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Section of Vascular Medicine, Divisions of 1 Cardiovascular Medicine and 2 Pediatric Cardiology, Stanford University, Stanford, California 94305
We tested
whether supplementation with L-arginine can augment aerobic
capacity, particularly in conditions where endothelium-derived nitric
oxide (EDNO) activity is reduced. Eight-week-old wild-type (E+) and apolipoprotein E-deficient mice (E
)
were divided into six groups; two groups (LE+ and
LE) were given L-arginine (6% in drinking
water), two were given D-arginine (DE+ and
DE), and two control groups (NE+ and
NE) received no arginine supplementation. At 12-16
wk of age, the mice were treadmill tested, and urine was collected
after exercise for determination of EDNO production. NE
mice demonstrated a reduced aerobic capacity compared with
NE+ controls [maximal oxygen uptake
(
O2 max) of NE = 110 ± 2 (SE) vs. NE+ = 122 ± 3 ml
O2 · min1 · kg1,
P < 0.001]. This decline in aerobic capacity was
associated with a diminished postexercise urinary nitrate excretion.
Mice given L-arginine demonstrated an increase in
postexercise urinary nitrate excretion and aerobic capacity in both
groups (O2 max of LE = 120 ± 1 ml
O2 · min1 · kg1,
P < 0.05 vs. NE;
O2 max of LE+ = 133 ± 4 ml
O2 · min1 · kg1,
P < 0.01 vs. NE+). Mice
administered D-arginine demonstrated an intermediate
increase in aerobic capacity in both groups. We conclude that
administration of L-arginine restores exercise-induced EDNO
synthesis and normalizes aerobic capacity in hypercholesterolemic mice.
In normal mice, L-arginine enhances exercise-induced EDNO
synthesis and aerobic capacity.
oxygen uptake; vascular reactivity; hypercholesterolemia; apolipoprotein E knockout; D-arginine; endothelium-derived relaxing factor
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