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Purpose: This study assessed the effects of upper-body rowing exercise on cardiorespiratory fitness, traditional cardiometabolic risk factors, and vascular health in individuals with spinal cord injury (SCI). Methods: Seventeen male and female adults with chronic (> 1 yr) motor-complete and incomplete SCI (level of injury: C4-L3) were randomized to control (CON, n = 9) or exercise (UBROW, n = 8). Participants in UBROW performed 12-week, 3 weekly sessions of 30-min upper-body ergometer rowing exercise, complying with current exercise guidelines for SCI. Cardiorespiratory fitness ( V ˙ O2peak), traditional risk factors (lipid profile, glycemic control) as well as inflammatory and vascular endothelium-derived biomarkers (derived from fasting blood samples) were measured before and after 6 (6W) and 12 weeks (12W). Brachial artery resting diameter and flow-mediated dilation (FMD) were determined by ultrasound as exploratory outcomes. Results: UBROW increased V ˙ O2peak from baseline (15.1 ± 5.1 mL/kg/min; mean ± SD) to 6W (16.5 ± 5.3; P < 0.01) and 12W (17.5 ± 6.1; P < 0.01). UBROW increased resting brachial artery diameter from baseline (4.80 ± 0.72 mm) to 12W (5.08 ± 0.91; P < 0.01), with no changes at 6W (4.96 ± 0.91), and no changes in CON. There were no significant time-by-group interactions in traditional cardiometabolic blood biomarkers, or in unadjusted or baseline diameter corrected FMD. Explorative analyses revealed inverse correlations between changes (∆12W-baseline) in endothelin-1 and changes in resting diameter (r = − 0.56) and FMD% (r = − 0.60), both P < 0.05. Conclusion: These results demonstrate that 12 weeks of upper-body rowing complying with current exercise guidelines for SCI improves cardiorespiratory fitness and increases resting brachial artery diameter. In contrast, the exercise intervention had no or only modest effects on traditional cardiometabolic risk factors. The study was registered at Clinicaltrials.gov (N-20190053, May 15, 2020). [ABSTRACT FROM AUTHOR]

Background: Humans display an age-related decline in cerebral blood flow and increase in blood pressure (BP), but changes in the underlying control mechanisms across the lifespan are less well understood. We aimed to; (1) examine the impact of age, sex, cardiovascular disease (CVD) risk, and cardio-respiratory fitness on dynamic cerebral autoregulation and cardiac baroreflex sensitivity, and (2) explore the relationships between dynamic cerebral autoregulation (dCA) and cardiac baroreflex sensitivity (cBRS). Methods: 206 participants aged 18–70 years were stratified into age categories. Cerebral blood flow velocity was measured using transcranial Doppler ultrasound. Repeated squat-stand manoeuvres were performed (0.10 Hz), and transfer function analysis was used to assess dCA and cBRS. Multivariable linear regression was used to examine the influence of age, sex, CVD risk, and cardio-respiratory fitness on dCA and cBRS. Linear models determined the relationship between dCA and cBRS. Results: Age, sex, CVD risk, and cardio-respiratory fitness did not impact dCA normalised gain, phase, or coherence with minimal change in all models (P > 0.05). cBRS gain was attenuated with age when adjusted for sex and CVD risk (young–older; β = − 2.86 P < 0.001) along with cBRS phase (young–older; β = − 0.44, P < 0.001). There was no correlation between dCA normalised gain and phase with either parameter of cBRS. Conclusion: Ageing was associated with a decreased cBRS, but dCA appears to remain unchanged. Additionally, our data suggest that sex, CVD risk, and cardio-respiratory fitness have little effect. [ABSTRACT FROM AUTHOR]

Introduction: Cocoa flavanols (CF) may exert health benefits through their potent vasodilatory effects, which are perpetuated by elevations in nitric oxide (NO) bioavailability. These vasodilatory effects may contribute to improved delivery of blood and oxygen (O2) to exercising muscle. Purpose: Therefore, the objective of this study was to examine how CF supplementation impacts pulmonary O2 uptake ( V ˙ O 2 ) kinetics and exercise tolerance in sedentary middle-aged adults. Methods: We employed a double-blind cross-over, placebo-controlled design whereby 17 participants (11 male, 6 female; mean ± SD, 45 ± 6 years) randomly received either 7 days of daily CF (400 mg) or placebo (PL) supplementation. On day 7, participants completed a series of 'step' moderate- and severe-intensity exercise tests for the determination of V ˙ O 2 kinetics. Results: During moderate-intensity exercise, the time constant of the phase II V ˙ O 2 kinetics ( τ V ˙ O 2 ) was decreased by 15% in CF as compared to PL (mean ± SD; PL 40 ± 12 s vs. CF 34 ± 9 s, P = 0.019), with no differences in the amplitude of V ˙ O 2 (A V ˙ O 2 ; PL 0.77 ± 0.32 l min−1 vs. CF 0.79 ± 0.34 l min−1, P = 0.263). However, during severe-intensity exercise, τ V ˙ O 2 , the amplitude of the slow component ( SC V ˙ O 2 ) and exercise tolerance (PL 435 ± 58 s vs. CF 424 ± 47 s, P = 0.480) were unchanged between conditions. Conclusion: Our data show that acute CF supplementation enhanced V ˙ O 2 kinetics during moderate-, but not severe-intensity exercise in middle-aged participants. These novel effects of CFs, in this demographic, may contribute to improved tolerance of moderate-activity physical activities, which appear commonly present in daily life. Trial registration: Registered under ClinicalTrials.gov Identifier no. NCT04370353, 30/04/20 retrospectively registered [ABSTRACT FROM AUTHOR]

Purpose: In this study, we examined whether the decrease in endothelial function associated with short-term exposure to elevated retrograde shear rate (SR), could be prevented when combined with a concurrent drop in transmural pressure in humans.Methods: Twenty-five healthy individuals reported to our laboratory on three occasions to complete 30-min experimental conditions, preceded and followed by assessment of endothelial function using flow-mediated dilation (FMD). We used cuff inflation for 30-min to manipulate retrograde SR and transmural pressure in the brachial artery. Subjects underwent, in randomised order: (1) forearm cuff inflation to 60 mmHg (distal cuff; causing increase in retrograde SR), (2) upper arm cuff inflation to 60 mmHg (proximal cuff; causing increase in retrograde SR + decrease in transmural pressure), and (3) no cuff inflation (Control).Results: The distal and proximal cuff conditions both increased brachial artery retrograde SR (p < 0.001) and oscillatory shear index (p < 0.001). The Control intervention did not alter SR patterns or FMD (p > 0.05). A significant interaction-effect was found for FMD (p < 0.05), with the decrease during distal cuff (from 6.9 ± 2.3% to 6.1 ± 2.5%), being reversed to an increase with proximal cuff (from 6.3 ± 2.0 to 6.9 ± 2.0%). The proximal cuff-related increase in FMD could not be explained by the decrease in antegrade or increase in retrograde shear.Conclusion: This study suggests that a decrease in transmural pressure may ameliorate the decline in endothelial function that occurs following exposure to elevated retrograde shear in healthy individuals. [ABSTRACT FROM AUTHOR]

Background: Repeated exposure to remote ischaemic preconditioning (rIPC; short bouts of non-lethal ischaemia) enhances peripheral vascular function within 1 week; whereas, longer periods of rIPC (~ 1 year) may improve cerebral perfusion. Increasing the 'dose' of rIPC may lead to superior effects. Given the similarities between exercise and rIPC, we examined whether adding exercise to the rIPC stimulus leads to greater adaptation in systemic vascular function. Methods: Nineteen individuals with increased risk for cardiovascular disease (CVD) were randomly allocated to either 8 weeks of rIPC (n = 9) or 8 weeks of rIPC + exercise (rIPC + Ex) (n = 10). rIPC was applied three times per week in both conditions, and exercise consisted of 50 min (70% heart rate max) of cycling 3 times per week. Peripheral endothelial function was assessed using flow-mediated dilation (FMD) before and after ischaemia–reperfusion (IR). Cerebrovascular function was assessed by dynamic cerebral autoregulation (dCA) and cerebrovascular reactivity (CVR), and cardio-respiratory fitness (VO2peak) using a maximal aerobic capacity test. Results: FMD% increased by 1.6% (95% CI, 0.4, 2.8) following rIPC + Ex and by 0.3% (− 1.1, 1.5) in the only rIPC but this did not reach statistical significance (P = 0.65). Neither intervention evoked a change in dCA or in CVR (P > 0.05). VO2peak increased by 2.8 ml/kg/min (1.7, 3.9) following the rIPC + Ex and by 0.1 ml/kg/min (− 1.0, 1.4) following the rIPC only intervention (P = 0.69). Conclusion: Combining exercise with rIPC across an 8-week intervention does not lead to superior effects in cerebrovascular and peripheral vascular function compared to a repeated rIPC intervention in individuals at risk of CVD. [ABSTRACT FROM AUTHOR]

Purpose: Remote ischaemic preconditioning (RIPC) refers to the protection conferred to tissues and organs via brief periods of ischaemia in a remote vascular territory, including the brain. Recent studies in humans report that RIPC provides neuroprotection against recurrent (ischaemic) stroke. To better understand the ability of RIPC to improve brain health, the present study explored the potential for RIPC to acutely improve cerebrovascular function.Methods: Eleven young healthy (females n = 6, age; 28.1 ± 3.7 years) and 9 older individuals (females n = 4, age 52.5 ± 6.7 years) at increased risk for stroke (cardiovascular disease risk factors) underwent assessments of cerebrovascular function, assessed by carbon dioxide (CO2) reactivity and cerebral autoregulation during normo- and hypercapnia (5% CO2) following 40 mins of bilateral arm RIPC or a sham condition. Squat-to-stand manoeuvres were performed to induce changes in blood pressure to assess cerebral autoregulation (0.10 Hz) and analysed via transfer function.Results: We found no change in middle cerebral artery velocity or blood pressure across 40 mins of RIPC. Application of RIPC resulted in no change in CO2 reactivity slopes (sham vs RIPC, 1.97 ± 0.88 vs 2.06 ± 0.69 cm/s/mmHg P = 0.61) or parameters of cerebral autoregulation during normocapnia (sham vs RIPC, normalised gain%, 1.27 ± 0.25 vs 1.22 ± 0.35, P = 0.46).Conclusion: This study demonstrates that a single bout of RIPC does not influence cerebrovascular function acutely in healthy individuals, or those at increased cardiovascular risk. Given the previously reported protective role of RIPC on stroke recurrence in humans, it is possible that repeated bouts of RIPC may be necessary to impart beneficial effects on cerebrovascular function. [ABSTRACT FROM AUTHOR]

32445849 2 Hansen RK, Samani A, Laessoe U. Rowing exercise increases cardiorespiratory fitness and brachial artery diameter but not traditional cardiometabolic risk factors in spinal cord-injured humans. It is thus indisputable that retainment of sympathetic nervous system function is critical for a variety of exercise and health-related outcomes, including the normal hemodynamic adjustments to exercise that ensure redistribution of blood flow and O SB 2 sb to the active muscles (Rowell [5]). [Extracted from the article]

Purpose: No previous study has explored the importance of exercise-induced changes in vascular function to prolonged adaptations. Therefore, the purpose was to explore the within-subject relationship between the acute post-exercise change in brachial artery endothelial function (flow-mediated dilation, FMD) and the change in resting FMD after a 2-week exercise training in healthy volunteers.Methods: Twenty one healthy, young men (24 ± 5 years) underwent assessment of brachial artery FMD using high-resolution ultrasound before and after 30-min of moderate-intensity cycle exercise (80% maximal heart rate). Subsequently, subjects performed five 30-min cycle exercise bouts at 80% maximal heart rate across a 2-week period, followed by repeat assessment of resting brachial FMD post-training.Results: Correcting for changes in diameter and shear, FMD did not change after the initial exercise bout (P = 0.26). However, a significant correlation was found between post-exercise changes in FMD and adaptation in resting FMD after training (r = 0.634, P = 0.002), where an acute decrease in post-exercise FMD resulted in a decrease in baseline FMD after 2 weeks and vice versa. We also found a positive correlation between antegrade shear rate during exercise and change in FMD% after acute exercise and after exercise training (r = 0.529 and 0.475, both P < 0.05).Conclusion: Our findings suggest that acute post-exercise changes in vascular function are related to changes in resting FMD after a 2-week endurance exercise training period in healthy men, an effect that may be related to exercise-induced increases in antegrade shear rate. This provides further insight into the relevance of acute changes in shear and FMD for subsequent adaptation. [ABSTRACT FROM AUTHOR]

Objective: Little is known about the impact of exercise training on conduit artery wall thickness in type 2 diabetes. We examined the local and systemic impact of exercise training on superficial femoral (SFA), brachial (BA), and carotid artery (CA) wall thickness in type 2 diabetes patients and controls. Methods: Twenty patients with type 2 diabetes and 10 age- and sex-matched controls performed an 8-week training study involving lower limb-based combined aerobic and resistance exercise training. We examined the SFA to study the local effect of exercise, and also the systemic impact of lower limb-based exercise training on peripheral (i.e. BA) and central (i.e. CA) arteries. Wall thickness (WT), diameter and wall:lumen(W:L)-ratios were examined using automated edge detection of ultrasound images. Results: Exercise training did not alter SFA or CA diameter in type 2 diabetes or controls (all P > 0.05). BA diameter was increased after training in type 2 diabetes, but not in controls. Exercise training decreased WT and W:L ratio in the SFA and BA, but not in CA in type 2 diabetes. Training did not alter WT or W:L ratio in controls ( P > 0.05). Conclusion: Lower limb-dominant exercise training causes remodelling of peripheral arteries, supplying active and inactive vascular beds, but not central arteries in type 2 diabetes. [ABSTRACT FROM AUTHOR]

Purpose: Exercise training in healthy volunteers rapidly improves vascular function, preceding structural remodelling. No study examined the time-course of such adaptations in subjects with a priori endothelial dysfunction. Methods: We examined brachial artery endothelial and smooth muscle function using flow-mediated dilation (FMD) and glyceryl trinitrate (GTN) administration in 13 type 2 diabetes patients (59 ± 6 years) and 10 healthy subjects (58 ± 7 years) before, during (2-weekly) and after an 8-week training programme. Arterial structure was assessed via peak blood flow and artery diameter. Results: Training increased peak oxygen uptake ( P = 0.03), comparable between groups ( P = 0.276). We observed a similar impact of training on brachial artery vasomotor function across the training period in diabetes patients and controls (FMD/GTN-ratio), with a higher FMD/GTN-ratio at 2, 6 and 8 weeks ( P = 0.036). Artery diameter, peak blood flow or peak diameter had not changed after training. Conclusion: Training leads to rapid improvement in brachial artery vascular function in diabetes patients and controls. In contrast to previous observations in healthy young subjects, the increase in function was preserved after 8 weeks of training in middle-aged diabetes patients and controls, suggesting a different time-course in vascular adaptations in subjects with endothelial dysfunction. [ABSTRACT FROM AUTHOR]

Purpose: Short-to-moderate duration exercise training improves fitness and lowers cardiovascular risk in type 2 diabetes (T2DM). However, the impact of long-term compliance to an active lifestyle of T2DM patients on cardiovascular risk factors has never been studied but could provide information on the maximal achievable health effect of physical activity in T2DM. This study examined the impact of a life-long active lifestyle by comparing physical fitness, cardiovascular risk and vascular function between long-term physically active T2DM patients versus sedentary T2DM patients and controls. Methods: Fitness, HOMA-IR, brachial artery flow-mediated dilation (FMD) and lifetime risk for cardiovascular disease were assessed in 15 exercising T2DM patients, 12 age-, sex- and weight-matched sedentary T2DM patients and 9 sedentary men free of established cardiovascular and metabolic disease as controls. Long-term regular exercise was defined as self-reported participation of >2.5 h of (predominantly) endurance exercise per week, which was performed for 18-47 years. Results: Sedentary T2DM patients showed lower fitness (21.8 ± 2.3, 32.6 ± 6.0 and 31.1 ± 3.2 ml O/kg/min), higher HOMA-IR (8.3 ± 5.0, 2.0 ± 1.8 and 1.1 ± 0.5 100/%S) and higher lifetime risk scores (17.3 ± 5.4, 9.3 ± 5.0 and 8.9 ± 3.9 %) compared to active peers and controls, respectively. Brachial artery FMD was lower in sedentary T2DM patients compared with active peers, but not in controls (3.3 ± 1.2, 5.2 ± 2.1 and 3.8 ± 1.2 %). Conclusions: Life-long active T2DM patients have superior fitness levels, HOMA-IR, cardiovascular risk and FMD compared to sedentary peers, whilst no differences were found when compared to controls. This study provides evidence that a life-long active lifestyle, even in T2DM, may be able to effectively normalize cardiovascular risk. [ABSTRACT FROM AUTHOR]

Exercise training is associated with rapid changes in endothelium-dependent vasodilation, which occur within days of training. Whilst long-term physical inactivity has potent effects on vascular structure, little is known about the immediate impact of inactivity on vascular function. Aim of this study was to measure vascular function before, during (day 4) and after 8 days of unilateral forearm inactivity. Thirteen healthy male subjects (22 ± 1 years) were instructed to wear a sling on the non-dominant arm to induce local inactivity. Before, during (at 4 days) and after the 8-day intervention, we used echo Doppler to measure bilateral brachial artery dilator response to 5-min ischaemia [i.e. flow-mediated dilation (FMD)], ischaemic handgrip exercise (iEX) and endothelium-independent dilation to a NO donor [i.e. glyceryl trinitrate (GTN)]. Maximal handgrip strength of the inactive forearm significantly decreased after 8 days ( t tests P = 0.03 for Day 0 vs. Day 8), confirming physical deconditioning in the inactive forearm. A significant decrease in peak blood flow was found in the intervention arm (sling: 539 ± 236, 528 ± 184, 384 ± 142 ml/min) relative to the control arm (559 ± 181, 591 ± 219, 613 ± 169 ml/min; 2-way ANOVA interaction: P = 0.05). Analysis revealed no significant change in brachial artery baseline diameter, FMD %, iEX or GTN across the 8 days in either arm ( P > 0.05). Eight days of forearm physical inactivity induced a significant decrease in post-ischaemic limb blood flow, suggestive of remodelling of forearm resistance vessels. However, measures of conduit artery endothelium-dependent vasodilation were not altered across an 8-day period of inactivity, suggesting that initial remodelling occurs at distal ends of the vascular tree. [ABSTRACT FROM AUTHOR]

Physical inactivity in response to a spinal cord injury (SCI) represents a potent stimulus for conduit artery remodelling. Changes in conduit artery characteristics may be induced by the local effects of denervation (and consequent extreme inactivity below the level of the lesion), and also by systemic adaptations due to whole body inactivity. Therefore, we assessed the time course of carotid (i.e. above lesion) and common femoral artery (i.e. below lesion) lumen diameter and wall thickness across the first 24 weeks after an SCI. Eight male subjects (mean age 35 ± 14 years) with a traumatic motor complete spinal cord lesion between T5 and L1 (i.e. paraplegia) were included. Four subjects were measured across the first 6 weeks after SCI, whilst another four subjects were measured from 8 until 24 weeks after SCI. Ultrasound was used to examine the diameter and wall thickness from the carotid and common femoral arteries. Carotid artery diameter did not change across 24 weeks, whilst femoral artery diameter stabilised after the rapid initial decrease during the first 3 weeks after the SCI. Carotid and femoral artery wall thickness showed no change during the first few weeks, but increased both between 6 and 24 weeks ( P < 0.05). In conclusion, SCI leads to a rapid and localised decrease in conduit artery diameter which is isolated to the denervated and paralyzed region, whilst wall thickness gradually increases both above and below the lesion. This distinct time course of change in conduit arterial diameter and wall thickness suggests that distinct mechanisms may contribute to these adaptations. [ABSTRACT FROM AUTHOR]

Elevated cardiac troponin I (cTnI), a marker for cardiac damage, has been reported after high-intensity exercise in healthy subjects. Currently, little is known about the impact of prolonged moderate-intensity exercise on cTnI release, but also the impact of obesity on this response. 97 volunteers (55 men and 42 women), stratified for BMI, performed a single bout of walking exercise (30-50 km). We examined cTnI-levels before and immediately after the exercise bout in lean (BMI < 25 kg/m, n = 30, 57 ± 19 years), overweight (25 ≤ BMI < 30 kg/m, n = 29, 56 ± 11 years), and obese subjects (BMI ≥ 30 kg/m, n = 28, 53 ± 9 years). Walking was performed at a self-selected pace. cTnI was assessed using a high-sensitive cTnI-assay (Centaur; clinical cut-off value ≥0.04 μg/L). We recorded subject characteristics (body weight, blood pressure, presence of cardiovascular risk) and examined exercise intensity by recording heart rate. Mean cTnI-levels increased significantly from 0.010 ± 0.006 to 0.024 ± 0.046 μg/L ( P < 0.001). The exercise-induced increase in cTnI was not different between lean, overweight and obese subjects (two-way ANOVA interaction; P = 0.27). In 11 participants, cTnI was elevated above the clinical cut-off value for myocardial infarction. Logistic regression analysis identified exercise intensity ( P < 0.001), but not BMI, body fat percentage or waist circumference to significantly relate to positive troponin tests. In conclusion, prolonged, moderate-intensity exercise results in a comparable increase in cTnI-levels in lean, overweight and obese subjects. Therefore, measures of obesity unlikely relate to the magnitude of the post-exercise elevation in cTnI. [ABSTRACT FROM AUTHOR]

The effects of inactivity and exercise training on established and novel cardiovascular risk factors are relatively modest and do not account for the impact of inactivity and exercise on vascular risk. We examine evidence that inactivity and exercise have direct effects on both vasculature function and structure in humans. Physical deconditioning is associated with enhanced vasoconstrictor tone and has profound and rapid effects on arterial remodelling in both large and smaller arteries. Evidence for an effect of deconditioning on vasodilator function is less consistent. Studies of the impact of exercise training suggest that both functional and structural remodelling adaptations occur and that the magnitude and time-course of these changes depends upon training duration and intensity and the vessel beds involved. Inactivity and exercise have direct "vascular deconditioning and conditioning" effects which likely modify cardiovascular risk. [ABSTRACT FROM AUTHOR]

Repeated episodes of ischemia followed by reperfusion, commonly referred to as ischemic preconditioning (IPC), represent an endogenous protective mechanism that delays cell injury. IPC also increases blood flow and improves endothelial function. We hypothesize that IPC will improve physical exercise performance and maximal oxygen consumption. The purpose of the study was to examine the effect of ischemic preconditioning in leg skeletal muscles on cycling exercise performance in healthy individuals. Fifteen healthy, well-trained subjects performed two incremental maximal exercise tests on a bicycle ergometer. Power output, oxygen consumption, ventilation, respiratory quotient, and heart rate were measured continuously. Blood pressure and blood lactate were measured before and after the test. One exercise test was performed after the application of ischemic preconditioning, using a protocol of three series of 5-min ischemia at both legs with resting periods of 5 min in between. The other maximal cycling test served as a control. Tests were conducted in counterbalanced order, at least 1 week apart, at the same time of the day. The repeated ischemic periods significantly increased maximal oxygen consumption from 56.8 to 58.4 ml/min per kg (P = 0.003). Maximal power output increased significantly from 366 to 372 W (P = 0.05). Ischemic preconditioning had no effect on ventilation, respiratory quotient, maximal heart rate, blood pressure or on blood lactate. Repeated short-term leg ischemia prior to an incremental bicycle exercise test improves maximal oxygen consumption by 3% and power output by 1.6%. This protocol, which is suggested to mimic the effects of ischemic preconditioning, may have important implications for exercise performance. [ABSTRACT FROM AUTHOR]

This study was performed to assess the effect of resistive vibration exercise during bed rest deconditioning on venous vascular dimension and function, as measured with ultrasound in the popliteal vein. Sixteen men were assigned to bed rest (BR-Ctrl) or bed rest with resistive vibration exercise (BR-RVE). Before and at 25 and 52 days of bed rest, popliteal vein diameter was measured at increasing cuff pressures. Venous capacitance and compliance were calculated from the pressure-volume curve. After 52 days of bed rest, BR-Ctrl showed no change in baseline popliteal vein diameter or compliance, while venous capacitance decreased. Resistive vibration exercise had no effect on the response in venous diameter, capacitance or compliance to 52 days of bed rest. The decline in venous capacitance due to long-term bed rest is not effectively counteracted by resistive vibration exercise, indicating that an alternative factor during bed rest deconditioning is responsible for venous changes. [ABSTRACT FROM AUTHOR]