Premium
Enhanced nitric oxide mediated blunting of sympathetic vasoconstriction following 4 weeks of exercise training
Author(s) -
Jendzjowsky Nicholas G,
DeLorey Darren Scott
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.645.1
The hypothesis that exercise training (ET) would up‐regulate nitric oxide (NO) mediated blunting of skeletal muscle sympathetic vasoconstriction was investigated. Sprague‐dawley rats were randomized to sedentary (S; n=8), mild‐ (M; 20m/min5% grade; n=10) or heavy‐intensity (H; 40m/min5% grade; n=6) ET groups and trained 5d/week for 4 weeks. ET volume was matched in M and H. Rats were anesthetised and instrumented with indwelling catheters and a femoral artery flow probe. Changes in femoral vascular resistance (FVR; arbitrary resistance units (RU)) in response to lumbar sympathetic chain stimulation delivered continuously at 2Hz or in patterns of 20 and 40Hz was determined before and after NO synthase inhibition (L‐NAME 5mg/kg IV). Basal blood flow and MAP were similar across groups. Prior to NOS inhibition, stimulations induced larger increases (p<0.05) in FVR in M (2Hz: 15±4; 20Hz: 17±4; 40Hz: 17±4 RU) and H (2Hz: 20±5; 20Hz: 26±6; 40Hz: 27±4 RU) compared to S (2Hz: 7±2; 20Hz: 9±3; 40Hz: 11±3RU). L‐NAME augmented the vascular response to sympathetic stimulation in S, M and H groups. However, the magnitude of the increase in FVR during NO inhibition was smaller (p<0.05) in S (2Hz: 11±6; 20Hz: 22±10; 40Hz: 25±10 RU) compared to M (2Hz: 30±18; 20Hz: 43±27; 40Hz: 50±32 RU) and H (2Hz: 43±18; 20Hz: 63±26; 40Hz: 73±31 RU). These data suggest that ET enhances NO mediated blunting of sympathetic vasoconstriction. NSERC Canada.