The purpose of this study was to evaluate the effectiveness of two exercise modalities for improving glycosylated hemoglobin (HbA1c) and associated clinical outcomes in Polynesian adults diagnosed with type 2 diabetes and visceral obesity. Twenty-six adults were randomized to receive resistance training or aerobic training, 3×/week, for 16 weeks. Dependent variables collected before and after intervention included: diabetes markers including HbA1c, blood lipids, relevant cytokines (C-reactive protein, adiponectin), and anthropometric and hemodynamic indices. Eighteen participants (72% female; age: 49.3 ± 5.3 years; waist circumference: 128.7 ± 18.7 cm) completed the intervention and follow-up assessments. Body mass index in the whole cohort at baseline indicated Class III (morbid) obesity (43.8 ± 9.5 kg/m(2)). Compliance to training was 73 ± 19 and 67 ± 18% in the aerobic and resistance training groups, respectively. HbA1c remained elevated in both groups after training. Aerobic training reduced systolic and diastolic blood pressure and increased serum triglycerides (all P < 0.05). No other exercise-induced adaptations were noted within or between groups. Post hoc analysis using pooled data indicated that higher adherence to training (≥75% attendance, n = 8) significantly reduced waist circumference (P < 0.001) and tended to reduce body weight and fasting insulin (all P ≤ 0.11) versus lower adherence (<75% attendance, n = 10). In conclusion, this study did not demonstrate an improvement in HbA1c with exercise in morbidly obese Polynesian people. Future investigations involving exercise regimens that are more practicable and which involve greater frequency and duration of training may be required to induce significant and clinically meaningful adaptations in this unique diabetes population.

Epigenomic regulation of the transcriptome by DNA methylation and posttranscriptional gene silencing by miRNAs are potential environmental modulators of skeletal muscle plasticity to chronic exercise in healthy and diseased populations. We utilized transcriptome networks to connect exercise-induced differential methylation and miRNA with functional skeletal muscle plasticity. Biopsies of the vastus lateralis were collected from middle-aged Polynesian men and women with morbid obesity (44 kg/m(2) ± 10) and Type 2 diabetes before and following 16 wk of resistance (n = 9) or endurance training (n = 8). Longitudinal transcriptome, methylome, and microRNA (miRNA) responses were obtained via microarray, filtered by novel effect-size based false discovery rate probe selection preceding bioinformatic interrogation. Metabolic and microvascular transcriptome topology dominated the network landscape following endurance exercise. Lipid and glucose metabolism modules were connected to: microRNA (miR)-29a; promoter region hypomethylation of nuclear receptor factor (NRF1) and fatty acid transporter (SLC27A4), and hypermethylation of fatty acid synthase, and to exon hypomethylation of 6-phosphofructo-2-kinase and Ser/Thr protein kinase. Directional change in the endurance networks was validated by lower intramyocellular lipid, increased capillarity, GLUT4, hexokinase, and mitochondrial enzyme activity and proteome. Resistance training also lowered lipid and increased enzyme activity and caused GLUT4 promoter hypomethylation; however, training was inconsequential to GLUT4, capillarity, and metabolic transcriptome. miR-195 connected to negative regulation of vascular development. To conclude, integrated molecular network modelling revealed differential DNA methylation and miRNA expression changes occur in skeletal muscle in response to chronic exercise training that are most pronounced with endurance training and topographically associated with functional metabolic and microvascular plasticity relevant to diabetes rehabilitation.

Exercise, regardless of specific modality, can improve many aspects of QoL in this population. Robust trials are required to investigate factors mediating improvements in QoL, and create greater advocacy for exercise as a QoL intervention in this and other indigenous populations with T2DM.

Murphy RM, Goodman CA, McKenna MJ, Bennie J, Leikis M, Lamb GD. Calpain-3 is autolyzed and hence activated in human skeletal muscle 24 h following a single bout of eccentric exercise.