(Mis-)Managing Hypothyroidism: 7% Reduction in Energy Expenditure & Fat Oxidation in Patients on Levothyroxin (T4) Mono Therapy. Plus: Alternative Dessicated Thyroid?

The thyroid is a real diva. You better treat her with utmost care (learn more)

I guess, ... no, I know that a couple of you have to deal with all sorts of thyroid problems. I know you won't like to hear that, but if you read the SuppVersity Athlete's Triad Series you should know that there is more than just the remote possibility, that food and rest would be everything to "heal" your underactive ductless gland (=thyroid). Good indicators are you train everyday, (1) you eat a high protein, low carb, low to at best medium fat diet with a constant caloric deficit, and (b) your TSH level is low to normal, your free T4 level is low to normal but your free T3 level is sub-par. In consequence you will feel sluggish, look sluggish, train sluggish and won't achieve either your fat loss, performance or muscle building goals.

If that's you, there is need for meditation, not medication, for stress management, not pills. In fact, throwing the "inactive" precursor T4, the textbook treatment for hypothyroidism into the equation, could make things even worse, as your body is going to convert the lion's share of it to the metabolic emergency break rT3, to avoid that increasing levels of the active metabolite T3 start gnawing away on your undernourished muscle and exacerbate the chronic stress you are exposing yourself to.

Is being "euthyroid" really the same as having normal TSH levels?

Data from the The Colorado Thyroid Disease Prevalence Study indicates the risk of suboptimal thyroid function & hypothyroidism is more pronounced in women (Canaris. 2000); associations w/ certain contraception meds, pregnancy & menopause in other studies point towards estrogen / progesteron issues as confounding factors.

Interestingly enough, a recent study from Division of Endocrinology and Metabolic Medicine, Policlinico di Monza and the Department of Biomedical Sciences for Health at the Università degli Studi di Milano, both obviously in Italy, did now reveal that it does note necessarily take overtraining + undereating to end up in a 'metabolically and mentally sluggish euthyroid state'. This became evident, when the Italian researchers compared the body composition and resting energy expenditures of 30 hypothyroid women with an average BMI >25 kg/m² and normal serum TSH levels (<3.5 μU/ml; text-book says: "Your patient has optimal thyroid function, doctor!") who had been on the "gold standard" (*rofl*) replacement therapy with L-T4 (levothyroxin = synthyroid; mean dose: 73±34 μg/d) for at least 2 years to the same parameters in a control group with matched age, BMI, menopausal state and life-style habits (P>0.3 for all).

While neither the average TSH levels, which were 1.92±1.06 µU/ml in the T4 and 1.87±0.89 μU/ml in the control group (P=0.91), nor the body composition (body fat: 41.4±7.4 vs 42.1±8.3%; LBM 58.6±7.4 vs 57.8±8.3%; P>0.7 for all) revealed a statistically significant inter-group difference, the resting energy expenditure of the the hypo- / after medication "euthyroid" women on levothyroxin did:

• 

  Click on the image to learn how to calculate (I should rather say estimate) your resting energy expenditure using different scientifically verified formulas and why it is important not to go below a certain threshold (learn more)

  In absolute terms, the women in the T4 group had a -7% lower REE than the controls (1347±171 vs 1447±154 kcal/d; P<0.05).
• The -7% difference remained the same and had an even higher statistical significance (P<0.02 vs. P<0.05), when the resting energy expenditure was expressed relative to the the subjects lean body mass (28.3±2.6 vs 30.5±3.0 kcal/kg LBM die; P<0.02).
• A smaller yet still significant difference was observed when the actual resting energy expenditure was compared to the "supposed" resting energy expenditure calculated by the means of the Harris-Benedict Equation (91±7 vs 95±7%; P<0.05).

The most significant difference (P<0.01) was yet observed, when the scientists analyzed the respiratory quotient (also respiratory exchange rate, short: RER) of their subjects. The latter is a direct measure of the ratio of glucose to fat your body is using a substrate to fulfill its energy requirements, in particular,...

• 

  Suggested read: Maximal Intra- & Post- Workout Fat Oxidation With Pause or 90min LISS Between 2x40min Incremental Exercise Bouts? (read more)

  higher RER levels indicate a greater contribution of glucose, while
• lower RER levels indicate a greater contribution of fats
• A RER of ~1.0 would be observed in healthy individuals, only, when they are engaging in highly glycolytic + brief exercise bouts like sprinting.
• Many "fat burners" work in part by decreasing the RER. When you are in a caloric deficit (and only then) this is an advantage because you will spare glucose and burn fat. 
• Other supplements like creatine, for example,  gear your metabolism towards an increase in glucose expenditure, which can be beneficial in all sorts of activities that rely heavily on short sprints / brief muscle contraction

In fact, the women on T4 (only) had a 11% higher respiratory exchange ratio (0.92±0.07 vs 0.86±0.06; P<0.01), of which even the scientists have to admit that it's clearly suggesting an "impaired fasting lipid oxidation in hypothyroid women" and would thus support "the view that additional interventions may be necessary to fully revert the entire set of hypothyroidism-related metabolic alterations." (Martucci. 2013)

Aren't there better alternatives? T4+T3 or dessicated thyroid?

In a way it is funny - or should I say tragic(?) - that this is the first study in years that bothers with the metabolic and often psychological downsides of T4 only regimen in a way that goes beyond the analysis of TSH levels. After all, the Internet and the waiting rooms of medical practitioners all over the world are full of (mostly female) patients complaining about the non-existent benefits and / or side effects of levothyroxin, only, therapies.

It should be obvious that some of those patients may belong to the initially referred to group of people who suffer from self-induced hypothyrodism in response to undereating and/or overtraining, while others may have confounding, often undetected pathologies that are responsible for their compromised metabolism, their inability to lose weight, their sluggishness, brain fog etc.

Suggested read: "Dietary Thyroid Treatment: Beef, Green Vegetables, Full-Fat Milk & Butter Normalize TSH in Subclinical Hypothyroidism " (read more)

If you do however put the results of the study at hand in perspective with previous studies comparing "T4 only" vs. "T4+T3" treatments and the overall patient-preference of the latter, and combine that with the results of a very recent comparison of levothyroxin vs. natural dissicated thyroid treatment, in the course of which researchers from the Department of Endocrinology at the Walter Reed National Military Medical Center and the University of Health Sciences in Bethesda observed significant weight (I highly suspect fat) loss in the 70 18–65 year-old patients with primary hypothyroidism who had been on a stable dose of T4 for 6 months, when the subjects were given desiccated thyroid extract (DTE) instead of levothyroxin (1 mg DTE ~ 1.667 g L-T4; cf. Hoang. 2013).

Interestingly, the patients had significantly lower rT3 levels, higher total T3 levels, lower otal and free T4 levels and that in the presence of higher, but normal TSH levels (inter-group difference p=0.032) during the DTR part of the 2x16 week cross-over trial. A health hazard, as it is often argued that it would be the result of depressed TSH levels is thus a weak argument against using an alternative treatment strategy, of which I would highly suspect that it could resolve part of the metabolic dysadvantages arising in the context of T4 monotherapy and which was preffered by 34 of the patients in the Hoang study.

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Bottom line: Whether using T4 + T3 or natural dessicated thyroid as the treatment method of choice is necessary or the best strategy for everyone is something that remains to be seen. Something that stands out of question, though, is that the stubborn adherence to the textbook standards, the blind reliance on TSH tests and the ignorance doctors display towards the complaints of their patients is not going to solve an increasingly prevalent problem (+3% increase in congenital hypothyrodism per year in the US, esp. in white and hispanic newborns; cf. Hintnon. 2010)

References

• Canaris GJ, Manowitz NR, Mayor G, Ridgway E. The Colorado Thyroid Disease Prevalence Study. Arch Intern Med. 2000;160(4):526-534.
• Hinton CF, Harris KB, Borgfeld L, Drummond-Borg M, Eaton R, Lorey F, Therrell BL, Wallace J, Pass KA. Trends in incidence rates of congenital hypothyroidism related to select demographic factors: data from the United States, California, Massachusetts, New York, and Texas. Pediatrics. 2010 May;125 Suppl 2:S37-47.
• Hoang TD, Olsen CH, Mai VQ, Clyde PW, Shakir MK. Desiccated Thyroid Extract Compared With Levothyroxine in the Treatment of Hypothyroidism: A Randomized, Double-Blind, Crossover Study. J Clin Endocrinol Metab. 2013 Mar 28.
• Martucci F, Manzoni G, Lattuada G, Perseghin G. Overweight/obese women with primary acquired hypothyroidism in appropriate levothyroxine replacement therapy are characterized by impaired whole body energy metabolism. Endocrine Abstracts (2013) 32 P1004 | DOI:10.1530/endoabs.32.P1004 Share on facebook Share on twitter Share on digg Share on stumbleupon Share on delicious Share on linkedin | Share on email Share on print

Full ROM = More Growth, More Strength, More Structural Changes & More Sustainable Gains & Fat Loss - Insights from Realistic 8 Weeks Leg Training + 4 Weeks Detraining

"That's not 90°, yet. Do deeper!"

I guess you will be remembering last week's post on the superior growth effects of full vs. partial squats, hah? Now, the results of the Bloomquist study certainly raise the question, whether the same or similar effects must be observe with different exercises or even different body parts, as well. After all, it would be bro-science at its best to generalize the result "full squat = full quad development" to "partial ROM  = partial strength and hypertrophy response" without the least hint of evidence that this hypothesis is more than just the "proposition or principle put forth or stated (without any reference to its correspondence with fact) merely as a basis for reasoning or argument" ("hypothesis, n.". OED) the word "hypothesis" implies - right?

The good news is that it appears as someone has heard my lamentations about the scarcity of respective research, or - what's in this case more probably - feel the same about the necessity to generate data that would be necessary to base our workout protocols on more than just "hearsay", hypothesis and "N=1 experiences" and a single study.

Ok, enough kiddin' around let's get to the facts

Table 1: McMahon's interpretation of an "ecologically valid resistance training program"; * denotes static holds for time in s, DL = double, SL = single legged (McMahon. 2013)

Despite the fact that the study I tried to make tempting to you in the introduction is again build around a leg training routine, it has two major advantages compared to the Bloomquist study: (1) The participants performed a complex, multi-exercise leg-training protocol, (2) the study used the vastus lateralis as yardstick for the size gains, (3) the effect of full vs. short ROM (range of motion) on strength, muscle structure and body fat were also measured and (4) the study had an active training part (8 weeks on the protocol outlined in table 1) and - and this is pretty unique - a subsequent 4-week follow-up in which the subjects did not train (detraining) that allow us to determine whether the persistency of the gains will also depend on whether you achieved the training with a limited 50° vs. a "full" 90° specific angle of knee flexion (McMahon. 2013).

With the the specified angle being defined as the "position at which the training load is held isometrically for two seconds",

• the 50° regimen involved a shorter ROM (SR) in the dynamic phase of the exercise and thus a shorter ‘average muscle length’, whereas
• the 90° regimen involved a longer ROM (LR) in the dynamic phase of the exercise and thus a longer ‘average muscle length’
  *you will learn more about the importance of muscle lengthening later this week, so stay tuned!

McMahon & Onambélé-Pearson hypothesized that the group training "at longer muscle length" (90°) would undergo a greater amount of skeletal muscle hypertrophy and concomittant strength development and that these differences would be "due to increased physiological stress and stretch on sarcomeres compared to the group training at 50°" (McMahon. 2013) and that these effects would be evident even during / after the deloading phase.

Figure 1: Cross sectional area (CSA) of the vastus lateralis measured at 25, 50 and 75% of the femur length for the full range (LR), partial range (SR) and a non-exercised control group (McMahon. 2013)

If we take a peak at changes in muscle cross sectional area (CSA) in figure 1 this hypothesis appears to be roughly accurate. There are however significant differences in the growth response the scientists measured at 25%, 50% and 75% of total femur length (VL25-75), with a statistically non significant advantage for the high(er) load, short-ROM approach (the higher load is a natural consequence of the RM prescription) and a highly significant advantage for the low(er) load, full-ROM approach, when it comes to that part of the muscle you want to shine, as it contributes to that massive "tear-drop look".

"CSA increased significantly (p<0.05) relative to baseline following training at all sites in both training groups. The significant training effect remained during the whole detraining period in both training groups at both 50% and 75%, but was not evident at 25% of femur length after week 10. There was a trend for LR to exhibit greater relative gains in a CSA compared to SR at all sites, which was significant at week 8 at 75% of femur length. It was found that there was not only a main training effect (p<0.05) but a main group effect after week 8 (p<0.05) with LR exhibiting a 59±15% compared to SR showing 16±10% increment in VL CSA." (McMohan. 2013)

To the surprise of the researchers, the "following the first two weeks of detraining the group effect was no longer evident (p=0.07)" (McMohan. 2012). In the end, the existing advantage of training over the full-ROM, as pronounced as it may be at the CSA75 site, is thus short lived in this group of previously non-resistance-traind 26 volunteers (14 males and 12 females). The fasicle length, which increased by
23±5%, 19±4%, 16±4% at weeks 8, 10 and 12 in the LR and by only 10±2%, 6±2% and 2±2% in the SR group (data not shown), on the other hand, were persistent - yet only in the full range (LR) group.

"And body fat? What about the body fat"

Crossfit doesn't fit well with everyone. In  fact, you have to be pretty fit already if you intend to benefit - specifically if you don't have someone who tailors the workouts to your specific needs. If you the shed 8% of your already low 16% body fat in 10 weeks workout routine I wrote about in February, chance is you'll just get injured or burned out (learn more)

The local reduction in subcutaneous fat that was likewise assessed based on the ultra-sound images the scientists used to evaluate the structural changes and CSA increases did not show significant group effects at 25%. The relative changes of 5% in the partial (SR) and 22% at the 50% measuring mark in the full ROM (LR) groups, clearly suggest that "going all the way" would still be the way to go if you don't want to look hypermuscular, but lean (ladies?). The latter is particularly true in view of the facts that the ...

"[...] main effect of group remained during weeks 10 and 12, as SR regressed toward baseline by week 12, whereas LR still possessed significant losses at this phase (-10±6%)" (McMahon. 2013)

and that there was a similar trend seen at 75% where a main effect of both group and training existed at week 8 (p<0.05) - even if the latter vanished in the course of the 4-week detraining period 7±3% SL and 9±1% LR).

Regional growth and angle-specific strength gains

Contrary to all previously reported values, which were - if they were group specific at all - regionally different, the changes in strength showed - as you would expect it - an angular specificity. While both groups did increase their strength, there were more than just minute differences between the partial (SR) an the full ROM (LR) groups:

• at the end-ranges, the maximal volunary contractive force increased 5±10 for SR at 50° and 30±5% for LR at 90°, respectively
• there was evidence of angular specificity of training in both groups with SR significantly (p>0.05) increasing MVCs at 50, 60, 65, and 70° , only, wheres the participants in the LR increased their MVCs values over the entire angular range.

What's remarkable, yet non necessarily beneficial, is the fact that the angle of peak torque which had been 75° at the beginning of the training intervention decreased to 70° within 8 weeks of training over the short ROM (SR) and remained there for the duration of the detraining (i.e. the change was at least persistent, if not permanent). No such effect was observed in the LR group.

"By week 10, both groups displayed an average 6±2% strength reduction (relative to the post-training strength values), with SR not significantly above baseline (0±2%) in contrast to LR remaining significantly above both baseline (p<0.05) and SR (p=0.027) at weeks 10 and 12."

Overall, the changes in contractile force and the angle at which they were elicited reflect the structural changes that were brought about by the more pronounced muscle lengthening that's a prerogative of training over the full range of motion (ROM).

To ensure that all participants conducted the complex exercises at the correct knee angle a goniometer was attached to their knees (photo velamed.com)

Bottom line: As far as the practical implications of his findings are concerned McMahon and Onambélé-Pearson reemphasizes that the specific muscle mechanics are of paramount importance, "when choosing a range of motion for a resistance training protocol." (McMahon. 2013). With resistance training protocols that enforce a full range of motion having the ability to influence force and power production to a greater extent than protocols where the range of motion is not as extensive, the authors are right to point out that it would be a mistake to allow your ROM to be compromised "in order to accommodate a greater absolute external load, in an attempt to increase the stress of mechanical loading". Accordingly they advice coaches to "reinforce a more complete ROM, even when absolute load maybe reduced, in order to provide a greater internal stress and more potent stimulus for adaptation" (McMahon. 2013).

Although this advise is obviously as relevant for trainees, like yourself, I would like to add one thing to McMahon et al's "bottom line", which relates to the previously described structural changes that accompany the hypertrophy response to exercise. These changes I discussed in the context of domain sizes and satellite cell recruitemen (see "Getting Big Means Growing Beyond Temporary Physiological Limits" | re-read it) are important for both continuous muscle and strength gains and your ability to maintain the gains you've made. Therefore, you would in fact be ill-advised not to "leave your ego at the door" if you want continious and persistent size gains and increases in strength over the full range of motion that do not vanish, when you are taking 2 weeks off.

Handpicked suggested reads:

• 

  The Jack-of-All-Traits Leg Workout from the Sáez de Villarreal study I discussed on July 15, 2012, would also be something you may want to look into if you need some inspiration for your own routine.

  You Want Maximal Performance & Size Gains + Complete Thigh Development? Then Full Squats are For You! (read more)
• SuppVersity EMG Series - Gluteus maximus, Quadriceps femoris, Gastrocnemius, Soleus & More: The Very Best Exercises for Tree-Trunk Legs and Herculean Calves (read more)
• The Step-By-Step to Your Own Workout Routine Guide (read it)
• All posts leg training at the SuppVersity (read them)

References:

•  "hypothesis, n.". OED Online. March 2013. Oxford University Press. 6 May 2013 <http://www.oed.com/view/Entry/90588?redirectedFrom=hypothesis>.
• Eugene McMahon G, Onambélé-Pearson G. Impact of range-of-motion during ecologically valid resistance training protocols, on muscle size, subcutaneous fat and strength. J Strength Cond Res. 2013 Apr 26.[Epub ahead of print]
  

Fish Oil Compromises, Fish Improves Adiponectin Levels in "Overweight, But Healthy" Individuals. Neither Promotes Weight or Fat Loss Within a 4-Week Study Period

Fish are smart, they tell you about the good things "omega-3" fatty acids will do, without pointing you to the fact that eating them will yield a more favorable DHA:EPA ratio than popping pills that are made from the same remnants of their deceased relatives the fishery industry has dumbed for decades.

With the vitamin D news the other day (go back), you are now probably thinking "hell, no Adel's other favorite topic to rant about"... an yes! You are right: I just like to rant against mainstream stupidity and one-size-fits-it all approaches everybody loves because they are so "easy"! Take your fish oil! And everything is going to be all right. Much easier and so much more compelling, than my advice to eat fatty fish at least once, better twice or thrice a week to promote, not magically achieve metabolic health.

And while you've heard about the anabolic and blood pressure lowering benefits of fish protein in previous articles, here at the SuppVersity, it is more than unlikely that you've already gotten wind of the latest study from the Smart Foods Centre, School of Health Sciences (you got to love that name!) at the University of Wollongong, New South Wales, Australia (Neale. 2013)... and that despite the fact that it took - just as with the egg study, showing only beneficial effects on blood lipids (learn more) - suspiciously long for the study to make it from an "accepted manuscript" into a print article in the scientific journal Metabolism.

Scaled fish or capped oils - is that even a question?

In what is by no means the first, and certainly not going to be the last paper comparing the metabolic effects of fish oil caps to the food item, the oil is supposed to be delivered with (the fish ;-), Elizabeth P. Neale and her colleagues recruited 18–65 year old volunteers, who were willing to consume fish, but had a low- or moderate habitual fish intake to begin with (<3x per week). The subjects had to have a BMI somwhere in-between 25 and 37 kg/m² and a chubby midline with awaist circumference of >94 cm for men, >80 cm for women. Exclusion criteria were pregnancy, diabetes mellitus, impaired renal function, smoking, not weight stable for the past six months, food allergies or habits inhibiting compliance with the study design, illiteracy and inadequate conversational English; plus, they were excluded if they were currently taking medications including thiazolidinediones, valproic acid, ACE in-hibitors, and glucocorticoids.This left the researchers with N=30 subjects who were randomized to consume either

• fish providing 1.86 g of LC n-3 PUFA (812mg EPA +1044 mg DHA)per day -- three serves of 135 g salmon (Birds Eye Atlantic Salmon Fillets, Simplot Australia), two serves of 66 g sardines (adjusted for percentage fish in total canned product; John West Sardines in Tomato Sauce, Simplot Australia) and one serve of 55.1 g tuna (adjusted for percentage fish; John West Tuna Tempters Lemon and Cracked Pepper, Simplot Australia) per week, or
• supplemental fish oil (Blackmores Omega Daily) containing the same amount of LC n-3 PUFAs, yet - and this is a consequence of the low DHA/EPA ratio in fish oil vs. real fish - 1055.1 mg EPA and only 744.9 mg DHA

for 4 weeks, on a daily basis. And while the participants in the supplement group were "not expressly told to avoid fish", they were not "encouraged to consume it in preference to other protein sources", either (Neale. 2013).

What did the scientists want to measure?

The primary outcome parameter of the study were the differential effects of fish and fish oil on the plasma total and high molecular weight adiponectin levels in overweight humans and, secondary, to identify the genetic variations in participant's ADIPOQand FTO genes that may influence that response.

Figure 1: Relative changes in weight, BMI, waist, body fat (%), glucose, insulin and EPA + DHA levels in serum from t = -2 weeks (i.e. before the 2-week run in in which the diets and activity levels were standardized to 25% protein, 45% carbohydrate, and 30% fat) to t = 4 weeks (Neale. 2013)

As the data in figure 1 goes to show you this did not stop the scientists from evaluation the effects the intervention had on anthropometric parameters (waist, body fat, etc.) of their subjects, as well. Neither of these, nor the effects on blood glucose and insulin showed any significant inter-group difference. If we discard the identical changes in the EPA and DHA levels of the subjects, the dietary / supplement intervention had absolutely zero effects on any of these "extra-parameters" - no weight loss, no visible improvement in glucose metabolism.

No reduction in body fat or waist circumference in with fish or fish oil

Reason enough to ask yourself, whether we should not go back to baseline and ask "is fish / fish oil even good for you"? Certainly not - or I should say, only if you put faith in the hilarious promises of "instant weight loss, improvements in glucose metabolism" and what not, if you finally jump aboard and take your "essential fish oil supplements" that are plastered all over the Internet. If you discard these advertisment claims or simply apply some critical thinking skills, it should be obvious that you got to content yourself with changes in your potential to shed fat / improve glucose metabolism by simultaneously committing to lifestyle that's juxtaposed to the way of living that has gotten you into all the trouble to begin with.

Figure 2: Total and high molecular weight adiponectin levels expressed relative to the levels after the 2-weeks run-in (left) and the ratio of the absolute values after 4 weeks (right; Neale. 2013)

The changes in adiponectin expression in figure 2 are such an indicator of a change in the potential of getting rid of the blubber, the high blood glucose - and it is obvious to see that fish oil is inferior to fish, when it comes to inducing these changes.

"The results of this study suggest that short-termconsumption of fish and fish oil supplements does not have the same effect on HMW adiponectin levels in overweight humans. [...] This was due to a small increase in HMW adiponectin in the ‘fish’ group, whilst the ‘supplement’ group exhibited a significant decrease in HMW adiponectin concentrations. A similar pattern was seen for total adiponectin; however this did not reach statistical significance." (Neale. 2013)

As mentioned in the previous paragraph, these changes were not associated with differential effects on body weight, insulin levels and body fat mass, all of which "remained relatively constant" (Neale. 2013)

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Fatty acid content in g/100g of wild and farmed salmon (left) and respective omega-3 to omega-6 ratios; learn more about making the "right fish choices", here

Unfortunately(?), the underlying mechanisms behind the differential effects on HMW adiponectin are as of now not known. Neale et al. do yet also subscribe to the "synergy hypothesis" I alluded to earlier in the first paragraphs of this article. The proven benefits of fish protein on insulin sensitivity and chronic inflammation (Soucy. 1999; Ouellet. 2007; Pilon. 2011), as well as the "other components present in fish such as selenium and vitamin D [, which] have also been associated with a range of health benefits in humans" [Rayman. 2000; Garland. 2006)...

...Oh, no! I know what you are thinking now. "I got all those in my multi! And I guess whey will do just as well as fish protein..." - come on, are you serious? Synergy is about ratios, about competition, about ups and downs, about co-factors and adjuvants. It's not about a kitchen sink supplementation approaches that try to reunite what has been ripped apart in a helpless effort to "make things easier" for the lazy consumer who does not like his fish and does not want to spend some of his daily screen time on buying fresh foods and preparing them... sorry, now I am really ranting ;-)

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Handpicked suggested reads:

• Study on Krill Powder Suggests: There is More to Seafood Than Fat - Can Krill Give You What Fish Oil Can't? Plus: Krill Protein's EAA Content More Than an Able Match to Whey (read more)
• Phospholipid or Triglyceride? What's in Your Fish Oil Caps? Only Phospholipid Based DHA+EPA Reduces Fat Cell Growth & Elevated Insulin Levels Despite Obesogenic Diet (read more)

References:

• Moroi M, Akter S, Nakazato R, Kunimasa T, Masai H, Furuhashi T, Fukuda H, Koda E, Sugi K, Jesmin S. Lower ratio of high-molecular-weight adiponectin level to total may be associated with coronary high-risk plaque. BMC Res Notes. 2013 Mar 6;6:83. 
• Neale EP, Muhlhausler B, Probst YC, Batterham MJ, Fernandez F, Tapsell LC. Short-term effects of fish and fish oil consumption on total and high molecular weight adiponectin levels in overweight and obese adults. Metabolism. 2013 May;62(5):651-60.
• Ouellet V, Marois J, Weisnagel S, et al. Dietary cod protein improves insulin sensitivity in insulin-resistant men and women: a randomized controlled trial. Diabetes Care 2007;30(11):2816.
• Pilon G, Ruzzin J, Rioux L-E, et al. Differential effects of various fish proteins in altering bodyweight, adiposity, inflammatory status, and insulin sensitivity in high-fat–fed rats. Metabolism 2011;60(8):1122–30. 
• Rayman MP. The importance of selenium to human health. Lancet 2000;356(9225):233–41.
• Soucy J, LeBlanc J. The effects of a beef and fish meal on plasma amino acids, insulin and glucagon levels. Nutr Res 1999;19(1):17–24.

300mg CoQ10 Boost Peak Power Increases in Young Elite Athletes. Plus: 140ml of Beet Root Juice, That's all it Takes to Minimize the Oxygen Demands During a Workout

Athletes from various sports train at the Olympic Camp, where the CoQ10 study was conducted.

As unfortunate as it may sound, the number of "next big things" in the area of performance enhancing (legal) substances - at least in large parts - a line-up of supplemental non-starters. Against that background it is all the more surprising that today' SuppVersity article features not one, but two already available supplements that could in fact make a valuable contribution to your workout regimen. And while we are going to take a brief look at the latest research on the ergogenic effects of beet root juice later, we will start out with a study the results of which did actually surprise me - in a positive sense, that is.

• Reduced CoQ10 (ubiquinol) increases peak power in trained athletes (Alf. 2013) -- While previous studies on the efficiacy of CoQ10 demonstrated at best inconclusive and statistically, but mostly practically insignificant benefits, the latest study from the Olympiastützpunkt Rhein-Ruhr in Essen, Germany, reports a whopping +11% increase in peak power per kg body mass in the 53 males and 47 females young German athletes (average age 19.2 years, height 181 cm, weight 78 kg) who consumed 5x 60mg ubiquinol, the completely reduced form of CoQ10, which comes in three redox states, i.e. fully oxidized (ubiquinone), semiquinone (ubisemiquinone), and fully reduced (ubiquinol), on a daily basis day as a supplemental adjunct to their 6-week training regimen.
  

  

  Figure 1: Progress of absolute peak power in the placebo and 5x60mg ubiquinol group (Alf. 2013)

  While it is not possible to tell, whether it was the comparatively long study period (CoQ10 needs week to build up in the tissue; cf. Cooke 2008), the high dose of ubqiuinol (previous studies with 150mg did not yield comparable results, cf. Svensson. 1999) or a combination of both thats responsible for the ergogenic effects you see in figure 1 cannot be said for sure. What is however certain and actually pretty remarkable, if you take into account that these young athletes were all training regularly at the Olympic Training Camp Rhein-Ruhr in Essen and that many of them have been competing at the Olympic Games 2012 in London., is that the supplemented athletes did make 2.5% more out of  their 6 weeks at the camp.
  Addendum: In view of the fact, that Rick just asked about potential side effects on facebook and I assume that, smart as you are, you will immediately spot the 2009 study by Sumien et al. talking about detrimental effects on cognitive function, I want to point out that the human equivalent of 2.6mg/g chow the high dose group received would exceed an ubiquinol intake of >6g even for the lightweights of you. With 1/4 of the dosage not producing any long-term negative sides in the same rodent study, you are thus probably on the save side w/ 300mg/day. This hypothesis is by the way backed by a 2008 review by Hidaka who report a no-observed-adverse-effect level (NOAEL) of 1200 mg/kg/day derived from a 52-week chronic toxicity study in rats that would translate to 720 mg/day for a person weighing 60 kg (Hidaka. 2008)
  Moreover, the way in which the gap between the supplement and placebo group widens only in the last weeks of the intervention seem to support the previously mentioned "pre-loading hypothesisand raises the hope that the ergogenic effects will persist for more than just 6 weeks.
  
  

  

  CoQ10 did work in previous studies, but affected mostly serum markers not performance (learn more)

  The researchers also speculate that "older athletes and “weekend warriors” might profit even more from CoQ10 supplementation than young, well-trained athletes", as both age and the lack of training are associated with a lower mitochondrial density, of which Alf et al. suspect that it may be compensated for by the provision of CoQ10. In view of it's purported beneficial effects on ATP and creatinine phosphate synthesis, this may well be the case. I would yet still refrain from buying a year-long supply of the ubiquinol before respective evidence from independent trials is available. I mean, with the current price tag on ubiquinol, even an N=1 experiment with a 6-weeks supply of 300mg of ubiquinol per day would cost you ~$60 which is not exactly cheap, but could be worth a try - assuming you have the patients to wait for the results.

• 280ml beet root concentrate have well-established ergogenic effects, more is not necessary (Wylie. 2013) -- Right from the Exeter University comes a new study on the ergogenic effects of beet root juice. While the main message of the paper is that beet root juice supplementation can effectively increase nitric oxide levels and physical performance, the real interesting part of the paper deals with the dose-response relationship.
  
  

  

  There are a couple of important confounding factors which will determine whether or not you or anyone else can benefit from nitrate supplementation. Sex is yet - as far as I know know - not one of them... ah, by the way, there may be other benefits to nitrates that are "sex-specific", but in this case the semantics are somewhat different (learn more in a previous post on beet root  juice here at the SuppVersity ;-)

  Lee J. Wylie and his colleagues found that the provision of 70, 140 or 280 ml of concentrated beet root juice (BR), with 4.2, 8.4 and 16.8 mmol NO3- on six separate occasions increased the plasma concentration of NO2- in a dose-dependent manner, with the peak changes occurring at ~2-3 h. Of the three dosing regimen,
  

  "[...] only the higher dosages (140ml and 280ml) reduced the steady-state VO₂ during moderate-intensity exercise by 1.7% (P=0.06) and 3.0% (P<0.05), whilst time to task failure was extended by 14% and 12% (both P<0.05), respectively" (Wylie. 2013)

  As the scientists point out, these results indicate that "there is no additional improvement in exercise tolerance after ingesting BR containing 16.8 compared to 8.4 mmol NO3-".
  
  The dreaded carb overload that may have popped in your head, whenever you heard about using a natural NO3- supplement should not keep you from taking advantage of nature's very own "nitric oxide supplement" ;-)

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Bottom line: In view of the fact that ubiquinol and beet root juice act via totally different pathways, a direct comparison of the two obviously doesn't make sense. A combination of both on the other hand would. I would not expect any synergistic affects, but it is relatively save to assume that the effects will add up.One thing you should keep in mind, thoug,h is that only the beets will have acute effects and provide the instant gratification everybody seems to be striving for, these days. The effects of coqu10 n the other hand will manifest only weeks after you started taking it, so that you will - for want of an independent control you will thus simply have to beleive that its working ... after all, you don't know how much progress you wouls make without it.

References:

• Alf D, Schmidt ME, Siebrecht SC. Ubiquinol supplementation enhances peak power production in trained athletes: a double-blind, placebo controlled study. J Int Soc Sports Nutr. 2013 Apr 29;10(1):24. 
• Cooke M, Iosia M, Buford T, Shelmadine B, Hudson G, Kerksick C, Rasmussen C, Greenwood M, Leutholtz B, Willoughby D, Kreider R: Effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained anduntrained individuals. J Int Soc Sports Nutr2008, 5:8.  
• Hidaka T, Fujii K, Funahashi I, Fukutomi N, Hosoe K. Safety assessment of coenzyme Q10 (CoQ10). Biofactors. 2008;32(1-4):199-208.
• Sumien N, Heinrich KR, Shetty RA, Sohal RS, Forster MJ. Prolonged intake of coenzyme Q10 impairs cognitive functions in mice. J Nutr. 2009 Oct;139(10):1926-32. doi: 10.3945/jn.109.110437.
• Svensson M, Malm C, Tonkonogi M, Ekblom B, Sjodin B, Sahlin K: Effect of Q10 supplementation on tissue Q10 levels and adenine nucleotide catabolism during high-intensity exercise. Int J Sport Nutr1999, 9:166–180. 
• Wylie LJ, Kelly J, Bailey SJ, Blackwell JR, Skiba PF, Winyard PG, Jeukendrup AE, Vanhatalo A, Jones AM. Beetroot juice and exercise: pharmacodynamic and dose-response relationships. J Appl Physiol. 2013 May 2.

Sex-Dependent Low GI Advantage(s) & Vasodilating Effects of Insulin. Diet-Dependant Effects of Active Vitamin D on Glucose Metabolism. Plus: Supplemental Flaxseed Oil?

It seems as if the glycemic index of her diet during puberty could determine on which side of this photoshopped divide a will end, when she's a young woman. Intriguingly, the association between high GI diets and high waist circumferences and obesity risk was not observed in the boys whose 5-year follow up data the researchers analyzed.

"145mm" that's the SuppVersity figure of the Week and the number of additional millimeters the waist circumference of a 12-year old girl is going to increase until she's 17 for each 1-SD increase in dietary GL. In conjunction with the observation that each 1-SD increase in dietary fiber intake was associated with a concurrent 0.44 kg/m² decrease in mean BMI, in girls and a 145mm lower increase in waist circumference, in boys, these results from a soon-to-be-published paper clearly support the notion of the fattening high GI carbs for girls (Gopinath. 2013).

The data does yet also raise the question, whether a higher activity level, a greater muscle mass or whatever something totally different is responsible for the non-significant effect the consumption of a high GI diet appears to have on the "strong sex". After all, even the devilish sugar sweetened soft-drinks which were associated with 4.45% higher body fat levels in girls who consumed one or more servings of the sugary glue per day, did not make a difference for the "young men" (suggested read: "Women Have a Much Higher Time Losing Body Fat Than Men")... ok, so let's see what else we've got "in the news today".

The vasodilatory effects of insulin could be life saving 

 (Hornstra. 2013) -- As a SuppVersity reader you are way beyond the stage of bro-science and thus fully aware that insulin not the villain everybody believes it was. Aside from the fact that it prevents catabolism, which is probably the only thing the average bro knows about, it helps nourish your cells, it keeps your blood from turning into a sweet slurry and has potent vasodilatory effects (ever wondered why you cannot get a decent pump ever since you went low carb?)

You don't still believe in the urban myth that adding fat to a high carb meal would blunt, the subsequent insulin spike, do you? Oh, you do? Well, in that case I recommend you take a look at one of the more recent installments of True or False (learn more)!

There is just one downside to it: Insulin does these and all the other good things only to people like yourself. People who work out, eat clean and remain insulin sensitive. In that, you do however have overweight company, that's at least what the results of a recent study from the Department of Internal Medicine at the VU University Medical Center in Amsterdam clearly suggest. In order to elucidate the hitherto only partially understood local microvascular vasoactive effects of insulin and their impact on systemic vascular resistance. J.M. Hornstra and colleagues conducted a cross-sectional studied in 37 healthy, overweight subjects (age 25 – 55 years, BMI 25 - 30 kg/m²), in whom they measured the local insulin-mediated vasodilation in response and transcutaneous iontophoresis of insulin and compared them to the local effects of acetylcholine and sodium nitroprusside, a potent pharmacological vasodilator.

What the researchers found was a clearcut inverse relationship between insulin-mediated vasodilation (r=-0.50; p<0.01) and the subjects' vascular resistance - a finding that was maintained after adjustment for age, sex, blood pressure and smoking and was not associated with local microvascular effects of acetylcholine.

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Bottom line: The results of the study at hand do thus corroborate to the notion... or I should better write "the proven fact" that insulin is not solely the fattening villain the current mainstream Internet paradigm says it was. It is a powerful hormone with physiological importance well beyond it's role in glucose management and the increased risk of cardiovascular diseases in type II diabetics and the average non-insulin sensitive overweight Westerner is not due to having too much insulin floating around in the system, but due to the non-responsiveness of the cells of the ever-increasing number of pre-diabetics.

Low GI diets helps to shed >10% more during three months exercise intervention 

(Solomon. 2003) -- In a way, you could say that the results of a soon-to-be-published study from the Department of Pathobiology at the Cleveleand Medical Clinic stands in line with both the SuppVersity Figure of the Week and the previous post on insulin's role in peripheral and systemic vascular resistance.

In the study at hand, the ingestion of a low glycemic index diet, as it was prescribed to the 20 older, obese individuals who participated in a 3-months fully-supervised aerobic exercise program will did (a) improve the weight loss success of the subjects in the low GI (LoGIX) vs. high GI (HiGIX) groups by +10.5%, (b) improved their insulin sensitivity and should (this was not measured) thus have have had a beneficial impact on the vascular resistance of the overweight individuals and (c) promoted a lower respiratory exchange ratio (a low RER which is the ratio of glucose / fat oxidation is an indicator of in creased fatty acid and/or lowered glucose oxidation) during exercise and did thus help them to decrease the amounts of lipids floating around in their system.

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Study probes whether "Hitting Your Macros" is all that counts (read more)

Bottom line: In the end, the results of the study at hand are not new, they only confirm what you will probably have known all along: The modulatory effects of low GI diets on the substrate utilization during exercise is highly relevant for the overweight and/or insulin resistant individual (skinny fat people included). With it's ability to improve and conserver insulin sensitivity, it is yet likewise important for the active individual and/or athlete trying to maintain his insulin naturally high insulin sensitivity without having to compromise his/her performance and endocrine health by running around glycogen depleted 24/7.

All of you who did not see the discussion revolving around the necessity of high GI carbs and thus insulin spikes for glycogen repletion after a workout, I suggest you take a peak at the corresponding graph on I posted on Facebook earlier this week (go to the SuppVersity Facebook Wall). One thing you should keep in mind though, is the fact that "high GI diets" are not characterized by the occasional ingestion of "fast carbs" in the postworkout window - this alone is thus unlikely to cause the same ill health effects as a dietary protocol that does not even give your body the chance to clear the steady and rapid influx of glucose from the bloodstream (the "GL", i.e. the glycemic load may in fact be a better measure here, learn more)

Diet- and tissue-specific effects on transcriptional regulation of glucose metabolism 

(Alharfy. 2013) -- In what is unfortunately yet another rodent study on vitamin D, researchers from the College of Pharmacy at the , King Saud University in Riyadh, Saudi Arabia, took a closer look at the differential effect vitamin D (1,25-(OH)2D3, Rocaltrol(R)) supplementation exerts on the transcriptional regulation of insulin-sensitive in liver, muscle and adipose tissue in Male C57BL/6J mice on regular low fat or obesogenic high fat (+high carb) chow.

Figure 1: Effect of vitamin D treatment on transcript levels of insulin sensitive genes in low-fat diet (LFD)- and high-fat diet (HFD)-fed mice (Alharfy. 2013)

If you take a closer look at the data in figure 1, you see that in muscle tissue of LFD-fed mice, vitamin D treatment increased vitamin D receptor (VDR, not shown) to 2.03-fold and insulin receptor substrate (IRS-1) to 1.5-fold. An even more pronounced increase in IRS-1 (+140%; IRS proteins play a key role in transmitting signals from  insulin receptors to the intracellular pathways, as well as growth promotion) expression occurred in the mice that were fed the obesogenic high fat diet - in this case, the increase was yet accompanied by a -50% reduction in VDR expression (not shown) without having downstream effects on GLUT4 expression.

Maybe some of you remember that I covered a study in which vitamin D3 lead to increased obesity levels in rodents back in October 2011 (learn more)

In the liver of the mice receiving the species-appropriate low-fat diet, the provision of supplemental 150 IU/kg calcitriol (the active form of vitamin D!) did not induce any statistically significant trancriptional changes, whereas the -85% decrease in exogenous IRS-1 level in the HFD group and the concomittant upregulation of the hepatic vitamin D receptor expression (+260%) show that the liver could be a major target for the previously observed anti-obesity effects of active vitamin D (see "Active vitamin D does what vitamin D3 doesn't do"; read more). In lean mice, on the other hand, similar effects were absent and the expression of glucose transporters /GLUT-4) decreased by -30%.

The decrease in hepatic GLUT-4 was yet still small compared to the rapid decline in GLUT-4 expression in the adipose tissue of the LFD group. Whether this could precipitate high blood glucose levels is yet about as uncertain as the implications of the highly elevated GLUT-4 expression in the HFD group. Theoretically the latter would help reduce blood glucose levels, but at an expense of profound increases in adipose tissue - that this is not very unlikely, is something you have read about here at the SuppVersity in October 2011, already (go back)

So what do the scientists say?

In view of the necessity to convert supplemental vitamin D3 to it's active form, it is questionable, whether the provision of the former would induce any of the changes Alharfy observed in the study at hand - learn more in a previous installment of the short news!

As Alharfy et al. point out the absence of significant changes in GLUT-4 expression in response to the adminstration of physiologically highly significant amounts of the active form of vitamin D provides further evidence that the "insulin action in mammalian tissue is not a direct one" but are brought about by "intracellular mechanisms of insulin action mediated by IRS-1 and VDR" in the absence of any immediate effects on "glucose transport across major insulin-sensitive tissues, including adipose and liver in mice under LFD and HFD conditions". Consequently, the...

"[...] antidiabetic effect of vitamin D may be directed through its anti-inflammatory action in obese conditions. Reduction in inflammatory cytokines production by vitamin D may play a role in decreasing insulin  resistance." (Alharfy. 2013)

The scientists' conclusion does therefore stand in line with the observations of Waldron et al. about which you've probably read on the SuppVersity Facebook Wall about a month ago (Waldron. 2013).

Based on the 25OHD response (remember: 25OHD is the precursor to calcitriol and will thus be lowered, when more calcitriol is produced from this 'storage form') the researchers from the New Cross Hospital, in Wolverhampton in the UK observed in response to inflammatory assaults, they were among the first to propose that "serum 25-(OH)D is a negative acute phase reactant [... and h]ypovitaminosis D may be the consequence rather than cause of chronic inflammatory diseases" (Waldron. 2013)

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Bottom line: While we are still far away from a proper understanding of the exact mechanisms which underly the observed correlations between low vitamin D levels and all sorts of (eventually) inflammatory diseases, the results of the study at hand corroborate the notion that D3 levels (=passive storage) have little to no direct effects on the etiology of the diabetes, cancer, and what not.

Figure 2: Reductions (!) in all risk mortality calculated on the basis of NHANES data for each 10ng/ml increase in vitamin D up to the "magic" 21ng/ml margin from the Amer study (Amer. 2013)

This would also explain why the vitamin D deficient ballet dancers from yesterday's SuppVersity Facebook news did benefit from supplementation, while the 10,000 participants in the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2004 in another recent study by Amer et al. did not have lower risks of all cause mortality, once their 25OHD levels were just above lowest margin of the normal range (see figure 2 + today's SuppVersity Facebook news; Amer. 2013). What it does not explain, though, is the fact that we see similarly increased risk of all-cause mortality among women with low (20 ng/mL) as well as high (50 ng/mL) levels of serum 25(OH)D (Melamed. 2008) or the 50% increase in mortality Michaëlsson et al. observed in 1194 elderly men (mean age at baseline, 71 years) with vitamin D levels below 18.5ng/mL and above 39.4 ng/mL during a median follow-up of 12.7 years (Michaelsson. 2010).

In the end, studies such as the one at hand, would have to be conducted over long enough periods in human beings to finally identify the mechanism behind the non-linear effects of vitamin D on mortality and metabolic health in the these and other studies. Personally, I would hope that studies like the one by Amer et al. get some more mainstream attention and raise people's awareness of the simple paradigm "test first, supplement second".

Flaxseed oil does not offer metabolic advantages over olive oil  

If you don't like the feminine look and the size of certain body parts of this Greek statuette, you just found another reason to avoid flaxseed - at least if you are and want to stay male (learn more)

(Kontogianni. 2013) -- With all the hype around fish oil, flaxseed oil has more or less been forgotten. If you ask the average Joe or Jane, about whether you should rather use olive or flaxseed oil if you wanted to improve your lipid metabolism and reduce inflammation, many of them will probably still answer: "Flaxseed, of course!"

According to a recent study from the Harokopio University in Greece this is yet nothing but another urban myth. In their randomized cross-over study (2x6 weeks + 6 weeks washout in-between), the scientists found that it did not make a physiologically significant difference whether the 37 normal weight young subjects (age: 22 years) consumed 15 mL/day of either flaxseed oil or extra virgin olive oil.

When it comes to the differences the scientists observed in response to the olive oil vs. flaxseed oil supplemented diet, you better have a magnifying glass ready, as the only highly visible change was allegedly not significant:

Figure 3: Relative levels of inflammatory and biochemical parameters before and after the interventions; all data expressed relative to baseline / after washout = pre-crossover values (Kontagianni. 2013)

Even the fatty acid composition in the cell membranes differed only in terms of the amount of alpha linoleic acid (short-chain omega-3), while the amount of what people often falsely label as "fish oil", namely the long-chain omega-3 fatty acids, DHA and EPA, did not change in either group.

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Oleuropein in olive oil is a natural testosterone booster (learn more)

Bottom line: Aside from statistically non-significant decreases in total and LDL cholesterol in the flaxseed oil group and a physiologically irrelevant increase in the ALA content of the in the erythrocyte membranes,  there were surprisingly little differences between the two study arms.

Now, you can certainly argue that the changes and potential benefits would have been more evident if the amount of flaxseed oil in the diet had been higher. On the other hand, you all should be aware that flaxseed oil goes rancid in no time, cannot be heated and tastes like a$$... this limits it's use as a regular part of your diet. What's more, if you take close look at the levels of hs-CRP in figure 3, you will have to admit that more flaxseed oil could also equal an increase in inflammation.

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That's it for today: Why? Well, I simply had no time to write more earlier today and other than briefly posting this no additional time to spend writing up additional short-news... but judged by the visitor counts on the last weekends, you are probably busy enjoying the weekend, as well. Enjoy your weekend, everyone!

References:

• Amer M, Qayyum R. Relationship between 25-Hydroxyvitamin D and All-cause and Cardiovascular Disease Mortality. Am J Med. 2013 Apr 17. 
• Brown LJ, Midgley AW, Vince RV, Madden LA, McNaughton LR. High versus low glycemic index 3-h recovery diets following glycogen-depleting exercise has no effect on subsequent 5-km cycling time trial performance. J Sci Med Sport. 2012 Nov 12.  
• Gopinath B, Flood VM, Rochtchina E, Baur LA, Louie JC, Smith W, Mitchell P. Carbohydrate nutrition and development of adiposity during adolescence. Obesity (Silver Spring). 2013 Mar 21.
• Hornstra JM, Serné EH, Eringa EC, Wijnker MC, de Boer MP, Yudkin JS, Smulders YM. Insulin's microvascular vasodilatory effects are inversely related to peripheral vascular resistance in overweight, but insulin-sensitive subjects. Obesity (Silver Spring). 2013 Mar 20.
• Kontogianni MD, Vlassopoulos A, Gatzieva A, Farmaki AE, Katsiougiannis S, Panagiotakos DB, Kalogeropoulos N, Skopouli FN. Flaxseed oil does not affect inflammatory markers and lipid profile compared to olive oil, in young, healthy, normal weight adults. Metabolism. 2013 May;62(5):686-93.
• Melamed ML, Michos ED, Post W, Astor B. 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med. 2008;168(15):1629-1637. 
• Michaëlsson K, Baron JA, Snellman G, et al. Plasma vitamin D and mortality in older men: a community-based prospective cohort study. Am J Clin Nutr. 2010;92(4):841-848.
• Solomon TP, Haus JM, Cook MA, Flask CA, Kirwan JP. A low glycemic diet lifestyle intervention improves fat utilization during exercise in older obese humans. Obesity (Silver Spring). 2013 Mar 20. 
• Waldron JL, Ashby HL, Cornes MP, Bechervaise J, Razavi C, Thomas OL, Chugh S, Deshpande S, Ford C, Gama R. Vitamin D: a negative acute phase reactant. J Clin Pathol. 2013 Mar 1.

Breaking the Fast, Cardio & Your Brain: Cardio on Empty is Fatiguing. Fasting Without Exercise, However, is Nootropic

Boring: Every endurance athletes knows and fears it, so wouldn't just that happen when you do your cardio on empty in the morning? And what about the effects on your brain power? Will your gray matter bonk, as well? And if so, what can be done about it?

Today's SuppVersity post is a little different from the usual "Training on empty? Yes / No / Maybe!" debate that flares up every now and then on almost every fitness related bulletin board of the World Wide Web. And in as much as I would like to say that this was all the credits belong to me, the fact that the the following dissertation may actually make a practically relevant contribution is due to the experimental design of the latest study from the Northumbria University in Newcastle, Tyne and Wear, in the UK (Veasey. 2013).

Why is that? Well, contrary to the majority of breakfast "yes or no" studies this one has both an exercise and and a cognitive performance aspect. Since I suppose that most of you are not living to train, but training to live, this is practically highly relevant. I mean, what's the use of "looking good naked" due to the purported benefits of working out "on empty" first thing in the morning if that reduces your cognitive performance in a way that you risk being fired?

Now that I've got everyone's attention, let's look at what exactly R.C Veasey and her colleagues did to find out whether having / not having breakfast before morning cardio or rest will impact cognitive performance and mood later in the morning. To this ends, the researchers recruited 12 healthy, active men in their early 20s with an average BMI of 24.5 ± 2.0 kg/m², who had to abstain from rigorous exercise and alcohol consumption prior to the exercise trials before they reported back to the lab after a 12h fast.

Do the online stroop test to get an idea of what the subjects in the study had to do and why it may in fact not be ideal to have breakfast when you are not exercising. After all, the results of the study at hand clearly suggest that the the accuracy in the stroop performance test decreases significantly in the "no exercise, but breakfast" condition.

"After confirming compliance to the study restrictions, a baseline completion of the cognitive tasks and mood scales was then undertaken, before participants were administered the test breakfast or remained fasted. During the 2 h rest period which followed, cognitive performance and mood were measured at 60 and 120 min. In between these periods, participants were allowed to read, write or watch a DVD. In the exercise trials (NB E and B E), participants then completed a treadmill run at 60% of their VO2, until 2.9MJ had been expended with heart rate and rate of perceived exertion (RPE) measured at 10 min intervals throughout. [...] On rest days (NB NE and B NE), participants rested for the equivalent amount of time. Cognitive performance and mood were reassessed before participants were administered a test drink, followed by a 90 min rest period where cognitive performance and mood was assessed at 30 and 75 min. This was followed by an ad libitum lunch where participants were asked to consume enough food to feel satisfied to a normal level. After lunch, they completed the cognitive tasks and mood scales for a final time and were then free to leave the laboratory." (Veasey. 2013)

"Hah?" Yeah, that was my initial reaction to the overcomplicated study protocol, but don't worry, after you've taken a peak at the following overview I guess, you will be able to identify how this corresponds to getting up, driving to the gym, working out and head to your working place with or without breakfast.

Illustration 1: Outline of the allegedly somewhat difficult to understand study protocol (Veasey. 2013)

You see? It's not so complicated as the scientists description of the protocol made it appear. Four conditions, total, two conditions with and two without 72g syrup flavor porridge oats with 360ml milk, each repeated twice with or without exercise after the initial rest period - that's all.

"Ok, whatever... what were the results? "

As the scientists had expected, the consuming breakfast prior to exercise did in fact elicit the most beneficial cognitive performance and mood effects following in the exercise conditions.

Figure 1: Cognitive performance, mental fatigue and tension in the four trials (Veasey. 2013)

The data in figure 1 does yet also reveal that having breakfast before rest had detrimental effects on the ability of the study participants' ability to rapidly process visual information and omitting breakfast improved their performance on Four Choice Reaction Time test.

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Whey and carbs as cognition booster and stress buffer for breakfast: In view of the results of a soon-to-be-published paper from the University of Helsinki clearly shows that a combination of whey and carbs for breakfast improves coping with mental tasks in healthy subjects compared to the "breakfast" used in the study at hand (Sihvola . 2013), it would appear prudent to remember that, when you rise and shine and decide to have breakfast - regardless of whether you intend to work out, or not (the increased protein intake may even help with the performance decline in the "breakfast, no exercise" condition - emphasis on may and assuming you don't ingest it in isolation just to end up hypoglycemic). Apropops, don't forget: Low GI carbs are your brain's friends (e.g. Micha. 2010; Cooper. 2012)

Bottom line: According to the results of the study at hand, you do have two options to maintain / optimize your "desk performance" (cognitive performance at the job) in the morning hours:

• either you fast and refrain from working out or
• you have breakfast and work out

It goes without saying that even minor changes in the protocol, e.g. the omission of the 120min rest period (I gather you don't need that long in the bathroom before you either leave the house and go for a jog, sit on your cycle ergometer or drive to the gym), for example could skew the results in a favorable way for the "non-breakfast condition", if  you don't stick to a meager 250ml of chocolate milk after your workout but indulge a real breakfast (see box on the right for a scientifically warranted suggestion)...

The latter is by the way a practice that has always worked pretty well for me. I did however have to realize that this does only work if you really eat and don't just down a protein, let alone whey shake that will only spike your insulin and send you down into the abyss of borderline hypoglycemia. A state which is certainly nothing your cognitive performance can benefit from (Lindgren. 1996).

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Highly suggested read: "Circadian Rhythmicity - "Breakfast" or "Breaking the Fast"? Fasting as Zeitgeber & All About King, Prince & Pauper" (read more)


References:

• Cooper SB, Bandelow S, Nute ML, Morris JG, Nevill ME. Breakfast glycaemic index and cognitive function in adolescent school children. Br J Nutr. 2012 Jun;107(12):1823-32. 
• Lindgren M, Eckert B, Stenberg G, Agardh CD. Restitution of neurophysiological functions, performance, and subjective symptoms after moderate insulin-induced hypoglycaemia in non-diabetic men. Diabet Med. 1996 Mar;13(3):218-25. 
• Micha R, Rogers PJ, Nelson M. The glycaemic potency of breakfast and cognitive function in school children. Eur J Clin Nutr. 2010 Sep;64(9):948-57.
• Sihvola N, Korpela R, Henelius A, Holm A, Huotilainen M, Müller K, Poussa T, Pettersson K, Turpeinen A, Peuhkuri K. Breakfast high in whey protein or carbohydrates improves coping with workload in healthy subjects. Br J Nutr. 2013 Apr 16:1-10.
• Veasey RC, Gonzalez JT, Kennedy DO, Haskell CF, Stevenson EJ. Breakfast consumption and exercise interact to affect cognitive performance and mood later in the day: a randomized controlled trial. Appetite. 2013 Apr 19.

Adelfo Cerame: Simple Recipes to Go With a Sensible Diet. A Practical Follow Up on the "Beach Ready Program"

Adelfo's latest pictures... believe it or not - after the Jr. Bacon Cheeseburger ;-)

With the last installment of his blogpost series here at the SuppVersity in the back of your heads, you should actually have a decent idea of how to train and split your macros to get "beach ready" in time. There is yet one thing of enormous practical importance that did remain somewhat in the dark. Where do you get those macros from? As Adelfo did of course point out, you are supposed to put a primer on whole foods, but I guess few of you will be happy with eating everything raw out of bag you carried with yourself home when you did your groceries at the farmer's market, supermarket or wherever you like to buy your foods... Are you the gal/guy who still feels that "healthy eating" equals downing blunt chicken breast, tuna and rice an nibbling on rice cakes as a "cheat"?!

Then today's follow up on Adelfo's highly popular "Adelfo Cerame's Beach Ready Program: A Blueprint to Shed The Winterfat in Time. Sample Workout + Diet Guide" from April, 18 2012 is for you and there is little for me (=Adel) to do, but lean back and have you enjoy Adelfo Cerame's cookery & nutrition class ;-)

Simple recipes to go with a sensible diet…

Now that you've got an idea of your daily overall energy requirements (depending on your goals) and the corresponding macronutrient goals, that you have internalized that you are supposed to prioritize protein and fiber in all of your meals and have - hopefully - finally realized that all foods are “OK” to eat - including those that contain carbohydrates! You don’t have to deprive yourself any more of certain foods because they are deemed evil.

My off-season macros

• Kcal: 2570
• Fats: 45-55g
• Carbohydrates: 250-300g
• Protein: 190-220g
• Fiber: 25-55g

Vegetables + fruits: At least 1 serving of both per day (and that doesn’t mean one cherry tomato!)

My current goals: Packing on lean muscle (off-season)

If you approach your nutrition with balance, moderation and consistency, you will be succeed - whatever your goals may be and no matter how long it takes!

I will take my own current dietary intake as an example to illustrate how to put all these important principles into practice. A sensible and above all flexible approach to what is - in my case - an off season diet.

I have outlined my current macro-nutrient intake as well as a handful of stats and my current goal in the infobox on the right hand side of this paragraph. It's advisable that you write a similar "primer" for yourself, especially when this is the first time you are dieting this way. This help you stay accountable and combine foods in a way that will allow you to "hit your macros" and grow, lose fat and/or increase your performance (or whatever other goals you had in mind, when you came up with the "rules") - for me the net result of this process looked like that:

• This was my food log from yesterday
  
  Meal 1 – Pre-Workout Meal/ Macros: 24g fat/ 51g carbs/ 44g protein/ 5g fiber
  
  
  
  I was out meeting with a client at a local coffee shop and by the time it was over I realized that it was time for me to train in an hour or so. So I knew that I would be caught for time and wouldn’t have time to cook, so I stopped by the nearest fast food spot and grabbed myself a jr. bacon cheeseburger that I knew would fit within my macronutrient goals for the day… went home and made myself a quick protein shake and grabbed an apple to go with that as well, along with my multivitamins, fish oil and vitamin D3, so still prioritizing protein and fiber and getting in my serving of fruit when breaking my fast. (don’t let the cheeseburger fool ya!) And it’s off to train I go!
  
  Meal #2 Post-Workout meal/ 20g fat/ 142g carbs/ 68g protein/ 11g fiber 
  
  
  
  After my workout, I was having the urge for some loco moco (it’s a Hawaiian dish) it’s pretty simple to make but can be pretty fattening if you order from a restaurant, so I made my own so to make sure that I would stay within my fat intake for the day. Your traditional loco moco dish uses white rice, burger patties, whole eggs and brown gravy – the only adjustments I made was using a leaner burger patty (96/4 extra lean) and used brown rice instead of white because more fiber in brown rice (again… prioritizing fiber!) I also threw in 200g of mixed greens on the side so I can get my serving of vegetables for the day as well ;-)
  
  Meal #3 before bed/ 7g fat/ 104g carbs/ 78g protein/ 22g fiber
  
  
  
  By the end of the night, I pretty much hit my goals for getting at least one serving of fruit, at least one serving of veggies and the majority of the 25-55g of fiber listed in the info-box a couple of paragraphs above.
  
  The only thing I had left to hit was my protein intake and that’s usually pretty easy - if nothing else, you just grab a protein shake or quest bar.
  
  Once I hit my goals for the day I usually use the rest of my energy allotment for the day to eat I have left in the fats and carbs department from whatever I feel like on a given day.
  

So at first glance, especially with the Jr. Bacon Cheeseburger I ate pre-workout…. You’re probably thinking ...

"WTF?! He eats like shit!!!"

An overview of my macronutrient intake for the day - de facto intake vs. goals.

But hold on there kemosabe… If you look below at my totals I stayed well within my macronutrient goals and hit more than enough fiber for the day.

In the end you will have to concide that "my approach" definitely has it's beauty, right? After all, I ate the foods I wanted, just as long as I stayed within my goals for the day.

Ah, and in case you're asking yourselves "What happened to the intermittent fasting? Didn't Adelfo follow an IF routine so successfully?" I still incorporate an intermittent fasting meal protocol into my regimen, because I love having my big Viking style feasts!

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Bonus: Adelfo's recipe of the week

Before signing off, I leave you with the recipe to one of my favorite post-workout meals. I call it the “Ahi Tuna Bacon Sashimi Bowl” – don't worry it sounds complicated, but is in fact very simple to make:

Healthy food does not have to taste blatant, it does not have to be difficult to prepare and it does not have to consist of chicken, broccoli and rice only. Adelfo's Ahi Tuna Bacon Sashimi Bowl is an excellent example, but by no means the only delicious and healthy food you can prepare in no time even if you are no Michelin-starred chef.

Ingredients (*):

• 10 oz. sashimi grade wild caught Ahi Tuna
• 1 strip of center cut bacon
• 400g of mixed greens (romaine, spinach, herb, slaw…)
• 2 (85g) baby beets
• 100g of sliced roma tomatoes
• rice wine vinegar, Ponzu sauce, Sriracha sauce
• 1 tbsp. sesame oil, sesame seeds

• Directions: (1) Throw in all your greens in bowl (2) Pour some rice wine vinegar and ponzu sauce with the mix and toss (3) Layer the baby beets and diced tomatoes on top of the greens (4) Layer the sliced and diced ahi tuna next (5) Sprinkle the bacon that you fried and cut into pieces (6) Pour your tbsp. of sesame oil on top of everything (7) Top it off with sriracha hot sauce and sesame seeds (8) Eat (9) Wash it down with a shot of sake and a cold Sapporo ;-)

*These portions are based on my macronutrient goals for the day, so measure accordingly to yours… and shot of sake and glass of Sapporo is optional ;-)

You Want Maximal Performance & Size Gains + Complete Thigh Development? Then Full Squats are For You!

So you got to squat?! But how?

I guess that many of you will be missing more recent news on training programming and exercise selection. And I would in fact love to write about these topics more often, but with 37% of the US population being overweight, 99% of the studies deal with the question: "How can exercise help the overweight, obese and morbidly obese survive?" The interest or rather the funds for research as into such profane things as the effect of range of motion in heavy load squatting on muscle and tendon adaptations, on the other hand, are so scarce that K. Bloomquist's, H. Langberg's, S. Karlsen's, S. Madsgaard's, M. Boesen's, T. Raastad's latest paper is almost an exotic bird and that in a journal with the auspicious title the European Journal of Applied Physiology.

Interesting studies on specific exercises are rare

In their latest study, the researchers from the Copenhagen University Hospital in Denmark and the Norwegian School of Sport Sciences tried to elucidate, whether the deep (DS) and shallow (SS) squatting would have a differential effect on specific adaptations in the front thigh muscles, the patellar tendon and the 17 male particpants in their early twenties.

Table 1: After an initial familiarization (week 1) and pretesting week (week 2) the subjects preformed the above workout; submax exercises were preformed for 8 reps with a weight the subjects could lift for 13-14 reps (Bloomquist. 2013)

Yet while all subjects were sports students, the scientists excluded those who had been squatting regularly within the last six months (probably to see statistical significant effects):

Learn about the efficacy of other exercises in the SuppVersity EMG Series (learn more)

"During the intervention, subjects were requested not to participate in endurance sports more than three times per week, or to engage in strength training of the lower extremities. After a 1-week familiarization period, subjects were tested and paired according to their initial DS strength. From each pair one subject was drawn, by envelope, into either the DS or SS group with the other member of the pair allotted to the opposite group."

After the 14-week (effectively only 12w) training period the subjects performed a follow up test in the course of which the researchers evaluated the 1-RM and isometric strength, the cross sectional area of the front thigh muscle, the total lean body mass, the collagen synthesis in the patellar tendon and the jump performance.

Figure 1: Changes in muscle power / performance (jump squat & counter movement jump) and size in the shallow squat and deep squat group (Bloomquist. 2012)

I guess a brief glance at data figure 1 should suffice to see that performance wise the full-squat (0–120 ° of knee flexion vs. 0-60° for shallow squats) play in a whole different league:

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• much higher torques (not shown), slightly more pronounced gains in 1RM strength (not shown)
• greater increase in leg mass, significantly higher increase in CSA with increases in CSA on all not just the proximal sites
• greater jump squat & counter movement jump (CMJ) performance increases

In view of these favorable results the only reason not to deep squat would probably be that it could hurt your patellar tendon, but contrary to what the scientists had expected,...

"[...] neither group elicited gains in patellar tendon CSA or collagen synthesis.[...] Though not expected, these results are in accordance with several resistance training studies that have shown that increases in strength were not accompanied by increases in tendon CSA. Rather, a markedly altered elastic modulus was found in these studies, implying a change in the composition of the tendon structure instead of the size."

In trained athletes / sport students a picture perfect deep squat may thus be considered a save and highly efficient way to build bigger and stronger wheels.

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Did you know that you can use your 1-RM squat to calculate your training weight on hamstring exercises? Ebben et al. found the following equations to yield reliable results: (1) seated leg curl load = squat load (0.186) + 10.935 kg, (2) stiff leg deadlift load = squat load (1.133) - 86.331 kg, (3) single leg stiff leg deadlift load = squat load (0.443) - 3.425 kg, and (4) good morning load = squat load (0.961) - 105.505 kg (Ebben. 2010). I have my doubts that this will work for all of you, but give it a try, it's free ;-)

Bottom line: So if you "got to squat" as the imagine next to the introductory paragraph clearly suggests, the deep squat is the way to go? Well... compared to the shallow squat to a knee angle of 90°, I would fully subscribe to that (as long as you know what you are doing and not hurting yourself by squatting with improper form), when it comes to the "to parallel" vs. 90° knee angle questions, the advantage of the full squat may well start to melt away.

Yet while the data in the SuppVersity EMG Series suggests that this is the case for the quads, it is highly questionable if the glute development the aformentioned slightly sexist image is unmistakably hinting at will not still suck if you don't squat to a 120° knee angle. Try it for yourself and feel the glutes working. If it's the pretty behind you are after, you won't get around squatting "deep" as far as the squat is concerned. But hey, who says you got to do that with weights that are so heavy that they put you at risk of injury?

References:

• Bloomquist K, Langberg H, Karlsen S, Madsgaard S, Boesen M, Raastad T. Effect of range of motion in heavy load squatting on muscle and tendon adaptations. Eur J Appl Physiol. 2013 Apr 20.  
• Ebben WP, Long NJ, Pawlowski ZD, Chmielewski LM, Clewien RW, Jensen RL. Using squat repetition maximum testing to determine hamstring resistance training exercise loads. J Strength Cond Res. 2010 Feb;24(2):293-9.