Dark chocolate supplementation reduces the oxygen cost of moderate intensity cycling

Dietary supplementation with sodium nitrate or nitrate rich beetroot juice has become increasingly popular and has consistently been shown to reduce oxygen demands during submaximal exercise and resting blood pressure (BP) [1, 2]. The physiological mechanisms underpinning these enhancements in contractile efficiency have been attributed to the breakdown of nitrate to the substantial elevation of circulating nitrite, which is subsequently converted into the bioactive nitric oxide (NO), that may potentially increase vasodilation, glucose uptake and regulate muscular contraction [3‐7].

Although supplementation with beetroot juice has become popular as an ergogenic aid, it is renowned for its poor palatability and lack of energy provision. Recent studies reported similar vascular improvements in NO levels from consumption of dark chocolate (DC) [8, 9]. This is of great interest given the popularity of DC often associated with food categories of high palatability and indulgence. Dark chocolate mechanistically unique to other dietary nitrate supplements augments NO production through endothelium-dependent influences [10, 11]. The abundant amount of (-)-epicatechin found within DC signals release of vasoactive components from the endothelial cells increasing the bioavailability of NO [12, 13]. The increased bioavailability and activity of NO have been demonstrated to statisitically increase flow-mediated dilation in healthy patients (46 g/day for fifteen days) [14], hypertensive patients (100 g/day for fifteen days) [15], pre-hypertensive patients (30 g/day for fifteen days) [13], and stage 1 hypertension patients (6.3 g/day for eighteen weeks) [16].

To date, the research surrounding DC has predominantly focused on its beneficial influences on cardiovascular health and has received limited focus towards the effects on exercise performance. Berry et al. [17] demonstrated attenuation in exercise-induced blood pressure through consumption of flavanol rich cocoa within overweight participants, demonstrating DC may decrease cardiovascular risk and enhance the cardiovascular benefits of moderate intensity exercise in at-risk individuals. Allgrove et al. [18] reported consumption of DC (40 g) for two weeks was associated with reduced oxidative-stress markers following prolonged exhaustive exercise and increased mobilization of free fatty acids after exercise. Allgrove et al. [18] and Berry et al. [17] also suggested that increased NO levels resulted in lower RER and improvements in moderate intensity.

To date, no studies have addressed the link between the reported increases in NO and nitrate levels resulting from consumption of DC and for its potential to lower oxygen demand during moderate intensity exercise and enhance performance during high-intensity exercise. Therefore, the purpose of this study was to examine whether commercially available DC, will elicit an improvement in gas exchange threshold (GET), lower oxygen consumption during moderate intensity cycling (80 % GET) and improve performance in a time trial in comparison to white chocolate.

To date, this is the first study to investigate the effects of Dark Chocolate (DC) on \( \overset{.}{V}{O}_{2 max} \), GET, oxygen demand during moderate intensity cycling, and a maximal performance time trial. The main finding was that regular consumption of DC daily (40 g) for fourteen days resulted in a significantly higher GET (21 and 11 %) and the total distance covered (17 and 13 %) during a maximal two minute maximal sprint compared to both baseline and WC conditions. Consumption of DC increased \( \overset{.}{V}{O}_{2 max} \) compared to baseline (P = 0.037). However, WC also marginally increased \( \overset{.}{V}{O}_{2 max} \) compared to baseline and this increase reduced the difference between WC and DC resulting in statistical significance not attaining the determined critical threshold (P = 0.071). There were no differences in the moderate intensity cycling in \( \overset{.}{V}{O}_2 \) RER, BLa, and heart rate between conditions. Furthermore there was no difference on systolic BP and diastolic BP between conditions.

While the specific mechanisms underlying this increase in GET and 2-min maximal sprint remains elusive it can be proposed that flavanol a subclass of DC is a particular compound of interest and may be responsible for eliciting the observed effects [3, 5, 19‐21]. Dark Chocolate (DC), unique to other dietary nitrate supplements is hypothesised to mediate NO production through endothelium-dependent effects; related to flavanols’ ability to supress vascular arginase enzyme activity, thus increasing the production of NO [4, 13, 22, 23]. Dark chocolate’s vasodilatative properties can be attributed to the increase in levels of (-)-epicatechin, which are further converted to 0-methylated metabolites that are potent inhibitors of NADPH oxidase. This suppreses oxygen free radical generation which increases the bioavailability of NO [10, 11]. Fisher et al. [24] and Sudarma et al. [13] both reported increased (-)-epicatechin within the blood following DC consumption; however both obtained DC which was manufactured to be precisely rich in flavanols by limiting the degradation, alkylation, and roasting of the cocoa seeds. The present study used Dove DC as Engler et al. [14] reported high associated polyphenol and (-)-epicatechin values; although, it was not stated whether the DC was specifically manufactured or was identical to the commercially available brand, as this may well contribute to a potentially lower flavanol and (-)-epicatechin concentration, thus may have potentially attenuated observed effects within this study. A caveat of the present study was that flavanol and NO were not directly measured thus the causation of the observed effects is speculated around flavanol and NO.

After 14 days consumption of DC, GET significantly increased by 11 % compared to WC and increased by 21 % compared to baseline. Similarly, \( \overset{.}{V}{O}_2 \) during moderate intensity cycling was consistently lower throughout the entire duration of cycling following consumption of DC (Fig. 2) compared to baseline and WC. However, \( \overset{.}{V}{O}_2 \) did not reach the threshold associated with statistical significance. The increases in GET complements findings by previous research using dietary nitrate supplementation which have been attributed to increased NO, which has been extensively shown to increase following regular consumption of DC [1, 2, 6].

Respiratory exchange ratio (RER) did not significantly differ between conditions (Fig. 4). These results conflict with Allgrove et al. [18], which reported lower RER values during exercise at 60 % \( \overset{.}{V}{O}_{2 max} \), also indicating increased fat oxidation. Furthermore, consumption of DC was also reported to increase free fatty acid mobilisation during prolonged cycling following DC consumption, which could be viewed beneficial to those with goals tailored towards weight loss and athletes in need of conserving carbohydrate stores. However, the duration of the tests in this study were probably too short to elicit a decrease in RER. Moreover, DC does contain trace elements of caffeine and theobromine, which can independently increase free fatty acid mobilisation; although, the dose found is relatively small to make a substantial alteration in metabolism [25].

Unlike previously reported studies by Faridi et al. [26] and Sudarma et al. [13] systolic and diastolic BP was not seen to be significantly different between DC and WC. Systolic BP was attenuated by 6 % following the ingestion of DC to a healthier range (124 ± 7 mmHg), and diastolic BP increased by 6 % following ingestion of DC (74 ± 9 mmHg), which was also associated with healthier ranges. However, Faridi et al. [26] and Sudarma et al. [13] the participants in the present study were all healthy and had no irregular BP, possibly hindering the chance of finding a significant difference.

This is the first study that has investigated the effects of DC consumption on GET, oxygen demands during a twenty-minute moderate cycle, \( \overset{.}{V}{O}_{2 max} \) and performance of a two-minute maximal sprint. The primary outcome observed was DC consumption increased the work rate achieved at GET by 11 % compared to WC and 21 % compared to baseline (P < 0.05). Time trial distances following DC consumption were higher compared to baseline and WC (P < 0.05). Maximal oxygen consumption also increased following DC compared to baseline (P < 0.05), but was not significantly different to WC. However, despite oxygen consumption and RER being consistently lower throughout the twenty minutes of moderate intensity cycling, no significant difference was observed. Consequently, it can be concluded that ingestion of DC for 14 days reduced the oxygen cost of moderate intensity exercise and may be an effective ergogenic aid for short-duration moderate intensity exercise. However, future double-blinded studies will need to confirm this effect.