<scp>l</scp>-Arginine enhances aerobic exercise capacity in association with augmented nitric oxide production

Maxwell, Andrew J.; Ho, Hoai Ky V.; Le, Christine Q.; Lin, Patrick S.; Bernstein, Daniel; Cooke, John P.

doi:10.1152/jappl.2001.90.3.933

Cited by 57 publications

(45 citation statements)

References 31 publications

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“…36) affect V O 2 max . On the other hand, the two studies investigating V O 2 max and RER in C57BL/6J, age and test protocol as the present study, found similar results (12,27).…”

Section: Discussionsupporting

confidence: 86%

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Kemi

Loennechen

Wisløff

et al. 2002

Journal of Applied Physiology

243

265

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. Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy. J Appl Physiol 93: 1301-1309. First published May 24, 2002 10.1152/japplphysiol.00231.2002-Whereas novel pathways of pathological heart enlargement have been unveiled by thoracic aorta constriction in genetically modified mice, the molecular mechanisms of adaptive cardiac hypertrophy remain virtually unexplored and call for an effective and wellcharacterized model of physiological mechanical loading. Experimental procedures of maximal oxygen consumption (V O2 max) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent V O2 max with 0.98 test-retest correlation was found at 25°treadmill grade. Running for 2 h/day, 5 days/wk, in intervals of 8 min at 85-90% of V O2 max and 2 min at 50% (adjusted to weekly V O2 max testing) increased V O2 max to a plateau 49% above sedentary females and 29% in males. Running economy improved in both sexes, and echocardiography indicated significantly increased left ventricle posterior wall thickness. Ventricular weights increased by 19-29 and 12-17% in females and males, respectively, whereas cardiomyocyte dimensions increased by 20-32, and 17-23% in females and males, respectively; skeletal muscle mass increased by 12-18%. Thus the model mimics human responses to exercise and can be used in future studies of molecular mechanisms underlying these adaptations. maximal oxygen uptake; work economy; respiratory exchange ratio; cardiomyocyte; allometric scaling SEVERAL NOVEL SIGNALING PATHWAYS of pathological cardiac hypertrophy have been unveiled in the powerful model of mechanical overloading by thoracic aorta constriction in genetically modified mice (8,22). Thus far, the molecular mechanisms of adaptive cardiac hypertrophy in response to physiological stimuli remain virtually unexplored because of a paucity of effective and well-controlled experimental models in this species. Ideally, the outcome should mimic typical results of exercise training in humans, e.g., increased maximal oxygen uptake (V O 2 max ) and work economy (21). In healthy individuals, increased exercise capacity is dependent on functional and structural adaptations in skeletal muscle, blood vessels, and heart. Cardiac adaptation includes increased ventricular chamber volumes and weights, cardiomyocyte hypertrophy, increased cardiac output, and improved contractile function measured in isolated cardiomyocytes and in the intact heart (2, 3).At present, there are few well-controlled endurance training studies in mice. Training is usually carried out as voluntary exercise regimens, with little control of exercise intensity and the individual's fitness level. Voluntary wheel running is most frequently used. V O 2 max has been shown to increase by 12-30% after a 7-to 12-wk period of free wheel running (11,40). The latter study also demonstrated a 6% decreased respiratory exchange ratio (RER) at V O 2 max in trained mice. Exercise capacity and adaptations have al...

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“…36) affect V O 2 max . On the other hand, the two studies investigating V O 2 max and RER in C57BL/6J, age and test protocol as the present study, found similar results (12,27).…”

Section: Discussionsupporting

confidence: 86%

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Kemi

Loennechen

Wisløff

et al. 2002

Journal of Applied Physiology

243

265

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“…In these animals, L-arginine supplementation increases exercise capacity in association with an increase in limb blood flow and urinary nitrogen oxides. 36 In addition to its action as a vasodilator, NO mediates angiogenesis. In the NO synthase-deficient mouse, angiogenesis in response to limb ischemia is impaired, as demonstrated by capillary densitometry.…”

Section: Wilson Et Al L-arginine In Peripheral Arterial Diseasementioning

confidence: 99%

l -Arginine Supplementation in Peripheral Arterial Disease

et al. 2007

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Background-L-Arginine is the precursor of endothelium-derived nitric oxide, an endogenous vasodilator. L-Arginine supplementation improves vascular reactivity and functional capacity in peripheral arterial disease (PAD) in small, short-term studies. We aimed to determine the effects of long-term administration of L-arginine on vascular reactivity and functional capacity in patients with PAD. Methods and Results-The Nitric Oxide in Peripheral Arterial Insufficiency (NO-PAIN) study was a randomized clinical trial of oral L-arginine (3 g/d) versus placebo for 6 months in 133 subjects with intermittent claudication due to PAD in a single-center setting. The primary end point was the change at 6 months in the absolute claudication distance as assessed by the Skinner-Gardner treadmill protocol. L-Arginine supplementation significantly increased plasma L-arginine levels. However, measures of nitric oxide availability (including flow-mediated vasodilation, vascular compliance, plasma and urinary nitrogen oxides, and plasma citrulline formation) were reduced or not improved compared with placebo. Although absolute claudication distance improved in both L-arginine-and placebo-treated patients, the improvement in the L-arginine-treated group was significantly less than that in the placebo group (28.3% versus 11.5%; Pϭ0.024). Conclusions-In patients with PAD, long-term administration of L-arginine does not increase nitric oxide synthesis or improve vascular reactivity. Furthermore, the expected placebo effect observed in studies of functional capacity was attenuated in the L-arginine-treated group. As opposed to its short-term administration, long-term administration of L-arginine is not useful in patients with intermittent claudication and PAD.

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“…17). Administration of L-arginine normalizes aerobic capacity (18) and reduces fat mass in Zucker diabetic fatty rats (19). The lack of appropriate generation of endogenous NO is an important progression factor of atherosclerosis in mice (20) and L-arginine may reduce atherogenesis in hypercholesterolemic mice (21).…”

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confidence: 99%

Physical training and metabolic supplementation reduce spontaneous atherosclerotic plaque rupture and prolong survival in hypercholesterolemic mice

Napoli

Williams-Ignarro²,

Nigris³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Moderate physical exercise (PE) combined with metabolic treatment (MT) (antioxidants and L-arginine) are well known to reduce atherosclerotic lesion formation in hypercholesterolemic mice. However, the long-term beneficial effects on unstable atheroma remain poorly understood. We started early PE training in large groups of 6-week-old hypercholesterolemic mice (by graduated swimming) alone or in combination with nutritional supplementation (1.0% vitamin E added to the chow and 0.05% vitamin C and 6% L-arginine added to the drinking water). Inactive controls did not receive PE. The spontaneous development of atherosclerotic plaque rupture (associated with advanced atherosclerosis) and survival rates were evaluated. Moderate PE elicited an increase in plasma levels of nitric oxide. Early combined treatment with PE and MT in the hypercholesterolemic mice significantly reduced lesions (also detected noninvasively at 10 months) and spontaneous atherosclerotic plaque rupture and prolonged survival more effectively than each intervention alone. Thus, early concerted actions of MT and PE improve the natural history of atherosclerotic lesions and reduce the plaque instability in hypercholesterolemic mice.antioxidants ͉ nitric oxide ͉ physical exercise ͉ L-arginine

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l-Arginine enhances aerobic exercise capacity in association with augmented nitric oxide production

Cited by 57 publications

References 31 publications

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

l -Arginine Supplementation in Peripheral Arterial Disease

Physical training and metabolic supplementation reduce spontaneous atherosclerotic plaque rupture and prolong survival in hypercholesterolemic mice

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