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The article discusses the findings of a study which demonstrated how nitric oxide (NO) and prostaglandins (PG) contribute to increased blood flow during hypoxic exercise. The experiment involved 10 young healthy adults who were measured for forearm blood flow (FBF), and vascular conductance responses at moderate exercise intensity. The study concluded that NO and PG inhibition can reduce hypoxic exercise hyperaemia and eliminate hypoxic vasodilatation at rest.

Acute ascorbic acid (AA) administration increases muscle blood flow during dynamic exercise in older adults, and this is associated with improved endothelium-dependent vasodilation. We directly tested the hypothesis that increase in muscle blood flow during AA administration is mediated via endothelium-derived vasodilators nitric oxide (NO) and prostaglandins (PGs). In 14 healthy older adults (64 ± 3 yr), we measured forearm blood flow (FBF; Doppler ultrasound) during rhythmic handgrip exercise at 10% maximum voluntary contraction. After 5-min steady-state exercise with saline, AA was infused via brachial artery catheter for 10 min during continued exercise, and this increased FBF ~25% from 132 ± 16 to 165 ± 20 ml/min (P < 0.05). AA was infused for the remainder of the study. Next, subjects performed a 15-min exercise bout in which AA + saline was infused for 5 min, followed by 5 min of the nitric oxide synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) and then 5 min of the cyclooxygenase inhibitor ketorolac (group 1). The order of inhibition was reversed in eight subjects (group 2). In group 1, independent NOS inhibition reduced steady-state FBF by ~20% (P < 0.05), and subsequent PG inhibition had no impact on FBF (Δ 3 ± 5%). Similarly, in group 2, independent PG inhibition had little effect on FBF (Δ -4 ± 4%), whereas subsequent NO inhibition significantly decreased FBF by ~20% (P < 0.05). In a subgroup of five subjects, we inhibited NO and PG synthesis before AA administration. In these subjects, there was a minimal nonsignificant improvement in FBF with AA infusion (Δ 7 ± 3%; P = nonsignificant vs. zero). Together, our data indicate that the increase in muscle blood flow during dynamic exercise with acute AA administration in older adults is mediated primarily via an increase in the bioavailability of NO derived from the NOS pathway. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that aging is associated with an impaired contraction-induced rapid vasodilation in healthy adults. We reasoned that employing single contractions of a small muscle mass would allow us to isolate the local rapid vasodilatory responses independent of systemic hemodynamic and sympathetic neural influences on forearm hemodynamics. We measured forearm blood flow (Doppler ultrasound) and arterial blood pressure (Finapres) on a beat-by-beat basis and calculated the changes in forearm vascular conductance (L~FVC) in response to forearm contractions in 18 young (24 ± 1 yr) and 13 older (62 ± 2 yr) healthy subjects. Single, 1-s dynamic forearm contractions were performed with the experimental arm slightly above heart level at 5, 10, 20, and 40% of the subjects' maximal voluntary contraction (MVC) in random order. In general, muscle contractions evoked a rapid increase in FVC that reached a peak within approximately four to five cardiac cycles postcontraction in both age groups. At 5% MVC, there were no significant age-related differences in contraction-induced forearm vasodilation. However, the peak vasodilatory responses were impaired -40-45% in older adults at 10, 20, and 40% MVC, as were the total vasodilatory responses (area under curve -40-50%; all P < 0.05). Additionally, the immediate vasodilation (first cardiac cycle postcontraction) for the 20% and 40% MVC trials was also impaired -50% with age (P < 0.05). There were no significant age-group differences in MVC or forearm fat-free mass, and these variables were not correlated with local vasodilation within a given exercise intensity. Under the experimental conditions employed, the blunted responses with age reflect impaired local contraction-induced rapid vasodilation. [ABSTRACT FROM AUTHOR]

Muscle sympathetic vasoconstrictor nerve activity increases with advancing age, but does not result in elevated forearm vasoconstrictor tone due to a selective reduction in α1-adrenergic receptor responsiveness. In contrast, the leg circulation of older adults is under greater tonic sympathetic vasoconstriction, but it is unclear whether leg α-receptor responsiveness is altered with age. We tested the hypothesis that α-adrenergic receptor responsiveness is not reduced in the leg circulation with age. In 12 young (24±1 yrs) and 7 healthy older men (62±2 yrs), we measured femoral blood flow (FBF; Doppler ultrasound) and calculated the vascular conductance (FVC) responses to alpha-adrenergic receptor stimulation via intra-femoral artery infusions of tyramine (evokes endogenous NE release), phenylephrine α1-agonist), and dexmedetomidine (α2-agonist) during local blockade of β-adrenergic receptors. At rest, femoral blood flow and vascular conductance were ∼30% lower in older compared with young men. Maximal vasoconstrictor responses (%ΔFVC) to tyramine (-30±3 vs -41±3%), phenylephrine (-25±4 vs -45±5%), and dexmedetomidine (-22±4 vs -44±3%) were significantly reduced in older compared with young men (all P<0.05). We conclude that aging is associated with impaired leg α-adrenergic receptor responsiveness at rest, and that this involves both α1- and α2-adrenergic receptors. [ABSTRACT FROM AUTHOR]