Anti-fatigue effect of oat peptide in mice: an experimental study

  Objective  To study whether the oat-peptide has anti-fatigue effect and possible mechanism of the effect.

  Methods  A total of 192 male specific pathogen free (SPF) ICR mice were randomly divided into 6 groups: a control group, a whey protein (0.22 g/kg) group, and four oat-peptide groups (0.50, 1.00, 2.0, and 4.00 g/kg body weight); all the mice were treated with intragastric administration for 30 days. Loading swimming time was determined; blood lactic acid was measured with absorption spectrophotometry; hepatic glycogen and muscle glycogen were detected with glycogen kit; and serum urea nitrogen and lactate dehydrogenase activity were determined with automatic biochemical analyzer.

  Results  The mean loading swimming time of mice in the control and whey protein group was 3.90 ± 1.38 and 4.91 ± 2.21 minutes, and there was no significant difference in the time between the two groups (P > 0.05). The loading swimming time of the mice in the four oat-peptide groups, compared with that in whey protein group, were prolonged significantly by 2.58, 1.40, 2.18, and 1.90 times, respectively (P < 0.05 for all). There were no significant differences between the control and whey protein group in the area under the blood lactate curve, the content of glycogen in liver and muscle, and the activity of lactate dehydrogenase. The under curve area of blood lactic acid of mice in all oat- peptide groups were significantly less than that in control group and whey protein group (both P < 0.05). Compared with those in the whey protein group, the area of blood lactic acid curve in each of oat-peptide groups decreased significantly but the content of liver glycogen increased significantly (all P < 0.05). Compared with those of the whey protein group, the muscle glycogen content and lactate dehydrogenase activity of 2.00 g/kg oat-peptide group increased.

  Conclusion  Oat-peptide can relieve physical fatigue to some extent and its mechanism may relate to reducing the accumulation of blood lactic acid and increasing the content of liver glycogen.