Journal Title (Medline/Pubmed accepted abbreviation): Int J Sport Nutr Exerc Metab
Page numbers: 124-134
doi (if applicable): N/A
Background: Physical exercise is known to cause increased formation of reactive oxygen species (ROS), which can potentially overreach antioxidant capacity. The resultant oxidative stress leads to damaged DNA, lipids, proteins, and carbohydrates, and may result in cell dysfunction or death. Enhancing the endogenous antioxidant defense system may reduce oxidative stress and potentially minimize or prevent cell damage. Superoxide dismutase (SOD) catalyzes the reduction of superoxide anions to less reactive hydrogen peroxide and is, therefore, a key component for intracellular antioxidant defense. It is found in many plants; however, its use in dietary supplements has thus far been limited because the enzyme is inactivated upon ingestion. The development of GliSODin is a SOD-rich melon extract that is coupled with a biodegradable wheat-based gliadin biopolymer and is, therefore, delivered efficiently by ingestion.
Hypothesis/purpose of study: The authors hypothesized that supplementation with orally effective vegetable SOD would enhance endogenous antioxidant defense and limit oxidative stress, muscle injury, and inflammatory response during exercise in professional rowers.
Subjects: Study participants (N = 19) were male members of the Polish rowing team. Ten members were assigned to the supplementation group and 9 to the control arm (mean age, 21.3 ± 1.1 yr, 20.3 ± 1.0 yr; mean mass, 89.3 ± 5.3 kg, 86.1 ± 10.2 kg; training, 7.2 ± 1.6 yr, 5.7 ± 1.7 yr, respectively).
Experimental design: Double-blind
Treatments and protocol: Subjects were given 2 capsules of either GliSODin (500 mg) or maltodextrin daily for 6 weeks. Subjects performed a controlled 2,000-m time trial on a rowing ergometer on Day 1 and after 6 weeks of supplementation. The entire study was conducted during a training camp, thus allowing daily monitoring of exercise and limitation of external dietary sources. Blood samples were taken before each 2,000-m trial, 1 minute after exercise, and 24 hours postrecovery, and multiple redox parameters were assessed, including total antioxidant capacity, SOD activity, glutathione peroxidase activity, C-reactive protein, thiobarbituric acid reactive substances (TBARS), lactate dehydrogenase (LDH), and creatine kinase (CK).
Supplementation with GliSODin did increase SOD activity, but did not alter glutathione peroxidase (another antioxidant enzyme) or TBARS (a marker of oxidative stress). Further, markers of muscle damage (eg, CK, LDH) were not reduced by supplementation. Thus, the physiologic significance of the increase in SOD activity regarding oxidative stress or muscle cell damage is not clear. An additional point is that the authors did not assess the intensity of exercise or the maximum oxygen consumption during the exercise tests, both of which are critical pieces of information. Of note, the observed decrease in C-reactive protein levels after supplementation with GliSODin suggests that melon extract may have anti-inflammatory effects to protect against increased inflammation in the serum of professional rowers. As with the other biomarkers measured, the physiologic significance of a decline in C-reactive protein of the magnitude observed in this study is not known.
One potential limitation of this supplement is that, because of the gliadin coating, it may not be appropriate for athletes with celiac disease or other gluten intolerances.