Research Articles

Arginine

Acute amino acids supplementation enhances pituitary responsiveness in athletes.

di Luigi L, Guidetti L, Pigozzi F, Baldari C, Casini A, Nordio M, Romanelli F.

Endocrine Research Laboratory, Sports Medicine Unit, University Institute of Motor Sciences, Rome, Italy.

PURPOSE: The purpose of this study was to determine the effect of a mixture of amino acids on pituitary responsiveness to a stimulation test (GnRH + CRH) in athletes. METHODS: In a double blinded counterbalanced experimental protocol, 10 moderately trained male athletes performed the pituitary stimulation test 60 min after a single oral administration of a placebo (P1-AS) or an amino acid mixture solution (AS) (L-arginine hydrochloride 100 mg x kg(-1) + L-ornithine hydrochloride 80 mg x kg(-1) + L-branched chain amino acids 140 mg x kg(-1): 50% L-leucine, 25% L-isoleucine, 25% L-valine) on two different occasions. Plasma ACTH, LH, FSH, GH, and cortisol were evaluated before (-60, -30, 0 min) and after (+15, +30, +45, +60, +90 min) the stimulation test. RESULTS: The ACTH, LH and FSH response to CRH + GnRH was significantly higher in AS group both as absolute values and area under curve (AUC) values than in P1-AS group. Pre-test and post-test cortisol AUC levels were significantly higher in P1-AS group although a higher percent increase in post-test cortisol was found in AS group. The total GH-AUC was higher in AS group and, as expected, the absolute GH concentrations at different time points were not influenced by CRH + GnRH administration. CONCLUSION: The amino acid mixture used enhanced the ACTH, LH, and FSH response to CRH + GnRH.

The effect of a carbohydrate--arginine supplement on postexercise carbohydrate metabolism.

Yaspelkis BB 3rd, Ivy JL.

Department of Kinesiology and Health Education, University of Texas, Austin, TX 78712, USA.

The effect of a carbohydrate-arginine supplement on postexercise muscle glycogen storage was investigated. Twelve well-trained cyclists rode for 2 hr on two separate occasions to deplete their muscle glycogen stores. At 0, 1, 2, and 3 hr after each exercise bout, the subjects ingested either a carbohydrate (CHO) supplement (1 g carbohydrate/kg body weight) or a carbohydrate-arginine (CHO/AA) supplement (1 g carbohydrate/kg body mass and 0.08 g arginine-hydrochloride/kg body weight). No difference in rate of glycogen storage was found between the CHO/AA and CHO treatments, although significance was approached. There were also no differences in plasma glucose, insulin, or blood lactate responses between treatments. Postexercise carbohydrate oxidation during the CHO/AA treatment was significantly reduced compared to the CHO treatment. These results suggest that the addition of arginine to a CHO supplement reduces the rate of CHO oxidation postexercise and therefore may increase the availability of glucose for muscle glycogen storage during recovery.

 
L-arginine in the management of cardiovascular diseases.

Cheng JW, Baldwin SN, Balwin SN.

Arnold & Marie Schwartz College of Pharmacy and Health Sciences, 75 DeKalb Ave., Brooklyn, NY 11201-5497, USA. jcheng@liu.edu

OBJECTIVE: To examine the role of L-arginine in the management of cardiovascular diseases. DATA SOURCES: A MEDLINE search (1966-April 2000) of review articles, using the search terms arginine, nitric oxide, and cardiovascular diseases, was conducted. After reviewing these articles, primary studies using the search terms arginine, hypercholesterolemia, hypertension, diabetes, smoking, ischemic heart disease, and heart failure were reviewed. STUDY SELECTION: English-language human studies were selected and evaluated based on quality of review. DATA SYNTHESIS: Small-scale studies have demonstrated that intravenous L-arginine augments endothelial function by enhancing vasodilation and reducing monocyte adhesion. Oral supplementation demonstrated similar effects as well as improvement of exercise ability in patients with cardiovascular diseases. CONCLUSIONS: L-arginine improves the management of multiple cardiovascular diseases. However, most published human studies are small. Before therapy can be routinely recommended, larger, well-designed studies are required to confirm its effect.

 
Short-term oral administration of L-arginine improves hemodynamics and exercise capacity in patients with precapillary pulmonary hypertension.

Nagaya N, Uematsu M, Oya H, Sato N, Sakamaki F, Kyotani S, Ueno K, Nakanishi N, Yamagishi M, Miyatake K.

Department of Internal Medicine and Department of Pharmacy, National Cardiovascular Center, and Osaka Seamen's Insurance Hospital, Osaka, Japan.

We sought to assess the effects of oral supplementation of L-arginine, the precursor of nitric oxide (NO), on hemodynamics and exercise capacity in patients with pulmonary hypertension. Acute hemodynamic responses to oral L-arginine (0.5 g/10 kg body weight) or placebo were examined in 19 patients with primary or precapillary secondary pulmonary hypertension. Cardiopulmonary exercise tests were performed to measure peak oxygen consumption (peak V O(2)) and the ventilatory response to carbon dioxide production (V E-V CO(2) slope) before and 1 wk after treatment with L-arginine (1.5 g/10 kg body weight/d) or placebo. Oral supplementation of L-arginine significantly increased plasma L-citrulline, which indicated enhancement of NO production. Supplemental L-arginine produced a 9% decrease in mean pulmonary arterial pressure (53 +/- 4 to 48 +/- 4 mm Hg, p < 0.05) and a 16% decrease in pulmonary vascular resistance (14.8 +/- 1.5 to 12.4 +/- 1.4 Wood units, p < 0.05). L-arginine modestly decreased mean systemic arterial pressure (92 +/- 4 to 87 +/- 3 mm Hg, p < 0.05). A 1-wk supplementation of L-arginine resulted in a slight increase in peak V O(2) (831 +/- 88 to 896 +/- 92 ml/min, p < 0.05) and a significant decrease in the V E- V CO(2) slope (43 +/- 4 to 37 +/- 3, p < 0.05) without significant systemic hypotension. Hemodynamics and exercise capacity remained unchanged during placebo administration. These results suggest that oral supplementation of L-arginine may have beneficial effects on hemodynamics and exercise capacity in patients with precapillary pulmonary hypertension.

 
Correction of endothelial dysfunction in chronic heart failure: additional effects of exercise training and oral L-arginine supplementation.

Hambrecht R, Hilbrich L, Erbs S, Gielen S, Fiehn E, Schoene N, Schuler G.

University of Leipzig, Heart Center, Division of Cardiology, Germany. hamr@server3.medizin.uni-leipzig.de

OBJECTIVES: The aim of this study was to analyze whether L-arginine (L-arg.) has comparable or additive effects to physical exercise regarding endothelium-dependent vasodilation in patients with chronic heart failure (CHF). BACKGROUND: Endothelial dysfunction in patients with CHF can be corrected by both dietary supplementation with L-arg. and regular physical exercise. METHODS: Forty patients with severe CHF (left ventricular ejection fraction 19 +/- 9%) were randomized to an L-arg. group (8 g/day), a training group (T) with daily handgrip training, L-arg. and T (L-arg. + T) or an inactive control group (C). The mean internal radial artery diameter was determined at the beginning and after four weeks in response to brachial arterial administration of acetylcholine (ACh) (7.5, 15, 30 microg/min) and nitroglycerin (0.2 mg/min) with a transcutaneous high-resolution 10 MHz A-mode echo tracking system coupled with a Doppler device. The power of the study to detect clinically significant differences in endothelium-dependent vasodilation was 96.6%. RESULTS: At the beginning, the mean endothelium-dependent vasodilation in response to ACh, 30 microg/min was 2.54 +/- 0.09% (p = NS between groups). After four weeks, internal radial artery diameter increased by 8.8 +/- 0.9% after ACh 30 microg/min in L-arg. (p < 0.001 vs. C), by 8.6 +/- 0.9% in T (p < 0.001 vs. C) and by 12.0 +/- 0.3% in L-arg. +/- T (p < 0.005 vs. C, L-arg. and T). Endothelium-independent vasodilation as assessed by infusion of nitroglycerin was similar in all groups at the beginning and at the end of the study. CONCLUSIONS: Dietary supplementation of L-arg. as well as regular physical exercise improved agonist-mediated, endothelium-dependent vasodilation to a similar extent. Both interventions together seem to produce additive effects with respect to endothelium-dependent vasodilation.

Oral arginine does not stimulate basal or augment exercise-induced GH secretion in either young or old adults.

Marcell TJ, Taaffe DR, Hawkins SA, Tarpenning KM, Pyka G, Kohlmeier L, Wiswell RA, Marcus R.

Department of Exercise Science, University of Southern California, Los Angeles, USA. marcellt@grc.nia.nih.gov

BACKGROUND: Growth hormone (GH) helps maintain body composition and metabolism in adults. However, basal and peak GH decline with age. Exercise produces a physiologic GH response that is subnormal in elderly people. Arginine (Arg) infusion can augment GH secretion, but the efficacy of oral Arg to improve GH response to exercise has not been explored. We investigated whether oral Arg increases GH secretion in young and old people at rest and during exercise. METHODS: Twenty young (Y: 22.1 +/- 0.9 y; SEM) and 8 old (O: 68.5 +/- 2.1 y) male and female subjects underwent three different trials following determination of their one-repetition maximum strength (1-RM); exercise only (EO; 3 sets, 8-10 reps at 85% of 1-RM; on 12 separate resistive lifts), Arg only (5.0 g), or Arg + exercise. Blood samples were collected between successive lifts, and GH (ng x ml(-1)) was determined via RIA. RESULTS: In Y vs O: Basal GH secreted (area under the curve) was 543.6 +/- 84.0 vs 211.5 +/- 63.0. During EO, values were 986.6 +/- 156.6 and 517.8 +/- 85.5. Both were significantly lower in the older individuals (p < .05). Oral Arg alone did not result in any increase in GH secretion at rest (310.8 +/- 73.2 vs 262.9 +/- 141.2). When Arg was coadministered during exercise, GH release was not affected in either the young or old and appeared to be blunted in the young compared to the exercise only trial in the young. CONCLUSION: Based upon these findings, we concluded that oral Arg does not stimulate GH secretion and may impair GH release during resistive exercise.

 
Acute supplementation with the nitric oxide precursor L-arginine does not improve cardiovascular performance in patients with hypercholesterolemia.

Wennmalm A, Edlund A, Granstrom EF, Wiklund O.

Department of Clinical Physiology, Goteborg University, Sahlgrenska University Hospital, Sweden.

Endothelial dysfunction based on lack of nitric oxide (NO) may contribute to several settings of cardiovascular disorder. Chronic oral supplementation with the NO precursor L-arginine counteracts the development of aortic atherosclerosis in cholesterol-fed rabbits, and i.v. infusion of L-arginine may acutely improve endothelium-dependent coronary epicardial vasodilation in patients with hypercholesterolemia (HC). To clarify whether excess NO precursor may also improve general cardiovascular performance in HC, we measured working capacity indices of myocardial ischemia, and basal and post-occlusive forearm and skin blood flow in nine patients with elevated plasma cholesterol (9.1 +/- 0.2 mumol/l) following random double-blinded administration of L-arginine (16 g i.v.) or placebo. Infusion of L-arginine raised the plasma concentration of this amino acid from 85 +/- 12 to 2460 +/- 230 mumol/l but did not change the plasma level of the major NO metabolite nitrate. Maximal working capacity, indices of myocardial ischemia, and basal and post-occlusive blood flow in the skin or forearm did not differ between the treatments. The lack of positive effect of L-arginine compared to placebo indicates that excess NO precursor did not improve microvascular endothelial function in the patients, or alternatively, that the indices measured in the present study were not dependent on endothelial microvessel function. Thus, in patients with HC, deficiency of precursor for NO formation does not seem to impair either maximal exercise capacity myocardial perfusion during maximal exercise, or maximal vasodilator capacity in skeletal muscle or skin.

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