Carotid stiffness, intima-media thickness and aortic augmentation index among adults with SARS-CoV-2.

NEW FINDINGS: What is the central question of this study? We sought to investigate whether carotid stiffness, carotid intima-media thickness and the aortic augmentation index are altered in young adults 3-4 weeks after contraction of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) compared with young healthy adults. What is the main finding and its importance? We found that carotid stiffness, Young's modulus and the aortic augmentation index were greater in young adults who tested positive for SARS-CoV-2 compared with healthy young adults. These findings provide additional evidence for detrimental effects of SARS-CoV-2 on young adult vasculature, which might have implications for cardiovascular health. ABSTRACT: Contracting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been observed to cause decrements in vascular function of young adults. However, less is known about the impact of SARS-CoV-2 on arterial stiffness and structure, which might have additional implications for cardiovascular health. The purpose of this study was to assess the carotid artery stiffness and structure using ultrasound and the aortic augmentation index (AIx) using applanation tonometry in young adults after they tested positive for SARS-CoV-2. We hypothesized that carotid artery stiffness, carotid intima-media thickness (cIMT) and aortic AIx would be elevated in young adults with SARS-CoV-2 compared with healthy young adults. We evaluated 15 young adults (six male and nine female; 20 ± 1 years of age; body mass index, 24 ± 3 kg m-2 ) 3-4 weeks after a positive SARS-CoV-2 test result compared with young healthy adults (five male and 10 female; 23 ± 1 years of age; body mass index, 22 ± 2 kg m-2 ) who were evaluated before the coronavirus 2019 pandemic. Carotid stiffness, Young's modulus and cIMT were assessed using ultrasound, whereas aortic AIx and aortic AIx standardized to 75 beats min-1 (AIx@HR75) were assessed from carotid pulse wave analysis using SphygmoCor. Group differences were observed for carotid stiffness (control, 5 ± 1 m s-1 ; SARS-CoV-2, 6 ± 1 m s-1 ), Young's modulus (control, 396 ± 120 kPa; SARS-CoV-2, 576 ± 224 kPa), aortic AIx (control, 3 ± 13%; SARS-CoV-2, 13 ± 9%) and aortic AIx@HR75 (control, -3 ± 16%; SARS-CoV-2, 10 ± 7%; P < 0.05). However, cIMT was similar between groups (control, 0.42 ± 0.06 mm; SARS-CoV-2, 0.44 ± 0.08 mm; P > 0.05). This cross-sectional analysis revealed higher carotid artery stiffness and aortic stiffness among young adults with SARS-CoV-2. These results provide further evidence of cardiovascular impairments among young adults recovering from SARS-CoV-2 infection, which should be considered for cardiovascular complications associated with SARS-CoV-2.

Altered central and peripheral haemodynamics during rhythmic handgrip exercise in young adults with SARS-CoV-2.

NEW FINDINGS: What is the central question of this study? Are central and peripheral haemodynamics during handgrip exercise different in young adults 3-4 weeks following infection with of SARS-CoV-2 compared with young healthy adults. What is the main finding and its importance? Exercising heart rate was higher while brachial artery blood flow and vascular conductance were lower in the SARS-CoV-2 compared with the control group. These findings provide evidence for peripheral impairments to exercise among adults with SARS-CoV-2, which may contribute to exercise limitations. ABSTRACT: The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can have a profound impact on vascular function. While exercise intolerance may accompany a variety of symptoms associated with SARS-CoV-2 infection, the impact of SARS-CoV-2 on exercising blood flow (BF) remains unclear. Central (photoplethysmography) and peripheral (Doppler ultrasound) haemodynamics were determined at rest and during rhythmic handgrip (HG) exercise at 30% and 45% of maximal voluntary contraction (MVC) in young adults with mild symptoms 25 days after testing positive for SARS-CoV-2 (SARS-CoV-2: n = 8M/5F; age: 21 ± 2 years; height: 176 ± 11 cm; mass: 71 ± 11 kg) and were cross-sectionally compared with control subjects (Control: n = 8M/5F; age: 27 ± 6 years; height: 178 ± 8 cm; mass: 80 ± 25 kg). Systolic blood pressure, end systolic arterial pressure and rate pressure product were higher in the SARS-CoV-2 group during exercise at 45% MVC compared with controls. Brachial artery BF was lower in the SARS-CoV-2 group at both 30% MVC (Control: 384.8 ± 93.3 ml min-1 ; SARS-CoV-2: 307.8 ± 105.0 ml min-1 ; P = 0.041) and 45% MVC (Control: 507.4 ± 109.9 ml min-1 ; SARS-CoV-2: 386.3 ± 132.5 ml min-1 ; P = 0.002). Brachial artery vascular conductance was lower at both 30% MVC (Control: 3.93 ± 1.07 ml min-1  mmHg-1 ; SARS-CoV-2: 3.11 ± 0.98 ml min-1  mmHg-1 ; P = 0.022) and 45% MVC (Control: 4.74 ± 1.02 ml min-1  mmHg-1 ; SARS-CoV-2: 3.46 ± 1.10 ml min-1  mmHg-1 ; P < 0.001) in the SARS-CoV-2 group compared to control group. The shear-induced dilatation of the brachial artery increased similarly across exercise intensities in the two groups, suggesting the decrease in exercising BF may be due to microvascular impairments. Brachial artery BF is attenuated during HG exercise in young adults recently diagnosed with mild SARS-CoV-2, which may contribute to diminished exercise capacity among those recovering from SARS-CoV-2 like that seen in severe cases.

COVID-19 is getting on our nerves: sympathetic neural activity and haemodynamics in young adults recovering from SARS-CoV-2.

KEY POINTS: The impact of SARS-CoV-2 infection on autonomic and cardiovascular function in otherwise healthy individuals is unknown. For the first time it is shown that young adults recovering from SARS-CoV-2 have elevated resting sympathetic activity, but similar heart rate and blood pressure, compared with control subjects. Survivors of SARS-CoV-2 also exhibit similar sympathetic nerve activity and haemodynamics, but decreased pain perception, during a cold pressor test compared with healthy controls. Further, these individuals display higher sympathetic nerve activity throughout an orthostatic challenge, as well as an exaggerated heart rate response to orthostasis. If similar autonomic dysregulation, like that found here in young individuals, is present in older adults following SARS-CoV-2 infection, there may be substantial adverse implications for cardiovascular health. ABSTRACT: The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can elicit systemic adverse physiological effects. However, the impact of SARS-CoV-2 on autonomic and cardiovascular function in otherwise healthy individuals remains unclear. Young adults who tested positive for SARS-CoV-2 (COV+; n = 16, 8 F) visited the laboratory 35 ± 16 days following diagnosis. Muscle sympathetic nerve activity (MSNA), systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were measured in participants at rest and during a 2 min cold pressor test (CPT) and 5 min each at 30° and 60° head-up tilt (HUT). Data were compared with age-matched healthy controls (CON; n = 14, 9 F). COV+ participants (18.2 ± 6.6 bursts min-1 ) had higher resting MSNA burst frequency compared with CON (12.7 ± 3.4 bursts min-1 ) (P = 0.020), as well as higher MSNA burst incidence and total activity. Resting HR, SBP and DBP were not different. During CPT, there were no differences in MSNA, HR, SBP or DBP between groups. COV+ participants reported less pain during the CPT compared with CON (5.7 ± 1.8 vs. 7.2 ± 1.9 a.u., P = 0.036). MSNA was higher in COV+ compared with CON during HUT. There was a group-by-position interaction in MSNA burst incidence, as well as HR, in response to HUT. These results indicate resting sympathetic activity, but not HR or BP, may be elevated following SARS-CoV-2 infection. Further, cardiovascular and perceptual responses to physiological stress may be altered, including both exaggerated (orthostasis) and suppressed (pain perception) responses, compared with healthy young adults.

Vascular alterations among young adults with SARS-CoV-2.

While SARS-CoV-2 primarily affects the lungs, the virus may be inflicting detriments to the cardiovascular system, both directly through angiotensin-converting enzyme 2 receptor and initiating systemic inflammation. Persistent systemic inflammation may be provoking vascular dysfunction, an early indication of cardiovascular disease risk. To establish the potential effects of SARS-CoV-2 on the systemic vasculature in the arms and legs, we performed a cross-sectional analysis of young healthy adults (control: 5 M/15 F, 23.0 ± 1.3 y, 167 ± 9 cm, 63.0 ± 7.4 kg) and young adults who, 3-4 wk prior to testing, had tested positive for SARS-CoV-2 (SARS-CoV-2: 4 M/7 F, 20.2 ± 1.1 y, 172 ± 12 cm, 69.5 ± 12.4 kg) (means ± SD). Using Doppler ultrasound, brachial artery flow-mediated dilation (FMD) in the arm and single passive limb movement (sPLM) in the leg were assessed as markers of vascular function. Carotid-femoral pulse wave velocity (PWVcf) was asvsessed as a marker of arterial stiffness. FMD was lower in the SARS-CoV-2 group (2.71 ± 1.21%) compared with the control group (8.81 ± 2.96%) (P < 0.01) and when made relative to the shear stimulus (SARS-CoV-2: 0.04 ± 0.02 AU, control: 0.13 ± 0.06 AU, P < 0.01). The femoral artery blood flow response, as evidenced by the area under the curve, from the sPLM was lower in the SARS-CoV-2 group (-3 ± 91 mL) compared with the control group (118 ± 114 mL) (P < 0.01). PWVcf was higher in the SARS-CoV-2 group (5.83 ± 0.62 m/s) compared with the control group (5.17 ± 0.66 m/s) (P < 0.01). Significantly lower systemic vascular function and higher arterial stiffness are evident weeks after testing positive for SARS-CoV-2 among young adults compared with controls.NEW & NOTEWORTHY This study was the first to investigate the vascular implications of contracting SARS-CoV-2 among young, otherwise healthy adults. Using a cross-sectional design, this study assessed vascular function 3-4 wk after young adults tested positive for SARS-CoV-2. The main findings from this study were a strikingly lower vascular function and a higher arterial stiffness compared with healthy controls. Together, these results suggest rampant vascular effects seen weeks after contracting SARS-CoV-2 in young adults.

Arterial stiffness and carotid distensibility following acute formaldehyde exposure in female adults.

Formaldehyde (FA) is a ubiquitous organic preservative used in several industries and represents an occupational health hazard. Short-term exposure to FA can increase oxidative stress and cause a decrease in conduit vessel function. These decrements in vascular function may extend to the arterial architecture, predisposing individuals to increased risk of cardiovascular disease. The purpose of this study was to investigate the impact of an acute 90-minute FA exposure period (259 ± 95 ppb) on indices of arterial architecture. Arterial stiffness and carotid distensibility as determined by central pressures, augmentation index (AIx), and carotid-femoral pulse wave velocity (cfPWV) (n=13F, 24 ± 1 year) as well as carotid stiffness and intima media thickness (IMT) (n = 9F, 23 ± 1 year) were assessed prior to (Pre-FA) and immediately following (Post-FA) exposure to FA in human cadaver dissection laboratories. Central pressures and cfPWV (Pre-FA: 5.2 ± 0.8 m.s-1, Post-FA: 5.2 ± 1.1 m s-1) were unchanged by acute FA exposure (p > 0.05). Carotid stiffness parameters and distension were unchanged by acute FA exposure (p > 0.05), although distensibility (Pre-FA: 33.9 ± 10.5[10-3*kPa-1], Post-FA: 25.9 ± 5.5[10-3*kPa-1], p < 0.05), and IMT (Pre-FA: 0.42 ± 0.05 mm, Post-FA: 0.51 ± 0.11 mm, p < 0.05) decreased and increased, respectively. Individual Pre- to Post-FA changes in these markers of arterial architecture did not correlate with levels of FA exposure ([FA]: 20-473 ppb) (p > 0.05). Our group previously found vascular function decrements following acute FA exposure in human cadaver laboratories; here we found that carotid distensibility and intima media thickness are altered following FA exposure.

Attentional focus does not impact locomotor-respiratory coupling in trained runners.

PURPOSE: The purpose of this study was to explore relationships between attentional strategies and LRC, running economy, perceived exertion, and dyspnea. METHODS: 25 endurance-trained males ([Formula: see text]O2max = 68.2 ± 4.7 mL kg-1 min-1) ran for 5 min each at two different submaximal speeds, during which LRC and oxygen consumption ([Formula: see text]O2) were measured. The degree of LRC was calculated as the percentage of breaths occurring during the same decile of the step cycle. Attentional focus was assessed at the end of exercise using an Attentional Focusing Questionnaire, with subscales for association, dissociation, and distress. RESULTS: We found no significant relationships between attentional focus measures and LRC. However, dissociation scores were positively correlated with [Formula: see text]O2 (r = 0.404), as well as  %[Formula: see text]O2max (r = 0.474), at the slower running speed. Distress scores were the only attentional focus subscale related to perceived exertion and dyspnea (r = 0.378 to 0.654). CONCLUSION: These findings suggest attentional focus is not driving the high levels of LRC seen in trained endurance athletes but may relate to running economy and perceptual responses.

Endurance exercise performance in acute hypoxia is influenced by expiratory flow limitation.

PURPOSE: We sought to determine if expiratory flow limitation influences intensive aerobic exercise performance in mild hypoxia. METHODS: Fourteen trained male cyclists were separated into flow-limited (FL, n = 7) and non-FL (n = 7) groups based on the extent of expiratory flow limitation exhibited during maximal exercise in normoxia. Participants performed two self-paced 5-km cycling time trials, one in normoxic (F IO2 = 0.21) and one in mild hypoxic (F IO2 = 0.17) conditions in a randomized, balanced order with the subjects blinded to composition of the inspirate. Percent change from normoxia to hypoxia in average power output (%ΔP TT) and time to completion (%ΔT TT) were used to assess performance. RESULTS: Hypoxia resulted in a significant decline in estimated arterial O2 saturation and decrements in performance in both groups, although FL had a significantly smaller %ΔP TT (-4.0 ± 0.5 vs. -9.0 ± 1.8 %) and %ΔT TT (1.3 ± 0.3 vs. 3.7 ± 0.9 %) compared to non-FL. At the 5th km of the time trial, minute ventilation did not change from normoxia to hypoxia in FL (3.4 ± 3.1 %) or non-FL (2.3 ± 3.7 %), but only the non-FL reported a significantly increased dyspnea rating in hypoxia compared to normoxia (~9 %). Non-FL athletes did not utilize their ventilatory reserve to defend arterial oxygen saturation in hypoxia, which may have been due to an increased measure of dyspnea in the hypoxic trial. CONCLUSION: FL athletes experience less hypoxia-related aerobic exercise performance impairment as compared to non-FL athletes, despite having less ventilatory reserve.

Runners maintain locomotor-respiratory coupling following isocapnic voluntary hyperpnea to task failure.

INTRODUCTION: Evidence has long suggested that mammalian ventilatory and locomotor rhythms are linked, yet determinants and implications of locomotor-respiratory coupling (LRC) continue to be investigated. Anecdotally, respiratory muscle fatigue seen at the end of heavy exercise may result in an uncoupling of movement-ventilation rhythms; however, there is no scientific evidence to substantiate this claim. PURPOSE: We sought to determine whether or not fatigue of the respiratory muscles alters locomotor-respiratory coupling patterns typically observed in highly trained individuals while running. A related query was to examine the relationship between the potential changes in LRC and measures of running economy. METHOD: Twelve male distance runners ran at four submaximal workloads (68-89 % VO2peak) on two separate days while LRC was quantified. One LRC trial served as a control (CON), while the other was performed following an isocapnic voluntary hyperpnea to task failure to induce respiratory muscle fatigue (FT+). LRC was assessed as stride-to-breathing frequency ratios (SF/fB) and degree of LRC (percentage of breaths occurring during the same decile of the step cycle). RESULT: Hyperpnea resulted in significant declines in maximal voluntary inspiratory (MIP) and expiratory (MEP) mouth pressures (ΔMIP = -10 ± 12 cm H2O; ΔMEP = -6 ± 9 cm H2O). There were no differences in minute ventilation between CON and FT+ (CON, all speeds pooled = 104 ± 25 L min(-1); FT+ pooled = 106 ± 23 L min(-1)). Stride frequency was not different between trials; however, breathing frequency was significantly greater during FT+ compared to CON at all speeds (CON pooled = 47 ± 10 br min(-1); FT+ pooled = 52 ± 9 br min(-1)), resulting in smaller corresponding SF/fB. Yet, the degree of LRC was the same during CON and FT+ (CON pooled = 63 ± 15 %; FT+ pooled = 64 ± 18 %). CONCLUSION: The results indicate that trained runners are able to continue entraining breath and step cycles, despite marked changes in exercise breathing frequency, after a fatiguing hyperpnea challenge.

Operating lung volumes are affected by exercise mode but not trunk and hip angle during maximal exercise.

INTRODUCTION: Despite VO2peak being, generally, greater while running compared to cycling, ventilation (VE) during maximal exercise is less while running compared to cycling. Differences in operating lung volumes (OLV) between maximal running and cycling could be one explanation for previously observed differences in V E and this could be due to differences in body position e.g., trunk/hip angle during exercise. PURPOSE: We asked whether OLV differed between maximal running and cycling and if this difference was due to trunk/hip angle during exercise. METHODS: Eighteen men performed three graded maximal exercise tests; one while running, one while cycling in the drop position (i.e., extreme hip flexion), and one while cycling upright (i.e., seated with thorax upright). Resting flow-volume characteristics were measured in each body position to be used during exercise. Tidal flow-volume loops were measured throughout the exercise. RESULTS: V E during maximal running (148.8 ± 18.9 L min(-1)) tended to be lower than during cycling in the drop position (158.5 ± 24.7 L min(-1); p = 0.07) and in the upright position (158.5 ± 23.7 L min(-1); p = 0.06). End-inspiratory and end-expiratory lung volumes (EILV, EELV) were significantly larger during drop cycling compared to running (87.1 ± 4.1 and 35.8 ± 6.2 vs. 83.9 ± 6.0 and 33.0 ± 5.7% FVC), but only EILV was larger during upright cycling compared to running (88.2 ± 3.5% FVC). OLV and V E did not differ between cycling positions. CONCLUSION: Since OLV are altered by exercise mode, but cycling position did not have a significant impact on OLV, we conclude that trunk/hip angle is likely not the primary factor determining OLV during maximal exercise.

Static respiratory mechanics are unaltered in males and females with obesity.

We tested the hypothesis that independent of the obesity-related shift in lung volume subdivisions, obesity would not reduce the interrelationships of expiratory flow, lung volume, and static lung elastic recoil pressure in males and females. Simultaneous measurements of expiratory flow, volume, and transpulmonary pressure were continuously recorded while flow-volume loops of varying expiratory efforts were performed in a pressure-corrected, volume-displacement body plethysmograph in males and females with obesity. Static compliance curves were collected using the occlusion technique. Flow-volume, static pressure-volume, and static pressure-flow relationships were examined. Isovolume pressure-flow curves were constructed for the determination of the critical pressure for maximal flow. Data were compared with that collected in lean males and females. Individuals with obesity displayed a notable decrease in functional residual capacity. The interrelationships of flow, lung volume, static elastic recoil pressure, and the minimum pressure required for maximal expiratory flow in males and females with obesity were not different from that in lean males and females (all P > 0.05). Obesity does not alter the interrelationships of flow-volume-pressure of the lung in adult males and females (all P > 0.05). We further explored potential sex differences in static mechanics independent of obesity and observed that females have lower maximal expiratory flow due to a combination of smaller lungs and greater upstream flow resistance compared with males (all P ≤ 0.05).NEW & NOTEWORTHY The potential influence of obesity on the interrelationships between maximal expiratory flow, lung volume, and static lung elastic recoil pressure is unclear. These data show that the presence of obesity does not alter the relationship of flow and pressure across the mid-expiratory range in males and females. In addition, independent of obesity, females have smaller lungs and greater upstream flow resistance, which contributes to reduced maximal flow, when compared with males.

Monthly transthoracic echocardiography in young adults for 6 months following SARS-CoV-2 infection.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can elicit acute and long-term effects on the myocardium among survivors, yet effects among otherwise healthy young adults remains unclear. Young adults with mild symptoms of SARS-CoV-2 (8M/8F, age: 21 ± 1 years, BMI: 23.5 ± 3.1 kg·m-2 ) underwent monthly transthoracic echocardiography (TTE) and testing of circulating cardiac troponin-I for months 1-6 (M1-M6) following a positive polymerase chain reaction test to better understand the acute effects and post-acute sequelae of SARS-CoV-2 on cardiac structure and function. Left heart structure and ejection fraction were unaltered from M1-M6 (p > 0.05). While most parameters of septal and lateral wall velocities, mitral and tricuspid valve, and pulmonary vein (PV) were unaltered from M1-M6 (p > 0.05), lateral wall s' wave velocity increased (M1: 0.113 ± 0.019 m·s-1 , M6: 0.135 ± 0.022 m·s-1 , p = 0.013); PV S wave velocity increased (M1: 0.596 ± 0.099 m·s-1 , M6: 0.824 ± 0.118 m·s-1 , p < 0.001); the difference between PV A wave and mitral valve (MV) A wave durations decreased (M1: 39.139 ± 43.715 ms, M6: 18.037 ± 7.227 ms, p = 0.002); the ratio of PV A duration to MV A duration increased (M1: 0.844 ± 0.205, M6: 1.013 ± 0.132, p = 0.013); and cardiac troponin-I levels decreased (M1: 0.38 ± 0.20 ng·ml-1 , M3: 0.28 ± 0.34 ng·ml-1 , M6: 0.29 ± 0.16 ng·ml-1 ; p = 0.002) over time. While young adults with mild symptoms of SARS-CoV-2 lacked changes to cardiac structure, the subclinical improvements to cardiac function and reduced inflammatory marker of cardiac troponin-I over 6 months following SARS-CoV-2 infection provide physiologic guidance to post-acute sequelae and recovery from SARS-CoV-2 and its variants using conventional TTE.

Plasma UCHL1, GFAP, Tau, and NfL Are Not Different in Young Healthy Persons With Mild COVID-19 Symptoms Early in the Pandemic: A Pilot Study.

Elevated levels of brain injury biomarkers have been found primarily in middle-aged or older persons experiencing moderate-to-severe COVID-19 symptoms. However, there is little research in young adults, and there is concern that COVID-19 causes brain injury even in the absence of moderate-to-severe symptoms. Therefore, the purpose of our study was to investigate whether neurofilament light (NfL), glial fibrillary acidic protein (GFAP), tau, or ubiquitin carboxyl-terminal esterase L1 (UCHL1) are elevated in the plasma of young adults with mild COVID-19 symptoms. Twelve participants diagnosed with COVID-19 had plasma collected 1, 2, 3, and 4 months after diagnosis to determine whether NfL, GFAP, tau, and UCHL1 concentrations increased over time or whether plasma concentrations were elevated compared with COVID-19-naïve participants. We also compared plasma NfL, GFAP, tau, and UCHL1 concentrations between sexes. Our results showed no difference between NfL, GFAP, tau, and UCHL1 concentrations in COVID-19-naïve participants and COVID-19-positive participants at any of the four time points (p = 0.771). Within the COVID-19-positive participants, UCHL1 levels were higher at month 3 after diagnosis compared to month 1 or month 2 (p = 0.027). Between sexes, females were found to have higher UCHL1 (p = 0.003) and NfL (p = 0.037) plasma concentrations compared to males, whereas males had higher plasma tau concentrations than females (p = 0.024). Based on our data, it appears that mild COVID-19 in young adults does not increase plasma NfL, GFAP, tau, or UCHL1.

Repeatability of dyspnea measurements during exercise in women with obesity.

While the 0-10 Borg scale to rate perceived breathlessness (RPB) is widely used to assess dyspnea on exertion, the repeatability of RPB in women with obesity is unknown. We examined the repeatability of RPB in women with obesity during submaximal constant-load cycling following at least 10 weeks of normal daily life. Seventeen women (37 ± 7 yr; 34.6 ± 4.5 kg/m2) who rated their breathlessness as 3 on the Borg scale (i.e., "moderate") during 60 W submaximal cycling repeated the same test following 19 ± 9 weeks of normal living. Mean body weight (93.8 ± 16.1 vs. 93.6 ± 116.8 kg, p = 0.94) and RPB (3.0 ± 0.0 vs. 3.1 ± 1.4, p = 0.80) did not differ between pre- and post-normal living periods. We demonstrate that subjective ratings of breathlessness are repeatable for the majority of subjects and can be used to accurately assess DOE during submaximal constant-load cycling in women with obesity.

Six-month longitudinal tracking of arterial stiffness and blood pressure in young adults following SARS-CoV-2 infection.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can increase arterial stiffness 3-4 wk following infection, even among young, healthy adults. However, the long-term impacts of SARS-CoV-2 infection on cardiovascular health and the duration of recovery remain unknown. The purpose of this study was to elucidate potential long-lasting effects of SARS-CoV-2 infection on markers of arterial stiffness among young adults during the 6 mo following infection. Assessments were performed at months 1, 2, 3, 4, and ∼6 following SARS-CoV-2 infection. Doppler ultrasound was used to measure carotid-femoral pulse wave velocity (cfPWV) and carotid stiffness, and arterial tonometry was used to measure central blood pressures and aortic augmentation index at a heart rate of 75 beats·min-1 (AIx@HR75). Vascular (VCAM-1) and intracellular (ICAM-1) adhesion molecules were analyzed as circulating markers of arterial stiffness. From months 1-6, a significant reduction in cfPWV was observed (month 1: 5.70 ± 0.73 m·s-1; month 6: 4.88 ± 0.65 m·s-1; P < 0.05) without any change in carotid stiffness measures. Reductions in systolic blood pressure (month 1: 123 ± 8 mmHg; month 6: 112 ± 11 mmHg) and mean arterial pressure (MAP; month 1: 97 ± 6 mmHg; month 6: 86 ± 7 mmHg) were observed (P < 0.05), although AIx@HR75 did not change over time. The month 1-6 change in cfPWV and MAP were correlated (r = 0.894; P < 0.001). A reduction in VCAM-1 was observed at month 3 compared with month 1 (month 1: 5,575 ± 2,242 pg·mL-1; month 3: 4,636 ± 1,621 pg·mL-1; P < 0.05) without a change in ICAM-1. A reduction in cfPWV was related with MAP, and some indicators of arterial stiffness remain elevated for several months following SARS-CoV-2 infection, possibly contributing to prolonged recovery and increased cardiovascular health risks.NEW & NOTEWORTHY We sought to investigate potential long-lasting effects of SARS-CoV-2 infection on markers of arterial stiffness among young adults for 6 mo following infection. Carotid femoral pulse wave velocity was significantly reduced while carotid stiffness measures remained unaltered over the 6-mo period. These findings suggest several months of recovery from infection may be necessary for young adults to improve various markers of arterial stiffness, possibly contributing to cardiovascular health and recovery among those infected with SARS-CoV-2.

Longitudinal observations of sympathetic neural activity and hemodynamics during 6 months recovery from SARS-CoV-2 infection.

Cross-sectional data indicate that acute SARS-CoV-2 infection increases resting muscle sympathetic nerve activity (MSNA) and alters hemodynamic responses to orthostasis in young adults. However, the longitudinal impact of contracting SARS-CoV-2 on autonomic function remains unclear. The aim of this study was to longitudinally track MSNA, sympathetic transduction to blood pressure (BP), and hemodynamics over 6 months following SARS-CoV-2 infection. Young adults positive with SARS-CoV-2 reported to the laboratory three times over 6 months (V1:41 ± 17, V2:108 ± 21, V3:173 ± 16 days post-infection). MSNA, systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were measured at rest, during a cold pressor test (CPT), and at 30° head-up tilt (HUT). Basal SBP (p = 0.019) and DBP (p < 0.001) decreased throughout the 6 months, whereas basal MSNA and HR were not different. Basal sympathetic transduction to BP and estimates of baroreflex sensitivity did not change over time. SBP and DBP were lower during CPT (SBP: p = 0.016, DBP: p = 0.007) and HUT at V3 compared with V1 (SBP: p = 0.041, DBP: p = 0.017), with largely no changes in MSNA. There was a trend toward a visit-by-time interaction for burst incidence (p = 0.055) during HUT, wherein at baseline immediately prior to tilting, burst incidence was lower at V3 compared with V1 (p = 0.014), but there were no differences between visits in the 30 HUT position. These results support impairments to cardiovascular health, and potentially autonomic function, which may improve over time. However, the improvements in BP over 6 months recovery from mild SARS-CoV-2 infection are likely not a direct result of changes in sympathetic activity.

Tracking peripheral vascular function for six months in young adults following SARS-CoV-2 infection.

SARS-CoV-2 infection is known to instigate a range of physiologic perturbations, including vascular dysfunction. However, little work has concluded how long these effects may last, especially among young adults with mild symptoms. To determine potential recovery from acute vascular dysfunction in young adults (8 M/8F, 21 ± 1 yr, 23.5 ± 3.1 kg⋅m-2 ), we longitudinally tracked brachial artery flow-mediated dilation (FMD) and reactive hyperemia (RH) in the arm and hyperemic response to passive limb movement (PLM) in the leg, with Doppler ultrasound, as well as circulating biomarkers of inflammation (interleukin-6, C-reactive protein), oxidative stress (thiobarbituric acid reactive substances, protein carbonyl), antioxidant capacity (superoxide dismutase), and nitric oxide bioavailability (nitrite) monthly for a 6-month period post-SARS-CoV-2 infection. FMD, as a marker of macrovascular function, improved from month 1 (3.06 ± 1.39%) to month 6 (6.60 ± 2.07%; p < 0.001). FMD/Shear improved from month one (0.10 ± 0.06 AU) to month six (0.18 ± 0.70 AU; p = 0.002). RH in the arm and PLM in the leg, as markers of microvascular function, did not change during the 6 months (p > 0.05). Circulating markers of inflammation, oxidative stress, antioxidant capacity, and nitric oxide bioavailability did not change during the 6 months (p > 0.05). Together, these results suggest some improvements in macrovascular, but not microvascular function, over 6 months following SARS-CoV-2 infection. The data also suggest persistent ramifications for cardiovascular health among those recovering from mild illness and among young, otherwise healthy adults with SARS-CoV-2.

Recruitment and Retention of Healthy Women with Obesity for a Psychophysiological Study before and After Weight Loss: Insights, Challenges, and Suggestions.

OBJECTIVE: The objective of this paper is to present data on participant recruitment, retention, and weight loss success during a psychophysiological study in women with obesity. METHODS: Volunteers were women with obesity, 20 - 45 yr, with a BMI between 30 - 45 kg/m2. The study was approximately 20 weeks in duration, including a 12-week weight loss program. RESULTS: Recruitment was not completed until 8 months past the original projected date of 12 months. The study was not completed until 11 months past the original projected completion date of 14 months. On average 4.4 ± 2.1 (mean ± SD) volunteers were consented per month (N = 99) and 2.5 ± 1.1 participants started the weight loss program per month. 24% of consented volunteers were lost due to exclusion criteria, withdrawals, and unresponsive behavior before starting the weight loss program. Attrition of participants who started the weight loss program was 45%. Only 11% of those who started the program were unable to lose weight (N = 6). CONCLUSION: Recruiting and/or weight loss success do not always present the most challenging aspects of completing a psychophysiological weight loss intervention. While participant attrition during a weight loss program can occur for a wide range of reasons supportive efforts in the early phases of the intervention may maximize retention.

Dysanapsis in men and women with obesity.

Obesity alters chest wall mechanics, reduces lung volumes, and increases airway resistance. In addition, the luminal area of the larger conducting airways is smaller in women than in men when matched for lung size. We examined whether differences in pulmonary mechanics with obesity and sex were associated with the dysanapsis ratio (DR), an estimate of airway size when the expiratory flow is maximal, in men and women with and without obesity. In addition, we examined the ability to estimate DR using predicted versus measured static recoil pressure at 50% forced vital capacity (FVC; Pst50FVC). Participants completed pulmonary function testing and measurements of pulmonary mechanics. Flow, volume, and transpulmonary pressure were recorded while completing forced vital capacity (FVC) maneuvers in a body plethysmograph. Static compliance curves were collected using the occlusion technique. DR was calculated using measured values of forced midexpiratory flow and Pst50FVC. DR was also calculated using Pst predicted from previously reported data. There was no significant group (lean vs. obese) by sex interaction or main effect of group on DR. However, women displayed significantly larger DR compared with men. Predicted Pst50FVC was significantly greater than measured Pst50FVC. DR calculated from measured Pst was significantly greater than when using predicted Pst. In conclusion, although obesity does not appear to alter airway size, women may have larger airways compared with men when midexpiratory flow is maximal. In addition, DR estimated using predicted Pst should be used with caution.NEW & NOTEWORTHY It is unclear whether obesity in combination with sex influences the dysanapsis ratio (DR). These data indicate that DR is unaltered in adults with obesity and is greater in women than in men but similar between sexes when matched for lung volume. We also report a significant difference between predicted and measured static recoil pressure. Thus, we caution against predicting static recoil pressure in the calculation of DR.