This is not going to be a long in-depth blog. In fact, it will simply provide a very condensed review of the paper recently published by Churchward-Venne et al (2016) in the Sports Medicine journal where they discuss: “the current state of evidence regarding the dose-dependent relationship between dietary protein ingestion and changes in skeletal muscle protein synthesis during recovery from resistance-type exercise in older adults. They provide recommendations on the amount of protein that may be required to maximize skeletal muscle reconditioning in response to resistance-type exercise in older adults.”
With an approximately $US50 cost to access this article, most will simply not be willing to fork out that sort of money. So I wanted to outline the key points that were made in this article and provide a little bit more than what appears in the below online abstract. If you have any questions or want further information just leave a comment at the end of the article and I’ll get back to you as soon as possible.
Whey Protein Increases Myofibrillar Protein Synthesis Rates
ABSTRACT: Hyperaminoacidemia following protein ingestion enhances the anabolic effect of resistance-type exercise by increasing the stimulation of muscle protein synthesis and attenuating the exercise-mediated increase in muscle protein breakdown rates. Although factors such as the source of protein ingested and the timing of intake relative to exercise can impact post-exercise muscle protein synthesis rates, the amount of protein ingested after exercise appears to be the key nutritional factor dictating the magnitude of the muscle protein synthetic response during post-exercise recovery. In younger adults, muscle protein synthesis rates after resistance-type exercise respond in a dose-dependent manner to ingested protein and are maximally stimulated following ingestion of ~20 g of protein. In contrast to younger adults, older adults are less sensitive to smaller doses of ingested protein (less than ~20 g) after exercise, as evidenced by an attenuated increase in muscle protein synthesis rates during post-exercise recovery. However, older muscle appears to retain the capacity to display a robust stimulation of muscle protein synthesis in response to the ingestion of greater doses of protein (~40 g), and such an amount may be required for older adults to achieve a robust stimulation of muscle protein synthesis during post-exercise recovery. The aim of this article is to discuss the current state of evidence regarding the dose-dependent relationship between dietary protein ingestion and changes in skeletal muscle protein synthesis during recovery from resistance-type exercise in older adults. We provide recommendations on the amount of protein that may be required to maximize skeletal muscle reconditioning in response to resistance-type exercise in older adults.
Key points
The key question often posed in relation to diet and resistance training is: “How much protein should I consume after a workout/training session to maximise the adaptive response to resistance-type exercise?”
Whilst the answer to this question is not entirely clear what is known is that this depends on 4 key things: age, bodyweight, energy balance and possibly training status.
Evidence shows that maximising skeletal muscle protein synthesis rates during recovery from resistance training exercise in younger adults is sufficiently accommodated by the ingestion of ∼20 g of protein or ∼0.25 g protein/kilogram bodyweight.
Older adults demonstrate a blunted post-prandial muscle protein synthetic response.
However, older adults as opposed to younger adults require higher amounts of protein during recovery from resistance training exercise to optimally stimulate muscle protein syntheis. Intakes even up to ∼40 g appear necessary.
No consensus currently exists regarding the amount of protein required to maximally stimulate skeletal muscle protein synethsis rates during recovery from resistance training exercise in older adults.
The Future Treatment For Sarcopenia-induced Muscle Atrophy?
Given that older adults not involved in resistance training or vigourous physical activity require an increased intake of protein relative to younger adults, a higher protein intake seems warranted post-exercise after performing resistance training.
Leucine-enriched whey protein or increased EAA providing 3.5 g leucine have prolonged the duration of the increase in myofibrillar protein synthesis rates following resistive exercise in older men.
Technically, the capacity of older skeletal muscle to robustly respond with increased protein synthetic response post-resistive exercise may relate to leucine-mediated increases in p70S6K1 (Thr389) phosphorylation and/or amino acid transporter expression.
The availability of dietary protein-derived amino acids within the circulation following protein ingestion is reduced in older adults.
The ‘optimal’ dose of ingested protein as previously mentioned may therefore be double (∼40 g) that required by younger adults.
The dose of ingested protein to induce a maximal stimulation of muscle protein synethesis following resistive exercise appears to increase during energy deficit versus energy balance.
Greater rates of muscle protein synethesis have been demonstrated when 30 g versus 15 g of whey protein were consumed after training in younger adults when under conditions of mild energy deficit.
Older adults in energy deficit and engaged in resistive exercise may require even higher amounts of post-exercise protein >40 g but <50 g; however, this is based entirely from extrapolating from younger adults and is therefore speculative at this point in time
There is a lack of data as to the amount of ingested protein required to maximally stimulate skeletal muscle protein synthesis after resistance-type exercise in younger and older women.
Continued research is required to unravel the contribution of ageing versus age-related decreases in physical activity on anabolic resistance and whether or not resistive exercise and/or increases in physical activity can reduce age-related anabolic resistance to protein feeding.
Work on masters athletes with above-average fitness and muscular strength will hopefully help researchers decipher the exact nature of anabolic age-related resistance.
It is envisaged that this will provide valuable guidance on how best to attenuate these changes through resistive exercise and/or physical activity in addition to nutritional strategies aimed at facilitating maximal muscle protein synthesis.
Reference
Churchward-Venne TA. et al. (2016) “What is the Optimal Amount of Protein to Support Post-Exercise Skeletal Muscle Reconditioning in the Older Adult?” Sports Medicine (see here for publication)
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to improve muscular strength, physical function (how you move around during the day) and quality of life or programs to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
FitGreyStrong fact: Weight gain occurs when total caloric daily consumption exceeds total daily energy expenditure. To achieve weight or fat loss there must be an energy or caloric deficit. Over 80 years of scientific research has confirmed this to be fact.
FitGreyStrong Advice: Don’t believe the hype. Food quality is a must and essential to good health. However, weight or fat loss will not be realised no matter how good your diet is unless an energy deficit exists. Increased total physical activity during all waking hours and an energy-deficit diet that is wholesome, natural, minimally-processed and nutrient-dense will provide a significant opportunity for weight loss to be achieved.
I’m going to make a confession. I have laboured over the last month to write this blog. I’ve spent hour upon hour trying my best to explain what I think is a simple concept. The strangest thing is the evidence published so far is conclusive but with so much shit floating around anyone looking to lose a few kilo’s in the New Year is faced with a major challenge. What info is good and what is bad? How does one decipher what advice to act on and what advice to send to the computer’s recycle bin?
As I explained recently the media and ‘rogue’ researchers have, in some ways, muddied the weight loss debate by promoting the idea that exercise doesn’t help (see here). There are many examples of the media misleading consumers by sensationalising material that has been poorly researched, lacks objectivity and obfuscates the facts.
Ironically, it is this type of questionable and controversial material that gains the most traction with the public. The confusion created by such reporting has had a truly dreadful impact on the public’s perception regarding the role of exercise for weight loss. Many health care professionals working in the field have also raised serious concerns about this too because there is the feeling that some people may simply avoid physical activity altogether.
Notwithstanding that compensatory mechanisms mitigate the efficacy of exercise in some people (see here), widespread consensus remains elusive regarding the very basic underpinnings of weight loss. It seems incredible in fact that in the year 2016 vigorous debate and disagreement continues to swirl. However, I believe that the writing was on the wall when Generation X’s were still kids. There was sufficient scientific research carried out from the 1930s to the 1980s to put to bed and move on from some of the most hotly contested questions relevant to weight loss. The two questions which continue to inspire fierce debate are:
1. Do calories really matter?
2. Is weight loss simply a matter of expending more energy than you consume?
Before outlining what the specific focus of this blog is I need to digress. I want to make clear that it is not my intention here to assess whether manipulating the macronutrient makeup of the diet – e.g. high fat versus high carb diets – yields superior benefits on metabolic outcomes such as fasting blood glucose or lipid profile. Of course, this is a very important question to address but I’ll have bitten off way more than I can chew to do this justice, so I’ll come back to this another time.
The only thing I will say is that the actual published research is mixed. Three meta-analyses and systematic reviews have been completed over the last 18 months assessing whether metabolic outcomes are affected by manipulating macronutrient composition. Two of the these (see hereand here) concluded that there were no differences on metabolic outcomes when the protein, carbohydrate and fat composition of the diet was varied; whilst the other paper (see here) suggested the opposite stating that dietary manipulation did alter metabolic outcomes.
Ok, let’s get back to what the focus of this blog is then.
Is obesity a disease?
The aim of the following is to shine a spotlight on and explore the mechanistic aspect of weight loss. You may be wondering…………. what the bloody hell does that mean? What I mean by ‘mechanistic’ is the basic physiological state required – in our species, Homo sapiens – to bring about weight loss.
To state this as simply as possible, when it comes to weight loss the single most important factor from a physiological perspective is that there exists an energy or caloric deficit. Eighty-five years of scientific research and investigation has demonstrated without equivocation that for weight loss to occur an energy deficit must exist. Total daily energy expenditure has to exceed total daily energy intake for any reduction in body mass to occur or vice versa for any increase to occur. Regardless of one’s age, race or gender this holds true. This really is the only conclusion you can draw if you actually read the studies that have been published in reputable peer-reviewed medical journals relevant to this area (see here).
Now some of you may disagree with me on this and you are not alone. Unfortunately, in my view, there are a number of dissenting voices from a variety of quarters that simply don’t believe this to be true. They passionately dispute this and contend that the total energy provided by the diet matters very little. What really counts is the metabolic effect food has on our body. An example of this type of thinking can be found here.
Supporters of such thinking, decouple weight loss and calories. They propose that the “metabolic propensity” to increase and store fat in the adipose cells is driven primarily by the quality of the foodstuffs ingested and the proportion of protein, carbohydrates and fat in the diet. “A calorie is not a calorie” because different foods of different qualities have different effects on our digestion, hormones, biochemistry, metabolism, thermogenesis, physiology and associated internal feedback loops.
Whilst the total energy or calorie content of food matters, what is significantly more important is the metabolic effect that food has on our body. All calories are not created equal, therefore, with the quality and type of food choices made and the subsequent metabolic effect that such choices have on our body ultimately determining if fat loss is successful or not.
The most significant and telling problem with this line of thinking is that there are virtually no respected and acknowledged researchers who believe it. I see this as a telltale sign that the dissenters are simply barking up the wrong tree. Virtually all leading obesity experts worldwide concur that unless there is an energy deficit, decreases to weight or fat mass are not possible irrespective of how good the diet is. The question needs to be asked, why is this the case?
FitGreyStrong’s take-home message to you up to this point is:
Unless you expend more than you take-in you ain’t going to see any changes to your weight or fat.
Resistance and weight training shows great promise to maximise fat loss
There exists consensus amongst nearly all scientists because of the following. Research undertaken with participants confined to an in-patient hospital setting or in facilities known as metabolic units are currently the most accurate way to scientifically determine the specific energy requirements needed for weight change. Such studies are usually expensive because they are very resource and equipment intensive. However, what they allow researchers to do is measure what is being consumed (energy in) and what is being expended (energy out) quite precisely – or at least, a lot more precisely than studies that involve free-living subjects.
In brief, the methodology of such studies looks something like this:
For the duration of the trial subjects have to remain in the hospital or unit.
Participants of these studies are allocated and given all consumables (food and drink) for the duration of the intervention.
The caloric content of what is consumed is a known entity and has been prepared and accurately measured.
The macronutrient percentages of the diet for protein, carbs and fat has been determined.
Physical activity is closely monitored, measured and accounted for.
Resting energy expenditure (REE) and total daily energy expenditure (TDEE) is estimated as accurately as possible based on the equipment utilised and methods employed in the study.
With energy intake and energy expenditure measured as close to actual as possible, investigators can now establish whether the prerequisite for weight loss is an energy deficit. Over the last 80 years or so there have been over 20 studies carried out that have assessed the effect of calorie and macronutrient manipulation on weight loss whilst in the strict confines of hospital or metabolic unit.
Evaluation of such research has shown that no major differences have been found for weight or fat loss when diets of different macronutrient composition but with the same amount of energy (i.e. isoenergetic diets) were compared. Results from these studies show beyond dispute that the key determinant for decreased weight is a caloric or energy deficit, not diet composition.
To look at the evidence another way, not one of these trials – not even one – has ever demonstrated an increase in body weight when daily energy intake is less than daily energy expenditure. Likewise, no such study has ever shown a decrease in body weight when daily energy intake exceeds daily energy expenditure. This remains so irrespective of the macronutrient breakdown.
To give you a taste of the studies that have incorporated some of the methods referred to above, let’s take a quick look at a few of these:
Study 1 – Graves and colleagues conducted a randomized trial comparing an energy-restricted high-protein versus high-carbohydrate, low-fat diet in the morbidly obese which was published in the Obesity Journal (see here). Eighty-eight obese participants (mean age, 46.7; mean BMI, 45.6 kg m squared) were enrolled in a 3-week inpatient and 48-week outpatient treatment. The study was novel in that it included cognitive behaviour therapy in the treatment. All subjects consumed a restricted diet (1,200 kcal/day for women, 1,500 kcal/day for men; 20% energy from fat, <10% saturated fat). The high-protein diet derived 34% energy from proteins, 46% from carbohydrates; the high carb diet derived 17% from proteins, 64% from carbohydrates. The primary outcome was 1-year percent weight loss and secondary outcomes were attrition rates, changes in cardiovascular risk factors and psychological profile. The three week in-patient period closely monitored and provided all food with the total energy content and macronutrient composition known.
No difference in BMI or weight reduction was detected for this period between each diet.
The authors concluded (pg.1774) that:
“the relative carbohydrate and protein content of the diet, when combined with intensive CBT, does not significantly affect attrition rate, weight loss and psychosocial outcome in patients with severe obesity”.
Study 2 – Golay and co-workers compared diets equally low in energy (1000 kcal) but widely different in relative amounts of fat and carbs on body weight reduction in 43 obese adults during a 6-week period of hospitalisation (see here). The diets were composed of 32% protein, 15% carb and 53% fat versus 29% protein, 45% carb and 26% fat. The first diet could be described quite well as a low-carb, high-fat diet and the second diet as a more balanced diet. After 6 weeks no significant differences were seen for weight loss, fat loss or waist-to-hip circumference. Energy intake, not nutrient composition, determined weight loss in response to low-energy diets.
Study 3 – Leibel and co-workers established in 1992 that even during very wide variations in the fat-to-carbohydrate ratio (fat energy varied from 0% to 70% of total intake) there was no significant variation in energy need and changes in body weight (see here). Sixteen human subjects were confined to a metabolic ward for an average of 33 days and fed precisely known liquid diets with protein derived from milk and fat varied from different amounts of corn oil. Total energy intake, not diet composition was once again the key determinant in modulating energy balance.
I could continue and summarise the other studies published but the overall findings are much the same as that described above. For a more extensive review of these type of studies please see here.
Confusion around this topic, I think, has been created by other research and weight loss trials that don’t take place in the confines of a hospital or metabolic unit, but rather use free-living subjects. These studies cannot accurately quantify energy intake and expenditure and they are hence plagued by problems.
Firstly, participants often have to record or attempt to recall what they ate and drank. It probably doesn’t surprise you then that this has been shown to be notoriously inaccurate. Even those studies that provide free-living subjects with their allotment of food and drink can’t completely prevent or control for individuals eating or not eating the food on their assigned ‘menu’. Secondly, energy expenditure is estimated via physical activity logs, diaries, pedometers or fancy equipment like activPAL (see here). Consequently, energy expenditure can often be under- or over-estimated so such data can be terrible misleading. To state the obvious, deriving definitive results and conclusions from these types of studies is going to be challenging.
In spite of the caveats mentioned above, the results from the many studies using free-living subjects concurs with the hospitalisation and metabolic unit studies. Two meta-analyses and systematic reviews published in 2014 and 2015 concluded the same thing:
“Both types of macronutrient-centered weight loss diets produced weight loss. Manipulation of macronutrient composition of weight loss diets does not appear to be associated with significantly different weight loss or metabolic outcomes.”
The massive 2014 review by Naude and colleagues (see here) assessed 228 studies making it one of the largest meta-analyses and systematic reviews available. Provided one reads and reviews such research with an objective and impartial mind it is implausible to reach any other conclusion.
A final comment: The one thing that I believe provides the biggest hint that total calories are indeed fundamental to weight loss is something that is noticeable in the methodology of the more scientifically robust studies. Of the research that has taken place in a hospital or metabolic unit setting there is one key characteristic that most of these studies determine before proceeding to the weight loss phase of the trial. Can you guess what it is? Researchers establish energy requirements (i.e. total daily caloric intake) for weight maintenance over a period of 1 to 2 weeks (see here). If for arguments sake, calories were not important for inducing weight loss, then establishing energy requirements for weight maintenance in these studies would be a pointless exercise.
Before I finish up I need to make some clarifying comments.
1. Those that make the claim that calories are not important in relation to the obesity problem or when trying to decrease body fat are doing, I think, either one of two things. They are ignoring the data produced from hospital/metabolic unit-based studies and/or they are misinterpreting and taking at face value the results of research conducted with free-living subjects.
2. There will be those that read this and conclude that what I am advocating or all that I think matters is calories, with diet quality just a cursory concern. I can hear some of you saying right now “….but surely 2500 calories of jelly beans or junk food is different to 2500 calories of atlantic salmon, walnuts, broccoli and berries.” Really? Well, yes, of course it is, thanks for pointing that out. A diet consisting of wholesome, natural, minimally processed and nutrient-dense foods is paramount to ensuring good health. I should state now that I am not suggesting for one moment that the quality of the diet is not important.
Food quality is key for health and weight management
3. Irrespective of how good a diet is in optimising the metabolic effect on your body, the fact remains nonetheless that it is still possible to gain weight eating a wholesome, natural, minimally processed and nutrient-dense diet. It is probably more difficult to do so, but regardless, you cannot escape the fact that you have to be in a consistent calorie deficit to lose fat or a chronic caloric surplus to gain fat.
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to lose weight, improve muscular strength, physical function (how you move around during the day) and quality of life or programs to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
In my article titled “It can’t possibly be true, can it?” I questioned whether there was any foundation to the claim that inactivity is not a chief cause obesity and provided scientific evidence suggesting otherwise. Today I will try explain to you what the bottom-line is as to why exercise doesn’t work for everybody trying to lose weight. One thing I have noticed is that there isn’t enough time or effort – either in the media or on the net – dedicated to informing the public about why exercise does not work for some people and what can be done about.
Exercise has been successfully applied as an essential ingredient of many weight loss programs. By increasing total daily energy expenditure, creating a caloric deficit state is theoretically, at least, more likely. It naturally follows that the weight loss achieved will be correlated to the magnitude of the energy deficit created. In practice however this does not always happen. In fact, there are a number of studies and anecdotal evidence that show a significant proportion of exercisers eating an ad libitum diet (possibly as high as 50%) do not achieve the weight loss expected with as many as 15% actually gaining weight. These individuals are often referred to as ‘non–responders‘. Those on the other hand that do achieve weight loss from exercise are referred to as ‘responders‘. The question is, how is this possible and are there any practical solutions?
Energy compensation and exercise-induced fat loss
People respond differently to exercise:
Non-responders vs responders
These differences in response to exercise include:
Non-responders increase whilst responders decrease, total daily energy intake (all the food and drinks you consume on a daily basis).
Some of these differences apparently occur unbeknownst to the exerciser so there is some sort of compensation going on to offset the extra energy expended from exercise.
Non-responders increase their consumption of fat.
Non-responders experience much greater subjective sensations of fasted hunger (upon waking) and hunger across the day compared to responders.
Non-responders demonstrate an increased whereas responders show a decreased, desire to eat.
Non-responders satisfaction or feelings of fullness from meals is significantly reduced whilst there are no changes in responders.
Behavioural compensatory adjustments to exercise training in overweight women showed the loss of weight/fat mass or lack thereof, was attributable to an increase or decrease in spontaneous physical activity, respectively.
Resting metabolic rate may be reduced in non-responders but not in responders.
Brain function and weight control is poorly understood
If you are struggling to lose weight after starting an exercise regimen then you could be classified as a non-responder and should consider the following:
If possible, have some measurements taken by a knowledgeable professional that includes girths (such as hips, waist, thighs etc) and skinfolds where the subcutaneous fat can be approximately measured by calipers. By doing this you will be able to work out more precisely what changes are actually taking place. This is pretty important because some ‘non-responders’ will lose a considerable amount of fat but total weight loss may be only slight or actually increase (see King et al 2008). This will affect roughly 10% of exercisers that are trying to lose weight but these body composition changes are in fact desirable and favourable.
Monitor energy intake more closely and consider recording actual food and beverage intakes so you can keep tabs on this as you go. Given that ad libitum diets don’t seem to work too well for non-responders, recording your intake is a good place to start. Assuringly, research shows that those that diarise what they are eating and drinking are much more successful at weight loss and weight management compared to those that don’t, so start recording.
Recognise that if you keep accurate records of these things and create an energy deficit – the research that has been conducted in metabolic-ward studies suggests – that weight loss is highly probable. Based on an account of energy intake and energy expenditure, if the creation of an energy deficit does not elicit any change in body composition, it is likely that there has been an over-estimation of energy expenditure or an under-estimation of energy intake, or a combination of both. However, this now allows subtle changes to be made to energy expenditure or intake so that body fat mass reduction can be realised (see here and herefor great discussions on the crucial role calories play when it comes to fat loss or fat gain).
Ensure that your exercise program includes some resistance or weight training. The response to exercise of non-responders as outlined above is related specifically to 1-2 hours of aerobic exercise (i.e. walking, running, cycling etc). You may ironically achieve better weight loss if you back off the aerobic exercise but place a bit more emphasis on weight training or resistance-type exercise. Some researchhas shown that appetite is suppressed more so with resistance versus aerobic exercise and it is the changes of increased appetite in non-responders that presents a major problem when attempting to bring about sustainable weight loss. With respect to adults who are overweight or obese, Drenowatz& colleagues clearly demonstrated that resistance exercise but not aerobic exercise reduced fat mass.
Resistance training is very effective to facilitate fat loss
This form of activity also substantially reduces the risk of losing LBM (lean body mass = muscle tissue) in older adults (see Villarealet al). It is very common to see exercisers lose significant amounts of LBM when only aerobic exercise is undertaken while in an energy deficit state.
The loss of LBM is not desirable for 2 key reasons. Firstly, functional physical capacity could be affected in both the short and long term (see Villrealet al). Secondly, resting metabolic rate will be reduced thereby making weight loss more difficult and weight regain more likely (see herefor further discussion).
“Don’t put the cart before the horse.” By that I mean, the quality of what you decide to eat will have a massive impact on your success. A caloric deficit is the goal but it should be achieved with a diet consisting of wholesome, natural, minimally processed and nutrient-dense foods. Not only is this essential to weight loss success but more importantly generating good health.
No caloric deficit = no fat loss
To combat increased subjective sensations of hunger, then, as a start please make sure that the diet is high in a variety of vegetables, has several serves of fruit each day, contains sufficient and varied sources of protein and includes things like nuts, seeds and oils. This is pretty commonsense stuff but you need to put into practice what actually works. The make-up or quality of the diet appears to impact on subsequent appetite, sensations of hunger and feelings of fullness, so anything that assists in keeping the physiological drives to eat at bay are only going to be helpful (see Blundellet al).
References (in no particular order)
Drenowatz, C. et al. (2015) “The prospective association between different types of exercise and body composition” Medicine & Science in Sports & Exercise. 47(12): 2535-2541.
Manthou, E. and Gill, J.M.R. and Wright, A. and Malkova, D. (2010) Behavioural compensatory adjustments to exercise training in overweight women. Medicine and Science in Sports and Exercise, 42 (6). pp. 1121- 1128.
Melanson, E.L. et al. (2013) “Resistance to exercise-induced weight loss: compensatory behavioural adaptations” Med Sci Sports Exerc.August; 45(8): 1600-1609.
King N.A. et al. (2008) “Individual variability following 12 weeks of supervised exercise: identification and characterization of compensation for exercise-induced weight loss.” International Journal of Obesity. 32: 177-184
King N.A. et al. (2009) “Dual-process action of exercise on appetite control: increase in orexigenic drive but improvement in meal-induced satiety.” Am J Clin Nutr. 90: 921-927
Peterson N.D. et al. (2014) “Dietary Self-Monitoring and Long-Term Success with Weight Management”. Obesity 22, 1962–1967
Broom, D.R. (2008) “Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males” American Journal of Physiology. 296(1): R29-R35.
King, N.A. et al (2012) “Exercise, appetite and weight management: understanding the compensatory responses in eating behaviour and how they contribute to variability in exercise-induced weight loss.”British Journal of Sports Medicine 46(5):315-22.
Villareal D.T. et al. (2011) “Weight Loss, Exercise, or Both and Physical Function in Obese Older Adults.” N Engl J Med 364(13): 1218-1229
Blundell J. et al. (2010) “Appetite control: methodological aspects of the evaluation of foods.” Obe Rev 11(3): 251-270
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to achieve the above-mentioned benefits or to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
The following article is a long review and appraisal of a study that investigated the effects that sitting had – with and without caloric restriction – on metabolic health and compared this to a group that was physically active. This was designed in an attempt to independently tease out just what effect – firstly, the action of sitting and secondly, the state of energy surplus – has on metabolic health. The take-home message is very simple; prolonged sitting is very bad for you. Period.
In summary, the following conclusions can be made:
Just one day of prolonged sitting had a profound effect on insulin action.
Sitting therefore has a direct effect on metabolic health by substantially reducing the body’s ability to dispose of, or “metabolise” the foods we consume.
These negative effects occurred in young, healthy and non-obese individuals.
Future research is required to determine if factors such as aging, obesity, health comorbidities and inactivity interact independently or synergistically to cause further metabolic dysfunction.
Decreasing energy or caloric intake to more closely match the energy requirements of prolonged sitting only reduced – by approximately half – the harmful effects of sitting on insulin action.
Inactivity and sedentariness causes substantial metabolic dysfunction with sitting a primary driver of poor insulin action and pivotal contributor to increased risk for more serious health complications.
Now for those that want the in-depth analysis, please read on………………………………..
A few years ago, researchers Dr Brooke Stephens, Dr Barry Braun and colleagues from the Department of Kinesiology, University of Massachusetts (USA) reported on an intriguing studyin the journal, Metabolism – Clinical and Experimental. In fact this piece of research was acknowledged with the top cited paper awardfor this journal in 2012 and was essential in highlighting the insidious dangers that inactivity and in particular, sitting, has on metabolic health. What they showed was that inactivity appears to negatively affect metabolic health and insulin action independently of diet. In fact, dietary manipulation whereby total energy intake is reduced – to match low energy expenditure requirements when primarily sitting all day long – was unable to fully mitigate the detrimental consequences of inactivity. What this suggests is that physical movement in and of itself is integral to metabolic function and health. The exact mechanisms that cause prolonged sitting to be so bad for our health are yet to fully understood but there is certainly some evidence that low to very low stimulation of skeletal muscle is central to this issue.
Whilst this seems to pass the common sense test, this is quite significant because many of the themes on the net and in the mass media that discuss ways of improving metabolic health focus heavily on diet, but relatively less time and energy seems to be dedicated to exploring the detrimental effects of inactivity largely accumulated by spending long periods of time sitting. I call this the
diet fixation syndrome
and it manifests in a utopian idea that diet and nutrition can fix almost anything. Enhancing health and wellbeing via diet is certainly a worthwhile cause but many pontificate their beliefs in such a manner whereby they assume some moral high ground lost in an idea that the consumption of “their” diet is as nature intended and then maintain with religious fervidness that any deviation from this ‘correct’ dietary approach will be somehow toxic, dangerous and unhealthy. “They” can’t all be right, can they? By “They” I mean the paleos, the vegans, the High-Fat Low-Carbers, the High-Carb Low Fat crowd, etc etc. I am not saying that the food we feed our body is unimportant but I do think that there needs to be more acknowledgment and discussion of the diabolical impact inactivity has as demonstrated by a significant body of scientific evidence. Otherwise, we will continue to see the oxygen sucked from, and being straggled and muffled by, the nutrition “hype”.
What is the best diet?
OK, well that’s enough with the popular culture critique; now let’s look at some of the science behind what happens to metabolic health when we are sedentary and I’m afraid to say the picture is pretty ugly. In this study Stephens and co. recruited fourteen recreationally active men (n=7) and women (n=7) between the age of 19 and 32 participated, of whom none were obese, all were in good health, non-smoking, free of known disease, not following a very low or very high carbohydrate diet (<30% or >70%), and none were taking any medications or supplements known to alter carb or fat metabolism. The intention of the study was to compare all participants for each test condition.
The 3 test conditions were: (1) an active condition with minimal sitting (energy expenditure and intake were both high) referred to as NO-SIT; (2) Prolonged sitting with no change in energy intake meaning that there was low activity but high energy intake i.e energy surplus referred to as SIT; (3) Prolonged sitting but energy intake was adjusted downward and accordingly to body weight (approximately 1000 kcal reduction) and this was referred to as SIT-BAL. Insulin action was defined as whole-body rate of glucose disappearance normalised to mean plasma insulin and this was determined following a continuous infusion of glucose after an overnight fast (13-14 hours) after each of the test conditions outlined above.
Insulin action was used as a proxy measure of metabolic health with better metabolic function reflected by lower insulin production, higher glucose metabolism and storage. Subjects completed each 24-hour laboratory condition with at least a week between visits. For the 2 days before each 24-hour test condition, attempts were made to ensure that eating and activity behaviour were standardised. Once in the laboratory room each subject was provided access to a computer, internet, books, magazines, or movies throughout the day and evening. Lunch and dinner during the test was standardised. Average energy intake and expenditure across each condition was approximately as follows (please click image for larger and clearer view):
Activity or inactivity was quantified using an activPAL professional physical activity monitor and this has been shown to be an accurate and reliable measurement tool to determining motion. Standardised meals based on body weight were provided. Total sitting, standing, and stepping time, and number of steps during the three 24-hour conditions was as follows:
So basically picture this. When subjects did the SIT and SIT-BAL experiment they sat and lounged around all day in a lab room, watching video’s, surfing the net and reading mags and doing as little as possible, with SIT able to indulge and eat well over what they needed whilst SIT-BAL had their food intake dramatically reduced so it matched the low energy they had burnt. Interestingly, it is the SIT condition which probably represents a significant portion of how many people spend their day so the results would provide some insight to what is really going on in those who are grossly sedentary and in energy surplus on a day-to-day basis.
In comparison, the NO-SIT ensured that subjects were on the go: stood while reading, talking on the phone, whilst on the computer; made subjects walk and accumulate at least 10,000 steps/day, perform tasks such as dish washing, sweeping, dusting etc. After spending 24 hours in the lab after each test condition, they were then injected and hooked up to a machine that pumped in different amounts of glucose (sugar) and blood samples were taken to measure insulin and glucose concentrations. These parameters were then assessed to work out how much insulin was produced in response to the glucose infusion and how well the body was then able to dispose of the glucose that was given. Generally higher insulin concentrations and reduced glucose disposal was indicative of impaired metabolic health and function.
What were the results?
The following parameters were significantly different between each test condition:
1. Mean plasma insulin (during glucose infusion)
Compared with NO-SIT, mean plasma insulin was 41% higher in SIT, whilst 18% greater levels were seen for SIT compared to SIT-BAL.
2. Total glucose disposal
During the glucose load, total disposal was lower in SIT compared with both NO-SIT and SIT-BAL.
3. Whole-body insulin action (glucose disposal normalised to mean plasma insulin)
SIT was 39% lower relative to NO-SIT and SIT was 17.7% lower compared to SIT-BAL.
4. Carbohydrate oxidation rate
SIT-BAL was 22% lower compared to NO-SIT and 19% lower compared to SIT.
5. Average energy intake and expenditure
a) Energy intake for SIT-BAL was approximately 32% lower than NO-SIT and SIT.
b) Energy expenditure for SIT and SIT-BAL was approximately 26% lower compared to NO-SIT.
c) Energy balance was different for all conditions. NO-SIT was in energy surplus by +162 kcal/day vs. SIT which was in surplus by +938 kcal/day vs. SIT-BAL which was in energy deficit by approximately -30 kcal/day.
6. Total sitting, standing and stepping time and number of steps
NO-SIT was significantly different to SIT and SIT-BAL but there was no difference between SIT and SIT-BAL.
Please refer to tables 2, 3 and 4 for a full report of the results of this study.
So what is the take-home message?
Prolonged sitting is very, very bad for us. This study showed that just one day of prolonged sitting had a massive impact on insulin action and therefore compromises metabolic function and health quite dramatically. Even if you reduce the food you eat – to lower your energy intake to more closely match your low energy expenditure when sitting for prolonged periods – insulin action is not fully restored to that seen when activity levels are high. The logical inference to make from this is that sitting for prolonged periods of time is not natural for our species. One of the obvious features of what makes ‘us’ who and what ‘we’ are, is the fact that we have a musculoskeletal system that is designed for physical movement and it is the lack of stimulation of this during waking hours that has very dire consequences.
The results also suggest that energy surplus (i.e. consuming food/beverages beyond energy requirements) plays a key role in the harmful effects of sitting on insulin action. As shown in previous studies energy surplus or an overabundance of fatty acids, glucose and/or amino acids inhibits key components of the insulin signalling pathway. Therefore, it is important that we look beyond just excessive carbohydrates or sugar – notwithstanding that reducing sugar intake remains an important dietary change to make – and acknowledge that a chronic state of energy surplus will reek havoc on our metabolic health irrespective of the macronutrient basis of any excess consumed. Currently, there is no scientific consensus for the notion that one macronutrient poses more risk to metabolic health when in energy surplus if you are healthy and insulin-sensitive. Until such time that evidence proves otherwise, it is the state of being in energy surplus that causes insulin action and metabolic health to be compromised not the source of the excess.
There are 2 more very important things to take note of to put this study into perspective. Firstly, if you refer to the results above and table 2 specifically, you will notice that NO-SIT was in energy surplus by approximately +162 kcal/day versus SIT-BAL which was in energy deficit by approximately -30 kcal/day. You may be wondering why this is important and worthy of comment. Basically due to this difference, the true impact of sitting on insulin action could have actually been underestimated with the real difference between these 2 condition possibly even larger than what was found. Had NO-SIT been in energy balance and not energy surplus, insulin action could have been better than that measured and hence when compared to SIT-BAL a greater difference would have been observed. Secondly, the study subjects were young, healthy and non-obese so it is difficult to extrapolate the findings to other less healthy, older and/or obese populations. What can be said is that prolonged sitting or inactivity would certainly not enhance insulin action and metabolic health in those that that are older and/or suffer from chronic health conditions. So pretty much the advice would be the same.
Finally, I would like to make some big picture comments that can possibly be deduced from this study. It is pretty obvious, I think, why health conditions such as obesity and insulin resistance have become endemic. To make clear:
this study showed that nutritional manipulation by reducing energy intake to match low energy expenditure of inactivity (SIT-BAL) only reduced approximately one half of the harmful effects of sitting on insulin action.
It is therefore feasible that impaired glucose metabolism and insulin resistance could be developed in the non-obese who are normal weight or Body Mass Index (BMI) if there is gross long-term inactivity. Consequently, we should be cognisant of the dangers of inactivity and refocus some of our energy and attention away from diet and nutrition as being the only answer to these problems. The solution seems very simple indeed but that would mean that people would have to move a whole lot more as well as modify and show greater restraint in their eating habits but that unfortunately seems very unlikely to occur anytime soon.
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to achieve the above-mentioned benefits or to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
