Effect of Chronic Caffeine Consumption on Cardiac Tissue Metabolism in the Rabbit

E W Nabofa, A R A Alada
2018 Nigerian Journal of Physiological Sciences  
Previous studies on the ability of caffeine to enhance endurance and boost performance have focused on theenergy substrates that are utilized by the skeletal muscle and the brain but nothing of such has been reported on cardiactissue. This study was designed to investigate the effect of caffeine on cardiac tissue metabolism in the rabbit. The study wascarried out on adult male New Zealand rabbits divided into 3 groups (n=5). Group I rabbits served as control and were given0.5ml/Kg of normal
more » ... ml/Kg of normal saline while group II and III rabbits were administered with 2mg/Kg and 6mg/kg of caffeine respectivelyfor 28 days. Blood samples were collected by retro orbital puncture for biochemical analysis. Animals were sacrificed bycervical dislocation and cardiac tissue biopsies were collected for biochemical and immunohistochemical analysis. Cardiactissue glycogen concentration was determined by anthrone reagent method. Cardiac tissue CPT 1 activity and cAMPconcentration were determined by immunohistochemistry and colorimetry techniques respectively, with assay kits obtainedfrom Biovision Inc. The results showed that Caffeine at 2 and 6 mg/kg significantly inhibited MPO activity from 0.72±0.05to 0.164±0.045 and 0.46±0.12 U/L respectively (p<0.05). Caffeine at 2mg/kg had no effect on serum nitric oxide but at6mg/Kg, it significantly increased serum nitric oxide form 28.01±6.53 to 45.25±3.88µM of nitrite (p<0.05). Also, Caffeineat 2 and 6mg/kg increased cardiac tissue glycogen from 15.62±0.73 to 40.69±6.35 and 38.82±6.91mg/100g respectively andcarnitine palmytol transferase 1 activity from 18.3 to 20 and 25.2% respectively. In conclusion, the study showed that caffeineconsumption increased CPT 1 activity suggesting increased utilization of free fatty acids for energy metabolism and sparingof cardiac tissue glycogen by mechanism(s) which probably involved blockade of A1 adenosine receptors and cAMPsignaling pathway.
pmid:30091728 fatcat:puipzofuwjh7tbjnofxwfsud4q