Fat and carbohydrate are the two primary fuels for endurance-type exercise. However, the capacity for endurance-type exercise performance is generally limited by the availability of skeletal muscle glycogen (6). As such, much research in the area of sports nutrition has been directed toward improving fat oxidative capacity by dietary modulation to stimulate fat use during exercise (13,19,32).
Astaxanthin has been identified as a nutritional compound that may strongly stimulate fat oxidation during exercise (4,17,33). Astaxanthin is a naturally occurring lipid-soluble carotenoid, synthesized primarily by marine microalgae, with powerful antioxidant (24,25) and anti-inflammatory (2,26) properties. Astaxanthin is most known as a feed additive for farm-raised salmon, giving salmon its reddish tissue color. Using a mouse model, 4–5 wk of astaxanthin supplementation (6–30 mg·kg−1 body weight) has been reported to improve fat use during exercise and subsequently increase swimming and treadmill running time to exhaustion (4,16). The observed increase in fat oxidation was suggested to be attributed to a greater capacity for fatty acyl–CoA uptake into the mitochondria via an improvement in carnitine palmitoyltransferase 1 (CPT1) function. Astaxanthin supplementation may improve CPT1 function by inhibiting the accumulation of damaging reactive oxygen species (ROS) on the mitochondrial membrane (24,25). In line with this observation, astaxanthin supplementation has been shown to attenuate the exercise-induced rise in plasma lactate and reduce muscle glycogen use (4). Taken together, these results suggest that astaxanthin may have strong ergogenic properties. Research on the proposed properties of astaxanthin supplementation to modulate skeletal muscle fuel use and/or to improve performance in vivo in humans is scarce (11).
Recently, Earnest et al. (11) observed no significant changes in the rate of fat oxidation during submaximal cycling exercise after 4 wk of astaxanthin supplementation (4 mg·d−1). However, astaxanthin was supplemented in a much smaller relative dose than what had previously been administered to mice. Therefore, we wanted to test the potential ergogenic properties of astaxanthin supplementation using a fivefold higher supplementation dose in a larger cohort of well-trained cyclists. We hypothesized that prolonged astaxanthin supplementation (20 mg·d−1) increases fat oxidation rates during submaximal cycling exercise and improves subsequent time trial performance in trained cyclists.
Thirty-two trained male cyclists or triathletes were recruited to participate in the study (age = 25 ± 1 yr, weight = 73 ± 1 kg, V˙O2peak = 60 ± 1 mL·kg−1·min−1, W max = 395 ± 7 W; mean ± SEM). Because of medical reasons unrelated to the study, one subject (in the PLA group) had to discontinue participation in the study. All subjects were competitive cyclists or triathletes who had been engaged in regular cycling training (more than three sessions per week) for at least 2 yr. After being advised of the purpose and potential risks of the study, all subjects provided written, informed consent. The study was approved by the Medical Ethical Committee of the Academic Hospital Maastricht, The Netherlands.
Overview of study design.
The study was designed to investigate whether 4 wk of astaxanthin supplementation (20 mg·d−1) modulates whole-body fuel selection at rest, during 1 h of submaximal cycling exercise, and/or improves subsequent time trial performance. Subjects visited the laboratory on two occasions before the start of the main experimental period. The first visit consisted of an incremental cycling exercise test to exhaustion to determine subjects’ maximal workload capacity (W max) and peak oxygen uptake (V˙O2peak). The second visit consisted of a familiarization test that was identical in design as the main experimental test days. The procedures included the assessment of resting metabolic rate using indirect calorimetry with a ventilated hood system, followed by indirect calorimetry measurements during 60 min of submaximal cycling exercise at a workload corresponding to 50% W max. Subsequently, a simulated time trial of approximately 1 h was performed in which a set amount of work was required to be completed in as fast a time as possible. All exercise tests were carried out on an electronically braked cycle ergometer (Lode Excalibur, Groningen, the Netherlands).
Physical activity and dietary standardization.
All subjects refrained from any strenuous physical labor and/or sports activities during the 48-h period before each experimental test day. Subjects were instructed to maintain dietary and activity records during the 2 d before the familiarization test day and to replicate their diet and activities during the pre- and postsupplementation test days. All subjects received a standardized dinner the evening before each experimental test day (62 ± 4 kJ·kg BW−1, consisting of 50 energy percent [En%] carbohydrate, 10 En% protein, and 40 En% fat) (5). Subjects were provided with all food products to consume before 2200 h the evening before each test day. Subjects kept their training schedule as consistent as possible during the 4-wk supplementation period.
Maximal workload capacity.
To determine subjects’ maximal workload capacity (W max) and peak oxygen uptake (V˙O2peak), all subjects performed an incremental cycling test to exhaustion on an electronically braked cycle ergometer. After a 5-min warm-up at 100 W, workload was set at 150 W and increased by 50 W every 2.5 min until voluntary exhaustion (21). Workload (W), cadence (rpm), and HR (Polar Electro Oy, Kempele, Finland) were recorded at every interval. The appropriate seat position, handlebar height, and orientation were determined for each subject and replicated for each subsequent visit. Indirect calorimetric measurements were performed using an Omnical gas analysis system (Omnical, Maastricht University, the Netherlands). The gas analyzers were calibrated before every measurement, and the function of the ventilated hood system was checked weekly (1). V˙O2peak was calculated as the average oxygen uptake of the three highest sequential oxygen uptake values during the last 60 s of the cycling test. Maximal workload (W max) was calculated as the last completed stage (W) + time in last incomplete stage in seconds / 150 (s) × 50 (W).
In a double-blind fashion, subjects were randomly assigned to receive either astaxanthin (ASTA) or placebo (PLA) supplementation. The astaxanthin supplementation consisted of an algae (Heamotococcus pluvialis) extract high in astaxanthin, dissolved in sunflower oil in gelatin capsules, with added vitamin C (60 mg per capsule) and vitamin E (10 mg per capsule) (BioReal, Gustavsberg, Sweden). Subjects ingested two capsules (4 mg astaxanthin/capsule) with breakfast and three capsules with dinner throughout the 4-wk intervention period to ascertain an intake of 20 mg astaxanthin per day. The placebo treatment consisted of soy oil in gelatin capsules, which were similar in appearance and taste. The placebo group followed the same supplementation regime as the astaxanthin group. Supplementation compliance was measured by the amount of pills that were remaining in the pill bottle after the 4-wk supplementation period.
During the main experimental period, subjects consumed either 20 mg astaxanthin per day (ASTA) or a placebo (PLA; gelatin capsules with soy oil) for 4 wk. Subjects were tested before and immediately after the supplementation period. During the morning of the pretest and posttest, subjects arrived at the laboratory at 0800 h by car or public transportation after a 10-h overnight fast. Subjects were weighed, fitted with a HR monitor (Polar Electro Oy), and familiarized with the traditional 6–20 Borg scale of perceived exertion (7). Using a ventilated hood system (Omnical), resting metabolic rate was measured for 30 min while subjects were lying in a supine position. The last 20 min of data collection were used for the calculation of resting metabolic rate (1). Subsequently, a Teflon catheter was inserted into an antecubital vein for venous blood sampling. After a resting blood sample was obtained, subjects initiated the 60 min of cycling exercise at a workload corresponding with 50% W max (197 ± 3 W). Blood samples were obtained at 15, 30, 45, and 60 min into the exercise bout, and cardiorespiratory data were collected during the 5-min periods commencing at 10, 25, 40, and 55 min into the exercise bout. Gas analyses were performed with an Omnical gas analyzer (Omnical), and values of V˙O2 and V˙CO2 were averaged during the last 3 min of each sampling period to calculate rates of whole-body fat and carbohydrate oxidation. Ratings of perceived exertion using the Borg scale were recorded after each respiratory measurement.
After the completion of the submaximal exercise bout, subjects rested for 3 min before commencing a simulated time trial of approximately 1 h, whereby a set amount of work (see calculations) was completed in the shortest time possible. Time trials have been proven to be a more accurate and practical measurement of endurance performance capacity compared with time to exhaustion trials (18). During the time trial, no temporal, verbal, or physiological feedback was provided. The only information visible to the subjects was the absolute amount of work performed and the percentage of work performed relative to the set amount of work, which was displayed on a computer screen in front of the ergometer. HR was recorded continuously throughout the test. Immediately after the completion of the time trial, a final blood sample was obtained. The pre- and postsupplementation tests were performed on the same time and day of the week for each subject.
From respiratory measurements, total fat and carbohydrate oxidation rates were calculated using the following nonprotein respiratory quotient (27):
with V˙O2 and V˙CO2 in liters per minute and oxidation rates in grams per minute. Total work to be performed during the time trial was calculated to be 1 h if subjects cycled at 60% W max (18):
where W max is the maximal workload capacity determined during visit 1 and 3600 is the duration in seconds (equivalent to 1 h). The ergometer was set to linear mode (5) so that 60% W max was obtained when subjects cycled at their preferred cadence (93 ± 2 rpm), which had been determined during the familiarization test.
Plasma and serum analyses.
Blood samples (8 mL) were collected in ethylenediaminetetraacetic acid and serum separating tub containing tubes and centrifuged at 1000g for 10 min at 4°C. Aliquots of plasma and serum were frozen in liquid nitrogen and stored at –80°C for the subsequent analysis of plasma astaxanthin, glucose, lactate, trolox equivalent antioxidant capacity (TEAC), uric acid, malondialdehyde (MDA), and serum insulin and free fatty acid concentrations. Plasma astaxanthin concentrations were analyzed by reverse phase high-performance liquid chromatography (HPLC; Alliance 2690; Waters, Milford, MA) (23). Plasma glucose and lactate were analyzed with the COBAS-PENTRA semiautomatic analyzer (Roche Diagnostics Ltd., Basel, Switzerland). Total plasma free fatty acid concentrations were analyzed using automated enzymatic techniques on the COBAS-MIRA (Roche Diagnostics Ltd.). Insulin levels were measured on an AutoDELFIA automatic immunoassay system using time resolved fluorometry (B080-101; PerkinElmer, Turku, Finland). The TEAC was determined in plasma that was deproteinized with a final concentration of 5% trichloroacetic acid (TCA). The samples were then incubated with the ABTS (2,2’-Azinobis [3-ethylbenzothiazoline-6-sulfonic acid]-diammonium salt) radical solution for 5 min, followed by an absorbance reading at 734 nm. TEAC is expressed as micromolar trolox equivalents. Uric acid was determined in plasma deproteinized with a final concentration of 5% TCA using HPLC. A Hypersil BDS C-18 end-capped column, 125 × 4 mm, particle size 5 km (Agilent, Palo Alto, CA), was used, with a mobile phase of 0.1% trifluoroacetic acid (v/v) in water. UV detection was performed at 292 nm. The relative contribution of uric acid to the TEAC is calculated, using the TEAC value of 1 for uric acid (12). MDA was determined in plasma by quantification of the formation of a colored adduct of MDA-like breakdown products of lipids with 2-thiobarbituric acid (TBA). Plasma (100 μL) was added to 1 mL of reagent (containing 12 mmol·L−1 TBA, 0.32 mol·L−1 o-phosphoric acid, 0.68 mmol·L−1 BHT, and 0.01% ethylenediaminetetraacetic acid), and the mixture was incubated for 1 h at 100°C in a water bath. After cooling, the TBA product was extracted with 500 mL of butanol. A portion (30 mL) of the butanol layer was injected into an HPLC system (Agilent) equipped with a fluorescence detector, set at an excitation wavelength of 532 nm and emission wavelength of 553 nm, and a Nucleosil C18 column (150 × 3.2 mm; particle size, 5 mm; Supelco, Bellefonte, PA). Samples were eluted with 35% (v/v) methanol containing 0.05% trifluoric acid. A calibration curve was constructed using MDA bis(diethylacetal) as a standard.
All data are presented as mean ± SEM (n = 31). Time trial performance was analyzed using a two-factor (treatment × time) repeated-measures ANOVA. Resting respiratory and plasma data were analyzed using a two-factor (treatment × time) repeated-measures ANOVA. Submaximal respiratory and plasma data were calculated as area under the curve and then also analyzed using a two-factor (treatment × time) repeated-measures ANOVA. The level of significance for all analyses was set at P < 0.05. Data were analyzed using the Statistical Package for the Social Sciences (version 15.0; SPSS Inc., Chicago, IL).
Subjects’ characteristics are presented in Table 1. No differences in age, body weight, V˙O2peak, W max, or average hours of training per week were observed between the PLA and the ASTA groups.
Significant treatment– time interactions were observed for plasma astaxanthin concentrations. At baseline, plasma astaxanthin concentrations were undetectable. In the PLA group, after 4 wk of placebo supplementation, plasma astaxanthin concentrations remained undetectable. In the ASTA group, plasma astaxanthin concentrations averaged 187 ± 19 μg·kg−1 after 4 wk of supplementation (P < 0.001). No adverse effects were reported after astaxanthin supplementation.
No significant differences in resting V˙O2, V˙CO2, and RER were observed over time or between groups (Table 2). In line with these observations, resting energy expenditure and calculated rates of carbohydrate and fat oxidation did not differ between pre- and postsupplementation measurements or between treatments. Resting energy expenditure averaged 5.20 ± 0.13 and 5.23 ± 0.12 kJ·min−1 before and 5.33 ± 0.11 and 5.29 ± 0.14 kJ·min−1 after 4 wk of supplementation in the PLA and ASTA groups, respectively (P = 0.69). Fat oxidation rates at rest averaged 0.060 ± 0.005 and 0.064 ± 0.004 g·min−1 before supplementation and 0.055 ± 0.004 and 0.051 ± 0.005 g·min−1 after 4 wk of supplementation in the PLA and ASTA groups, respectively (P = 0.35).
During submaximal exercise at 50% W max, subjects cycled at 61% ± 1% of their individual V˙O2peak. During submaximal exercise, V˙O2, V˙CO2, and RER did not differ between pre- and postsupplementation measurements or between groups (Table 2). During submaximal exercise, energy expenditure averaged 53.7 ± 1.6 and 53.6 ± 1.2 kJ·min−1 preintervention and 53.8 ± 1.5 and 54.0 ± 1.3 kJ·min−1 postintervention in the PLA and ASTA groups, respectively (P = 0.69). Fat oxidation rates during submaximal exercise averaged 0.71 ± 0.04 and 0.66 ± 0.03 g·min−1 preintervention and 0.68 ± 0.04 and 0.61 ± 0.05 g·min−1 postintervention in the PLA and ASTA groups, respectively (P = 0.73; Fig. 1). HR and RPE did not differ over time or between groups (Table 2).
No significant differences in plasma glucose (Fig. 2A), insulin (Fig. 2B), lactate (Fig. 2C), or free fatty acid (Fig. 2D) concentrations were observed between pre- and postintervention measurements or between groups (treatment–time interaction, P > 0.05). In addition, antioxidant capacity markers including TEAC, uric acid, TEAC–uric acid, and MDA did not differ between pre- and postintervention measurements or between groups (treatment–time interaction, P > 0.05; Fig. 3).
Time trial performance.
Time trial performance averaged 59.43 ± 1.37 and 60.38 ± 1.20 min in the PLA and ASTA groups, respectively. In addition, average power output (236 ± 9 and 238 ± 6 W), average HR (167 ± 3 and 164 ± 2 bpm), and RPE recorded after the time trial (18.2 ± 0.4 and 18.1 ± 0.5) did not differ between groups. After 4 wk of supplementation, time to complete the time trial had not changed in either group and averaged 58.57 ± 1.39 and 59.14 ± 1.21 min in the PLA and ASTA groups, respectively. In addition, average power output (239 ± 7 and 244 ± 6 W), average HR (165 ± 3 and 167 ± 2 bpm), and RPE recorded after the time trial (17.9 ± 0.4 and 18.3 ± 0.4) did not differ over time or between treatments. No treatment–time interaction of time trial performance was observed (Fig. 4; P = 0.63). The percent difference in time trial performance (from pre- to postsupplementation) was 5.9% ± 1.2% and 3.5% ± 0.7% for the PLA and ASTA groups, respectively.
In the present study, we demonstrate that 4 wk 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. Furthermore, prolonged astaxanthin supplementation did not improve approximately 1 h cycling time trial performance in trained cyclists.
Astaxanthin is a naturally occurring component found in a variety of aquatic organisms and is available as an over-the-counter nutritional supplement. Astaxanthin supplementation has been demonstrated to stimulate fatty acid β-oxidation (4) and to improve exercise performance in vivo in a mouse model (4,16). More specifically, 4 wk of astaxanthin supplementation (6–30 mg·kg−1·d−1) in mice was demonstrated to increase fat oxidation rates during exercise and prolong subsequent running and swimming time to exhaustion (4,16). Although the precise mechanism by which astaxanthin supplementation improves exercise time to exhaustion remained unclear, a greater fat oxidative capacity during exercise after astaxanthin supplementation was suggested as the most likely mode of action.
Aoi et al. (4) hypothesized that prolonged astaxanthin supplementation augments fat oxidation through an improvement in the function of CPT1. CPT1 is located on the mitochondrial membrane and is regarded as the rate-limiting enzyme of fatty acid metabolism (22,29). Prolonged astaxanthin supplementation has been demonstrated to result in an accumulation of astaxanthin in the mitochondrial membrane (3,31), thereby providing astaxanthin with the opportunity to scavenge ROS (24,25). Consequently, astaxanthin supplementation may improve CPT1 function by inhibiting the accumulation of damaging ROS, thereby improving the efficiency of long chain fatty acid transport through the mitochondrial membrane. In line with this purported mechanism, prolonged astaxanthin supplementation in mice has been demonstrated to increase co-immunoprecipitation of CPT1 with fatty acyl–CoA (FAT)/CD36, resulting in increased rates of fat oxidation in vivo in a mouse model (4). In the present study, we did not find any evidence to support this hypothesis in an in vivo human model. Although plasma astaxanthin had markedly increased after 4 wk of supplementation, we did not detect any measurable changes in plasma MDA levels (a marker of fatty acid peroxidation), plasma antioxidant capacity, or whole-body fat oxidation rates at rest and/or during moderate-intensity exercise. Although plasma MDA levels were higher after the time trial compared with during exercise, astaxanthin supplementation did not attenuate this elevation of MDA, suggesting that there was no inhibition of fatty acid peroxidation. The apparent lack of any improvement in antioxidant capacity, despite substantial increases in plasma astaxanthin concentrations, seems to be at odds with previous work showing improvements in antioxidant capacity and a subsequent attenuation in oxidative damage after prolonged astaxanthin supplementation (9,10,20). More specifically, 12 wk of astaxanthin supplementation has been demonstrated to improve total antioxidant capacity and decrease MDA in sedentary, obese subjects (10) and lower levels of lipid peroxidation in healthy untrained men (20). In the current study, the apparent absence of any antioxidant properties may be attributable to the high fitness level of our subjects or the shorter supplementation time (4 wk compared with 12 wk). Endurance-type exercise training has been shown to increase endogenous antioxidant capacity (14,28), which may reduce the likelihood for any additional improvements through astaxanthin supplementation.
Despite the proposed properties of prolonged astaxanthin supplementation to augment fat oxidative capacity during exercise (4,16), we could not detect any effect of 4 wk of astaxanthin supplementation on fat oxidation rates at rest and/or during moderate-intensity exercise in vivo in humans (Table 2 and Fig. 1). The latter seems to be in line with recent work by Earnest et al. (11), who also failed to detect any improvements in the rate of fat oxidation during moderate-intensity exercise after 4 wk of supplementation with 4 mg d−1 of astaxanthin in well-trained men. The authors speculated that their applied dose of astaxanthin (4 mg·d−1) might have been too small to augment rates of fat oxidation. We provided a fivefold greater dose of astaxanthin (20 mg·d−1) throughout the 4-wk supplementation period. Regardless, the greater daily dose of astaxanthin administered in the present study also did not modulate the rate of fat oxidation at rest or during moderate-intensity exercise. We conclude that prolonged (4 wk) astaxanthin supplementation (20 mg·d−1) does not augment fat oxidative capacity in vivo in humans.
Prolonged astaxanthin supplementation has been reported to improve both swimming and running time to exhaustion in vivo in mice (4,16). As such, astaxanthin has been identified as a potential novel ergogenic aid. As time to exhaustion is not a representative measure of performance in a competitive setting, we applied a time trial of approximately 1 h to assess endurance performance capacity before and after astaxanthin or placebo supplementation. Despite strict dietary standardization and the application of familiarization tests, we were unable to observe any improvements in time trial performance within or between treatments (Fig. 4). In line with this observation, no differences were observed in average power output, HR, or time to complete the set workload within or between treatments. These findings are in line with the absence of any effect of 4 wk of astaxanthin supplementation on fat oxidative capacity, which had previously been suggested as the mechanism responsible for any proposed ergogenic benefits of astaxanthin supplementation (4). However, our findings seem to be at odds with previous work recently published by Earnest et al. (11), who reported a significant 5% improvement in the 20-km time trial performance after 4 wk of astaxanthin supplementation (4 mg·d−1) in seven trained cyclists. Subjects were reported to have exercised for 2 h at approximately 70% of their individual V˙O2peak, followed by a 20-km time trial. Only 14 of the 21 included subjects were able to complete the entire testing protocol, and improvements in time trial performance were reported in the remaining seven subjects in the astaxanthin supplemented group. Although there is no explanation for the apparent discrepancy, the present study does not show any ergogenic properties of astaxanthin supplementation. On the basis of the large cohort of subjects in our current study, the high fitness level of the athletes, and the use of a time trial of approximately 1 h, we conclude that astaxanthin supplementation does not improve exercise performance in endurance trained cyclists. Interestingly, some athletes currently use astaxanthin for a purpose other than its proposed ergogenic properties. Astaxanthin is currently being used by triathletes as a natural sun-blocking agent, which is supported by the observation that astaxanthin supplementation protects against UVA skin damage by providing a photo-protective effect of the dermal layer (8,15,30).
In conclusion, prolonged astaxanthin supplementation (20 mg·d−1) does not augment plasma antioxidant capacity, increase fat oxidative capacity at rest and/or during moderate-intensity exercise, or improve performance capacity in endurance trained athletes.
The authors gratefully acknowledge the assistance of Olaf Henselmans, Steven Meex, Åke Lignell, Janneau van Kranenburg, and Antoine Zorenc and the subjects who volunteered to participate in this study. The astaxanthin and placebo pills were a kind gift of BioReal Sweden.
None of the authors declared any conflict of interest, and this study did not receive funding.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
1. Adriaens MP, Schoffelen PF, Westerterp KR. Intra-individual variation of basal metabolic rate and the influence of daily habitual physical activity before testing. Br J Nutr. 2003; 90 (2): 419–23.
2. Andersen LP, Holck S, Kupcinskas L, et al. Gastric inflammatory markers and interleukins in patients with functional dyspepsia treated with astaxanthin. FEMS Immunol Med Microbiol. 2007; 50 (2): 244–8.
3. Aoi W, Naito Y, Sakuma K, et al. Astaxanthin limits exercise-induced skeletal and cardiac muscle damage in mice. Antioxid Redox Signal. 2003; 5 (1): 139–44.
4. Aoi W, Naito Y, Takanami Y, et al. Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification. Biochem Biophys Res Commun. 2008; 366: 892–7.
5. Beelen M, Berghuis J, Bonaparte B, Ballak SB, Jeukendrup AE, van Loon LJ. Carbohydrate mouth rinsing in the fed state: lack of enhancement of time-trial performance. Int J Sport Nutr Exerc Metab. 2009; 19 (4): 400–9.
6. Bergstrom J, Hermansen L, Hultman E, Saltin B. Diet, muscle glycogen and physical performance. Acta Physiol Scand. 1967; 71 (2): 140–50.
7. Borg G. Ratings of perceived exertion and heart rates during short-term cycle exercise and their use in a new cycling strength test. Int J Sports Med. 1982; 3 (3): 153–8.
8. Camera E, Mastrofrancesco A, Fabbri C, et al. Astaxanthin, canthaxanthin and beta-carotene differently affect UVA-induced oxidative damage and expression of oxidative stress-responsive enzymes. Exp Dermatol. 2009; 18 (3): 222–31.
9. Choi HD, Kim JH, Chang MJ, Kyu-Youn Y, Shin WG. Effects of astaxanthin on oxidative stress in overweight and obese adults. Phytother Res. 2011; 25 (12): 1813–8.
10. Choi HD, Youn YK, Shin WG. Positive effects of astaxanthin on lipid profiles and oxidative stress in overweight subjects. Plant Foods Hum Nutr. 2011;66(4):363–9.
11. Earnest CP, Lupo M, White KM, Church TS. Effect of astaxanthin on cycling time trial performance. Int J Sports Med. 2011; 32 (11): 882–8.
12. Fischer MA, Gransier TJ, Beckers LM, Bekers O, Bast A, Haenen GR. Determination of the antioxidant capacity in blood. Clin Chem Lab Med. 2005; 43 (7): 735–40.
13. Goedecke JH, Christie C, Wilson G, et al. Metabolic adaptations to a high-fat diet in endurance cyclists. Metabolism. 1999; 48 (12): 1509–17.
14. Gomez-Cabrera MC, Domenech E, Vina J. Moderate exercise is an antioxidant: upregulation of antioxidant genes by training. Free Radic Biol Med. 2008; 44 (2): 126–31.
15. Hama S, Takahashi K, Inai Y, et al. Protective effects of topical application of a poorly soluble antioxidant astaxanthin liposomal formulation on ultraviolet-induced skin damage. J Pharm Sci. 2012; 101 (8): 2909–16.
16. Ikeuchi M, Koyama T, Takahashi J, Yazawa K. Effects of astaxanthin supplementation on exercise-induced fatigue in mice. Biol Pharm Bull. 2006; 29 (10): 2106–10.
17. Ikeuchi M, Koyama T, Takahashi J, Yazawa K. Effects of astaxanthin in obese mice fed a high-fat diet. Biosci Biotechnol Biochem. 2007; 71 (4): 893–9.
18. Jeukendrup A, Saris WH, Brouns F, Kester AD. A new validated endurance performance test. Med Sci Sports Exerc. 1996; 28 (2): 266–70.
19. Josse AR, Sherriffs SS, Holwerda AM, Andrews R, Staples AW, Phillips SM. Effects of capsinoid ingestion on energy expenditure and lipid oxidation at rest and during exercise. Nutr Metab (Lond). 2010; 7: 65.
20. Karppi J, Rissanen TH, Nyyssonen K, et al. Effects of astaxanthin supplementation on lipid peroxidation. Int J Vitam Nutr Res. 2007; 77 (1): 3–11.
21. Kuipers H, Verstappen FT, Keizer HA, Geurten P, van Kranenburg G. Variability of aerobic performance in the laboratory and its physiologic correlates. Int J Sports Med. 1985; 6 (4): 197–201.
22. McGarry JD, Brown NF. The mitochondrial carnitine palmitoyltransferase system. From concept to molecular analysis. Eur J Biochem. 1997; 244 (1): 1–14.
23. Mercke Odeberg J, Lignell A, Pettersson A, Hoglund P. Oral bioavailability of the antioxidant astaxanthin in humans is enhanced by incorporation of lipid based formulations. Eur J Pharm Sci. 2003; 19 (4): 299–304.
24. Mortensen A, Skibsted LH, Truscott TG. The interaction of dietary carotenoids with radical species. Arch Biochem Biophys. 2001; 385 (1): 13–9.
25. Naguib YM. Antioxidant activities of astaxanthin and related carotenoids. J Agric Food Chem. 2000; 48 (4): 1150–4.
26. Ohgami K, Shiratori K, Kotake S, et al. Effects of astaxanthin on lipopolysaccharide-induced inflammation in vitro and in vivo. Invest Ophthalmol Vis Sci. 2003; 44 (6): 2694–701.
27. Peronnet F, Massicotte D. Table of nonprotein respiratory quotient: an update. Can J Sport Sci. 1991; 16 (1): 23–9.
28. Radak Z, Chung HY, Goto S. Systemic adaptation to oxidative challenge induced by regular exercise. Free Radic Biol Med. 2008; 44 (2): 153–9.
29. Schenk S, Horowitz JF. Coimmunoprecipitation of FAT/CD36 and CPT I in skeletal muscle increases proportionally with fat oxidation after endurance exercise training. Am J Physiol Endocrinol Metab. 2006; 291 (2): E254–60.
30. Suganuma K, Nakajima H, Ohtsuki M, Imokawa G. Astaxanthin attenuates the UVA-induced up-regulation of matrix-metalloproteinase-1 and skin fibroblast elastase in human dermal fibroblasts. J Dermatol Sci. 2010; 58 (2): 136–42.
31. Takahashi K, Watanabe M, Takimoto T, Akiba Y. Uptake and distribution of astaxanthin in several tissues and plasma lipoproteins in male broiler chickens fed a yeast (Phaffia rhodozyma
) with a high concentration of astaxanthin. Br Poult Sci. 2004; 45 (1): 133–8.
32. Venables MC, Hulston CJ, Cox HR, Jeukendrup AE. Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans. Am J Clin Nutr. 2008; 87 (3): 778–84.
33. Yang Y, Seo JM, Nguyen A, et al. Astaxanthin-rich extract from the green alga Haematococcus pluvialis
lowers plasma lipid concentrations and enhances antioxidant defense in apolipoprotein E knockout mice. J Nutr. 2011; 141 (9): 1611–7.
Keywords:©2013The American College of Sports Medicine
SUBSTRATE USE; CYCLING; FAT OXIDATION; EXERCISE; ERGOGENIC AIDS; ANTI-OXIDANTS