Metabolic implications of resistive force selection for oxidative stress and markers of muscle damage during 30�s of high-intensity exercise

Abstract

The purpose of this study was to compare power outputs, and blood concentrations of lipid hydroperoxides (LH), malondialdehyde (MDA), creatine kinase (CK), myoglobin (Mb) and lactate ([La-]B) following 30 s of maximal cycle ergometry when resistive forces were derived from total-body mass (TBM) or fat-free mass (FFM). Alpha-tocopherol (AT), retinol (R) and uric acid (UA) concentrations were also measured to qualify the activity of antioxidants. Cardiac troponin levels were determined to exclude myocardial damage and to verify that any CK was predominantly derived from skeletal muscle. Differences (P<0.05) in peak power output, pedal velocity and resistive forces were observed when the TBM and FFM protocols were compared [953 (114) W vs 1,020 (134) W; 134 (8) rpm vs 141 (7) rpm; 6 (1) kg vs 5 (1) kg respectively). LH and MDA concentrations increased immediately post-exercise during the TBM protocol only (P<0.05) and were greater when compared to FFM (P<0.05). LH and MDA values decreased 24 h post-exercise. Increases in CK concentrations were recorded immediately post-exercise for both the TBM and FFM protocols with greater concentrations recorded for TBM (P<0.05). Decreases were observed 24 h post-exercise. Mb concentrations were greater immediately post-exercise for the TBM protocol and were greater than those recorded for FFM (P<0.05). Values decreased 24 h later (P<0.05). AT and UA concentrations decreased immediately post-exercise for both protocols (P<0.05) and increased 24 h later (P<0.05). There were no changes observed in R concentrations at any of the blood sampling stages. [La-]B increased (P<0.05) immediately post-exercise for both protocols, and decreased 24 h later (P<0.05). The results of the study suggest that greater power outputs are obtainable with significantly less oxidative stress and muscle disruption when resistive forces reflect FFM mass as opposed to TBM.

Impact of single anaerobic exercise on delayed activation of endothelial xanthine oxidase in men and women

“…Changes in UA concentration in the blood have been used in previous studies as an indicator of oxidative stress occurring after anaerobic exercise [3,6,[16][17][18][19]. The results of the previous studies are not conclusive because UA is a product of purine metabolism and, at the same time, non-enzymatic antioxidant that affects the total antioxidant capacity of the blood [20].…”

“…A significant increase in the blood concentration of UA beginning at various times after the completion of anaerobic exercise could be found (3, 10, 15, 60 minutes) [3,16,18,19]. Peak concentration of UA in the blood occurred 1 hour after the end of anaerobic exercise, with a subsequent decrease in concentration up to 24 hours [3], or the UA concentration decreased immediately after exercise and increased after 24 hours of rest [17]. In other studies, no significant changes in UA concentration in the blood 24 hours after anaerobic exercise were found [6].…”

“…Owing to the presence of intracellular XO, we assessed whether anaerobic exercise caused micro-injury to muscle fibers, as in the case of other studies [17,44]. Damage to cell membranes could result in the outflow of cytoplasmic proteins to the extracellular fluid, and among others, may cause an increase in XO activity in the blood which is not the result of the Table 5.…”

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

“…In fact, many studies have reported that an acute exhaustive maximal exercise task lasting only 30s (i.e. the Wingate test) is capable of inducing systemic changes in redox homeostasis (Groussard et al, 2003a;Groussard et al, 2003b;Baker et al, 2004;Cuevas et al, 2005;Cooke et al, 2008;Bloomer and Smith, 2009;Arent et al, 2010). For example, Groussard et al (Groussard et al, 2003b), employing electron paramagnetic resonance (EPR) spectroscopy, reported a twofold increase in lipid-derived radicals in plasma after 30s of cycling.…”

The Effect of Soybean Trypsin Inhibitor on the Generation of Oxygen Free Radical in Pancreas of Mice during Different Growth Periods

“…Overproduction of ROS (arising either from mitochondrial electrontransport chain or excessive stimulation of NAD(P)H) results in oxidative stress (Marian et al, 2007), a deleterious process that has been implicated in various pathological conditions involving cardiovascular disease, cancer, neurological disorders, diabetes, ischemia/reperfusion, other diseases and ageing (Baker et al, 2004;Valko et al, 2007;Stadtman, 2004;Dalle-Donne et al, 2005;Gupte & Mumper, 2009;Khandrika et al, 2009). Free radicals react with lipid and cause peroxidative changes that result in enhanced lipid peroxidation (Zwart et al, 1999;Girotti, 1985).…”