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Endogenous neurotransmitter release and sympathetic vasoconstriction during prolonged exercise
Author(s) -
DeLorey Darren S,
Hamann Jason J,
Valic Zoran,
Kluess Heidi A,
Clifford Philip S,
Buckwalter John B
Publication year - 2006
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.20.5.a1400-b
Our laboratory has previously reported a decline in sympathetic nervous system restraint of skeletal muscle blood flow during prolonged mild‐intensity (3 miles/h) exercise. This decline may be explained by: 1) a decrease in α‐adrenergic receptor responsiveness over time; and/or 2) a decline in endogenous norepinephrine bioavailability. Thus, the purpose of the present study was to investigate the effect of exercise duration on the vasoconstrictor response to pharmacologically evoked endogenous norepinephrine release. Mongrel dogs (n=5) were instrumented chronically with transit‐time flow probes on the external iliac arteries and an indwelling catheter in a branch of the femoral artery. Tyramine (3 μg/ml hindlimb flow) was infused following 5, 30 and 50 min of treadmill exercise at 3 mph. Hindlimb blood flow (HBF) and mean arterial pressure (MAP) were monitored continuously. Vascular conductance (VC) was calculated as HBF/MAP. During treadmill running at 3 mph, infusion of tyramine resulted in similar decreases in VC following 5 (55 ± 15 %), 30 (51 ± 10 %) and 50 (50 ± 7 %) min of exercise. These results demonstrate that sympathetic vasoconstriction in response to endogenous norepinephrine release does not decline during prolonged mild‐intensity exercise. Thus, a decrease in α‐adrenergic receptor responsiveness over time and/or a decrease in norepinephrine bioavailability do not appear to be responsible for the decrease in sympathetic restraint of muscle blood flow during prolonged exercise. Supported by NHLBI, VA Research and NSERC, Canada