Abstract

Introduction While it is known that acute intense exercise promotes the generation of oxidative stress (OS), the role of intermittency in this paradigm is unclear. Thus, the aim of the present study was to assess the impact of exercise intermittency on markers of OS. Methods Nine (n = 9) healthy males of an average age of 22.6 yrs (range 21 – 27 yrs) volunteered for the study. Participants were randomly assigned to complete a low (80s work:rest) moderate (20s work:rest) or high (5s work:rest) intermittent exercise protocol using a cross-over design on a non-motorised treadmill. The total work completed was equivalent across each of the conditions in terms of mean speed and duration (45mins). Fasted venous blood samples were collected pre, 1-h, 2-h and 24-h post exercise for the analysis of lipid hydroperoxides (LOOHs), superoxide dismutase (SOD), and glutathione (GSH) via plate reader methods while 8-Oxo-2'-deoxyguanosine (8-oxo-dG) was analysed using LC-MS. Results Analysis of DNA damage showed no detectable levels of 8-oxo-dG across all exercise protocols. LOOHs increased on average by 69% (range -6 − 427%), SOD by 52% (range -49 − 590%) and GSH by 99% (range -47.7 − 179%) in the low intermittent group 2hrs post exercise, whereas moderate and high intermittency did not demonstrate any relevant changes. Discussion It is presented that OS was found to increase 2hrs after a bout of high intensity/low intermittent exercise. It is plausible that the higher intermittent modes were not of sufficient duration to trigger the signaling cascade associated with exercise, free radical formation and subsequent OS. It was also further determined that plasma concentrations of 8-oxo-dG were below the limit of detection of LC-MS (0.25nM) and further consideration should be given to choice of sample type when investigating this important biological marker.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call