Green Tea Extract Reduces the Amount of Insulin You Need to Store Your PWO Carbs by ~20% + Discussed: What are the Potential Benefits During Bulking and Cutting?

The beneficial effects of green tea won't occur if you just put some GTE into your post-workout shake... well, at least they didn't occur in response to acute supplementation in the study at hand, where 3x350mg/d consumed for 7 days before a std. exercise + oral glucose tolerance test did the insulin lowering trick.

While green tea has a record of promoting the metabolic and overall health of the obese and sick, its benefits in healthy individuals are still an object of ongoing research. Research such as the latest study from the McMaster University, in which Brian J. Martin et al. (2016) evaluated the effect of supplementation with green tea extract (GTE) on the plasma glucose kinetics of eleven healthy, sedentary men (21±2 y; BMI=23±4 kg/m², VO2peak=38±7 ml/kg/min; mean±SD).

Now, this alone would probably not be SuppVersity newsworthy, but unlike other studies that assessed the effects of GTE on glucose management, Martin's study tested the effects specifically during the post-workout window - a fact that makes the study particularly interesting for SuppVersity readers.

Another important determinant of your 24h insulin levels is your meal frequency:

Grazin' Bad For the Obese!

Largest Meal For Lunch = Winner!?

Regularity is Key to Leanness

Optimal Meal Freq. 4 Kids?

8 Meals = Stable, But High Insulin

Are 6 Meals Better Than 2?

In contrast to what the study's title, "Green tea extract does not affect exogenous glucose appearance but reduces insulinemia with glucose ingestion in exercise recovery", suggests, we are not talking about an acute response study, here.

Simply adding some green tea extract to your PWO drink, alone, is thus unlikely to produce the same results. Rather than that you'd  better mirror the study protocol by consuming 350 mg of a standardized green tea extract thrice daily. After 7 days, which was the timespan after which Martin et al. conducted their oral glucose tolerance test, you should then be able to stash away a significantly larger amount of glucose with a given insulin load than before.

Figure 1: Post-workout glucose kinematics in response to a beverage containing 75g of glucose after 7 days of thrice daily green tea extract supplementation at a dosage of 3x350 mg (Martin. 2016).

As you can see in Figure 1 the chronic intake of GTE decreased the amount of insulin that was required to stash away the 75g of glucose the subjects consumed after participating in a graded exercise test (=cycling to exhaustion at ever-increasing intensities) was reduced by a statistically significant and practically relevant ~20%.

Why did GTE not improve the glucose AUC and the rates of glucose appearance and disappearance? Even though the experiment was not designed to elucidate this hypothesis, it is very likely that the lack of decreases of the amount of glucose in the blood, as well as its absorption kinetics, is probably the logical consequence of the fact that the uptake and storage already took place at the maximal physiological pace - though at sign. lower insulin levels w/ GTE.

Even though neither the glucose AUC, i.e. the amount of glucose that appeared in the blood, nor the glucose rate of appearance and disappearance decreased / increased significantly, said reduction in insulin is a clear indicator of a significantly improved insulin sensitivity - and that during a time-window where your cells' ability to take up and store glucose is already especially high, anyway.

Figure 2: Insulin is the most potent anabolic hormone known, and promotes the synthesis and storage of carbohydrates, lipids and proteins, while inhibiting their degradation and release into the circulation. Insulin stimulates the uptake of glucose, amino acids and fatty acids into cells, and increases the expression or activity of enzymes that catalyse glycogen, lipid and protein synthesis, while inhibiting the activity or expression of those that catalyse degradation (Saltiel. 2001).

In conjunction with the likewise improved oxidation of fatty acids during the workout, said reduction in insulin requirements may be an advantage during both cutting and bulking:

• cutting - during the former part of a "get jacked"-cycle, the reduced insulin excursions could shorten the time period during which elevated insulin levels suppress the release and oxidation of fatty acids from your fat stores while being in a caloric deficit
• bulking - during the latter part of the cycle, a reduced level of insulin could reduce the risk of fat storage while being in a caloric surplus

Eventually, it is important to note the italicization of "could" in the previously outlined hypotheses. Until their accuracy will have been proven in future studies, you better don't overestimate the results you may see from taking GTE supplements. Insulin is, after all, not half as obesogenic as Gary Taubes and co would have it... speaking of insulin: you probably don't have to be afraid to miss out on its beneficial effects on satiety and its ability to inhibit skeletal muscle protein breakdown - if the glucose AUC didn't change, it is after all very unlikely that the efficacy of insulin on other target organs wasn't increased to a similar degree so that you will experience the same satiety improving anti-catabolic effects with 20% less insulin; and yes, this means that, eventually, you could also experience the same degree of fat storage (luckily, though, PWO lipogenesis is → ZERO, anyway).

It may sound boring, but the classic combination of GTE and caffeine is probably the best fat burner left on the OTC supplement market | more

Bottom line: While future studies are, as so often, highly warranted, the study at hand provides initial evidence of the potential usefulness of green tea supplements in people who exercise regularly.

Whether the potential benefits, i.e. increased fat loss during cuts and decreased fat storage during bulks will actually occur in the everyday practice of athletic training and bodybuilding, however, is something that needs further research - research of which I'd hope that the guys at the McMaster University conduct it in the not all-too-distant future. After all, most of you will probably be more interested in the real world results than the mechanism of which Martin et al. write in the conclusion of the study at hand that it warrants further study | Comment on Facebook!

References:

• Martin, B.J. et al. "Green tea extract does not affect exogenous glucose appearance but reduces insulinemia with glucose ingestion in exercise recovery." Journal of Applied Physiology Published ahead of print on October 7, 2016 - DOI: 10.1152/japplphysiol.00657.2016
• Saltiel, Alan R., and C. Ronald Kahn. "Insulin signalling and the regulation of glucose and lipid metabolism." Nature 414.6865 (2001): 799-806.

Paleo Goes "Real Science" - First Meta-Analysis of Available RCTs Shows Improvements in Health + Body Composition

The good thing about paleo is that you can eat a broad range of foods. An advantage that makes paleo versatile and tasty enough to adhere to.

I know that I will probably have annoyed some of you by implicitly calling "paleo" non-scientific. If we are honest, though, the whole paleo concept is based on extrapolating data from modern hunter gatherer populations, infusing them with a minimal amount of real evidence of what our ancestors ate and mixing that with the intrinsically flawed assumption that the way our ancestors ate (which was 100% opportunistic and 0% "optimized") was the optimal way for us to eat... and no, I am not going to apologize for what some of you may consider an assault on respected scientists who have published more than a dozen of papers which constitute the theoretical backbone of an experimentally still mostly unverified, but promising approach to "healthy dieting".

Meat is an essential part of the "paleo diet" | Learn more about meat at the SuppVersity

You May Eat Pork, too!

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Meat Packaging = Problem?

Grass-Fed Pork? Is it Worth it?

Just to make sure there's no confusion. I am not saying that everything that Eaton, Cordain and others wrote is bogus. I am just saying that their papers are above everything else the material based on which others have formulated research hypothesis and done experimental research. Research that has been reviewed in a soon-to-be-published paper in the influential American Journal of Clinical Nutrition, by Eric W Manheimer, Esther J van Zuuren, Zbys Fedorowicz, and Hanno Pijl. A paper that leaves its readers with a generally positive conclusion, but state that "[t]he available data warrant additional evaluations of the health benefits of Paleolithic nutrition" (Manheimer. 2015). Now that does not sound like much, but in view of the scarcity of evidence it is more than you'd usually expect from a review that was partly financed by the National Center for Complementary and Alternative Medicine of the US.

When they decided on the methodology, inclusion and exclusion criteria, Manheimer et al. began with the simple, but important question "Does paleo-nutrition improve risk factors for chronic disease more than other dietary interventions in people with the metabolic syndrome?" To answer this question, the authors searched the following bibliographic databases for reports of controlled trials without any language restriction (likewise included were relevant results from the following ongoing trials databases):

• 

  Figure 1: Details of the selection process in January 2015 (Manheimer. 2015).

  The Cochrane Central Register of Controlled Trials (CENTRAL) 2014
• MEDLINE via OVID (from 1946)
• EMBASE via OVID (from 1974)
• LILACS (Latin American and Caribbean Health Science Information database, from 1982)
• Science Citation Index (from 1988 to the present).
• The metaRegister of Controlled Trials 
• The U.S. National Institutes of Health Ongoing Trials Register
• The Australian and New Zealand Clinical Trials Registry 
• The World Health Organization International Clinical Trials Registry platform 

The reference lists of all identified RCTs and key review articles were also reviewed and squared with the following selection criteria:

"Randomised controlled trials will be included. Any other study design will be excluded. We will only include cross-over trials if we are able to extract the relevant data from the first phase (i.e., before the crossover occurred) because we consider the risk for carryover effects to be prohibitive" (Manheimer. 2015).

In addition, the scientists looked for dietary interventions which were designed to emulate as much as possible, for the modern time, the diet of plants and animals eaten by human beings during the Paleolithic era. More precisely, Manheimer et al. included only studies with diets with...

• large amounts of vegetables (including root vegetables), 
• fruits (including fruit oils e.g., olive oil, coconut oil, palm oil), 
• nuts, fish, meat, and eggs

To make sure to get relevant data, the duration of the dietary intervention had to be at least one week. Studies showing only acute improvement in blood pressure, glucose levels or whatever from eating more veggies and fruit and calling that "the paleo diet" were thus not included in the meta-analysis. The same goes for two uncontrolled clinical trials, as well as all studies where the dietary protocols included one or several of the following "paleo-nono-foods": dairy, grain-based foods, legumes, extra sugar, nutritional products of industry (including refined fats, refined carbohydrates).

This is the macronutrient composition (in g/day) of what Eaton describes as the "paleo diet" in his 1985 seminal paper - needless to say that this is based solely on hypothetical extrapolations of sample data from modern hunter gatherer populations and the little actual evidence we have of what our ancestors ate (Eaton. 1985).

So what's paleo, and what was it compared to? For those who are too lazy to read the full article, here's the gist. The "paleo diets in the four RCTs that were analyzed in Manheimer's meta-analysis used diets that were high in vegetables (including root vegetables), fruits (including "fruit oils", i.e. olive oil, palm oil, coconut oil) and nus, fish, meat and eggs. Dairy, grains, legumes, extra-sugar and processed foods were a no-go in all studies Manheimer et al. included in their analysis. The control diets in all 4 RCTs that were concluded in the meta-analysis were based on distinct national nutrition guidelines, but still broadly similar. Obviously that's interesting, because the results of this meta-analysis are thus going to be a comparison of the "paleo diet" and the recommended "healthy diet" according to what experts on certain advisory boards think would be the one and only way for us to eat.

Important side note: I would like to use the chance to highlight that this diet - if it was not for the (imho) unnecessarily rigid exclusion of dairy and legumes - is actually very similar to what fitness experts have been suggesting for decades. If you do the math on the macros in Eaton's recommendation you end up with 32.5% protein, 22.8% fat, 43.7% carbohydrates and the rest of the energy in form of fiber. With this common macro ratio from the fitness community and the requirement to "get all of that from whole foods" you end up eating almost the same diet.

The number of studies all these search efforts brought to light was - as you, as someone who's heard about all the pertinent trials on www.facebook.com/SuppVersity, already, will know - not exactly extensive. All in all, only four RCTs that involved 159 participants were included. This were four RCTs with very similar results, as the researchers' meta-analysis revealed:

"In this systematic review and meta-analysis of 4 RCTs, Paleolithic nutrition resulted in greater short-term pooled improvements on each of the 5 components of the metabolic syndrome than did currently recommended guideline-based control diets. However, the greater pooled improvements did not reach significance for 2 of the 5 components (i.e., HDL cholesterol and fasting blood sugar). For each metabolic syndrome component, the quality of the evidence for the pooled estimate for improvement was moderate" (Manheimer. 2015).

I guess what these results mean is much easier to grasp if you take a look at the plot of the data I've created for you. Keep in mind: What you see in Figure 1 are the differences compared to the allegedly "optimal" recommended diets in the respective studies, not differences to the habitual diets of the subjects which were probably significantly more pronounced.

Figure 2: Improvements in  triglycerides, HDL, fasting blood sugar, waist circumference, systolic and diastolic blood pressure with "paleo" diets vs. nationally recommended diets (Manheimer. 2015).

The most significant and probably practically relevant benefits of the paleo diet can be seen in the graph on the right hand side: Compared to the relatively small (and practically probably almost irrelevant, if not already stat. non-significant) advantages in terms of blood lipids and glucose, the improvements in blood pressure and waist circumferences are what I would use to argue in favor of paleo-esque dietary recommendations in front of any expert panel.

Meat vs. beans - what's more satiating? A recent study from the University of Minnesota did a "paleo-relevant" comparison of the satiety effects of meat- and bean-based meals. More specifically, Bonnema and her colleagues compared the satiety response to a beef meal providing 26 g of protein and 3 g of fiber to a bean meal providing 17 g of protein and 12 g of fiber. What they found may surprise the non-paleo-lovers out there: "[The] beef-based meal with high protein and [the] bean-based meal with moderate protein and high fiber produced similar satiety, while the bean-based meal resulting in higher, yet moderate, gas and bloating" (Bonnema. 2015). Since both lead to a reduced energy intake on subsequent meals, both the anti-paleo legume-based and the paleo meat-based meal "could equate to weight loss and/or management over time" (ibid.).

After all, more than 50 million people in the US alone are suffering from full-blown hypertension (high blood pressure). In view of the fact that even pre-hypertension is associated with an 80% increased risk of cardiovascular morbidity (learn more), the consumption of a paleo-esque diet could thus save the lives of millions of people. In view of the fact that this would also save us billions of dollars that are spent on managing hypertension every year, this is probably the strongest argument in favor of the "paleo diet" (Note: It's not an exclusive advantage, though. The DASH diet with a similar if not higher vegetable and fruit content has similar effects).

Figure 3: Increase in all-cause mortality risk among 48 500 men and 56 343 women, 50 years or older, in the Cancer Prevention Study II Nutrition Cohort according to BMI and waist circumference (Jacobs. 2010).

A bit less convincing for the average panel member, but practically as relevant are the significant decreases in waist circumference. With studies showing a 2-fold elevated all-cause mortality risk in average American men and women with WC ≥120 cm (compared with <90 cm) and WC ≥110 cm (compared with <75 cm), respectively (see Figure 3 for details), there's yet little doubt that an improvement in this often overlooked health-marker is just as important as the reduction in blood pressure.

Bottom line: Even though we have to rely exclusively on the evidence of the four studies (Lindeberg. 2007; Jönsson. 2009; Boers. 2014; Mellberg. 2014), there's little doubt that paleo-esque diets are superior to many of the recommended "low fat + whole grain, ..."-diets. Unfortunately, the number of pertinent studies is small and the existing studies have short-comings the critics will always bring up as an objection when someone dares questioning the current recommendations:

• Three out of the four existing RCTs, i.e. Lindeberg, Jönssen and Boers, either didn't account for inter-group differences at baseline or didn't report whether they did that or didn't do it (you can safely assume that they didn't, so that everyone can easily say that the paleo group had an unfair advantage and we cannot tell if this was or wasn't the case).
• Adverse events were assessed only in one out of the four existing RCTs (in the Boers study) and otherwise completely ignored (in view of the accusations against "paleo" from the proponents of the current guidelines that's an important shortcoming).
• The quality of life was not assessed by any of the studies (I don't say that the quality of life will suffer, but it is unquestionably important to assess it, also in view of the likeliness that people will adhere to the diet in the long run).

These issues, as well as the short the duration of three out of the four existing studies (only the Mellberg study lasted 2 years) are problems the "paleo research" will still have to overcome before any of the governing bodies / councils will say "paleo is the new recommended diet for XY" (insert "the average citizen of the European Union", "the average US citizen", etc. for XY).

No, there are not neg. side effects of high protein intakes. On the contrary, the major source of acids in the Western diets are grains which are obviously not allowed on "paleo diets" | more

In view of the fact that the analysis of secondary outcomes, like body weight development [subjects on paleo lost 2.69 (0.52-4.87) kg more], inflammation [subjects on paleo reduced their CRPs by 0.28 (0.21-0.76) mg/L more], fasting insulin [subjects on paleo had 13.03 (6.52-32.59) pmol/L lower levels], and total cholesterol [subjects on paleo had 0.24 (0.09- 0.56) mmol/L levels], yielded similar "pro-paleo" results, I personally think that it is very unlikely that future trials that avoid these problems would find very fundamentally different results and/or ill health effects of a liberal paleo-esque dietary template.

The fact that longer-term studies that account for baseline differences, measure adverse events and assess the quality of life of their subjects are not available, yet, is still holding "paleo" back from greater acceptance within the medical / research community. Plus: What I would like to see are studies that compare the different paleo varieties, as in "strict paleo" vs. "paleo + dairy" or "paleo + legumes"... but who knows, maybe someone is already working on one or several of these studies at the very moment today's SuppVersity article is published. | Comment on Facebook!

References:

• Boers, Inge, et al. "Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-study." Lipids Health Dis 13.1 (2014): 160. 
• Eaton, S. Bovn, M. Konner, and N. Paleolithic. "A consideration of its nature and current implications." N Engl j Med 312.5 (1985): 283-9.
• Jacobs, Eric J., et al. "Waist circumference and all-cause mortality in a large US cohort." Archives of internal medicine 170.15 (2010): 1293-1301.
• Jönsson, Tommy, et al. "Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study." Cardiovasc Diabetol 8.35 (2009): 1-14.
• Lindeberg, Staffan, et al. "A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease." Diabetologia 50.9 (2007): 1795-1807.
• Manheimer, et al. "Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis." American Journal of Clinical Nutrition (2015): Ahead of print.
• Mellberg, Caroline, et al. "Long-term effects of a Palaeolithic-type diet in obese postmenopausal women: a 2-year randomized trial." European journal of clinical nutrition 68.3 (2014): 350-357.

Is Low Blood Sugar Obesogenic? Hypoglycemic Episodes Characteristic of Weight Loss Plateaus & Weight Regain - What to Do? Diet, Sleep, Exercise & Mental Work Matter

Tip: Restore your muscle and liver glycogen after workouts and before long fasts to ensure a smooth transition from glucose to fat utilization.

In view of the diabetes pandemic it sounds stupid, when J-P Chaput and A Tremblay write that low blood sugar levels could contribute to the ever-increasing obesity rates in the US and other Western countries.

Their reasoning, however, is sound: An increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect.

Chronically low levels of glucose, as well as the glucose excursions we see in the few (still) healthy people after shoveling down packages of twinkies and dingdongs, would thus precipitate overeating and eventually obesity and diabetes.

Use alternatives to sugar sweetened beverages if you want to stabilize your blood glucose!

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Stevia, Much More Than Sweet?

Artif. Sweetened Foods Good, Not Bad for Fat Loss.

Compared to the way the hypothesis was originally formulated by Jean Mayer in the 1950s, the theory Chaput & Tremblay present in a 2009 review of the literature is significantly more complex (Mayer. 1953 & 1955. Chaput. 2009) and more of a glucose homeastasis hypothesis of obesity.

In contrast to the mainstream version of the "bad blood sugar spikes", Mayer and later Chaput and Tremblay focus on the role of the blood sugar troughs, we rarely think about. It all goes back to the classic glucostatic theory of food intake which postulates that

"that reduced glucose utilization in critical brain regions leads to perception and expression of hunger, and increased glucose utilization in these same glucosensitive sites leads to decreased hunger and cessation of eating." (Chaput. 2009)

In a state of decreased glucose utilization aka "metabolic hypoglycemia" (Mayer. 1955), there is a point at which the peripheral arteriovenous difference in blood glucose becomes negligible and glucose is no longer entering ‘metabolizing cells’ - this, according to Mayer, is the the signal for meal
initiation.

Does this mean that fasting is counter-indicated? For most of you probably not. If your liver gylcogen levels are well-stocked at the onset of the fast and assuming that you have a decent degree of metabolic flexibility, the transition into the fast will not put you at risk of metabolic (temporary glucose shortage at the cellular level) and / or full-blown hypoglycemia (really low blood glucose levels). So, fasting is ok, if you don't turn it into "starving" by extending the fast indefinitely and/or not restocking your glycogen levels in the feeding windows.

Interestingly, Mayer argued in his previously cited 1955 paper, already that the glucostatic theory would explain the short-term control of hunger and food intake, whereas a lipostatic mechanism would control the long-term regulation of body weight and energy balance.

There is nothing static about the glucostatic theory

Today, the role of glucose in the control of food intake is thought to be dynamic: it is a satiety factor and an initiation signal that has been associated with body fat by Chaput and Tremblay in two studies, which examined the effects of low glucose concentrations on long-term energy balance and weight gain in (Boulé. 2008)

Figure 1: Surprisingly linear increase in weight and body fat regain in prospective study and experimantal trial with lower blood glucose levels after OGGT (Boulé. 2008)

• 259 participants between 20 and 67 years of age involved in the Quebec Family Study - A study which revealed a closeassociation between glucose concentrations at the end of anoral glucose challenge and changes in body mass over the course of a 6-year follow up (Boulé . 2008).

• 44 obese participants on a 15-week weight-loss programme in either a drug therapy group or a placebo group coupled with energy intake restriction - A study which showed a higher propensity for weight regain over a follow up period of 83 weeks in those who had glucose levels below fasting values at the end of the oral glucose tolerance test during the weight loss intervention (Boulé. 2008)

In view of the fact that it would be easy to over-read the significance of these results: The researchers found that (1) lower glucose concentrations at the end of an OGTT were correlated with weight gain over time, that (2) large amounts of weight loss were associated with low glycemia at the end of an OGTT, and that (3) these low glucose concentrations were strong predictors of the amount of weight regained after weight loss.

The GI does matter - but only before and after you try to lose weight

Of these findings (2) is particularly interesting as it would support the notion that low glycemia can do both: It supports weight loss, when the energy intake is restricted and it increases the risk and extend of weight (re-)gain, when there is no energy restriction.

Figure 2: When the dietary energy intake is tightly controlled, there is hardly a difference in weight loss and body fat loss with high GI, low GI and high fat dieting in obese men & women (Raatz. 2005)

These observations would support previous evidence that a high glycemic index of foods, which would obviously be connected to higher glucose excursions after meals, figures large on ad-libitum (Alfenas. 2005), but only marginally on tightly controlled diets (Raatz. 2005).

It is thus no wonder that Chaput & Tremblay write in their latest review that their results are relevant only in phases without deliberate (significant) energy restriction. In these phases, the present research clearly suggests that weight-reduced obese individuals are at particular risk of weigh (re-)gain; an observation of which the scientists say that it is brought about by a destabilization of the "body homeostasis" that occurs, whenever the weight loss exceeds 10% of the initial body weight. And indeed: Tremblay et al. have observed in 1999, already that the mean glycemia of participants who had reached the point where their weight loss stagnated had reached an all-time low of 3.3 mmol/ l, of which studies by LeBlanc show that that it is significant enough to evoke a significant counter-regulatory hormonal response (LeBlanc. 1982; Tremblay. 1999).

Hypoglycemia and depression? The reduced glycemia could also be the underlying cause of diet induced increases in symptoms of depression as they were observed by Chaput et al. in a previous trial (2005), in the course of which their male volunteers became increasingly depressed, when they had surpassed the 10% weight loss margin (Chaput. 2007a). A direct association between low glycemia and depression in weight loss was confirmed in a follow up that used a low calorie diet (700kcal/day) + aerobic exercise. (Chaput. 2007b). Intriguingly, depression peaked, when the subjects finally hit a weight loss plateau in both studies.

These "significant counter-regulatory hormonal responses", which manifest in form of blunted growth hormone and epinephrine responses and appear to be controllable by regular exercise, are of particularly interest for those of you whose weight loss efforts have plateaued. A better glucose control with a focus on avoiding low glucose levels and regular physical activity could thus help you solve this problem... switching to a ketogenic diet which guarantees 100% glucose stability since the glucose is no longer used as a substrate, would be a another option.

Exercise to the rescue!

Another and eventually probably the most promising way of increasing glucose stability, facilitating further weight loss and forestalling future weight (re-)gain would be regular workouts.

"Physical exercise can be described as a stimulus contributing to optimal body functioning. This is discretely expressed at many levels of regulatory processes, be it by stimulating the effect of key enzymes, by increasing the sensitivity to hormones, by facilitating substrate transport through the membranes, by influencing cell receptors in a tissue-specific manner and probably many others.  The participation in regular physical activity has also been shown to prevent both hyperglycemia and hypoglycemia, which is concordant with the idea that exercise enhances the accuracy of substrate balance regulation." (Chaput. 2008)

It's thus not best to sit around all day to avoid your blood glucose levels from plummeting. On the contrary, individuals who are physically engaged in their daily schedule may expect a better control of both high and low glucose levels and better overall glucose homeostasis. And in fact, previous research also suggests that physically fit individuals are less likely to experience feelings of hunger associated with declines in blood glucose (Chaput. 2008).

The unbeatable benefits of exercise include both improved glucose control in the traditional sense of avoiding hyperglycemia and improved glucose control in the more comprehensive sense of avoiding both high and low glucose levels.

Chaput and Tremblay do yet add another factor to the discussion: Mental exercise! The glucose demands of our brain during cognitive activity are a commonly overlooked factor, when it comes to both glucose and energy control and that in spite of the fact that we all know that (with the exception of full ketosis) carbohydrate represents a critical energy substrate for the brain. Against that background,...

"the low capacity of the body to store carbohydrate might be perceived as a paradox of nature, particularly when cognitive activities are dominant in the daily activity schedule. This limitation is exacerbated by the inability of the body to synthesize glucose from free fatty acids." (Chaput. 2009)

It is thus not surprising that Cognitively and thus energetically demanding tasks will influence the ad-libitum meal intake, even if the measured energy expenditure during sitting at the desk doing nothing and performing a reading–writing task for 45 min is practically the same (13kj difference in Chaput. 2007c).

The brain may be your hungriest muscle

Figure 3: In contrast to both high (HIE) and low intensity exercise (LIE) 45 minutes of knowledge-based work will increase energy intake at a subsequent buffet (McCann. 1990)

In that the results presented in Figure 3 are not a statistical artifact. They agree with the results with the results of a study involving scientists from the University of Washington who increased their energy and fat intake at the time of the preparation of NIH grant applications (the additional influence of stress should be considered, here, as well | McCann. 1990)

In conjunction with the increase in the variability of glycemia, Chaput et al. observed in a 2008 follow up (Chaput. 2008), this may well explain the increased food intake the researchers observed in response to "cognitive work" in the broadest sense in all three studies.

Unquestionably, Chaput & Tremblay are right, when they warn that these observations raise the question as to whether other sedentary leisure activities (for example, video game playing, television viewing, chatting on internet) are also hyperphagic stimuli. In other words, whether they will make you overeat similar toknowledge-based work; and whether associations with glucose instability, as they were observed by Chaput et al. in 2008 exist for "texting", as well.  And even if that wasn't the case, the mere fact that knowledgebased work represents the main working modality in the current way of living, alone, would warrant further research in this direction.

Apropos "modern lifestyle", sleep or rather a lack thereof figures, as well

If you take a look at the data in Figure 4, you will realize that another feature of the modern way of living, i.e. a lack of sleep quantity and quality is associated with glucose excursions into hypoglycemia as well.

Figure 4: Mean glucose area below fasting glucose concentrations (GABF | higher values increase more severe / longer episodes of hypoglycemia) in men and women according to their habitual sleep duration (Chaput. 2007d)

The mean glucose area below fasting glucose concentrations (GABF) Chaput et al. measured in a yet another study they conducted in 2007 (Chaput. 2007d) clearly indicate that border line hypoglycemia is much less pronounced in long vs. short sleepers.

In that, it is interesting to see that the differences in mean glucose area below fasting glucose concentrations reflect the contemporary evidence of associations between sleep duration, obesity and type II diabetes - both sleeping too short (Xi. 2013) and too long is associated with increased risk of metabolic syndrome and/or type II diabetes (Ohkuma. 2014).

Bottom line: I doubt that hypoglycemia is the ultimate weight loss tool, but I hope you will agree that the previously presented evidence is significant enough to argue that you better keep an eye on both overtly high and overtly low glucose levels.

Table 1: Overview of factors that are believed to directly influence glucose homeostasis (Chaput. 2009)

As I've pointed out before, the latter damaging effects of low glucose levels are particularly pronounced, when you're not dieting. Yet even if you're calorically restricted, it's certainly a wise advise to keep the number and duration of episodes with borderline low glucose levels to a minimum to (a) reduce cravings, specifically for sweets, (b) minimize the negative long(er) term effects on the production of catecholamine and thyroid hormone (Leung. 1975), testosterone (Oltmanns. 2001) and the rest of the hormones the production of which depends on an intact hypothalamic signalling that is disrupted as a consequence of low glucose availability in the brain | Comment on Facebook!

References:

• Alfenas, Rita CG, and Richard D. Mattes. "Influence of glycemic index/load on glycemic response, appetite, and food intake in healthy humans." Diabetes Care 28.9 (2005): 2123-2129.
• Boulé NG, Chaput JP, Doucet E, Richard D, Despre´s JP, Bouchard Cet al. Glucose homeostasis predicts weight gain: prospective and clinical evidence.Diabetes Metab Res Rev 2008;24: 123–129. 
• Chaput, Jean-Philippe, et al. "Psychobiological impact of a progressive weight loss program in obese men." Physiology & behavior 86.1 (2005): 224-232.
• Chaput, Jean‐Philippe, et al. "Psychobiological effects observed in obese men experiencing body weight loss plateau." Depression and anxiety 24.7 (2007a): 518-521.
• Chaput, Jean-Philippe, et al. "Increase in depression symptoms with weight loss: association with glucose homeostasis and thyroid function." Applied Physiology, Nutrition, and Metabolism 33.1 (2007b): 86-92.
• Chaput, Jean-Philippe, and Angelo Tremblay. "Acute effects of knowledge-based work on feeding behavior and energy intake." Physiology & behavior 90.1 (2007c): 66-72. 
• Chaput, J-P., et al. "Association of sleep duration with type 2 diabetes and impaired glucose tolerance." Diabetologia 50.11 (2007d): 2298-2304.
• Chaput, Jean-Philippe, et al. "Glycemic instability and spontaneous energy intake: association with knowledge-based work." Psychosomatic medicine 70.7 (2008): 797-804. 
• Chaput, J. P., and A. Tremblay. "The glucostatic theory of appetite control and the risk of obesity and diabetes." International journal of obesity 33.1 (2008): 46-53.
• LeBlanc, J., et al. "Variations in plasma glucose, insulin, growth hormone and catecholamines in response to insulin in trained and non-trained subjects." Metabolism 31.5 (1982): 453-456.
• Leung, Yan, et al. "The effect of hypoglycemia on hypothalamic thyrotropin-releasing hormone (TRH) in the rat." Endocrinology 97.2 (1975): 380-384.
• Mayer J. Glucostatic mechanism of regulation of food intake. N Engl J Med1953;249: 13–16.
• Mayer J. Regulation of energy intake and the body weight, the glucostatic theory and the lipostatic hypothesis.Ann NY Acad Sci 1955;63: 15–43.
• McCann, Barbara S., G. Russell Warnick, and Robert H. Knopp. "Changes in plasma lipids and dietary intake accompanying shifts in perceived workload and stress." Psychosomatic medicine 52.1 (1990): 97-108. 
• Ohkuma, Toshiaki, et al. "U-shaped association of sleep duration with metabolic syndrome and insulin resistance in patients with type 2 diabetes: The Fukuoka Diabetes Registry." Metabolism 63.4 (2014): 484-491.
• Oltmanns, Kerstin M., et al. "Hypoglycemia, but not insulin, acutely decreases LH and T secretion in men." The Journal of Clinical Endocrinology & Metabolism 86.10 (2001): 4913-4919.
• Raatz, Susan K., et al. "Reduced glycemic index and glycemic load diets do not increase the effects of energy restriction on weight loss and insulin sensitivity in obese men and women." The Journal of nutrition 135.10 (2005): 2387-2391. 
• Tremblay, Angelo, et al. "Metabolic Fitness in Active Reduced‐Obese Individuals." Obesity research 7.6 (1999): 556-563. 
• Xi, Bo, et al. "Short sleep duration predicts risk of metabolic syndrome: A systematic review and meta-analysis." Sleep medicine reviews (2013).

Stevia - Natural Sweetener With Anti-Diabetes + Anti-Obesity Effects? Research Update: GLP-1, Insulin, Glucose Transport and Uptake, Inflammation, Bitterness & Safety

Stevia is certainly one of the best choices to use as a sweetening agent. It is yet important to point out that this has nothing to do with the fact that it is "natural" - as "natural" as the white stevioside powder ism anyway.

You may remember from the Facebook News that Ripken et al. reported in a recent paper in the  Journal of Agricultural and Food Chemistry (2014) that Stevia will stimulate the release of the satiety (and pro-metabolic) hormones GLP-1 and PYY in the stomach of our (digestion- & nutrition-wise) next relatives, the pigs.

The results Ripken et al. presented about 3 weeks ago are yet only the tip of a whole heap of studies of which Nabilatul Hani Mohd-Radzman and colleagues believe that it is sufficient to postulate that the Stevia rebaudiana Bertoni plant "could benefit the community medicinally through several different pathways, all eventually leading to its antihyperglycemic qualities." (Mohd-Radzman. 2014)

You can learn more about sweeteners at the SuppVersity

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Stevia, Much More Than Sweet?

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But is there really convincing  evidence that the beneficial effects of the consumption / use of stevia and its main sweetening agent stevioside go beyond the mere reduction in sugar consumption? Yes, there is; and here is a brief overview of what we've learned so far:

• Anti-inflammatory effects -- Some scientists believe that Stevia’s utility in diabetes protection is due to its antioxidant properties; a hypothesis that is supported by analysis of the phenols that may be extracted from the plant.
  
  Stevia has a large overall proportion of phenols, up to 91 mg/g; it is proposed that these constituents extracted from the leaves are the major agents contributing towards the anti- hyperglycemic activities exerted by the plant (Shivanna. 2013). This is further supported by the fact that the leaves have a greater ability to scavenge free radicals and prevent lipid peroxidation than controls such as butylated hydroxytoluene, butylated hydroxyanisole, and tertiary butyl hydroxyquinone.
  

  

  Figure 1: Effect of Stevia on lipid peroxidation in liver in STZ treated rats (n = 8; Shivanna. 2013).

  The mere presence of anti-oxidants does not ensure anti-diabetic effects, though. Against that background it's important that corresponding experimental evidence from streptozotocin-induced diabetic rats, in which phenolic compounds prevented several diabetic complications is already available. In addition, Shivanna et al. (2013) observed a significant decrease (about 30%) in peroxidation in the livers of Stevia-pre-fed rats, compared to those of their control groups. In view of the previously discussed involvement of the liver in the etiology of the metabolic syndrome, this is a good indicator of reduction in the progression of diabetic complications.
  
  The same goes for the levels of the pro-inflammatory cytokine NF-kappaB and TNF-alpha of which researchers from the Shanghai Institute of Endocrine and Metabolic Diseases report that it was significantly downregulated in a study on a C57BL6J mouse model of insulin-resistance, when the rodents received stevioside supplemented chow (Wang. 2012).
• Direct beneficial effects on blood glucose levels --  Whether the beneficial effects of stevia on blood glucose management are mediated solely via its anti-inflammatory effects is not yet certain. The initially mentioned effects on GLP-1, for example, could (and probably will) also contribute to the significant decrease in blood-glucose levels Susuki et al. observed in a study from 1977 that was published in the Japanese science journal Nippon Nogei Kagaku Kaishi (Susuki. 1977).  The Japanese researchers fed rats a stevia enriched high carbohydrate + high fat diet and observed "a significant reduction in glycemia" after four weeks on the otherwise highly prodiabetic rodent equivalent of the Western diet. 

You cannot stand the bitter taste of stevia? Unlucky you! You've simply got the wrong genes. As scientists from the Laboratory of Molecular Anthropology and Centre for Genome Biology at the University of Bologna observed in a very recent study, men and women with the TAS2R4 gene polymorphism rs2234001 and /or the TAS2R14 (TAS = taste receptor) gene polymorphism rs3741843 will never understand how the rest of us can ignore the obnoxious bitterness of steviosides - I know, that's bitter ;-)

• That these benefits are not rodent specific and don't arise in response to an interaction with certain components in the rodent chow was demonstrated 27 years later by Gregersen, et al.  (2004). In their paper in the January issue of Metabolism, the scientists report that they observed a similar, highly significant reduction (an average of 18%) in postprandial glucose levels in Type II diabetic patients given test meals supplemented with stevioside..
  
  A 2010 study by Anton et al. confirmed this (Anton. 2010) this; postprandial glucose levels were significantly lowered in patients supplemented with Stevia, compared to those
  given aspartame (a type of synthetic sweetener) or sucrose (normal table sugar). In that, the slightly increased insulin levels in the stevia vs. aspartame group provides further support for the involvement of GLP-1, which is likewise involved in health insulin function (Kjems. 2003)
  

  

  Figure 2: Total energy intake of type II diabetics in kcal/day on days with aspartame, setvia or sucrose sweetened foods (left); corresponding plasma insulin levels (Anton. 2010)

  In addition, patient satiety as an aftereffect of the different sweeteners was also tested; it was found that subjects given lower-calorie sweeteners (Stevia or aspartame) did not compensate by eating more than those given sucrose. Any potential increase in insulin did thus have the proven, but largely ignored satiety effect insulin is supposed to have (Vanderweele. 1994). 
• Possible interactions with the gut & its microbiome -- The research on the interactions of stevia with the microbes in our gut is still in its infancy.
  

  

  Table 1: Effects of non-nutritive sweeteners on gut hormones and glucose absorption:in vivo effects on animals (Brown. 2014)

  Nevertheless, the repeatedly mentioned effects on GLP-1, as well as evidence from animal studies which show a decrease in glucose uptake, when carbohydrates are fed in the presence of stevia (Brown. 2012) clearly indicate that there is more to the anti-diabetic & -obesity effects of stevia (and maybe other non-nutritive sweeteners) than direct antioxidant effects (Payne,. 2012).

Is stevia even safe? At "sane" intake levels toxic effects appear unlikely (Aze. 1990); studies show no detrimental effects on female reproduction, when consumed in amounts equivalent to those you would use in food products (Yodyingyuad. 1991; Saenphetet. 2006); there are minimal negative effects on seminal vesicle weight in high dose study with male rodents (Oliveira-Filho. 1989); studies show no genotoxic effects or DNA interactions (Brusick. 2008); stevia even appears to have a limited anti-viral activity (Takahashi 2000 & 2001)

"Natural and good", not "good since natural": As the previous elaborations have shown stevia really appears to be one of the best sugar replacements to chose. This is yet not due to the "naturalness" of stevia, but due to the specific molecular structure of the the glycosides the food industry extracts from the leaves of a plant.

Accordingly, the white substance we wrongfully call "stevia", when it's eventually only an extract of the sweet(est) tasting steviosides wouldn't be less effective or unhealtier if it was synthesized in the laboratories of Monsanto or extracted from the poop of genetically modified bacteria. And you know what? I guess, when the market keeps growing the way it does, this is soon going to be the white-washed sterile environment of a laboratory is probably soon going to be where 90% of the stevia is going to come from.

Reference:

• Anton, Stephen D., et al. "Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels." Appetite 55.1 (2010): 37-43. 
• Aze, Y., et al. "Subchronic oral toxicity study of stevioside in F344 rats." Eisei Shikenjo hokoku. Bulletin of National Institute of Hygienic Sciences 109 (1990): 48-54.
• Brown, Rebecca J., and Kristina I. Rother. "Non-nutritive sweeteners and their role in the gastrointestinal tract." The Journal of Clinical Endocrinology & Metabolism 97.8 (2012): 2597-2605. 
• Brusick, D. J. "A critical review of the genetic toxicity of steviol and steviol glycosides." Food and Chemical Toxicology 46.7 (2008): S83-S91.
• Gregersen, Søren, et al. "Antihyperglycemic effects of stevioside in type 2 diabetic subjects." Metabolism 53.1 (2004): 73-76.
• Kjems, Lise L., et al. "The Influence of GLP-1 on Glucose-Stimulated Insulin Secretion Effects on β-Cell Sensitivity in Type 2 and Nondiabetic Subjects." Diabetes 52.2 (2003): 380-386.
• Oliveira-Filho, Ricardo M., et al. "Chronic administration of aqueous extract of< i> Stevia rebaudiana</i>(Bert.) Bertoni in rats: Endocrine effects." General Pharmacology: The Vascular System 20.2 (1989): 187-191.
• Payne, A. N., C. Chassard, and C. Lacroix. "Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity." obesity reviews 13.9 (2012): 799-809.
• Ripken, Dina, et al. "Stevia Glycoside Rebaudioside A Induces GLP-1 and PYY Release in a Porcine Ex Vivo Intestinal Model." Journal of agricultural and food chemistry (2014).
• Shivanna, Naveen, et al. "Antioxidant, anti-diabetic and renal protective properties of  Stevia rebaudiana." Journal of Diabetes and its Complications 27.2 (2013): 103-113.
• Suzuki, H., et al. "Influence of oral administration of stevioside on levels of blood glucose and liver glycogen of intact rats." Journal of the Agricultural Chemical Society of Japan (1977).
• Takahashi, K., et al. "Extracts from Stevia rebaudiana is a potent anti-rotavirus inhibitor in vitro and in vivo." Antiviral Research. Vol. 46. No. 1. PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS: ELSEVIER SCIENCE BV, 2000.
• Takahashi, Kazuo, et al. "Analysis of anti-rotavirus activity of extract from< i> Stevia rebaudiana</i>." Antiviral research 49.1 (2001): 15-24.
• Vanderweele, Dennis A. "Insulin is a prandial satiety hormone." Physiology & behavior 56.3 (1994): 619-622.
• Wang, Zhiquan, et al. "Stevioside ameliorates high-fat diet-induced insulin resistance and adipose tissue inflammation by downregulating the NF-kappaB pathway." Biochemical and biophysical research communications 417.4 (2012): 1280-1285.
• Yodyingyuad, Vithaya, and Supranee Bunyawong. "Effect of stevioside on growth and reproduction." Human Reproduction 6.1 (1991): 158-165.

SuppVersity World Cup Special: What Football Can Do For Your Health & Performance Now & As You Age - It's Better for Heart & Bones (!) Than Lifting

Soccer! For Young & Old, Heart & Bones, Blood Sugar & Body Fat Now & Beyond World Cup 2012

Ok, I have to admit, in spite of the fact that the World Cup starts today, I wouldn't have produced this article, if the editor(s) of the Scandinavian Journal of Medicine & Science in Sports didn't have a similar idea and I wouldn't have "early view" access to a bunch of soon-to-be-published on the beneficial and not so beneficial effects of what I call "football" and most of you call "soccer".

But enough of the prelude, let's take a look at what I have to report, here: Schmidt et al. present the amazing cardiovascular adaptations they observed in response to 4 and 12 months of football or strength training in 65- to 75-year-old untrained men.

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The study was conducted at the Copenhagen Centre for Team Sport and Health of the University of Copenhagen and involved, as you would have guessed, 26 untrained men (age: 68.2 ± 3.2 years). The guys were randomized to football training (FTG; n = 9), strength training (STG; n = 9), or control (CG; n = 8).

Football (soccer), older hearts will love it!

Maximum oxygen consumption (VO2max; L/min) and resting heart rate (RHR; bpm) in elderly healthy 65- to 75-yearold men at baseline, after 4 & 12 months of football training (FTG), strength training (STG), and control (CG) - Schmidt. 2014

Aside from the impressive improvements in VO2max (vs. no improvement in either the strength training or the control group; see Figure 1), the researchers observed the following beneficial structural changes of the heart:

• increases in left ventricular diastolic diameter +8%
• increases in end-diastolic volume +21%
• increases in ventricular mass index +18%

Unlike the improvements in ejection fraction (+8% in FTG vs. +5% in STG), these changes were "football"-exclusive.The systolic longitudinal two-dimensional strain increased by 8% (FTG) and 6% (STG), whereas the right ventricular systolic function improved (P < 0.05) by 22% in FTG, but not in STG and CG.

In conjunction with the football-exclusive increases in diastolic mitral inflow (E/A) ratio and peak early diastolic velocity (E') improved (25% and 12%, respectively), your 3x1h of training may thus be better spend on football than on resistance training if your main goal is to improve your VO2max and kick heart disease's ass.

If we look at the benefits the older guys in the Schmidt study derived from their soccer training it can hardly be surprising that Anderson et al. (2014a) report similarly "hearty" benefits in 31 untrained males with mild-to-moderate hypertension who were randomized 2:1 to a football training group (n = 20) and a control group receiving traditional recommendations on healthy lifestyle (n = 11).

While the football group exhibited significant (P < 0.05) changes in cardiac dimensions and function after just 3 months similar to those in the Schmidt study, as well as significant reduction in arterial blood pressure, the results in the "traditional take this *bs* advice" group were mediocre tat best. Consequently, the researchers conclude that even in the short term (3-6 months)...

"football training improves LV diastolic function in untrained men with mild-to-moderate arterial hypertension [and] improve longitudinal systolic function of both ventricles." (Anderson. 2014a)

 Now, SuppVersity readers are not generally hypertensive, and I am gathering that the few highly appreciated "best agers" in my readership are also in the minority. Against that background it's worth mentioning that the heart is not the only part of your body that will benefit from soccer practices - your bones will, too. Ok, I see you laughin' cause you're hittin' the weights, regularly, but what would you say if I told you that ...

"4 months of recreational football for elderly men had an osteogenic effect, which was further developed after 12 months, whereas resistance training had no effect."  (Helge. 2014)

I see, I've got your attention, now! Well, the authors, again researchers from the Copenhagen Centre for Team Sport and Health speculate that the anabolic response may be due to increased bone turnover, especially improved bone formation which was obviously promoted to a greater extent in those 9 of the initially 26 healthy sedentary men (age 68.2 ± 3.2 years) who had been randomized to the  football (F; n = 9) and not the resistance training (R; n = 9) group - and that despite the fact that both trained two to three times weekly for a total of 45–60 min training.

Playing soccer is good for your health, watching it... well, watching it can increase your risk of being hospitalized for acute myocardial infarction minimally (+1%; cf. Barone-Adesi. 2010), unless, of course, your team wins! During the 1998 World Cup, which was won by France, the myocardial infarction risk of French men was actually reduced by 35% (Berthier. 2003)

When it comes to improving the functional ability and physiological response to submaximal exercise, in older men, however, it's difficult to pinpoint a difference between three football and three resistance training sessions per week. Unsurprisingly, study #4 in today's review did yet report that only football trainign "additionally elevates maximal aerobic fitness and exhaustive exercise performance." (Anderson. 2014b).

What's left to discuss, oh yes! Anderson. 2014c and the effects on glucose management!

Yeah, with 21 middle-aged men (49.8 ± 1.7 years ± SEM) with T2DM as subjects, this study will certainly appeal to all the Average Joes out who unfortunately don't get their daily dose of SuppVersity wisdom, yet (Anderson. 2014c).

The said middle-aged subjects were divided into a football training group (FG; n = 12) and an inactive control group (CG; n = 9) - the absence of a strength training "control" is a pity... but alas, after the 24-week intervention period, in the course of which the sick guys covered only During 4.7 ± 0.2 km at a mean heart reate of 83 ± 2% of HRmax per 1h soccer training, they experienced a 11% increase in VO2peak and lost 1.7 kg and 12.8% of their total fat and android fat, respectively.

Against that background it's not that surprising that Anderson et al. report concomitant improvements in plasma glucose and an increased expression of the glucose transporters (GLUT-4). Most importantly, however, the Danish researchers did also observe an overall time effect for glycosylated hemoglobin (HbA1) and thus significant and continuous improvements in glucose management in the soccer group.

Bottom line: "There you have it" ... that's actually something my good friend Carl Lanore from www.superhumanradio.com like to say. There you have the benefits of playing soccer. Improved heart health, fat loss and reductions in blood glucose in type II diabetes are probably nothing, you wouldn't have expected, anyways, right?

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Well, what about the benefits on bone health, then? I personally was surprised that the impact of soccer training was more pronounced than the one of strength training. In the end, I would yet expect equal results if the latter, i.e. the strength training had included free-weight squats and/or deadlifts. Those and not sissy curls and lat pulldowns are true bone builders, but honestly - when I see some of the 60+ agers at my gym do them I think to myself: You better leave that to true physical culturists, like my previously mentioned friend Carl Lanore (www.superhumanradio.com) and head over to the soccer training, folks ;-)

References:

• Andersen, L. J., Randers, M. B., Hansen, P. R., Hornstrup, T., Schmidt, J. F., Dvorak, J., Søgaard, P., Krustrup, P. and Bangsbo, J. (2014a), Structural and functional cardiac adaptations to 6 months of football training in untrained hypertensive men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12237 
• Andersen, T. R., Schmidt, J. F., Nielsen, J. J., Randers, M. B., Sundstrup, E., Jakobsen, M. D., Andersen, L. L., Suetta, C., Aagaard, P., Bangsbo, J. and Krustrup, P. (2014b), Effect of football or strength training on functional ability and physical performance in untrained old men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12245
• Andersen, T. R., Schmidt, J. F., Thomassen, M., Hornstrup, T., Frandsen, U., Randers, M. B., Hansen, P. R., Krustrup, P. and Bangsbo, J. (2014b), A preliminary study: Effects of football training on glucose control, body composition, and performance in men with type 2 diabetes. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12259
• Barene, Svein, et al. "Soccer and Zumba as health-promoting activities among female hospital employees: a 40-weeks cluster randomised intervention study." Journal of sports sciences ahead-of-print (2014): 1-11. 
• Barone-Adesi, Francesco, et al. "It is just a game: lack of association between watching football matches and the risk of acute cardiovascular events." International journal of epidemiology 39.4 (2010): 1006-1013.
• Berthier, Fabrice, and Frédéric Boulay. "Lower myocardial infarction mortality in French men the day France won the 1998 World Cup of football." Heart 89.5 (2003): 555-556.
• Helge, E. W., Andersen, T. R., Schmidt, J. F., Jørgensen, N. R., Hornstrup, T., Krustrup, P. and Bangsbo, J. (2014), Recreational football improves bone mineral density and bone turnover marker profile in elderly men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12239.
• Ramírez-Campillo, Rodrigo, et al. "Effects of In-Season Low-Volume High-Intensity Plyometric Training on Explosive Actions and Endurance of Young Soccer Players." The Journal of Strength & Conditioning Research 28.5 (2014): 1335-1342.
• Schmidt, J. F., Hansen, P. R., Andersen, T. R., Andersen, L. J., Hornstrup, T., Krustrup, P. and Bangsbo, J. (2014), Cardiovascular adaptations to 4 and 12 months of football or strength training in 65- to 75-year-old untrained men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12217