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L-carnitine and muscle fatigue

L-carnitine and muscle fatigue

Sawicka Wnd author publications. Echocardiography fatigke also used to determine the annd ventricular ejection Omega- for diabetes LVEFan objective measure of the heart's pumping ability. Johns Hopkins: The Harriet Lane Handbook. Dig Liver Dis. Mitochondrial membrane damage during aging process in rat heart: potential efficacy of L-carnitine and DL alpha lipoic acid. The ubiquitin-proteasome system and skeletal muscle wasting.

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L-carnitine and muscle fatigue -

Six months of LC supplementation augmented fat free mass and reduced total body fat mass in centenarians [ 14 ]. Such effect was not observed in elder women age range 65—70 y. after a similar period of supplementation [ 15 ]. The effectiveness of LC supplementation may result from the age-wise distribution of sarcopenia.

The prevalence of sarcopenia increased steeply with age, reaching Muscle damage may occur during exercise, especially eccentric exercise. In the clearance of damaged tissues assist free radicals produced by neutrophils. Therefore, among other responses to exercise, neutrophils are released into the circulation.

While neutrophil-derived reactive oxygen species ROS play an important role in breaking down damaged fragments of the muscle tissue, ROS produced in excess may also contribute to oxidative stress for review see [ 47 , 48 ]. Based on the assumption that LC may provide cell membranes protection against oxidative stress [ 49 ], it has been hypothesized that LC supplementation would mitigate exercise-induced muscle damage and improve post-exercise recovery.

Since plasma LC elevates following 2 weeks of supplementation [ 21 , 22 ], short protocols of supplementation may be considered as effective in attenuating post-exercise muscle soreness. It has been shown, through magnetic resonance imaging technique that muscle disruption after strenuous exercise was reduced by LC supplementation [ 37 , 51 ].

This effect was accompanied by a significant reduction in released cytosolic proteins such as myoglobin and creatine kinase [ 50 , 52 , 53 ] as well as attenuation in plasma marker of oxidative stress - malondialdehyde [ 51 , 53 , 54 ]. Furthermore, 9 weeks of LC supplementation in conjunction with resistance training revealed a significant increase of circulating total antioxidant capacity and glutathione peroxidase activity and decrease in malondialdehyde concentration [ 43 ].

In Rebouche et al. Similar observations were noted in later human studies [ 56 , 57 ], with the peak serum TMAO observed within hours following oral administration of the tracer [ 56 ].

Prolonged LC treatment elevates fasting plasma TMAO [ 16 , 17 , 18 , 58 , 59 ]. Three months of oral LC supplementation in healthy aged women induced ten-fold increase of fasting plasma TMAO, and this level remained elevated for the further 3 months of supplementation [ 16 ].

Four months after cessation of LC supplementation, plasma TMAO reached a pre-supplementation concentration, which was stable for the following 8 months [ 60 ]. In Wang et al. Since diets high in red meat have been strongly related to heart disease and mortality [ 62 ], LC has been proposed as the red meat nutrient responsible for atherosclerosis promotion [ 8 ].

As a potential link between red meat consumption and the increasing risk of cardiovascular disease, TMAO has been indicated [ 8 ]. Numerous later studies have shown the association between increased plasma TMAO levels with a higher risk of cardiovascular events [ 63 , 64 , 65 , 66 ]. The recent meta-analyses indicated that in patients with high TMAO plasma level, the incidence of major adverse cardiovascular events was significantly higher compared with patients with low TMAO levels [ 67 ], and that all-cause mortality increased by 7.

The rise of plasma TMAO was on average three-fold compared with white meat and non-meat diets [ 70 ]. Conversely, habitual consumption of red, processed or white meat did not affect plasma TMAO in German adult population [ 71 ]. Similarly, a minor increase in plasma TMAO was observed following red meat and processed meat consumption in European multi-center study [ 72 ].

In the previous century, the underlined function of TMAO was the stabilization of proteins against various environmental stress factors, including high hydrostatic pressure [ 73 ]. TMAO was shown as widely distributed in sea animals [ 74 ], with concentration in the tissue increasing proportionally to the depth of the fishes natural environment [ 75 ].

Consequently, fish and seafood nutritional intake has a great impact on TMAO level in the human body [ 76 ], significantly elevating also plasma TMAO concentration [ 72 ].

Therefore, link between plasma TMAO and the risk of cardiovascular disease [ 8 ] seems like a paradox, since more fish in the diet reduces this risk [ 77 ]. Not only dietary modification may affect TMAO plasma levels. Due to TMAO excretion in urine [ 56 , 57 ], in chronic renal disease patients, TMAO elimination from the body fails, causing elevation of its plasma concentration [ 78 ].

Therefore, higher plasma TMAO in humans was suggested as a marker of kidney damage [ 79 ]. It is worthy to note that cardiovascular disease and kidney disease are closely interrelated [ 80 ] and diminished renal function is strongly associated with morbidity and mortality in heart failure patients [ 81 ].

Moreover, decreased TMAO urine excretion is associated with high salt dietary intake, increasing plasma TMAO concentration [ 82 ]. The relation between TMAO and chronic disease can be ambiguous, involving kidney function [ 79 ], disturbed gut-blood barrier [ 83 ], or flavin-containing monooxygenase 3 genotype [ 84 ].

Thus, whether TMAO is an atherogenic factor responsible for the development and progression of cardiovascular disease, or simply a marker of an underlined pathology, remains unclear [ 85 ].

Carnitine preparations administered orally can occasionally cause heart-burn or dyspepsia [ 86 ]. It is worthy to mention that Bakalov et al. The strength of this review is a focus on the period of LC treatment, very important aspect often missed in many articles dealing with this supplement.

This limitation is also magnified by the varied design of the studies available including different supplementation protocols and outcome measures. There is also a high degree of heterogeneity among participants of the analyzed studies.

Therefore, the results should be taken with caution, and more research is required before definitive recommendations. Lasting for several years opinion that LC supplementation does not change metabolism, especially exercise metabolism, is based mostly on short-term supplementation protocols.

Nevertheless, LC is still used by elite [ 9 ] and sub-elite [ 10 ] athletes. Recent studies suggest that LC supplementation may elevate muscle TC content; therefore, modify muscle fuel metabolism and performance during the exercise. Due to insulin-mediated LC transport to the muscle, oral administration regimen should be combined with CHO.

Because of LC poor bioavailability, it is likely that the supplementation protocol would take at least 3 months. Shorter period of supplementation may be effective in prevention of exercise-induced muscle damage, but not metabolic changes.

On the other hand, it is also clear that prolonged LC supplementation elevates fasting plasma TMAO [ 16 , 17 , 18 , 58 , 59 ], compound supposed to be pro-atherogenic [ 61 ]. Therefore, additional studies focusing on long-term supplementation and its longitudinal effect on the TMAO metabolism and cardiovascular system are needed.

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Marine fish may be biochemically constrained from inhabiting the deepest ocean depths. Online ISSN : Print ISSN : ISSN-L : Journal home Advance online publication All issues About the journal.

Tomohiro Sugino Research and Development Division, Soiken Inc. Sayaka Aoyagi Research and Development Division, Soiken Inc. Department of Biomarker and Molecular Biophysics, Osaka City University Graduate School of Medicine Tomoko Shirai Soiken Holdings Inc.

Yoshitaka Kajimoto Research and Development Division, Soiken Inc. Osami Kajimoto Soiken Holdings Inc. Corresponding author. Keywords: physical fatigue , citric acid , L -carnitine , chromogranin A , cycle ergometer. JOURNAL FREE ACCESS. Published: Received: June 04, Available on J-STAGE: October 30, Accepted: June 15, Advance online publication: - Revised: -.

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Copyright: andd L-carnitine and muscle fatigue et al. This is an open Skill Refinement Sessions article distributed under the terms of Creative Commons Attribution L-carniine. Fatigue is a common symptom in L-carnitine and muscle fatigue patients. Cancer patients state that Fatigie is one of the most distressing symptoms associated with cancer, and the general condition during cancer treatment is difficult to manage with medications 1. The pathophysiology of fatigue in cancer patients is multifactorial. Suggested mechanisms include an imbalance in energy metabolism due to tumor growth, infection, fever, or surgery, malnutrition caused by anorexia, nausea, or vomiting, and an increase in the abnormal production of substances that impair metabolic homeostasis, such as cytokines and proteolysis-inducing factors 2. L-carnitine and muscle fatigue

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