No description available.

There is some evidence to suggest that oxygen consumption (VO2) and oxygen delivery to muscle are reduced at exercise onset and steady state in individuals with type 2 diabetes (T2D), although no studies have combined measurements of both muscle blood flow and VO2 during exercise in this population. OBJECTIVES: 1) To determine whether a reduction in VO2 during exercise would be accompanied by reduced leg blood flow (LBF). 2) To examine the dynamic response characteristics of LBF to determine whether feedforward and/or feedback control systems of blood flow regulation are impaired. METHODS: Four men with T2D and six healthy, activity matched controls (CON) performed supine, two-leg knee extension/flexion exercise tests involving progressive increase in exercise intensity to exhaustion and step increases to a low intensity equivalent to lifting 7.5 kg (LO7.5kg), and a moderate intensity equivalent to 90% of ventilatory threshold (VT90%). MEASUREMENTS: LBF, VO2, mean arterial pressure, heart rate, and stroke volume were measured continuously. RESULTS: Means ± SE, CON vs. T2D. 1) ∆VO2 was not different between groups during the incremental test (P= 0.264), ∆LBF in T2D tended to be lower (P = 0.098). 2) ∆VO2 was not different between groups at any time during LO7.5kg (P = 0.351). Individuals with T2D demonstrated a lower ∆LBF at time = 15 s (3435.6 ± 275.0 vs. 2120.4 ± 218.4 ml/min, P = 0.018). 3) Gains for baseline (G0) and phase I (G1) LBF adaptation to LO7.5kg were lower in T2D compared to CON (G0: 959.8 ± 111.3 vs. 617.0 ± 22.1 ml/min, P = 0.044; G1: 3662.1 ± 229.0 vs. 2128.1 ± 161.6 ml/min, P = 0.002). 4) The time required to achieve 63% of the total response magnitude tended to be slower in T2D (LO7.5kg: 14.3 ± 1.7 vs. 23.1 ± 4.2 s; VT90%: 26.2 ± 3.5 vs. 40.0 ± 7.5 s; P = 0.095). CONCLUSIONS: 1) The initiatory rise in LBF is significantly lower in individuals with T2D, likely due to impairments in feedforward control mechanisms of blood flow regulation, 2) Individuals with T2D do not demonstrate lower VO2 responses to exercise despite an impaired LBF response. / Thesis (Master, Kinesiology & Health Studies) -- Queen's University, 2009-10-09 17:52:31.708

To optimize muscle blood flow to the skeletal muscle during exercise, the vascular bed of the muscle is partially protected from sympathetic nervous activity (SNA) vasoconstriction via a phenomenon termed functional sympatholysis. Functional sympatholysis has been documented during exercise periods in human skeletal muscle. However, it remains unknown whether functional sympatholysis is specific to the exercising period, or if it may persist for a period of time following skeletal muscle exercise. Through this study, we aimed to confirm the presence and duration of post-exercise functional sympatholysis in the human skeletal muscle. The cold pressor test (CPT) was administered to 9 male (mean age = 21.1 ± 0.8 years) participants at various time points during four different experimental trials (Rest, Exercise, Recovery 1 and Recovery 2). Exercise consisted of 7 minutes of moderate isometric handgrip exercise (15% below critical power). Heart rate (HR) and mean arterial pressure (MAP) were recorded continuously throughout each trial. Brachial artery mean blood velocity measurements as well as brachial artery diameter measurements were recorded on each participant’s exercising arm throughout each trial. Deep venous blood samples were drawn pre- and post-CPT administration from a catheter inserted into an antecubital vein of each participant’s non-experimental arm. The cardiovascular response to the CPT was repeatable across experimental days as it consistently resulted in MAP elevations regardless of the experimental time point of administration. The CPT also resulted in a significant elevation in plasma norepinephrine concentration from 0.49 ± 0.04 ng/mL at “pre-CPT” measurement to 0.66 ± 0.05 ng/mL at the end of the CPT in the Rest trial (P < 0.05). The percentage reduction in forearm vascular conductance (FVC) due to CPT administration during Exercise (4.5 ± 6.6%) and Recovery 1 (4 minutes post-exercise; -11.6 ± 8.8%) was significantly blunted in comparison to that measured during Rest (-34.8 ± 7.4%) (P < 0.05). The percentage change in FVC during the Recovery 2 trial (10 minutes post-exercise; -20.1 ± 7.1%) was not significantly different from that measured at Rest. These findings support the concept of a lingering presence of functional sympatholysis 4 minutes, but not 10 minutes, post-moderate exercise. / Thesis (Master, Kinesiology & Health Studies) -- Queen's University, 2011-12-21 17:17:09.037

We sought to determine if compensatory vasodilator and/or pressor responses protect exercising muscle O2 delivery (O2D) under conditions of reduced arterial perfusion pressure, if this is exercise intensity-dependent, and if distinct cardiovascular response phenotypes exist. Ten healthy male subjects (19.5±0.4 years) completed two trials of a ramp protocol forearm isometric handgrip exercise test to exhaustion (2.5 kg increments every 3.5 minutes) in each of forearm above and below heart level (forearm arterial perfusion pressure (FAPP) difference of 29.5±0.97 mmHg). Forearm blood flow ((FBF (ml/min; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (MAP; finger photoplethysmography), and exercising forearm venous effluent (ante-cubital vein catheter) measurements at the end of each work rate (WR) revealed the following. Group level (n=10) Δ FBF was compromised beyond 5 kg WR in above vs. below (P<0.05). There was no evidence of compensatory vasodilator (P=0.21) or pressor (P=0.63) responses. Peak O2D, WR and VO2 were significantly compromised by reduced FAPP (115.6±16.8 vs. 152.0±13.4 mlO2/min, 25.5±1.22 vs. 28.94±1.50 kg and 75.9±5.3 vs. 100.2±8.6 ml/min; P<0.05). In contrast, examination of individual responses revealed distinct cardiovascular response groups with (n=6) vs. without (n=4) compensatory vasodilation with the former having less compromise to submaximal O2D and peak WR (-94.12±23.42 vs. -223.40±36.01 mlO2/min), P<0.05 and -2.5±0.32 vs. -5.32±0.79 kg, P<0.05). In conclusion, exercising forearm muscle hypoperfusion due to reduced FAPP is not compensated for by pressor responses. However, there appear to be distinct phenotypes in which vasodilatory compensation does vs. does not occur, which in the former partially protects O2D and exercise performance. / Thesis (Master, Kinesiology & Health Studies) -- Queen's University, 2012-09-13 16:42:41.751

Dissertation submitted in partial compliance with the requirements for the Master’s Degree in Technology: Chiropractic Durban University of Technology, 2009 / Aim: To investigate the effect of therapeutic and sham ultrasound on radial artery blood flow (m.s-1) and radial arterial lumen diameter (mm). Subjects: Fifty healthy asymptomatic volunteers between the ages of 18-38 years. Methodology: The subjects were randomly allocated into one of five intervention groups (A-E). Group A received continuous ultrasound at 0.2 W.cm-² for 5 minutes, Group B received pulse ultrasound at 0.2 W.cm-² for 5 minutes, Group C received continuous ultrasound at 1.5 W.cm-² for 5 minutes, Group D received pulse ultrasound at 1.5 W.cm-² for 5 minutes and Group E received sham ultrasound at 0 W.cm-² for 5 minutes. Baseline radial artery blood flow (m.s-1) and radial artery lumen diameter (mm) readings were taken prior to the commencement of the therapeutic or sham ultrasound application using a Doppler ultrasound. At four minutes of application (during the therapeutic or sham ultrasound application), another set of blood flow and arterial lumen diameter measurements were taken. The final blood flow and arterial lumen diameter measurements were taken one minute after the therapeutic or sham ultrasound application was stopped. Results: The mean (± SD) radial artery blood flow and radial artery lumen diameter at baseline was 0.197 (± 0.060) m.s-1 and 2.4 (± 0.6) mm respectively. In Group A, the mean (± SD) radial artery blood flow during ultrasound application and one-minute after ultrasound application was 0.193 (± 0.070) m.s-1 and 0.179 (± 0.073) m.s-1 respectively. The mean (± SD) radial artery lumen diameter in Group A at the two time intervals was 2.2 (± 0.5) mm and 2.2 (± 0.3) mm respectively. In Group B, the mean (± SD) radial artery blood flow during ultrasound application and one-minute after ultrasound application was 0.187 (± 0.067) m.s-1 and 0.195 (± 0.041) m.s-1 respectively. The mean (± SD) radial artery lumen diameter in Group B at the two time intervals was 2.4 (± 0.4) mm and 2.3 (± 0.5) mm respectively. In Group C, the mean (± SD) radial artery blood flow during ultrasound application and one-minute after ultrasound application was 0.225 (± 0.088) m.s-1 and 0.186 (± 0.071) m.s-1 respectively. The mean (± SD) radial artery lumen diameter in Group C at the two time intervals was 2.4 (± 0.7) mm and 2.7 (± 0.8) mm respectively. In Group D, the mean (± SD) radial artery blood flow during ultrasound application and one-minute after ultrasound application was 0.215 (± 0.080) m.s-1 and 0.200 (± 0.081) m.s-1 respectively. The mean (± SD) radial artery lumen diameter in Group iv D at the two time intervals was 2.4 (± 0.8) mm and 2.4 (± 0.7) mm respectively. In Group E, the mean (± SD) radial artery blood flow during ultrasound application and one-minute after ultrasound application was 0.200 (± 0.067) m.s-1 and 0.182 (± 0.075) m.s-1 respectively. The mean (± SD) radial artery lumen diameter in Group E at the two time intervals was 2.5 (± 0.7) mm and 2.3 (± 0.5) mm respectively. There was no significant change in radial artery blood flow and radial artery lumen diameter over time in any individual group or between groups (p > 0.05; repeated measures ANOVA). There was an overall weak positive correlation between radial artery blood flow and radial artery lumen diameter at baseline (r = 0.508), during (r = 0.541) and after (r = 0.532) the therapeutic or sham ultrasound application. Conclusion: The results of this study showed that continuous, pulse or sham ultrasound had no significant effect on radial artery blood flow and radial artery lumen diameter. Furthermore, active ultrasound (continuous and pulse) was not superior to sham ultrasound in significantly affecting blood flow in a muscular artery.

No description available.

No description available.

No description available.

No description available.

No description available.