RESEARCH PAPER
Dose-Dependent Effects of Astaxanthin on Exercise-Induced Muscle Damage in Exercising Males
1
Department of Physical Education and Sports Teaching, Faculty of Sport Sciences, Sabahattin Zaim University, Istanbul, Turkiye.
2
Department of Coaching Education, Faculty of Sport Sciences, Dumlupinar University, Kutahya, Turkiye
3
Department of Medical Pharmacology, School of Medicine, Onyedi Eylul University, Bandirma, Balikesir, Turkiye.
4
Division of Exercise Nutrition and Metabolism, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkiye.
Submission date: 2024-09-05
Final revision date: 2025-05-26
Acceptance date: 2025-09-02
Publication date: 2026-04-02
Corresponding author
Muhammed M. Atakan
Division of Exercise Nutrition and Metabolism, Faculty of Sport Sciences, Hacettepe University, Beytepe Campus, 06690, Ankara, Turkey
Division of Exercise Nutrition and Metabolism, Faculty of Sport Sciences, Hacettepe University, Beytepe Campus, 06690, Ankara, Turkey
Journal of Human Kinetics 2026;101:103-117
KEYWORDS
TOPICS
ABSTRACT
Astaxanthin (AX) is a potent antioxidant and an anti-inflammatory carotenoid. Research examining whether AX could counteract exercise-induced muscle damage and improve exercise capacity has reported inconsistent results. The aim of this study was to test the efficacy of high-dose versus low-dose AX supplementation for four weeks on muscle damage markers, total antioxidant status, and a subjective marker of muscle pain following exhaustive exercise. A total of 24 active males were randomly assigned to one of the three groups: an AX12 group (12 mg·day−1; n = 8), an AX36 group (36 mg·day−1; n = 9) or a placebo group (PLC, n = 7). After four weeks of supplementation, blood samples were collected at rest, and at 2, 24, 48, and 72 h following eccentric arm exercise performed at 85% of the predetermined one-repetition maximum to assess muscle damage markers and total antioxidant status, and muscle pain levels were evaluated using a Numerical Visual Pain Scale0–10. Creatine kinase activity was significantly lower in AX groups compared to the PLC group at 24, 48, and 72 h post-exercise (p < 0.05), with no difference between both AX groups (p > 0.05). At 24, 48, and 72 h post-exercise, lactate dehydrogenase activity in the PLC group was higher than in AX12 and AX36 groups, averaging 2.2 and 2.8 times higher, respectively; however, these differences were not statistically significant (p > 0.05). A significant time effect of the muscle pain score was noted at 2, 24, 48, and 72 h post-exercise (p < 0.001), with no significant differences among the supplementation protocols (p > 0.05). In conclusion, four-week AX supplementation at a dose of 12 or 36 mg·day−1 similarly reduces plasma creatine kinase activity following exhaustive exercise, yet its impact on muscle pain and antioxidant status remains limited.
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