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Altered vasodilatory mechanisms during exercise in aging humans
Author(s) -
Schrage William G,
Eisenach John H,
Dietz Niki M,
Joyner Michael J
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.20.4.a812-c
Subject(s) - vasodilation , medicine , ketorolac , forearm , reactive hyperemia , brachial artery , nitric oxide , blood flow , endocrinology , anesthesia , blood pressure , surgery , analgesic
Aging humans exhibit lower exercise blood flow (exercise hyperemia), but the vascular mechanisms mediating this remain unknown. In aging humans, agonist infusions suggest endothelial dysfunction, due in part to less nitric oxide (NO) and prostaglandin (PG) mediated vasodilation. Notably, in young adults inhibition of NO or PGs decreases exercise hyperemia by 20% and 12%, respectively. We tested the hypothesis that aging humans would exhibit an attenuated reduction in exercise hyperemia following inhibition of NO or PGs, due to less vasodilation from these signals. Eleven older males and females (55–76 years) performed dynamic forearm exercise for 20 minutes. Forearm blood flow (FBF) was measured beat‐to‐beat with Doppler ultrasound while saline or drugs were infused sequentially via brachial artery catheter in the exercising forearm. After achieving steady state exercise (min 5), L‐NAME (25 mg) was infused for 5 minutes to inhibit NO synthase. After 2 more minutes of exercise (saline), ketorolac (6 mg) was infused for 5 minutes to inhibit PGs, followed by 3 more minutes of exercise with saline. L‐NAME reduced exercise hyperemia by 13–18% in older subjects, whereas ketorolac had no net effect on blood flow. In the reverse drug order (n=6), ketorolac did not effect FBF, but L‐NAME reduced FBF by 10–13%. Our results suggest that in aging humans, the contribution of NO to exercise hyperemia may be modestly reduced, but the role of PGs mediating vasodilation is completely lost. Loss of vasodilating PGs along with diminished NO may contribute to lower blood flow in aging humans. Grant support: HL‐69692, HL‐46493, and GCRC RR‐00585.