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It was hypothesized that muscle injury would be greater with eccentric than with all-out or prolonged exercise, and that immune changes might provide an indication that supplements the information provided by traditional markers such as creatine kinase (CK) or delayed-onset muscle soreness. Eight healthy males [mean (SE): age?=?24.9?(2.3) years, maximum oxygen consumption ( V?O 2max)=43.0?(3.1)?ml?·?kg -1?·?min -1] were each assigned to four experimental conditions, one at a time, using a randomized-block design: 5?min of cycle ergometer exercise at 90% V?O 2max (AO), a standard circuit-training routine (CT), 2?h cycle ergometer exercise at 60% V?O 2max (Long), or remained seated for 5?h. Blood samples were analyzed for CK, natural killer (NK) cell counts (CD3 -/CD16 +56 +), cytolytic activity and plasma levels of the cytokines interleukin (IL)-6, IL-10, and tissue necrosis factor a (TNF-a). CK levels were only elevated significantly 72?h following CT. NK cell counts increased significantly during all three types of exercise, but returned to pre-exercise baseline values within 3?h of recovery. Cytolytic activity per NK cell was not significantly modified by any type of exercise. Prolonged exercise induced significant increases in plasma IL-6 and TNF-a. We conclude that the lack of correlation between traditional markers of muscle injury (plasma CK concentrations and muscle soreness rankings) and immune markers of the inflammatory response suggests that, for the types and intensities of exercise examined in this study, the exercise-induced inflammatory response is modified by humoral and cardiovascular correlates of exercise.

This study examined the impact of heat exposure and moderate, intermittent exercise on the CD16+ and CD56+ cell counts and cytolytic activity. Eleven healthy male subjects [mean (SD): age = 27.1(3.0) years, peak oxygen intake, VO2maxO2 peak = 47.6 (6.2) ml · kg-1 · min-1] were assigned to each of four different experimental conditions according to a randomized-block design. While in a climatic chamber maintained at a comfortable temperature (23°C) or heated (40°C, 30% relative humidity, r.h.), subjects performed either two 30-min bouts of cycle-ergometer exercise at ˜50% VO2maxO2 peak (separated by a 45-min recovery interval), or remained seated for 3 h. Blood samples were analyzed for CD16+ and CD56+ cell counts, cytolytic activity and the concentrations of various exercise stress hormones (norepinephrine, epinephrine and cortisol). Heat exposure alone had no significant effect on cytolytic cells. The (CD16+ and CD56+) cell count increased significantly (P < 0.0001) during each exercise bout under both environmental conditions, but returned to baseline levels 15–45 min following each exercise bout. Total cytolytic activity (determined by a standard 51Cr release assay using K562 cells) followed a similar pattern, but cytolytic activity per CD16+ or CD56+ cell was not significantly modified by exercise. Our findings show a strong association between hemodynamic factors and recruitment of cytolytic cells into the peripheral circulation. Alterations in cytolytic activity of the whole blood during and following moderate exercise seem to be the result of changes in CD16+ and CD56+ cell counts.