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 (VO2 max) of NE- = 110 ± 2 (SE) vs. NE+ = 122 ± 3 ml O2 · min-1 · kg-1, 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 (VO2 max of LE- = 120 ± 1 ml O2 · min-1 · kg-1, P < 0.05 vs. NE-; VO2 max of LE+ = 133 ± 4 ml O2 · min-1· kg-1, 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.
- Apolipoprotein E knockout
- Endothelium-derived relaxing factor
- Oxygen uptake
- Vascular reactivity
ASJC Scopus subject areas
- Orthopedics and Sports Medicine
- Physical Therapy, Sports Therapy and Rehabilitation