L-Carnitine
L-Carnitine (levocarnitine) is an amino-acid derivative that shuttles long-chain fatty acids into the mitochondrion for beta-oxidation, studied for fat metabolism, energy and exercise recovery.
Total Price
฿950
For research & laboratory use only. Not for human consumption.
Half-Life
~17.4 hours (oral single dose); shorter for parenteral administration
Administration Route
Intramuscular or intravenous injection (ready-to-use 500 mg/ml solution)
Fatty-Acid Transport
Carries long-chain fatty acids into the mitochondrion for beta-oxidation
Energy Metabolism
Rate-limiting step of fat oxidation — links lipid supply to ATP production
Exercise Recovery
Studied for reduced muscle damage and soreness after exertion (Fielding 2018)
Effect Timeline
Fatty-acid transport into mitochondria for beta-oxidation on each dose
Fuel-selection and fat-oxidation endpoints assessed during exercise
Muscle total-carnitine content rises with sustained protocols (Wall 2011)
Recovery markers — muscle damage, soreness, oxidative stress — evaluated
Start — Acute
Fatty-acid transport into mitochondria for beta-oxidation on each dose
Weeks 1-4
Fuel-selection and fat-oxidation endpoints assessed during exercise
Weeks 4-12
Muscle total-carnitine content rises with sustained protocols (Wall 2011)
Post-exertion
Recovery markers — muscle damage, soreness, oxidative stress — evaluated
Mechanism of Action
Scientific Research
Why Researchers Study L-Carnitine
L-Carnitine (levocarnitine) is the biologically active form of carnitine, a small amino-acid derivative the body makes from lysine and methionine. Its central function is the carnitine shuttle — the only route by which long-chain fatty acids reach the mitochondrial matrix to be burned for energy. Because that shuttle is the rate-limiting step of fat oxidation, carnitine availability is a natural lever for research into fuel selection, energy metabolism and exercise recovery.
Mechanism of Action
Long-chain fatty acids cannot cross the inner mitochondrial membrane on their own. Carnitine palmitoyltransferase I (CPT1) attaches the fatty acyl group to carnitine, carnitine-acylcarnitine translocase (CACT) moves the resulting acylcarnitine across the membrane, and CPT2 hands the acyl group back to CoA inside the matrix for beta-oxidation. Stephens, Constantin-Teodosiu and Greenhaff (2007) showed that free-carnitine availability can become limiting to fat oxidation during higher-intensity submaximal exercise, establishing carnitine as an active regulator of muscle fuel selection rather than a passive carrier.
Beyond transport, carnitine buffers the mitochondrial acetyl-CoA/CoASH ratio by exporting excess acetyl groups as acetylcarnitine, freeing CoA for pyruvate dehydrogenase and the TCA cycle.
Research Context
Wall et al. (2011) demonstrated that muscle total-carnitine content can actually be raised in humans and that doing so shifts fuel use — sparing glycogen at low intensity and improving work output at high intensity. Separately, Fielding et al. (2018) reviewed evidence that carnitine supplementation attenuates markers of exercise-induced muscle damage, free-radical formation and soreness during recovery. Investigational interest therefore spans fat-oxidation models, exercise performance and post-exertion recovery.
Handling & Storage
Supplied as a sterile, ready-to-use 500 mg/ml aqueous solution in a 10 ml vial (5000 mg total) — no reconstitution or bacteriostatic water is required. Store refrigerated at 2–8 °C and protect from light; allow the vial to reach room temperature before drawing. A 500 mg research dose corresponds to 1 ml.
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