Oxidative Metabolism Efficiency Research Articles

Tilapia protein hydrolyzate improves growth performance, protein absorption and antioxidant status in Silver catfish ( Rhamdia quelen )

This study evaluated the substitution of fish meal with tilapia protein hydrolyzate (TPH) in diets for Silver catfish (Rhamdia quelen) by verifying the effects on growth, body composition, blood and biochemical parameters, and biomarkers of oxidative stress. Five isoproteic and isoenergetic diets (37% crude protein, 3,800 kcal/kg) were produced with different substitution levels of TPH (0%, 5%, 10%, 15% and 20%) for fishmeal. The hydrolyzate was obtained by enzymatic hydrolysis from carcasses of Nile tilapia (Oreochromis niloticus), which were exposed to swine pepsin enzyme at 36°C for four hours. The experimental design was completely randomised with five treatments and four replications. The inclusion of 20% TPH in diets for silver catfish increased the growth of Silver catfish juveniles. At levels above 5%, there was an increase in body protein deposition and the efficiency of oxidative metabolism.

Intensive aerobic training improves motor performances and oxidative metabolism efficiency in chronic polymyositis: A case report

We describe the case of a 64-year-old woman affected by chronic polymyositis with gait disturbance, fatty replacement and swelling of thigh muscles. She achieved significant clinical improvement after 5 weeks intensive aerobic training. In particular the patient improved in motor performance tests, showed an improvement in the efficiency of oxidative metabolism and quality of life. Furthermore, analysis of creatinephosphokinase levels showed a reduction of muscle damage susceptibility. In conclusion, a specific intensive exercise program can be safely used with beneficial effects on muscle function in patients with chronic polymyositis.

Nitric oxide and efficiency of the right heart

See article by Setty et al. (pages 431–436) in this issue . Several differences between right and left heart are known: the effect of cardiac contraction on coronary arterial inflow, autoregulation, and oxygen extraction. Setty et al. [1] show in their study the relationships between function and oxygen consumption of the right heart under control and ischemic conditions and the role of nitric oxide (NO). It turns out that these relationships also differ between left and right heart. Coronary flow depends on perfusion pressure and cardiac oxygen consumption [2]. NO decreases vascular smooth muscle tone and thus modulates flow. NO also promotes vascular growth and affects cardiac function in terms of metabolism, contractility, rhythmicity, and growth [3]. Early studies on ischemia and the role of NO mainly emphasized the vasodilatory effect on the coronary vasculature and thus a protective role of NO. At higher concentrations, NO has a cGMP-independent negative inotropic effect [4]. NO synthase inhibition impairs the efficiency of oxidative metabolism and cardiac function, while during moderate ischemia, NO synthase appears not to be involved in cardiac metabolism … *Tel.: +31 20 4448111; fax: +31 20 4448255. Email address: n.westerhof{at}vumc.nl

Effect of NO synthase inhibition on myocardial metabolism during moderate ischemia.

Nitric oxide (NO) is involved in the control of myocardial metabolism. In normoperfused myocardium, NO synthase inhibition shifts myocardial metabolism from free fatty acid (FFA) toward carbohydrate utilization. Ischemic myocardium is characterized by a similar shift toward preferential carbohydrate utilization, although NO synthesis is increased. The importance of NO for myocardial metabolism during ischemia has not been analyzed in detail. We therefore assessed the influence of NO synthase inhibition with N(G)-nitro-l-arginine (l-NNA) on myocardial metabolism during moderate ischemia in anesthetized pigs. In control animals, the increase in left ventricular pressure with l-NNA was mimicked by aortic constriction. Before ischemia, l-NNA decreased myocardial FFA consumption (MV(FFA); P < 0.05), while consumption of carbohydrate and O(2) (MVo(2)) remained constant. ATP equivalents [calculated with the assumption of complete oxidative substrate decomposition (ATP(eq))] decreased with l-NNA (P < 0.05), associated with a decrease of regional myocardial function (P < 0.05). In contrast, aortic constriction had no effect on MV(FFA), while MVo(2) increased (P < 0.05) and ATP(eq) and regional myocardial function remained constant. During ischemia, alterations in myocardial metabolism were similar in control and l-NNA-treated animals: MV(FFA) decreased (P < 0.05) and net lactate consumption was reversed to net lactate production (P < 0.05). Regional myocardial function was decreased (P < 0.05), although more markedly in animals receiving l-NNA (P < 0.05). We conclude that the efficiency of oxidative metabolism was impaired by l-NNA per se, paralleled by impaired regional myocardial function. During ischemia, l-NNA had no effect on myocardial substrate consumption, indicating that NO synthases were no longer effectively involved in the control of myocardial metabolism.