Abstract
PURPOSE:Obesity is associated with over activation of the pro-apoptotic pathway, implicating in the development of various comorbidities, such as insulin resistance and cardiovascular disease. While autophagy has been recently discovered as a critical molecular process in promoting cell survival against apoptosis, increased autophagic activation in obese individuals may serve as a pro-survival regulator to eliminate damaged proteins, organelles, or aggregates, and/or to enhance the cellular metabolic responses associated with physical stressors. Therefore, the purpose of this study was to examine whether or not maximal aerobic exercise-mediated apoptosis in obesity might be underlying the involvement of autophagy in the peripheral blood mononuclear cells (PBMCs). METHODS: Twelve healthy male subjects (6 obese and 6 normal-weight) were recruited to participate in a maximal graded exercise test on a treadmill. Western blot analysis was used to determine the level of apoptotic and autophagic markers (Bax/Bcl-2 and LC3-II/LC3-I; respectively) in PBMCs prior to, immediately following exercise, and one and two hours into recovery from exercise. RESULTS: Obese subjects exhibited a significantly lower Bax (p = 0.028), but a higher Bcl-2 protein level (p = 0.006) in conjunction with a reduced Bax/Bcl-2 area-under-the-curve “with respect to increase” (AUCi) (p = 0.024) compared to normal-weight subjects following maximal aerobic exercise. Furthermore, a greater LC3-II/LC3-I ratio and LC3-II/LC3-I AUCi was observed in obese subjects compared to normal-weight subjects in response to exercise (p = 0.003 and p = 0.005; respectively). LC3-II/LC3-I AUCi was also positively associated with obesity-associated parameters (BMI, waist/hip circumference, and fasting insulin level), but was negatively correlated with Bax/Bcl-2 AUCi (r = -0.835, p = 0.001). CONCLUSIONS: These findings demonstrate that maximal aerobic exercise differentially mediates the intrinsic apoptotic pathway and autophagic activity in human PBMCs isolated from obese compared to normal-weight individuals, suggesting the importance of autophagy as a critical molecular process in promoting cell survival against exercise-induced apoptosis.
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