Abstract
Both positive and negative aspects of sport performance are currently considered. The aim of our study was to determine time- and intensity-dependent effects of a single exercise bout on redox and inflammatory status. The experiment was performed on 40 male Wistar rats subjected to treadmill running for 30 min with the speed of 18 m/min (M30) or 28 m/min (F30), or for 2 h with the speed of 18 m/min (M120). Immunoenzymatic and spectrophotometric methods were applied to assess the levels of pro-inflammatory and anti-inflammatory cytokines, chemokines, growth factors, the antioxidant barrier, redox status, oxidative damage products, nitrosative stress, and their relationships with plasma non-esterified fatty acids. Treadmill running caused a reduction in the content of monocyte chemoattractant protein-1 (MCP1) and nitric oxide (M30, M120, F30 groups) as well as macrophage inflammatory protein-1α (MIP-1α) and regulated on activation, normal T-cell expressed and secreted (RANTES) (M30, F30 groups). We also demonstrated an increase in catalase activity as well as higher levels of reduced glutathione, advanced oxidation protein products, lipid hydroperoxides, malondialdehyde (M30, M120, F30 groups), and advanced glycation end products (F30 group). The presented findings showed the activation of antioxidative defense in response to increased reactive oxygen species’ production after a single bout of exercise, but it did not prevent oxidative damage of macromolecules.
Highlights
Regular physical activity has been acknowledged a pivotal component of a healthy lifestyle and recommended in the management and treatment of atherosclerosis, insulin resistance, type 2 diabetes, cardiovascular diseases, cognitive disorders, and cancer [1]
In order to better define the immune response to a single exercise bout, rats were subjected to treadmill running for 30 min with the speed of 18 m/min (M30) or 28 m/min (F30) or for 2 h with the speed of 18 m/min (M120)
A tendency toward diminished IL-1β and IL-7 was noticed in M120 group (−31%, −31%, M120 vs. control, respectively, p > 0.05; Figure 1B,G)
Summary
Regular physical activity has been acknowledged a pivotal component of a healthy lifestyle and recommended in the management and treatment of atherosclerosis, insulin resistance, type 2 diabetes, cardiovascular diseases, cognitive disorders, and cancer [1]. Acute training triggers alterations in the cellular status of Ca2+ and superoxide anion (O2−), the ratio of oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD+/NADH), AMP/ATP ratio, as well as influences the release of numerous hormones and neurotransmitters [3]. Exercise is an initiator of signal-transmitting cascades involved in the regulation of glucose tolerance and cellular repair as well as the transcriptional modulation of redox and cytokine signaling [4]. Exercise-induced nuclear factor-like 2 (Nrf2) regulates nuclear factor κB (NF-κB)-dependent mechanisms that control downstream antioxidant and inflammatory responses [5,6]. The effects of training rely on reduced expression of Toll-like receptors (TLRs) on monocytes and macrophages that subsequently diminish pro-inflammatory cytokines’ production [1]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
