Carnitine requirement of vascular endothelial and smooth muscle cells in imminent ischemia

Hülsmann, W.C.; Dubelaar, Marie-Louise

doi:10.1007/978-1-4615-3514-0_18

Cited by 11 publications

(14 citation statements)

References 28 publications

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“…Carnitine has been shown to stimulate fatty acid oxidation in vascular endothelial cells (14). Ischemia in endothelial cells results in release of carnitine, increased oxidative stress, and compromised blood flow regulation, which can be overcome by intravascular carnitine administration (5,15). Our working hypothesis was that carnitine supplementation could protect against carnitine deficiency in vascular endothelial cells and thereby improve blood flow regulation and delivery of oxygen to muscle tissue during and after exercise (18).…”

mentioning

confidence: 99%

l-Carnitinel-tartrate supplementation favorably affects markers of recovery from exercise stress

Volek

Kraemer

Rubin

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

129

109

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nor. L-Carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress. Am J Physiol Endocrinol Metab 282: E474-E482, 2002; 10.1152/ajpendo. 00277.2001.-We examined the influence of L-carnitine L-tartrate (LCLT) on markers of purine catabolism, free radical formation, and muscle tissue disruption after squat exercise. With the use of a balanced, crossover design (1 wk washout), 10 resistance-trained men consumed a placebo or LCLT supplement (2 g L-carnitine/day) for 3 wk before obtaining blood samples on six consecutive days (D1 to D6). Blood was also sampled before and after a squat protocol (5 sets, 15-20 repetitions) on D2. Muscle tissue disruption at the midthigh was assessed using magnetic resonance imaging (MRI) before exercise and on D3 and D6. Exercise-induced increases in plasma markers of purine catabolism (hypoxanthine, xanthine oxidase, and serum uric acid) and circulating cytosolic proteins (myoglobin, fatty acid-binding protein, and creatine kinase) were significantly (P Յ 0.05) attenuated by LCLT. Exerciseinduced increases in plasma malondialdehyde returned to resting values sooner during LCLT compared with placebo. The amount of muscle disruption from MRI scans during LCLT was 41-45% of the placebo area. These data indicate that LCLT supplementation is effective in assisting recovery from high-repetition squat exercise. hypoxia; ergogenic aid; resistance exercise; muscle damage GIVEN THE OBLIGATORY ROLE of the carnitine system in transporting long-chain fatty acids to the mitochondrial matrix for oxidation (16), it is not surprising that there has been a great deal of research examining the potential of carnitine supplementation to enhance lipid oxidation, spare muscle glycogen, and improve exercise performance (3, 10). Despite the theoretical basis for usage of carnitine, the scientific literature has provided few "metabolic" benefits of carnitine supplementation for skeletal muscle during exercise, perhaps because of the difficulty of increasing carnitine concentrations in muscle with oral supplementation (2, 25). Using a different approach to study the effects of carnitine supplementation, Giamberardino et al. (7) demonstrated that eccentric exercise-induced delayed-onset muscle soreness and accumulation of creatine kinase during recovery was attenuated in subjects that supplemented with L-carnitine (3 g/day for 3 wk). Their findings indicate that carnitine supplementation may have a favorable effect on recovery from exercise. The study by Giamberardino et al., however, provided no data regarding potential mechanisms to explain the beneficial effect of carnitine supplementation.This study was designed to further examine the role of carnitine supplementation in acute exercise stress and its influence on biochemical events during recovery. Carnitine has been shown to stimulate fatty acid oxidation in vascular endothelial cells (14). Ischemia in endothelial cells results in release of carnitine, increased oxidative stress, and compromised blood flow regulation, wh...

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mentioning

confidence: 99%

l-Carnitinel-tartrate supplementation favorably affects markers of recovery from exercise stress

Volek

Kraemer

Rubin

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

129

109

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“…Three studies reported an increase in VO 2max [21,44,50] and two demonstrated no effect of carnitine [48,51]. The study of Vecchiet et al [50] demonstrated that a single dose of carnitine an hour before exercise increased VO 2max .…”

Section: Methodologic Considerationsmentioning

confidence: 95%

“…The mechanism for these effects of carnitine and its derivatives are unclear and may be indirect. For example, carnitine may modify endothelial cell function [44], leading to changes in vascular dynamics. Again, the relevance of these observations to human physiology or exercise performance are unclear.…”

Section: Carnitine and Exercisementioning

confidence: 99%

The Role of Carnitine and Carnitine Supplementation During Exercise in Man and in Individuals with Special Needs

Brass

Hiatt

1998

Journal of the American College of Nutrition

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Carnitine is critical for normal skeletal muscle bioenergetics. Carnitine has a dual role as it is required for long-chain fatty acid oxidation, and also shuttles accumulated acyl groups out of the mitochondria. Muscle requires optimization of both of these metabolic processes during peak exercise performance. Theoretically, carnitine availability may become limiting for either fatty acid oxidation or the removal of acyl-CoAs during exercise. Despite the theoretical basis for carnitine supplementation in otherwise healthy persons to improve exercise performance, clinical data have not demonstrated consistent benefits of carnitine administration. Additionally, most of the anticipated metabolic effects of carnitine supplementation have not been observed in healthy persons. The failure to demonstrate clinical efficacy of carnitine may reflect the complex pharmacokinetics and pharmacodynamics of carnitine supplementation, the challenges of clinical trial design for performance endpoints, or the adequacy of endogenous carnitine content to meet even extreme metabolic demands in the healthy state. In patients with end stage renal disease there is evidence of impaired cellular metabolism, the accumulation of metabolic intermediates and increased carnitine demands to support acylcarnitine production. Years of nutritional changes and dialysis therapy may also lower skeletal muscle carnitine content in these patients. Preliminary data have demonstrated beneficial effects of carnitine supplementation to improve muscle function and exercise capacity in these patients. Peripheral arterial disease (PAD) is also associated with altered muscle metabolic function and endogenous acylcarnitine accumulation. Therapy with either carnitine or propionylcarnitine has been shown to increase claudication-limited exercise capacity in patients with PAD. Further clinical research is needed to define the optimal use of carnitine and acylcarnitines as therapeutic modalities to improve exercise performance in disease states, and any potential benefit in healthy individuals.

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“…Previous publications of studies have discussed the positive effects of positive L -carnitine therapy and have stated that these effects could be brought about by an increase in blood flow velocity, reduction of PAI-1 activity, and an increase in red blood cell deformability [45,46] . It is likely that at least some of the beneficial effects of PLC can be attributed to its role as an antioxidant [47,48] . To this end, our results also showed improvements in the endothelial balance and shed further light on its mechanism of action.…”

Section: Discussionmentioning

confidence: 99%

Propionyl-<i>L</i>-Carnitine Therapy: Effects on Endothelin-1 and Homocysteine Levels in Patients with Peripheral Arterial Disease and End-Stage Renal Disease

Signorelli¹,

Fatuzzo

Rapisarda

et al. 2006

Kidney Blood Press Res

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Background/Aims: Recent data have addressed the issue of higher levels of homocysteine (Hcy) and endothelin-1 (ET-1) in end-stage renal disease (ESRD) that may be considered an independent predictor for cardiovascular disease. The prevalence of peripheral arterial disease (PAD) in patients with ESRD has been reported to be relevant, highlighting its clinical importance. We aimed to explore the therapeutic role of propionyl-L-carnitine (PLC) in hemodialysis patients with PAD by measuring ankle/brachial index (ABI), ET-1 and Hcy. Design: Randomized, double-blind, placebo-controlled trial. Methods: Sixty-four patients on hemodialysis with chronic renal insufficiency and PAD were assigned to receive either intravenous PLC (600 mg) or placebo 3 times weekly for 12 months. The ABI and plasma levels of ET-1 and Hcy were measured at baseline, 6 and 12 months. Results: In the PLC-treated group, progressive increases in ABI were observed, while in the placebo group the reverse trend was seen. Highly significant and progressive reductions in plasma levels of ET-1 and Hcy, compared to baseline, were also seen in the PLC-treated group. Conclusions: Hemodynamic flow, endothelial profile and Hcy levels were ameliorated by the administration of PLC in hemodialysis patients with ESRD and PAD.

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Carnitine requirement of vascular endothelial and smooth muscle cells in imminent ischemia

Cited by 11 publications

References 28 publications

l-Carnitinel-tartrate supplementation favorably affects markers of recovery from exercise stress

l-Carnitinel-tartrate supplementation favorably affects markers of recovery from exercise stress

The Role of Carnitine and Carnitine Supplementation During Exercise in Man and in Individuals with Special Needs

Propionyl-<i>L</i>-Carnitine Therapy: Effects on Endothelin-1 and Homocysteine Levels in Patients with Peripheral Arterial Disease and End-Stage Renal Disease

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