馬拉松賽對淋巴細胞自發性死亡以及脂質過氧化的影響

Effects of Marathon Race on Both Apoptosis of Lymphocytes and Lipid Peroxidations

徐台閣 ； 徐廣明 ； 蘇文和 ； 張永政

《北體學報》 9期 (2001/12) Pp. 195-205

https://doi.org/10.6167/TPEC/2001.9.16

摘要

Several Studies have indicated that have indicated that an overproduction of reactive oxygen species (ROS) may be associated with endurance running. And other specialists have proposed that increasing free radical activities may cause a number of human diseases and aging. Strenuous exercise predisposes the untrained individual to increase free radical damages. Long distance running, due to the large amounts of oxygen uptake they cause, may lead to the generation of ROS, and oxidative stresses and damages that include aopotosis. High intensity endurance running inducing immune suppression is well documented. Recent studies have demonstrated exhaustive exercise and high intensity exercise induced DNA damage in leukocytes and lymphocytes apoptosis. The purpose of this study was to investigate the effects of a 42.2 KM marathon run (MR) on apoptosis of lymphocytes in blood. Twelve subjects (age = 34.4 ± 12.5 yrs, ht = 166.4 ± 4.8 cm, wt = 62.0 ± 4.1 Kg, train 102.km per week for 7.6 yrs on average) competed in the 1998 Taipei International Marathon Championship. Venous blood samples were taken before, and at 30 mins and 24 hrs after the race. Lymphocytes were prepared for flow cytometry to determine apoptosis. It is using the terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) method to analysis apoptosis. Whole blood lymphocytes were also determined. The results indicated that lymphocyte apoptosis rose significantly (p ＜. 05) at 30 mins (32.9 %), 24 hrs (25.0%) and 72 hrs (8.7%) after MR, as compared with the pre-race levels (1.39%). Lymphocytes cell count significantly decreased (p ＜. 05) at 30 mins (1395 cells/mm^3) after MR as compared to the pre-race levels (2183 cells/mm^3). It is concluded that MR induced apoptosis specific for lymphocytes may in part account for MR induced lymphocytopenia and reduced immunity.

關鍵字

馬拉松賽 ； 淋巴細胞 ； 細胞自發性死亡

並列摘要

Several Studies have indicated that have indicated that an overproduction of reactive oxygen species (ROS) may be associated with endurance running. And other specialists have proposed that increasing free radical activities may cause a number of human diseases and aging. Strenuous exercise predisposes the untrained individual to increase free radical damages. Long distance running, due to the large amounts of oxygen uptake they cause, may lead to the generation of ROS, and oxidative stresses and damages that include aopotosis. High intensity endurance running inducing immune suppression is well documented. Recent studies have demonstrated exhaustive exercise and high intensity exercise induced DNA damage in leukocytes and lymphocytes apoptosis. The purpose of this study was to investigate the effects of a 42.2 KM marathon run (MR) on apoptosis of lymphocytes in blood. Twelve subjects (age = 34.4 ± 12.5 yrs, ht = 166.4 ± 4.8 cm, wt = 62.0 ± 4.1 Kg, train 102.km per week for 7.6 yrs on average) competed in the 1998 Taipei International Marathon Championship. Venous blood samples were taken before, and at 30 mins and 24 hrs after the race. Lymphocytes were prepared for flow cytometry to determine apoptosis. It is using the terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) method to analysis apoptosis. Whole blood lymphocytes were also determined. The results indicated that lymphocyte apoptosis rose significantly (p ＜. 05) at 30 mins (32.9 %), 24 hrs (25.0%) and 72 hrs (8.7%) after MR, as compared with the pre-race levels (1.39%). Lymphocytes cell count significantly decreased (p ＜. 05) at 30 mins (1395 cells/mm^3) after MR as compared to the pre-race levels (2183 cells/mm^3). It is concluded that MR induced apoptosis specific for lymphocytes may in part account for MR induced lymphocytopenia and reduced immunity.

並列關鍵字

marathon race ； apoptosis ； lymphocytes