Age-associated impairments in contraction-induced rapid-onset vasodilatation within the forearm are independent of mechanical factors

Abstract

New findings: What is the central question of this study? We examined whether the mechanical contribution to contraction-induced rapid-onset vasodilatation (ROV) differed with age and whether ROV is associated with peripheral artery stiffness. Furthermore, we examined how manipulation of perfusion pressure modulates ROV in young and older adults. What is the main finding and its importance? The mechanical contribution to ROV is similar in young and older adults. Conversely, peripheral arterial stiffness is not associated with ROV. Enhancing perfusion pressure augments ROV to a similar extent in young and older adults. These results suggest that age-related attenuations in ROV are not attributable to a mechanical component and that ROV responses are independent of peripheral artery stiffness.

Abstract: Contraction-induced rapid-onset vasodilatation (ROV) is modulated by perfusion and transmural pressure in young adults; however, this effect remains unknown in older adults. The present study examined the mechanical contribution to ROV in young versus older adults, the influence of perfusion pressure and whether these responses are associated with arterial stiffness. Forearm vascular conductance (in millilitres per minute per 100 mmHg) was measured in 12 healthy young (24 ± 4 years old) and 12 older (67 ± 3 years old) adults during: (i) single dynamic contractions at 20% of maximal voluntary contraction; and (ii) single external mechanical compression of the forearm (200 mmHg) positioned above, at and below heart level. Carotid-radial pulse-wave velocity characterized upper limb arterial stiffness. Total ROV responses to single muscle contractions and single external mechanical compressions were attenuated in older adults at heart level (P < 0.05); however, the relative mechanical contribution to contraction-induced peak (46 ± 14 versus 40 ± 18%; P = 0.21) and total (37 ± 21 versus 32 ± 18%; P = 0.27) responses were not different between young and older adults. Reducing or enhancing perfusion pressure altered ROV responses to a similar extent between young and older adults (P < 0.05). Upper limb arterial stiffness was not associated with peak (r = 0.02; P = 0.93) or total vascular conductance (r = -0.01; P = 0.96) in the group as a whole. Our data suggest that: (i) age-associated attenuations in ROV are not attributable to a mechanical component; (ii) enhancing perfusion pressure augments ROV to a similar extent between young and older adults; and (iii) basal upper limb arterial stiffness is not associated with the vasodilator responses after a single skeletal muscle contraction in young and older adults.

Keywords: ageing; contraction-induced vasodilatation; skeletal muscle pump.

Figure 1

Experimental Timeline. Hatch marks indicate 15 minutes of rest between each trial. Order was randomized and counter-balanced within subjects.

Figure 2

Change in vascular conductance (Δ vascular conductance) over 30 cardiac cycles following a single forearm contraction (20% MVC; A & B) and single mechanical compression (200 mmHg; C & D) with changes in arm position relative to heart level (above, at, and below-heart level) in young (A & C) and older adults (B & D).

Figure 3

Peak (A & B) and total (C & D) hyperaemic and vasodilator responses following a single skeletal muscle contraction and single mechanical compression of the forearm in young and older adults across experimental trials (above-, at-, and below-heart level). * P < 0.05 vs. at-heart level during single skeletal muscle contraction. † P < 0.05 vs. at-heart level during single external compression. ‡P < 0.05 vs. young adults during single skeletal muscle contraction. # P < 0.05 vs. young adults during single external compression.

Figure 4

Relative mechanical contribution to peak (A & B) and total (C & D) hyperaemic and vasodilator responses in young and older adults across experimental trials (above-, at-, and below-heart level). * P < 0.05 vs. at-heart level.