12 - Dec - 2009

7/21/2019 12 - Dec - 2009

1/17

ean

Alan Aragons Research Review December, 2009 [Back to Contents] Page 1

Copyright December 1st, 2009 by Alan Aragon

Home:www.alanaragon.com/researchreview

Correspondence:[email protected]

2 An objective look at the paleo diet.

By Alan Aragon

6 The effect of glycaemic index of high carbohydratediets consumed over 5 days on exercise energymetabolism and running capacity in males.

Hamzah S, et al. J Sports Sci. 2009 Dec 3:1-10. [Epub

ahead of print] [Medline]

7 Resistance exercise training lowers HbA1c morethan aerobic training in adults with type 2diabetes.

Diabetol Metab Syndr.;1(1):27. [Epub ahead of print]

[Medline]

8 Effects of agonist-antagonist complex resistancetraining on upper body strength and powerdevelopment.J Sports Sci. 2009 Dec 3:1-9. [Epub ahead of print][Medline]

9 Ergogenic and Antioxidant Effects of SpirulinaSupplementation in Humans.

Med Sci Sports Exerc. 2010 Jan;42(1):142-51. [Medline]

10 Increased p70s6k

phosphorylation during intake ofa proteincarbohydrate drink following resistanceexercise in the fasted state (guest analysis by MattPerryman)

Deldicque L, et al. Eur J Appl Physiol. 2009 Nov 18. [Epubahead of print] [Medline]

16 20 things I learned in 2009 (random editi on).

By Alan Aragon
http://alanaragon.com/researchreviewhttp://www.alanaragon.com/researchreviewmailto:[email protected]://www.ncbi.nlm.nih.gov/pubmed/19967585?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/20003276?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19967584?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/20010119?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ncbi.nlm.nih.gov/pubmed/19921243?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://alanaragon.com/researchreviewhttp://www.ncbi.nlm.nih.gov/pubmed/19921243?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ncbi.nlm.nih.gov/pubmed/20010119?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19967584?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/20003276?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19967585?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1mailto:[email protected]://www.alanaragon.com/researchreview

7/21/2019 12 - Dec - 2009

2/17


A

n objective look at the paleo diet.

By Alan Aragon

Introduction

The paleolithic diet is also called the ancestral diet, stone agediet, caveman diet, and hunter-gatherer diet. From this point on,Ill use its popular abbreviation, the paleo diet. The beginning of

the paleolithic period is characterized by our prehistoricancestors initial use of stone tools, dating back approximately2.5 million years. Our genus homo is thought to have beenexisting since 2.4 million years ago. The main premise of paleodieting is that the agricultural revolution, occurring about 10,000years ago, represents less than 1% of the human evolutionarytimeline. Proponents of paleo dieting thus blame the relativelyrecent widespread consumption of grain foods for the chronicdiseases of modern man, or the so-called diseases ofcivilization. Technological advancements in food refinement,packaging, and distribution have presented humans with a dietthat supposedly violates our genetic profile. In this article Illattempt to define what the paleo diet is, discuss its well-

supported aspects, its ill-supported aspects, and then tie thingstogether with some practical recommendations.

W

hat exactly wasthe paleo diet?

One of the fundamental problems with paleo dieting other thanthe primary issue of a lack of direct evidence is defining thediet in the first place. Gowlett addresses this question in aneloquent review.1 Illustrating the disparity of intakes acrossgeographic regions, Ill quote the text directly:

Despite the wide range of differences, Gowlett mentions acouple of key commonalities. Prior to the past 5000 years or so,our ancestors were not likely to be heavily dependent on milkor other dairy products. He adds to this that a heavydependence on cereal grains is also a relatively recentphenomenon in the human timeline.

T

he modern adaptation of paleo dieting

Paleo dieting has been brought to mainstream attention in largepart by Dr. Lauren Cordain, a professor in the Health andExercise Science Department at Colorado State University.Cordains personal website describes him as the worldsleading expert on Paleolithic diets. Indeed, Cordain ispublished in the peer-reviewed literature, and his nameimmediately pops up when an authoritative opinion on paleo

dieting is called for. Cordains broad interpretation of paleodieting is a relatively simple matter of adhering to a food list thancludes:i Lean meats (eggs are fine) Sea food (particularly those rich in omega-3 fatty acids) Fruits Vegetables (particularly the leafy/non-starchy ones)Nuts

F oods to avoid or aggressively minimize are:

All starch-based foods except for roots and tubers (grainsand legumes are the bad guys)

Dairy (milk & milk products) Refined sugar (honey on rare occasion is fine, because thats

how it was way back in the cave days) Salt

The above outline is straight from Cordains website. Howevera review paper by Cordain and others adds the following foodso the no-no list:2t Alcohol Fatty domestic meats (as opposed to the leaner meat of wild

animals) Refined vegetable oils (trans fats produced byhydrogenation)

W

ell-supported principles of paleo dieting

An emphasis on lean meats rather than fatty ones is beneficialfrom the standpoint of controlling caloric intake. Furthermorethe fat of land animals generally offers no special benefit otherthan making foods more palatable (and enjoyable). Cordain et alalso make the case that fatty meats from domesticated livestockare more likely to be higher in saturated fatty acids and omega-6fatty acids, and lower in omega-3 fatty acids, which isnt idealrom a cardiovascular risk standpoint.

Ancestorsofmodernhumansarenowbelievedtohaveevolvedin

the tropics, probably in Africa, from about 200,000 years ago.

Their diet was, therefore, probably largely (perhaps 70%) plant

based

like

that

of

modern

hunters

and

gatherers

in

the

region

[20]. [] In contrast, modern humans entering Europe 40,000

years ago would have adopted ameatbased diet by necessity,

and maintained this over hundreds of generations. [] Modern

huntersandgatherersechothevarietyofpastdiets,rangingfrom

largelyplantbasedinthetropics,tobeingalsoheavilymeatbased

inthearctic.

fReducing added sugar intake also benefits caloric control, as

does the elimination or reduction of any food type. An additionalbenefit is the reduction of the risk for micronutrient dilutionwhich is the potential for empty calories to displace the ofessential vitamins and minerals and cause deficiencies.3 Itsimportant to note, however, that micronutrient dilution is nolikely to occur unless total calories are restricted (as in a weightloss scenario), and added sugars constitute more than 20% of thetotal calories in the diet.4 As a sidenote for review, Ivediscussed sugar misconceptions in the opening articles of the

ugust 2008 and July 2009 AARR issues.AA substantial body of literature correlates higher intakes of fruitand vegetable with a decreased risk of cardiovascular disease,5,

stroke,7 type 2 diabetes,8and certain types of cancer.9,10Theresalso a growing body of evidence that nuts can improve (amongother things) blood lipid profiles and reduce cardiovascular riskfactors.11,12 Increasing the dietary proportion of omega-3 fattyacids through fish and/or fish oil has been seen to benefit a widerange of clinical parameters, but most consistently theimprovement of blood lipids13 and blood pressure,14 andprevention various cardiovascular diseases.15 In contrastpartially hydrogenated oils rich in trans fats have been seen to

dversely impact multiple cardiovascular risk factors.16a
http://www.thepaleodiet.com/aboutus/http://www.thepaleodiet.com/aboutus/http://www.thepaleodiet.com/paleolithic-diet.htmhttp://www.thepaleodiet.com/aboutus/http://www.thepaleodiet.com/paleolithic-diet.htmhttp://www.thepaleodiet.com/paleolithic-diet.htm

7/21/2019 12 - Dec - 2009

3/17


From a weight loss standpoint, it goes without saying that anydiet with a list of foods to avoid (and in paleos case, theavoidance of entire food groups) can potentially result in adefault reduction in total calories. In this sense, paleo dieting canfunction as a calorie cutting for dummies method. If the foodscut from the diet happen to comprise the majority of what thedieter overeats, then you have a successful weight loss protocol.Additionally, the food groups cut out in paleo nutrition arelargely carbohydrate-dominant. This has the potential to defaulttoward increased protein intake, which in turn can increasethermogenesis (to a small degree) and also the retention or gainof muscle tissue. This effect would be more pronounced in folks

ho switched to paleo from a formerly protein-deficient diet.wA strong testament to the level of interest generated by the paleodieting is an emerging body of peer-reviewed literaturecomparing its effects with more conventional diets. Thus far it

as all been positive:h Frasetto et al found that compared to the subjects usual

dietary habits, paleo dieting improved blood pressure,glucose tolerance, insulin sensitivity, and lipid profiles inonly 10 days, even without weight loss.17However, this waspredictable given poor quality of the usual dietary habits of

sedentary subjects. Not to mention, protein in the paleotreatment was nearly double the control treatment.

In a trial on type 2 diabetics, Jnsson et al found the paleotreatment to be superior to the standard-issue diabetes dietfor improving glycemic control and other cardiovascularrisk factors.18These results were also predictable since thepaleo treatment involved significantly less total kcals perday, and 60g (36%) less carbohydrate.

Lindeberg et al found the paleo diet more effective atimproving glucose tolerance in patients with ischemic heartdisease.19 However, the paleo diet had 97 g lesscarbohydrate (42%).

Its important to note that a common theme among these trials isa lack of matching of macronutrition, making it difficult todetermine the relative impact of the food choices, as opposed tomerely a more ideal amount of protein and/or carbohydrate forthe given population.

P

oorly supported principles of paleo dieting

Based on the above body of research, its clear that paleo dietingcan have positive effects, but is yet to be proven superior to amacronutrient-matched comparison arm, let alone amacronutrient-matched, fiber-matched treatment in nonsedentaryor athletic subjects. Hopefully future trials will provide moredefinitive answers to just how useful the food group omissions

f paleo dieting is, given a more level playing field.oAnother disadvantage of paleo dieting is the missed benefits ofthe omitted foods not to mention the lack of research dataindicting these foods as harmful to begin with. In a recentsystematic review of randomized controlled trials, whole-graincereals (oats in particular) were found to lower risk factors forcoronary heart disease.20 Take note that the authors of thisreview caution that the trial periods were short, and most of thetudies were funded by commercially vested sponsors.s

Dairy, another omitted food group from paleo dieting, has asizable body of evidence showing its effectiveness for improvingbone health,21-24 muscle mass and strength,25-28and even weighmanagement.29A case can be made that the majority of positive-result studies are industry-funded, but with scant exception,30themajority of negative reviews done on milk have been led byresearchers with vegetarian agendas.31,32

Legumes have also been blacklisted as a non-paleo foodHowever, their detriment to human health is yet another claim

without strong support in the literature. A recent meta-analysisby Bazzano et al determined that non-soy legumes decrease totaand LDL cholesterol.33 Similar positive outcomes have beenseen in a meta-analysis of the effect of soy isoflavones on bloodlipids.34Is this really any surprise? Soy has been a staple food ofAsian Pacific populations with some of the most favorablehealth profiles in the world.

Another recurrent assertion made by paleo proponents is that thediet promotes alkalinity, which can prevent calcium excretionand thus osteoporosis. This idea is based on work by Remer andManz who determined the potential renal acid load (PRAL) ofvarious foods.35Quoting Cordains website,

Because the average American diet is overloaded with grains

cheeses, salted processed foods, and fatty meats at the expense

of fruits and vegetables, it produces a net acid load and

promotes bone demineralization.

Read the above quote carefully and notice how Cordain ignoresthe possibility of moderating the intake of the supposedlyoffending foods while consuming sufficient amounts of fruitsand vegetables. Paleo proponents tend to position theirarguments in black and white terms; its always an either-orproposition. This is false because a range of healthy possibilitiesexists between the extremes. Furthermore, the acid-alkalinehypothesis of bone health has not been supported by studies thatlook beyond PRAL. Ill quote a recent meta-analysis by Fenton

t al that refutes Cordains assertion:

36

eThis meta-analysis did not find evidence that phosphate intake

contributes to demineralization of bone or to bone calcium

excretion in the urine. Dietary advice that dairy products, meats

and grains are detrimental to bone health due to "acidic"

phosphate content needs reassessment.

Fundamental flaws in the paleo diets ideology

A cornerstone principle of paleo dieting is to avoid foods thawerent available to our prehistoric ancestors. This line ofthinking is overassumptive to begin with, but lets oblige it for asecond. Grains are one of the prime foods were supposed toavoid, but a recent archaeological discovery challenges this ideaMercader retrieved a large amount of starch granules from thesurfaces of tools dating back to the Middle Stone Age, indicatingthat early homo sapiens relied on grass seeds starting at least105,000 years ago.37 This calls into question the popularassumption that grain consumption only began 10,000 years agowith the advent of agriculture.

This brings me to perhaps the most important shortcoming opaleo dieting, which is its massively speculative nature. Simplyput, its based on an incomplete set of archaeological data

7/21/2019 12 - Dec - 2009

4/17

combined with observations of modern hunter-gatherer societies(who arent necessarily accurate representations of prehistorichunter-gatherers). Allow me to quote myself from the paleochapter in Girth Control (which by the way, is not as up-to-dates this article):a

Examinations of the dietary habits of Paleolithic humans can

only be made by indirect means such as ethnographic,

archaeological, or fossil records. These methods inevitably

place the burden of accuracy upon the records in question.

Furthermore, the indirect nature of studying pre-historynecessitates a certain degree of speculation and assumption in

the midst of considerable room for error.

Populations who violate paleo rules and live to tell about it

Okinawans are famous for having the longest life expectancy onthe planet. Its safe to assume that although many factors areinvolved with their longevity, diet is a major contributor. Hereare some interesting details about their eating habits, Ill quotethe conclusion of a review paper by Sho directly:38


Although its not listed in the papers conclusion, Sho also citesa white rice intake (of all social classes combined) averagingroughly 840 g, the equivalent of 3 bowls of white rice per day.So much for the paleo rules of avoiding sugar, grains, andlegumes for optimal health. There must be something in theOkinawan water protecting them from the evils of consumingoods that are not paleo-approved.f

While the Okinawans break some key paleo rules, the Frenchmake a mockery of them with their regular intake of whitebread, red wine, and full-fat cheese. In whats known as theFrench Paradox, low coronary heart disease death rates are seendespite a high intake of dietary cholesterol and saturated fat.39Although this paradox has not been explained definitively, itsclear that the French did not get the memo that they are grosslyviolating paleo law. I could go on in this vein with otherpopulations besides Okinawa and the France, but Im sure youget the picture.

S

ummary points

Its impossible to universally define the diet of ourpaleolithic ancestors because intakes varied widelyaccording to food availability dictated by geographicalocation.

Modern adaptations of the paleo diet, such as Cordainshave distinct pros and cons. The foods that arerecommended generally have plenty of supporting literatureHowever, the blacklisted foods do not have adequate

scientific justification for avoidance. In fact, many of thebad foods have multiple research-supported benefits.

The emerging experimental evidence supporting paleo dietsover traditional diets have thus far not matchedmacronutrient or fiber intake, so its difficult to attribute thepaleo benefits to specific food choices versus moreoptimized macronutrition for the populations studied.

Paleo proponents tend to think in extremes, ignoring the facthat healthy diets can consist of moderated amounts of foodson both the good and bad list (which are not alwayssupportable as good or bad in the first place).

The acid-alkaline hypothesis of bone health has not beensupported by multiple studies that look beyond PRAL.

AroughsummaryoftheOkinawanlongevityfoodculture

m

ightincludethefollowingpoints:

1. Inmodern

pork

cuisine,

unlike

in

the

past,

saturated

fats

are

carefullyremoved in theprocessofboilingorakunuki.Clever

useismadeofcollagenrichpigsfeetandinternalorgans.

2. Largeamountsofvarious typesof seaweed, rich inminerals,

dietaryfibreandessentialfattyacids(EPA,DPAandDHA),are

includedintheirdiet.

3. Leafy vegetables and herbs that are rich in dietary fibre,

chlorophyll and Vitamins A and C, are part of the everyday

diet.

4. Okinawan tofu, which is receiving worldwide attention as

containing isoflavones for the prevention of lifestyle related

diseases,isconsumedinlargeamounts.

5. Rawsugariseateninhealthysnackswithteaandkohencha(a

semifermentedtea)isapopulardrink.

6. Saltconsumption

is

the

lowest

in

Japan.

7. Thediet isalsorich inseveralother importantnutrients,such

ascurcumin (yellowishsubstancefound incurrypowder)and

anthocyanin(foundinredsweetpotatoes).

Recent archaeological findings have challenged the idea thatpaleolithic man did not consume grains. Paleo dieting principles are based on the false assumption

that the archaeological records combined with observationsof modern hunter-gatherer societies are accurate enough toextrapolate into rigid nutritional recommendations.

I thought it might be fun to use the real-world example ofthe Okinawans, who regularly consume grains, added sugarand legumes, but still manage to outlive the rest of theworld. Similar principles apply to the French, who completethe intake of supposed non-paleo foods.

C

onclusions & applications

The underlying take-home point here is that paleo proponentstend to be dogmatically inflexible about a set of guidelines thatare not rooted in unshakable fact. Combine this illogic withignorance of research data supporting the supposed bad foodsand you end up with a set of dietary principles that are sub-optimal and incomplete at best. To quote a study led by Cordain

imself,40hUnfortunately, not a single comprehensive study evaluating the

macronutrient and trace nutrient contents of the wild plant and

animal foods actually consumed in completely un-Westernized

unter-gatherer diets was ever conducted.hThe most practical way to apply the data in this article is to eat areasonable variety of foods within and across the food groupsand maintain a predominance of unprocessed (or minimallyprocessed foods) while getting enough protein andessential/beneficial fat. For those who dont eat fish, considersupplementing with fish oil to cover your bases. Eat anabundance of vegetables and fruit, sticking with the ones thasuit your personal taste. Speaking of fruit, ignore the mythicalsuperfoods concept. If you like grains and dairy (and canproperly digest them), by all means have as much as will allowyou to maintain a healthy body composition, staying aware of
http://alanaragon.com/fish-oil.htmlhttp://alanaragon.com/fish-oil.html

7/21/2019 12 - Dec - 2009

5/17


the caloric density of some of these foods. Theres no goodreason to put any food on an avoid list, even classic junk foodand desserts. Why give any food all that power and taboomystique? Eat it when you want to, but moderate the amountconsumed. Stay physically active. Stay vigilant about the latestdiet rules, even if they come from highly decoratedacademicians. Focusing on personal dietary optimization insteadof prehistoric speculation just might increase your lifeexpectancy.

References

1. Gowlett J. What actually was the stone age diet? J Nutr EnvironMed. 2003 Sep;13(3):143-7. [JNEM, full PDF]

2. Cordain L, et al. Origins and evolution of the Western diet: healthimplications for the 21st century. Am J Clin Nutr. 2005Feb;81(2):341-54. [Medline]

3. Livingstone MB, Rennie KL. Added sugars and micronutrientdilution. Obes Rev. 2009 Mar;10 Suppl 1:34-40. [Medline]

4. Gibson SA. Dietary sugars intake and micronutrient adequacy: asystematic review of the evidence. Nutr Res Rev. 2007Dec;20(2):121-31.[Medline]

5. He FJ, et al. Increased consumption of fruit and vegetables isrelated to a reduced risk of coronary heart disease: meta-analysis ofcohort studies. J Hum Hypertens. 2007 Sep;21(9):717-28.

[Medline]6. Hu FB. Plant-based foods and prevention of cardiovascular

disease: an overview. Am J Clin Nutr. 2003 Sep;78(3 Suppl):544S-551S. [Medline]

7. He FJ, et al. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet. 2006 Jan 28;367(9507):320-6.[Medline]

8. Hamer M, Chida Y. Intake of fruit, vegetables, and antioxidantsand risk of type 2 diabetes: systematic review and meta-analysis. JHypertens. 2007 Dec;25(12):2361-9. [Medline]

9. Van Duyn MA, Pivonka E. Overview of the health benefits of fruitand vegetable consumption for the dietetics professional: selectedliterature. J Am Diet Assoc. 2000 Dec;100(12):1511-21. [Medline]

10. Steinmetz KA, Potter JD. Vegetables, fruit, and cancer prevention:a review. J Am Diet Assoc. 1996 Oct;96(10):1027-39. [Medline]

11. Banel DK, Hu FB. Effects of walnut consumption on blood lipidsand other cardiovascular risk factors: a meta-analysis andsystematic review. Am J Clin Nutr. 2009 Jul;90(1):56-63. Epub2009 May 20. [Medline]

12. Sabat J, Ang Y. Nuts and health outcomes: new epidemiologicevidence. Am J Clin Nutr. 2009 May;89(5):1643S-1648S.[Medline]

13. Eslick GD, et al. Benefits of fish oil supplementation inhyperlipidemia: a systematic review and meta-analysis. Int JCardiol. 2009 Jul 24;136(1):4-16. Epub 2008 Sep 6. [Medline]

14. Cicero AF, et al. Omega-3 polyunsaturated fatty acids: theirpotential role in blood pressure prevention and management. CurrVasc Pharmacol. 2009 Jul;7(3):330-7. [Medline]

15. Lavie CJ, et al. Omega-3 polyunsaturated fatty acids and

cardiovascular diseases. J Am Coll Cardiol. 2009 Aug11;54(7):585-94. [Medline]16. Mozaffarian D, et al. Health effects of trans-fatty acids:

experimental and observational evidence. Eur J Clin Nutr. 2009May;63 Suppl 2:S5-21. [Medline]

17. Frassetto LA, et al. Metabolic and physiologic improvements fromconsuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr.2009 Aug;63(8):947-55. [Medline]

18. Jnsson T, et al. Beneficial effects of a Paleolithic diet oncardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovasc Diabetol. 2009 Jul 16;8:35. [Medline]

19. Lindeberg S, et al. A Palaeolithic diet improves glucose tolerancemore than a Mediterranean-like diet in individuals with ischaemicheart disease. Diabetologia. 2007 Sep;50(9):1795-807. [Medline]

20. Kelly SA, et al. Wholegrain cereals for coronary heart diseaseCochrane Database Syst Rev. 2007 Apr 18;(2):CD005051[Medline]

21. Heaney RP. Dairy and bone health. J Am Coll Nutr. 2009 Feb;28Suppl 1:82S-90S. [Medline]

22. Huth PJ, et al. Major scientific advances with dairy foods innutrition and health. J Dairy Sci. 2006 Apr;89(4):1207-21[Medline]

23. Heaney RP. Protein and calcium: antagonists or synergists? Am Clin Nutr. 2002 Apr;75(4):609-10. [Medline]

24. Heaney RP. Calcium, dairy products and osteoporosis.J Am ColNutr. 2000 Apr;19(2 Suppl):83S-99S. [Medline]

25. Josse AR, et al. Body Composition and Strength Changes inWomen with Milk and Resistance Exercise. Med Sci Sports Exerc2009 Dec 9. [Epub ahead of print] [Medline]

26. Kammer L, et al. Cereal and nonfat milk support muscle recoveryfollowing exercise. J Int Soc Sports Nutr. 2009 May 14;6:11[Medline]

27. Hartman JW, et al. Consumption of fat-free fluid milk afterresistance exercise promotes greater lean mass accretion than doesconsumption of soy or carbohydrate in young, novice, maleweightlifters. Am J Clin Nutr. 2007 Aug;86(2):373-81. [Medline]

28. Tipton KD, et al. Ingestion of casein and whey proteins result inmuscle anabolism after resistance exercise. Med Sci Sports Exerc2004 Dec;36(12):2073-81. [Medline]

29. Van Loan M. The role of dairy foods and dietary calcium in weightmanagement. J Am Coll Nutr. 2009 Feb;28 Suppl 1:120S-9S[Medline]

30. Barba G, Russo P. Dairy foods, dietary calcium and obesity: ashort review of the evidence. Nutr Metab Cardiovasc Dis. 2006Sep;16(6):445-51. [Medline]

31. Lanou AJ, et a. Calcium, dairy products, and bone health inchildren and young adults: a reevaluation of the evidencePediatrics. 2005 Mar;115(3):736-43. [Medline]

32. Lanou AJ, Barnard ND. Dairy and weight loss hypothesis: anevaluation of the clinical trials. Nutr Rev. 2008 May;66(5):272-9[Medline]

33. Bazzano LA, et al. Non-soy legume consumption lowerscholesterol levels: A meta-analysis of randomized controlled trialsNutr Metab Cardiovasc Dis. 2009 Nov 23. [Epub ahead of print[Medline]

34. Taku K, et al. Soy isoflavones lower serum total and LDLcholesterol in humans: a meta-analysis of 11 randomizedcontrolled trials. Am J Clin Nutr. 2007 Apr;85(4):1148-56[Medline]

35. Remer T, Manz F. Potential renal acid load of foods and itsinfluence on urine pH. J Am Diet Assoc. 1995 Jul;95(7):791-7[Medline]

36. Fenton TR, et al. Phosphate decreases urine calcium and increasescalcium balance: a meta-analysis of the osteoporosis acid-ash diehypothesis.Nutr J.2009 Sep 15;8:41. [Medline]

37. Mercader J. Mozambican grass seed consumption during the

Middle Stone Age. Science. 2009 Dec 18;326(5960):1680-3[Medline]

38. Sho H. History and characteristics of Okinawan longevity foodAsia Pac J Clin Nutr. 2001;10(2):159-64. [Medline]

39. Ferrires J. The French paradox: lessons for other countries. Heart2004 Jan;90(1):107-11. [Medline]

40. Cordain L, et al. Plant-animal subsistence ratios and macronutrienenergy estimations in worldwide hunter-gatherer diets. Am J Clin

Nutr 2000;71:682-92. [Medline]
http://pcwww.liv.ac.uk/~gowlett/GowlettCJNE_13_03_02.pdfhttp://www.ncbi.nlm.nih.gov/pubmed/12081815?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/19207534?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumhttp://www.ncbi.nlm.nih.gov/pubmed/19079865?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumhttp://www.ncbi.nlm.nih.gov/pubmed/17443205?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4http://www.ncbi.nlm.nih.gov/pubmed/12936948?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/16443039?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=1&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/17984654?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/11138444?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3http://www.ncbi.nlm.nih.gov/pubmed/17984654?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/19458020?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=9http://www.ncbi.nlm.nih.gov/pubmed/19321572?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=11http://www.ncbi.nlm.nih.gov/pubmed/18774613?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=10http://www.ncbi.nlm.nih.gov/pubmed/19601857?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19660687?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4http://www.ncbi.nlm.nih.gov/pubmed/19424218?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/19209185?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19209185?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/17583796?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=10http://www.ncbi.nlm.nih.gov/pubmed/17443567?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3http://www.ncbi.nlm.nih.gov/pubmed/19571166?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3http://www.ncbi.nlm.nih.gov/pubmed/16537954?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/11916747?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/10759135?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/19997019?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19442266?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4http://www.ncbi.nlm.nih.gov/pubmed/17684208?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=2http://www.ncbi.nlm.nih.gov/pubmed/15570142?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/19571169?ordinalpos=&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.SmartSearch&log$=citationsensorhttp://www.ncbi.nlm.nih.gov/pubmed/16928440?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/15741380?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/18454813http://www.ncbi.nlm.nih.gov/pubmed/19939654?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/17413118?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedarticles&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/7797810?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=5http://www.ncbi.nlm.nih.gov/pubmed/19754972?dopt=AbstractPlus&holding=f1000,f1000m,isrctnhttp://www.ncbi.nlm.nih.gov/pubmed/20019285?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/11710358?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/14676260?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=7http://www.ncbi.nlm.nih.gov/pubmed/10702160?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/10702160?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/14676260?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=7http://www.ncbi.nlm.nih.gov/pubmed/11710358?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/20019285?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19754972?dopt=AbstractPlus&holding=f1000,f1000m,isrctnhttp://www.ncbi.nlm.nih.gov/pubmed/7797810?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=5http://www.ncbi.nlm.nih.gov/pubmed/17413118?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedarticles&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/19939654?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/18454813http://www.ncbi.nlm.nih.gov/pubmed/15741380?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/16928440?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19571169?ordinalpos=&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.SmartSearch&log$=citationsensorhttp://www.ncbi.nlm.nih.gov/pubmed/15570142?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/17684208?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=2http://www.ncbi.nlm.nih.gov/pubmed/19442266?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4http://www.ncbi.nlm.nih.gov/pubmed/19997019?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/10759135?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/11916747?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/16537954?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/19571166?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3http://www.ncbi.nlm.nih.gov/pubmed/17443567?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3http://www.ncbi.nlm.nih.gov/pubmed/17583796?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=10http://www.ncbi.nlm.nih.gov/pubmed/19209185?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19209185?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19424218?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/19660687?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4http://www.ncbi.nlm.nih.gov/pubmed/19601857?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/18774613?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=10http://www.ncbi.nlm.nih.gov/pubmed/19321572?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=11http://www.ncbi.nlm.nih.gov/pubmed/19458020?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=9http://www.ncbi.nlm.nih.gov/pubmed/17984654?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/11138444?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3http://www.ncbi.nlm.nih.gov/pubmed/17984654?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/16443039?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=1&log$=relatedreviews&logdbfrom=pubmedhttp://www.ncbi.nlm.nih.gov/pubmed/12936948?dopt=Abstracthttp://www.ncbi.nlm.nih.gov/pubmed/17443205?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4http://www.ncbi.nlm.nih.gov/pubmed/19079865?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumhttp://www.ncbi.nlm.nih.gov/pubmed/19207534?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumhttp://www.ncbi.nlm.nih.gov/pubmed/12081815?dopt=Abstracthttp://pcwww.liv.ac.uk/~gowlett/GowlettCJNE_13_03_02.pdf

7/21/2019 12 - Dec - 2009

6/17


The effect of glycaemic index of high carbohydratediets consumed over 5 days on exercise energy

etabolism and running capacity in males.mHamzah S, et al. J Sports Sci. 2009 Dec 3:1-10. [Epub ahead of

print] [Medline]

PURPOSE: The aim of this study was to determine whether

rates of total fat and carbohydrate oxidation and endurancecapacity during running conducted in the fasted state areinfluenced by the glycaemic index (GI) of high carbohydratediets consumed over 5 days. METHODS: Nine healthy malesperformed three treadmill runs to exhaustion at 65% ofmaximum oxygen uptake ([Vdot]O(2max)): after a habitual diet(control trial), after 5 days on a high carbohydrate/highglycaemic index diet, and after 5 days on a highcarbohydrate/low glycaemic index diet in randomizedcounterbalanced order. RESULTS:No significant differences inrates of fat and carbohydrate oxidation, concentrations of plasmainsulin, glucose, non-esterified fatty acids and glycerol, or timeto exhaustion were observed between the high carbohydrate/highglycaemic index and high carbohydrate/low glycaemic indextrials. Compared with the control trial, the concentration ofplasma glycerol and rate of fat oxidation were lower (P < 0.05)and the rate of carbohydrate oxidation higher (P < 0.05) in boththe high carbohydrate/high glycaemic index diet and highcarbohydrate/low glycaemic index trials during the run toexhaustion. CONCLUSION:In conclusion, the extent by whicha high carbohydrate diet consumed over 5 days reduces rate offat oxidation during subsequent running exercise in the fastedstate is not influenced by the glycaemic index of the diet.SPONSORSHIP:None listed.

Study strengths

Subjects were healthy and involved in endurance sports for atleast 4 years. It seems elementary for studies like this to chooseappropriate samples, but this isnt always the case. During the 5days leading up to the first treadmill run, subjects recorded allplanned and structured exercise and were asked to replicate thisbefore their subsequent runs. For 2 days before the runningtrials, the participants were asked to limit themselves to non-exercise activities of daily living. All the food and detailedmenus were provided by the lab. Digital food scales and writteninstructions explaining how to cook and prepare the foods werealso provided. The menus contained a predominance ofprocessed and easy-to-prepare foods in order to minimize theeffect of cooking time variation on glycemic index. Theresearchers kept in close communication with the subjects, who

were encouraged to contact the lab if they had any questionsabout the diet procedures.

Study limitations

As noted by the authors, the calculation of the glycemic index(GI) and glycemic load of the diets was based on published GItables rather than direct measurements of the foods consumed.This raises the concern that foods with contrasting GI do notalways induce a proportionally comparable difference in plasma

glucose response. Furthermore, the wide range of variationamong the GI of the same food types listed in the published datacalls overall reliability into question. For example, glucosewhich should be the simplest and most straight-forward food tomeasure, has a GI ranging from 85-111 (a 23.4% margin).1Thisdegree of variance in a monosaccharide with minimal potentiaconfounders in assessing metabolic response can only beamplified with the more complex foods.

Another limitation common to this type of research is that thesubjects completed the main exercise trials on an empty stomachafter a 12-hour fast. This simply is not the case in real-worldendurance events. A breakfast or pre-test meal should have beenproportionally standardized. Furthermore, a time-to-exhaustiontest was done, as opposed to a time trial. The advantage of thelatter is that it more closely mimics real-world race conditionswhere, the winner is one who completed the course in the leastamount of time not the one who ran for the longest amount oftime before collapsing after the race was over.

C

omment/application

The main findings of the present study are 3-fold: 1) The exten

to which high-carbohydrate diets consumed for 5 days reducethe rate of fat oxidation during running in the fasted state is noinfluenced by the GI of the diet, 2) the GI of high-carbohydratediets consumed for 5 days has no impact on running capacity inthe fasted state, and 3) there was no significant difference inendurance capacity between the experimental treatments and thecontrol. The lack of effect of GI on fat oxidation is in agreemenwith previous research by Chen et al, who found that theamount, rather than the GI of the carbohydrate consumed duringthe 3-day loading phase was the overriding factor influencingsubsequent metabolism and endurance run performance.2

Surprising the authors of the present study was the lack of

difference in endurance capacity between the control group andthe two experimental groups. This occurred despite asignificantly higher carbohydrate intake in the experimentagroups (Control: 349 g, HGI: 511 g, LGI: 508 g). This was anunexpected outcome, since the literature indicates theeffectiveness of increased carbohydrate intake for elevating liverand muscle glycogen, thereby prolonging time to exhaustion intrials longer than 90 minutes. The authors speculate that this lackof difference was perhaps because the diet in the control tria(supposed to reflect the subjects habitual diet) was not strictlycontrolled. And although the carbohydrate intake in theexperimental groups was higher than the control group, theactual difference was not great enough to impact endurancecapacity. At 349 g/day, the control group was far from being

carb-restricted. Another point of speculation was that theintensity of the trial (65% of VO2max) was not high enough forthe difference in carbohydrate intakes to matter. As a take-home

oint, Ill quote the authors directly:pFrom a practical perspective, our findings suggest that when

high carbohydrate diets are consumed for 35 days leading up

to an endurance event, consideration of the glycaemic index is

not necessary.
http://www.ncbi.nlm.nih.gov/pubmed/19967585?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19967585?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1

7/21/2019 12 - Dec - 2009

7/17


Resistance exercise training lowers HbA1c more thanerobic training in adults with type 2 diabetes.a

Diabetol Metab Syndr.;1(1):27. [Epub ahead of print] [Medline]

BACKGROUND: The aim of this study was to compare theeffects of 10 weeks of resistance or treadmill exercises onglycemic indices levels prior to and immediately followingexercise in adults with type 2 diabetes. DESIGN: Twentyinactive subjects (mean age 53.5 years) with type 2 diabetes

enrolled in the study. Baseline HbA1c, blood glucose levels,heart rate, and blood pressure were measured for each subjectprior to the initiation of the exercise program. Subsequently,subjects were matched to age, waist circumference and sex andassigned to either isocaloric resistance or treadmill exercisegroups, which met 3 times per week for 10 weeks. RESULTS:Both groups showed a reduction in pre and post-exercise bloodglucose and HbA1c values. There was no change in restingblood pressure or heart rate in either group during the course ofthe 10 week intervention. The group receiving resistanceexercises showed significant differences in the daily pre-exerciseblood glucose readings between the beginning and end of theexercise protocol (p < 0.001). There were significantimprovements in the mean HbA1c reading pre and post trainingin both groups (p

7/21/2019 12 - Dec - 2009

8/17


Effects of agonist-antagonist complex resistancetraining on upper body strength and power

evelopment.dJ Sports Sci. 2009 Dec 3:1-9. [Epub ahead of print] [Medline]

PURPOSE: The objective of this study was to examine thechronic effects on strength and power of performing complexversus traditional set training over eight weeks. DESIGN:Fifteen trained males were assessed for throw height, peak

velocity, and peak power in the bench press throw and one-repetition maximum (1-RM) in the bench press and bench pullexercises, before and after the eight-week programme. Thetraditional set group performed the pulling before the pushingexercise sets, whereas the complex set group alternated pullingand pushing sets. The complex set training sessions werecompleted in approximately half the time. Electromyographic(EMG) activity was monitored during both test sessions in anattempt to determine if it was affected as a result of the trainingprogramme. RESULTS:Although there were no differences inthe dependent variables between the two conditions, bench pulland bench press 1-RM increased significantly under the complexset condition and peak power increased significantly under thetraditional set condition. Effect size statistics suggested that thecomplex set was more time-efficient than the traditional setcondition with respect to development of 1-RM bench pull andbench press, peak velocity and peak power. The EMG activitywas not affected. CONCLUSIONS: Complex set trainingwould appear to be an effective method of exercise with respectto efficiency and strength development. SPONSORSHIP:Nonelisted.

Study strengths

Although resistance-based machine circuits have been studiedfor some time, this is perhaps the first (published) study to-dateto examine the effect of this particular brand of complex set

raining over a chronic period. Heres the authors definition:tFor the purposes of this research, a complex set refers to

agonistantagonist pairs of either two heavy resistance exercises

or a heavy resistance and ballistic exercise performed over

repeated trials, in an alternating manner, with rest intervals

between sets.

Subjects had at least one years strength training experience. Allparticipants had experience with complex set-type training. Therepetition range of 3-6 properly reflected the goal of increasingmaximal strength and power. To help qualify and explain anydifferences in 1-RM, throw height, peak velocity, and peakpower, the EMG responses of four muscles (pectoralis major,

anterior deltoid, latissimus dorsi, and trapezius) were monitoredduring the pre- and post-training tests.

Study limitations

As commonly seen in exercise research, there was a lack ofdietary control. In fact, dietary intake wasnt even measured orreported. This is a considerable design flaw since chronic effectswere observed. No mention was made of what point in the daythe testing was done (fed vs. fasted state), nor whether this was

kept constant across the groups. Inter-set rest (between the sameexercises not between each successive exercise) was 4minutes. Although this rest length is in line with whats beenseen as effective for increasing maximal strength, there are alsoreports showing a lack of significant difference between 2-minute and 4-minute interest rest periods.11,12Given that not alathletes seeking to increase maximal strength have lots of sparetime to train, a practical alternative would have been to keep therest periods at 2-3 minutes, with the rest times between sets inthe complex group being 1-1.5 minutes. Since a major aspect ofthis trial was to investigate time efficiency, I feel the envelopecould have been pushed further in this regard. Another limitationis that these results may or may not be smoothly extrapolated tolower-body exercises. Finally, the authors themselves concedethat the small sample size may have compromised the detectionof statistically significant differences.

Comment/application

The main findings in the present study were a lack of significantdifferences in throw height and peak velocity between groupsHowever, the truly interesting finding was that the maximastrength measures (1-RM in both the bench pull and bench

press) increased significantly in the complex group. Peak powerincreased significantly traditional group. Complex training wasmore time-efficient for the development of 1-RM bench pull andbench press, peak velocity and peak power. EMG activity wasnot significantly different in either group throughout the courseof the program. In sum, complex-type training may be moreEffective for building strength than power, whereas traditionatraining may be more effective at building power than strength.

A valid point made by the authors of the present study is thattraining methods that are time-efficient without sacrificingeffectiveness are beneficial to both the general population aswell as athletes. Another valid point mentioned is that the time

saved building strength and power can be re-allotted forsharpening the technical aspects of the given sport, allowingbetter competition preparation.

A practical issue regarding complex training is that in a typicacommercial gym setting, its not always possible to take up morethan one station or piece of equipment without either a) losingthe station you abandoned in order to complete the other half ofthe complex, or b) pissing off the other gym members who arewaiting for the particular station you appear to be reserving foryour special training. A possible solution to this would requirea training partner who switched off sets with you while you bothtook up 2 stations. This would garner less complaints from thesurrounding gym members. Another solution would be to build

your own home gym where you have free reign over how manystations you want to simultaneously occupy.

The authors concluded by deeming complex training anefficacious means of developing strength and an efficient method

of training both strength and power. Complex training is alsolikely to have an advantage over traditional training in terms ofenhancing cardio-respiratory adaptations. Perhaps futureresearch will compare each type of trainings effect on not juststrength and power, but endurance measures as well.

7/21/2019 12 - Dec - 2009

9/17


Ergogenic and Antioxidant Effects of Spirulinaupplementation in Humans.S

Med Sci Sports Exerc. 2010 Jan;42(1):142-51. [Medline]

PURPOSE:Spirulina is a popular nutritional supplement that isaccompanied by claiMSS for antioxidant and performance-enhancing effects. Therefore, the aim of the present study was to

examine the effect of spirulina supplementation on (i) exerciseperformance, (ii) substrate metabolism, and (iii) blood redoxstatus both at rest and after exercise. METHODS: Ninemoderately trained males took part in a double-blind, placebo-controlled, counterbalanced crossover study. Each subjectreceived either spirulina (6 g x d(-1)) or placebo for 4 wk. Eachsubject ran on a treadmill at an intensity corresponding to 70%-75% of their VO2max for 2 h and then at 95% VO2max toexhaustion. Exercise performance and respiratory quotientduring exercise were measured after both placebo and spirulinasupplementation. Blood samples were drawn before,immediately after, and at 1, 24, and 48 h after exercise. Reducedglutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG,thiobarbituric acid-reactive substances (TBARS), proteincarbonyls, catalase activity, and total antioxidant capacity (TAC)were determined. RESULTS:Time to fatigue after the 2-h runwas significantly longer after spirulina supplementation (2.05 +/-0.68 vs 2.70 +/- 0.79 min). Ingestion of spirulina significantlydecreased carbohydrate oxidation rate by 10.3% and increasedfat oxidation rate by 10.9% during the 2-h run compared withthe placebo trial. GSH levels were higher after the spirulinasupplementation compared with placebo at rest and 24 h afterexercise. TBARS levels increased after exercise after placebobut not after spirulina supplementation. Protein carbonyls,catalase, and TAC levels increased similarly immediately afterand 1 h after exercise in both groups. CONCLUSIONS:Spirulina supplementation induced a significant increase in

exercise performance, fat oxidation, and GSH concentration andattenuated the exercise-induced increase in lipid peroxidation.SPONSORSHIP:This study was supported by funds from theCenter of Research and Technology Thessaly.

Study strengths

The subjects were recreational runners who had trained for atleast 1 year, at least two times per week, and at least 45 minutesper session. Choosing this population minimizes the broaderoutcomes associated with rank novices and deconditioned folks.A crossover design was used to help alleviate the statisticalweakness of the small sample size (9 subjects). This study is

unique in that its the first to examine the effect of spirulina onexercise performance, substrate metabolism (fat andcarbohydrate oxidation), and redox status (relative oxidation &antioxidation) in humans. Subjects took 3-day diet recordsbefore their first lab visit, and were instructed to keep their dietsconstant throughout the study. Subjects were provided with awritten set of guidelines for monitoring dietary consumption anda journal for recording intake. Diet records were analyzed withnutritional software. A capsule count after bottles were returned

showed that compliance with ingesting the spirulina supplementsand placebo was high (96.4% and 97.6%, respectively).

Study limitations

Overall, this study was well-designed and executed, so theresnot a lot to nitpick, other than a small aspect of the testing. Theexercise testing protocol was different from whats commonlyseen with time-to-exhaustion tests. 2 hours at 70-75% VO 2maxpreceded 95% VO2max to exhaustion. While this format is more

reflective of an actual endurance event than the more traditionatime-to-exhaustion protocols (i.e., 60-70% VO2max toexhaustion), a time trial would have been more appropriate. Inother words, completing a fixed distance (or fixed energyexpenditure) in the shortest time possible would most closelyreflect actual race conditions, as opposed to attempting tomaximally prolong the exercise bout. An obvious limitation, bunot necessarily a design flaw, is that these results might notapply to events that are longer (or shorter) than the duration ofthe testing protocol.

Comment/application

The above chart illustrates the decreased carbohydrate oxidationrate and increased fat oxidation rate during the 2-hour runcompared to placebo. Statistical significance is one thing, but Ialways question how meaningful the difference is in real-worldterms. 10.3% less carbohydrate kcal and 10.9% more fat kcalburned in this case boils down to roughly 1 kcal per minute foreach, or 60 kcal per hour for each substrate. To athletes whoseevents span 2 hours and beyond, this may have some real-worldsignificance. However, for those whose training bouts last aboutan hour (& certainly less), this glycogen-sparing/fat-oxidativeeffect is minimal. Nevertheless, the authors speculate that thismore favorable use of substrates (a better glycogen-sparingeffect) in combination with the increased levels of reducedglutathione (GSH) can potentially explain the performance

enefit caused by spirulina.b

Another thing to look closely at is the actual time to exhaustionat 95% VO2max after the 2-hour steady-state period. Thespirulina treatment allowed subjects to last roughly 40 moreseconds before fatigue terminated the bout. Although that was astatistically significant difference, in the grand scheme of the 2hour test, thats only a 0.005% advantage. These results areintriguing, but too preliminary to get excited about. Replicationof these results in time trial protocols would strengthen the casefor endurance athletes to give spirulina supplementation a try.

7/21/2019 12 - Dec - 2009

10/17


Increased p70s6k

phosphorylation during intake of aproteincarbohydrate drink following resistanceexercise in the fasted state (guest analysis by Matt

Increased p70s6k

phosphorylation during intake of aproteincarbohydrate drink following resistanceexercise in the fasted state (guest analysis by MattPerryman).

Deldicque L, et al. Eur J Appl Physiol. 2009 Nov 18. [Epubahead of print] [Medline]

PURPOSE: The present study aimed at comparing theresponses of myogenic regulatory factors and signalingpathways involved in muscle protein synthesis after a resistancetraining session performed in either the fasted or fed state.DESIGN: According to a randomized crossover study design,six young male subjects participated in two experimentalsessions separated by 3 weeks. In each session, they performed astandardized resistance training. After the sessions, they receivedduring a 4-h recovery period 6 ml/kg b.w. h of a solutioncontaining carbohydrates (50 g/l), protein hydrolysate (33 g/l),and leucine (16.6 g/l). On one occasion, the resistance exercisesession was performed after the intake of a carbohydrate-richbreakfast (B), whereas in the other session they remained fasted(F). Needle biopsies from m. vastus lateralis were obtainedbefore (Rest), and 1 h (+1h) and 4 h (+4h) after exercise.Myogenin, MRF4, and MyoD1 mRNA contents weredetermined by RT-PCR. Phosphorylation of PKB (protein kinaseB), GSK3, p70(s6k) (p70 ribosomal S6 kinase), eIF2B, eEF2(eukaryotic elongation factor 2), ERK1/2, and p38 was measuredvia western blotting. RESULTS: Compared with F, the pre-exercise phosphorylation states of PKB and p70(s6k) werehigher in B, whereas those of eIF2B and eEF2 were lower.During recovery, the phosphorylation state of p70(s6k) waslower in B than in F (p = 0.02). There were no differences inbasal mRNA contents between B and F. However, comparedwith F at +1h, MyoD1 and MRF4 mRNA contents were lower inB (p < 0.05). CONCLUSIONS:Our results indicate that prior

fasting may stimulate the intramyocellular anabolic response toingestion of a carbohydrate/protein/leucine mixture following aheavy resistance training session. SPONSORSHIP: This studywas supported by grants from the Onderzoeksraad K.U.-Leuven(grant # OT04/45), the Fonds voor Wetenschappelijk OnderzoekVlaanderen (grant # G.0233.05) and the Fonds de la RechercheScientiWque Mdicale (grant # 3.4574.03).___________________________________________________

Introduction

Normally I'm not the diet/nutrition guy. As I've said before, Itend to focus my specialty on training-related material, whichincludes all the exercise physiology elements of geekdom. Don'tget me wrong, I still follow the latest research in digested form -it's just easier to listen to other smart guys you trust when youdon't have the time or motivation to immerse yourself in it.

In contrast, I like to wrap myself up in the research concerningexercise-related neuroscience and muscular physiology. That'swhere my interest really lies - understanding how the braininteracts with the hormonal and motor systems of the body, andhow those motor systems adapt to changes in the environment.

To dumb that down a little, I'm the "muscle and strength"labcoat guy.If there's one thing I've taken away from that particularknowledge base, it's that the body's systems all tend to overlapIt's hard to separate say the central nervous system fromendocrine and immune functions; when you discuss one, youautomatically have to include cross-talk and feedbackmechanisms and account for a cascade of effects that rippleacross the entire body. Needless to say, nothing about it isimple or clear-cut.s

Which also means it's getting harder and harder to separate theelements of pure exercise physiology from pure nutrition. Thiswas an easier distinction 10-15 years ago, back when the bitsand pieces of both fields were really coming together. When itwas all about the building blocks, you could look at things inisolation. Nowadays, it's nearly impossible to separate the two.

This flies in the face of sound-bite wisdom where it's still invogue to talk about how diet is 80% of your results, or whateverthe favored percentage is these days. That's a naive viewpointmind you, but it does convey how most people think about thesubject. Your diet fulfills some magical criteria, while yourtraining routine does something else. The reality of the situation

is that you can't separate out the importance of either training ordiet in the discussion of adaptation to exercise - or your resultsThe picture emerging from the research is that both nutritionand exercise-mediated factors are equally important.a

Instead of talking about the relative importance of eithernutrition or training, we have to consider them as an integratedsynergistic system; when we're discussing real-worldapplications (as opposed to the constraints of researchmethodology), you need to model things as close to the real-world as you can. It's about context, in other words.

And just to go off on a brief rant, this is also why "researchsupports anything". Research actually doesn't support just any

conclusion; papers only observe and report the outcome ofspecific events. When you lack context, of course studies seemto be in conflict. When you apply critical thinking and considerthe big picture, nutrition and exercise research rarely sayanything trulysurprising. I realize I say something to this effectin just about everything I write; that means it's important.

Getting back on topic, this brings me to the paper I want to lookat this time. This one was so good I actually came to Alan andtold him I wanted to tear it apart, because it's just that juicy

B

reakdown and First Impressions

If you read that abstract, I've little doubt that your eyes glazed

over from all the acronyms. Most of that won't mean anything toyou, I'm sure, but here's the gist of it: the took six guys and hadthem perform two experimental sessions. Each session involveda resistance-training workout, followed by a 4-hour recoverywindow in which they were given your standard post-workourecovery drink containing carbs, protein, and the amino acidleucine - which is pretty much the common expectation for whayou get post-workout amongst your average gym-rats. Thedifference between each session was the pre-workout feeding
http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ncbi.nlm.nih.gov/pubmed/19921243?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ncbi.nlm.nih.gov/pubmed/19921243?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/http://www.ampedtraining.com/

7/21/2019 12 - Dec - 2009

11/17


One session was performed with "a carbohydrate-rich breakfast",hile the other was done fasted.w

All the acronyms that they tested for here are known asmyogenic regulatory factors. In lay-speak, it means that they'rethe biochemical signals that control muscular growth right downat the cellular level. The intuitive reaction to that is prettyobvious: something that positively impacts these regulatoryfactors is desirable, as switching on muscular growth in the cellsis what's ultimately going to make your muscles bigger. This is

interesting from a medical standpoint as it can help in thetreatment of muscle-wasting conditions, which is the mainreason much of this is funded, but let's be honest - it's alsointeresting to all the vain people out there trying to get biggermuscles.

What this study found is that pre-exercise, some of theseregulatory factors were higher in the "ate breakfast" condition,compared to the fasting condition. During post-workoutrecovery, p70s6k was lower in the "ate breakfast" condition,compared to fasting. At one hour post-workout, MyoD1 andMFR4 mRNA were lower in the "ate breakfast" condition againas compared to the fasted condition. I'll explain what this meanshortly.s

Based on these results, the authors conclude that fasting prior toa resistance-exercise session may increase the anabolic responseto a standard post-workout drink.

Why This is Important

Okay, just so we're on the same page, I want to give a littleprimer on muscle growth. A bigger muscle is the result ofprotein accretion in your muscle fibers. The more protein theyhold, the bigger and stronger they are. Getting bigger is thereforell about stimulating muscle protein synthesis.a

All of those growth factors listed in the study there areresponsible for this to some degree or another. We've known for

awhile now that there are two main factors responsible for thesignaling of muscle growth: resistance exercise and ingestion ofamino acids. To put this in Bro-speak, the most anabolic thingsyou can do are lifting weights and eating protein.

This goes right back to what I said earlier about looking at thisas an integrated process. In fact, while amino acids andresistance exercise will each signal muscle growthindependently, doing both at the same time tends to have asynergistic effect. Not to put too fine a point on it, but having aprotein meal before and after a resistance-training workout isabout as anabolic as you can get short of shooting up a 500mg ofest.t

As the title indicates, they're particularly interested in the actionof p70s6k, which is a nifty little compound that directly governsprotein synthesis in muscle fibers. It's arguably one of the moreimportant signals of growth, as it lies directly downstream ofcompounds called Protein Kinase B (also known as PI3K) andmTOR, which have long been known as pretty much the signalsfor muscle hypertrophy. It might be better to describe them as abottleneck or central switch, though; the actual signals comefrom elsewhere in the muscle (say the membrane, when it'sstretching, or certain other signals that are responsive to

environmental changes). PI3K and mTOR just take all thosesignals and then switch on the protein-synthesizing machinery inesponse.r

In particular mTOR is widely thought to be the big boy, affectedby just about everything else, and thus almost exclusivelyresponsible for the instigation of protein synthesis. That makesp70s6k, mTOR's workhorse, pretty intimately connected to thewhole process, and thus something you want to have a closeook at.l

They also look at MyoD, MRF4, and myogenin, which doslightly different things. These growth factors are moreassociated with the development of satellite cells, which maketheir own contribution to muscle growth. That's a whole separatedigression which I don't really want to get into. Let's just leave itat this: they aren't directly related to the processes of geneexpression and protein synthesis, but they are very importantndicators of the anabolic process all the same.i

The implication, at least from the first glance, is that noteatingbefore your workout can improve your sensitivity to the postworkout recovery drink. The abstract notes that at one hour post-exercise, the fasted condition seems to indicate a superior

response. I know your first instinct is to see that and thenimmediately stop eating anything before you go to the gymhat's what happens when you jump to conclusions too quickly.T

I'll just say that this is one of those cases where you really, reallyhave to stop and read the whole paper before making any hastyconclusions. I was skeptical of confounds even before I read thefull paper, and seeing the entire thing only confirmed what I'dhought.t

Let's see why.

A Closer Look

First of all, I do want to give props to the authors for even doing

this in the first place. As they note, most studies of this natureare done in fasted-state subjects, but the reality of the situation isthat most weight-training folks are going to be exercising withfood in them. I know I for one very rarely come into a sessionwithout something in my stomach; I don't imagine most peoplewith any halfway serious intent would different. Bodybuilderswho are already obsessive about the timing of their food intakeand tend to eat every 2-3 hours, will basically never have aasted workout.f

Given the effects that diet can have on both exercise andrecovery, it's a good idea to compare "fed" and "fasted"conditions just to see what differences there might be in the

rowth-chemistry.g

As far as the study itself is concerned, the most regrettable thingis apparent right up front: the sample size is only six males. Thatby itself gives it only limited statistical power even with thecrossover design, so we have to be careful generalizing this righoff the bat. That said, we can likely take away the general theme

f the paper even if the effect sizes are harder to control for.oAll six subjects were physically active males, listed as physicaeducation students involved in a variety of activities, althoughnone were consistently involved in a specific resistance training

7/21/2019 12 - Dec - 2009

12/17


program. Two weeks prior to the start of the study, the subjectswere familiarized with the exercises involved, which consistedof seven exercises to train the entire body. This was another

ood choice on the part of the authors.gEach session was separated by a three-week interval, and to keepdiet under control, all food and drink was provided by theresearchers for three days prior to each test. The subjects arrivedearly in the morning after an 11-hour overnight fast, and werethen assigned to either breakfast (B) or fasted (F) conditions.

The (B) condition was given "a standardized carbohydrate-richbreakfast" containing 722 kcal, 85% carb, 4% fat, 11% protein.If you do the math, that works out to be ~153g carbs, 3g fat, and

0g protein. The (F) condition obviously didn't eat anything.2Muscle biopsies and blood samples were drawn before theworkout session. The session itself consisted of 3 sets of 8 repson each exercise, with three-minute rest intervals and alternatingupper and lower body movements. The workout took 90 minutesto complete. After the session, the subjects had a 4-hoursupervised recovery period in which they were all given arecovery drink at 6ml per kg of body weight (i.e., a 90kg subjectwould get 540ml) each hour. The drink itself had 50g per liter ofa carb solution (listed as 50% glucose and 50% maltodextrin),

16.6 g/L of leucine, and 33.3 g/L of protein hydrolysate, so againour 90kg subject would get 27g carbs, 9g of leucine, and 18g ofprotein hydrolysate. In short, it's your standard post-workout

rotein-carb recovery drink.pAt both +1hour and +4hours (the end of the recovery interval),new biopsies and blood samples were taken, and these weresubjected to the usual boring lab-work to determine levels of theelevant compounds.r

Pre-exercise insulin levels were roughly 13 times higher in the(B) condition, which isn't a shock; insulin drops off in a hurry infasting conditions. Likewise pre-exercise free fatty acids (FFA)were higher in the (F) condition. This is again no surprise, since

FFA levels tend to be negatively correlated with insulin levels.The higher insulin levels in the (B) condition increased theactivity of PKB and p70s6k (and there was certainly some effectfrom amino acid intake, even though the authors didn't mentiont).i

Where these guys got all excited is at the +1hour time point - atthis point in time, p70s6k was higher in the (F) condition. Looksgreat if you just consider that alone. However, I do have to notethat there was no statistically significant difference between anyother growth factorat either +1hour or +4hours. In fact, if youlook at their data set, by +4hours, p70s6k is actually slightlylower in the (F) condition. The MyoD1 and MRF4 genesshowed some (very slight and non-significant) advantage in the

(F) condition at +1hour as well, though again by the time4hours rolls around, the differences have vanished.+

Based on these outcomes, the authors speculate that pre-exercisefasting may be a way to increase stimulation of p70s6k, and thusmuscle protein synthesis, with a post-workout recovery drink.They note that the mechanism works via insulin-independentactivation of mTOR, and that lack of feeding for several hourscould "create a favorable environment" for activation of bothmTOR and p70s6k by amino acids.

The authors do recognize the limitations of this, however, byacknowledging that the apparent advantage of the (F) conditionvanishes by the +4hour time point, and by questioning therelevance to realized muscular anabolism. They note that whilep70s6k levels correlate with protein synthesis in some studies, itdoes not in others, and indeed there may be no connectionbetween p70s6k and real protein remodeling. Which is to sayshort-term post-workout spikes may not actually translate to rea

uscle growth.m

What is somewhat interesting and might (might) be worth a lookis the effect of feeding on the MyoD1 and MRF4 genes. Theauthors cite several studies that show an effect on these geneswith respect to the timing of nutrients, and there may actually besomething to it. Then again, there's a rule of thumb I adhere towhen talking about these slices of the whole: if you're doingeverything right, and then some fine point of biochemistry seemsto be in disagreement, the odds are that the biochemistry isn'going to be a game-changer. What's more likely is that we justaren't seeing the big picture.

M

att's Commentary

It's been fairly common knowledge for awhile now that both pre-

and post-exercise nutrition can play a huge role in the effects ofresistance-training workouts. That's not in dispute, nor is thereanything here that's going to change the playing field. Ifanything, this just tells us that eating before a workout doesmake a real difference at the local muscular level. The questionas always, is whether or not this makes an ounce of difference to

s at the practical level.uAs far as the conclusion presented in the abstract, I'll be blunt: Ithink it's wrong. On analysis, it's not actually incorrect as muchas it's simply misleading, to be fair to the authors. It's somisleading in fact that it's the main reason I wanted to do thisreview. It's not wrong, but you just know every supplemencompany and guru with a blog is sitting out there ready to talk

about the merits of fasting before your workouts. Unfortunatelythe actual data in the paper doesn't back that up. Firstly, the fedcondition showed a better anabolic response pre-workoutSecondly, the only significant advantage to the fasted group wasat +1hour, and even there you're talking about one factor. By+4hours, there's no significant difference, and in fact there's alight advantage to the fed condition.s

This is not unlike the Bro-wanking about post-workouhormonal spikes. I've said it about that topic, and I'll say it abouthis: transient spikes of activity mean nothing. The remodelingof a muscle fiber is a process that takes days and even weeks bysome indicators; a burst of activity that lasts less than one hour issimply not significant to that process. What gave it away to meeven before I read the full paper is the fact that only one datapoint was significantly different, that being p70s6k. While it's animportant factor to be sure, it doesn't always correlate to realizedgrowth. What sealed the deal was the fact that this differencewas only observed at +1hour. Anything that's going to trulyaffect muscle growth is going to have to operate on a muchlonger time-frame, considering that elevated protein synthesisalone will continue for at least 48 hours post-training.

7/21/2019 12 - Dec - 2009

13/17


What's most likely happened here is simple, and the authorsthemselves examined the possibility in their own discussion. Thefasted condition simply primed the muscle for a stimulus. Thosein the fed condition, in contrast, already had their growthchemistry humming along nicely. The body's known for sharpresponses to new, unaccustomed stimuli. In my mind, that's allthat happened here. The fasted group was briefly less-accustomed to amino acids and/or insulin than the fed group, andhe spike was simply a response to that.t

To those saying "Oh yeah? An anabolic spike is still an anabolicspike!", I'd also note that the fed subjects actually spent moretime "anabolic" simply because, well, they weren't fasted goinginto the workout. If growth is a matter of net time anabolic vs.net time catabolic, it becomes pretty clear what protocol you'dwant to follow. A brief spike that might be anabolic is probablynot going to balance out the drawbacks of remaining fasted longenough to make it happen (although there may be someloopholes in that premise; keep reading).

That brings me to another point - this study didn't actuallymeasure fractional protein synthesis rates, nor did it measureprotein loss. Without having some idea of net protein turnover,measuring the myogenic regulatory factors alone is leaving out a

big chunk of useful data. Simply put, we have no idea of theactivity of the growth factors correlates to anything that wouldbe of value to us. Worse, even if they had observed increasedprotein synthesis rates, that alone doesn't even mean that much,because we've seen that protein loss tends to scale up to match

ny increases.aWorkouts are one of the biggest causes of protein loss that thereis, yet nobody considers working out to be a bad thing forgrowth. Protein synthesis ramps up to compensate, and as longas the rate of synthesis is greater than the rate of breakdown,you're still in a net positive protein balance. In order to bepredictive of realized muscle growth, you'll need some measureof both. And of course even that is assuming you can note the

relevance within four hours of a training session - which isquestionable.

At best these regulatory factors and signaling pathways are aproxy indicator for what's actually happening. We know they'reassociated with good wholesome anabolic muscle growth. Westill don't understand the process well enough to accuratelymodel the actual growth of muscle tissue based on the chemistrylone. Them's the breaks.a

Of course, there is another angle to consider as well.

It's been suggested that low-carb diets mimic many of thepositive effects of fasting, largely due to effects on insulinactivity, resting levels of FFAs, catecholamine levels, and fattyacid oxidation. It's not out of the realm of possibility that we'dsee something similar here as well. Insulin has effects on themyogenic chemistry through at least two pathways I can thinkof: AMPK and GSK3, if you're interested. Indeed GSK3 wasone of the factors tested for in this paper. Insulin has a mildeffect on protein synthesis, though it's weak compared to aminoacids. The main function of insulin so far as I've seen is to fill an"anti-catabolic" role - it tends to blunt protein breakdown,mainly through AMPK and GSK3.

It's not in question that carb intake post-workout will help withrecovery, mainly due to the impact on insulin levels and onrestoring any glycogen that may have been depleted. However, Ihave to say that personally I've been questioning the necessity ofcarb intake before/after workouts for a number of years now. tend to train with a relatively low volume of work; I don't dovery many exercises, and while I tend to average 4-6 sets, Igenerally tend to keep the reps in the 1-6 range. That kind ofraining isn't very glycogen-depleting.t

On the other hand, if you're an endurance athlete, or one of theold-school bodybuilders that does 100 sets per part (which is tosay, an endurance athlete), you're eating up a ton of glycogen inyour workouts and will certainly benefit from replacing it. Ingeneral the more work you do, or the longer you train without a

reak, the more likely you are to need carbs in your workout.bThe authors don't really touch on the possibility, but I do have towonder if a protein-only feeding before the workout might noshow similar effects to the fasted subjects, if there is some carbor insulin-mediated effect going on. The only problem with thatis that I can't think of anything that would do this. That doesn'tmean there is no such thing, just that I can't think of it right thisinstant. Insulin doesn't really have any effects I can think of tha

would cause a negative response from the "anabolic" standpoint- which is one of the reasons I'm taking my position on the

atter.mSomething else that may be relevant here is the concept of"protein pulse feeding". Some relatively recent research byLayne Norton and others has indicated that keeping chronicallyelevated levels of amino acids may be a bad thing; it seems thatdoing this may actually create a lesser anabolic response to anyfeeding. Instead, Layne's suggested that it might be better to"pulse" your protein feedings, getting a larger amount at eachmeal while spacing the meals farther apart - at least every 3-5hours, compared to the Standard Bodybuilding Suggestion ofhaving meals every 2-3 hours.

Now this could have an interesting effect, if you time it so thayou work out at the tail end of a protein "pulse". If there is anybeneficial effect to it, this could exploit it without actuallyhaving to starve yourself. So you'd eat say 4-5 hours beforelifting, do your workout fasted, then slam your recovery drinkafter the fact. If you're convinced it matters, that is. It might bean interesting strategy to toy with, even though I'm still playinghe skeptic for now.t

Then there's the whole Intermittent Fasting concept. Our buddyMartin Berkhan over at Leangainshas been getting great resultswith this approach, by having people fast 16 hours and eat 8hours per day. If there is anything to the added "anabolic

sensitivity" of fasting, the IF strategy may well be takingadvantage of it. It's really too soon to say if the IF approach toeating is really superior or just a convenient way of dieting, butit does get results.

T

he Occam's Razor Test: Will it matter in a year?

For those of you wondering why I'm so skeptical about all thisstuff, you have to remember that I've been trying most of it ouon myself for over 10 years now. If there's one thing that's been
http://www.leangains.com/http://www.leangains.com/

7/21/2019 12 - Dec - 2009

14/17


consistent between all of it, it's the fact that none of it seems toake a damn bit of difference.m

As far as I'm concerned, I don't think there is any hard and fastrule here - at least if you're looking for a Comprehensive MagicFormula to Meet All Your Needs. Which most everyone is, let'sface it.

My hunch is that this particular effect may seem to offer anadvantage if you just look at the short-term slices of activity, butwhen you average it out over 24 hours the magic vanishes. Ifthere's one thing your body is good at, it's balancing things outover the long-term. You may well get bigger spikes of anabolismby fasting going into your workout, but I'd bet money that it'smatched by longer periods of catabolism and protein breakdown.

he net result? No real difference.TAs with training routines, people diet all different ways and stillsee good results from it. As far as wanking over this particularstudy, just don't. There's nothing here that provides any solidbacking to the idea that you should intentionally go out of yourway to fast before lifting weights. Remember, it's not the theorythat shapes reality. Reality shapes the theory. Even without anyacademic support, what makes more sense from an intuitive

standpoint? Making sure your body has an adequate supply ofnutrients, or starving it? Without any other input, the logicalonclusion is to feed yourself.c

That said, if you find room for protein pulsing or intermittentfasting, then why not? Even though this paper doesn't imply youshould go and fast before training,

12 - Dec - 2009

Documents

Transcript of 12 - Dec - 2009