TY - JOUR
AU - Willis, Monte
AB - Introduction The effects of exercise on the heart and its resistance to disease are well-documented. Recent studies have identified that exercise-induced resistance to arrhythmia is due to the preservation of mitochondrial membrane potential. Objectives To identify novel metabolic changes that occur parallel to these mitochondrial alterations, we performed non- targeted metabolomics analysis on hearts from sedentary and exercise-trained rats challenged with isolated heart ischemia– reperfusion injury (I/R). Methods Eight-week old Sprague–Dawley rats were treadmill trained 5 days/week for 6 weeks (exercise duration and intensity progressively increased to 1 h at 30 m/min up a 10.5% incline, 75–80% V O ). The recovery of pre-ischemic 2max function for sedentary rat hearts was 28.8 ± 5.4% (N = 12) compared to exercise trained hearts, which recovered 51.9% ± 5.7 (N = 14) (p < 0.001). Results Non-targeted GC–MS metabolomics analysis of (1) sedentary rat hearts; (2) exercise-trained rat hearts; (3) sedentary rat hearts challenged with global ischemia–reperfusion (I/R) injury; and (4) exercise-trained rat hearts challenged with global I/R (10/group) revealed 15 statistically significant metabolites between groups by ANOVA using Metaboanalyst (p < 0.001). Enrichment analysis of these metabolites for pathway-associated metabolic sets indicated a > 10-fold enrichment for ammo- nia recycling and protein 
TI - Untargeted metabolomics analysis of ischemia–reperfusion-injured hearts ex vivo from sedentary and exercise-trained rats
JF - Metabolomics
DO - 10.1007/s11306-017-1303-y
DA - 2017-12-04
UR - https://www.deepdyve.com/lp/springer-journals/untargeted-metabolomics-analysis-of-ischemia-reperfusion-injured-nmw2OyHmkQ
SP - 1
EP - 15
VL - 14
IS - 1
DP - DeepDyve
ER -