This is likely due to the limited inflammatory response and lack of a clear indicator of muscle damage as measured by CK. There was a significant elevation in serum concentrations of IL-6 at IP compared to BL, DHY and 24P learn more and at RHY compared to BL and 24P. This response is consistent with previous studies that have shown significant elevations following prolonged endurance [33, 35, 38] and eccentric exercise [34]. IL-6 is produced in

active skeletal tissue [39] and in the central nervous system [40]. Exercise is a potent stimulator of IL-6 production, with elevations greater than 100-fold reported [41]. It is thought that increases in IL-6 modulates CRP production in the liver [42] and operate synergistically to enhance the inflammatory response to exercise. The potential outcome from this inflammatory Gemcitabine response is the risk for significant tissue damage and reduced recovery capability. Several investigations have examined the ability of nutritional intervention to attenuate the post-exercise inflammatory response [43, 44]. Carbohydrate ingestion [44] and a vitamin E and omega-3 fatty acid combination [43] have been successful in attenuating the IL-6 response to exercise. In contrast, glutamine supplementation has been shown to enhance plasma IL-6 production [38], while an AG dipepide has shown to have no effect on cytokine production in healthy individuals [45]. Hiscock and colleagues [38] suggested

that the enhanced glutamine uptake by skeletal muscle would increase or maintain the production of IL-6. This hypothesis may be more consistent with the anti-inflammatory role suggested of IL-6 during exercise [46]. Increases in IL-6 concentrations have been consistently reported without corresponding muscle damage [46], and is supported by the results of this present study. The difference between this study and the results of Hiscock et al., [38] may be related to the length of exercise and the training experience of the subjects. In the present study the duration of exercise ranged from

5 – 47 minutes following the ~60 minute active dehydration protocol, in recreationally BCKDHB trained individuals, while the subjects in Hiscock’s study were untrained and required to perform a 2-hr time trial using the same exercise intensity as employed in this study. However, those subjects were euhydrated and allowed to drink ad libitum. It is unlikely that dosing impacted these results, considering that the glutamine dose used in Hiscock’s study (3.5 g) was similar to the low dosing trial (T4). [MDA] were significantly elevated from baseline for all trials. This is not Cell Cycle inhibitor surprising considering that exercise is a potent stimulator of the formation of reactive oxygen species [47]. The results of this study are also consistent with previous research demonstrating elevated oxidative stress following a mild dehydration and exercise to exhaustion protocol [48].