Femoral Blood Flow Research Articles

Relationship between regional sympathetic vascular transduction and sympathetic transduction of blood pressure in young adults at rest.

A burst of muscle sympathetic nerve activity (MSNA) induces vasoconstriction that transiently reduces regional vascular conductance and increases systemic blood pressure (BP) over the subsequent 4-8 cardiac cycles. These responses are termed sympathetic neurovascular transduction and sympathetic transduction of BP, respectively. Sympathetic transduction of BP is commonly calculated and interpreted as a proxy measure for regional sympathetic neurovascular transduction despite the systemic nature of BP regulation. The present analysis tested whether the peak change in signal-averaged sympathetic transduction of BP was correlated to the change in regional sympathetic vascular transduction at rest. Fourteen adults (5 females, 23 ± 3 yr) arrived at the laboratory, ate a standardized meal, and rested for 90-120 min. MSNA (fibular nerve microneurography), heart rate (electrocardiography), beat-to-beat BP (finger photoplethysmography), and superficial femoral artery blood flow (Doppler ultrasound) were obtained continuously for 10 min in the supine position. Femoral vascular conductance (FVC) was calculated as blood flow divided by mean arterial BP. The peak change in diastolic BP following a burst of MSNA was correlated to the corresponding nadir change in femoral vascular conductance (r = -0.58 [-0.07 to -0.85], P = 0.03) and superficial femoral artery blood flow (r = -0.54 [-0.17 to -0.83], P = 0.04). The nadir change in diastolic BP in cardiac cycles not following an MSNA burst was correlated to the peak change in femoral vascular conductance (r = -0.42 [-0.83 to 0.00], P = 0.05), but not superficial femoral artery blood flow (r = 0.41 [-0.77 to 0.15], P = 0.14). In conclusion, more commonly assessed sympathetic transduction of BP provides moderate insight into regional sympathetic neurovascular transduction.NEW & NOTEWORTHY The majority of studies have used signal-averaged sympathetic transduction of blood pressure as a generalized measure of transduction. In this analysis, we show that sympathetic transduction of blood pressure and regional sympathetic vascular transduction were moderately correlated in healthy adults at rest. The moderate strength of this relationship highlights potential differences between regional and systemic assessments of sympathetic transduction and suggests that future work should choose the transduction measure best aligned with the research question.

Post-exercise hot or cold water immersion does not alter perception of effort or neuroendocrine responses during subsequent moderate-intensity exercise.

Post-exercise hot (HWI) and cold (CWI) water immersion are popular strategies used by athletes in a range of sporting contexts, such as enhancing recovery or adaptation. However, prolonged heating bouts increase neuroendocrine responses that are associated with perceptions of fatigue. Fourteen endurance-trained runners performed three trials consisting of two 45-min runs at 95% lactate threshold on a treadmill separated by 6h of recovery. Following the first run, participants completed one of HWI (30min, 40°C), CWI (15min, 14°C) or control (CON, 30min rest in ambient conditions) in a randomised order. Perceived effort and recovery were measured using ratings of perceived exertion (RPE) and the Acute Recovery and Stress Scale (ARSS), whilst physiological responses including venous concentrations of a range of neuroendocrine markers, superficial femoral blood flow, heart rate and rectal temperature were measured. Exercise increased neuroendocrine responses of interleukin-6, adrenaline and noradrenaline (all P <0.001). Additionally, perceptions of overall recovery (P <0.001), mental performance capacity (P =0.02), physical performance capability (P =0.01) and emotional balance (P =0.03) were reduced prior to the second run. However, there was no effect of condition on these variables (P>0.05), nor RPE (P =0.68), despite differences in rectal temperature, superficial femoral blood flow following the first run, and participants' expected recovery prior to the intervention (all P <0.001). Therefore, athletes may engage in post-exercise hot or cold-water immersion without negatively impacting moderate-intensity training sessions performed later the same day.

Central and peripheral haemodynamics at exercise onset: the role of central command

PurposeThe involvement of central command in central hemodynamic regulation during exercise is relatively well-known, although its contribution to peripheral hemodynamics at the onset of low-intensity contractions is debated. This study sought to examine central and peripheral hemodynamics during electrically-evoked muscle contractions (without central command) and voluntary muscle activity (with central command).MethodsCyclic quadriceps isometric contractions (1 every second), either electrically-evoked (ES; 200 ms trains composed of 20 square waves) or performed voluntarily (VC), were executed by 10 healthy males (26 ± 3 years). In both trials, matched for force output, peripheral and central hemodynamics were analysed.ResultsAt exercise onset, both ES and VC exhibited equal peaks of femoral blood flow (1276 ± 849 vs. 1117 ± 632 ml/min, p > 0.05) and vascular conductance (15 ± 11 vs. 13 ± 7 ml/min/mmHg, p > 0.05), respectively. Similar peaks of heart rate (86 ± 16 bpm vs. 85 ± 16 bpm), stroke volume (100 ± 20 vs. 99 ± 27 ml), cardiac output (8.2 ± 2.5 vs. 8.5 ± 2.1 L/min), and mean arterial pressure (113 ± 13 vs. 113 ± 3 mmHg), were recorded (all, p > 0.05). After ~ 50 s, all the variables drifted to lower values. Collectively, the hemodynamics showed equal responses.ConclusionThese results suggest a similar pathway for the initial (first 40 s) increase in central and peripheral hemodynamics. The parallel responses may suggest an initial minimal central command involvement during the onset of low-intensity contractions, likely associated with a neural drive activation delay or threshold.

Ultrasound vector mapping of common femoral artery blood flow in normal and early-stage stenosis

It is assumed that the wall shear stress (WSS), which determines the function of the endothelium, is constant along the arterial bed. The assessment of turbulence, blood flow velocity in the arterial system in healthy (13 patients) and in patients with the initial form of atherosclerosis in the femoral artery (42 patients) was discussed. The study quantified blood flow in the common femoral artery using V Flow with visualization of blood flow with a high frame rate. The results obtained in the femoral arteries were evaluated by the wall shear rate, velocity profile and oscillation index (OSI). It was shown that the average value of WSSmean in the femoral artery in healthy and in patients with stenosis &lt;30–35% is 0.9± 0.4 – 0.91±0.4 Pa and does not significantly differ. The wall thickness in the common femoral artery in patients with the initial form of atherosclerosis was 0.9–1.1 mm, and in healthy patients 0.8–0.9 mm. The correlation between the parameters was evaluated by nonparametric analysis of Kendall’s Taub. It was revealed that there is no correlation between WSSmean and blood flow velocity (Vs) in both healthy and patients with the initial form of atherosclerosis.

Interactions Between Reproductive Hormones and Neuro-Vascular Regulation During the Cold Pressor Test in Young Females

Recently, we reported that muscle sympathetic nerve activity (MSNA) is not predictive of vascular nor blood pressure outcomes during the cold pressor test (CPT) in young healthy females. Instead, we observed substantial variability in vascular responses to the CPT which ranged widely from decreases in blood flow and vascular conductance to increases in these same outcomes. Interindividual differences in circulating reproductive hormones may account for this female-specific variability in vascular responses to acute elevations in MSNA. Therefore, the purpose of this study was to test the hypothesis that reproductive hormones account for variability in MSNA, femoral blood flow (FBF), and femoral vascular conductance (FVC) during the CPT in females. We retrospectively assessed data from 9 young healthy females (age: 24±3 years) in the low hormone phase of their menstrual cycle (days 1-5). Intravenous blood samples were obtained and prospectively analyzed to assess concentrations of circulating reproductive hormones (radioimmunoassay). Integrated peroneal MSNA (microneurography; NeuroAmpEX, ADI) was quantified at rest and during a 3-minute hand CPT. Mean arterial pressure (MAP) was measured beat-by-beat (Finometer Midi, FMS) and duplex vascular ultrasound was used to measure FBF; FVC was quantified as FBF/MAP (mL/min/mmHg). All variables are expressed as the difference between the average CPT value and the average baseline value. CPT-induced changes in MSNA burst incidence (bursts/100hb) were not related to [17-beta-estradiol] (R2=0.05; P=0.60), [progesterone] (R2=0.11, P=0.47), or [free testosterone] (R2=0.01, P=0.81). Similarly, changes in FBF and FVC were not related to [17-beta-estradiol] (FBF: R2=0.04, P=0.67; FVC: R2=0.01, P=0.80) or [progesterone] (FBF: R2=0.04, P=0.67; FVC: R2=0.09, P=0.51). However, there was a negative correlation between [free testosterone] and the changes in both FBF (R2=0.69, P=0.02) and FVC (R2=0.66, P=0.03). In other words, females with higher free testosterone demonstrated larger decreases in FBF and FVC during the CPT relative to those with lower free testosterone concentrations. These data suggest that circulating free testosterone may act to increase the vasoconstrictive consequences of MSNA in females, and may account for the previously observed variability in vascular responses to MSNA during acute stress. This project was funded by: NSERC and FRQ-S. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Novel Use of 1-methylhistamine as a Biomarker of the Histamine Response to Exercise

Histamine is released within skeletal muscle during exercise, promoting a sustained post-exercise vasodilation and contributing to adaptive responses to exercise training. Tracking this response is complicated by the short half-life and localization of histamine, requiring invasive methods such as intramuscular microdialysis or arteriovenous catheterization. Surrogates based on regional blood flow to assess post-exercise vasodilation require skilled use of expensive equipment, such as ultrasonography. These approaches may not be available in many research or athletic settings. Therefore, we explored the use of 1-methylhistamine (1-MH), a primary metabolite of histamine, as a novel biomarker of histamine’s release in response to aerobic and resistance exercise. We hypothesized that urinary 1-MH production would increase following exercise and that it would be positively correlated with post-exercise femoral artery blood flow and vascular conductance. Six healthy (1F, 5M; 22±4y; 24.3±1.9 kg·m2) trained participants (VO2peak: 51.8±7.7 ml·kg−1·min−1; back squat 1-repetition maximum, 1-RM: 1.66±0.27 kg·bodyweight−1) completed two exercise sessions separated by 1-wk: Aerobic, 30-min of cycling exercise at 70% VO2peak; Resistance, 6 sets of 10 repetitions of back squat exercise at 70% 1-RM. Femoral artery blood flow and vascular conductance were measured and venous blood samples were obtained before, immediately after, and throughout 2-h of post-exercise recovery. Urine was collected during the 24-h before and 2-, and 24-h post-exercise. Histamine and 1-MH concentrations were measured via high-performance liquid chromatography. Results are presented as mean ± SD and were compared by repeated-measures ANOVA and Pearson’s correlations. Blood flow increased immediately after exercise vs before (Aerobic: 442±60 vs 184±58 mL·min−1, p&lt;0.05; Resistance: 626±190 vs 194±54 mL·min−1, p&lt;0.05) and remained elevated 30-min into recovery (Aerobic: 273±63, p&lt;0.05; Resistance: 396±99 mL·min−1, p&lt;0.05). The area under the curve for blood flow after exercise tended to be greater following resistance (16117±5504 mL) vs aerobic (8732±5360 mL, p=0.06) exercise. When averaged across exercise modes, urine 1-MH production was elevated 2-h post-exercise vs before (23.6±15.9 vs 9.2±5.9 μg/h, p&lt;0.05). Urine 1-MH production tended to correlate with percent elevation in femoral artery blood flow (r=0.59, p=0.09) and correlated with the percent elevation in vascular conductance following exercise (r=0.53, p&lt;0.05). These results demonstrate that both aerobic and resistance exercise elicit a histamine response and support the utility of urinary 1-MH production as a biomarker of histamine’s release in response to exercise. Supported by NIH grant R01 AG072805. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Spontaneous Bursts of Muscle Sympathetic Nerve Activity Reduce Femoral Arterial Compliance in Humans

Previous studies in rodents have demonstrated tonic sympathetic restraint of arterial compliance. To date, studies in humans have examined sympathetic restraint of compliance via either reflexively or pharmacologically manipulating sympathetic vasoconstriction and measuring resultant changes in compliance. The extent to which spontaneous bursts of muscle sympathetic nerve activity (MSNA) dynamically regulate arterial compliance in humans on a beat-by-beat basis remains unknown. Herein, we hypothesized that femoral arterial compliance would be transiently reduced following spontaneous bursts of MSNA. Further, we hypothesized that the magnitude of reduction in arterial compliance would be graded to the MSNA burst amplitude (index of net neural outflow). Beat-to-beat blood pressure (BP; Finometer), heart rate (ECG), MSNA (peroneal microneurography), and femoral artery blood flow (duplex Doppler ultrasound) were continuously measured over 10-20 minutes of quiet supine rest in 27 young, healthy men (age: 22 ± 1 years, resting MSNA burst frequency: 11 ± 5 bursts/minute). Customized labview programs were used to time-align neural cardiovascular variables with ultrasound data sampled at 30Hz, enabling the quantification of arterial compliance on a beat-by-beat basis defined as the change in arterial cross-sectional area divided by the change in blood pressure over the cardiac cycle. Bursts of MSNA were tracked for 10 cardiac cycles and changes in arterial compliance were quantified using signal-averaging for all bursts, and subsequently, for bursts of MSNA when sub-classified based on amplitude into quartiles (Q1= smallest 25% of bursts, Q4= largest 25% of bursts). Reductions in arterial compliance were significantly greater following cardiac cycles with bursts of MSNA compared to cardiac cycles without bursts of MSNA (bursts: -5.1 ± 0.6% vs. non-bursts: -0.8 ± 0.2%, p&lt;0.001). Further, reductions in compliance appeared to be graded to MSNA burst amplitude (Q1: -6.5 ± 0.8%; Q4: -9.1 ± 1.3%, P=0.051). The latency (i.e., number of heartbeats) to nadir arterial compliance following bursts of MSNA was 4.2 ± 0.6 cardiac cycles. Collectively, these findings suggest that the sympathetic nervous system dynamically regulates femoral arterial compliance on a beat-to-beat basis. College of Nursing and Health Innovation, University of Texas at Arlington. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Ischemic Conditioning Improves the Microvascular Hyperemic Response to Passive Limb Movement in Young Adults

Background: Passive limb movement (PLM) of the lower extremity is a simple and clinically relevant approach to measure peripheral microvascular health. PLM causes an acute increase in hyperemic leg blood flow (LBF) without an increase in skeletal muscle metabolism, and the hyperemic response is ~80% nitric oxide-mediated. A known therapeutic stimulus to increase large conduit artery vascular health is ischemic conditioning (IC). Whether a single session of IC can improve the hyperemic response to PLM remains unknown. Objective: To quantify the microvascular response to PLM after a single session of IC in young adults. Hypothesis: The hyperemic response to PLM, measured as a change in peak femoral artery blood flow, will be greater following IC vs. sham-IC. Methods: This was a prospective, cross-over, blinded clinical trial (NCT05935670). Young adults aged 18-30 years who were free of cardiovascular disease were recruited, and study participants completed two study visits. Participants were seated in a Biodex dynamometer and superficial femoral artery resting blood flow and diameter were measured in the dominant leg using ultrasonography. The dynamometer then passively moved the knee 90 degrees at a frequency of 1 Hz for a single PLM while blood flow was continuously measured. The ΔLBF was calculated as the absolute (ml/min) and relative (% change) difference in LBF from rest to peak. Participants were then randomized to receive either IC or sham-IC, and the vascular assessor was blinded to the condition. For IC, the cuff was placed around the proximal dominant thigh and repetitively inflated to 225 mmHg for 5 min then deflated for 5 min, for a total of 5 cycles. For sham-IC, the thigh cuff was inflated to only 25 mmHg. Fifteen minutes after IC or sham-IC the hyperemic response to PLM was re-assessed. The pre-/post- change in the PLM hyperemic response was calculated as the difference from pre- vs. post-IC or sham-IC. Statistical analysis included one-sided paired t-tests. Results: Seven individuals (3 female, age 26 ± 4 years old) completed the study. Compared to pre-IC, the relative peak hyperemic response to PLM was augmented post-IC (%ΔLBF = 89 ± 42% pre- vs. 136 ± 49% post-IC, p=0.001). Conversely, there was no change in the relative peak hyperemic response in the sham-IC condition (%ΔLBF = 108 ± 61% pre- vs. 108 ± 77% post-sham-IC, p=0.50). The pre-/post- change score of absolute peak hyperemic response to PLM was also higher after IC vs. sham-IC (change in ΔLBF = 50 ± 78 IC ml/min vs. -44 ± 127 ml/min sham-IC, p = 0.03). Conclusion: These results show an improvement in the peripheral microvascular response to PLM following IC. Future studies should examine the mechanistic pathways responsible for an improved PLM response as well as the potential benefits of IC on microvascular health in clinical populations with underlying peripheral microvascular dysfunction. AAW was supported by the National Heart, Lung and Blood Institute (T32HL13464) and Cardiovascular Center’s A.O. Smith Fellowship Scholars Program. Research was supported by the Eunice Kennedy Shriver National Institute of Child Health &amp; Human Development R01-HD099340 (ASH and MJD) and R01-HD112258 (MJD and ASH). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Pharmacological Targeting of Endothelial KCa Channels In Vivo Augments Vasodilatory Responses in Rat Femoral and Coronary Arteries in Health and Disease

As the primary interface between the blood and organs, the vascular endothelium functions as a key regulator of tissue blood flow by sensing chemical and mechanical stimuli and producing vasoactive signals to dynamically control intraluminal diameter in local arterioles and upstream arteries. Flow-mediated dilation (FMD) is an important physiological mechanism to modify local tissue perfusion in response to dynamic metabolic conditions, and reduced FMD responses are indicative of endothelial dysfunction, the latter being a major risk factor for cardiovascular disease. We have previously reported that pharmacological enhancement of endothelial KCa2.3 and KCa3.1 channel activity by SKA-31 augmented vasodilatory responses in small resistance arteries and intact hearts isolated from healthy and Type 2 Diabetic (T2D) rats (RC Mishra et al, 2014, 2021). In the present study, we have investigated the ability of SKA-31 to enhance endothelium-dependent vasodilation in vivo in femoral and coronary arteries of healthy and T2D male rats. Methods: FMD responses associated with reactive hyperemia were measured in a side branch of the femoral artery by high sensitivity Doppler ultrasound following release of an inflated pressure cuff placed on the distal hind limb of male Sprague Dawley (SD) and T2D Goto-Kakizaki (GK) rats (26-32 weeks of age). Rats were injected i.p. with either 10 mg/kg SKA-31 or drug vehicle ~ 3 hours prior to cuff inflation. M-mode echocardiographic imaging was used to visualize intraluminal diameter changes in the left main coronary artery in the same four treatment groups in response to an increase in inhalational isoflurane from 2% to 5%. Results: Femoral artery blood flow increased ~2-fold during reactive hyperemia in vehicle treated SD rats, as quantified by velocity-time integral, and did not increase further with SKA-31 treatment. In contrast, the FMD response in vehicle treated T2D GK rats was substantially blunted vs. SD rats, and SKA-31 administration restored this response to the level observed in healthy controls, which was still observable 15-24 hours later. In vehicle treated SD rats, exposure to 5% isoflurane increased left main coronary arterial diameter by 50-60%, which reversed to baseline following return to the original 2% isoflurane condition. SKA-31 treatment of SD rats increased basal arterial diameter by ~30%, but did not significantly modify the observed increase in arterial diameter evoked by 5% isoflurane inhalation, compared with vehicle treatment. In vehicle treated T2D GK rats, exposure to 5% isoflurane did not increase coronary artery diameter over a 10 min period, which is suggestive of endothelial dysfunction. However, SKA-31 treatment significantly increased basal coronary arterial diameter by 40-50%, and promoted a rapid and robust increase in diameter following exposure to 5% isoflurane (80-90% increase above that observed in vehicle treated T2D rats), which reversed to baseline upon return to 2% isoflurane inhalation. No enhancement of isoflurane evoked coronary vasodilation was observable in T2D GK rats 15-24 hrs post-SKA-31 treatment. In summary, these data provide the first direct demonstration that low dose administration of a KCa channel activator can enhance vasodilatory responses in vivo. This study was supported by research funding to APB from the Canadian Institutes of Health Research (MOP-142467) and NSERC (RGPIN 2017-04116). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

BLUNTED SKELETAL MUSCLE MICROVASCULAR BLOOD FLOW IS A POTENTIAL UNDERLYING MECHANISM FOR EXERCISE INTOLERANCE IN ADULTS WITH ATRIAL FIBRILLATION

INTRODUCTION &amp; AIMS Approximately 45% of adults living with atrial fibrillation (AF) experience exercise intolerance (EI). However, the mechanisms of EI in AF are not well understood. We aimed to determine whether impaired skeletal muscle microvascular blood flow (MBF), not macrovascular, responses to peak exercise is a plausible explanation for EI in adults with AF. METHODS Adults with AF and healthy controls completed a Modified Bruce treadmill protocol to obtain peak oxygen uptake (V̇O2peak). Skeletal muscle microvascular blood volume, velocity, and flow in the vastus lateralis muscle was assessed using contrast enhanced ultrasound. Superficial femoral artery diameter, blood velocity and flow were assessed using 2D and Doppler ultrasound. Vascular measurements were collected at rest, immediately post-exercise, and 30 minutes post-exercise. RESULTS Nine adults with AF (age: 62±5 years, 66% females, BMI: 29.7±4.2 kg/m2, V̇O2peak: 24.3±6.1 mL/kg/min) and seven controls (age: 63±10 years, 57% females, BMI: 26.7±1.7 kg/m2, V̇O2peak: 31.0±7.5 mL/kg/min) participated. One participant was in AF during testing. A significant group x time interaction in skeletal muscle MBF (p=0.04) and near significant interaction in blood volume (capillary recruitment, p=0.08) was observed. Post-hoc analysis revealed adults with AF had a significantly blunted MBF at 30 minutes post-exercise (-1.3 fold versus control, p=0.01) and reduced microvascular blood volume (i.e. capillary recruitment) pre- and 30 minutes post-exercise (-6.6 fold [p=0.01] and -9.4 fold [p=0.01] versus controls). No differences were observed for changes in skeletal muscle microvascular blood velocity, or femoral artery diameter, blood velocity or flow. CONCLUSION Despite similar femoral artery blood flow responses, adults with AF have lower skeletal muscle MBF responses to peak exercise which may be driven by a reduced capillary recruitment in the skeletal muscle. Our findings provide new insight into vascular complications which may partially explain EI in those with AF.

The effect of underwater massage during hot water immersion on acute cardiovascular and mood responses

PurposeThere is emerging evidence that demonstrates the health benefits of hot water immersion including improvements to cardiovascular health and reductions in stress and anxiety. Many commercially available hot tubs offer underwater massage systems which purport to enhance many benefits of hot water immersion, however, these claims have yet to be studied. MethodsTwenty participants (4 females) completed three, 30-min sessions of hot-water immersion (beginning at 39 °C) in a crossover randomized design: with air massage (Air Jet), water massage (Hydro Jet) or no massage (Control). Cardiovascular responses comprising; heart rate, blood pressure and superficial femoral artery blood flow and shear rate were measured. State trait anxiety, basic affect, and salivary cortisol were recorded before and after each trial. Data were analysed using a mixed effects model. ResultsPost immersion, heart rate increased (Δ31bpm, P < 0.001, d = 1.38), mean arterial blood pressure decreased (Δ16 mmHg, P < 0.001, d = −0.66), with no difference between conditions. Blood flow and mean shear rate increased following immersion (P < 0.001, Δ362 ml/min, d = 1.20 and Δ108 s−1, d = 1.00), but these increases were blunted in the Air Jet condition (P < 0.001,Δ171 ml/min, d = 0.43 and Δ52 s−1, d = 0.52). Anxiety and salivary cortisol were reduced (P = 0.003, d = −0.20, P = 0.014, d = −0.11), but did not vary between conditions. Enjoyment did not vary between conditions. ConclusionThese data demonstrate positive acute responses to hot water immersion on markers of cardiovascular function, anxiety, and stress. There was no additional benefit of water-based massage, while air-based massage blunted some positive vascular responses due to lower heat conservation of the water.

Reducing femoral flow artefacts in radial magnetic resonance fingerprinting of the prostate using region-optimised virtual coils.

High acceleration factors in radial magnetic resonance fingerprinting (MRF) of the prostate lead to strong streak-like artefacts from flow in the femoral blood vessels, possibly concealing important anatomical information. Region-optimised virtual (ROVir) coils is a beamforming-based framework to create virtual coils that maximise signal in a region of interest while minimising signal in a region of interference. In this study, the potential of removing femoral flow streak artefacts in prostate MRF using ROVir coils is demonstrated in silico and in vivo. The ROVir framework was applied to radial MRF k-space data in an automated pipeline designed to maximise prostate signal while minimising signal from the femoral vessels. The method was tested in 15 asymptomatic volunteers at 3 T. The presence of streaks was visually assessed and measurements of whole prostate T1, T2 and signal-to-noise ratio (SNR) with and without streak correction were examined. In addition, a purpose-built simulation framework in which blood flow through the femoral vessels can be turned on and off was used to quantitatively evaluate ROVir's ability to suppress streaks in radial prostate MRF. In vivo it was shown that removing selected ROVir coils visibly reduces streak-like artefacts from the femoral blood flow, without increasing the reconstruction time. On average, 80% of the prostate SNR was retained. A similar reduction of streaks was also observed in silico, while the quantitative accuracy of T1 and T2 mapping was retained. In conclusion, ROVir coils efficiently suppress streaking artefacts from blood flow in radial MRF of the prostate, thereby improving the visual clarity of the images, without significant sacrifices to acquisition time, reconstruction time and accuracy of quantitative values. This is expected to help enable T1 and T2 mapping of prostate cancer in clinically viable times, aiding differentiation between prostate cancer from noncancer and healthy prostate tissue.

Oral Vitamin C Supplementation and its Impact on Endothelial Function in Obstructive Sleep Apnea Patients

Background – Obstructive Sleep Apnea (OSA) is a prevalent condition associated with endothelial dysfunction, a precursor to cardiovascular disease. Passive Leg Movement (PLM) has emerged as a simple method to assess endothelial function. The role of oral vitamin C in improving endothelial function in OSA patients, however, has been underexplored. Materials and Methods This study recruited 26 male subjects, 13 with OSA and 13 healthy controls, aged 18-55 years. PLM was utilized to assess endothelial function by measuring femoral artery blood flow (FBF) and velocity (FBV) using Doppler ultrasound, pre- and post-administration of 1000mg of oral vitamin C. The intervention aimed to compare endothelial function responses between OSA patients and healthy controls, and to evaluate the impact of oral vitamin C on these responses. Results Baseline comparisons revealed a significant difference in FBF between OSA patients (76.6 ml/min) and healthy controls (162.1 ml/min, p &lt; 0.05), indicating endothelial dysfunction in OSA. Post-vitamin C intervention, the peak FBF responses in OSA patients showed no significant difference (Pre-vitamin C: 76.6 ml/min, Post-vitamin C: 79.9 ml/min, p &gt; 0.05), suggesting that oral vitamin C did not significantly improve endothelial function in OSA patients. Conclusion PLM effectively distinguished between healthy subjects and those with OSA through differences in FBF, confirming its utility as a diagnostic tool for endothelial dysfunction. However, oral vitamin C supplementation did not significantly enhance endothelial function in OSA patients, indicating the need for further research into alternative or adjunctive therapies.

Passive Leg Movement as a Diagnostic Tool for Distinguishing Healthy Individuals from Those with Obstructive Sleep Apnea

Background – Obstructive Sleep Apnea (OSA) is linked with endothelial dysfunction, posing a significant risk for cardiovascular diseases. The non-invasive assessment of endothelial function through passive leg movement (PLM) offers a novel diagnostic avenue. This study explores PLM's efficacy in differentiating between healthy individuals and those with OSA, alongside evaluating the impact of oral vitamin C on endothelial function within these groups. Materials and Methods: The study enrolled 26 male subjects, divided equally into healthy and OSA groups. PLM was performed using an isokinetic machine to assess femoral artery blood flow (FBF) and blood velocities (FBVs) via Doppler ultrasound. Subjects consumed 1000mg of oral vitamin C, with measurements repeated post-consumption. Data analysis involved repeated measures ANOVA to evaluate the diagnostic capability of PLM and the effect of vitamin C on FBF responses. Results: A significant difference in FBF was observed between OSA and healthy groups (healthy: 162.1 ml/min, OSA: 76.6 ml/min; p &lt; 0.05), confirming PLM's diagnostic potential. However, vitamin C administration did not significantly alter FBF responses in OSA patients (pre-vitamin C: 76.6 ml/min, post-vitamin C: 79.9 ml/min; p &gt; 0.05), challenging the anticipated benefits of oral vitamin C on endothelial function. Conclusion: PLM effectively distinguishes between healthy individuals and those with OSA, highlighting its diagnostic utility. Nonetheless, oral vitamin C did not improve endothelial dysfunction in OSA patients, suggesting the need for further research on alternative administration methods or dosages.

The Improvement in Exercise Performance during Reduced Muscle Mass Exercise is Associated with an Increase in Femoral Blood Flow in Older and Younger Endurance-Trained Athletes.

This study investigated whether the improved performance observed with maximal self-paced single-leg (SL), compared with double-leg (DL) cycling, is associated with enhanced femoral blood flow and/or altered tissue oxygenation. The hyperaemic response to exercise was assessed in younger and older athletes. Power output was measured in 12 older (65 ± 4 y) and 12 younger (35 ± 5 y) endurance-trained individuals performing 2 x 3 min maximal self-paced exercise using SL and DL cycling. Blood flow (BF) in the femoral artery was assessed using Doppler ultrasound and muscle oxygenation was measured using near-infrared spectroscopy on the vastus lateralis. SL cycling elicited a greater power output (295 ± 83 vs 265 ± 70 W, P < 0.001) and peak femoral BF (1749.1 ± 533.3 vs 1329.7 ± 391.7 ml/min, P < 0.001) compared with DL cycling. Older individuals had a lower peak BF in response to exercise (1355.4 ± 385.8 vs 1765.2 ± 559.6 ml/min, P = 0.019) compared with younger individuals. Peak BF in response to exercise was correlated with power output during SL (r = 0.655, P = 0.002) and DL (r = 0.666, P = 0.001) cycling. The greater exercise performance during SL compared with DL cycling may be partly explained by a greater hyperaemic response when reducing active muscle mass. Despite regular endurance training, older athletes had a lower femoral BF in response to maximal self-paced exercise compared with younger athletes.

Mechanism involved of post-exercise cold water immersion: Blood redistribution and increase in energy expenditure during rewarming

ABSTRACT Thermogenesis is well understood, but the relationships between cold water immersion (CWI), the post-CWI rewarming and the associated physiological changes are not. This study investigated muscle and systemic oxygenation, cardiorespiratory and hemodynamic responses, and gastrointestinal temperature during and after CWI. 21 healthy men completed randomly 2 protocols. Both protocols consisted of a 48 minutes heating cycling exercise followed by 3 recovery periods (R1-R3), but they differed in R2. R1 lasted 20 minutes in a passive semi-seated position on a physiotherapy table at ambient room temperature. Depending on the protocol, R2 lasted 15 minutes at either ambient condition (R2_AMB) or in a CWI condition at 10°C up to the iliac crest (R2_CWI). R3 lasted 40 minutes at AMB while favoring rewarming after R2_CWI. This was followed by 10 minutes of cycling. Compared to R2_AMB, R2_CWI ended at higher V ˙ O2 in the non-immersed body part due to thermogenesis (7.16(2.15) vs. 4.83(1.62) ml.min−1.kg−1) and lower femoral artery blood flow (475(165) vs. 704(257) ml.min−1) (p < 0.001). Only after CWI, R3 showed a progressive decrease in vastus and gastrocnemius medialis O2 saturation, significant after 34 minutes (p < 0.001). As blood flow did not differ from the AMB protocol, this indicated local thermogenesis in the immersed part of the body. After CWI, a lower gastrointestinal temperature on resumption of cycling compared to AMB (36.31(0.45) vs. 37.30(0.49) °C, p < 0.001) indicated incomplete muscle thermogenesis. In conclusion, the rewarming period after CWI was non-linear and metabolically costly. Immersion and rewarming should be considered as a continuum rather than separate events.

Effects of Electronic Cigarette Vaping on Cardiac and Vascular Function, and Post-myocardial Infarction Remodeling in Rats

The effect of electronic cigarette (E-cig) vaping on cardiac and vascular function during the healing phase of myocardial infarction (MI), and post-MI remodeling was investigated. Sprague Dawley rats were subjected to left coronary artery ligation to induce MI. One week later, rats were randomized to receive either 12 weeks of exposure to purified air (n = 37) or E-cig vapor (15 mg/ml of nicotine) (n = 32). At 12 weeks, cardiac and vascular function, and post-MI remodeling were assessed. Baseline blood flow in the femoral artery did not differ between groups, but peak reperfusion blood flow was blunted in the E-cig group (1.59 ± 0.15 ml/min) vs. the air group (2.11 ± 0.18 ml/min; p = 0.034). Femoral artery diameter after reperfusion was narrower in the E-cig group (0.54 ± 0.02 mm) compared to the air group (0.60 ± 0.02 mm; p = 0.023). Postmortem left ventricular (LV) volumes were similar in the E-cig (0.69 ± 0.04 ml) and air groups (0.73 ± 0.04 ml; p = NS); and myocardial infarct expansion index did not differ between groups (1.4 ± 0.1 in E-cig group versus 1.3 ± 0.1 in air group; p = NS). LV fractional shortening by echo did not differ between groups at 12 weeks (E-cig at 29 ± 2% and air at 27 ± 1%; p = NS). Exposure to E-cig during the healing phase of MI was associated with altered vascular function with reduced femoral artery blood flow and diameter at reperfusion, but not with worsened LV dilation or worsened cardiac function.

The vascular response to acute sauna heating is similar in young and middle-aged adults.

Sauna has been linked to a reduction of cardiovascular disease risk and is a promising nonpharmacological treatment for populations at risk of cardiovascular disease. This study examined the vascular response to an acute bout of sauna heating in young and middle-aged individuals. Ten young (25 ± 4 yr, 6 males and 4 females) and eight middle-aged adults (56 ± 4 yr, 4 males and 4 females) underwent 40 min of sauna exposure at 80°C. Esophageal and intramuscular temperatures, brachial and superficial femoral artery blood flow, artery diameter, and shear rates were recorded at baseline and following heat exposure. Brachial artery flow-mediated dilation (FMD) was measured at baseline and following 90 min of recovery. Esophageal and muscle temperatures increased similarly in the young and middle-aged adults by 1.5 ± 0.53 and 1.95 ± 0.70°C, respectively (P < 0.05). The shear rate increased by 170-200% (P < 0.001), while blood flow increased by 180-390% (P < 0.001) in the superficial femoral and brachial arteries, respectively, and did not differ between age groups (P = 0.190-0.899). Systolic blood pressure was reduced from 135 ± 17 to 122 ± 20 mmHg (P = 0.017) in middle-aged participants. These data indicate that young and middle-aged adults have similar vascular responses to acute sauna heating.NEW & NOTEWORTHY Sauna therapy has been shown to improve cardiovascular health and function in older adults and individuals with cardiovascular disease risk factors. Specifically, improvements in vascular function have been reported and have been attributed to the increased hemodynamic stimuli on the vasculature associated with thermal stress. The present study quantified this hemodynamic response to a sauna protocol associated with improved cardiovascular health across the lifespan. Our data show that middle-aged adults have the same shear rate and blood flow response to sauna as young adults.

Thermo-haemodynamic coupling during regional thigh heating: Insight into the importance of local thermosensitive mechanisms in blood circulation.

A positive relationship between local tissue temperature and perfusion exists, with isolated limb-segment hyperthermia stimulating hyperaemia in the heated region without affecting the adjacent, non-heated limb segment. However, whether partial-limb segment heating evokes a heightened tissue perfusion in the heated region without directly or reflexly affecting the non-heated tissues of the same limb segment remains unknown. This study investigated, in 11 healthy young adults, the lower limb temperature and haemodynamic responses to three levels of 1h upper-leg heating, none of which alter core temperature: (1) whole-thigh (WTH; water-perfused garment), (2) quadriceps (QH; water-perfused garment) and (3) partial-quadriceps (PQH; pulsed shortwave diathermy) heating. It was hypothesised that perfusion would only increase in the heated regions. WTH, QH and PQH increased local heated tissue temperature by 2.9±0.6, 2.0±0.7 and 2.9±1.3°C (P<0.0001), respectively, whilst remaining unchanged in the non-heated hamstrings and quadriceps tissues during QH and PQH. WTH induced a two-fold increase in common femoral artery blood flow (P<0.0001) whereas QH and PQH evoked a similar ∼1.4-fold elevation (P≤0.0018). During QH and PQH, however, tissue oxygen saturation and laser-Doppler skin blood flow in the adjacent non-heated hamstrings or quadriceps tissues remained stable (P>0.5000). These findings in healthy young humans demonstrate a tight thermo-haemodynamic coupling during regional thigh heating, providing further evidence of the importance of local heat-activated mechanisms on the control of blood circulation.

Role of Rho Kinase in Regulating Arterial Stiffness in Anesthetized Rabbits.

The effects of Rho kinase inhibitors fasudil and ripasudil on arterial stiffness were assessed using anesthetized rabbits, where the aortic β and femoral β were measured as a stiffness parameter at each arterial region. Intravenous administration of fasudil and ripasudil dose-dependently decreased blood pressure and femoral vascular resistance and increased femoral arterial blood flow, which appeared according to their in vitro potencies for Rho kinase inhibition. Both drugs increased the aortic β but decreased the femoral β at hypotensive doses. These results suggest that the inhibition of Rho kinase contributes to reducing elastic recoil in the aorta and an increase in compliance in the femoral artery. In addition, the Rho kinase-associated Ca2+-independent mechanism of arterial vascular smooth muscle contraction may be essential in the regulation of femoral arterial stiffness.