Exercise as a model to study redox homeostasis in blood: the effect of protocol and sampling point

Abstract

Twenty males ran either on a level treadmill (nonmuscle-damaging condition) or on a downhill treadmill (muscle-damaging condition). Blood and urine samples were collected before and after exercise (immediately after, 1h, 4h, 24h, 48h, and 96h). The following assays were performed: F(2)-isoprostanes in urine, protein carbonyls in plasma, glutathione, superoxide dismutase, glutathione peroxidase, and catalase in erythrocytes. The main finding was that monophasic redox responses were detected after nonmuscle-damaging exercise compared to the biphasic responses detected after muscle-damaging exercise. Based on these findings, muscle-damaging exercise may be a more appropriate experimental model to induce physiological oxidative stress.

Alterations in Redox Homeostasis in the Elite Endurance Athlete

“…Unfortunately, there is no single time point that best describes the post-exercise changes in OS across a spectrum of OS assays [135]. The ideal sampling point will depend on the assay used [135], the mode of exercise [58] and the training status of the subjects [23]. For the GSH, GSSG, GSH/GSSG and TAC assay, 2-hour post-aerobic exercise (no muscle damage) in untrained individuals captures the peak changes in blood; 1-hour post-exercise for TBARS, F2-isoprostanes, and immediately post-exercise for CAT, and 4-hour post-exercise for PC as reported by Michailidis et al [135].…”

“…Those with relevance to the athletes' training and competition environment include aerobic and anaerobic training [21,22], tissue ischaemia and re-oxygenation [21], red cell haemolysis [46], iron deficiency [47], dehydration [48], altitude [49], sunlight and associated ultraviolet radiation (UVB and UVA) [50], heat stress [51], diet poor in fruit and vegetables [52], psychological stress [53,54], infection [55,56], use of anti-inflammatory drugs [57], sterile tissue trauma and associated inflammation resulting from a contact injury, or muscle damage resulting from eccentric exercise [58,59]. Sleep deprivation in animals causes OS and ARH [60,61], and given recent evidence of mild sleep deprivation increasing inflammation in humans [62], a lack of sleep and long haul travel may be anticipated to be a further cause of OS and ARH in the athlete.…”

Effects of exercise on alterations in redox homeostasis in elite male and female endurance athletes using a clinical point-of-care test

“…Unfortunately there is no single time point post-exercise which best describes the response across a spectrum of OS assays (Michailidis et al 2007). The ideal sampling point will depend on the assay used (Michailidis et al 2007), the mode of exercise (Nikolaidis et al 2012a), and the training status of the participants (Bloomer and Fisher-Wellman 2008). Given that we chose to assess elite athletes, we selected a sampling point immediately post-maximal exercise and 20 minutes into recovery, as used by other studies in elite athletes (Palazzetti et al 2003, Tanskanen et al 2010.…”

“…Exercise is known to be a source of reactive nitrogen and oxygen species (RNOS), leading to post-exercise alterations in redox homeostasis (ARH) (Nikolaidis et al 2012b). Initially, RNOS were thought to be detrimental to athlete recovery, but it is now clear that RNOS are important for adaptation to endurance training (Finaud et al 2006, Ristow et al 2009, Powers et al 2010a, skeletal muscle hypertrophy and protein signaling (Makanae et al 2013, Paulsen et al 2014).…”

The Effects of Eccentric Exercise on Muscle Damage and Blood Redox Status in Men and Women

“…Despite the many human studies investigating the effects of acute concentric non-muscle-damaging exercise on blood redox status (reviewed in [7]), our group focused on the effects of acute eccentric muscle-damaging exercise on blood redox status [3,[8][9][10][11]. The main finding of these studies was that eccentric exercise provoked large and uniform alterations in several oxidative stress indices and antioxidant molecules, indicating increased oxidative stress, probably arising from increased free radical production in the damaged skeletal muscle fibers.…”