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Dark Chocolate May Boost Cardiovascular Performance

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I expect by now we've all heard the news that beets and beet juice boost cardiovascular performance. I love beets, but for those who don't it appears you now have another, more palatable option - dark chocolate!


This recent study [1] (popular press story) found in a randomized crossover design that daily consumption of dark chocolate (40g Dove Dark Chocolate, 50-60% cacao) for two weeks, but not the equivalent calories of white 'chocolate' <sic> (0% cacao), resulted in a 6%  increase in VO2max relative to baseline in nine trained cyclists. These cyclists were able to cover 17 percent greater distance on average in a two minute maximum effort time trial relative to controls, but the effect wasn't statistically significant due to small sample size.


It looks like the mechanism involved might be the same as beets - namely that the epicatechins in cacao increases nitric oxide levels in the blood, and boosting cardiovascular performance.





[1] J Int Soc Sports Nutr. 2015 Dec 15;12:47. doi: 10.1186/s12970-015-0106-7.

eCollection 2015.
Dark chocolate supplementation reduces the oxygen cost of moderate intensity
Patel RK(1), Brouner J(1), Spendiff O(1).
BACKGROUND: Dark chocolate (DC) is abundant in flavanols which have been reported
to increase the bioavailability and bioactivity of nitric oxide (NO). Increasing 
NO bioavailability has often demonstrated reduced oxygen cost and performance
enhancement during submaximal exercise.
METHODS: Nine moderately-trained male participants volunteered to undertake
baseline (BL) measurements that comprised a cycle V̇O(2max) test followed by
cycling at 80% of their established gas exchange threshold (GET) for 20-min and
then immediately followed by a two-minute time-trial (TT). Using a randomised
crossover design participants performed two further trials, two weeks apart, with
either 40 g of DC or white chocolate (WC) being consumed daily. Oxygen
consumption, RER, heart rate and blood lactate (BLa) were measured during each
RESULTS: DC consumption increased GET and TT performance compared to both BL and 
WC (P < 0.05). DC consumption increased V̇O(2max) by 6% compared to BL
(P < 0.05), but did not reach statistical significance compared to WC. There were
no differences in the moderate-intensity cycling for V̇O₂, RER, BLa and heart
rate between conditions, although, V̇O₂ and RER exhibited consistently lower
trends following DC consumption compared to BL and WC, these did not reach
statistical significance.
CONCLUSION: Chronic supplementation with DC resulted in a higher GET and enhanced
TT performance. Consequently, ingestion of DC reduced the oxygen cost of moderate
intensity exercise and may be an effective ergogenic aid for short-duration
moderate intensity exercise.
PMCID: PMC4678700
PMID: 26674253
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This assumes that we prioritize CV efficiency during exercise. So, like a performance enhancing drug (except, hopefully without negative health side effects). Fine. But what about those who only care about health and longevity and not about how efficiently their heart works when they bike/run/jump - can we therefore surmise that regular dark chocolate consumption might be good for CV health in general, as some studies indicate? And if the answer is "yes", then is there any advantage to actually consuming the actual chocolate, or is it enough to cold brew the cacao beans as discussed in the "So Why Don't We Brew Our Chocolate?" thread? If the effect described in this paper is due to flavanols that boost NO, aren't we getting them from the brew just as well, without the additional calories, fat, heavy metals etc.? Or do we need some other elements for this NO effect - or more accurately the cardiac effect described in this paper - and that is why we need to eat the actual chocolate mass?

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Boy you are the skeptic. 


But what about those who only care about health and longevity and not about how efficiently their heart works when they bike/run/jump  - can we therefore surmise that regular dark chocolate consumption might be good for CV health in general, as some studies indicate? 


Notice from the paper they mention increased nitric oxide activity in the cardiovascular system as the likely cause of the improved cycling performance. Here, let me google that for you. Oh, lookie there - a page full of review publications like this one [1], showing a mountain of evidence that increased nitric oxide activity is associated with reduced CVD risk, as well as a host of other health benefits:


A healthy vasculature depends on the integrity of the endothelium with a dynamic autocrine and paracrine organ with vasodilator, anti-inflammatory,  and  antithrombotic  effects.1  Injuries or  dysfunctional  endothelial  cells,  with  a  loss  of endothelium-derived  nitric  oxide  (NO),  are  major critical  factors  in  the  pathogenesis  of  vascular  diseases,  including  hypertension,  atherosclerosis,  and vasospasm with compromised blood flow.


In addition to its discovery as a vasodilator, NO mediates several protective functions of the endothelium by inhibiting (1) neutrophil activation and adhesion, (2) platelet adhesion and aggregation, (3) vascular smooth muscle pro-liferation, and  (4)  expression  of  proinflammatory cytokines. Thus, a healthy endothelium with normal generation of NO acts to prevent atherosclerosis development and its complications.


In short, if you want smooth, pliable arteries, and therefore avoid increase in blood pressure with age, maintaining NO signalling is very important. It's also implicated in brain health as well [2], and interestingly, curcumin may prevent cognitive decline by increasing NO signalling in neurons [4]. Exercise helps with cardiovascular health in part by upregulating NO signalling [3], and as this and other recent evidence suggest, the phytochemicals in dark chocolate and beets appear to potentiate this effect.


As to whether this and other benefits of chocolate will result if we drink brewed cacao beans (like we do coffee) rather than eat them in processed form as chocolate, is a question I investigated ad nauseum in the So Why Don't We Brew Our Chocolate? thread you refer to. You'll have to read that thread for details. But based on the demonstrated water solubility of polyphenols like the ones in chocolate and the fact that coffee and tea are health-promoting due to their high polyphenol content despite the fact we brew them and then throw out the solids, my conclusion is yes - you can get the beneficial effects of chocolate without the downsides of saturated fat, added sugar, cadmium and other heavy metals, by brewing rather than eating chocolate.






[1] J Clin Hypertens (Greenwich). 2008 Apr;10(4):304-10.

Vascular system: role of nitric oxide in cardiovascular diseases.
Bian K(1), Doursout MF, Murad F.
In contrast with the short research history of the enzymatic synthesis of nitric 
oxide (NO), the introduction of nitrate-containing compounds for medicinal
purposes marked its 150th anniversary in 1997. Glyceryl trinitrate
(nitroglycerin) is the first compound of this category. On October 12, 1998, the 
Nobel Assembly awarded the Nobel Prize in Medicine or Physiology to scientists
Robert Furchgott, Louis Ignarro, and Ferid Murad for their discoveries concerning
NO as a signaling molecule in the cardiovascular system. NO-mediated signaling is
a recognized component in various physiologic processes (eg, smooth muscle
relaxation, inhibition of platelet and leukocyte aggregation, attenuation of
vascular smooth muscle cell proliferation, neurotransmission, and immune
defense), to name only a few. NO has also been implicated in the pathology of
many inflammatory diseases, including arthritis, myocarditis, colitis, and
nephritis and a large number of pathologic conditions such as amyotrophic lateral
sclerosis, cancer, diabetes, and neurodegenerative diseases. Some of these
processes (eg, smooth muscle relaxation, platelet aggregation, and
neurotransmission) require only a brief production of NO at low nanomolar
concentrations and are dependent on the recruitment of cyclic guanosine
monophosphate (cGMP)-dependent signaling. Other processes are associated with
direct interaction of NO or reactive nitrogen species derived from it with target
proteins and requires a more sustained production of NO at higher concentrations 
but do not involve the cGMP pathway.
PMID: 18401228
[2] Oxid Med Cell Longev. 2015;2015:721514. doi: 10.1155/2015/721514. Epub 2015 Jun
Age-Related Cognitive Impairment as a Sign of Geriatric Neurocardiovascular
Interactions: May Polyphenols Play a Protective Role?
Jagla F(1), Pechanova O(1).
Author information: 
(1)Institute of Normal and Pathological Physiology, Slovak Academy of Sciences,
Sienkiewiczova 1, 813 71 Bratislava, Slovakia.
It is known that endothelial dysfunction plays an important role in the
development and progression of cardiovascular diseases implicated also in
cognitive decline. Experimental studies pointed to the fact that the modification
of NO levels via NOS activity may affect the blood pressure level as well as
several higher nervous functions-for example, learning and memory. There are
emerging evidences from in vitro and animal studies suggesting that polyphenols
may potentially have a protective effect on the development of neurodegenerative 
diseases and may improve cognitive function as well as positively affecting the
blood pressure regulatory mechanisms. This review accentuates the need for
precisely defined clinically controlled studies as well as for use of adequate
experimental procedures discriminating between the human higher brain functions
and the only overall activation of the brain cortex. The physiological
neurocardiovascular interactions are implicated in the increased healthy life
span as well.
PMCID: PMC4477224
PMID: 26180593
[3] Sports Med. 2003;33(14):1013-35.
Exercise and the nitric oxide vasodilator system.
Maiorana A(1), O'Driscoll G, Taylor R, Green D.
Author information: 
(1)Department of Human Movement and Exercise Science, The University of Western
Australia, Crawley, Western Australia, Australia.
In the past two decades, normal endothelial function has been identified as
integral to vascular health. The endothelium produces numerous vasodilator and
vasoconstrictor compounds that regulate vascular tone; the vasodilator, nitric
oxide (NO), has additional antiatherogenic properties, is probably the most
important and best characterised mediator, and its intrinsic vasodilator function
is commonly used as a surrogate index of endothelial function. Many conditions,
including atherosclerosis, diabetes mellitus and even vascular risk factors, are 
associated with endothelial dysfunction, which, in turn, correlates with
cardiovascular mortality. Furthermore, clinical benefit and improved endothelial 
function tend to be associated in response to interventions. Shear stress on
endothelial cells is a potent stimulus for NO production. Although the role of
endothelium-derived NO in acute exercise has not been fully resolved, exercise
training involving repetitive bouts of exercise over weeks or months up-regulates
endothelial NO bioactivity. Animal studies have found improved
endothelium-dependent vasodilation after as few as 7 days of exercise. Consequent
changes in vasodilator function appear to persist for several weeks but may
regress with long-term training, perhaps reflecting progression to structural
adaptation which may, however, have been partly endothelium-dependent. The
increase in blood flow, and change in haemodynamics that occur during acute
exercise may, therefore, provide a stimulus for both acute and chronic changes in
vascular function. Substantial differences within species and within the
vasculature appear to exist. In humans, exercise training improves
endothelium-dependent vasodilator function, not only as a localised phenomenon in
the active muscle group, but also as a systemic response when a relatively large 
mass of muscle is activated regularly during an exercise training programme.
Individuals with initially impaired endothelial function at baseline appear to be
more responsive to exercise training than healthy individuals; that is, it is
more difficult to improve already normal vascular function. While improvement is 
reflected in increased NO bioactivity, the detail of mechanisms, for example the 
relative importance of up-regulation of mediators and antioxidant effects, is
unclear. Optimum training schedules, possible sequential changes and the duration
of benefit under various conditions also remain largely unresolved. In summary,
epidemiological evidence strongly suggests that regular exercise confers
beneficial effects on cardiovascular health. Shear stress-mediated improvement in
endothelial function provides one plausible explanation for the cardioprotective 
benefits of exercise training.
PMID: 14599231
[4] Prog Neuropsychopharmacol Biol Psychiatry. 2013 Aug 1;45:47-53. doi:
10.1016/j.pnpbp.2013.05.001. Epub 2013 May 8.
Curcumin ameliorates memory deficits via neuronal nitric oxide synthase in aged
Yu SY(1), Zhang M, Luo J, Zhang L, Shao Y, Li G.
Author information: 
(1)Department of Physiology, Shandong University, School of Medicine, Wenhuaxilu 
Road, Jinan, Shandong Province 250012, PR China.
A number of neuroprotective effects of curcumin have been demonstrated in recent 
years. However, whether curcumin exerts any beneficial effects on age-related
impaired cognition and memory has not been well characterized; nor was there any 
detailed data on the molecular pathways activated by curcumin. The present study 
attempts to investigate the effects of curcumin on memory decline of aged mice
with a focus upon the possible contribution of the neuronal nitric oxide synthase
(nNOS)/nitric oxide (NO) pathway in the memory amelioration effect of curcumin.
The results showed that chronic administration of curcumin (50mg/kg, i.p., 21
days) significantly ameliorated the memory acquisition ability of aged male mice 
in the novel object recognition and passive avoidance tasks. Immunoblotting
revealed that chronic treatment of curcumin increased nNOS expression in the
prefrontal cortex, amygdala and hippocampus, as well as the enhancement of nNOS
activity and NO concentration. This enhancement was suppressed by pre-treatment
with 7-nitroindazole (7-NI), a specific inhibitor of neuronal nitric oxide
synthase (nNOS). Furthermore, inhibition of nNOS synthase by 7-NI also prevented 
the memory improvement effects of curcumin in aged mice. Taken together, the
results of the present study suggest that the amelioration of memory deficits by 
curcumin in aged mice was mediated, at least in part, by activating the nNOS
activity in specific brain regions. These findings reveal the therapeutic
potential of curcumin as a preventive agent upon the deterioration of cognitive
Copyright © 2013 Elsevier Inc. All rights reserved.
PMID: 23665290
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  • 3 months later...

The dark chocolate-exercise benefit reported also by the last of the below papers seemed blind to the elephant in the room -- the stimulants caffeine and theobromine.

Combined caffeine and ephedrine ingestion improves run times of Canadian Forces Warrior Test.
Bell DG, Jacobs I.
Aviat Space Environ Med. 1999 Apr;70(4):325-9.
PMID: 10223267


The ingestion of a combination of caffeine © and ephedrine (E) has been reported to prolong exercise time to exhaustion during cycle ergometry at 85% VO2max. The present study was undertaken to investigate whether this enhancement would occur in a field setting and if drug ingestion on 1 d would affect performance 1 d later. Two hours after ingesting either a combination of 375 mg of C and 75 mg E (C+E), or a placebo (P), 9 healthy male recreational runners completed six balanced and double-blind trials of the Canadian Forces Warrior Test (WT), a 3.2 km run wearing "fighting order" which weighed about 11 kg. The trials were performed in sets of two runs, i.e., two runs were done 24 h apart, and these sets were separated by a minimum of 7 d. The sets were: C+E trial on day 1 (D1), placebo on day 2 (P2); placebo first (P1), C+E second (D2); and placebo first (P3), placebo second (P4). In addition, 1 wk before the treatment trials the subjects performed a control trial WT. During the WT, heart rates (HR) were recorded every minute. Plasma C and E levels immediately before the WT were similar for both C+E trials, but were undetectable for all P trials. Run times (mean+/-SD) were 15.3+/-0.6, 15.4+/-0.9, 15.5+/-1.2, 15.4+/-0.9, 15.4+/-0.9, 14.8+/-0.7, and 14.6+/-0.8 min for control, P1, P2, P3, P4, D1, D2 trials, respectively. The two C+E trial run times were similar and both were significantly faster (p < 0.05) than control and all placebo trials. HR during the WT was significantly higher (p < 0.05) for the C+E trials compared with the other trials. WT performance was not impaired by C+E ingestion 24 h earlier. In conclusion, performance of the WT was improved by ingestion of C+E.

The metabolic and performance effects of caffeine compared to coffee during endurance exercise.
Hodgson AB, Randell RK, Jeukendrup AE.
PLoS One. 2013;8(4):e59561. doi: 10.1371/journal.pone.0059561. Epub 2013 Apr 3.
PMID: 23573201
Free PMC Article


There is consistent evidence supporting the ergogenic effects of caffeine for endurance based exercise. However, whether caffeine ingested through coffee has the same effects is still subject to debate. The primary aim of the study was to investigate the performance enhancing effects of caffeine and coffee using a time trial performance test, while also investigating the metabolic effects of caffeine and coffee. In a single-blind, crossover, randomised counter-balanced study design, eight trained male cyclists/triathletes (Mean ± SD: Age 41 ± 7 y, Height 1.80 ± 0.04 m, Weight 78.9 ± 4.1 kg, VO2 max 58 ± 3 ml • kg(-1) • min(-1)) completed 30 min of steady-state (SS) cycling at approximately 55% VO2max followed by a 45 min energy based target time trial (TT). One hour prior to exercise each athlete consumed drinks consisting of caffeine (5 mg CAF/kg BW), instant coffee (5 mg CAF/kg BW), instant decaffeinated coffee or placebo. The set workloads produced similar relative exercise intensities during the SS for all drinks, with no observed difference in carbohydrate or fat oxidation. Performance times during the TT were significantly faster (~5.0%) for both caffeine and coffee when compared to placebo and decaf (38.35 ± 1.53, 38.27 ± 1.80, 40.23 ± 1.98, 40.31 ± 1.22 min respectively, p<0.05). The significantly faster performance times were similar for both caffeine and coffee. Average power for caffeine and coffee during the TT was significantly greater when compared to placebo and decaf (294 ± 21 W, 291 ± 22 W, 277 ± 14 W, 276 ± 23 W respectively, p<0.05). No significant differences were observed between placebo and decaf during the TT. The present study illustrates that both caffeine (5 mg/kg/BW) and coffee (5 mg/kg/BW) consumed 1 h prior to exercise can improve endurance exercise performance.

Beneficial effects of dark chocolate on exercise capacity in sedentary subjects: underlying mechanisms. A double blind, randomized, placebo controlled trial.
Taub PR, Ramirez-Sanchez I, Patel M, Higginbotham E, Moreno-Ulloa A, Román-Pintos LM, Phillips P, Perkins G, Ceballos G, Villarreal F.
Food Funct. 2016 Aug 5. [Epub ahead of print]
PMID: 27491778


In heart failure patients the consumption of (-)-epicatechin ((-)-Epi)-rich cocoa can restore skeletal muscle (SkM) mitochondrial structure and decrease biomarkers of oxidative stress. However, nothing is known about its effects on exercise capacity and underlying mechanisms in normal, sedentary subjects. Twenty normal, sedentary subjects (∼50 years old) were randomized to placebo or dark chocolate (DC) groups and consumed 20 g of the products for 3 months. Subjects underwent before and after treatment, bicycle ergometry to assess VO2 max and work, SkM biopsy to assess changes in mitochondrial density, function and oxidative stress and blood sampling to assess metabolic endpoints. Seventeen subjects completed the trial. In the DC group (n = 9), VO2 max increased (17% increase, p = 0.056) as well as maximum work (watts) achieved (p = 0.026) with no changes with placebo (n = 8). The DC group evidenced increases in HDL levels (p = 0.005) and decreased triglycerides (p = 0.07). With DC, SkM evidenced significant increases in protein levels for LKB1, AMPK and PGC1α and in their active forms (phosphorylated AMPK and LKB1) as well as in citrate synthase activity while no changes were observed in mitochondrial density. With DC, significant increases in SkM reduced glutathione levels and decreases in protein carbonylation were observed. Improvements in maximum work achieved and VO2 max may be due to DC activation of upstream control systems and enhancement of SkM mitochondria efficiency. Larger clinical studies are warranted to confirm these observations.

The Hershey® Company  provided  the  products  used  and  financial  support  for  the  study.  Drs.  Ceballos  and Villarreal are stockholders in Cardero Therapeutics Inc.

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The dark chocolate-exercise benefit reported also by the last of the below papers seemed blind to the elephant in the room -- the stimulants caffeine and theobromine.


According to the USDA, the 20g of dark chocolate per day eaten by the subjects in your "last paper below" (PMID: 27491778) contained in the neighborhood of 10mg of caffeine. That is the amount in 1/8th of a cup of coffee, and about 1/30th as much as the subjects received per day (in your first study) or shortly before the exercise test (in your second study). Not only that, but according to the full text, the subjects in PMID 27491778 were prohibited from ingesting any form of caffeine (including chocolate) or alcohol for 18h before the exercise test.


It therefore seems quite unlikely to me that the exercise benefits of the dark chocolate were a result of the direct, stimulatory effects of caffeine, or theobromine, which is a 10x weaker stimulant that caffeine. 


That's not to say the caffeine or theobromine may not have been involved in the cardiovascular benefits observed, but if they were appears to have been through their indirect effects on more fundamental processes involved in energy metabolism. In particular, chocolate consumption appears to have influenced expression of several genes association with mitochondria metabolism (AMPK and PGC1α) and the Kreb's Cycle (citrate synthase). This suggests something pretty fundamental is going on.


In addition to the observed effects on mitochondria, I thought you might have mentioned this other chocolate study you recently posted [1] as another possible explanation. It found frequent chocolate consumption makes arteries more supple (i.e. reduces arterial stiffness), which would be expected to improve cardiovascular performance during exercise. 





[1] Pulse (Basel). 2016 Jul;4(1):28-37. doi: 10.1159/000445876. Epub 2016 May 3.
Relation of Habitual Chocolate Consumption to Arterial Stiffness in a Community-Based Sample: Preliminary Findings.
Crichton GE, Elias MF, Alkerwi A, Stranges S, Abhayaratna WP.
The consumption of chocolate and cocoa has established cardiovascular benefits. Less is known about the effects of chocolate on arterial stiffness, a marker of subclinical cardiovascular disease. The aim of this study was to investigate whether chocolate intakes are independently associated with pulse wave velocity (PWV), after adjustment for cardiovascular, lifestyle and dietary factors.
Prospective analyses were undertaken on 508 community-dwelling participants (mean age 61 years, 60% women) from the Maine-Syracuse Longitudinal Study (MSLS). Habitual chocolate intakes, measured using a food frequency questionnaire, were related to PWV, measured approximately 5 years later.
Chocolate intake was significantly associated with PWV in a non-linear fashion with the highest levels of PWV in those who never or rarely ate chocolate and lowest levels in those who consumed chocolate once a week. This pattern of results remained and was not attenuated after multivariate adjustment for diabetes, cardiovascular risk factors and dietary variables (p = 0.002).
Weekly chocolate intake may be of benefit to arterial stiffness. Further studies are needed to explore the underlying mechanisms that may mediate the observed effects of habitual chocolate consumption on arterial stiffness.
Arterial stiffness; Chocolate; Cocoa; Pulse wave velocity
PMID: 27493901
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