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<blockquote data-quote="Gene Devine" data-source="post: 2630" data-attributes="member: 4"><p>Attached is one of the best research papers I've found to date on L-Arginine usage. Let it be known, and the author agrees, there just has not been enough research on the use of L-Arginine and L-Citrulline to make any conclusions...but this paper helps.</p><p></p><p>I've cut and pasted sections of interest here and <strong>bold highlight below</strong> may shed light on the pic of my forearm earlier in this thread...which was new news for me LOL!</p><p></p><p>Enjoy fellows!</p><p></p><p>Effects of L-arginine supplementation on exercise metabolism</p><p>Glenn K. McConell</p><p></p><p><strong>Acute L-arginine supplementation and</strong></p><p><strong>exercise</strong></p><p>Although infusion of L-arginine, NO donors and NOS</p><p>inhibitors has effects on blood pressure, heart rate and</p><p>to clarify the role of L-arginine/NOS in skeletal-muscle</p><p>glucose uptake during exercise.</p><p></p><p></p><p>Since local muscle infusion of L-arginine [25] and</p><p>femoral-artery infusion of L-arginine [24] have no effect</p><p>on leg blood flow during exercise in humans, we feel that</p><p>it is likely that L-arginine infusion increases glucose</p><p>uptake during exercise by increasing glucose transporter</p><p>4 (GLUT-4) translocation to the plasma membrane</p><p>rather than increasing skeletal-muscle blood flow. It</p><p>should be kept in mind, however, that L-arginine/NOS</p><p>inhibitors might effect the distribution of blood flow (the</p><p>extent of capillary blood flow) during exercise without</p><p>effecting total blood flow [25,38,39].</p><p></p><p></p><p>We also found that L-arginine infusion increased hepatic</p><p>glucose output during exercise to a greater extent than</p><p>exercise with saline infusion [30]. The mechanism(s)</p><p>behind this response are unclear but may relate, in part, to</p><p>the relative hypoglycaemia caused by L-arginine infusion</p><p>during exercise. Liver glucose output is exquisitely sensitive</p><p>to small changes in plasma glucose levels during</p><p>exercise in humans, so the decrease in plasma glucose</p><p>would be expected to increase liver glucose output [40].</p><p></p><p></p><p>Therefore, it is possible that greater glucose uptake with</p><p>L-arginine infusion causes a decrease in the plasma</p><p>glucose concentration which then stimulated glucose</p><p>output from the liver. It is also possible that L-arginine</p><p>infusion increases plasma glucagon concentration during</p><p>exercise, which then stimulates liver glucose output,</p><p>since this has been shown to occur at rest in humans</p><p>[17]. </p><p></p><p>Finally, L-arginine infusion may augment the</p><p>exercise-induced increases in hepatic glucose output</p><p>by increasing NO, since NO donors have been shown</p><p>to potentiate the effect of noradrenaline to increase</p><p>liver glucose output in rats and cats [41]. Plasma noradrenaline</p><p>increases during exercise in humans [42]. No</p><p>study has examined the influence of L-arginine on</p><p>hormonal responses to exercise, with the exception</p><p>of insulin.</p><p></p><p></p><p>Lipolysis is reduced by L-arginine infusion during exercise,</p><p>based on an attenuation of the increase in plasma</p><p>glycerol and lower non-esterified fatty acid concentration</p><p>[30]. The lower lipolysis may have been due to greater</p><p>NO production with L-arginine infusion since NO</p><p>inhibits catecholamine-induced stimulation of lipolysis</p><p>[43,44]. NOreduces glycerol release from isolated human</p><p>adipocytes in vitro [45].</p><p></p><p></p><p>We found that L-arginine infusion has no effect on</p><p>exercise performance which involved completion of a</p><p>set amount of work as quickly as possible following</p><p>120 min of exercise [30]. The set amount of work took</p><p>around 15 min. Similarly, acute L-arginine infusion has</p><p>been found to have no effect on VO2max-test exercise time</p><p>in patients with chronic heart failure [46] and patients</p><p>with hypercholesterolaemia [47].</p><p></p><p></p><p>It is necessary to now determine whether oral L-arginine</p><p>supplementation, like L-arginine infusion, increases</p><p>glucose disposal during exercise. Unfortunately several</p><p>studies in humans involving oral supplementation of</p><p>L-arginine have not used L-arginine on its own but rather</p><p>have used L-arginine in combination with various other</p><p>metabolites/salts, which makes interpretation of results</p><p>difficult since the effects could be due to the L-arginine,</p><p>the other metabolite or a combination. In addition, studies</p><p>have sometimes involved very small numbers of</p><p>participants. Ingestion of 20 g of L-arginine glutamate</p><p>salt before exercising at 75&#8211;80% VO2max caused a significant</p><p>attenuation of the increase in plasma ammonia</p><p>levels at the cessation of exercise (60 min) [48]. </p><p></p><p>A concern about this study is that it only involved three participants.</p><p>However, Schaefer et al. [49] also found lower plasma</p><p>ammonia (and lactate) after maximal exercise when</p><p>L-arginine was infused prior to exercise compared with</p><p>a placebo infusion. These results suggest that L-arginine</p><p>may decrease muscle energy imbalance during exercise;</p><p>however, we found no effect of L-arginine infusion on</p><p>plasma lactate during prolonged exercise in endurancetrained</p><p>individuals [30]. Studies with muscle biopsies</p><p>are required to examine mechanisms in this regard.</p><p></p><p></p><p><strong>Effects of chronic L-arginine supplementation</strong></p><p><strong>at rest.</strong></p><p><strong></strong></p><p></p><p>It is obviously not possible to infuse L-arginine into</p><p>humans for days or weeks. Therefore chronic effects of</p><p>L-arginine supplementation are confined to studies</p><p>utilizing oral L-arginine supplementation. <strong>Chronic oral</strong></p><p><strong>L-arginine supplementation reduces cardiovascular disease</strong></p><p><strong>risk factors. Four weeks of oral L-arginine supplementation</strong></p><p><strong>(2 g, three times per day) improves angina</strong></p><p><strong>class, lowers systolic blood pressure,<u> increases maximum</u></strong><strong><u>forearm blood flow</u> and improves quality of life in hypertensive</strong></p><p><strong>patients with microvascular angina [50].</strong> It also</p><p>raised the plasma L-arginine and cGMP concentration</p><p>and increased the L-arginine/asymmetric dimethylarginine</p><p>ratio [50].</p><p></p><p></p><p>In addition, long-term oral L-arginine supplementation</p><p>improves insulin sensitivity and endothelial function in</p><p>nonobese people with type 2 diabetes [51]. Recently, in a</p><p>follow-up study, this group found that 21 days of oral</p><p>L-arginine treatment augmented the beneficial effects of</p><p>a hypocaloric diet and exercise training program on</p><p>glucose metabolism, insulin sensitivity and markers of</p><p>oxidative stress in obese type 2 diabetics [52]. </p><p></p><p>It is possible that L-arginine supplementation improves insulin</p><p>sensitivity, at least in part, by increasing skeletalmuscle</p><p>mitochondrial biogenesis. Mitochondrial volume</p><p>is reduced in skeletal muscle of people with type 2</p><p>diabetes [53]. NO donors increase mitochondrial biogenesis</p><p>in L6 myocytes and eNOS-knockout mice have</p><p>reduced muscle mitochondrial biogenesis markers [54].</p><p>We have recently found that 2 days of NOS inhibition</p><p>reduces basal skeletal muscle mitochondrial biogenesis</p><p>markers in rats [55].</p><p></p><p></p><p>Exercise training and a combination of antioxidants and</p><p>L-arginine reduce athererosclerotic lesions and spontaneous</p><p>athererosclerotic plague rupture in hypercholesterolemic</p><p>mice [56]. Importantly, the combined therapy of</p><p>exercise training and supplementation improved these</p><p>outcomesmore than either treatment alone [56]. Six weeks</p><p>of oral L-arginine supplementation in rats potentiates the</p><p>exercise-training-induced increases in angiogenesis in</p><p>skeletal muscle and the left ventricle by, it appears,</p><p>increasing vacular endothelial growth factor expression</p><p>[57]. Indeed, NOS inhibition has been shown to attenuate</p><p>the increases in skeletal-muscle vacular endothelial</p><p>growth factor mRNA with exercise in rats [58].</p><p></p><p></p><p><strong>Chronic L-arginine supplementation and exercise.</strong></p><p></p><p></p><p>Chronic dietary L-arginine supplementation increases</p><p>aerobic capacity during treadmill exercise (8&#8211;9%</p><p>increase in VO2max) in hypercholesterolemic and normal</p><p>mice, which was linked to increases endothelial NO</p><p>function [59]. In humans, results have been contradictory</p><p>[60], but on balance it would appear that chronic oral</p><p>L-arginine supplementation improves maximal (VO2max</p><p>test) exercise capacity in patients with cardiovascular</p><p>disease, congestive heart failure, stable angina, and pulmonary</p><p>hypertension [61&#8211;64]. In patients with stable</p><p>angina pectoris, oral supplementation of L-arginine</p><p>(6 g/day for 3 days) increased exercise capacity, as determined</p><p>by a maximum exercise test [61]. </p><p></p><p>In addition, Doutreleau et al. [65] found that 6 weeks of oral L-arginine</p><p>supplementation improved a standard enduranceexercise</p><p>tolerance test in patients with heart failure</p><p>(compared with a placebo group). Heart rate and plasma</p><p>lactate concentration were also lower during exercise</p><p>after chronic L-arginine supplementation.</p><p>Several studies have examined the effect of chronic</p><p>L-arginine ingestion on aspects of metabolism during</p><p>exercise in humans. In one study 10 days of arginine</p><p>aspartate supplementation resulted in a reduction in</p><p>plasma ammonia levels at 15 min during 45 min of cycling</p><p>at 80% VO2max [66]. </p><p></p><p>However, in another study 2 weeks of</p><p>arginine aspartate supplementation had no effect on</p><p>plasma ammonia concentration during or 2 h after a</p><p>marathon run [67]. It also had no effect on plasma</p><p>glucose, lactate, pyruvate, free fatty acids, glycerol,</p><p>b-hydroxybutyrate, cortisol, insulin, lactate dehydrogenase</p><p>or creatine kinase, although it increased growth</p><p>hormone, glucagon, urea and L-arginine itself [67].</p><p>Campbell et al. [68] examined the effect of 8 weeks</p><p>of oral L-arginine a-ketoglutarate supplementation on</p><p>strength and other measures in resistance-trained men.</p><p>Twenty men ingested L-arginine a-ketoglutarate three</p><p>times per day (12 g/day) and 15 men ingested a placebo.</p><p>The L-arginine a-ketoglutarate group had significantly</p><p>greater gains in strength during the bench-press exercise</p><p>and during a predominantly anaerobic 30-s sprint test on</p><p>a bicycle ergometer (the Wingate peak power test).</p><p>L-arginine a-Ketoglutarate did not influence body composition,</p><p>muscular strength endurance or aerobic capacity</p><p>[68]. </p><p></p><p>The finding that L-arginine a-ketoglutarate supplementation</p><p>did not improve aerobic capacity supports</p><p>earlier findings that L-arginine improves VO2max in various</p><p>disease populations but not in healthy individuals [69].</p><p></p><p></p><p><strong>Conclusion</strong></p><p></p><p></p><p>It is clear that L-arginine supplementation improves</p><p>aerobic exercise capacity in various cardiovascular disease</p><p>states which are associated with endothelial dysfunction.</p><p>It is likely that the improvement in exercise capacity is</p><p>due to L-arginine increasing the production of NO in</p><p>these individuals with reduced basal NO production.</p><p></p><p></p><p>Accordingly, in healthy individuals with normal NO</p><p>production it appears that L-arginine administration has</p><p>little impact on aerobic exercise capacity.</p><p></p><p></p><p>Little research has been conducted to examine the effect</p><p>of L-arginine supplementation on exercise metabolism.</p><p><strong>There is some evidence that L-arginine infusion increases</strong></p><p><strong>glucose uptake during prolonged exercise and reduces</strong></p><p><strong>lipolysis. It is possible that these effects are due to</strong></p><p><strong>increases in NO production but more research is required</strong></p><p><strong>to confirm this. </strong>[ATTACH]329[/ATTACH]</p></blockquote><p></p>
[QUOTE="Gene Devine, post: 2630, member: 4"] Attached is one of the best research papers I've found to date on L-Arginine usage. Let it be known, and the author agrees, there just has not been enough research on the use of L-Arginine and L-Citrulline to make any conclusions...but this paper helps. I've cut and pasted sections of interest here and [B]bold highlight below[/B] may shed light on the pic of my forearm earlier in this thread...which was new news for me LOL! Enjoy fellows! Effects of L-arginine supplementation on exercise metabolism Glenn K. McConell [B]Acute L-arginine supplementation and[/B] [B]exercise[/B] Although infusion of L-arginine, NO donors and NOS inhibitors has effects on blood pressure, heart rate and to clarify the role of L-arginine/NOS in skeletal-muscle glucose uptake during exercise. Since local muscle infusion of L-arginine [25] and femoral-artery infusion of L-arginine [24] have no effect on leg blood flow during exercise in humans, we feel that it is likely that L-arginine infusion increases glucose uptake during exercise by increasing glucose transporter 4 (GLUT-4) translocation to the plasma membrane rather than increasing skeletal-muscle blood flow. It should be kept in mind, however, that L-arginine/NOS inhibitors might effect the distribution of blood flow (the extent of capillary blood flow) during exercise without effecting total blood flow [25,38,39]. We also found that L-arginine infusion increased hepatic glucose output during exercise to a greater extent than exercise with saline infusion [30]. The mechanism(s) behind this response are unclear but may relate, in part, to the relative hypoglycaemia caused by L-arginine infusion during exercise. Liver glucose output is exquisitely sensitive to small changes in plasma glucose levels during exercise in humans, so the decrease in plasma glucose would be expected to increase liver glucose output [40]. Therefore, it is possible that greater glucose uptake with L-arginine infusion causes a decrease in the plasma glucose concentration which then stimulated glucose output from the liver. It is also possible that L-arginine infusion increases plasma glucagon concentration during exercise, which then stimulates liver glucose output, since this has been shown to occur at rest in humans [17]. Finally, L-arginine infusion may augment the exercise-induced increases in hepatic glucose output by increasing NO, since NO donors have been shown to potentiate the effect of noradrenaline to increase liver glucose output in rats and cats [41]. Plasma noradrenaline increases during exercise in humans [42]. No study has examined the influence of L-arginine on hormonal responses to exercise, with the exception of insulin. Lipolysis is reduced by L-arginine infusion during exercise, based on an attenuation of the increase in plasma glycerol and lower non-esterified fatty acid concentration [30]. The lower lipolysis may have been due to greater NO production with L-arginine infusion since NO inhibits catecholamine-induced stimulation of lipolysis [43,44]. NOreduces glycerol release from isolated human adipocytes in vitro [45]. We found that L-arginine infusion has no effect on exercise performance which involved completion of a set amount of work as quickly as possible following 120 min of exercise [30]. The set amount of work took around 15 min. Similarly, acute L-arginine infusion has been found to have no effect on VO2max-test exercise time in patients with chronic heart failure [46] and patients with hypercholesterolaemia [47]. It is necessary to now determine whether oral L-arginine supplementation, like L-arginine infusion, increases glucose disposal during exercise. Unfortunately several studies in humans involving oral supplementation of L-arginine have not used L-arginine on its own but rather have used L-arginine in combination with various other metabolites/salts, which makes interpretation of results difficult since the effects could be due to the L-arginine, the other metabolite or a combination. In addition, studies have sometimes involved very small numbers of participants. Ingestion of 20 g of L-arginine glutamate salt before exercising at 75–80% VO2max caused a significant attenuation of the increase in plasma ammonia levels at the cessation of exercise (60 min) [48]. A concern about this study is that it only involved three participants. However, Schaefer et al. [49] also found lower plasma ammonia (and lactate) after maximal exercise when L-arginine was infused prior to exercise compared with a placebo infusion. These results suggest that L-arginine may decrease muscle energy imbalance during exercise; however, we found no effect of L-arginine infusion on plasma lactate during prolonged exercise in endurancetrained individuals [30]. Studies with muscle biopsies are required to examine mechanisms in this regard. [B]Effects of chronic L-arginine supplementation[/B] [B]at rest. [/B] It is obviously not possible to infuse L-arginine into humans for days or weeks. Therefore chronic effects of L-arginine supplementation are confined to studies utilizing oral L-arginine supplementation. [B]Chronic oral[/B] [B]L-arginine supplementation reduces cardiovascular disease[/B] [B]risk factors. Four weeks of oral L-arginine supplementation[/B] [B](2 g, three times per day) improves angina[/B] [B]class, lowers systolic blood pressure,[U] increases maximum[/U][/B][B][U]forearm blood flow[/U] and improves quality of life in hypertensive[/B] [B]patients with microvascular angina [50].[/B] It also raised the plasma L-arginine and cGMP concentration and increased the L-arginine/asymmetric dimethylarginine ratio [50]. In addition, long-term oral L-arginine supplementation improves insulin sensitivity and endothelial function in nonobese people with type 2 diabetes [51]. Recently, in a follow-up study, this group found that 21 days of oral L-arginine treatment augmented the beneficial effects of a hypocaloric diet and exercise training program on glucose metabolism, insulin sensitivity and markers of oxidative stress in obese type 2 diabetics [52]. It is possible that L-arginine supplementation improves insulin sensitivity, at least in part, by increasing skeletalmuscle mitochondrial biogenesis. Mitochondrial volume is reduced in skeletal muscle of people with type 2 diabetes [53]. NO donors increase mitochondrial biogenesis in L6 myocytes and eNOS-knockout mice have reduced muscle mitochondrial biogenesis markers [54]. We have recently found that 2 days of NOS inhibition reduces basal skeletal muscle mitochondrial biogenesis markers in rats [55]. Exercise training and a combination of antioxidants and L-arginine reduce athererosclerotic lesions and spontaneous athererosclerotic plague rupture in hypercholesterolemic mice [56]. Importantly, the combined therapy of exercise training and supplementation improved these outcomesmore than either treatment alone [56]. Six weeks of oral L-arginine supplementation in rats potentiates the exercise-training-induced increases in angiogenesis in skeletal muscle and the left ventricle by, it appears, increasing vacular endothelial growth factor expression [57]. Indeed, NOS inhibition has been shown to attenuate the increases in skeletal-muscle vacular endothelial growth factor mRNA with exercise in rats [58]. [B]Chronic L-arginine supplementation and exercise.[/B] Chronic dietary L-arginine supplementation increases aerobic capacity during treadmill exercise (8–9% increase in VO2max) in hypercholesterolemic and normal mice, which was linked to increases endothelial NO function [59]. In humans, results have been contradictory [60], but on balance it would appear that chronic oral L-arginine supplementation improves maximal (VO2max test) exercise capacity in patients with cardiovascular disease, congestive heart failure, stable angina, and pulmonary hypertension [61–64]. In patients with stable angina pectoris, oral supplementation of L-arginine (6 g/day for 3 days) increased exercise capacity, as determined by a maximum exercise test [61]. In addition, Doutreleau et al. [65] found that 6 weeks of oral L-arginine supplementation improved a standard enduranceexercise tolerance test in patients with heart failure (compared with a placebo group). Heart rate and plasma lactate concentration were also lower during exercise after chronic L-arginine supplementation. Several studies have examined the effect of chronic L-arginine ingestion on aspects of metabolism during exercise in humans. In one study 10 days of arginine aspartate supplementation resulted in a reduction in plasma ammonia levels at 15 min during 45 min of cycling at 80% VO2max [66]. However, in another study 2 weeks of arginine aspartate supplementation had no effect on plasma ammonia concentration during or 2 h after a marathon run [67]. It also had no effect on plasma glucose, lactate, pyruvate, free fatty acids, glycerol, b-hydroxybutyrate, cortisol, insulin, lactate dehydrogenase or creatine kinase, although it increased growth hormone, glucagon, urea and L-arginine itself [67]. Campbell et al. [68] examined the effect of 8 weeks of oral L-arginine a-ketoglutarate supplementation on strength and other measures in resistance-trained men. Twenty men ingested L-arginine a-ketoglutarate three times per day (12 g/day) and 15 men ingested a placebo. The L-arginine a-ketoglutarate group had significantly greater gains in strength during the bench-press exercise and during a predominantly anaerobic 30-s sprint test on a bicycle ergometer (the Wingate peak power test). L-arginine a-Ketoglutarate did not influence body composition, muscular strength endurance or aerobic capacity [68]. The finding that L-arginine a-ketoglutarate supplementation did not improve aerobic capacity supports earlier findings that L-arginine improves VO2max in various disease populations but not in healthy individuals [69]. [B]Conclusion[/B] It is clear that L-arginine supplementation improves aerobic exercise capacity in various cardiovascular disease states which are associated with endothelial dysfunction. It is likely that the improvement in exercise capacity is due to L-arginine increasing the production of NO in these individuals with reduced basal NO production. Accordingly, in healthy individuals with normal NO production it appears that L-arginine administration has little impact on aerobic exercise capacity. Little research has been conducted to examine the effect of L-arginine supplementation on exercise metabolism. [B]There is some evidence that L-arginine infusion increases[/B] [B]glucose uptake during prolonged exercise and reduces[/B] [B]lipolysis. It is possible that these effects are due to[/B] [B]increases in NO production but more research is required[/B] [B]to confirm this. [/B][ATTACH]329[/ATTACH] [/QUOTE]
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