Dark chocolate reduces exercise induced oxidative stress:

Jacob Schor

August 11, 2011

www.DenverNaturopathic.com 

 

Dark chocolate reduces exercise induced oxidative stress: is this a good thing or not?

 

A study by Allgrove et al on chocolate’s effect on bicyclists that was published last April has given me something to chew on over the last few months. 

 

This was in fancy terms a randomized, counterbalanced, crossover designed trial,.  Twenty active men ate chocolate or a placebo [though I can’t imagine what pretend chocolate would look like] for two weeks and then performed a bout of prolonged cycling.  They cycled at 60% maximal oxygen uptake (VO2max) for 1.5 hr, with the intensity increased to 90% VO2max for a 30-second period every 10 minutes, followed by a ride to exhaustion at 90% VO2max.

[in less technical terms, as our neighbor the Pastor Jason might say, they biked until they puked, or pretty darn close to it]

 

Venous blood samples were taken immediately before exercise, post-exercise (fixed duration), post-exhaustion, and after 1 hour of recovery.

 

In the 2 week period prior to the exercise bout, these guys ate 40 grams of dark chocolate (DC) or a placebo containing equivalent quantities of carbohydrate and fat as in the chocolate, twice a day and once more 2 hours before starting the exercise bout.  For comparison the squares of Bakers chocolate that come individually wrapped in the white paper, 8 to a box weigh in at an ounce each, that is just under 30 grams.

 

Blood samples were taken immediately before starting the exercise bout, partway through the exercise (the fixed duration section), post-exhaustion and after 1 hour of recovery.  The blood was analyzed seeking changes associated with eating the chocolate, including,  F-2 isoprostanes, lipoproteins, free fatty acids, glucose, insulin, glucagon, cortisol and  various interleukins.

 

Those guys consuming the dark chocolate had lower F2-isoprostanes at exhaustion and during recovery.  Consuming dark chocolate lowered levels of oxidized low-density lipoproteins both before and after exercise.  Chocolate consumption was also associated with ~21% greater increase in free fatty acids during exercise.  Eating chocolate had no observed effect on exercise performance.  [1]

 

 

Implications:

 

These Allgrove et al results are similar to those from earlier studies on chocolate consumption’s effect on exercise-induced changes in blood chemistry.  This study was reminiscent of Wan et al’s 2001 trial of cocoa powder and dark chocolate, though the earlier study measured the effects without introduction of the exercise. [2]  Davison et al had a somewhat similar study published on April 5, 2011 though they examined the effect of chocolate consumption might have on neuroendocrine markers post cycling bout. [3]

 

 Testing the effect of antioxidant foods on blood chemistry before and after bouts of strenuous exercise has become a popular experimental model, especially using cyclists.   Dumke et al in 2009, used cyclists to gauge quercetin’s effect on blood parameters. [4]  Eichenberger has used cyclists to test the effects of both green tea extracts and Siberian ginseng on cycling performance without finding benefit from either. [4,5]

 

Before we rush to encourage every patient to eat vast amounts of chocolate, there are several nuances to blood fat oxidation that we might wish to consider.  The basic concept that blood fat, in particular LDL, oxidation is a contributing factor to atherosclerosis is well known (so well known that I’m going to see if I can mention this without my editors insisting on a citation).  Exercise, even a single relatively minor bout will increase oxidative damage in the muscles and blood thereby triggering, “… an adaptive increase in antioxidant capacity of blood and skeletal muscle.   [7]  As a result of this adaptive response, the amount of oxidative damage sustained from exercise actually decreases with repeated exercise bouts. [8]

 

There are researchers who argue that oxidative stress is useful for the organism’s overall health because it triggers an adaptive response.  For example, Ristow and Zarse argue in their 2010 paper that increased oxidative stress promotes longevity and metabolic health.  They introduced an idea they call ‘mitohormesis’ that describes how oxidative stressors will have a hormetic effect on the mitochondria.  Hormesis is a relatively rarely used term.  It describes the situation in which moderate to large concentrations of a particular substance have a toxic effect or damaging effect on an organism, that is are poisonous, while very low concentrations have a beneficial effect.  The theory is that these faint doses are enough to stimulate an adaptive response in the organism in effect making it better able to handle larger damaging exposures, or in simpler words, makes it stronger.  They use this to explain why caloric restriction often extends lifespan.  Back to Ristow and Zarse, they hypothesize that, “…these effects may be due to increased formation of reactive oxygen species (ROS) within the mitochondria causing an adaptive response that culminates in subsequently increased stress resistance assumed to ultimately cause a long-term reduction of oxidative stress.”

 

Their theory leads to a reasonable concern that, “…abrogation of this mitochondrial ROS signal by antioxidants impairs the lifespan-extending and health-promoting capabilities of glucose restriction and physical exercise, respectively.”   [9]

 

In other words, exercise induced oxidative damage may be why exercise is good for us.  If that is true, perhaps chocolate, by reducing exercise induced lipid peroxidation may reduce the benefit of exercise? Or another way,this would mean diet and exercise will not produce the health benefits we expect if we squelch the resulting oxidative damage by consuming antioxidants, like chocolate.  But this is kind of like opening a can of worms.  If oxidative stress is good and is what brings on the benefits of exercise, we have raised a host of questions.  Then we can argue that any food that we think is ‘good for us’ because it acts as an antioxidant, might negate the benefits of exercise.  We had better not go there.

 

There’s another theory that might be easier to swallow.  The antioxidant effects and life extending benefits of a number of polyphenol chemicals have been ascribed to their triggering a hormetic effect.  The phytonutrients that act via hormesis include quercetin, caffeic acid, rosemarianic acid, curcumin and sulforaphane from Brassica vegetables.      [10-12]  Why not chocolate?

 

Could dark chocolate lower LDL peroxidation levels post intense exercise, not because the chocolate is an antioxidant, but because the polyphenols themselves have an oxidant effect?  Though an intriguing thought, this does not appear to be the case.  No evidence supports the idea that chocolate is an oxidant in disguise.  In vitro experiments with chocolate clearly suggest that it acts solely as an antioxidant and protects LDL from oxidation. [13]

 

Which brings us back to the initial concern.  Will supplying the body with effective antioxidants reduce damage brought on by exercise and reduce the long term benefits typically elicited by the adaptive response brought on by initial oxidative damage? 

Though this may sound like a great question, it isn’t. 

 

That’s because we don’t know the answer.

 

References:

 

 

Allgrove J, Farrell E, Gleeson M, Williamson G, Cooper K. Regular dark chocolate consumption's reduction of oxidative stress and increase of free-fatty-acid mobilization in response to prolonged cycling.  Int J Sport Nutr Exerc Metab. 2011 Apr;21(2):113-23.

Wan Y, Vinson JA, Etherton TD, Proch J, Lazarus SA, Kris-Etherton PM.  Effects of cocoa powder and dark chocolate on LDL oxidative susceptibility and prostaglandin concentrations in humans. [Clinical Trial, Journal Article, Randomized Controlled Trial].  Am J Clin Nutr 2001 Nov; 74(5):596-602.

Davison G, Callister R, Williamson G, Cooper KA, Gleeson M.  The effect of acute pre-exercise dark chocolate consumption on plasma antioxidant status, oxidative stress and immunoendocrine responses to prolonged exercise. Eur J Nutr 2011 Apr 5.

Dumke CL, Nieman DC, Utter AC, Rigby MD, Quindry JC, Triplett NT, et al. Quercetin's effect on cycling efficiency and substrate utilization. Appl Physiol Nutr Metab 2009 Dec; 34(6):993-1000.

Eichenberger P, Mettler S, Arnold M, Colombani PC. No effects of three-week consumption of a green tea extract on time trial performance in endurance-trained men. Int J Vitam Nutr Res 2010 Jan; 80(1):54-64.

Eschbach LF, Webster MJ, Boyd JC, McArthur PD, Evetovich TK.   The effect of siberian ginseng (Eleutherococcus senticosus) on substrate utilization and performance. Int J Sport Nutr Exerc Metab 2000 Dec; 10(4):444-51.

Rietjens SJ, Beelen M, Koopman R, VAN Loon LJ, Bast A, Haenen GR.  A single session of resistance exercise induces oxidative damage in untrained men. Med Sci Sports Exerc 2007 Dec; 39(12):2145-51.

Nikolaidis MG, Paschalis V, Giakas G, Fatouros IG, Koutedakis Y, Kouretas D, Jamurtas AZ.  Decreased Blood Oxidative Stress after Repeated Muscle-Damaging Exercise.   Med Sci Sports Exerc 2007 Jul; 39(7):1080-1089.

Ristow M, Zarse K.  How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis). Exp Gerontol 2010 Mar 27.

Pietsch K, Saul N, Chakrabarti S, Stürzenbaum SR, Menzel R, Steinberg CE. Hormetins, antioxidants and prooxidants: defining quercetin-, caffeic acid- and rosmarinic acid-mediated life extension in C. elegans. Biogerontology. 2011 Aug;12(4):329-47.

Calabrese V, Cornelius C, Trovato A, Cavallaro M, Mancuso C, Di Rienzo L, et al. The hormetic role of dietary antioxidants in free radical-related diseases.  Curr Pharm Des. 2010;16(7):877-83.

Mattson MP. Dietary factors, hormesis and health. Ageing Res Rev. 2008 Jan;7(1):43-8.

Hirano R, Osakabe N, Iwamoto A, Matsumoto A, Natsume M, Takizawa T, et al. Antioxidant effects of polyphenols in chocolate on low-density lipoprotein both in vitro and ex vivo.  J Nutr Sci Vitaminol (Tokyo). 2000 Aug;46(4):199-204.