Resistance to Aerobic Exercise Training Causes Metabolic Dysfunction and Reveals Novel Exercise-Regulated Signaling Networks

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FIG. 2.
FIG. 2.

Whole-body metabolic dysfunction in LRT. Fasting blood samples were collected from sedentary and exercise-trained LRT/HRT. A: Plasma glucose and insulin values were used to calculate the homeostasis model of insulin resistance (HOMA-IR). B: Glucose tolerance was assessed in sedentary rats after an intraperitoneal (IP) injection of 2 g/kg glucose and the area under curve (AUC) was calculated. C: Insulin tolerance was assessed after IP injection of 0.75 units/kg insulin. Body weight (D) and gonadal fat pad weight (E) were measured in sedentary and exercise-trained LRT and HRT. Plasma triglycerides (F), TNF-α (G), and TGF-β1 (H) concentrations were analyzed by ELISA. I: Liver triglycerides were estimated from total liver glycerol content. *P < 0.05 for phenotype main effect; ^P < 0.05 for exercise main effect; °P < 0.05 for phenotype–exercise interaction by two-way ANOVA. P values obtained by Tukey post hoc testing are displayed. n = 10–12/group.

This Article

  1. Diabetes vol. 62 no. 8 2717-2727