Exercise -induced muscle damage and immune cell apoptosis

Kyung-Shin Park, Purdue University

Abstract

The purpose of this study was to examine the effect of unaccustomed downhill running on muscle damage, oxidative stress and leukocyte apoptosis. Additionally, four pro-/anti- apoptotic proteins, representing the receptor mediated or mitochondrial apoptotic pathway, were assessed to provide insight into the mechanisms involved in exercise-induced apoptosis. Twelve moderately trained subjects aged 18-26 yr performed three 40 min treadmill exercises eliciting ∼70% VO2max: a level running trial (L) and two downhill (-10%) running trials (DH1 and DH2). Blood samples were taken pre-exercise (PRE) and immediately (POST), 2 h, 24 h, and 48 h following each run and analyzed for creatine kinase (CK) activity, oxygen radical absorbance capacity (ORAC), anti-/pro apoptotic proteins (Bcl-2, Bax, sFas and FasL) and the percentage of apoptotic leukocytes (apoptotic index : AI). CK activity peaked at 24 h following DH1 and was significantly higher in DH1 than L and DH2 (P<0.01). ORAC at 24 h post in DH1 was significantly lower than pre-exercise and lower than L and DH2 at the same time point (p<0.01). AI for total leukocytes, lymphocytes and neutrophils showed a similar pattern. AI was significantly elevated at POST and 2 h post in L and DH2. In contrast, a significant elevation in AI was found up to 48 h post in DH1 trial. Moreover, AI in DH1 compared to L and DH2 was significantly greater at 24 h and 48 h post for total leukocytes, lymphocytes and neutrophils measured by morphological identification as well as in total leukocytes measured by TUNEL assay and flow cytometry. Total leukocyte AI was significantly greater with morphological identification from whole blood as compared to TUNEL assay from isolated leukocytes. Pro-apoptotic protein expression (Bax; p<0.05) and Bax/Bcl-2 ratio (p<0.01) were significantly elevated above PRE at 24 h following DH1 when significant increases were recognized in the markers of exercise-induced muscle damage and oxidative stress as well as the amount of apoptotic leukocytes, lymphocytes, and neutrophils. Meanwhile anti-apoptotic protein (Bel-2) was unaltered. Receptor-mediated apoptotic proteins sFas (p=.051) and FasL (p=.059) tended to increase following the runs. Bax/Bcl-2 ratio was significantly higher at 24 h post vs. PRE in DH1 and compared to L at 24 h post. Results of this study suggest that significant increases in leukocyte apoptosis can be induced at an exercise intensity < 75% VO2max. Moreover, increases in leukocyte apoptosis following eccentric exercise are coincident with changes in markers of oxidative stress and muscle damage.

Degree

Ph.D.

Advisors

Sedlock, Purdue University.

Subject Area

Physical education

COinS