Unaccustomed eccentric exercise, such as downhill walking, produces micro-structural damage to muscles resulting in reduced muscle strength and mobility. The mechanisms behind eccentric exercise-induced muscle damage is believed to be mediated, in part, by immune cells recruited to the site of injury.
Ten healthy male volunteers performed 30 minutes of single leg stepping exercise to induce muscle damage in the quadriceps muscles. Quadriceps muscle function, perceived soreness, circulating immune cell phenotyping and plasma cytokines were measured before, immediately after and 24h, 48h and 72h post exercise.
Six responders had statistically significant (p<0.05) decreases in eccentric, isometric and concentric muscle function immediately following the step-up exercise and persisting for 72h. The responders also reported increased soreness at 48h post exercise (p=0.01). The responders had significantly increased plasma CCL2 (p=0.032) immediately post exercise, and plasma CXCL10 (p=0.013) 24h post exercise. There was a trend towards an increase in circulating monocytes immediately post exercise that returned to baseline at 24h post exercise. There were no differences in circulating T cells or natural killer (NK) cells at any of the time points measured.
Previous contractile muscle damage studies have shown that CCL2 and CXCL10 are increased in the damaged muscle and there is increased infiltration of T cells and monocytes 24h to 48h following exercise. In this study we showed that we could detect increases in CCL2, CXCL10 and monocytes within the blood post damage, but not changes in T cells. These results indicate that contractile muscle damage mediated immune activation can be transiently quantified by plasma cytokine and circulating immune cell changes, mitigating the need for muscle biopsies to identify aspects of the immune response to muscle damage.