For Elite Athletes
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An introductory paper discussing how exercise depletes ribose, and how ribose restores energy in muscles. It also gets into ribose as an aid in reducing free radicals.

[6-11]

The role of ribose in human skeletal muscle metabolism.

Dodd SL, Johnson CA, Fernholz K, St Cyr JA.

Department of Exercise and Sports Sciences, University of Florida, P.O. Box 118205, Gainesville, FL 32611, USA. sdodd@hhp.ufl.edu

Bioenergetic pathways in muscle provide high-energy compounds that are required for cellular integrity and function. Increased cellular demand for adenosine triphosphate (ATP) or limitations in the rephosphorylation rate of adenosine diphosphate (ADP) can decrease the total adenine nucleotide (TAN) pool, which may take several days to recover or may not recover at all in cases of chronic ischemia. Total adenine nucleotide levels may be significantly decreased as a result of myocardial or skeletal muscle ischemia, certain metabolic diseases, repeated intense skeletal muscle contractions or in repetitive high-intensity exercise. Ribose, a naturally occurring pentose sugar, has been shown to enhance the recovery of myocardial or skeletal muscle ATP and TAN levels following ischemia or high-intensity exercise. Furthermore, ribose has been demonstrated to modulate the production of oxygen free radicals during and following exercise. The following paper reviews skeletal muscle energetics and the potential role of ribose during and following exercise.

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Here we see a study, including nine HEALTHY individuals, showing how ribose helped exercise performance.

[6-26]

Ribose administration during exercise: effects on substrates and products of energy metabolism in healthy subjects and a patient with myoadenylate deaminase deficiency.

Gross M, Kormann B, Zollner N.

Medizinische Poliklinik, Universitat Munchen, FRG.

Nine healthy men and a patient with myoadenylate deaminase deficiency were exercised on a bicycle ergometer (30 minutes, 125 Watts) with and without oral ribose administration at a dose of 2 g every 5 minutes of exercise. Plasma or serum levels of glucose, free fatty acids, lactate, ammonia and hypoxanthine and the urinary hypoxanthine excretion were determined. After 30 minutes of exercise without ribose intake the healthy subjects showed significant increases in plasma lactate (p less than 0.05), ammonia (p less than 0.01) and hypoxanthine (p less than 0.05) concentrations and a decrease in serum glucose concentration (p less than 0.05). When ribose was administered, the plasma lactate concentration increased significantly higher (p less than 0.05) and the increase in plasma hypoxanthine concentration was no longer significant. The patient showed the same pattern of changes in serum or plasma concentrations with exercise with the exception of hypoxanthine in plasma which increased higher when ribose was administered.

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This study supposes that part of why carnitine works so well is because it dilates arteries, thus increasing blood flow.

[5-18]

Propionyl-L-carnitine dilates human subcutaneous arteries through an endothelium-dependent mechanism.

Cipolla MJ, Nicoloff A, Rebello T, Amato A, Porter JM.

Department of Surgery, Division of Vascular Surgery, Oregon Health Sciences University, Portland 97201, USA.

PURPOSE: The vasoactive effects of propionyl-L-carnitine (PLC) on human arteries, including endothelial and smooth muscle cell influences, were studied. METHODS: Small (less than 200 microm) subcutaneous fat arteries (n = 19), obtained from human patients undergoing vascular surgery, were dissected and mounted in an arteriograph system that allowed measurement of lumen diameter and control of transmural pressure. To investigate the role of the endothelium, arteries were compared intact, intact and in the presence of either 0.3 mmol/L nitro-L-arginine (an inhibitor of nitric oxide synthesis) or 10 micromol/L indomethacin (an inhibitor of prostaglandin synthesis), or denuded of endothelium. After a 1-hour equilibration at a pressure of 50 mm Hg, arteries were precontracted 50% with an intermediate concentration of norepinephrine, and clinically relevant concentrations of PLC (0.1 to 100 micromol/L) were cumulatively added to the bath while the lumen diameter was continually measured. RESULTS: Intact arteries dose-dependently dilated to PLC, with the half maximal dilation occurring at 2.9 +/- 1.2 micromol/L, increasing diameter 91% +/- 5% at 100 micromol/L. In contrast, PLC had significantly less effect on deendothelialized arteries, increasing diameter only 24% +/- 11% at 100 micromol/L (P <.01 vs. intact). This indicates the endothelial dependency of this compound. Blockade of nitric oxide did not inhibit this vasodilation, with the half-maximal response occurring at 8.6 +/- 7 micromol/L, increasing diameter 85% +/- 8% at 100 micromol/L ( P >.O5 vs. intact). However, this vasodilation was significantly diminished in the presence of indomethacin, which dilated arteries only 53% +/- 18% at 100 micromol/L (P <.01 vs. intact; P >.O5 vs. denuded). CONCLUSION: PLC is an endothelium-dependent vasodilator, the mechanism of which is partially mediated by prostaglandin synthesis, not nitric oxide. The beneficial effects of this compound may, in part, be related to vasodilation and enhanced blood flow.

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Claudication is terrible leg pain brought on by physical exercise, due to oxygen starvation because the blood supply of the legs is compromised. Carnitine here allowed people walk faster and longer on a treadmill, and therefore would improve their QOL (Quality of Life).

[5-32]

Propionyl-L-carnitine improves exercise performance and functional status in patients with claudication.

Hiatt WR, Regensteiner JG, Creager MA, Hirsch AT, Cooke JP, Olin JW, Gorbunov GN, Isner J, Lukjanov YV, Tsitsiashvili MS, Zabelskaya TF, Amato A.

Department of Medicine, Section of Vascular Medicine, Divisions of Geriatrics and Cardiology, University of Colorado Health Sciences Center, Denver 80203, USA.

PURPOSE: We tested the hypothesis that propionyl-L-carnitine would improve peak walking time in patients with claudication. Secondary aims of the study were to evaluate the effects of propionyl-L-carnitine on claudication onset time, functional status, and safety. SUBJECTS AND METHODS: In this double-blind, randomized, placebo-controlled trial, 155 patients with disabling claudication from the United States (n = 72) or Russia (n = 83) received either placebo or propionyl-L-carnitine (2g/day orally) for 6 months. Subjects were evaluated at baseline and 3 and 6 months after randomization with a graded treadmill protocol at a constant speed of 2 miles per hour, beginning at 0% grade, with increments in the grade of 2% every 2 minutes until maximal symptoms of claudication forced cessation of exercise. Questionnaires were used to determine changes in functional status. RESULTS: At baseline, peak walking time was 331 +/- 171 seconds in the placebo group and 331 +/- 187 seconds in the propionyl-L-carnitine group. After 6 months of treatment, subjects randomly assigned to propionyl-L-carnitine increased their peak walking time by 162 +/- 222 seconds (a 54% increase) as compared with an improvement of 75 +/- 191 seconds (a 25% increase) for those on placebo (P <0.001). Similar improvements were observed for claudication onset time. Propionyl-L-carnitine treatment significantly improved walking distance and walking speed (by the Walking Impairment Questionnaire), and enhanced physical role functioning, reduced bodily pain, and resulted in a better health transition score (by the Medical Outcome Study SF-36 Questionnaire). The incidence of adverse events and study discontinuations were similar in the two treatment groups. CONCLUSIONS: Propionyl-L-carnitine safely improved treadmill exercise performance and enhanced functional status in patients with claudication.

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This is a more technical piece, of interest to doctors who specialize in muscle disorders and elite level athletes.

[6-7]

. Purine salvage to adenine nucleotides in different skeletal muscle fiber types.

Author: Brault, J J : Terjung, R L Citation: J-Appl-Physiol. 2001 Jul; 91(1): 231-8

Rates of purine salvage of adenine and hypoxanthine into the adenine nucleotide (AdN) pool of the different skeletal muscle phenotype sections of the rat were measured using an isolated perfused hindlimb preparation. Tissue adenine and hypoxanthine concentrations and specific activities were controlled over a broad range of purine concentrations, ranging from 3 to 100 times normal, by employing an isolated rat hindlimb preparation perfused at a high flow rate. Incorporation of [(3)H]adenine or [(3) H]hypoxanthine into the AdN pool was not meaningfully influenced by tissue purine concentration over the range evaluated (approximately 0.10-1.6 micromol/g). Purine salvage rates were greater (P less than 0.05) for adenine than for hypoxanthine (35-55 and 20-30 nmol x h(-1) x g(-1), respectively) and moderately different (P less than 0.05) among fiber types. The low-oxidative fast-twitch white muscle section exhibited relatively low rates of Abstract: purine salvage that were approximately 65% of rates in the high-oxidative fast-twitch red section of the gastrocnemius. The soleus muscle, characterized by slow-twitch red fibers, exhibited a high rate of adenine salvage but a low rate of hypoxanthine salvage. Addition of ribose to the perfusion medium increased salvage of adenine (up to 3- to 6-fold, P less than 0.001) and hypoxanthine (up to 6- to 8-fold, P less than 0.001), depending on fiber type, over a range of concentrations up to 10 mM. This is consistent with tissue 5-phosphoribosyl-1-pyrophosphate being rate limiting for purine salvage. Purine salvage is favored over de novo synthesis, inasmuch as delivery of adenine to the muscle decreased (P less than 0.005) de novo synthesis of AdN. Providing ribose did not alter this preference of purine salvage pathway over de novo synthesis of AdN. In the absence of ribose supplementation, purine salvage rates are relatively low, especially compared with the AdN pool size in skeletal muscle.