Saeid Ashtiyani , Mostafa Moosavi , Saman Hosseinkhani , Mehdi Shirazi ,
Volume 67, Issue 10 (1-2010)
Abstract
Background: Ureteral obstruction has been shown to induce renal oxidative stress, suppressed energy metabolism and defected acid excretion. This study was aimed to examine the improving effects of L-carnitine, a facilitating cofactor for mitochondrial oxidation of fatty-acids as well as a scavenger of free-radicals, and -tocopherol as the most potent antioxidant on these renal disorders at early hours following release of unilateral ureteral obstruction.
Methods: The left ureter was ligated in 60 anaesthetised rats, L-carnitine, -tocopherol, or their vehicles (normal saline and olive oil, respectively) were injected (i.p.) in four groups. Each rat was re-anesthetized and cannulated, and ureteral legation was released at exactly 24h after UUO-induction. A 30-min clearance period performed to separately collect urine from both kidneys. The collected urine and arterial blood samples were given to pH-gas analyzer and autoanalyzer, and malondialdehyde (MDA), ATP and ADP levels were assessed in preserved kidneys. There were also sham and control groups (n=8-10 in each).
Results: In the post-obstructed kidney of vehicle-treated groups with respect to the equivalent kidney of sham group, there were increases in MDA (p<0.001), ADP (p<0.01), urinary pH (p<0.001), absolute (p<0.05) and fractional bicarbonate excretions (p<0.01), but decreases in ATP, ATP/ADP (both p<0.001), and urinary PCO2 (p<0.01). -tocopherol could normalize MDA level but did not affect the altered amounts of energy metabolic indices and acid-base excretions, while L-carnitine improved all of them except of decreased urinary PCO2.
Conclusions: Increased bicarbonate-excretion in post-obstructed kidney is due to defected acid-secretion at collecting duct, which is not related to ureteral obstruction-induced renal oxidative stress and suppressed energy metabolism.
Arazi H, Rahmaninia F, Azali K, Mehrtash M,
Volume 71, Issue 1 (4-2013)
Abstract
Background: Probably L-Carnitine can induce increasing of Pyruvate dehydrogenase activity, decreasing of lactic acid production and performance improvements due to the reinforcement of long chain fatty acid oxidation and stabilize of Coenzyme A (CoASH) to free Coenzyme A (COA). Based on this, the aim of this study was to investigate the effect of acute L-Carnitine supplementation on blood lactate, glucose, VO2max and anaerobic power in trained men.
Methods: Sixteen trained men (aged 19-23) volunteers from University of Guilan, facul-ty of Physical Education and Sport Sciences participated as subjects in this investiga-tion. Subjects divided to aerobic (A) and anaerobic (An) group randomly. In a double blind design, subjects participated in two separated tests by one week. Subjects ingested 3 grams of L-Carnitine supplementation or placebo (maltodextrin) 90 minute before aerobic and anaerobic exercise. For aerobic activity used shuttle run 20 meter and for anaerobic activity used RAST test. Blood samples were collected 5 minute prior at rest and 4 minute post tests. Participants were asked in the morning to obtain fasting blood samples and perform tests. A t-test was used to detect differences between supplementa-tion and placebo groups in each exercise.
Results: L-Carnitine group ((A) 141.25±20.62 and (An) 145.38±55.47) significantly had lower lactate concentration than placebo ((A) 151.00±20.85 and (An) 152.50±28.59) after tests (P≤0.05). L-Carnitine group ((A) 136.00±19.74 and (An) 115.50±13.64) had significa-ntly higher blood glucose compared to placebo ((A) 121.62±15.65 and (An) 110.12±12.63) too (P≤0.05). Also, VO2max, mean and maximum anaerobic power in L-Carnitine group were significantly more than ones in placebo (P<0.05).
Conclusion: These findings indicate that acute oral supplementation of L-Carnitine can induce fatigue decreasing and improvement of aerobic and anaerobic performance.
