Abstract
ObjectiveTo investigate injury pattern during intense exercises in hot and humid environment particularly on liver in a rat exertional heat stroke model.MethodsWe randomly divided 30 rats into a control group (CG), a normal temperature (25±2°C, 60%±5% humidity) exercise group (NTEG) and a high temperature and high humidity (35±2°C, 80%±10% humidity) exercising group (HTEG), each comprising 10 animals. The NTEG and HTEG rats were forced to run in a treadmill for 1 hour maximum at 20 rpm. We analyzed liver cells of all three groups with JC-1 dye and flow cytometry for apoptosis rates in addition to liver tissue 8 - hydroxy deoxyguanosine (8 - OhdG) and blood serum IL–6, tumor necrosis factor alpha (TNF-α), alanine aminotransferase ALT, aspartate amino transferase (AST), serum creatinine (CREA), blood urea nitrogen (BUN), lactate dehydrogenase (LDH), creatine phosphate kinase (CK) concentrations.ResultCompared with NTEG rats, beside reduced exercise tolerance (60±5 vs. 15±3 minutes) (p = 0.002) the 8-OhdG liver tissue concentrations were significantly higher (p = 0.040) in the HTEG rats. The HTEG developed more organ tissue damage and cellular fragmentations of liver cells. In both exercise groups TNF-α and IL-6 serum concentrations were enhanced significantly (p<0.001) being highest in the HTEG animals. Serum ALT, AST, LDH, CREA, BUN and CK concentrations were significantly enhance in both exercise groups.ConclusionIn our exertional heat stroke rat model, we found tissue damage particularly in livers during exercises in hot and humid environment that was related to inflammation, oxidative stress and apoptosis.
Highlights
Heatstroke, which is a clinical emergency with high mortality and morbidity rates, can be divided into classic or non-exertional and exertional heat stroke (EHS)
Serum concentration of ALT, AST and lactate dehydrogenase (LDH), CREA, blood urea nitrogen (BUN) and creatine phosphate kinase (CK) were significantly different among all groups
BUN and CREA analyses revealed that the former was higher concentrated in sera of the NTEG (P,0.05) and the latter was higher concentrated in sera of the HTEG (P,0.05) (Table 1)
Summary
Heatstroke, which is a clinical emergency with high mortality and morbidity rates, can be divided into classic or non-exertional and exertional heat stroke (EHS) The former, is a clinical syndrome caused by exposure to high temperature and occurs mainly in children, elderly person and those with chronic diseases [1, 2], whereas the latter one, caused by excess heat production over heat loss during intensive exercises, occurs mainly in healthy young people such as athletes and soldiers [3]. Lipopolysaccharides (LPS) serum concentrations rose significantly up to 8.6 ng/ml in heat stroke patients, which was significantly higher than the conventional lethal concentration of 1 ng/ml [6] This has been confirmed in animal EHS experiments, in which the plasma concentration of lipopolysaccharides in an experimental group was 4.8 times (2.9–7 times) higher than in the control group and sepsis treatment could improve heat tolerance and the survival rates of heat exposed animals. We compared effects of exercises alone and in combination with heat on physiological and morphological changes in a rat model
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