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Lamprecht M, editor. Antioxidants in Sport Nutrition. Boca Raton (FL): CRC Press/Taylor & Francis; 2015.

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Antioxidants in Sport Nutrition.

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Chapter 5Well-Known Antioxidants and Newcomers in Sport Nutrition

Coenzyme Q10, Quercetin, Resveratrol, Pterostilbene, Pycnogenol and Astaxanthin

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Physical exercise induces an increase in production of free radicals and other reactive oxygen species (ROS) (Davies et al. 1982, Borzone et al. 1994, Halliwell and Gutteridge 1999). Current evidence indicates that ROS are the primary reason of exercise-induced disturbances in muscle redox balance. Severe disturbances in redox balance have been shown to promote oxidative injury and muscle fatigue (Reid et al. 1992, O’Neill et al. 1996) and thus impair the exercise performance. There are several potential sources of ROS that can be activated by exercise such as mitochondrial electron transfer chain, in the purine degradation pathway the reaction catalysed by xanthine oxidase, macrophage infiltration and metabolic degradation of catecholamines (Urso and Clarkson 2003, Finaud et al. 2006). The high production of ROS during exercise is also responsible for muscular damage (Aguiló et al. 2007). On the basis of the above-mentioned information, sportsmen have to improve their antioxidant defence systems to overcome the exercise-induced oxidative damage. Over the past few decades, many attempts have been made to improve antioxidant potential and therefore increase physical performance by improving nutrition, training programmes and other related factors.

An antioxidant is generally defined as any substance that significantly delays or prevents oxidative damage of a target molecule (Halliwell 2007). The antioxidant defence system of the body consists of antioxidant enzymes (superoxide dismutases, catalase and glutathione peroxidase, etc.) and non-enzymatic antioxidants (vitamins A, C and E, coenzyme Q10 (CoQ10) and glutathione, etc.) (Deaton and Marlin 2003). There is a cooperative interaction between endogenous antioxidants and dietary antioxidants; therefore, antioxidant supplementation may improve the muscle fibre’s ability to scavenge ROS and protect the exercising muscle against exercise-induced oxidative damage and fatigue. However, antioxidant nutrient deficiency could induce an increased susceptibility to exercise-induced damage and thus leads to impaired exercise performance (Stear et al. 2009). Recently, the problem of whether or not athletes should use antioxidant supplements is an important and highly debated topic. To prevent these hypothetically negative or side effects of physical exercise, supplementation with different types of antioxidants has been used in a great number of studies (Snider et al. 1992, Rokitzki et al. 1994, Reid et al. 1994, Margaritis et al. 1997, Aguiló et al. 2007, Bloomer et al. 2012). In the context of this chapter, information in brief about the well-known and recently used antioxidants such as CoQ10, quercetin, resveratrol, pterostilbene, pycnogenol and astaxanthine is given. The effects of these antioxidants on exercise performance and exercise-induced oxidative stress are also explained.


CoQ10 (2,3 dimethoxy-5 methyl-6-decaprenyl benzoquinone) is a fat-soluble, vitamin like quinone commonly known as ubiquinone, CoQ and vitamin Q10 (Bonakdar and Guarneri 2005). CoQ10 is an essential cofactor in mitochondrial oxidative phosphorylation, and is necessary for ATP production. It acts as a mobile electron carrier, transferring electrons from complex I to complex III or from complex II to complex III (Molyneux et al. 2008). CoQ10 also appears to increase ATP levels by preventing the loss of the adenine nucleotide pool from cardiac cells (Bonakdar and Guarneri 2005). Additionally, CoQ10 has evidenced activity in preventing lipid peroxidation as an antioxidant, and as an indirect stabiliser of calcium channels to decrease calcium overload (Sugiyama et al. 1980). The function of CoQ10 as an electron shuttle in the electron transport chain has been suggested as a rate limiting step in exercise where energy production is of great importance.

It was generally shown that oral CoQ10 supplementation at different doses led to a marked elevation of CoQ10 levels in various tissues such as skeletal muscle, liver, heart and kidney (Kwong et al. 2002, Kon et al. 2007) and in human plasma (Zuliani et al. 1989, Kaikkonen et al. 1998, Bonetti et al. 2000, Zhou et al. 2005, Kon et al. 2008, Mizuno et al. 2008, Bloomer et al. 2012). Supplementation with CoQ10 could therefore, hypothetically, ‘normalise’ or even enhance physical performance by increasing the CoQ10 content in the mitochondria and would potentially enhance the oxidative phosphorylation process (Zhou et al. 2005). Parallel to this, it has been speculated that increased ROS production during physical exercise could decrease the CoQ10 level in muscle tissue and negatively affect physical performance, at least in subjects undertaking strenuous physical training (Karlsson et al. 1996). A positive relationship between exercise capacity and the concentration of CoQ10 in the vastus lateralis muscle was reported in physically active males (Karlsson et al. 1996). Different investigators have consequently tested several related hypotheses regarding CoQ10 and physical performance and oxidative stress and these studies are summarised in Table 5.1.



Summary of Published Articles about the Effects of CoQ10 on Exercise Performance and Exercise-Induced Oxidative Stress in Humans

5.2.1. Effects on Performance

The studies which investigated the potential ergogenic value of CoQ10 have reported mixed results. These studies are categorised according to the type of exercise such as aerobic, anaerobic and muscle injury induced exercises. Although CoQ10 is being suggested to improve exercise capacity, this effect is not supported by empirical data. The previous studies investigating the effects of CoQ10 supplementation on physical performance in humans have found negative effects (Malm et al. 1997), no effect (Braun et al. 1991, Snider et al. 1992, Porter et al. 1995, Weston et al. 1997, Kaikkonen et al. 1998, Nielsen et al. 1999, Svensson et al. 1999, Zhou et al. 2005), positive effects (Cooke et al. 2008, Mizuno et al. 2008, Gökbel et al. 2010), decreased exercise-induced muscular injury in athletes (Kon et al. 2008, Tauler et al. 2008) and positive effects on aerobic and anaerobic threshold and maximal oxygen consumption (VO2max) in cross-country skiers (Ylikoski et al. 1997).

Contradictory results have been found regarding the effects of CoQ10 supplementation on aerobic performance (Laaksonen et al. 1995, Ylikoski et al. 1997, Zhou et al. 2005, Cooke et al. 2008, Bloomer et al. 2012). In placebo-controlled studies, it was shown that CoQ10 supplementation alone (Braun et al. 1991, Weston et al. 1997) or combined with vitamins C and E (Snider et al. 1992, Nielsen et al. 1999) had no significant effect on respiratory capacity and performed work or muscle metabolism. In untrained subjects, Porter et al. (1995) did not find any changes in VO2max, lactate threshold, heart rate and maximal workload during a cycle ergometer test after supplementation with CoQ10 for 2 months. Bonetti et al. (2000) observed that CoQ10 supplementation (100 mg·day–1 for 8 weeks) did not affect aerobic power. Similarly, Zhou et al. (2005) demonstrated that CoQ10 supplementation (150 mg·day–1 for 4 weeks) did not affect maximal oxygen consumption and ventilatory threshold in healthy sedentary males. In a study by Bloomer et al. (2012), no change in aerobic exercise performance was observed following 4 weeks of CoQ10 supplementation (300 mg·day–1) in physically active subjects. Laaksonen et al. (1995) found that CoQ10 supplementation (120 mg·day–1 for 6 weeks) did not affect aerobic performance in trained subjects. In a recent study, Ostman et al. (2012) observed no clear effect on physical capacity, including VO2max, heart rate and lactate threshold after 8 weeks of CoQ10 administration in moderately trained subjects. In contrast to these results, Ylikoski et al. (1997) demonstrated that CoQ10 supplementation (90 mg·day–1 for 12 weeks) caused an increase in VO2max in cross-country skiers.

Cooke et al. (2008) showed that both acute (200 mg-60 min before exercise test) and chronic (200 mg·day–1 for 14 days) CoQ10 supplementation did not affect time to exhaustion during the aerobic exercise. In contrast, Mortensen (2005) demonstrated that CoQ10 supplementation increased the 6-min walk distance from 269 m to 382 m in patients with chronic heart failure, and they suggested that CoQ10 supplementation increased performance improving the time to exhaustion. Mizuno et al. (2008) found that although 300 mg CoQ10 for 1 week improved physical performance during fatigue-inducing workload trials on a bicycle ergometer, 100 mg of CoQ10 did not affect exercise performance. According to the systemic review of Rosenfeldt et al. (2003), it appears that a modest improvement in the exercise capacity may be observed with CoQ10 supplementation, but this is not a consistent finding.

Studies investigating the effects of CoQ10 supplementation on anaerobic exercise performance (Malm et al. 1997, Cooke et al. 2008, Gökbel et al. 2010, Bloomer et al. 2012) are limited. Malm et al. (1997) demonstrated that 120 mg·day–1 for 22 days CoQ10 supplementation had no significant effect on four anaerobic cycling test performances. Similarly, Cooke et al. (2008) showed that CoQ10 supplementation of 200 mg·day–1 for 14 days caused no significant change on anaerobic power measured by peak power, mean power and fatigue index compared with placebo. In a study by Bloomer et al. (2012) no change in anaerobic exercise performance was observed following 4 weeks of CoQ10 supplementation. In a recent study (Gökbel et al. 2010), we demonstrated that CoQ10 supplementation 100 mg·day–1 for 8 weeks improved the mean power during repeated bouts of the supramaximal exercises. These results were attributed to the contribution of aerobic metabolism and key role of CoQ10 in energy metabolism during the repeated bouts of supramaximal exercises.

Effects of CoQ10 supplementation on exercise-induced muscle injury were investigated in both humans and animals (Shimamura et al. 1991, Kon et al. 2007, Kon et al. 2008). Shimamura et al. (1991) and Kon et al. (2007) reported that intravenous and oral CoQ10 supplementation, respectively, attenuates the rise in markers of muscle damage in rats following downhill running. In addition, Okamoto et al. (1995) provided evidence that CoQ10 protects cultured skeletal muscle cells from electrical stimulation-induced lactate dehydrogenase release. In human subjects, Kon et al. (2008) showed that CoQ10 supplementation prevents exercise-induced increase in creatine kinase (CK) activity and myoglobin levels in kendo athletes after muscle damaging exercise. In contrast, Kaikkonen et al. (1998) claimed that CoQ10 supplementation did not affect CK activity following a marathon run. From these results, it has been stated that CoQ10 supplementation may have the potential to reduce exercise-induced muscular cell damage.

5.2.2. Effects on Exercise-Induced Oxidative Stress

The antioxidant activity of CoQ10 appears only with the reduced form (ubiquinol). The oxidised form (ubiquinone) is readily reduced to ubiquinol enzymatically after dietary uptake (Mohr et al. 1992). CoQ10 inhibits the expression of free radicals from different sources (Sohet et al. 2009, Tsuneki et al. 2007), and therefore it can improve the antioxidant system in the body.

CoQ10 supplementation has been reported to attenuate biomarkers of oxidative stress when measured at rest (Niklowitz et al. 2007, Weber et al. 1994). Weber and his colleagues (1994) reported a decrease in lipid peroxidation in healthy subjects after 2 weeks of CoQ10 treatment (90 mg·day–1).

The effect of CoQ10 supplementation on exercise-induced oxidative stress has been investigated in humans, but the existing data are inconsistent (Braun et al. 1991, Cooke et al. 2008, Gül et al. 2011, Bloomer et al. 2012, Díaz-Castro et al. 2012, Ostman et al. 2012). Laaksonen et al. (1995) found that neither the CoQ10 supplementation nor the exercise affected serum malondialdehyde (MDA) concentration in endurance-trained athletes. Similarly, Cooke et al. (2008) showed that acute CoQ10 supplementation did not affect serum MDA levels and SOD activities during and following exercise. In a study by Bloomer et al. (2012), it has been indicated that, in physically active men and women, 30 days of CoQ10 supplementation (300 mg·day–1) did not affect resting or exercise-induced measures of oxidative stress. In a study by Ostman et al. (2012), it has been demonstrated that supplementation of 90 mg·day–1 CoQ10 for 8 weeks in moderately trained men did not affect oxidative stress indices. In contrast, in a study by Gül et al. (2011), we showed that supplementation of 100 mg·day–1 CoQ10 for 8 weeks decreased oxidative stress indices immediately after the repeated bouts of supramaximal exercises in sedentary men. In a recent study (Díaz-Castro et al. 2012), it has been reported that CoQ10 supplementation during high-intensity exercise is efficient in reducing the degree of oxidative stress (decrease membrane hydroperoxides, 8-hydroxy-2´-deoxyguanosine (8-OHdG) and isoprostanes), which would lead to the maintenance of cell integrity. Also in the same study, CoQ10 administration modulated inflammatory signalling associated with exercise by preventing over-expression of tumour necrosis factor (TNF)-α after the exercise.

The effect of CoQ10 administration on exercise-induced oxidative stress has been also investigated in rats, but the existing data are also inconsistent (Faff and Frankiewicz-Jóźko, 1997, Kon et al. 2007, Okudan et al. 2012). Faff and Frankiewicz-Jóźko (1997) demonstrated that 4 weeks of oral CoQ10 supplementation in a daily dose of 10 mg·kg–1 body mass markedly suppresses exercise-induced lipid peroxidation in the liver, heart and gastrocnemius muscle. In a recent study (Okudan et al. 2012), we showed that 6 weeks of intraperitoneal CoQ10 injection in a daily dose of 10 mg·kg–1 body mass and exercise training significantly inhibits exhaustive exercise-induced lipid peroxidation and DNA damage, but did not affect glutathione levels and SOD activity in the heart tissue of rats. As a result of the study, we concluded that CoQ10 supplementation and exercise training have interactive effects on lipid peroxidation and DNA damage. In contrast, Kon et al. (2007) reported that 4 weeks of oral CoQ10 supplementation in a daily dose of 300 mg·kg–1 body mass ameliorates exercise-induced oxidative damage in skeletal muscle, but not in the liver after the muscle damaging exercise.

CoQ10 is a relatively large hydrophobic molecule (Kaikkonen et al. 2002). Therefore, absorption of CoQ10 into tissues is often slow and limited. Additionally, ingestion of CoQ10 at fast-melt or in capsule form could affect its plasma availability. It has been suggested that ‘fast-melt’ CoQ10 formulations enhanced the absorption kinetics into the bloodstream (Joshi et al. 2003) and the increased bioavailability may enhance greater uptake into the muscle. The difference among the results in both human and animal studies is most likely dependent on the type, dosage and time frame of treatment of the antioxidant(s), the tissue sampled, the exercise protocol used to induce oxidative stress, the time of measurement, the assays used and the test subjects recruited (i.e. trained versus untrained, old versus young and healthy versus diseased), among other variables (Bloomer 2008).


Quercetin (3,4,5,7-pentahydroxylflavone) is a natural bioactive flavonoid found in a wide variety of natural foods, such as nuts, grapes, apples, berries, onions, broccoli and black tea (Boots et al. 2008, Kelly 2011). In vitro and animal studies indicate that quercetin has many biological effects such as antioxidant, antiinflammatory, anticarcinogenic, antiviral, psychostimulant, cardioprotective, neuroprotective, antipathogenic, immune regulatory and increasing mitochondrial biogenesis (Davis et al. 2009a). Antioxidant properties of quercetin are attributed to its chemical structure, particularly the presence and location of the hydroxyl (-OH) substitutions.

The beneficial effects of quercetin largely depend on its bioavailability after oral administration. Although initial reports indicated that bioavailability of quercetin was limited, recent evidence suggests that quercetin can be detected in plasma within 15–30 min of ingestion of a 250 or 500 mg quercetin chew preparation, reaching a peak concentration at approximately 120–180 min, returning to baseline levels at 24 h in humans (Boots et al. 2008, Davis et al. 2009a). Quercetin also has been shown to reach and accumulate in various tissues such as the colon, kidney, liver, lung, muscle and brain, though the tissue distribution has not yet been studied in humans (de Boer et al. 2005, Harwood et al. 2007).

Quercetin supplementation studies in athletes have focused on the potential effects of exercise-induced inflammation, oxidative stress, immune dysfunction and exercise performance (Nieman et al. 2012). The available evidence for a beneficial effect of quercetin on exercise performance, while encouraging, is limited by the lack of sophisticated clinical trials. The first human exercise study investigating quercetin supplementation was published in 2006 (MacRae and Mefferd 2006), with many more published in the past few years and continuing to be published. When athletes are studied, most of the researches have failed to find an ergogenic effect (Quindry et al. 2008, Utter et al. 2009), in contrast to that of a study of elite cyclists, who exhibited an improvement of their aerobic performance (MacRae and Mefferd 2006). MacRae and Mefferd (2006) indicated that administration of quercetin (1200 mg) for 6 weeks resulted in performance improvement in cyclists. Davis et al. (2010) examined the effects of 7 days of quercetin (1000 mg) supplementation on both VO2max and time to fatigue on a bicycle ergometer in healthy untrained men and women. Increases in both VO2max (3.9%) and time to fatigue (13.2%) were found.

In a recently published meta-analysis (Pelletier et al. 2013), it has been demonstrated that quercetin supplementation improves endurance performance by 0.74 ± 1.04% compared with placebo. However, no relationship was found between quercetin duration and percentage changes in endurance performance between groups. In this meta-analysis, it was demonstrated that quercetin confers an increase in performance which is much less than this efficacy threshold, thereby indicating that it is unlikely to confer any ergogenic value, at least within the length of supplementation used and quercetin doses provided by the actual studies. The authors concluded that quercetin is unlikely to improve performance, independent of the training state. Athletes may hope to benefit from use of a sport nutrition supplement during out of doors, real-world exercise conditions, if it produces an effect under laboratory-controlled exercise conditions that is 1.3–1.6% (Hopkins et al. 1999, Hopkins and Hewson 2001) greater than the effect of the placebo.

In a study by Dumke et al. (2009), no effect of quercetin supplementation (1000 mg·day–1) was observed on cycling time trial performance in elite cyclists. Quindry et al. (2008) reported that quercetin supplementation (1000 mg·day–1 for 3 weeks) had no effect on race performance at the Western States 100-mile race. A single, very high dose of quercetin (2 g) was also shown not to increase exercise performance in moderately fit military personnel during exercise in the heat (Cheuvront et al. 2009). Supplementation with quercetin and vitamin C for 8 weeks did not improve exercise performance but reduced muscle damage and body fat percent in athletes (Askari et al. 2012). Sharp et al. (2012) demonstrated that supplementation with quercetin (1000 mg·day–1 for 9 days) did not improve aerobic capacity, aerobic performance, steady state load carriage exercise and change the metabolic or perceptual responses to exercise. In a recent study, Casuso et al. (2013) suggested that quercetin supplementation showed no effect on VO2peak, speed at VO2peak or endurance time to exhaustion after 6 weeks of quercetin supplementation.

Some studies (MacRae and Mefferd 2006, Davis et al. 2010, Nieman et al. 2010) reported an improvement in exercise performance in humans after ingestion of quercetin, whereas most others failed to find statistically significant benefits in exercise capacity (Cureton et al. 2009, Utter et al. 2009, Bigelman et al. 2010, Ganio et al. 2010, Sharp et al. 2012, Askari et al. 2013).

The most important novel effect of quercetin related to a possible benefit on endurance performance comes from two recent in vitro and rodent studies (Rasbach and Schnellmann 2008, Davis et al. 2009b) that show a benefit on mitochondrial function. Davis et al. (2009b) found that quercetin feedings (12.5 and 25 mg·kg–1day–1) for 7 days improve running time to fatigue by stimulation of mitochondrial biogenesis, including peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and sirtuin 1 (SIRT1) gene expression, mitochondrial DNA (mtDNA) and cytochrome c enzyme concentration in both the brain and soleus muscle of rats. However, this effect has not yet been observed in humans. A study investigating markers of mitochondrial biogenesis in humans after quercetin administration (1000 mg·day–1 for 2 weeks) observed trends towards increased markers of mitochondrial biogenesis such as cytochrome c oxidase and muscle mtDNA but failed to reach statistical significance (Nieman et al. 2010).

Possible reasons for the inconsistent findings among these studies may include the range of subject fitness levels, differences in plasma quercetin concentration obtained via the various supplementation protocol/supplement types and differences in research design.

In accordance with anti-inflammatory properties, it has been shown that quercetin modulates intracellular signalling pathways, including the inflammatory signalling cascade, by inhibiting activation proinflammatory transcription factor and nuclear factor-kappa B (NF-κB) (Harwood et al. 2007). Strenuous exercise is capable of damaging muscle and initiating an inflammatory response. Nieman et al. (2007a,b,c) examined the effect of quercetin upon inflammation after three consecutive days of cycling and following an ultralong endurance run. Except for an attenuation of interleukin (IL)-8 and IL-10 mRNA in blood leukocytes following the cycling bouts, quercetin failed to attenuate any of the measured markers of muscle damage, inflammation, increases in plasma cytokines and alterations in muscle cytokine mRNA expression. Recently, Overman et al. (2011) reported that quercetin decreased expression of inflammatory cytokine TNF-α, interferon-γ, IL-6 and IL-1β transcripts in cultured human macrophages, which are known to be contributors to secondary muscle damage. O’Fallon et al. (2012), McAnulty et al. (2008) and Abbey and Rankin (2011) demonstrated no effect of quercetin supplementation on the markers of muscle damage and no effect of quercetin or eccentric exercise on biological markers of systemic inflammation (IL-6 and C-reactive protein) in untrained and trained individuals. Konrad et al. (2011) reported that ingestion of a quercetin-based supplement (1000 mg) 15 min before the 2 hours of treadmill run did not attenuate exercise-induced inflammation or immune changes or improve performance. In a study, quercetin feedings reduced self-reported symptoms of upper respiratory tract infection (URTI) following 3 days of exhaustive exercise (Nieman et al. 2007c). In this study, highly trained cyclists ingesting 1000 mg·day–1 of quercetin during a 3-week period experienced a significantly lower incidence of URTI during the 2-week period following the 3 days of intensified training. However, there was no beneficial effect of quercetin on any of the immune components measured, including natural killer (NK) cell lytic activity, polymorphonuclear respiratory burst or phytohaemagglutinin-stimulated lymphocyte proliferation, despite the reduced incidence of URTI symptoms that were observed after quercetin feedings. However, in a similar study, Henson et al. (2008) reported no benefit on illness rates following the Western States Endurance Run. Davis et al. (2008) reported that quercetin supplementation (12.5 mg·kg–1·day–1) for 7 days reduces susceptibility to influenza infection following stressful exercise in rats. No effects of quercetin were found on leukocyte subset counts, granulocyte respiratory burst activity and salivary immunoglobulin A following quercetin supplementation for 3 weeks before and 2 weeks after the Western States Endurance Run (Henson et al. 2008).

Another interesting property of quercetin which may enhance mental and physical performance is its caffeine-like psychostimulant effect. Psychostimulants, like caffeine, can delay fatigue during endurance exercise, because of their ability to block adenosine receptors in the brain, which results in an increase in dopamine activity (Davis et al. 2003). A psychostimulant effect of quercetin has also been reported in vitro (Alexander 2006) in a manner similar to that of caffeine (Ferré 2008), but this effect was not found in human subjects (Cheuvront et al. 2009).


Resveratrol (3,5,4´-trihydroxystilbene) is a natural polyphenolic flavonoid (Baur and Sinclair 2006). It is freely available in food supplements and is found in the seeds and skins of grapes, red wine, mulberries, peanuts and rhubarb (Baur and Sinclair 2006, Nieman et al. 2012). Many in vivo and in vitro studies (Brisdelli et al. 2009, Ventura-Clapier 2012) have provided evidence for neuroprotective, antiatherogenic, antithrombotic, antihypercholesterolemic, antiinflammatory, antioxidant, proangiogenic, vasorelaxing and anticancer effects of resveratrol. Interestingly, it has also been shown that resveratrol increases skeletal muscle mitochondrial biogenesis and fatty acid oxidation in many tissues as well as exercise performance in mice (Dolinsky et al. 2012).

Pharmacokinetic studies indicate that resveratrol has a poor bioavailability. Resveratrol, even at the high dosage of 750 mg (kg·body weight–1) per day for 13 weeks by the oral route, has been shown to have no adverse effects (Edwards et al. 2011). Pharmacological studies also suggest that therapeutic doses of resveratrol are non-toxic, easily absorbed and well tolerated by humans. A dose of 150 mg·kg–1·day–1 has been used in the study of Dolinsky et al. (2012), while other studies have shown that lower doses of 20 mg.kg–1.day–1 proved to be efficient in preventing cardiac dysfunction (Rimbaud et al. 2011) and pulmonary hypertension (Csiszar et al. 2009) and also in vasoprotection (Ungvari et al. 2007).

Interest in resveratrol in sport medicine arose after animal studies assessed endurance performance of mice and found a dose-dependent increase in exercise tolerance, improved motor skills and increased number and activity of mitochondria in muscle cells. Both exercise and resveratrol are thought to trigger biochemical cascades, leading to improved mitochondrial function and energy metabolism. Indeed, it has been shown that resveratrol enhances mitochondrial biogenesis and induces adenosine 5´ monophosphate-activated protein kinase (AMPK) in the skeletal muscle of mice (Baur and Sinclair 2006, Lagouge et al. 2006). However, when SIRT1 was knocked out, these effects were absent (Price et al. 2012). Resveratrol as a food supplement in sport medicine has not received much attention especially in human studies, despite some basic scientific evidence that this substance could have multiple indications related to high-performance sport (Nieman et al. 2012).

Resveratrol has been also touted as an exercise mimetic effect through its activation of SIRT1 and AMPK (Hart et al. 2013). To support this hypothesis, it has been demonstrated that resveratrol supplementation increases the exercise performance in aged mice (Murase et al. 2009) and mice fed by a Western diet (Lagouge et al. 2006) in the absence of exercise training, suggesting that resveratrol can stimulate pathways similar to exercise. Ryan et al. (2010) demonstrated that 10 days of resveratrol supplementation also diminishes the basal levels of oxidative stress associated with ageing. Functional measurements of maximal isometric force and rate of fatigue were unaffected by resveratrol supplementation in aged animals. Mice treated with resveratrol demonstrated elevations in AMPK activation and PGC-1α expression, along with increases in mitochondria in animals fed by a high fat diet (Baur and Sinclair 2006). Additionally, enhanced SIRT1 activity like exercise training decreases plasma glucose levels, improves insulin sensitivity, increases mitochondrial number and function, decreases adiposity, improves exercise tolerance and potentially lowers body weight (Elliott and Jirousek 2008). The induction of PGC-1α and activation of AMPK are commonly observed following both exercise and resveratrol administration (Ruderman and Prentki 2004, Baur and Sinclair 2006, Lagouge et al. 2006, Zang et al. 2006).

Menzies et al. (2013) demonstrated that SIRT1 protein is responsible for the partial maintenance of basal mitochondrial content and function, in addition to lowering mitochondrial ROS generation and improving fatigue in skeletal muscle. They also showed that resveratrol can activate both AMPK and p38 in temporally distinct stages, which could promote post-translational changes in PGC-1α, thereby altering its activity (Jäger and Nguyen-Duong 1999). These studies (Jäger and Nguyen-Duong 2007, Menzies et al. 2013) also demonstrated that high doses of resveratrol were necessary for AMPK-mediated activation of SIRT1. The resveratrol-induced improvement in energy metabolism is at least partly mediated by specific signal transduction pathways and resveratrol seems mediated by enhanced mitochondrial biogenesis with the activation of the AMPK-SIRT1-PGC-1α pathway (Ventura-Clapier 2012).

Resveratrol administration seems to induce a higher aerobic capacity in mice, as shown by the increased running time and oxygen consumption in muscle fibres (Menzies et al. 2013). Similarly, Hart et al. (2013) suggested that resveratrol supplementation enhanced the effects of exercise on endurance capacity, and this was shown in rats which already had a high level of aerobic endurance. These findings suggest that resveratrol could be used as a performance enhancer (Baur and Sinclair 2006, Lagouge et al. 2006). Dolinsky et al. (2012) demonstrated that a combination of resveratrol and exercise training increased time to exhaustion compared to exercise training. The authors suggested that resveratrol optimises fatty acid metabolism, which may contribute to the increased contractile force response of skeletal muscles.


Pterostilbene (trans-3,5-dimethoxy-4-hydroxystilbene) is a stilbenoid chemically similar to resveratrol and is found in grapes, wine and berries (Rimando et al. 2004). Pterostilbene is generated by plants in response to microbial infestation or exposure to ultraviolet light (Langcake 1981). Pterostilbene is closely related structurally to resveratrol (a naturally occurring dimethylether analogue of resveratrol) and shows many of the same characteristics, as well as its own unique therapeutic potential (Rimando et al. 2002).

Pterostilbene might show higher biological activity compared with resveratrol, because substitution of a hydroxy with a metoxy group increases the transport into cells and increases the metabolic stability of the molecule. Therefore, pterostilbene is not as quickly glucuronidated and sulphated as resveratrol.

Pterostilbene is known to have many pharmacological benefits for the prevention and treatment of a wide variety of diseases, including cancer (McCormack and McFadden 2012), dyslipidaemia (Rimando et al. 2005), diabetes (Amarnath Satheesh and Pari 2006), cardiovascular degeneration (Amarnath Satheesh and Pari 2008) and pain (Hougee et al. 2005). Antioxidant and antiinflamatory effects of pterostilbene are also demonstrated (Roupe et al. 2006, Perečko et al. 2010, Hsu et al. 2013). Pterostilbene possesses strong, dose-dependent antioxidant effects (Rimando et al. 2002, Amorati et al. 2004). The antioxidant activity of pterostilbene was first demonstrated in vitro by its inhibition of methyl linoleate oxidation (Roupe et al. 2006). It inhibits the production of hydroxyl radicals (Perečko et al. 2010). In terms of the antiinflamatory effect of pterostilbene, Hsu et al. (2013) demonstrated that pterostilbene downregulates inflammatory TNF-α, IL-6, cyclooxygenase-2, inducible nitric oxide synthase, IL-1β, monocyte chemotactic protein-1, C-reactive protein and plasminogen activator inhibitor-1 expression by inhibiting the activation of NF-κB.

According to our knowledge, to date no study has investigated the effects of pterostilbene supplementation on exercise performance, exercise-induced oxidative stress and inflammatory response in both sedentary and trained individuals. On the basis of the current studies, pterostilbene may improve athletic performance by activating and supporting both antioxidant and antiinflamatory cascades in untrained and trained subjects. However, detailed animal and human studies are needed in this subject.


Pycnogenol (also referred to as picnogel or pycnogel) is the registered trade name for a natural extract from the bark of a French maritime pine (Pinus Pinaster). It is a standardised extract composed of a mixture of flavonoids, mainly phenolic acids, catechin, taxifolin and procyanidins, and each component exerting a unique biological effect (Packer et al. 1999). Recommended doses of pycnogenol range widely and depend on the treatment aim. For example, to combat chronic venous insufficiency, recommended doses range from 150 to 360 mg·day–1, whereas others have recommended approximately 75–90 mg·day–1 to prevent oxidative tissue damage. In a majority of clinical trials, the duration of supplementation is generally 2–3 months. Side effects of pycnogenol supplementation are minimal (Gleeson et al. 2012). Studies indicate that pycnogenol components are highly bioavailable. Interestingly, pycnogenol displays greater biologic effects as a mixture than its purified components do individually, indicating that the components interact synergistically (Packer et al. 1999).

Pycnogenol supplementation has been reported to have a wide range of health benefits, including improved cognitive function, endothelial function, blood pressure regulation and venous insufficiency (Maimoona et al. 2011, Gleeson et al. 2012). Pycnogenol also acts as an antiinflammatory and antioxidant agent (Packer et al. 1999, Devaraj et al. 2002, Williamson and Manach 2005). The antioxidant effect of pycnogenol is attributed to the high procyanadin content (Grimm et al. 2004). Pycnogenol has also been reported to have cardiovascular benefits, such as a vasorelaxant activity, angiotensin-converting enzyme inhibiting activity and the ability to enhance the microcirculation by increasing capillary permeability (Packer et al. 1999).

There are a limited number of studies in the current literature about the effects of pycnogenol on exercise performance, exercise-induced oxidative stress and inflammatory response. In a previous study (Pavlovic 1999), examining the effect of pycnogenol on endurance performance demonstrated a significant increase in endurance performance in recreationally trained athletes. Mach et al. (2010) demonstrated that pycnogenol-rich antioxidant cocktail improves time to fatigue by increasing the serum NAD+ levels. In a recent study, Bentley et al. (2012) showed that an acute single dose of pycnogenol supplement is able to improve endurance performance in trained athletes. Additionally, Vinciguerra et al. (2006) demonstrated that pycnogenol ingestion reduces the number of events in subjects with cramps and muscular pain without causing negative effects. However, additional experiments are required to confirm these results, to examine the optimal timing and dose amount of this supplement, as well as to establish the physiological mechanisms that explain the increased time to exhaustion during intense endurance exercise.


Astaxanthin (3,3´-dihydroxy-β,β´-carotene-4,4´-dione) is a natural compound (one of the xantophyll carotenoids) found in algae, fish and birds (Aoi et al. 2008). Astaxanthin has been shown to be one of the most effective antioxidants against lipid peroxidation and oxidative stress in in vivo and in vitro systems (Chan et al. 2009, Tripathi and Jena 2009, Choi et al. 2011). It has potential health-promoting effects in the prevention and treatment of various diseases such as cancer, chronic inflammatory diseases, diabetes, cardiovascular and neurodegenerative diseases (Yuan et al. 2011). Astaxanthin also has immunomodulating, antiinflammatory actions (Park et al. 2010) and stimulates fat oxidation (Aoi et al. 2008, Res et al. 2013). In vitro studies (Kurashige et al. 1990) have demonstrated that astaxanthin is a several fold more active free radical scavenger than β-carotene and α-tocopherol.

In mammals, astaxanthin accumulates in muscle, liver and kidney tissues after oral administration and dietary astaxanthin attenuates muscle damage and inhibits peroxidation of DNA and lipids due to prolonged exercise (Aoi et al. 2003). Prolonged astaxanthin supplementation has been reported to improve both swimming and running time to exhaustion in mice (Aoi et al. 2003, Ikeuchi et al. 2006). Keisuke et al. (2002) observed that 4 weeks of astaxanthin supplementation showed performance enhancing effects by reducing the lactic acid build-up following 1200 m of running. Earnest et al. (2011) reported a significant 5% improvement in 20 km time trial performance following 4 weeks of astaxanthin supplementation (4 mg·day–1) in seven trained cyclists. In contrast to these reports, Res et al. (2013) demonstrated that astaxanthin supplementation did not improve exercise performance in endurance trained cyclists.

One possible explanation of the performance enhancing effect of astaxanthin is to increase the fat oxidation. In several studies (Ikeuchi et al. 2006, Aoi et al. 2008) using a mouse model, 4–5 weeks of astaxanthin supplementation (6–30 mg·kg body weight–1) has been reported to improve fat utilisation during exercise and subsequently increase swimming and treadmill running time to exhaustion. The observed increase in fat oxidation was attributed to a greater capacity for fatty acyl-CoA uptake into the mitochondria via an improvement in carnitine palmityol transferase 1 (CPT1) function. CPT1 is located on the mitochondrial membrane and is regarded as the rate limiting enzyme of fatty acid metabolism (McGarry and Brown 1997). Astaxanthin supplementation may improve CPT1 function by inhibiting the accumulation of damaging ROS on the mitochondrial membrane (Naguib 2000, Mortensen et al. 2001). Astaxanthin also inhibited the elevation of plasma lactate and reduced muscle glycogen catabolism during exercise, which supports the lipolytic effect of astaxanthin (Aoi et al. 2008). In a recent study, Res et al. (2013) demonstrated that 4 weeks of astaxanthin supplementation (20 mg·d–1) increases plasma astaxanthin levels, but this did not augment fat oxidation rates at rest and/or during submaximal exercise.

In accordance with antioxidant activity, 12 weeks of astaxanthin supplementation has been demonstrated to improve total antioxidant capacity and decrease MDA levels in sedentary, obese subjects (Choi et al. 2011) and lower levels of lipid peroxidation in healthy untrained males (Karppi et al. 2007). In a recent study, Res et al. (2013) observed the apparent absence of any antioxidant properties of astaxanthin in endurance trained athletes and they attributed this situation to the duration of the supplementation period. In a recent study, Baralic et al. (2013) demonstrated that astaxanthin supplementation had a beneficial effect on paraoxonase activity towards paraoxon and diazoxon, as well as total sulphydryl content in young soccer players. They suggest that astaxanthin might be of special interest for the athletes who are more susceptible to oxidative stress, providing additional support for enzymatic and non-enzymatic endogenous antioxidant defence systems in order to attenuate increases in ROS production. In a recent study, Park et al. (2010) demonstrated that dietary astaxanthin decreased biomarkers of oxidative DNA damage (8-OHdG) in young healthy females.

Studies (Jyonouchi et al. 1994, Chew et al. 1999, Bennedsen et al. 1999, Park et al. 2010) investigating the immunomodulatory effects of astaxanthin have demonstrated that astaxanthin stimulates immune response in both animals and humans. Dietary astaxanthin enhanced both cell-mediated and humoral immune responses in young healthy females (Park et al. 2010). The immune markers significantly enhanced after astaxanthin supplementation such as T-cell and B-cell mitogen-induced lymphocyte proliferation, NK cell cytotoxic activity, INF-γ and IL-6 production and leukocyte function antigen-1 expression (Park et al. 2010). Astaxanthin increased cytotoxic T-lymphocyte activity in mice (Jyonouchi et al. 2000) and inhibited stress-induced suppression of NK cell activity (Kurihara et al. 2002).

There are contradictory findings about the effects of astaxanthin on exercise-induced damage. Aoi et al. (2003) suggested that astaxanthin can attenuate aerobic exercise-induced damage in mouse skeletal and heart muscle, including the associated neutrophil infiltration that may potentiate further injury. However, Bloomer et al. (2005) demonstrated no benefit for astaxanthin on eccentric exercise-induced muscle damage. Interestingly, astaxanthin is currently being used by some athletes as a natural sun blocking agent. It has been reported that astaxanthin supplementation protects against UVA-skin damage by providing a photo-protective effect of the dermal layer (Camera et al. 2009, Suganuma et al. 2010, Hama et al. 2012).


In conclusion, antioxidant supplements are widely used in many sport fields, even though some of them are probably ineffective. There is insufficient evidence to recommend antioxidant supplements for exercising individuals who consume the recommended amounts of dietary antioxidants through food because of the contradictory findings. During the antioxidant supplementation, exercising individuals consider that not only type, but also dosage and duration of the supplement is important for effective prevention. However, further studies are needed to clarify the interactive effects of exercise training and antioxidant supplementation.


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