Abstract
BackgroundA large body of evidence shows that a single bout of strenuous exercise induces oxidative stress in circulating human lymphocytes leading to lipid peroxidation, DNA damage, mitochondrial perturbations, and protein oxidation.In our research, we investigated the effect of physical load on the extent of apoptosis in primary cells derived from blood samples of sixteen healthy amateur runners after marathon (a.m.).ResultsBlood samples were collected from ten healthy amateur runners peripheral blood mononuclear cells (PBMCs) were isolated from whole blood and bcl-2, bax, heat shock protein (HSP)70, Cu-Zn superoxide dismutase (SOD), Mn-SOD, inducible nitric oxide synthase (i-NOS), SIRT1, SIRT3 and SIRT4 (Sirtuins) RNA levels were determined by Northern Blot analysis. Strenuous physical load significantly increased HSP70, HSP32, Mn-SOD, Cu-Zn SOD, iNOS, GADD45, bcl-2, forkhead box O (FOXO3A) and SIRT1 expression after the marathon, while decreasing bax, SIRT3 and SIRT4 expression (P < 0.0001).ConclusionThese data suggest that the physiological load imposed in amateur runners during marathon attenuates the extent of apoptosis and may interfere with sirtuin expression.
Highlights
A large body of evidence shows that a single bout of strenuous exercise induces oxidative stress in circulating human lymphocytes leading to lipid peroxidation, DNA damage, mitochondrial perturbations, and protein oxidation.In our research, we investigated the effect of physical load on the extent of apoptosis in primary cells derived from blood samples of sixteen healthy amateur runners after marathon (a.m.)
Total TRaining IMPulse (TRIMP) score accumulated over the marathon race averaged 523 ± 67 arbitrary unit, equivalent to exercise at 80% of heart rate reserve for 200 to ~220 min
HSP70, HSP32, Cu-Zn-superoxide dismutase (SOD), and Mn-SOD, inducible nitric oxide synthase (i-NOS) levels Northern blot analysis demonstrated that the RNA content of HSP70, HSP32 increased substantially in the studied group after marathon (Figure 4)
Summary
A large body of evidence shows that a single bout of strenuous exercise induces oxidative stress in circulating human lymphocytes leading to lipid peroxidation, DNA damage, mitochondrial perturbations, and protein oxidation.In our research, we investigated the effect of physical load on the extent of apoptosis in primary cells derived from blood samples of sixteen healthy amateur runners after marathon (a.m.). A large body of evidence shows that a single bout of strenuous exercise induces oxidative stress in circulating human lymphocytes leading to lipid peroxidation, DNA damage, mitochondrial perturbations, and protein oxidation. Programmed cell death, is a normal physiological function essential for the homeostasis of immuno haemopoietic tissues. This process occurs via specific signaling pathways, eventually leading to DNA fragmentation, nuclear condensation, proteolysis and cell fragmentation [1]. It has been suggested that apoptosis contributes to the loss of blood lymphocytes after exercise possibly via the cell surface death receptor CD95 (Fas/Apo-1) signaling [8,9,10], resulting in postexercise lymphocytopenia, which could lead to lowered immunity in athletes performing frequent and physically demanding training regimens. Studies that have examined the effects of exercise on the extent of apoptosis in blood lymphocyte in humans are few, making it difficult to draw any definitive conclusions [8,9,10,11,12]
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