Stiffness In Healthy Young Adults Research Articles

High altitude sojourn elicits divergent effects in aortic and carotid stiffness in healthy-young adults

High altitude exposure challenges the cardiovascular system to compensate for barometric pressure-mediated reductions in arterial oxygen content. Reductions in oxygen content elicit simultaneous increases in sympathetic nervous system activity and vasodilation that may have competing effects on changes in large artery stiffness. The objective of this study was to examine changes in aortic and carotid stiffness during high altitude sojourn in healthy, young adults. We hypothesized that short-term high-altitude sojourn would increase both aortic and carotid stiffness. 17 Generally healthy adults (23±4 yrs, 25.0±3.0 BMI, n=9 females) underwent vascular assessments in the supine position at 1400 m and after an 8-day incremental ascent to 4300 m. Aortic stiffness and carotid β-stiffness were derived from carotid-femoral pulse wave velocity (cfPWV) via applanation tonometry and right common carotid artery ultrasonography, with blood pressure assessed via oscillometry. Ascent from 1400 m to 4300 m resulted in decreased arterial oxygen saturation (-11±4 %, p<0.001) and carotid β-stiffness (-4.48±2.73 au, p<0.001), and increased cfPWV, (+54.98±78.10 cm/s, p=0.01) and mean arterial pressure (+4±7 mmHg, p=0.02). Changes in cfPWV, arterial oxygen saturation, and blood pressure were moderately to strongly correlated (r=-0.425-0.503, p=0.09-0.04). Our data suggest that short term exposure to high altitude has differential effects on carotid versus aortic stiffness despite increases in mean blood pressure. Increases in aortic stiffness appear related to hypoxia-induced reductions in arterial oxygen saturation and concomitant increases in blood pressure, while reductions in carotid stiffness may stem, in-part, from compensatory carotid artery dilation necessary to increase cerebral blood flow at high altitude. Additional research is necessary to further understand mechanisms underlying differential changes in large artery stiffness during high altitude sojourn. 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.

Acute effects of the 4-4-8 breathing technique on arterial stiffness in healthy young men.

Increased arterial stiffness is a risk factor for cardiovascular disease. Slow, deep breathing decreases blood pressure related to arterial stiffness. The objective of the present study was to determine the acute effects of a single session of slow breathing on arterial stiffness, blood pressure, and cardiac autonomic function. Fifteen healthy men (20 ± 0 years) were administered (a) a slow breathing condition (12 consecutive breaths of 4 s of inhalation, 4 s of pause, and 8 s of exhalation through the nose, approximately 5 min per breath) and (b) a control, two-condition crossover design. Carotid-femoral artery pulse wave velocity (cfPWV), brachial-ankle PWV (baPWV), brachial blood pressure, high frequency (HF) and low frequency (LF) were measured at baseline, 30 min, 60 min and 24 h after respiratory control. Brachial-ankle PWV and brachial systolic pressure on the 4-4-8 breathing trial decreased after 30 min of respiratory control compared to baseline (p < 0.05), but did not change on the CON trial. Carotid-femoral PWV on both trials was unchanged; HF on the 4-4-8 breathing trial increased (p < 0.05) and LF decreased (p < 0.05) after 30 min of respiratory control compared to baseline, but was unchanged on the CON trial. These results suggest that slow breathing techniques may be effective in modulating autonomic function and improving arterial stiffness in healthy young adults.

Association between depressive symptomatology and central arterial stiffness in healthy young adults

Depression symptomology is linked with incident cardiovascular disease (CVD). Increased central arterial stiffness represents a potential mechanism connecting depression and increased cardiovascular risk. Therefore, the objective of this study was to examine the association between depressive symptomology and central arterial stiffness in healthy young adults without cardiovascular disease. The study tested the hypothesis that higher depressive symptomology is associated with greater central arterial stiffness. Using existing data from the Niagara Longitudinal Heart Study (NLHS), a sample of 293 young adults (22.5±1.71 years; 55% female) was included. Depressive symptomology (Centre for Epidemiological Studies Depression Scale; CESD), central arterial stiffness (carotid-femoral pulse wave velocity; cfPWV), beat-by-beat mean arterial pressure (MAP; finger photoplethysmography), and heart rate (HR; electrocardiogram) were measured. Multiple linear regression analyses were used to examine the association between depressive symptomology and cfPWV, adjusting for age, sex, body mass index, physical activity, smoking status, MAP, and HR. Depressive symptomology was categorized as low (CESD score &lt; 16), moderate (CESD score ≥16 and &lt; 26), and high (CESD score ≥ 26), where low symptomology was used as the reference group. After adjusting for covariates, high depressive symptomology was predictive of a faster cfPWV (β = 0.134, p = 0.026), whereas moderate depressive symptomology was not (β = 0.053, p = 0.365). These findings suggest that high depressive symptomatology is associated with a faster cfPWV, signifying elevated central arterial stiffness. Therefore, central arterial stiffness may act as a mechanism connecting depression to CVD. Future research should aim to decipher the causal direction between depression and cfPWV. This work was supported by the Canadian Institute of Health Research (CIHR) and Brock University. This is the full abstract presented at the American Physiology Summit 2023 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.

MyotonPro Is a Valid Device for Assessing Wrist Biomechanical Stiffness in Healthy Young Adults.

BackgroundThe MyotonPro is a portable device for measuring biomechanical and viscoelastic properties in superficial soft tissues. The aims of this study are firstly to validate the MyotonPro compared to a reliable gold-standard frame and secondly to observe the influence of MyotonPro measurement on the total wrist viscoelasticity.MethodsThree silicone polymers with different elastic properties were assessed with the MyotonPro and with a reference rheometer (Universal Tribometer Mod). Then, a free oscillations method was used to measure the passive elastic and viscous stiffness of the wrist and compared to MyotonPro forearm measurements.ResultsA one-way ANOVA demonstrated the validity of the MyotonPro's stiffness (p = 0.001), decrement (p < 0.001), and relaxation (p = 0.008) parameters for measuring the elastic stiffness (k) of the three polymers. The MyotonPro parameters demonstrated excellent reliability on the forearm. Proximal and distal anterior myofascial measurements of the MyotonPro were moderately correlated to the elastic stiffness (p = 0.0027–0.0275, absolute r = from 0.270 to 0.375) of the wrist while the postero-distal myofascial tissues of the forearm demonstrated a moderate correlation with the viscous stiffness of the wrist (p = 0.0096–0.0433, absolute r = from 0.257 to 0.326).DiscussionThe MyotonPro is a valid device for measuring elastic stiffness as well as a portable, affordable, and easy-to-use tool for quantifying the biomechanical properties and viscoelasticity of myofascial tissue in healthy subjects.

Cognitive Demands Influence Drop Jump Performance and Relationships With Leg Stiffness in Healthy Young Adults.

Holmes, HH, Downs Talmage, JL, Neely, KA, and Roper, JA. Cognitive demands influence drop jump performance and relationships with leg stiffness in healthy young adults. J Strength Cond Res 37(1): 74-83, 2023-Sports-relevant cognition influences neuromuscular control and sports performance. This study assessed the influence of cognition on (a) drop jump performance and (b) commonly researched relationships between lower extremity stiffness, ground contact time (GCT), peak vertical ground reaction force (vGRF), and leg deformation. Active adults (n = 33, 13 men, 20 women, 21 ± 2 years, height = 1.71 ± 0.81 m, body mass = 70.5 ± 10.6 kg) participated in decisions to perform drop jumps or lands of a 30-cm box in 4 conditions: (a) standard, explicit instructions; (b) choice, internally driven decisions; and (c and d) visual and audio, external visual or audio cues reducing time for motor planning. Significance was set at p < 0.05. Ground contact time with audio (M ± SD: 0.62 ± 0.14 seconds) and visual cues (0.59 ± 0.10 seconds) was longer than standard instructions (0.54 ± 0.10 seconds). Standard condition jump height was higher (0.49 ± 0.10 m) than audio (0.435 ± 0.10 m) and choice (0.44 ± 0.09 m). Standard condition reactive strength index was higher (1.03 ± 0.35) than audio (0.76 ± 0.23), visual (0.82 ± 0.27), and choice (0.84 ± 0.33). Visual and audio conditions did not demonstrate significant relationships between leg stiffness and GCT, and relationships between vGRF and leg deformation were not significant with visual cues (p > 0.05). Cognition did not significantly change stiffness and vGRF, indicating alternative force strategies. Understanding how cognition influences performance can positively affect coaching practices, sports-specific assessments, and rehabilitation applications.

Influence of Axial Load and a 45-Degree Flexion Head Position on Cervical Spinal Stiffness in Healthy Young Adults

Background: Neck pain is a major cause of disability worldwide. Poor neck posture such as using a smartphone or work-related additional cervical axial load, such headgear of aviators, can cause neck pain. This study aimed at investigating the role of head posture or additional axial load on spinal stiffness, a proxy measure to assess cervical motor control.Methods: The posterior-to-anterior cervical spinal stiffness of 49 young healthy male military employees [mean (SD) age 20 ± 1 years] was measured in two head positions: neutral and 45-degree flexed head position and two loading conditions: with and without additional 3 kg axial load. Each test condition comprised three trials. Measurements were taken at three cervical locations, i.e., spinous processes C2 and C7 and mid-cervical (MC).Results: Cervical spinal stiffness measurements showed good reliability in all test conditions. There was a significant three-way interaction between location × head position × load [F(2, 576) = 9.305, p < 0.001]. Significant two-way interactions were found between measurement locations × loading [F(2, 576) = 15.688, p < 0.001] and measurement locations × head position [F(2, 576) = 9.263, p < 0.001]. There was no significant interaction between loading × head position [F(1, 576) = 0.692, p = 0.406]. Post hoc analysis showed reduction of stiffness in all three measurement locations in flexion position. There was a decrease in stiffness in C2 with loading, increase in stiffness in C7 and no change in MC.Discussion: A flexed head posture leading to decreased stiffness of the cervical spine might contribute to neck pain, especially if the posture is prolonged and static, such as is the case with smartphone users. Regarding the additional load, stiffness decreased high cervical and increased low cervical. There was no change mid cervical. The lower spinal stiffness at the high cervical spine might be caused by capsular ligament laxity due to the buckling effect. At the lower cervical spine, the buckling effect seems to be less dominant, because the proximity to the ribs and sternum provide additional stiffness.

Actigraphy-derived Sleep Metrics Are Not Related To Central Hemodynamics Or Arterial Stiffness In Healthy Adults

Insufficient sleep is an emerging risk factor for cardiovascular disease. PURPOSE: To evaluate the hypothesis that decrements in vascular function, due to poor sleep, may serve as a mechanistic link between sleep and cardiovascular disease, we explored relationships of actigraphy-derived sleep metrics with central hemodynamics and arterial stiffness in healthy young adults. METHODS: A total of 23 women and 27 men (23 ± 5 yrs), free of known cardiovascular, metabolic, and renal disease, and not using sleep medication, participated in this study. ActiGraph GT9X wrist-worn accelerometers were used to measure sleep efficiency, total sleep time, wake after sleep onset, and number of awakenings over a seven-day period. Vascular health measures including central pressures and augmentation index at a heart rate of 75 beats per minute (AIx75) were quantified via pulse wave analysis, and carotid femoral pulse wave velocity (cf-PWV) was assessed using applanation tonometry. Gender-specific z-scores for each of the sleep metrics were summed to assign each participant a “sleep score” (higher score = better sleep), and relationships between sleep scores and vascular health measures were explored using Pearson correlation coefficients. RESULTS: In men, sleep score (range: -4.92 to 9.10) was not related (P > 0.05) to central systolic (114 ± 15 mmHg, r = -0.26) or diastolic (72 ± 7 mmHg, r = -0.21) pressures. Similarly, in women, sleep score (range: -5.02 to 5.34) was not related (P > 0.05) to central systolic (103 ± 11 mmHg, r = -0.09) or diastolic (72 ± 10 mmHg, r = -0.21) pressures. Sleep score also failed to predict (P > 0.05) indices of arterial stiffness, AIx75 (men = 3.1 ± 12.3%, r = 0.04; women = 5.2 ± 9.5%, r = -0.25) and cf-PWV (men = 6.2 ± 0.8 m/s, r = -0.12; women = 5.7 ± 0.5 m/s, r = -0.10). CONCLUSIONS: In young healthy individuals, actigraphy-derived sleep characteristics were not related to central hemodynamics or non-invasive indices of arterial stiffness. Previously documented relationships between sleep and vascular function may be limited to less healthy populations, poorer sleepers, or only for certain sleep metrics.

071 Actigraphy-Derived Sleep Metrics are Not Related to Central Hemodynamics or Arterial Stiffness in Healthy Adults

Abstract Introduction Insufficient sleep is an emerging risk factor for cardiovascular disease. To evaluate the hypothesis that decrements in vascular function, due to poor sleep, may serve as a mechanistic link between sleep and cardiovascular disease, we explored relationships of actigraphy-derived sleep metrics with central hemodynamics and arterial stiffness in healthy young adults. Methods A total of 23 women and 27 men (23±5 yrs), free of known cardiovascular, metabolic, and renal disease, and not using sleep medication, participated in this study. ActiGraph GT9X wrist-worn accelerometers were used to measure sleep efficiency, total sleep time, wake after sleep onset, and number of awakenings over a seven-day period. Vascular health measures including central pressures and augmentation index at a heart rate of 75 beats per minute (AIx@75) were quantified via pulse wave analysis, and carotid femoral pulse wave velocity (cf-PWV) was assessed using applanation tonometry. Gender-specific z-scores for each of the sleep metrics were summed to assign each participant a “sleep score” (higher score = better sleep), and relationships between sleep scores and vascular health measures were explored using Pearson correlation coefficients. Results In men, sleep score (range: -4.92 to 9.10) was not related (P&amp;gt;0.05) to central systolic (114±15 mmHg, r=-0.26) or diastolic (72±7 mmHg, r=-0.21) pressures. Similarly, in women, sleep score (range: -5.02 to 5.34) was not related (P&amp;gt;0.05) to central systolic (103±11 mmHg, r=-0.09) or diastolic (72±10 mmHg, r=-0.21) pressures. Sleep score also failed to predict (P&amp;gt;0.05) indices of arterial stiffness, AIx@75 (men = 3.1±12.3, r=0.04; women = 5.2±9.5, r=-0.25) and cf-PWV (men = 6.2±0.8 m/s, r=-0.12; women = 5.7±0.5 m/s, r=-0.10). Conclusion In young healthy individuals, actigraphy-derived sleep characteristics were not related to central hemodynamics or non-invasive indices of arterial stiffness. Previously documented relationships between sleep and vascular function may be limited to less healthy populations, poorer sleepers, or only for certain sleep metrics. Support (if any):

Acute Effects of Self-myofascial Release using a Foam Roller on Arterial Stiffness in Healthy Young Adults

This study aimed to investigate whether a single bout of Self-myofascial Release (SMR) has a beneficial effect on peripheral and central Blood Pressure (BP) and different parameters of arterial stiffness. Twenty nine healthy male recreational athletes (26.1 ± 2.9 years, BMI 23.4 ± 1.5 kg/m2) completed an instructed SMR using a foam roller. Peripheral and central BP and different parameters of arterial stiffness were measured noninvasively before SMR and at different time points (t1, t15, t30) during a subsequent 30-min recovery phase. There was a significant decrease in both systolic (t15, −2.36 ± 4.45 mmHg, p = 0.05; t30, −4.01 ± 4.47 mmHg, p = 0.003) and diastolic (t30, −2.45 ± 5.45 mmHg, p = 0.025) peripheral pressure during the recovery phase after SMR. Regarding central BP, only systolic pressure showed a significant decrease (t30, −3.64 ± 5.83 mmHg, p = 0.003). Mean arterial pressure (t15, −1.91 ± 3.36, p = 0.03; t30, −3.05 ± 2.88 mmHg, p < 0.001), augmentation pressure (t30, −1.60 ± 2.40 mmHg, p = 0.009), peripheral resistance (t30, −0.09 ± 0.10 s* mmHg/ml, p < 0.001), and stiffness index β0 (t30, −0.33 ± 0.55, p = 0.021) were significantly reduced after SMR. No significant changes were determined for reflection coefficient, augmentation index, cardiac output, and heart rate, respectively. SMR showed effects on peripheral and central BP and different parameters of arterial stiffness in healthy young adults.

The effects of repeated binge drinking on arterial stiffness and urinary norepinephrine levels in young adults.

The aim of this study was to investigate the effect of repeated binge drinking and moderate alcohol consumption in young adults on arterial stiffness and sympathetic activity. We enrolled 49 healthy young adults, free of cardiovascular diseases (25 men; age: 23.5 ± 0.4 years; BMI: 23.4 ± 0.4 kg/m; mean ± S.E). Individuals included were those with a history of repeated binge drinking (>2 years duration; n = 20), drank at moderate levels (MODs, >5 years duration; n = 16) and abstained from alcohol (last 2-3 years; n = 13). Arterial stiffness was assessed using carotid to femoral pulse wave velocity (cfPWV) and sympathetic activity was assessed using 24-h urinary norepinephrine levels. Also measured was aortic SBP and augmentation index (AIx), a measure of wave reflection. Binge drinkers and MODs had higher cfPWV than alcohol abstainers (0.6 and 0.5 m/s, respectively; P ≤ 0.04). In addition, binge drinkers had higher urinary norepinephrine levels than MODs and alcohol abstainers (P < 0.05). Higher cfPWV were correlated with higher norepinephrine levels (r = 0.35. P = 0.02). Aortic SBP (P = 0.2) and AIx (P = 0.96) were similar among binge drinkers, MODs and alcohol abstainers. Our findings suggest that repeated exposure to alcohol, regardless of drinking pattern, may increase aortic arterial stiffness in healthy young adults. In addition, sympathetic activation, reflected by increased 24-h urinary norepinephrine levels, may contribute to alcohol-induced arterial stiffening in young adults.

Influence of body position and axial load on spinal stiffness in healthy young adults.

This study aimed at investigating the effects of different body positions and axial loads on spinal stiffness to better understand spinal stabilisation mechanisms. The posterior-to-anterior lumbar and thoracic spinal stiffness of 100 young healthy adults (mean age 23years; 50 females) were measured in three test situations: prone, standing and standing while carrying a load equal to 50% of the subject's body weight. Each test situation comprised three trials. Spinal stiffness in all test situations showed good reliability. Repeated measures analysis of covariance showed significantly higher spinal stiffness in standing than in the prone position [F(1/1694) = 433.630, p < 0.001]. However, spinal stiffness was significantly lower when standing while carrying a load of 50% of the body weight than when standing without additional load [F(1/1494) = 754.358, p < 0.001]. This study showed that spinal lumbar and thoracic stiffness increases when body position is changed from prone to standing. Additional axial load of 50% of the subject's body weight results in reduced spinal stiffness during standing. These slides can be retrieved under Electronic Supplementary Material.

Remote Ischemic Preconditioning Has No Short Term Effect on Blood Pressure, Heart Rate, and Arterial Stiffness in Healthy Young Adults.

ObjectiveRemote ischemic preconditioning (RIPC) are short episodes of ischemia and reperfusion applied to remote tissue to trigger responses in a specific organ or cardiovascular bed. This study investigates whether RIPC has a short-term effect on blood pressure (BP), heart rate, and arterial stiffness.Patients and MethodsFrom March 2018 to August 2018, we included 40 healthy volunteers (23 female, age 25.6 ± 2.8 years) into this single-blinded randomized-controlled crossover trial. After measuring BP, heart rate, and arterial stiffness in supine position participants were randomized into intervention or SHAM group. The intervention group then underwent a RIPC protocol (3 cycles of 5 min of 200 mmHg ischemia followed by 5 min reperfusion) at the thigh. The SHAM group followed the same protocol just on the upper arm with 40 mmHg pressure inflation. Directly after this 30-min procedure a reassessment of hemodynamic measures was conducted.ResultsThere were no significant changes in all five outcome parameters when comparing the effect of RIPC to SHAM. In peripheral systolic BP the mean difference between groups was Δ1.14 ± 6.5 mmHg (p = 0.672), and for diastolic BP Δ−0.69 ± 4.5 mmHg (p = 0.507). Heart rate shoed a Δ−0.8 ± 4.7 beats/min (p = 0.397). Regarding arterial stiffness measures, there was also no significant improvements thru RIPC. The mean difference between RIPC and SHAM for central systolic BP was Δ0.40 ± 7.2 mmHg (p = 0.951) and for PWV Δ0.01 ± 0.26 m/s (p = 0.563).ConclusionThis study could not find any short-term effects of RIPC on arterial stiffness, BP, and heart rate in a RCT in young healthy adults.

Characteristics of metabolic factors related to arterial stiffness in young and old adults

ABSTRACTIt has not been adequately studied which biomarkers for cardiovascular risk indicate changes of atherosclerosis by aging process. The current study aimed to investigate the characteristics of metabolic factors related to arterial stiffness in young and old adults. Our cross-sectional study enrolled 851 healthy young adults and 719 old adults. Metabolic biomarkers included glucose, lipid profiles, and liver enzymes. In young adults, additional biomarkers such as C-reactive protein, apolipoproteins, lipoprotein(a), ferritin, and 25-hydroxycholecalciferol were measured. Arterial stiffness was evaluated by measuring brachial-ankle pulse wave velocity (baPWV). The mean age was 37.8 and 65.1 years old in the young and old groups, respectively. Without adjustment, most parameters were significantly correlated with baPWV in both young and old groups. Mean baPWV was significantly different according to metabolic syndrome (MetS) in both groups (13.1 and 12.1 m/s in the young subjects with and without MetS, respectively; 17.4 and 15.8 m/s, respectively, in the old group). After adjusting for age, sex, and hemodynamic factors, the difference in baPWV according to MetS was significant only in the old group. The relationship between most biomarkers and baPWV was influenced by metabolic disorders such as hypertension and diabetes in old adults. Total cholesterol (TC), low-density lipoprotein cholesterol (LDLC), and apolipoprotein B were significant in young group. In conclusion, the metabolic biomarkers related to arterial stiffness were different between young and old adults. Contrary to old adults, TC, LDLC, and apolipoprotein B were independent biomarkers for arterial stiffness in healthy young adults.

Validity and reliability of carotid-toe pulse wave velocity as a measure of arterial stiffness in healthy individuals: Comparison to carotid-femoral pulse wave velocity

PurposeThe present investigation evaluated the validity and reliability of carotid-toe PWV (ctPWV) as a non-intrusive measure of systemic arterial stiffness in healthy young adults. MethodsThe Validity Trial examined the association and agreement between cfPWV and ctPWV in 33 adults (24 ± 2 years; 14 females), while the Reliability Trial assessed the variability in cfPWV and ctPWV in 13 adults (22 ± 2 years; 5 females) over repeat visits. Proximal pulse waves were acquired (applanation tonometry) from the left common carotid (CCA) for both measures, while distal pulse waves were acquired from the left femoral artery (applanation tonometry) and the second left toe (pulse oximeter) for cfPWV and ctPWV, respectively. ResultscfPWV (5.3 ± 0.7, 3.9–6.5 m/s) and ctPWV (5.4 ± 0.5, 4.6–6.3 m/s) demonstrated a moderate-to-strong positive linear correlation (r = 0.79, P < 0.01) and a strong intra-class correlation (ICC; ICC = 0.86, P < 0.01). The Bland–Altman plot demonstrated agreement between cfPWV and ctPWV with no fixed bias (0.1 m/s, ± 2SD: −0.8 to 0.9 m/s, P > 0.05) and all data points falling within ±2 SD of the mean difference between measures. cfPWV and ctPWV demonstrated reliability across visits as evidenced by low coefficients of variation (cfPWV: 3.4 ± 2.6%, ctPWV: 2.6 ± 2.5%) and strong ICCs (cfPWV: ICC = 0.91, ctPWV: ICC = 0.84, both P < 0.01). ConclusionsThrough comparison with cfPWV, this study provides evidence to suggest that ctPWV yields a valid and reliable index of arterial stiffness in healthy young adults.

Acute Effect of Interval Walking on Arterial Stiffness in Healthy Young Adults.

The purpose of this study was to determine the acute effects of interval walking (IW) on arterial stiffness. The participants in this study were 14 healthy men and women (age 27.5±3.8 y). Carotid-femoral pulse wave velocity (cfPWV) was measured using an automatic oscillometric device at 30 min before (baseline) and at 30 and 60 min after walking. Participants repeated five sets of 3-min walks at 30% and 70% of maximum aerobic capacity for a total of 6 min per set in the IW trial. The participants also walked for 30 min at 50% (moderate intensity) of maximum aerobic capacity in a continuous walking (CW) trial. cfPWV was significantly decreased from baseline at 30 min (P=0.02) after the IW trial, and this reduction in cfPWV persisted for 60 min (P=0.01). In contrast, cfPWV was significantly decreased from baseline at 30 min (P=0.03) after the CW trial, but the reduction did not persist for 60 min. Moreover, changes in cfPWV in the IW trial after 30 and 60 min were significantly lower than in the CW trial (P<0.05). These results suggest that IW acutely reduces central arterial stiffness more than CW in healthy young adults.

Acute Effect of Static Stretching Exercise on Arterial Stiffness in Healthy Young Adults.

Habitual stretching exercise increases carotid arterial compliance, and acute stretching exercise increases arterial compliance in patients with myocardial infarction. However, it is not known whether this arterial adaptation is sustained after exercise. The aim of this study was to examine the effect of a single bout of stretching exercise on the time course of systemic, central, and peripheral arterial stiffness in healthy young subjects. Twenty-six healthy young men performed static stretching exercise involving the entire body (trunk, upper limb, and lower limb) for 40 mins. Pulse-wave velocity (PWV; an index of arterial stiffness), blood pressure, and heart rate were measured before and 0, 15, 30, and 60 mins after stretching exercise. Femoral-ankle PWV and brachial-ankle PWV were reduced relative to baseline 15 and 30 mins after acute stretching (P < 0.05); however, these arterial responses were not sustained for longer periods, and both PWV values returned to the baseline levels within 60 mins. By contrast, carotid-femoral PWV was unchanged. These results suggest that chronic and sufficient repetition of muscle stretch stimulation may result in chronic high arterial compliance, although a single bout of stretch exercise acutely affects arterial compliance.

Abstract P206: Increased Short-term Dietary Sodium Intake Does Not Increase Blood Pressure or Measures of Aortic Stiffness in Young Healthy Adults

Background: Sodium (Na) sensitivity is defined as the short-term increase in blood pressure (BP) after increased Na intake. The impact of Na sensitivity on measures of aortic stiffness has not been previously characterized in non-hypertensives. We tested the feasibility of an oral Na loading protocol to characterize the effects of increased dietary Na on blood pressure and measures of aortic stiffness in health young adults. Methods: In an open-label repeated measures pilot study, we enrolled 40 healthy adults age 21-30 years (18 females). Subjects were evaluated before and after 7 days of oral Na loading (12g (205 mmol) of salt tablets/day). BP (mmHg, cuff method) was measured in supine, seated and standing positions. Radial artery tonometry (Sphygmacor) was used to assess measures of aortic stiffness: aortic BP (mmHg), aortic pulse pressure (mmHg), aortic augmentation index (%) and adjusted Tr, time of return of the reflected pressure wave as an index of aortic pulse wave velocity (m/s). Serum aldosterone, urine Na and potassium (K) were measured. Results: Nine subjects dropped out due to GI intolerance of the salt pills. In the remaining 31 subjects, Na loading did not change BP in any position, aortic BP, aortic pulse pressure, or Tr (Table: mean±SD for seated R arm BP and measures of aortic stiffness). There was no measurable aortic augmentation in the cohort. Na loading decreased serum aldosterone (9.1±1.5 to 5.2±0.8 ng/dl, p=0.02), and increased urine Na:K ratio (1.8±0.2 to 3.5±0.5, p=0.002). Conclusion: Oral Na loading was associated with suppression of the renin-angiotensin aldosterone system, did not increase BP, or measures of aortic stiffness in healthy young adults.

Postprandial effects on arterial stiffness parameters in healthy young adults.

Postprandial lipemia has been associated with acute endothelial dysfunction. Endothelial dysfunction, in turn, is associated with increased arterial stiffness. However, the relationship between postprandial lipemia and acute changes in arterial stiffness has not been extensively investigated. Therefore, we conducted a pilot study on the effects of postprandial lipemia on arterial stiffness in 19 healthy young adults before and after consumption of a high-fat mixed meal. Arterial stiffness was assessed locally with echo-tracking carotid arterial strain (CAS) and globally with carotid-femoral pulse wave velocity (PWV). As assessed by these two benchmark parameters, arterial stiffness did not differ significantly postprandially. However, the arterial distension period (ADP) was significantly lower 2 hours after mixed meal ingestion. In addition, slopes of carotid artery area (CAA) curves were significantly steeper postprandially. Therefore, we concluded that ADP may be a more sensitive marker of arterial stiffness in healthy young adults when compared to PWV and CAS.

Acute Sleep Deprivation is Associated with Increased Arterial Stiffness in Healthy Young Adults

PP-042 Arterial stiffness and its hemodynamic consequences are known to be associated with increased cardiovascular morbidity and mortality. Pulse wave velocity (PWV) and augmentation index (AIx) are non-invasive indicators of the arterial stiffness and wave reflection. Sleep deprivation (SD) is

Acute sleep deprivation is associated with increased arterial stiffness in healthy young adults

Arterial stiffness and its hemodynamic consequences are known to be associated with increased cardiovascular morbidity and mortality. Pulse wave velocity (PWV) and augmentation index (AIx) are noninvasive indicators of the arterial stiffness and wave reflection. Sleep deprivation (SD) is known to be associated with increased incidence of adverse cardiovascular events. The aim of this study was to investigate whether there is an association between acute SD and arterial stiffness parameters in healthy adults, which has not been studied previously. The study population consisted of 42 healthy volunteers (18 males, mean age 30.0 ± 4.5 years). Measurements of arterial stiffness were carried out by using a Mobil-O-Graph arteriograph system. Arterial stiffness measurements were obtained both after a night with regular sleep (RS) and after a night with SD. Mean sleep time was significantly lower after the night of SD when compared after RS (0.73 ± 1.39 versus 7.33 ± 0.52 h, p<0.001). Peripheral systolic blood pressure, peripheral pulse pressure, and cardiac output were significantly higher after SD when compared after RS (p=0.032, 0.007, and 0.003, respectively). PWV was significantly higher (5.33 ± 0.46 versus 5.15 ± 0.26 m/s, p=0.001), and AIx was significantly lower (20.5 ± 11.9 versus 26.0 ± 8.4 %, p=0.008) after the night of SD when compared after the RS. While PWV was significantly higher (p=0.008), and AIx was significantly lower (p=0.039) in male subjects, only PWV was significantly higher (p=0.009) in female subjects. Sleep time correlated with AIx (p=0.034; r=0.233) and inversely correlated with PWV (p=0.044; r=-0.222). In the present study, we demonstrated that even one night of SD is associated with increased arterial stiffness in healthy adults. The present findings suggest that adverse effects of SD on cardiovascular system might be at least in part due to increased arterial stiffness which needs to be tested with large-scale studies and in the chronic SD setting.