Delayed Onset of Muscle Soreness: Creatine Kinase as a Marker for Tissue Damage (Pgf(2a) Metabolite).
Date of Award
Doctor of Philosophy (PhD)
Twenty college age males participated in a weight-lifting experiment, 3 sets of 10 repetitions at 70% 1RM for the squat, to examine the time courses between creatine phosphokinase (CPK), prostaglandin F(,2) alpha metabolite (PGF(,2a) met) and ratings of perceived soreness (RPS). Both groups, aspirin (n = 10) and placebo (n = 10), received medication (3g/day) for four consecutive days, starting 1 day prior to workout. Ratings of soreness and blood samples were taken pre- and immediately post-exercise, and at 24 h intervals for 3 days after exercise. There was no significant difference (p < 0.05) between the groups for CPK and RPS across time, but the prostaglandins were significantly different (p < 0.01) at all time intervals between groups. Changes seen across time were quadratic for all variables. The 24 h prostaglandin level was significantly higher (p < 0.05) than the pre-, post-exercise and 72 h levels, but not significantly different from the 48 h level. Ratings of soreness were not significantly different (p < 0.05) at the 24 and 48 h intervals, but both were significantly higher than at all other time intervals. The mean CPK levels at 24 and 48 h were not significantly different (p < 0.05), but the 24 h CPK level was significantly higher (p < 0.05) from the other time intervals. There was a significant correlation (p < 0.01) between the time courses of CPK and RPS. It was concluded that CPK can be used as a marker for tissue damage and that prostaglandins did not influence the subjects' perception of muscle soreness or the release or uptake of CPK.
Boatwright, John Douglas, "Delayed Onset of Muscle Soreness: Creatine Kinase as a Marker for Tissue Damage (Pgf(2a) Metabolite)." (1986). LSU Historical Dissertations and Theses. 4174.