Abstract
Multiple organ dysfunction syndrome can follow severe infection or injury, but its relationship to exercise is not well understood. Previous studies have observed that prolonged strenuous exercise can lead to transiently increased level and/or activity of markers for systemic inflammatory response and multiple organ damage. However, few studies have analyzed the pathogenesis of the inflammatory response and subsequent multi-organ injury in exhaustive exercise conditions. In this study, we established a rat model of repetitive bouts of exhaustive running (RBER) and investigated its effects on multiple organ damage. Rats were subjected to RBER in either uphill or downhill running modes daily for a period of 7 days. Morphologically, RBER causes tissue structural destruction and infiltration of inflammatory cells in the skeletal muscles and many visceral organs. RBER also causes sustained quantitative changes in leukocytes, erythrocytes, and platelets, and changes in the concentration of blood inflammatory factors. These inflammatory alterations are accompanied by increases in serum enzyme levels/activities which serve as functional markers of organ damage. In general, RBER in the downhill mode seemed to cause more damage evaluated by the above-mentioned measures than that produced in the uphill mode. A period of rest could recover some degree of damage, especially for organs such as the heart and kidneys with strong compensatory capacities. Together, our data suggest that, as a result of multi-organ interactions, RBER could cause a sustained inflammatory response for at least 24 h, resulting in tissue lesion and ultimately multiple organ dysfunction.
Highlights
Exercise is highly regarded as a lifestyle modification which can significantly benefit one’s health; lack of exercise has been shown to be a contributing factor in a variety of disease processes including metabolic syndrome, type 2 diabetes mellitus, heart disease/failure, vascular disease, and cognitive decline (Booth et al, 2012)
In addition to identifying morphologic alterations consistent with organ injury, damage caused by exhaustive exercise was evaluated by changes in the serum levels and activities of specific enzymes, such as creatine kinase (CK), ALT, CK-MB, and cardiac troponin I (cTnI)
The serum cTnI levels groups followed a similar pattern with levels significantly higher than those in the S group (P < 0.05, P < 0.05, and P < 0.01 respectively), with its activity in both exercise modes being decreased at 24 h after exercise (Figure 5B)
Summary
Exercise is highly regarded as a lifestyle modification which can significantly benefit one’s health; lack of exercise has been shown to be a contributing factor in a variety of disease processes including metabolic syndrome, type 2 diabetes mellitus, heart disease/failure, vascular disease, and cognitive decline (Booth et al, 2012). Adoption of an exercise regimen is often an early strategy for Exhaustive Exercise Causes Systemic Inflammation reversing or preventing disease progression This is perhaps most well documented in the setting of cardiovascular disease, where enhanced physical activity has been shown to be effective in primary prevention of coronary artery disease (CAD) as well as in the secondary reduction in progression and impact of the disease (Alves et al, 2016). Skeletal muscle damage induces an inflammatory response to the muscle necrosis that results in activation and migration of immune cells While this response is important for muscle regeneration following normal exercise, excessively damaging or exhaustive exercise induces a larger, systemic inflammatory response with release of a variety of cytokines and chemokines which can induce multi-organ effects (Yang and Hu, 2018). Beyond the direct damage to skeletal muscle, exhaustive exercise is known to induce systemic phenomena such as heat stress (American College of Sports Medicine et al, 2007; Heytens et al, 2017), visceral organ ischemia via splanchnic hypoperfusion (van Wijck et al, 2012), and alterations in blood cell counts and inflammatory mediator levels (Gannon et al, 1997; Weinstock et al, 1997; Ronsen et al, 2001)
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