Ergogenic and Antioxidant Effects of Spirulina Supplementation in Humans

Maria Kalafati; Athanasios Z. Jamurtas; Michalis G. Nikolaidis; Vassilis Paschalis; Anastasios A. Theodorou; Giorgos K. Sakellariou; Yiannis Koutedakis; Dimitris Kouretas

Disclosures

Med Sci Sports Exerc. 2010;42(1):142-151. 

In This Article

Discussion

To our knowledge, this is the first attempt to examine the effects of spirulina supplementation on exercise performance, substrate metabolism, and blood redox status at rest and after exercise in humans. The results showed that spirulina supplementation for 4 wk induced a significant increase in exercise performance, fat oxidation, and glutathione concentration as well as attenuated exercise-induced increases in lipid peroxidation. This provides evidence that increased levels of fat oxidation and GSH may contribute to enhanced exercise performance.

Exercise Performance and Increased Fat Oxidation Rate

Probably the most interesting finding of the present study is the increase in exercise performance after spirulina supplementation. Despite the fact that the mechanism behind the ergogenic effect of spirulina is difficult to be identified, the most plausible explanation implicates fat oxidation, the rate of which was found substantially increased (15.8%) during the 2-h exercise trial in spirulina-supplemented individuals. The maintenance of maximal aerobic power output requires that carbohydrates are oxidized as well as fats.[15] Because carbohydrates come from the glycogen stores, the time that maximal aerobic power can be sustained depends on the amount of glycogen stored initially.[15] In fact, it was found that the time to exhaustion when working at 75% of maximal aerobic power (almost equal to 70% V·O2max that was used in the present study) correlated with the initial muscle glycogen concentration.[15] Moreover, there is evidence that increasing fat oxidation leads to sparing of glycogen[15]); thus, at least in principle, the increased fat oxidation could have spared glycogen or glucose to allow high-intensity exercise to be continued for a longer time.

We have no hint as to what biochemical mechanism may have led to increased fat oxidation after spirulina supplementation, partly because spirulina is a complex mixture of substances with different properties. Potential control points of fat oxidation include lipolysis in adipose tissue, transportation of fatty acids via blood, transportation of fatty acids to muscle, hydrolysis of myocellular triacylglycerols, transportation of fatty acids to mitochondria, and mitochondrial density.[30] We know very little about whether and how spirulina affects these processes. However, the high content of γ-linolenic acid in spirulina (21.7% of total fatty acids in dry spirulina)[33] may play a role in mediating the reported effects on fat metabolism in the present study. In fact, γ-linolenic acid has been shown to reduce body fat[47] and facilitate fatty acid β-oxidation in the liver as judged by the increased activities of carnitine palmitoyl-transferase,[24,47] acyl-CoA oxidase,[24] and peroxisomal β-oxidation[47] in rats.

Exercise Performance and Increased GSH Concentration

Except for the substrate-oriented explanation depicted in the previous paragraphs, the increased concentration of GSH may also explain to some extent the increased performance detected after spirulina supplementation. Several studies provided convincing data to support the view that cysteine is generally the limiting amino acid for GSH synthesis in humans and in other animals.[54] Thus, increasing the supply of cysteine or its precursors (e.g., N-acetylcysteine) via oral or intravenous administration enhances GSH synthesis,[21,23,38,48,52] we found only two studies that addressed the effects of spirulina supplementation on redox status in humans.[35,43] The two studies measured several indices of redox status in blood and reported contradictory results. For example, Park et al.[35] reported decreased levels of lipid peroxidation, whereas Shyam et al.[43] reported no change in lipid peroxidation after spirulina supplementation.

Effect of Spirulina Supplementation on Redox Status after Exercise

TBARS was the only biochemical variable that a significant group × time interaction was detected, with TBARS levels increasing after exercise after placebo but not after spirulina supplementation. The main probable mechanism through which exercise increased lipid peroxidation after its cessation is the increased susceptibility to peroxidation of unsaturated fatty acids[16] because exercise markedly increases the concentration and unsaturation degree of nonesterified fatty acids in blood.[32] The higher levels of GSH can partially explain the absence of an increase in lipid peroxidation after exercise in the spirulina-supplemented individuals. GSH can effectively scavenge several RONS that can cause lipid peroxidation (e.g., hydroxyl radical, lipid peroxyl radical, peroxynitrite, and hydrogen peroxide) directly and indirectly through enzymatic reactions.[54] In addition, GSH is a substrate for glutathione peroxidase, which catalyzes the reduction of peroxides, such as hydrogen peroxide and lipid hydroperoxides.[54] Another potential mechanism through which spirulina decreased lipid peroxidation might be the increased content of γ-linolenic acid in spirulina.[33] Indeed, it has been found that an increased ratio of γ-linolenic acid to arachidonic acid is capable of attenuating the biosynthesis of arachidonic acid metabolites (i.e., prostaglandins, leukotrienes, and platelet-activating factor) and exerts an anti-inflammatory effect.[9,19] Decreased inflammation via this route might have decreased the production of superoxide, hydrogen peroxide, and hypochlorous acid by the activated neutrophils[10] leading to less lipid peroxidation after spirulina supplementation.

Regarding the remaining indices of redox status (protein carbonyls, catalase, and TAC), all increased immediately and 1 h after exercise indicating oxidative stress. All redox status indices returned to their preexercise values at 24 h. Studies that have investigated the effects of aerobic exercise on serum protein carbonyls generally have reported increases similar to ours lasting up to 6 h of recovery.[8,29]

Evidence addressing the efficacy of antioxidant supplementation to decrease oxidative stress remains ambiguous. For example, it has been shown that supplementation for 4 wk with vitamin E prevented the increase of lipid peroxidation after exercise.[46] In addition, supplementation for 2 wk with vitamins C and E attenuated the rise in protein oxidation after exercise.[8] On the contrary, supplementation for 6 wk with vitamin C, vitamin E, and β-carotene did not prevent the exercise-induced increase of lipid peroxidation.[20] Moreover, supplementation for 5 wk with artichoke extract did not attenuate oxidative damage to erythrocytes after exercise.[45] These differences in results may be related, in part, to the different concentration of the antioxidants and the combination of ingredients.

Mobilization of tissue antioxidant stores into plasma, such as uric acid,[13] is probably one mechanism responsible for the marked increase (and not decrease, as might be expected intuitively) of TAC after exercise. This is a widely accepted phenomenon that helps maintain or even increase serum antioxidant status in times of need.[39] Increased catalase activity after exercise also could have contributed to the increased TAC. Nevertheless, this increase in the antioxidant capacity of serum did not prove efficient at inhibiting the increase in lipid and protein oxidation in the blood. Most studies agree that exercise increases TAC for some hours after exercise.[3,53] Perhaps the increased TAC could mean that the plasma gets enriched with antioxidant molecules that need to be transported into tissues where they can provide protection.

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