This study shows that high intensity training is required for induction of changes in cardiac substrate utilization and energetics, which may contribute to the superior effects of high compared with moderate intensity training in terms of increasing aerobic capacity.

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Hafstad AD, Khalid AM, How OJ, Larsen TS, Aasum E. Glucose and insulin improve cardiac efficiency and postischemic functional recovery in perfused hearts from type 2 diabetic (db/db) mice. Am J Physiol Endocrinol Metab 292: E1288 -E1294, 2007. First published January 9, 2007; doi:10.1152/ajpendo.00504.2006.-Hearts from type 2 diabetic (db/db) mice demonstrate altered substrate utilization with high rates of fatty acid oxidation, decreased functional recovery following ischemia, and reduced cardiac efficiency. Although db/db mice show overall insulin resistance in vivo, we recently reported that insulin induces a marked shift toward glucose oxidation in isolated perfused db/db hearts. We hypothesize that such a shift in metabolism should improve cardiac efficiency and consequently increase functional recovery following low-flow ischemia. Hearts from db/db and nondiabetic (db/ϩ) mice were perfused with 0.7 mM palmitate plus either 5 mM glucose (G), 5 mM glucose and 300 U/ml insulin (GI), or 33 mM glucose and 900 U/ml insulin (HGHI). Substrate oxidation and postischemic recovery were only moderately affected by GI and HGHI in db/ϩ hearts. In contrast, GI and particularly HGHI markedly increased glucose oxidation and improved postischemic functional recovery in db/db hearts. Cardiac efficiency was significantly improved in db/db, but not in db/ϩ hearts, in the presence of HGHI. In conclusion, insulin and glucose normalize cardiac metabolism, restore efficiency, and improve postischemic recovery in type 2 diabetic mouse hearts. These findings may in part explain the beneficial effect of glucose-insulin-potassium therapy in diabetic patients with cardiac complications. glucose; insulin; myocardial oxygen consumption; pressure-volume area TYPE 2 DIABETES IS THE MOST prevalent form (90%) of diabetes, resulting from a combination of insulin resistance and, eventually, a ␤-cell secretory defect. Increased cardiovascular disease is the most common complication of diabetes (10). Both clinical (4) and experimental (2, 35) studies have shown that type 2 diabetes and/or insulin resistance is associated with reduced myocardial tolerance to ischemia, which may explain the increased morbidity of ischemic heart disease in diabetes (10). Type 2 diabetes and/or insulin resistance are associated with increased cardiac fatty acid oxidation (FA ox ) and a concomitant decrease in glucose utilization (2,5,9,33). This change in substrate utilization has been considered a metabolic maladaptation that may contribute to the development of cardiac dysfunction and/or reduced ischemic tolerance in type 2 diabetes. In line with this notion, transgenic mice with increased cardiac fatty acid (FA) uptake/utilization show a diabetic phenotype with reduced ventricular function and/or reduced postischemic recovery (3, 6).There has been a long-standing interest in metabolic modulation as a means to improve functional recovery following myocardial ischemia, and administration of glucose and insulin, as part of glucose-insulin-potassium (GIK) treatment, ...

This study for the first time observed that in vivo administration of a synthetic PPARalpha ligand elevated FA oxidation, an effect that was also associated with decreased cardiac efficiency and reduced post-ischaemic functional recovery.

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