GEN-TEC NUTRACEUTICALS source, blend and package 100% pure pharmaceutical grade ACETYL L-CARNITINE powder. ACETYL L-CARNITINE supplementation is ideal for individuals with a goal of improving mental focus while reducing subcutaneous body fat levels.
SUGGESTED USE: Mix 2g (1/2 tsp) of ACETYL L-CARNITINE in 150mL water and consume 20 minutes before aerobic or anaerobic exercise. Store in a cool, dry, dark place.
INGREDIENTS: 100% Pharmaceutical grade ACETYL L-CARNITINE, Silicon Dioxide (2%).
May contain traces of milk, soybeans, cereals containing gluten, tree nuts, sesame seeds and their products.
DISCLAIMER: Formulated Supplementary Sports Food. This product is not a sole source of nutrition and should be consumed in conjunction with a nutritious diet and an appropriate physical training or exercise program. Not suitable for children under 15 years of age or pregnant women. Should only be used under medical or dietetic supervision.
Made in Australia from local and imported ingredients.
Fat metabolism, cognitive functions (ie reflex’s and co-ordination), vigilance,
fatloss, mind/muscle connection.
Acetyl L-Carnitine (ALC) plays a critical role in not only lipid and energy
metabolism but also within nerve cells of the central nervous system (CNS)
(Rebouche, 2012). Research shows that in the periphery skeletal muscle sites,
ALC is a co-factor for beta-oxidation (metabolism of fatty acids)whereby it
mops up available fats to be sent to the muscle cells for metabolism (Stephens
et al., 2007, Kido et al., 2001). More specifically it translocates long chain fatty
acids (LCFA) to the mitochondrial matrix where it can undergo beta –oxidation
and enter the Kreb cycle for fat derived ATP re-synthesis (Stephens et al.,
2007). This involvement in fat metabolism is also one way by which ALC assists
with energy levels during exercise.
It is important to understand that the mitochondria is an organelle within a
cell that functions to produce energy by ATP synthesis from primarily fats
and carbohydrates (Stephens et al., 2007). If the mitochondria is a factory to
burn fuel then ALC is the employee who transports that fuel into the factory
to be burned. If there is insufficient ALC (employees) then naturally there is a
reduced mitochondrial (factory) use of fats (fuel). In addition, ALC can reduce
the amount of muscle damage experienced by intense exercise by acting as
“mitochondrial antioxidant”, which if revisiting the previous factory analogy,
within every factory there must be some level of maintenance to ensure
the longevity and proper functioning of machinery, so ALC is like that ‘oil’ or
‘maintenance check’ to ensure a healthy and functioning environment for fats
(fuel) to be burned (Stephens et al., 2007).
Moreover, ALC crosses the blood brain barrier which means it exhibits activity
in not only the muscle cells for energy but also in the brain and nerve cells
(Kido et al., 2001). Over recent years research has revealed that ALC acts as a
neuro-protective agent against alcohol related nerve cell damage and glucose
transportation to the brain (Abdul Muneer et al., 2011). Furthermore, evidence
has indicated possible clinical benefit for ALC use in neurodegenerative
conditions such as Alzheimer’s disease, diabetic neuropathy and other
conditions resulting in nerve damage (Malaguarnera, 2012, Ruggenenti et
al., 2009). It appears that ALC assists with the activity of cholinergic neurons,
membrane stabilization and mitochondrial function (Palacios et al., 2011). To
further understand how, we must understand that the brain and nerve cells
also require adequate energy supply, so they too poses mitochondria within the
nerve cells (Palacios et al., 2011).
The difference between muscle cell mitochondria mentioned above and
neuronal cell mitochondria is that neuronal mitochondria are more vulnerable
to oxidative stress (wear and tear by producing energy), therefore a strong
mitochondrial antioxidant like ALC can provide ongoing maintenance checks to
all nerve cells (Palacios et al., 2011, Rebouche, 2012).
In addition to ALC ‘s use for increased metabolism of fats in the mitochondria
and its neuro-protective properties in a range of clinical settings, it is also
shown to assist with reproductive function and glucose tolerance (Showell et
al., 1996). Studies which have explored ALC’s use in patients with low sperm
count concluded that although ALC does not conclusively increase the quantity
of sperm, it does improve sperm motility and quality (Busetto et al., 2012). In
women who suffer from a neuroendocrine impairment, which adversely affects
their reproductive axis, ALC is reported to significantly improve Luteinizing
hormone (LH) profiles and stress induced abnormalities caused by the
condition resulting in improved well-being and energy levels (Genazzani et al.,
2011). Lastly in patients with abnormal glucose tolerance, ALC significantly
improved insulin sensitivity and glucose functioning with the cessation of ALC
resulting in immediate reversal of acquired benefits from ALC (Ruggenenti et
al., 2010, Ruggenenti et al., 2009). Once patients went back on ALC their glucose
tolerance improved again, thus demonstrating a multi-factorial benefit from
ALC in the body.
ABDUL MUNEER, P. M., ALIKUNJU, S., SZLACHETKA, A. M. & HAORAH, J. 2011. Inhibitory effects of
alcohol on glucose transport across the blood-brain barrier leads to neurodegeneration: preventive
role of acetyl-L: -carnitine. Psychopharmacology, 214, 707-18.
BUSETTO, G. M., KOVERECH, A., MESSANO, M., ANTONINI, G., DE BERARDINIS, E. & GENTILE, V.
2012. Prospective open-label study on the efficacy and tolerability of a combination of nutritional
supplements in primary infertile patients with idiopathic astenoteratozoospermia. Archivio Italiano
di Urologia, Andrologia, 84, 137-40.
GENAZZANI, A. D., LANZONI, C., RICCHIERI, F., SANTAGNI, S., RATTIGHIERI, E., CHIERCHIA, E.,
MONTELEONE, P. & JASONNI, V. M. 2011. Acetyl-L-carnitine (ALC) administration positively affects
reproductive axis in hypogonadotropic women with functional hypothalamic amenorrhea. Journal
of Endocrinological Investigation, 34, 287-91.
KIDO, Y., TAMAI, I., OHNARI, A., SAI, Y., KAGAMI, T., NEZU, J.-I., NIKAIDO, H., HASHIMOTO,
N., ASANO, M. & TSUJI, A. 2001. Functional relevance of carnitine transporter OCTN2 to brain
distribution of l-carnitine and acetyl-l-carnitine across the blood–brain barrier. Journal of
Neurochemistry, 79, 959-969.
MALAGUARNERA, M. 2012. Carnitine derivatives: clinical usefulness. Current Opinion in
Gastroenterology, 28, 166-76.
PALACIOS, H. H., YENDLURI, B. B., PARVATHANENI, K., SHADLINSKI, V. B., OBRENOVICH, M. E.,
LESZEK, J., GOKHMAN, D., GASIOROWSKI, K., BRAGIN, V. & ALIEV, G. 2011. Mitochondrion-specific
antioxidants as drug treatments for Alzheimer disease. CNS & Neurological Disorders Drug
Targets, 10, 149-62.
REBOUCHE, C. J. 2012. L-Carnitine. Present Knowledge in Nutrition. Wiley-Blackwell.
RUGGENENTI, P., CATTANEO, D., LORIGA, G., LEDDA, F., MOTTERLINI, N., GHERARDI, G., ORISIO,
S. & REMUZZI, G. 2009. Ameliorating hypertension and insulin resistance in subjects at increased
cardiovascular risk: effects of acetyl-L-carnitine therapy. Hypertension, 54, 567-74.
RUGGENENTI, P., VAN DER MEER, I. M. & REMUZZI, G. 2010. Oral acetyl-L-carnitine therapy and
insulin resistance. Hypertension, 55, e26.
SHOWELL, M. G., BROWN, J., YAZDANI, A., STANKIEWICZ, M. T. & HART, R. J. 1996. Antioxidants
for male subfertility. Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd.
STEPHENS, F. B., CONSTANTIN-TEODOSIU, D. & GREENHAFF, P. L. 2007. New insights concerning
the role of carnitine in the regulation of fuel metabolism in skeletal muscle. The Journal of
Physiology, 581, 431-444.
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