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;21(2):113-123.
In a randomized, counterbalanced, crossover designed trial, 20 active men consumed chocolate or a placebo for 2 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.
Venous blood samples were taken immediately before exercise, post-exercise (fixed duration), post-exhaustion, and after 1 hour of recovery.
20 active men
Study Medication and Dosage
In the 2-week period before the exercise bout, participants 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.
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 consuming the chocolate, including F-2 isoprostanes, lipoproteins, free fatty acids, glucose, insulin, glucagon, cortisol, and various interleukins.
Those consuming 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. Consuming chocolate had no observed effect on exercise performance.
These current results from Allgrove et al 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 the introduction of exercise.1 Davison et al had a somewhat similar study published on April 5, 2011, though they examined the effect chocolate consumption might have on neuroendocrine markers after a cycling bout.2
Testing the effect of antioxidant foods on blood chemistry before and after bouts of strenuous exercise, especially cycling, has become a popular experimental model. In 2009, Dumke et al used cyclists to gauge quercetin’s effect on blood parameters.3 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, we should consider several nuances to blood fat oxidation. The basic concept that blood fat, in particular LDL, oxidation is a contributing factor to atherosclerosis is well known. Even a single relatively minor bout of exercise will increase oxidative damage in the muscles and blood, thereby triggering “an adaptive increase in antioxidant capacity of blood and skeletal muscle.”6 As a result of this adaptive response, the amount of oxidative damage sustained from exercise actually decreases with repeated exercise bouts.7
Some researchers 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 or hormetic effects are the terms used to describe dose-response relationships in which something, often a toxic substance, that produces harmful biological effects at moderate to high doses, will produce beneficial effects at lower doses. Ristow and Zarse use this concept of hormesis to explain why caloric restriction often extends lifespan. 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.”8
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. 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.
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.
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.9-11 Why not chocolate?
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? In other words, is some small amount of damage good for us? Do we need it to make us stronger?
Great question. Unfortunately, we don’t know the answer.