The effect of exercise on the generation of ROS measured with several different methods was reported in a variety of exercises. The exercise-induced increase in the lipid peroxidation indices occurred in blood and other tissues of both trained and untrained humans and animals. The methods used for demonstration of the exercise-induced oxygen stress included direct measurement of the oxygen radicals using electron paramagnetic resonance (EPR) and chemiluminescence. Other methods consisted of the estimation of the products of free radical reactions with polyunsaturated fatty acids, such as ethane and pentane as well as malondialdehyde (MDA). Total thiobarbituric acid-reactive substances (TBARS) have also been widely used as a nonspecific measure of MDA.
Davies et al.29 demonstrated increased EPR signals in the liver and muscle homogenates obtained from animals subjected to exhaustive endurance exercise. The increased EPR signal was also seen in the stimulated contracting muscle30 and in the rat myocardium after exhaustive exercise.31 The exercise-stimulated enhanced generation of ROS was also detected in rat muscle using the chemiluminiscence method.22 It was demonstrated32 that expiratory pentane levels in humans increased after long-term submaximal exercise (50% of VO2max). It has been established that elevation in the lipid peroxidation indices is related to the intensity and duration of the exercise and is significantly less pronounced in trained compared to untrained subjects. Kanter et al.33 reported that both expiratory pentane and serum MDA increased as a result of the 60% VO2max intensity work and continued to rise proportional to the increasing work load. Similar results were reported by Leaf et al.34 who showed that in healthy, physically active men and women exposed to graded aerobic exercise, the expiratory ethane and pentane levels exceeded the lactic threshold at the resting levels, continued to rise to the VO2max, and then declined during recovery. In this study, however, the marked elevations in expiratory ethane and pentane were not accompanied by a comparable increase in the serum TBARS levels, which were not significantly different before and after maximal exercise. According to these authors, this discrepancy suggests that MDA is cleared from the plasma by several potential mechanisms including excretion, catabolism, or redistribution to body tissues. Alesio et al.35 demonstrated that increases in the MDA levels in skeletal muscle were more pronounced following a short-lasting exercise of high intensity than following longer exercise of lower intensity. Frankiewicz-Jozko et al.36 reported that in untrained rats, treadmill running until exhaustion led to elevation in TBARS in the liver, heart, and soleus muscle. In contrast, in trained animals that ran on the treadmill until exhaustion almost twice as long as the untrained animals, the rise in TBARS levels was detectable only in the liver but not in the heart or soleus. Alesio and Goldfarb37 demonstrated that an increased MDA concentration in the muscles following moderate treadmill exercise occurred only in the untrained but not in the trained rats. In human studies, Niess38 reported that both long distance runners as well as sedentary persons exhibit increases in their plasma MDA levels as a result of maximal exercise on a treadmill. However, the increase was substantially less pronounced in the former than in the latter group.
Was this article helpful?