Ultimately, this increase facilitates excessive cell damage, altered cell signaling, decreased cellular performance, lipid peroxidation, oxidation of proteins and glutathione, and subsequent DNA damage. As a result, this type of long duration mechanical muscle stress and high oxidative metabolic demand, significantly increases free radical production beyond the capacity of the endogenous antioxidant systems. Over the 48-h recovery period, P changes in medial quadriceps soreness from pre-run measures were smaller compared to TC.Īcute bouts of strenuous aerobic exercise facilitate a stress response characterized by mechanical muscle damage, oxidative stress, and inflammation that parallels the physiological stress response associated with many adverse traumatic cardiovascular events and illnesses. Soreness perception between the groups was different over time in the medial quadriceps ( p = 0.035) with 34 % lower pre-run soreness in TC compared to P. Inflammatory markers were 47 % lower in TC compared to P over time ( p = 0.053) coupled with a significant difference between groups ( p = 0.017). Despite lower antioxidant activity pre-run in TC compared to P, changes from pre-run levels revealed a linear increase in antioxidant activity at 24 and 48-h of recovery in TC that was statistically different (16–39 %) from P and pre-run levels. Attenuations in TC muscle catabolic markers were reported over time for creatinine ( p = 0.047), urea/blood urea nitrogen ( p = 0.048), total protein ( p = 0.081), and cortisol ( p = 0.016) compared to P. Subjects in the TC group averaged 13 % faster half-marathon race finish times ( p = 0.001) and tended to have smaller deviations from predicted race pace ( p = 0.091) compared to P.
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