Archive for the ‘General’ Category

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.


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


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.


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


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.


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


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’!


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.


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.


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


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.


  • 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


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.

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

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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!


  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)


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


  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.


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).


  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



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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!


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!

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Warming up and stretching before a workout (or a sports performance) is a routinely followed practice. A good warm-up routine followed by stretching prepares the athlete (physically as well as mentally) for the task at hand. Furthermore, anecdotal as well as scientific evidence supports the view that a cardio warm-up followed by stretching enhances performance and prevents injury 1;2.

Decreased flexibility leading to muscle strains (esp. hamstring strains) is a frequent occurrence in sports 3. Hamstring strains are a major reason for loss of playing time in international sport 4. Immense importance is, thus, attached to flexibility by athletes and their support staff.

Types of stretching

blog_pigeon_stretchSince a very long time, stretching has always been associated with preparing your body for exercise (or a ‘match-up’). Traditionally, gym goers and athletes and have learnt to stretch in two fundamental ways.

These are:

  • Static Stretching: a muscle is elongated to its longest possible length and then held for a pre-determined period of time (usually 30 seconds) 5, for e.g., a toe-touch stretch for the hamstrings.
  • Dynamic/ballistic Stretching: involves movement of a limb or the torso in a smooth and rapid (but under control) way from its normal, anatomical position to the fullest range and then back again. Ideally, dynamic stretches are performed for a pre-determined number of reps and sets (on either side in the case of limbs) 6. A brilliant example of dynamic stretching is ‘butt kicks’for the quadriceps.

What is good for you, dynamic or static stretching?

Most people believe that stretching is solely for increasing flexibility. While that is true for static stretching, not many realise that dynamic stretching improves agility, speed, power and strength as well – in addition to ‘warming’ you up. And, as we all know, these parameters define athletic ability more than flexibility alone. Thus, although static stretching is good for increasing flexibility’ dynamic stretching should be go to choice for exercisers and athletes.

  • If you want to increase flexibility:

Static stretching specifically increases flexibility. As such, it is recommended in injury rehab when increasing flexibility is the principle goal 7.

  • If you want to enhance sports performance:

Dynamic stretching has been shown to increase generation of muscle power during sports performance 8. More importantly, regular warm-up combined with dynamic stretching helps athletes learn new (and maintain known levels of) sensorimotor skills 9.

Static stretching, on the other hand, immediately prior to an exercise or a ‘match-up’ has been shown to be detrimental to performance 10;11. A number of theories have been proposed for this:

  1. decreased stability of joints caused by unduly excessive flexibility around joints (joint stability is required for twisting and turning; sacrificing joint stability is not such a great thing esp. in sports like soccer where one knee needs to be really stable while kicking with the other)
  2. inhibition of stretch reflex (which is crucial for storing kinetic energy in your muscles and thus, generation of power, esp. sports like weightlifting, track and field and basketball) – research has shown that static stretching reduces sprint times 12


The research community in sports medicine is totally divided with regards to the type of stretching most effective for enhancing performance and preventing injuries.

Research carried out in the past has favoured static stretching in preventing injuries 13. However, more recently, researchers have begun to report that static stretching may not improve performance or prevent injuries after all 14-16.

In a study conducted to find out the lasting effects of static stretching on muscle length, de Weijer et. al reported that static stretching may, in fact, be detrimental to sports performance 7.

Also, contrary to popular belief, the authors were of the opinion that a warm-up has no connection whatsoever with static stretches to be effective. Numerous others researchers also regard static stretching to be detrimental to athletic performance 11;17.


The latest recommendation, therefore, is to avoid static stretching immediate pre-performance. An aerobic, warm-up routine followed by dynamic stretching is the best strategy to prepare for an exercise session or a sporting encounter.


There is an exception to this recommendation though.

For excelling at any sport, the activation of the glutei is of utmost importance. This group of muscles provides stability to the torso as well as propulsive (jumping, running, etc) and rotational power (throwing, twisting and turning, etc). Keeping the antagonist (opposing) muscles relaxed thus makes sense in maximizing the involvement of the glutes.

Thus, static stretching of the hip flexors (iliopsoas) has been suggested as a good strategy to improve athletic performance.

Me personaly, I believe a movement-specific, loaded static stretch should help immensely, for example pause-squats prior to really loading up the bar should help!


Reference List

(1) McMillian DJ, Moore JH, Hatler BS, Taylor DC. Dynamic vs. static-stretching warm up: the effect on power and agility performance. J Strength Cond Res 2006; 20(3):492-499.

(2) Bishop D. Warm up I: potential mechanisms and the effects of passive warm up on exercise performance. Sports Med 2003; 33(6):439-454.

(3) Worrell TW, Perrin DH. Hamstring muscle injury: the influence of strength, flexibility, warm-up, and fatigue. J Orthop Sports Phys Ther 1992; 16(1):12-18.

(4) Orchard J, Seward H. Epidemiology of injuries in the Australian Football League, seasons 1997-2000. Br J Sports Med 2002; 36(1):39-44.

(5) Anderson B, Burke ER. Scientific, medical, and practical aspects of stretching. Clin Sports Med 1991; 10(1):63-86.

(6) Murphy DR. Dynamic range of motion training: An alternative to static stretching. Chiropractic sports medicine 1994; 8:59.

(7) de Weijer VC, Gorniak GC, Shamus E. The effect of static stretch and warm-up exercise on hamstring length over the course of 24 hours. J Orthop Sports Phys Ther 2003; 33(12):727-733.

(8) Reiman MP, Peintner AM, Boehner AL, Cameron CN, Murphy JR, Carter JW. Effects of dynamic warm-up with and without a weighted vest on lower extremity power performance of high school male athletes. J Strength Cond Res 2010; 24(12):3387-3395.

(9) Ajemian R, D’Ausilio A, Moorman H, Bizzi E. Why professional athletes need a prolonged period of warm-up and other peculiarities of human motor learning. J Mot Behav 2010; 42(6):381-388.

(10) Booth L. Mobility, stretching and warm-up: Applications in sport and exercise. SportEX Medicine 2008; 37:20-23.

(11) Shrier I. Does stretching improve performance? A systematic and critical review of the literature. Clin J Sport Med 2004; 14(5):267-273.

(12) Fletcher IM, Jones B. The effect of different warm-up stretch protocols on 20 meter sprint performance in trained rugby union players. J Strength Cond Res 2004; 18(4):885-888.

(13) Hartig DE, Henderson JM. Increasing Hamstring Flexibility Decreases Lower Extremity Overuse Injuries in Military Basic Trainees. The American Journal of Sports Medicine 1999; 27(2):173-176.

(14) Malliaropoulos N, Papalexandris S, Papalada A, Papacostas E. The role of stretching in rehabilitation of hamstring injuries: 80 athletes’ follow-up. Med Sci Sports Exerc 2004; 36(5):756-759.

(15) Mason DL, Dickens V, Vail A. Rehabilitation for hamstring injuries. Cochrane Database Syst Rev 2007;(1):CD004575.

(16) Pope RP, Herbert RD, Kirwan JD, Graham BJ. A randomized trial of preexercise stretching for prevention of lower-limb injury. Med Sci Sports Exerc 2000; 32(2):271-277.

(17) Winchester JB, Nelson AG, Landin D, Young MA, Schexnayder IC. Static stretching impairs sprint performance in collegiate track and field athletes. J Strength Cond Res 2008; 22(1):13-19.


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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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