Carnitine-Related Alterations in Patients With Intermittent Claudication

Brevetti, Gregorio; Lisa, Fabio Di; Perna, Stefano; Menabò, Roberta; Barbato, R; Martone, Vincenzo Domenico; Siliprandi, N.

doi:10.1161/01.cir.93.9.1685

Cited by 31 publications

(12 citation statements)

References 22 publications

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“…This explains the apparent paradox whereby the administration of L-carnitine to perfused rat heart increases glucose oxidation while decreasing FAO [142]. This biochemical rationale underlies the clinical evidence of L-carnitine protection [143][144][145].…”

Section: Metabolic Approachesmentioning

confidence: 99%

Mitochondria and cardioprotection

et al. 2007

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Major factors linking mitochondrial dysfunction with myocardial injury are analyzed along with protective mechanisms elicited by endogenous processes and pharmacological treatments. In particular, a reduced rate of ATP hydrolysis and a slight increase in ROS formation appear to represent the prevailing components of self-defense mechanisms, especially in the case of ischemic preconditioning. These protective processes are activated by signaling pathways, which converge on mitochondria activating the mitochondrial K(ATP) channels and/or inhibiting the mitochondrial permeability transition pore. These pathways can also be stimulated by pharmacological treatments. Another major goal for cardioprotection is decreasing the burst in mitochondrial ROS formation that characterizes post-ischemic reperfusion. Finally, mitochondrial targets for therapeutic intervention may include the switch of substrate being utilized, because inhibition of fatty acid oxidation is associated with cardioprotective effects.

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Section: Metabolic Approachesmentioning

confidence: 99%

Mitochondria and cardioprotection

et al. 2007

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“…The loss of walking performance in people with PAD is primarily because of the reduced blood flow to these active muscles (Green & Mehlsen, 1999). In addition, disturbances in metabolism in the calf muscles that might be independent of blood flow and which are responsive to exercise training or pharmacotherapy could also contribute to the walking impairment in PAD (Brevetti et al ., 1992, 1996; Hiatt et al ., 1992, 1996).…”

Section: Introductionmentioning

confidence: 99%

Skeletal muscle mitochondrial ATP production rate and walking performance in peripheral arterial disease

Hou

Green

Askew

et al. 2002

Clin Physio Funct Imaging

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This study tested the hypotheses that skeletal muscle mitochondrial ATP production rate (MAPR) is impaired in patients with peripheral arterial disease (PAD) and that it relates positively to their walking performances. Seven untrained patients, eight exercise-trained patients and 11 healthy controls completed a maximal walking test and had muscle sampled from the gastrocnemius medialis muscle. Muscle was analysed for its MAPR in the presence of pyruvate, palmitoyl-L-carnitine or both, as well as citrate synthase (CS) activity. MAPRs were not different between untrained PAD and controls. In contrast, MAPRs (pyruvate) were significantly higher in trained PAD vs. controls. MAPR (pyruvate combinations) was also significantly higher in trained than untrained PAD muscle. MAPR and CS activity were highly correlated with walking performance in patients, but not in controls. These data do not support the hypothesis that isolated mitochondria are functionally impaired in PAD and demonstrate that the muscle mitochondrial capacity to oxidize carbohydrate is positively related to walking performance in these patients.

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“…the decrease observed before treatment [50]. This implies that a corresponding amount of acetyl-CoA was removed from mitochondria with consequent stimulation of PDH.…”

Section: Effect Of Ischemiamentioning

confidence: 70%

“…Importantly, there is an inverse correlation between both plasma and muscle levels of acetylcarni- tine and subsequent assessments of peak exercise performance suggesting that in patients with IC, altered carnitine metabolism might be associated with the altered muscle energy metabolism [6,49]. Patients with mild functional impairment have low resting plasma levels of acetylcarnitine that normally increase with exercise, while the most affected patients have elevated resting levels of acetylcarnitine and do not form these esters with exercise [50]. Plasma concentration of acetylcarnitine depends, at least in part, on two factors, the rate of formation of acetyl-CoA and the availability of carnitine to remove if from mitochondria.…”

Section: Effect Of Ischemiamentioning

confidence: 99%

Impairment of microcirculation and energy metabolism in intermittent claudication: beneficial effects of exercise training

Laurenzano¹,

Spadera²,

Laurentis³

et al. 2016

Monaldi Arch Chest Dis

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Impairment of microcirculation and energy metabolism in intermittent claudication: beneficial effects of exercise training. E. Laurenzano, L. Spadera, M. De Laurentis, G. Brevetti.Although in peripheral arterial disease (PAD) the primary determinant of inadequate blood supply to the affected limb during exercise is a flow-limiting lesion of a conduit artery, there is a large body of evidence that impairment of microcirculation and skeletal muscle energy metabolism play a relevant role in the reduced working ability of affected individuals. This review was conceived to cast some light on this topic, paying special attention to the functional benefits of exercise training (ET) in the treatment of claudicant patients.In PAD, the ischemia induced by maximal exercise increases oxidative stress, inflammation and endothelial dysfunction. Perturbation of the endothelial homeostasis results in increased adhesiveness of leukocytes and platelets, and in reduced vasodilator capability. These events, expression of the interplay between inflammation and endothelium, provoke an obstacle in the microcirculation with a reduction in the nutritive blood flow, leading to acidosis and impaired energy metabolism in skeletal muscle, with consequent reduced exercise tolerance.ET counteracts these effects by improving walking ability and quality of life in patients with intermittent claudication, thus representing the gold standard in the treatment of PAD.

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Carnitine-Related Alterations in Patients With Intermittent Claudication

Abstract: In patients with intermittent claudication, assessment of plasma acetylcarnitine at rest and after exercise may be a means to select a target population for L-carnitine therapy.

Cited by 31 publications

References 22 publications

Mitochondria and cardioprotection

Mitochondria and cardioprotection

Skeletal muscle mitochondrial ATP production rate and walking performance in peripheral arterial disease

Impairment of microcirculation and energy metabolism in intermittent claudication: beneficial effects of exercise training

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