Eccentric Exercise IGF1 & Athlete's Heart; Long or Short Intervals, Both Improve Arterial Stiffness. Plus: Exercise Heals Wounds & Makes You Rust Proof Within One Year!

Controlled exhaustion = positive adaptation; continuous exhaustion = wear and tear = one out of 57,002 who suffer from cardiac arrest during a marathon (data based on Webner. 2012)

As announced on Saturday, already this is a "special edition" of the On Short Notice series, focusing exclusively on exercise related studies. With

• two studies on heart health, 
• one on wound healing and the last one on the 
• bullet proof endogenous anti-oxidant system of trained athletes, 

this installment of the "Exercise News Roundup" and two studies on different HIIT, it does however have both a health, as well as a HIIT focus.

I know that does not sound as sexy as being big and buffed, but what's the use of that if you don't fit the coffin, you're about to need, when your looks are more important to you than your health?

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IGF-Response to exercise implicated in "athletes heart" A group of polish researchers describes in their latest paper that's been published ahead of print in the International Journal of Sports Medicine, how the differential IGF-1 response to eccentric (ECC) and concentric (CON) arm exercise in 10 trained strength athletes (1.5-2.0 h on 3-5 days weekly) and 10 age-matched healthy non-trained subjects could explain the differences in the degree of left ventricular hypertrophy, the scientists had measure via M-mode and 2D Doppler echocardiography beforehand (Zebrowska. 2012).

IGF1 and left ventricular hypertrophy (LVH): The correlation stands out of question, but what about the implications? Is this a causative relationship? And what's more: How dangerous are LVH  and having an athlete's heart, at all?

The athletes with LVH did not only have higher IGF-1 levels at baseline (52±5 nM vs. 46±7 nM for controls, p<0.05), they also showed a significantly more pronounced IGF-1 response during the eccentric (ECC) exercise test, with athletes with LVH exhibiting 30% higher and athletes without LVH 15% higher IGF-1 levels than untrained controls (54±6 nM). Moreover, both CON and ECC exercise resulted in higher serum IGFBP-3 levels in LVH athletes compared to controls (242±57 and 274±58, athletes, vs. 215±63 and 244±67, controls, nM, p<0.05), while no differences in other hormones were found between groups. Yet though the scientists' conclusion that these findings would "suggest a role of IGF-1, possibly released from contracting muscle, in stimulating LV hypertrophy in resistance training" is certainly right, we would be ill-advised to jump to any conclusions, hastily by simply (and faultily) equating correlation and causation, here.

Moreover, we should acknowledge that the previously accepted paradigm that LVH, per se, is a bad thing that has to be avoided at all costs is actually not supported by empirical evidence, or as Florescu et al. have it "'Supranormal' cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with 'supranormal' cardiac function, and there are no markers of myocardial fibrosis." (Florescu. 2010)... in short: in the absence of myocardial fibrosis, a big heart is nothing you will die from - how IGF-1 could actually prevent the latter, i.e. the occurrence of fibrotic structures due to uncompensated growth of the heart muscle, would yet be the topic for another quite lengthy blogpost ;-)

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This image shows a study participant of another study during a VO2 max test on the exact same bike Rakobowchuk et al. used (WSCU.edu). Wrt to the protocols the researchers remark "the protocols involved an identical total training volume and time commitment but differed regarding metabolic stress" With the HIIT trial inducing greater metabolic stress due to the longer periods at supra-amaximal workloads (cf. Turner. 2006).

Heavy or moderate interval training equally heart healthy - at least if you take their effect on arterial stiffness and heart rate dynamics as a measure. That's the message of an article that was published ahead of print in the European Journal of Applied Physiology at then end of last week. During a six-week experiment, Mark Rakobowchuk and his colleagues from the University of Essex and the University of Leeds investigated which of the following protocols (all performed three times per week, for a total of 18 session; 2min warm-up for each; cf. Rakobowchuk. 2012),

• MIIT - moderate intensity interval training consisting of 10s : 20s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression), or
• HIIT - high intensity interval training consisting of 30s : 60s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression),

would elicit more favorable changes in carotid artery stiffness, blood pressure, and heart rate variability in a group of 20 healthy, previously untrained young men and women (n = 7 men and 13 women; age 23.5y; BMI 23).

Trainees who want to increase their VO2max should still do HIIT, because only the subjects in the HIIT training group achieved statistically significant increases with respect to this outcome measure (+14% in HIIT vs. +3% VO2 max in MIIT).

Just as the scientists had speculated, their hypothesis that irrespective of the metabolic stress, which would be higher in the HIIT vs. the MIIT trial, the total volume, which was identical would determine the overall adaptive response. For them it was therefore not surprising that all measured parameters of  heart health, i.e.blood pressure, heart rate dynamics and carotid arterial stiffness, improved without significant inter-group differences. Most notably, though, those with the highest arterial stiffness before the trial saw the greatest reductions!

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Figure 2: Additional exercise sped up the wound healing process only in the obese rodents, not the lean ones (Pence. 2012)

Exercise speeds healing of subcutaneous wounds in obesity. This was allegedly observed only in obese rodents, but since the underlying mechanism was neither mediated by gene or protein expression of proinflammatory cytokines interleukin-1A and tumor necrosis factor-alpha or the anti-inflammatory cytokine interleukin-10 in the wounds, I felt it was still worth mentioning, also because it is, as the scientists point out,

"the first report of an exercise effect on wound healing that is unrelated to alterations in wound site inflammation." (Pence. 2012) 

Future trials will have to elucidate whether clotting and homeostasis, which occur in the earliest stage of wound healing, approximately 30 min after the trauma may be involved in this phenomenon.

In this context, some of you will probably remember my recent post on the "Antithrombotic effects of caffeine blunt platelet activity in response to interval training" that exercise increases the tendency of your blood to clot - a tendency that does obviously come handy, when you are bleeding. That the increase in coagulation factors came into effect only in the obese, yet not in the normal weight control, in turn, could be related to the presence of existing hemostastic imbalances due to obesity which would have been corrected by the 30min of treadmill running the rodents in the exercise groups performed at a pace of 12 m/min on a 5% incline for the final 30 min of the light period (0930–1000 h), three days before until five days after the wounding.

A bunch of maggots on a diabetic wound.

Be that as it may, there are more than enough sedentary, "SAD dieting" (and the standard high fat diet rodents are fed in studies like this is nothing but a clone of the S-tandard A-merican D-diet) full-blown or pre-diabetic obese human beings who could likewise benefit from as little as 30min of daily aerobic activity. I mean think about it, if you could thus avoid having 50-100 maggots being placed on those nasty diabetic wounds (see picture on the right) that would never heal without those tiny critters secreting their salivary juices onto the wound to liquefy and subsequently ingest and further degrade the dead tissue in their gut, you can hardly argue that this is too much to ask for, can you?

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"Rust proof" athletes don't need vitamin pills with copious amounts of anti-oxidants and don't have to be afraid of fruit with their synergistic blend of small, but highly effective and synergistic amounts of vitamins and polyphenols, either.

Oxidation proof after 1 year+ of regular aerobic + anaerobic training. According to a paper that's soon going to be published in Medicine & Science in Sports & Exercise trained athletes between the ages of 21 and 35yrs who had been participating in a structured exercise training program (including both aerobic and anaerobic) for the past 12 months, with each session lasting no less than 45 min per session, as well as no less than three sessions per week, are virtually "rust proof".

That's at least my allegedly nonchalant interpretation of the non-existent increases in serum markers of oxidation the scientists from the University of Memphis observed in their 12 male subjects (BMI 25kg/m², body fat 12.8%; VO2Max 20 ml/kg/min) in response to four training sessions separated by 1 wk.

The Sessions were counterbalanced and included either a no-exercise condition (subjects simply rested for the entire period) or one of the these three:

• MISS - moderate intensity + duration steady state: 70% HR reserve for 60min; total time: 60min with 60min of actual work
• HIIT - high intensity + moderate duration interval sprints: 5x60s at 100% + 225s recovery yielding a 1:3.75 work-to-rest ratio ("Within each interval, subjects were instructed to pedal between 80 and 100 rpm for the first 45 s, and then for the final 15 s, subjects were instructed to pedal as fast as possible"); total time: 20 min with 300s of actual work
• MaxIIT - maximal intensity + short duration interval: 10x15s at a wattage of 200% of VO2max, followed by 116s of recovery (1:7.7 work-to-rest ratio); total time: 20 min with 150s of actual work

All exercise bouts were performed on the same cycle ergometer used for the GXT, and subjects reported to the laboratory in the morning (0600–0900 h) after a minimum 10-h overnight fast. The HR was continuously monitored via Polar (TM) HR monitors and blood was drawn at the end of the 20-min rest period  (corresponding to the immediate postexercise blood samples) and 30 and 60 min after the 20-min rest period (corresponding to the postexercise blood samples).

Figure 3: Total antioxidant capacity (TEAC), SOD, CAT and GPx values immediately (0min), 30min and 60min after the respective exercise bouts (data based on Farney. 2012)

The respective total work performed during the trials was 461.1kJ, 96.9kJ, 96.9kJ for the MISS, HIIT and MaxIIT trials, respectively, the perceived exertion was highest in the MaxIIT trial (16.7 vs. 15.6 for HIIT and 13.5 for MISS), while the maximal heart rate 171.7bpm was achieved in the HIIT trial. Still,

"No differences were noted in malondialdehyde, H2O2, advanced oxidation protein product, or NOx between conditions or across time (P > 0.05) [while the a]ntioxidant capacity was generally highest at 30 and 60 min after exercise and lowest at 0 min after exercise." (Farney. 2012; my emphases)

If you will, you could even go one step further and argue that the total antioxidant capacity increases in well-rested, well conditioned athletes in response to exhaustive exercise bouts. Though, this increase reaches statistical significance in the MaxIIT trial only (see figure 3).

Hungry for more news? Visit the SuppVersity on Facebook!

That's it for today, ... but only as far as SuppVersity posts go. In about 2h at 1PM (EST), to be precise you can - if you want - listen to me on Super Human Radio. I am going to pick up on the topic of the first hour which is "Moderate Alcohol Consumption how (Un-)Healthy is it really" and do my best to provide some insights into the discrepancy that exists between reliable scientific evidence, the media coverage on the topic and Mr Average Joe's interpretation of the latter. And if you ain't into booze, just work out ;-) [update: download the podcast]

References:

• Farney TM, McCarthy CG, Canale RE, Schilling BK, Whitehead PN, Bloomer RJ. Absence of blood oxidative stress in trained men after strenuous exercise. Med Sci Sports Exerc. 2012 Oct;44(10):1855-63.
• Pence BD, Dipietro LA, Woods JA. Exercise Speeds Cutaneous Wound Healing in High-Fat Diet-Induced Obese Mice. Med Sci Sports Exerc. 2012 Oct;44(10):1846-1854.
• Rakobowchuk M, Harris E, Taylor A, Cubbon RM, Birch KM. Moderate and heavy metabolic stress interval training improve arterial stiffness and heart rate dynamics in humans. Eur J Appl Physiol. 2012 Sep 16.
• Turner AP, Cathcart AJ, Parker ME, Butterworth C, Wilson J, Ward SA (2006) Oxygen uptake and muscle desaturation kinetics during intermittent cycling. Med Sci Sports Exerc 38:492–503.
• Webner D, Duprey KM, Drezner JA, Cronholm P, Roberts WO. Sudden cardiac arrest and death in United States marathons. Med Sci Sports Exerc. 2012 Oct;44(10):1843-5.
• Zebrowska A, Waśkiewicz Z, Zając A, Gąsior Z, Galbo H, Langfort J. IGF-1 Response to Arm Exercise with Eccentric and Concentric Muscle Contractions in Resistance-Trained Athletes with Left Ventricular Hypertrophy. Int J Sports Med. 2012 Sep 7.

Green Tea Extracts, Athletes and a Preliminary Answer to the Question: "Are Anti-Oxidants For Athletes Not?" No True Benefits or Negative Effects of 1g GTE in Sprinters

The supplement that was used in the study at hand was a commercially available product from Olimp Labs, a Polish producer of bodybuilding and fitness supplements.

Before I even go into more detail, I would like to point out that the study today's SuppVersity article will talk about is not able to answer the question whether anti-oxidants are for athletes once and for all. Why? Well, the subjects in the recently conducted experiment by Ewa Jówko, Barbara Długołecka, Beata Makaruk and Igor Cieslinski were sprinters from a University Sports Club, and they received a green tea supplement - so who can guarantee that a bodybuilder taking vitamin C would not have a totally different reaction to a totally different anti-oxidant?

No one can and that's why I'd like to ask you to go back to some of the previous articles on that matter and remind yourself that there is evidence that the provision of significant amounts of supplemental antioxidant can blunt the beneficial adaptive response to exercise (learn more and even more).

Learn more about hormesis and potential neg. effects of antioxidants at the SuppVersity

Is Vitamin E Good for the Sedentary Slob, Only?

NAC Impairs Anabolic Effects of Exercise

Vitamin C + E Hamper Gains in the Elderly

C+E Useless or Detrimental for Healthy People

Vitamin C and Glucose Management?

Antiox. & Health Benefits Don't Correlate

Apropos "significant amounts"! If we take a look at the amount of green tea extract, the 16 male sprinters (21.6 y; 76.9kg; 11.8% body fat) received, a question arises: Are 2x250 mg of standardized GTE (245 mg polyphenols, including 200 mg catechins, among them 137 mg epigallocatechin-3-galate) a "significant amount" of green tea extract (GTE) if they are consumed twice daily?

I guess there may be supplement junkies out there who consume way more than this 1g of green tea extract everyday. Based on the dosages in studies that report beneficial effects of GTE, 1g is yet already on the high(er) side of the dosing continuum and thus unquestionably a "significant amount" of green tea extract, which was administered in a randomized controlled crossover study that was conducted during preparatory phase of yearly training cycle (after transition period) of the sprinters all of whom had more than 4 years of training experience.

What do the latest reviews say about exercise + antioxidant supplementation? In spite of the fact that you will find reviews with different undertones, the vast majority of reviewers concludes that convincing evidence of the long-assumed benefits of anti-oxidant supplementation does not exist.Whether this warrants conclusions as the one Mari Carmen Gomez-Cabrera, Michael Ristow and Jose Viña formulate in their 2012 paper(s) and "the vast majority of experimental evidence clearly advises against this supplementation" (Gomez-Cabrera. 2014), however is still a matter of open debate (Holloszy. 2012).

The two 4-week treatment periods (during which half of the subjects received GTE and the other half PL, and vice versa) were separated by a 4-week washout period. The duration of the washout period was selected based on the results of one previous study (Brown. 2011), in which 6-week supplementation with higher amounts of catechins (800 mg/day) was used on obese subjects. In view of the fact that the plasma catechin concentration in this study returned to its baseline level after at least 2 weeks of washout period, we can safely assume that a 6-week washout in highly active non-obese individuals should be enough to get rid of all the effects of only 250mg of catechins.

Both GTE and PL were administered in the form of dark gelatin capsules (Olimp Labs, De˛bica, Poland), identical in appearance (i.e., size, shape, and color); the same dosage regimen was used (two capsules twice a day). One GTP capsule contained 250 mg of standardized GTE (245 mg polyphenols, including 200 mg catechins, among them 137 mg epigallocatechin-3-galate) and additional substances (maltodextrin, microcrystalline cellulose, and magnesium stearate). Therefore, each participant was administered 980 mg polyphenols daily. PL capsules contained microcrystalline cellulose, magnesium stearate, and maltodextrin instead of GTP."

Compliance was measured by counting the capsules the subjects returned. Participants who returned no more than 15 % of their capsule dose were classified as "compliant". At the end of each of the two 4-week treatment periods, the sprinters performed a repeated cycle sprint test (RST) on a cycle ergometer (Ergomedic 839E, Monark, Sweden).

Based on the food logs, the scientists decided that there were no significant nutritional differences between the two phases of the study (Jówko. 2014)

Dietary standardization: The participants were asked to not modify their diet for the duration of the study, except for refraining from consuming any products containing green tea and limiting the intake of caffeine-containing drinks to one cup per day. Moreover, they were asked to maintain a similar
diet for both treatment periods. During both the first and the second treatment periods (during 7 days preceding each RST), the participants filled out a 3-day dietary record (covering 2 week days and 1 day of the week end).

The test consisted of four consecutive 15-s bouts (4 x 15 s), each of them with base set according to the Wingate procedure and separated by 1-min rest intervals. The subjects were asked to cycle for 15 s, as fast as possible, against a constant load (75 g/kg body weight).

The performance tests were performed in the morning following 12-hovernight fast, at air temperature between 19 and 21°C and with 40–60 % relative humidity. The subjects were instructed to not perform hard physical training for 48 h and avoid drinking tea and caffeinated beverages within
24 h prior to each of the RSTs.

Figure 1: Changes in blood indices of acid–base balance & lactate concentration induced by the repeated sprint test (49 x15 s) in sprinters (n=16) after 4-week supplementation with placebo (PL) or green tea extract (GTE; Jówko. 2014)

As you can see in Figure 1, there were no treatment (only time) effects as far as the acute changes in blood indices of acid–base balance and plasma lactate concentration are concerned. Against that background it's not surprising that there were no changes in the performance results of the repeated sprint test, either. Peak power, mean power, total work output, and fatigue index during the Wingate protocol were identical.

Table 1: Changes in blood parameters of oxidative stress and muscle damage induced by the repeated sprint test (49 x15 s) in sprinters (n=16) after 4-week supplementation with placebo (PL) or green tea extract (GTE; Jówko. 2014)

An observation that certainly raises the question, whether the treatment effects that were observed for the total antioxidant capacity and Superoxide Dismutase (SOD) levels (see Table 2) are even physiologically significant. Personally, I'd say no, because higher TAC and SOD levels have no health or performance value on their own.

Previous studies suggest that NAC impairs the adaptive response to exercise | learn more

Bottom line: In spite of the fact that the study at hand does not provide evidence that the commonly assumed beneficial ergogenic effects of green tea supplements exists, the results are still good news for green tea supplement users. They do after all suggest that the provision of significant amounts of anti-oxidant catechins does not appear to hamper the adaptive response to exercise.

In that, it's important to mention that the study at hand acquits only green tea, yet not vitamin C, NAC & co which act via different mechanisms of the charge of having potentially detrimental effects on the adaptive response of athletes, average joes and/or obese type II diabetics... and just to remind you: Theoretically the response of all three of them could be totally different | comment on Facebook!

Reference:

• Brown, A. L., et al. "Health effects of green tea catechins in overweight and obese men: a randomised controlled cross-over trial." British Journal of Nutrition 106.12 (2011): 1880-1889.
• Gomez-Cabrera, Mari Carmen, Michael Ristow, and Jose Viña. "Antioxidant supplements in exercise: worse than useless?." American Journal of Physiology-Endocrinology and Metabolism 302.4 (2012): E476-E477. 
• Holloszy, J. O., et al. "Response to letter to the editor by Gomez-Cabrera et al." American Journal of Physiology Endocrinology and Metabolism 302 (2012): E478-E479.
• Jówko, Ewa, et al. "The effect of green tea extract supplementation on exercise-induced oxidative stress parameters in male sprinters." European Journal of Nutrition (2014): 1-9.

Sucralose is for Diabetics Not, Scientists say. But How Significant is the Cholesterol Increase They Observed?

This way of consuming Splenda is quite certainly going to increase your cholesterol levels ;-)

I guess, all of you will still remember the show Carl and I did on the "Pro-Insulinogenic Effects of Artificial Sweeteners" (read more), right? The one where I tried to point out that even if there was a meager change in the insulin response, this would only be a problem if there was any truth to  narrow-minded condemnation of insulin as the deadly obesity hormone, so that, in the end, the whole hoopla turned out to be way less daunting than some scare-mongers would have it.

Yet while something deep inside of me is telling me that the latter is probably going to be the same with the recently published study that's at the focus of today's SuppVersity article, cannot refute that the data from that very rodent study that was published in the Journal of Nutrition Sciences does clearly suggest that...

...sucralose increases cholesterols!

That certainly doesn't sound so scary to you, as it does to someone who still adheres to the "cholesterol is the root cause of all evil" paradigm, yet still. The fact that the administration of  11 mg/kg body weight of SPLENDA® over the course of 6 weeks to "intensifie[d the already existing] hypercholesterolemia in STZ-induced diabetic rats" (Saada. 2013) does sound as if there must be something to the rumors about sucralose being one of the main ingredients of devil's excrements.

Would having your coffee with Splenda instead of sugar make this cookie even more hazardous to your glucose levels and what about your waistline? Read more about the effects of artificial sweeteners on glucose-management, insulin and obesity in a previous article.

Now 130-150mg of sucralose per day is unquestionably a whoppy dose of artificial sweeteners. After all, this stuff is approximately 600x sweeter than sugar. Sounds like a total overkill, but if you do the math, i.e. 150mg x 600 = 90,000 mg, you will realize that this is not more than the non-caloric sweetness equivalent of ~1.5 Snickers bars. And if the figures a Scivation rep mentions in a post on the most popular bodybuilding website on the planet are correct this would be exactly 10 servings of their highly popular BCAA formula. Considering the fact that for most people Xtend is probably not the only dietary source of sucralose in the diet it is thus not a totally unrealistic dose (especially for those diabetic or non-diabetic sugar addicts, who are using splenda as a means to sweeten their tea, coffee and whetever else, as well).

Good you've made it past the introduction

That being said the message that sucralose "intensifie[d the already existing] hypercholesterolemia in STZ-induced diabetic rats" (Saada. 2013) appears to be even more scary.

Fortunately (or unfortunately for the "sweeteners are devil's excrements"-faction out there), this is not your average "Pubmed-Warrior blog", where the authors read a headline copy and paste the conclusion of the abstract and try to sell it as "science news" and I do not leave you hanging with the inappropriately overgeneralizing conclusion of the author's that

"[...] diabetic people consuming high amount of sucralose must check their lipid profile to avoid diabetic complications" (Saada. 2013)

Now, it is obviously right that diabetics should "check their lipid profile" on a regular basis, but if you look at the actual study outcomes, it is hard to argue that this would be particularly important for those of them who use SPLENDA® on a regular basis.

Figure 1: Changes in blood glucose, insulin, triglyceride and total (TC), HDL, and LDL cholesterol, as well as the TC/HDL levels after 6 weeks on 150mg/day sucralose (Saada. 2013)

After all, the "dangerous" increase in cholesterol the scientists observed in their lab animals (remember: we are not even 100% sure the same is going to happen in human beings) is not just accompanied by highly desirable desirable reduction in glucose (-22%) and triglycerides (-22%), it also leaves the CVD-relevant ratio of total to HDL cholesterol literally unchanged (+2%, n.s.).

Moreover, if you look at the way statins help managing cholesterol, but increase diabetes risk, you could even speculate that there is a yin and yang connecting the two metabolic pathways, where a lower strain on the one side will precipitate a higher strain on the other. Within this paradigm, the increase in cholesterol, which is by the way something many people who are "going paleo" will see, as well, could be a totally normal part of a "balancing" process that has nothing to do with the pathological overprodcution (always remember this is not about eating too much cholesterol) of highly oxidizable small and very small density lipoproteins people fear like the plague.

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In addition to reductions in blood glucose and triglyceride compared to cornflakes & co, the regular consumption of whole eggs increases HDL's ability to carry lipids out of the macrophages. If these accumulate, they will turn the macrophage into pro-atherogenic foam cells (learn more).

Bottom line: At least in my humble opinion, the results of this study don't imply that diabetics should stay away from sucralose. In the end, the benefits of lower glucose & triglyceride levels will outweigh the "downsides". This is all the more true, in view of the fact that we (a) the total-cholesterol-to-HDL-ratio remained essentially the same and (b) don't have data on the changes in lipoprotein particle profile. After all, improved glycemia and reduced triglyceride levels often go hand in hand with heat-healthy changes in the particle size distribution that is still totally ignored by way too many researchers.

That being said, the reduction in 10% reduction in TBARs, a marker of oxidative damage, clearly indicates that the rats with "increased" cholesterol levels were less inflamed than their sugar guzzling peers.

Needless to say that the same applies for the healthy rodents, where the changes in blood glucose, triglycerides and total, HDL and LDL cholesterol were much less pronounced, but the tendencies identical.

References:

• Saada H, Mekky N, Eldawy H, Abdelaal A. Biological Effect of Sucralose in Diabetic Rats. Food and Nutrition Sciences. 2013; 4(7a):82-89.

Meat Science: To Cook or Not to Cook? The Raw Truth About Antioxidants in Raw and Cooked Meat and Fish.

Image 1: Now, that we know that meat is not
bad for you. Let's get to the meat of the matter:
Is raw meat better than cooked meat?

"Eat Raw!" If its referring to peppers, tomatoes and salads, even the Vegan lobby won't disagree with this slogan, yet when it comes to eating raw meat, dairy and eggs, hell breaks lose. "Don't do that you will kill yourself!" is what you will hear even from respected scientists. Strangely, I am eating raw eggs and other raw stuff on a daily basis without noticing any detrimental health effects whatsoever. All bacteria-hysteria aside (this would be the topic for a whole new blogpost, cf. red info-box at the bottom), the idea that meat has to be cooked before it is eaten is actually counterintuitive. I do not want to bring up the "Look at the lion, does he cook his pray before savoring on his bloody prey?"-debate, but didn't you ever ask yourself, why the same people who are scared of a medium steak, order their veggies steamed, or even raw (again see red info box at the bottom of the page), so that the antioxidants in them do not get damaged by the heat. Assuming that these people are aware that raw meat is full of healthy antioxidants (I assume many or them are not, though), common wisdom about the effects of heat on anti-oxidants tells us that they should be eating all our foods raw. As it turns out, though, even that may not be the optimal strategy to boost your antioxidant defenses...

A recently published study by Serpen et al. (Serpen. 2011) showed that the total antioxidant capacity (TAC) of meat and fish actually peaked after brief (<5 min) heating at 180°C - intriguing, no?

The Turkish scientists had bought four samples of your favorite meats and fish - chicken (breast), pork (tenderloin), beef (tenderloin) and fish (Sea bream, fillet) - at a local market, determined the proximate composition (cf. fig 1) of the samples and cut identical cylindrical (5x2cm) slices from the samples.

Figure 1: Composition of raw meat extracts (data adapted from Serpen. 2011)

In the next step, Serpen and his colleagues determined the total antioxidant value of raw and thermally treated meat / fish samples using a process that is called the QUENCHER method. The method was described by the same authors in a previous paper (Gökmen. 2009) and has already become a widely used and generally accepted way of determining the total antioxidant content of foodstuff.

Figure 2: Total antioxidant capacity (calculated average from ADPS and DPPH probes) of meat and fish samples after 0, 5, 10, 15 and 20 minutes of heating at 180°C (data calculated based on Serpen. 2011)

As can be seen in figure 2, where I plotted the mean total antioxidant values of the meat / fish samples as measured by ABTS and DPPH challenges, heating at 180°C does not - as common wisdom would have it - lead to a linear or even exponential decline of the antioxidant capacity of raw meats and fish. The total anti-oxidant capacity rather peaks at around 5 minutes, decreases thereafter, just to rise again at about 20 min. According to the scientists, the highly non-linear effects of heating on the antioxidant value of various meats and the observable variety in heat responses among the different samples can be explained by the interaction of the following processes

1. denaturation and exposure of reactive sites of proteins; 
2. thermoxidation and degradation of endogenous antioxidants; 
3. formation of antioxidant MRPs (Maillard Reaction Products)

While some antioxidants are destroyed in the course of the heating process, others are created. This interplay appears to be most pronounced in the case of chicken (breast) and is the least obvious in fish (Sea bream fillet). Yet, despite the fact that short-fried <5 min meat and fish appears to be the best choice in terms of its overall antioxidant properties, specific anti-oxidants, amino acids and proteins, such as L-cysteine could get damaged even in the course of very brief heating processes. Furthermore it should be mentioned that other than a chef would do it, the scientists removed their probes from the oven and cooled them down immediately, in order to stop the continuing chemical processes. To see the same results as the scientists did for their 5min-steak, you would thus have to fry it for no more than let's say 2 minutes (this is just a very rough estimation) to make up for the ongoing reactions that won't stop if you do not shock-freeze your food before you eat it.

Note for the non-Europeans: Just in case you did not see it on CNN - the EHEC bacteria that killed people in Germany and all over Europe did not come from raw meats, but from sprouts. And it was the prejudice that raw meat, dairy and eggs were the worst (if not only) offenders, when it comes to food poisoning, that significantly hindered the investigations into the roots of an infection that has killed 37 people (according to Bild.de, 07-02-2011) in Germany, alone, when the first patients were hospitalized a few weeks ago.

Bottom line: While heating is obviously less detrimental to the overall antioxidant capacity of meat and fish, as some raw food eaters (and interestingly even the steam cooker faction) would have it, it remains questionable how you can reproduce the optimal fyring time of 5 minutes without immediately deep freezing your meat in a way, which would not leave you with your a steak that would be at least pretty rare. In turn, this means that a steak without a few drips of blood will not provide an optimal level of total antioxidants (TAC). Now, its up to you to decide whether a 2.3% decrease in mean TAC values are worth eating your steak rare - I would say no, but I don not love my steak rare, anyways, but I also read Sean Casey's formidable article on AGE formation, so if you cannot get over your socialized aversion against raw meat, dairy and eggs for what it does contain, i.e. antioxidants, then maybe for what it does not contain, which is advanced glycation end-products ;-)

Study Puts "?" Behind Beneficial Health Effects of Veggies! Is There No Correlation Between Antioxidant Content & Beneficial Health Effects of Cucumber, Lotus & Rape!?

Don't obsess about "optimal" antioxidant contents, just eat your veggies!

Over the past couple of weeks, ... no actually over the past years I have repeatedly written about the concept of (mito-)hormesis and its consequences for the well-established, but not necessarily accurate free radical theory of aging (and for some people everything else). ROS, i.e. reactive oxygen species, have been established as an important signalling molecule that is - among other things - heavily involved in the insulin sensitizing effects of exercise. "Inflammation" makes muscles grow and burns body fat and the "what doesn't kill me makes me strong" principle appears to reign everywhere you look.

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That being said, the latest study from the Institute of Health and Environmental Medicine in Tianjin, China, opens another "anti-antioxidant" Box of Pandora. One that puts a huge questionmark behind the implications of hundreds of thousands of scientific studies, when it says in it's title, already: "No correlation is found for vegetables between antioxidant capacity and potential benefits in improving antioxidant function in aged rats"

"Skin of Grape Tomatoes Contains Max. Amount of Antioxidants" - You can find this and dozens of other daily updated SuppVersity Science News on www.facebook.com/SuppVersity

This is a title that may in fact change the way we look at study results like those of a recent study by Valdez-Morales, et al. (2014) investigating the "best" = highest antioxidant tomato, the results of which you are about to find among the ~20/day SuppVersity Facebook News @ www.facebook.com/SuppVersity - don't forget to like it, or you'll miss out on the latest science news!

If the results of the study can be confirmed by an independent team for vegetables other than lotus root, rape or cucumber and if there is an identical mismatch between the in-vivo anti-oxidant capacity and the potential benefits in improving antioxidant function in (aged) humans.

This would be big and highly consequential news for nutrition experts, scientists and average Joes and Janes like you and me. Why? Well,...

• any ranking of "superfoods" that was based even partly on in vitro data derived with the good old ferric reducing antioxidant power (FRAP) assay would be invalid, ...
• every scientist who has been following up on "promising" data from FRAP assays would have been wasting his time, ...
• and you may have been eating all the wrong foods for years...

... hell no, as long as you ate your veggies over the past years, I wouldn't worry if you may have made a "suboptimal" selection (which would be different based on whatever new criteria you select).

Figure 1: FRAP value, vitamin C and vitamin E content and total amount phenolics in the powdered vegetables that were added to the rodent diets in the study at hand (Ji. 2014)

Honestly, I'd hope that you didn't select your foods only based on the orthorexic principle of maximal antioxidant content, anyways. 

Never forget the three principles of veggie eating: Variety, seasonality, colorfulness

Against that background I'd recommend you keep eating your lotus roots, if you like them, although, they have a significantly lower beneficial effect on SuperOxide Dismutase (SOD, a group of antioxidant enzymes) than rape and cucumber.

Figure 2: Serum markers of anti-oxidant status / oxidative damage after 6 weeks on the three experimental diets (Ji. 2014)

Moreover, if you look closely at the data in Figure 1+2, you will realize that lotus may suck at SOD and its ability to reduce hemolysis (the destruction of red blood cells), but will have the most profound beneficial effects on the levels of malondealdehyde (MDA), a marker of lipid oxidation, and the amount of plasma carbonyls, which have - just as in cellular regulation, aging, and disease (Levine. 2002). Just like their similarly radical cousins, carbonyls will thus play a dual role so that in the end, their reduction may not be beneficial in each and every case.

Figure 3: Blood mononuclear cell DNA damage expressed as total injury rate (%) and total tails low (% of all) in male Wistar rats on control and experimental diets (Ji. 2014)

The Take Away: Whatever the role of carbonyls, MDA & co may be and no matter what you believe which of the three tested vegetables may be the "best" one, if there is one definite message you can take home from today's SuppVersity article, it's not to overly rely on the abstract data from chemical tests the reliability of which appears to be inversely proportional to their accuracy.

Trust your instincts and go for a broad variety of vegetables. Eat seasonal! Eat colorful! And most importantly eat plenty. Optimal or not, none of the vegetables in the study at hand would harm you - all of them would help you defy diabesity and slow the aging process as best mother nature allows.

Reference: 

• Ji, Linlin, et al. "No correlation is found for vegetables between antioxidant capacity and potential benefits in improving antioxidant function in aged rats." Journal of Clinical Biochemistry and Nutrition 54.3 (2014): 198-203.
• Levine, Rodney L. "Carbonyl modified proteins in cellular regulation, aging, and disease^{2, 3}." Free Radical Biology and Medicine 32.9 (2002): 790-796.
• Valdez-Morales, Maribel, et al. "Phenolic content, and antioxidant and antimutagenic activities in tomato peel and seeds, and tomato by-products." Journal of Agricultural and Food Chemistry (2014). Accepted Manuscript.

Study Suggests: Frozen Veggies Worse Than Common Wisdom Says - Frozen Asparagus, Zucchini and Green Beans Lose More Antioxidants During Boiling

Green asparagus from the fridge and  from the market are not created equal - at least not when they finally end up on your plate after a short bath in hot water.

You just have to watch one of the consumer report shows on television to hear it: "Frozen veggies are way better than their reputation would suggest." Actually, here in Germany this sentence has been repeated to soften that I've even heard people say they'd buy the frozen broccoli because it contained "more vitamins and the other good stuff, you know." And you know what? For some veggies like spinach, for example, this may actually be the case. For others, like broccoli or peas, the nutrient status of the frozen and the raw uncooked vegetable appears to be more or less identical (Favell. 1998). But that's something you cannot say for the green asparagus stems, zucchini and green beans in a recent study from the Università degli Studi di Parma in Italy.

Warning: Don't take this article as an excuse and stop eating veggies completely. The frozen stuff may lose more vitamins, when you boil it, but (a) you can still blanch it and (b) even with significantly reduced antioxidant effects veggies are still among the healthiest things you can eat.

I am not an asparagus expert and can still tell that the cell structure of the Transverse  sections boiled (C - from raw | D - from frozen) is profoundly messed up compared to the raw (A) and blanched (B) variety | legend: c = collenchyma; vp = vascular bundle; p = parenchyma; f = fissure.

In the corresponding experiment, the Italian researchers bought Green asparagus stems (Asparagus officinalis L., var. Grande), zucchini (Cucurbita pepo L., va Quine) and green beans (Phaseolus vulgaris L., var. Giamaica) from a local producer and processed them within 24 hours from harvesting. For each of the veggies four samples were prepared: Raw/uncooked  (R), raw/boiled  (B), blanched (BL) and industrially frozen/boiled (FB)

The raw (ten kilograms of each vegetable), blanched (five kilograms of each vegetable) and industrially frozen  samples  (five  kilograms  of  each  vegetable) had been transported were  transported  to  the  University of  Parma laboratories  under  adequate  refrigerated conditions to avoid the exuberant nutrient loss that occurs upon inadequately slow (re-)freezing.

SuppVersity Suggested Read: " Conventional vs. Organic: It's Not About Getting More, But Getting Less For Your Money. Less Pesticides, Dioxins & Co" | read more if you want to know if the claim "organic is always better" is a similar misconcept as "frozen over fresh".

If you "freeze" your veggies in the freezer compartment of your fridge, this will make the cells blast, so that even before they are cooked, and the nutrients flow out. It is generally assume that the latter would not happen, if the veggies are shock-frosted.

Figure 1: Total antioxidant capacity of green asparagus, zucchini and green beans raw, blanched, boiled and frozen and boiled (Paciulli. 2014); as the data tells you frozen veggies with similar  icy grease on them like you see on the right may not really be a better source of antioxidants than fresh veggies from the farmers or even the supermarket.

If we look at the data in Figure 1, though, it would appear that the cells may have "cracked" already so that they are more susceptible to the subsequent heat assault and the frozen + boiled samples end up having consistently lower total antioxidant (Figure 2) and feric acid reducing capacity than their raw + boiled counterparts.

For a similar reason (nutrient retention), the blanched samples have been cooled immediately after blanching in an ice-water bath for 3 min before they have been transported to the laboratories, where their analysis shows that only the Zucchini lost a small, but significant amount of their total antioxidant activity.

Figure 2: It would be interesting to see if the negative effects of freezing and boiling occur in all vegetables. In view of the fact that previous studies compared raw vs. frozen, but nor raw + cooked vs. frozen + cooked, frozen Broccoli + cooked broccoli could be exactly as "bad" as asparagus, zucchini and green beans.

The thing that is of most practical relevance, tough, is the significant negative effect of freezing + boiling on both, the total antioxidant capacity (Figure 1) and the ferric reducing capacity (Figure 2) of all three vegetables.

The previously "cited" statement that you're better of with the "fresh" frozen veggies is thus probably only right, if you eat them raw. Compared to fresh veggies, the previously frozen asparagus, zucchini and green beans lost almost 11-30% of their antioxidant prowess during the cooking process - and the same may well happen to other veggies, including broccoli, which have been compared in previous studies only on a raw vs. frozen, but not on a cooked vs. frozen + cooked basis. Unless you're afraid that all the good veggies may limit your gains due to their potent anti-oxidant effects, it appears smart to stay away from their frozen varieties.

References:

• Paciulli, Maria, et al. "Impact of the industrial freezing process on selected vegetables Part I. Structure, texture and antioxidant capacity." Food Research International (2014).

The Overlooked Non-ROS-Scavenging Antioxidant Effects of Creatine Monohydrate: CM Works W/ & W/Out Exercise

Creatine, obviously monohydrate and no expensive and often impotent spinoff (Jäger. 2011) is useful for any athlete.

The number of items on the list of health and performance benefits of creatine is about as high as the number of boring articles about "the benefits of creatine" you can find all over the Internet. And even here at the SuppVersity they have been piling up in a way that has me ignore the majority of "creatine supplementation increases strength gains in XY" studies that appear on a monthly, sometimes weekly basis. Against that background I will cut today's creatine post short and get straight to the facts, Giuseppe Potrick Stefani et al. report in their latest paper in (how else could it be) the peer-reviewed Journal of the International Society of Sports Nutrition (Stefani. 2014).

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In what turns out to be another rodent study Stefani et al. investigated whether creatine supplementation exerts intra and/or extracellular antioxidant effects and if it plays a synergistic role in the adaptation of antioxidant enzymes associated with resistance training. The actual aim of the study was thus

"to evaluate the effects of monohydrate creatine supplementation associated, or not, with RT on oxidative stress and antioxidant enzymatic activity in the plasma, the heart, the liver and the gastrocnemius of rats." (Stefani. 2014)

And the results were unambiguous. As you can see in Figure 1, the anti-oxidant capacity of plasma, heart and liver of all 40 male Wistar rats which had been divided into four groups, i.e.

• sedentary (SED),
• sedentary + creatine  (SED-Cr), and
• resistance training (RT) and resistance training + creatine (RT-Cr),

increased significantly in response to the provision of creatine (0.3 g/kg/day of creatine for seven days, 0.05 g/kg for the rest of the 8-week study period).

Figure 1: Oxidative stress in heart, liver and muscle after 8 weeks of intervention.Concentrations of MDA and CAT activity. Values are mean ± SD; n = 10 for all groups (Stefani. 2014).

As you can see, both treatments, creatine-only and creatine + resistance training led to significant improvements in heart, liver and muscle antioxidant status - and that, this is important, in the absense of those direct free radical scavenging abilities that turn vitamin C, vitamin E & co into highly questionably agents with potential anti-adaptational effects (learn more).

Works w/ and w/out exercise, but with the latter creatine really excels

Compared to the sedentary animals the rats in the exercise group did yet significantly increased catalase levels (=good, because it catalyzes the decomposition of hydrogen peroxide - the bad stuff - to water and oxygen - the benign stuff) in the heart and - obviously - increased strength gains.

Figure 2: Absolute and relative 1RM strength before and after the intervention (Stefani. 2014).

What is (positively) surprising, at first, is the fact that the latter, i.e. the increases in 1-RM strength in response to creatine supplementation occurred even in the absence of resistance training.

If you look closely, you will yet realize that the relative increase in strength, a much better gauge for lasting real-world strength gains, in the sedentary rodents was ZERO. So that it is very likely that they would disappear with the increased water the rats were holding, as soon as the creatine supplementation is seized.

If you want to make your creatine even better, super-charge it with baking soda (NaHCO3) and build your own "buffered" creatine | learn more

Bottom line: If you are still not taking your 3-5g of creatine per day religiously, you are either in the last week of your contest prep and afraid of the potential increase in water retention, or you are a soccer mum who has been bamboozeled by the sensational reports about "kidney damage due to dangerous nutritional supplements" that pop up on one of the news channels every now and then.

I mean, what other invalid reason for not making use of this "non-enzymatic antioxidant" as a side-effect free health and performance promoter?

References:

• Jäger, Ralf, et al. "Analysis of the efficacy, safety, and regulatory status of novel forms of creatine." Amino Acids 40.5 (2011): 1369-1383.
• Stefani, Giuseppe Potrick, et al. "Effects of creatine supplementation associated with resistance training on oxidative stress in different tissues of rats." Journal of the International Society of Sports Nutrition 11.1 (2014): 11.