Exercise-Induced Muscle Damage and Immune Cell Apoptosis

Abstract

Muscle damage is evident following an acute bout of downhill running (i.e., eccentric ally-biased exercise) at moderate intensity whereas it does not occur following running on a level grade or after a second bout of downhill running. Muscle damage increases intracellular free radicals due to the phagocytic processes of white cells. This increase in reactive oxygen species reduces oxygen radical absorbance capacity (ORAC) which may elevate the number of apoptotic cells. PURPOSE: to examine the effect of muscle damaging exercise on immune cell apoptosis. METHODS: Twelve moderately trained subjects (mean±SE age=22.7±0.7yr, VO2max= 53.1±1.3ml·kg−1·min−1) performed three 40 min treadmill exercises at ∼70% VO2max: a level running trial (L) and two downhill (−10%) running trials (DH1 and DH2). Blood samples were taken at rest and immediately (POST), 2h, 24h, and 48h following each run, and analyzed for creatine kinase (CK) activity, ORAC and apoptotic cells (%) using morphological identification. Data were analyzed using a 2-way repeated measures ANOVA with post hoc Tukey tests. RESULTS: CK activity at 24h following exercise was significantly higher in DH1 than L and DH2 (p < 0.01). ORAC was significantly lower at 24h in DH1 as compared to L and DH2 (p < 0.01). Lymphocyte number peaked at POST and was significantly higher in DH1 than in L and DH2. The number of neutrophils was highest 2h following exercise and also significantly higher in DH1 vs L and DH2. Lymphocyte apoptosis was significantly greater at 24h and 48h following DH1 than L and DH2 (p < 0.01). Neutrophil apoptosis in DH1 was significantly higher at 2h, 24h and 48h than in L and significantly greater at 24h and 48h than in DH2 (p < 0.01). CONCLUSION: An initial bout of downhill running for 40 min at a moderate intensity, which likely induced muscle damage, significantly increased oxidative stress and the proportion of apoptotic lymphocytes and neutrophils in the blood compared to level running or a second downhill run. This suggests that increased oxidative stress following exercise-induced muscle damage may affect the amount of apoptosis in white cells, and perhaps play a role in immune suppression.