/10.1136/ard.2007.076232

Bleyer, A. J., & Hart, T. C. (2006). Genetic factors associated with gout and hyperuricemia. Advances in Chronic Kidney Disease. https://doi.org/10.1053/j.ackd.2006.01.008

Choi, H. K., Atkinson, K., Karlson, E. W., Willett, W., & Curhan, G. (2004). Purine-rich foods, dairy and protein intake, and the risk of gout in men. The New England Journal of Medicine, 350(11), 1093–1103. https://doi.org/10.1056/NEJMoa035700

Choi, H. K., & Curhan, G. (2008). Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ (Clinical Research Ed.), 336(7639), 309–12.https://doi.org/10.1136/bmj.39449.819271.BE

Doherty, M. (2009). New insights into the epidemiology of gout. Rheumatology (Oxford, England), 48 Suppl 2(suppl 2), ii2-ii8. https://doi.org/10.1093/rheumatology/kep086

Dunn, A. J. (2000). Cytokine activation of the HPA axis. Annals of the New York Academy of Sciences, 917, 608–17. Retrieved fromhttp://www.ncbi.nlm.nih.gov/pubmed/11268389

McCarty, D. J. (1994). Gout without hyperuricemia. JAMA, 271(4), 302–3. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8295290

Mikuls, T. R., Farrar, J. T., Bilker, W. B., Fernandes, S., Schumacher, H. R., & Saag, K. G.(2005). Gout epidemiology: results from the UK General Practice ResearchDatabase, 1990-1999. Annals of the Rheumatic Diseases, 64(2), 267–72.https://doi.org/10.1136/ard.2004.024091

Nakagawa, T., Hu, H., Zharikov, S., Tuttle, K. R., Short, R. A., Glushakova, O., … Johnson, R. J. (2006). A causal role for uric acid in fructose-induced metabolic syndrome. American Journal of Physiology – Renal Physiology, 290(3).

Nuki, G., & Simkin, P. A. (2006). A concise history of gout and hyperuricemia and their treatment. Arthritis Research & Therapy, 8 Suppl 1(Suppl 1), S1.
https://doi.org/10.1186/ar1906

Pineda, C., Amezcua-Guerra, L. M., Solano, C., Rodriguez-Henríquez, P., Hernández-Díaz, C., Vargas, A., … Gutiérrez, M. (2011). Joint and tendon subclinical involvement suggestive of gouty arthritis in asymptomatic hyperuricemia: an ultrasound controlled study. Arthritis Research & Therapy, 13(1), R4. https://doi.org/10.1186/ar3223

Puig, J. G., de Miguel, E., Castillo, M. C., Rocha, A. L., Martínez, M. A., & Torres, R. J. (2008). Asymptomatic hyperuricemia: impact of ultrasonography. Nucleosides, Nucleotides & Nucleic Acids, 27(6), 592–5. https://doi.org/10.1080/15257770802136040

Richette, P., & Bardin, T. (2010). Gout. Lancet (London, England), 375(9711), 318–28. https://doi.org/10.1016/S0140-6736(09)60883-7

Richette, P., & Bardin, T. Purine-rich foods: an innocent bystander of gout attacks?, 71Annals of the Rheumatic Diseases 1435–1436 (2012). BMJ Publishing Group Ltd and European League Against Rheumatism. https://doi.org/10.1136/ard-2011-201215.Pineda

Roubenoff, R., Klag, M. J., Mead, L. A., Liang, K. Y., Seidler, A. J., & Hochberg, M. C. (1991). Incidence and risk factors for gout in white men. JAMA, 266(21), 3004–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1820473

Star, V. L., & Hochberg, M. C. (1993). Prevention and Management of Gout. Drugs, 45(2), 212–222. https://doi.org/10.2165/00003495-199345020-00004

Teng, G. G., Pan, A., Yuan, J. M., & Koh, W. P. (2015). Food sources of protein and risk of incident gout in the Singapore Chinese Health Study. Arthritis and Rheumatology, 67(7), 1933–1942. https://doi.org/10.1002/art.39115

Urano, W., Yamanaka, H., Tsutani, H., Nakajima, H., Matsuda, Y., Taniguchi, A., … Kamatani, N. Inflammatory Process in the Mechanism of Decreased Uric Acid Conc during Acute Gouty Arthritis.pdf, 29The Journal of rheumatology 1950–3 (2002). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12233891

Wallace, K. L., Riedel, A. A., Joseph-Ridge, N., & Wortmann, R. (2004). Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. The Journal of Rheumatology, 31(8), 1582–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15290739

Wang, J., & Dunn, A. J. (1999). The role of interleukin-6 in the activation of the hypothalamo-pituitary-adrenocortical axis and brain indoleamines by endotoxin and interleukin-1 beta. Brain Research, 815(2), 337–48. https://doi.org/10.1016/s0006-8993(98)01091-9

Zhang, Y., Chen, C., Choi, H., Chaisson, C., Hunter, D., Niu, J., & Neogi, T. (2012). Purine-rich foods intake and recurrent gout attacks. Annals of the Rheumatic Diseases, 71(9), 1448–53. https://doi.org/10.1136/annrheumdis-2011-201215

Comical Cricket!


This is why I think cricket is the funniest game there ever was, is and will be…

McCrory, in The Wonderful World of Cricket 1reckons this is how you’d explain cricket to an American or a Canadian:

‘You have two sides, one out in the field and one in. Each man that’s in the side that’s in goes out, and when he’s out he comes in and the next man goes in until he’s out. When they are all out, the side that’s out comes in and the side that’s been in goes out and tries to get those coming in, out. 

Sometimes, you get men still in and not out. 

When a man goes out to go in, the men who are out try to get him out, and when he is out he goes in and the next man in goes out and goes in.

There are two men called umpires who stay out all the time and they decide when the men who are in are out. When both sides have been in and all the men have been out, and both sides have been out twice after all the men have been in, including those who are not out, that is the end of the game!’

This comical, traditional version explaining what cricket really is, is found on tea towels in most test cricket venues in England – especially Lords (the famous Lord’s ‘Cricket Explained’ tea towel).

Nothing comical about Lord’s Cricket Ground though – it is one of the most stunning sporting venues that you’ll ever come across!

..The Fitness Doc at Lord's Cricket Ground, 2012

Me..at Lord’s Cricket Ground, July 2009

Reference:

  1. McCrory, P. (2007). The wonderful world of cricket. Br.J Sports Med, 41, 467-468.

RE-BLOGGED FROM 2013

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?!

122121HOW RAMPANT IS THE USE OF PEDs?

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!

122121333

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.

UPHOLDING THE SPIRIT OF THE GAME

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’.

SO, WHAT’S WRONG WITH THE ANTI-DOPING CODE?

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’.

DISCUSSION

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.

QUESTIONS TO PONDER OVER

  • 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.

CONCLUSION

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’!

DISCLAIMER

REFERENCES

(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.


We’ve always known about the ‘dumbbell pullover’. But have you ever wondered what it exactly does for you – in terms of stimulating prime movers, stabilizers and what-have-you that it hits. If you ask around, you – most likely – will get many different answers – most of them way off the mark. The dumbbell pullover is one exercise which most gym- goers know about but don’t have a clue to what it actually does!

So, let’s try to set the record straight; let’s have a closer look at what the dumbbell pullover is, what it does for you and why it is a good idea to combine it with core training rather than the traditional way of hitting it on a ‘chest day’.


Well, as opposed to what most PTs will tell you and what most people think, the pullover isn’t strictly a ‘chest exercise’. Well, it is, in some ways but I have always held that the dumbbell pullover is an exercise which doesn’t do very much for your pectorals. Rather it is an exercise that helps you expand / elevate your rib cage and stretches your abdominals. In that sense, it is a very effective exercise and should be a part of almost everyone’s training arsenal, more so if you are a young athlete or into endurance sports.

Costal_cartilages_frontalAs is apparent, when you are young, your costal cartilages (cartilages that attach you ribs to the sternum in the front – red structures in the illustration on the left) are more pliable (compared to the adult ones) and hence can be stretched out more. This stretch will effectively – over time – lead to increased circumference and internal capacity of the thoracic cavity (rib cage): meaning more leeway for the lungs to expand and hence improved cardio-respiratory status!

Now, if you follow the method that I recommend (and described here), you will make the pullover exercise more effective.

Before we have a look at my way of executing the dumbbell pullover, let us have a look at how it is done traditionally!


EXERCISE EXECUTION – THE TRADITIONAL WAY9295333258_78ae47d714_b

  1. Starting position – lie down on a flat bench, holding a single dumbbell (with both hands) at arm’s length over your chest (barbell can also be used for more advanced athletes
  2. Execution – lower the dumbbell to a point well past your head; as deep and low are you can – pull it back up to the staring position to complete a repetition
  3. Breathing – traditionally, this is how you are supposed to breathe…breathe in while lowering the dumbbell and breathe out while pulling it up
  4. Muscles worked – chest, shoulders, arms (isometric)

EXERCISE EXECUTION – THE WAY I RECOMMEND IT

To get the most out of a dumbbell pullover, do it on your core day…this is what you do:

pullovers

  1. breathe in when the dumbbell is held with extended arms on top of your chest
  2. breathe out as you lower the dumbbell…so as the dumbbell passes your head, make sure that have totally exhaled
  3. hold the dumbbell just below the head with arms flexed at the elbows; hyper-extend your thoracic vertebral column while keeping glutes firmly planted on the bench. Keep holding here…while you take a couple of deep breaths
  4. push your core in….and exhale totally (and I mean the last bits of air in the lungs). After you’ve exhaled completely, form a ‘box’ of your abdominal wall (i.e. suck you tummy in – also called a ‘vacuum’)
  5. all this while the dumbbell is not moving….
  6. when you can’t hold the ‘vacuum’ any longer, pull the dumbbell up
  7. reach the top, breathe in …and repeat the whole sequence..
  8. the hold should be long enough so that you are done in 4 to 5 reps per set
  9. if you don’t feel your rib cage and abdominals being stretched you are either using too light a dumbbell or aren’t doing it right

Alternate dumbbell pull over with exercise hanging leg raises and sit ups (or even wood-choppers) for better results.


WHAT THE DUMBBELL PULLOVER DOES

As opposed to popular notion, chest pullover is not a strictly ‘muscle-building’ exercise, rather it works more towards stretching your rib cage out, in effect increasing the capacity of your thoracic cavity – this would help cardiorespiratory endurance in the long run. Also, the ‘lifting up’ of the rib cage may help improves posture. Another important but most often overlooked function is the stretching and flattening of your core (function of the transversus abdominis muscle).


TAKE HOME MESSAGE

  1. Expands rib cage in young athletes – improves cardiorespiratory status and posture
  2. NOT STRICTLY FOR MUSCULAR DEVELOPMENT ALONE but, more so for stretching and inducing isometric contraction of abdominals

DISCLAIMER

 


SONY DSC


The whole town and his wife seems to be using whey protein.

Whey protein isolate – everybody knows – works; you know it works. It is the best protein for improving body composition (reducing fat while improving lean mass)! Or is it really?!

Whey protein isolate may be the best protein for you in most instances, that may not be the case always! Depending on your fitness goal, whey protein concentrate (and, even casein!) can sometime give whey isolate a run for its money. How is that?!

Well, read on to find out!

However, before we get into the nitty-gritty of which type of whey will best serve your purpose, let us get to know a bit more about why you should supplement with whey, in the first place.


Why should I take whey supplements?

Resistance training causes increase in muscle mass. This is due to increased muscle protein synthesis (MPS) that resistance training induces (Hulmi et al., 2009; Hakkinen et al., 2001; Hulmi et al., 2007). However, intense workouts alone are not enough to keep packing on lean muscle mass; you have to ‘stay anabolic’ most of the time to be able to keep that MPS working for you.

Without complicating matters, here’s a look at how resistance training increases lean muscle mass: a resistance training session causes muscle protein breakdown. This is then followed by repair of the damaged muscle tissue so that the muscles come out stronger the next time you hit the weights. For the muscles to get stronger, however, proteins ingestion (over and above normal needs) is crucial. Needless to say, the process of repair will suffer if you aren’t loading up on proteins.

That resistance training combined with protein supplementation causes muscle hypertrophy is well-documented (Moore et al., 2009; Hulmi et al., 2009; Cribb, Williams, Carey, & Hayes, 2006).  Ingestion of a whey protein supplement either immediately before or after a training session is – considered by some – to be the best for this purpose; also whey increases muscle protein turnover like no other protein. Furthermore, whey protein seems to work equally well in women as well (Josse, Tang, Tarnopolsky, & Phillips, 2010).

Another benefit of supplementing with whey is, improved post-workout recovery  This is likely due to the ‘anti-catabolic’ action of essential amino acids (Bird, Tarpenning, & Marino, 2006; Hoffman et al., 2010; Etheridge, Philp, & Watt, 2008).


What is Whey Protein?

You most likely know that whey is one of the 2 milk proteins – the other being casein. Casein is the more abundant of the two and it is casein that gives milk that white colour. In commercially available cow’s milk, 20% of protein is whey while the rest of it is casein (Hulmi, Lockwood, & Stout, 2010; Ha & Zemel, 2003; Etzel, 2004; Krissansen, 2007).

Whey is produced in large amounts as a by-product in the cheese industry. However, this whey has loads of fat, milk sugar (lactose) and salts in it and is not suitable for improving body composition.

During the process of whey purification, whey concentrate and isolate are produced sequentially. During the initial steps, larger molecules are separated out resulting in formation of whey concentrate. These larger molecules are proteins, lactose, immunoglobulins, amongst other less important ones. To produce whey isolate, cheese whey is passed through an ultrafiltration process (ion exchange or other methods). The ultra membrane filters fat, milk sugar (lactose), salts and other unwanted ingredients leaving behind a pure form of whey (Barile et al., 2009).

Hydrolysates, on the other hand, are formulations where large protein molecules are broken down into smaller fragments. The hypothesis is that this might further increase the rate of absorption of whey. However, this might not be totally true and hydrolysates may not offer much of an advantage over isolates or concentrates.


Types of Whey Protein

Whey is available commercially as either isolate or concentrate. ‘So, what’s the difference between them and which one should I be using’, you might want to ask?

The main difference between the two is the quality and the amount of protein content – isolate is purer and thus will contain almost 100% protein (well, 90-94% to be precise) while whey concentrate will contain protein ranging from 70-85%.

‘Well, that settles it – I am going with whey isolate!’, you might say. Hang on, not so fast! There is more to it than just protein content.


Comparing Whey Isolate and Whey Concentrate

Since whey isolate is higher in protein content, has a better amino acid ratio and thus bioavailability, it is absorbed into your system way quicker than whey concentrate (or any other protein, for that matter). That makes whey isolate the ideal post-exercise anabolic drink (Hulmi et al., 2009). Some researchers have suggested taking whey protein isolate before workouts as well in addition to your routine post-workout shake for maximum benefits (Esmark et al., 2001; Cribb & Hayes, 2006). Quicker absorption will mean almost instantaneous rise in blood amino acids which are then taken up by ‘hungry muscles’.

Having said that, the need for immediate post-workout protein supplementation in now being increasingly questioned (more below).

High protein content and higher quality of protein, however, that does not clinch the deal in favour of whey isolate. Concentrate has something up its sleeve that will make sit up and take notice!

As stated earlier, in comparison to isolate, whey protein concentrate will contain lesser amount of protein (in the range of 70-85%). However, somewhat similar to casein, whey protein concentrate will get absorbed slowly – this helps you stay anabolic for longer! Slower absorption also helps with absorption of other important nutrients from food like calcium. Not a lot of people know this but calcium plays an important role in causing fat loss (in addition to keeping your bones healthy)! Add to that the added benefit of appetite suppression for longer and casein suddenly become an important tool for your fat-loss goals or intermittent-fasting health journey…

Furthermore, whey protein concentrate is loaded with immunoglobulins – this helps boost your immune system and therefore may be beneficial in dealing with the intense stresses of training (especially if you happen to overtrain!).


Whey Isolate

Pros

    • pure; contains 90-94% protein!
    • purity means that it is great for gaining / maintaining lean mass while getting ripped (ideal when nearing competition or a photo shoot)
    • contains all essential amino acids in the best possible ratios
    • bioavailability for humans is best amongst all proteins – meaning, of the amount ingested, more is likely to be absorbed. For instance, in a scoop containing 25 g of whey isolate, almost all of the protein in there, will be going into your muscle
    • lightening fast absorption; ideal post-exercise drink – helps you get into the anabolic mode almost immediately

Cons

    • pricier than whey protein concentrate – to ensure purity, the commercial production of whey necessitates use of complex filtration procedure, hence the price
    • although whey isolate will help recovery after workouts, it loses out to whey concentrate in some respects. This is so because immune boosting constituents of milk protein like alpha – lactoglobulins and lactoferrins are removed during the purification process

Whey Concentrate

Pros:

    • lot cheaper than whey isolate
    • has a slower absorption rate than whey protein isolates; thus ensures a steady state of elevated amino acids in the blood and helps you stay anabolic for longer. This also reduces the need for frequent dosing
    • slower absorption helps with absorption of other important minerals like calcium and reducing blood glucose and lipid levels
    • induces appetite suppression which may help longer fasting interval, thereby improving body composition and metabolic disease parameters
    • contains immune boosting complexes (alpha – lactoglobulins and lactoferrins) which help post-exercise muscle recovery
    • helps fight diseases – for instance, chronic hepatitis C (Elattar et al., 2010)

Cons:

    • some amount of fat will be present so not ideally suited during times when keeping body fat% down is desirable
    • if you have any degree of intolerance to milk and dairy products, you might want to forget using whey concentrate on account of its lactose content – which is missing from the more purer whey isolate

TAKE HOME MESSAGE

In conclusion, isolate and concentrate are equally good – however, your circumstances – price, training goals and lactose intolerance – should tip the scales in favour of one or the other.


Recent developments

  1. More recently, the presence of a post-workout anabolic window (of opportunity) is being increasing questioned. ‘Not only is nutrient timing research open to question in terms of applicability, but recent evidence has directly challenged the classical view of the relevance of post-exercise nutritional intake with respect to anabolism’ (Aragon and Schoenfeld, 2013). The amount and quality of protein that you consume throughout the day is, now, thought to be more important than immediate post-workout whey ingestion.
  2. BCAAs (branched-chain amino acids – leucine, isoleucine and valine) may be overrated and ‘data do not seem to support a benefit to BCCA supplementation during periods of caloric restriction’ (Dieter BP, Schoenfeld BJ and Aragon AA, 2016).

Reference List

Aragon AA, Schoenfeld BJ (2013). Nutrient timing revisited: is there a post-exercise anabolic window? Journal of the International Society of Sports Nutrition. 2013;10:5 /1550-2783-10-5.

Barile, D., Tao, N., Lebrilla, C. B., Coisson, J. D., Arlorio, M., & German, J. B. (2009). Permeate from cheese whey ultrafiltration is a source of milk oligosaccharides. Int Dairy J, 19, 524-530.

Bird, S. P., Tarpenning, K. M., & Marino, F. E. (2006). Liquid carbohydrate/essential amino acid ingestion during a short-term bout of resistance exercise suppresses myofibrillar protein degradation. Metabolism, 55, 570-577.

Cribb, P. J. & Hayes, A. (2006). Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci.Sports Exerc., 38, 1918-1925.

Cribb, P. J., Williams, A. D., Carey, M. F., & Hayes, A. (2006). The effect of whey isolate and resistance training on strength, body composition, and plasma glutamine. Int J Sport Nutr.Exerc.Metab, 16, 494-509.

Dieter BP, Schoenfeld BJ, Aragon AA.(2016). The data do not seem to support a benefit to BCAA supplementation during periods of caloric restriction. Journal of the International Society of Sports Nutrition;13:21. doi:10.1186/s12970-016-0128-9.

Elattar, G., Saleh, Z., El-Shebini, S., Farrag, A., Zoheiry, M., Hassanein, A. et al. (2010). The use of whey protein concentrate in management of chronic hepatitis C virus – a pilot study. Arch.Med Sci., 6, 748-755.

Esmarck, B., Andersen, J. L., Olsen, S., Richter, E. A., Mizuno, M., & Kjaer, M. (2001). Timing of postexercise protein intake is important for muscle hypertrophy with resistance training in elderly humans. J Physiol, 535, 301-311.

Etheridge, T., Philp, A., & Watt, P. W. (2008). A single protein meal increases recovery of muscle function following an acute eccentric exercise bout. Appl.Physiol Nutr.Metab, 33, 483-488.

Etzel, M. R. (2004). Manufacture and use of dairy protein fractions. J Nutr., 134, 996S-1002S.

Ha, E. & Zemel, M. B. (2003). Functional properties of whey, whey components, and essential amino acids: mechanisms underlying health benefits for active people (review). J Nutr.Biochem., 14, 251-258.

Hakkinen, K., Pakarinen, A., Kraemer, W. J., Hakkinen, A., Valkeinen, H., & Alen, M. (2001). Selective muscle hypertrophy, changes in EMG and force, and serum hormones during strength training in older women. J Appl.Physiol, 91, 569-580.

Hoffman, J. R., Ratamess, N. A., Tranchina, C. P., Rashti, S. L., Kang, J., & Faigenbaum, A. D. (2010). Effect of a proprietary protein supplement on recovery indices following resistance exercise in strength/power athletes. Amino.Acids, 38, 771-778.

Hulmi, J. J., Ahtiainen, J. P., Kaasalainen, T., Pollanen, E., Hakkinen, K., Alen, M. et al. (2007). Postexercise myostatin and activin IIb mRNA levels: effects of strength training. Med Sci.Sports Exerc., 39, 289-297.

Hulmi, J. J., Kovanen, V., Selanne, H., Kraemer, W. J., Hakkinen, K., & Mero, A. A. (2009). Acute and long-term effects of resistance exercise with or without protein ingestion on muscle hypertrophy and gene expression. Amino.Acids, 37, 297-308.

Hulmi, J. J., Lockwood, C. M., & Stout, J. R. (2010). Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein. Nutr.Metab (Lond), 7, 51.

Josse, A. R., Tang, J. E., Tarnopolsky, M. A., & Phillips, S. M. (2010). Body composition and strength changes in women with milk and resistance exercise. Med Sci.Sports Exerc., 42, 1122-1130.

Krissansen, G. W. (2007). Emerging health properties of whey proteins and their clinical implications. J Am Coll.Nutr., 26, 713S-723S.

Moore, D. R., Tang, J. E., Burd, N. A., Rerecich, T., Tarnopolsky, M. A., & Phillips, S. M. (2009). Differential stimulation of myofibrillar and sarcoplasmic protein synthesis with protein ingestion at rest and after resistance exercise. J Physiol, 587, 897-904.


WOW! Why this sudden change of topic? Why are we shifting focus and suddenly not talking of fitness, nutrition, medicine and what-have-you – you might want to ask?

Well, because lately, it has come to my notice – I’m sure everyone who has been in research for a decent amount of time, knows – that people tend to believe that everything that science says is gospel (funny that!). And, any suggestions or hinting towards alternative thinking / reasoning is branded as foolish!

When in reality, science is just a method of inquiry. And, what you think is gospel is questionable as well. Almost everything that you know as truth or proven, is either a theory or a hypothesis; just that it may be most accepted world-wide because we may not have a better model or explanation.

In case, you are confused, lemme put things in context:

Just the other day, I had posted a link to one of my blogs on my facebook page – on the potential curative abilities of marijuana (originally, released in December, 2013).  One of my well-meaning colleagues – after reading the blog post – thought that, ‘well, that doesn’t prove anything’. Because all you are saying is that marijuana MAY or is ASSOCIATED with…’ And, not that it WILL cure.. let’s say diabetes and cardiovascular disease.

The following excerpt was what, probably, was the area of contention:

‘…recent use of marijuana IS ASSOCIATED with lower fasting insulin levels, decreased insulin resistance and reduced waist circumferences. Additionally, marijuana MAY CAUSE an elevated level of high-density lipoprotein cholesterol (HDL-C), the good cholesterol. Thus, in addition to protection against obesity and diabetes, marijuana MAY also help protect from cardiovascular diseases.

National surveys reported that regular use of marijuana is ASSOCIATED WITH reduced BMI (body mass index) and obesity.’

Well, yes… because recent evidence is in favour of just such a SURMISE that marijuana MAY help in these conditions. No one can say for sure that IT DOES!

And, that is the thing with almost everything that science has told you about almost everything. What you have to understand is that almost everything is a theory or a hypothesis or a surmise. No one can say for sure that such and such a thing is proven to be effective!

As Rupert Sheldrake – researcher, biologist and author – so eloquently puts in his banned TED talk (video below), science has become a world-view or a belief system for most ‘educated’ people – where everyone believes that if science says so, it must have been proven beyond doubt! When in actuality, everything is a theory or a hypothesis and is questionable. What’s more, it is the questioning abilities of the people who don’t believe in dogmas that usually help progress science; not the resigning to the fact that ‘oh, it is ‘proven’ so let’s not look at it again’.

To make you understand this better, I’d like you to watch Rupert Sheldrake’s banned TED talk below: notice how he talks about the gravitational constant (G) and how people never entertain the surmise that the laws of nature may not be as rigid as we are made to believe. Also, maybe the universal constants are not as constant as we think they are and maybe their values change from time to time and from place to place – all of this just because the laws of nature and the universal constants have been ‘PROVEN‘ to be constant!

TAKE HOME MESSAGE

Everything in science is a theory, a hypothesis, a surmise, someone’s perspective or view… what looks like the best available option at a given moment may end up as ‘proven’ in the layman’s psyche. That – however – cannot be furthest from the truth. Although, ‘proven’, everything still remains questionable!