%0 Journal Article
%T N-Acetylcysteine Supplementation Controls Total Antioxidant Capacity, Creatine Kinase, Lactate, and Tumor Necrotic Factor-Alpha against Oxidative Stress Induced by Graded Exercise in Sedentary Men
%A Donrawee Leelarungrayub
%A Raphiphat Khansuwan
%A Prapas Pothongsunun
%A Jakkrit Klaphajone
%J Oxidative Medicine and Cellular Longevity
%D 2011
%I Hindawi Publishing Corporation
%R 10.1155/2011/329643
%X Aim of this study was to evaluate the effects of short-term (7 days) N-acetylcysteine (NAC) at 1,200£¿mg daily supplementation on muscle fatigue, maximal oxygen uptake ( ), total antioxidant capacity (TAC), lactate, creatine kinase (CK), and tumor necrotic factor-alpha (TNF-¦Á). Twenty-nine sedentary men (13 controls; 16 in the supplement group) from a randomized control were included. At before and after supplementation, fatigue index (FI) was evaluated in the quadriceps muscle, and performed a graded exercise treadmill test to induce oxidative stress, and as a measure of . Blood samples were taken before exercise and 20 minutes after it at before and after supplementation, to determine TAC, CK, lactate, and TNF-¦Á levels. Results showed that FI and increased significantly in the supplement group. After exercise decreased the levels of TAC and increased lactate, CK, and TNF-¦Á of both groups at before supplementation. After supplementation, lactate, CK, and TNF-¦Á levels significantly increased and TAC decreased after exercise in the control group. Whereas the TAC and lactate levels did not change significantly, but CK and TNF-¦Á increased significantly in the supplement group. Therefore, this results showed that NAC improved the muscle fatigue, , maintained TAC, controlled lactate production, but had no influence on CK and TNF-¦Á. 1. Introduction Exercise is promoted for improving general health and preventing many diseases such as cardiovascular disease, diabetes mellitus, and cancer [1]. However, several studies have shown that short heavy exercise may induce adverse effects associated with oxidative stress in untrained humans through various pathways such as electron leakage within mitochondria, auto-oxidation of the catecholamine, NADPH activity, or an ischemic-reperfusion [2]. Oxidative stress induces oxidation processes in proteins, lipids, or DNA. Oxidation of all biological molecules is a result of organ dysfunction [3]. During muscle contraction with a short heavy load, numerous free radicals are produced that induce microinjury or an inflammation process and tumor necrotic factor-alpha (TNF-¦Á), interleukin-6 (IL-6) [4], lactate dehydrogenase (LDH), and creatine phosphokinase (CPK) [5] are released. Thus, over-oxidative stress directly affects physical performance through the ability of muscles to contract to whole-body aerobic capacity [6]. Considerable interest has been shown in finding ways to prevent heavy exercise-induced free-radical production and muscle injury. Nutritional supplements, such as vitamin C (ascorbic acid) or vitamin E
%U http://www.hindawi.com/journals/omcl/2011/329643/