This study examined the effects of different resistance exercise protocols on markers of muscle damage, lipid peroxidation and nitric oxide response in the plasma of the sedentary men. One of the primary findings of this investigation was the increase of NO_x production in high resistance exercise (HR) group (p < 0.05). The response of the MDA to the two different resistance exercise protocols showed a significant increase between the values obtained before and immediately after the exercise in both groups (p < 0.05). Also there was a significant difference in the MDA level between the two groups in the values obtained immediately after cessation of the exercise (p < 0.05). CK activity increased significantly (p < 0.05) for all post exercise values in both HR and LR groups but there was no difference between them.

Vascular formation of NO_x is directly facilitated by increased shear stress (Cooke et al., 1991; Miller and Burnett, 1992). During a session of physical exercise, cardiac output increases and blood redistribute to the exercising muscles. The exercise-induced increase of blood flow elicits an increase in shear stress (Van Citters and Franklin, 1969), thereby providing a possible coupling between exercise and endogenous NO_x formation. Although the role of endothelium-derived NO_x in acute exercise has not been fully resolved, exercise training involving repetitive bouts of exercise over weeks or months up-regulates endothelial NO_x bioactivity (Maiorana et al., 2003). We saw that NO_x production increased in HR group (p < 0.05). There was a significant increase after the 6 hours of the exercise according to NO_x results in HR group and this increase continued after 24 and 48 hours (Figure 1). In agreement with these findings, it has also been reported that NO_x is increased in venous plasma after prolonged running, cycling (Jungersten et al., 1997) and after incremental cycling exercise to VO₂ max (Node et al., 1997). In contrast, some other studies have also shown no change of NO_x metabolism following an incremental treadmill test to exhaustion in healthy human subjects (Komiyama et al., 1997; Poveda et al., 1997; St Croix et al., 1999). In our study, there was no significant difference between measurement times in LR group (Figure 1). Our results suggest that the intensity of the resistance exercise increase NO_x production, only when it was performed at high intensities. According to result of the correlations comparing the same measurement times, there was a positive correlation between CK and NO_x in HR group (r = 0.557 p < 0.05)

Several different exercise models have been conducted to study the effect of acute physical activity on various oxidative stress indices and tissue damage markers and different results have been reported on different models (Alessio et al., 2000; Atalay et al., 1996; Khanna et al., 1999; Lovlin et al., 1987; McBride et al., 1998; Viitala et al., 2004; Simpson et al., 2005). Resistance training consists of repetitive, static muscle actions. These include concentric and eccentric muscle actions, which are considered as respectively, a low- or high- intensity resistance exercise protocol (Liu et al., 2005). Based on previous investigations, it was determined that the intensity of the exercise protocol used is a primary factor in creating a physiological environment for increased free radical production (Sahlin et al., 1992; Saxton et al., 1994). Few studies have assessed oxidative stress resulting from resistance exercise (McBride et al., 1998; Surmen-Gur et al., 1999). An increase in blood MDA was noted in 2 days following a full body resistance training protocol (McBride et al., 1998), whereas no change was reported in blood MDA 6 min following the performance of 20 eccentric/concentric actions with the knee extensors (Surmen-Gur et al., 1999). No change was also noted for TBARS following heavy full-body resistance exercise performed to failure. The differences in the protocols may have contributed to the discrepancy in the results. In this study both high and low intensity resistance exercise bouts resulted in significant increase in lipid peroxidation immediately after exercise (p < 0.05). But higher values were observed in HR group (Figure 2). Maughan et al., 1989 states that peak changes in MDA occur at 6 hours post exercise, while some studies have only examined immediate post exercise MDA values. Some of the investigations, which have examined resistance type exercise and free radical formation reported no increase in free radical formation (Ortenblad et al., 1997; Sahlin et al., 1992; Saxton et al., 1994). This may be a result of lighter loads and smaller amount of muscle tissue activation.

Intense muscle contractions associated with resistance exercise may result in ischemia-reperfusion at the site of the active muscles. The free radicals act as mediators of ischemia-reperfusion injury in skeletal muscles and result in muscle injury accompanied by increased amounts of CK. Kanter et al. (1993; 1988) have also shown that plasma MDA measurements correlate with CK activity during exercise. In this study, plasma MDA reached peak values immediately after the exercise in both groups, but plasma CK activity reached peak values at 24^th hrs post exercise in HR group, 6^th hrs post exercise in LR group and higher values were observed in HR group. But no difference was found between both groups according to same measurement times (Figure 3). The creatine kinase activity observed in this investigation showed that muscle tissue damage occurred well after the exercise in both resistance exercise protocols. The fact that the two types of exercise protocols predominantly used to study muscle damage, downhill running and high-force muscular contractions, show very different CK responses. For example, after downhill running, CK peaks about 12-24 hrs post-exercise, with increases in range from 100 to 600 IU (Byrnes et al., 1985; Clarkson and Hubal, 2002; Schwane et al., 1983), whereas after high-force eccentric exercise the increase does not begin until about 48 hrs post exercise, with peak activity (generally 2000-10000 IU) occurring about 4 to 6 days post exercise (Clarkson et al., 1992). The current findings confirm that the high-intensity whole body resistance exercise can result in the formation of free radicals. These free radicals may play a role in adaptation of the muscle tissues to the physiological stress caused by resistance exercise (Liu et al., 2005; Ramel et al., 2004). Ischemia-reperfusion during resistance exercise at the site of muscle, and post-exercise production of free radicals via oxidative burst from neutrophils, are key factors that must be taken to account while trying to decrease the muscle injury during this type of exercise (Pyne, 1994).