Dose-response analysis showed L-carnitine supplementation did change BMI and weight significantly based on the dose used in a nonlinear fashion, with higher doses increases the trend found for reduced BMI and weight . There were significant non-linear associations between trial duration and BMI , but not for any other outcomes.

There was a significant improvement in endurance exercise, as indicated by an increase in run to exhaustion following L-carnitine supplementation under normobaric normoxia (36%–39%) and hypobaric hypoxia (50%). L-carnitine supplementation improved exercise endurance in rats exposed to normobaric normoxic and hypobaric hypoxic conditions.

The effects of various concentrations of lcarnitine (15, 30 and 45 Ag/mL) on lipid peroxidation of linoleic acid emulsion are shown in Fig. 1 and was found to be 94.6%, 95.4% and 97.1%, respectively, and their activities are greater than that of a-tocopherol (88.8%) and trolox (86.2%) at the 45 Ag/mL concentration.

The extent of necrotic area in patients with a confirmed  diagnosis of acute myocardial infarction was evaluated. Within-group analysis showed that the increase in the sum of the pre- and post-treatment resting scores was highest in the area of the left anterior descending artery (70, p < 0.032) followed by the right coronary artery segment (45, p < 0.018) in the L-carnitine group. An increased score indicates an increase in viability. The data suggest that L-carnitine may have a significant role in the treatment of patients after myocardial infarction.

L-carnitine and BCAA promote lipolysis and glycogen synthesis via the replenishment of Acyl-CoA and a reactivation of the TCA cycle. L-carnitine and BCAA can protect mitochondrial integrity via subsequent recovery of CLs, as well as increase ATP production thus attenuating lipid peroxide production resulting in the overall protection of the cirrhotic liver.