This study examined whether acute inflammation was the mechanism underlying delayed muscle soreness (DMS) by assessing the effect of soreness-inducing exercise on blood levels of C-reactive protein (CRP), an acute inflammation marker. Sixteen female college students (= 20.6 +/- 2.6 years) performed three sets of 35 isokinetic contractions of the knee flexors and extensors at 120 degrees /set on a Biodex isokinetic dynamometer. Group 1 (N = 8) exercised eccentrically and Group 2 (N = 8) concentrically at an intensity of 80% of a concentric 120 degrees /set peak torque. Pre-exercise and 1, 24, 48 and 72 hours postexercise, DMS of the quadriceps femoris (QF) and hamstrings (HA) were assessed and blood samples were collected for creatine kinase (CK), an indicator of muscle damage, and CRP, which was measured by a radial immunodiffusion procedure. The mean CK values 72 hours postexercise were 14,856 and 360 IU/L for groups 1 and 2, respectively. No significant elevations of CRP occurred in either group. ANOVAs using a split plot factorial design found Group 1 to have significantly larger logarithmic CK elevations, ranked QF soreness, and ranked HA soreness than Group 2. In contrast to myocardial infarct patients and marathon runner investigations, this study did not demonstrate abnormal elevations of CRP when increases in CK were induced. With high-repetition submaximal isokinetic exercise, eccentric contractions induce higher levels of muscle damage and DMS than concentric contractions. Further, the hamstrings are more susceptible to DMS than the quadriceps femoris when eccentric isokinetic exercise is performed at the same relative intensity. J Orthop Sports Phys Ther 1992;16(5):208-214.