Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific

Abstract

Murias JM, Grise KN, Jiang M, Kowalchuk H, Melling CWJ, Noble EG. Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific. Am J Physiol Regul Integr Comp Physiol 304: R574 -R580, 2013. First published December 12, 2012 doi:10.1152/ajpregu.00508.2012.-The dynamic adjustment and amplitude of the endothelium-dependent vasorelaxation of the carotid, aorta, iliac, and femoral vessels were measured in response to acute low-(LI) or high-intensity (HI) endurance exercise. Vasorelaxation to 10 Ϫ4 M ACh was evaluated in 10 control, 10 LI, and 10 HI rats. Two-millimeter sections of carotid, aorta, iliac, and femoral arteries were mounted onto a myography system. Vasorelaxation responses were modeled as a monoexponential function. The overall (control, 10.5 Ϯ 6.0 s; LI, 10.4 Ϯ 5.7 s; HI, 11.0 Ϯ 6.9 s) and time-to-steady-state (control, 47.6 Ϯ 24.0 s; LI, 46.2 Ϯ 22.8 s; HI, 49.1 Ϯ 28.3 s) was similar in LI, HI, and control (P Ͼ 0.05). The overall (average of four vessel-type) % vasorelaxation was larger in LI (73 Ϯ 16%) and HI (73 Ϯ 16%) than in control (66 Ϯ 19%) (P Ͻ 0.05). The overall rate of vasorelaxation was greater in LI (1.9 Ϯ 0.9%·s Ϫ1) and HI (1.9 Ϯ 1.1%·s Ϫ1) compared with control (1.6 Ϯ 0.7%·s Ϫ1 ) (P Ͻ 0.05). The vessel-specific responses (average response for the three conditions) showed that carotid displayed a slower adjustment (, 18.9 Ϯ 4.4 s; time-to-steady-state, 80.4 Ϯ 18.4 s) compared with the aorta (, 10.3 Ϯ 3.8 s; time-to-steady-state, 46.3 Ϯ 15.2 s), the iliac (, 6.3 Ϯ 2.1 s; time-to-steady-state, 30.3 Ϯ 9.0 s), and the femoral (, 6.0 Ϯ 1.9 s; time-to-steady-state, 29.3 Ϯ 8.4 s). The % vasorelaxation was larger in the carotid (82 Ϯ 14%) than in the aorta (67 Ϯ 16%), iliac (61 Ϯ 13%), and femoral (71 Ϯ 19%) (P Ͼ 0.05). The rate of vasorelaxation was carotid (1.1 Ϯ 0.2%·s, and femoral (2.6 Ϯ 1.0%·s Ϫ1 ). In conclusion, an acute bout of endurance exercise increased vascular responsiveness. The dynamic and percent adjustments were vessel-specific with vessel function likely determining the response. endothelium-dependent vasorelaxation; vessel myography; vascular responsiveness; vascular kinetics THE MATCHING OF BLOOD FLOW to the metabolic demands for oxygen and other nutrients throughout different organs is of critical importance to maintain cellular energetics and homeostasis (2). In this regard, relaxation of the vascular smooth muscle through diffusion of nitric oxide (NO) produced in the endothelial cells through the activation of endothelial NO synthase (e-NOS) has been shown to be fundamental (6,9,29). Although the positive effects of endurance exercise training on vascular responsiveness (and more specifically endothelium-dependent vasodilation) have been demonstrated (12,13,15,28), the effects of an acute bout of exercise on vascular responsiveness are poorly understood. For instance, an early study by Delp and Laughlin (5) showed no changes in the vasorelaxation response to a given dose of ACh in the aorta arteries of rats 24 h after a single, 1-h bout of...

Effects of short‐term training and detraining on VO2 kinetics: Faster VO2 kinetics response after one training session

“…Our data support the idea that improvements in the matching of O 2 delivery to O 2 distribution were an important factor mediating the faster VO 2 kinetics observed within the first two training sessions (as indicated by a reduction in the "overshoot" in the HHb VO [ ] 2 ratio, reflecting microvascular fractional O 2 extraction per unit VO 2 and thus indicating the dynamic balance between O 2 delivery and muscle O 2 utilization in the area of NIRS interrogation). This observation is consistent with several studies showing that, even in young healthy individuals, improvement in O 2 provision to the active tissues plays an important role in regulating the speed of the VO 2 adjustment (Murias et al, 2010b(Murias et al, ,c, 2011c(Murias et al, , 2014, and is supported by other studies demonstrating a rapid improvement in vascular responsiveness even after an acute bout of exercise (Haram et al, 2006;Goto et al, 2007;Murias et al, 2013). For example, it has been demonstrated in rat vessels that improvements in endothelium-dependent responses after one session of endurance exercise result in a greater amplitude and sensitivity of the vessels as well as a greater rate of vasorelaxation (Haram et al, 2006;Murias et al, 2013).…”

“…This observation is consistent with several studies showing that, even in young healthy individuals, improvement in O 2 provision to the active tissues plays an important role in regulating the speed of the VO 2 adjustment (Murias et al, 2010b(Murias et al, ,c, 2011c(Murias et al, , 2014, and is supported by other studies demonstrating a rapid improvement in vascular responsiveness even after an acute bout of exercise (Haram et al, 2006;Goto et al, 2007;Murias et al, 2013). For example, it has been demonstrated in rat vessels that improvements in endothelium-dependent responses after one session of endurance exercise result in a greater amplitude and sensitivity of the vessels as well as a greater rate of vasorelaxation (Haram et al, 2006;Murias et al, 2013). These improved vasorelaxation responses were observed at higher (∼70-80% VO max 2 ; Haram et al, 2006;Murias et al, 2013) and lower (∼50-60% of VO max 2 ; Murias et al, 2013) intensities of exercise.…”

“…For example, it has been demonstrated in rat vessels that improvements in endothelium‐dependent responses after one session of endurance exercise result in a greater amplitude and sensitivity of the vessels as well as a greater rate of vasorelaxation (Haram et al., ; Murias et al., ). These improved vasorelaxation responses were observed at higher (∼70–80% ; Haram et al., ; Murias et al., ) and lower (∼50–60% of ; Murias et al., ) intensities of exercise. Similarly, short‐term exercise training (seven consecutive days, 1 h at 5.6 km/h twice daily) has been shown to enhance endothelium‐dependent vasorelaxation responses in pig conduit vessels (McAllister & Laughlin, ), and somewhat longer training interventions (2–4 weeks) in young rats have shown that training increases endothelial nitric oxide (NO) synthesis in skeletal muscle arterioles and improves the vasodilator responses (Sun et al., ).…”

Effects of Ginseng Supplementation and Endurance-Exercise in the Artery-Specific Vascular Responsiveness of Diabetic and Sedentary Rats

“…A portion of the carotid, abdominal aorta, and femoral artery were then divided into ∼2 mm long rings and, after removal of luminal blood clots, vessel rings were used for in vitro isometric tension measurements. These vessels were selected to represent a commonly used artery in this type of preparation that reflects more central delivery of blood (i.e., aorta), and more peripheral conduit arteries that, despite similar morphological characteristics, have been shown to display differential functional profiles (i.e., carotid and femoral) ( Murias et al, 2013a , c ).…”

Slower V˙O2 Kinetics in Older Individuals

“…Based on these results, the authors speculated that increases in ACh-mediated and flow-induced vasodilation might have mediated the faster V O 2 kinetics observed in response to exercise training. Indeed, improvements in ACh-mediated vasodilatory response have been reported to occur and peak between 24 and 48 h following an acute bout of exercise (42,56) and to remain elevated for 96 h after exercise (42) in young rats. Importantly, chronic exposure to exercise (6 wk) resulted in increases in vasodilatory responses that were twice as large and longer-lasting (È1 wk) compared with those observed with acute exercise (42).…”