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  • Kaspersen Kirk posted an update 1 year, 6 months ago

    Postural orthostatic tachycardia syndrome (POTS) is accompanied by reduced brain blood flow, autonomic dysfunction, and orthostatic intolerance. We hypothesized that wearing a neck compression collar would attenuate orthostatic symptoms, increase brain blood flow, and influence autonomic reflexes. Ten participants with POTS (9 women, age 36±10) underwent two trials of supine rest, paced deep breathing (6 breaths/min), Valsalva maneuver (40mmHg for 15s), and 70o upright tilt. For one trial participants wore a neck compression device (Q30 Innovations). Blood pressure, heart rate, brain blood flow velocity, stroke volume, respiratory rate, and end-tidal gases were continuously measured. The Vanderbilt Orthostatic Symptom Score was compiled at the end of tilt. The use of the collar reduced the orthostatic symptom score of participants with POTS during upright tilt (26.9±12.5 to 18.7±13.1, P=0.04). Collar compression, in the supine condition reduced the low frequency domain of heart rate variability (60±18 to 51±23nu, P=0.04) and increased the change in HR (15±5 to 17±6bpm, P=0.02) and EI ratio (1.2±0.1 to 1.3±0.1, P=0.01) during paced deep breathing. Throughout tilt, wearing the collar reduced respiratory rate (Baseline 13±3 to 12±4breath/min; Tilt 18±5 to 15±5breath/min; Main effect of collar P=0.048), end-tidal oxygen (Baseline 115±5 to 112±5mmHg; Tilt 122±10 to 118±11mmHg; Main effect of collar P=0.026). In participants with POTS wearing the Q-collar reduced orthostatic symptoms, increased the HR response to deep breathing, and decreased resting ventilation.This study investigated the effects of exercise training on cardiac inflammatory and cardiac fibrotic pathways in female spontaneously hypertensive rats (SHR) which were divided into a sham-operated sedentary hypertensive group (SHR-S), a sedentary hypertensive ovariectomized group (SHR-O), hypertensive ovariectomized group with treadmill exercise training (SHR-OT, 60 min/day, 5 days/week) for 8 weeks. Normotensive female Wistar Kyoto rats (WKY) served as controls. SOD and CAT activities were significantly increased in the SHR-OT group, when compared with the SHR-S or SHR-O groups. The protein levels of ERα and ERβ became decreased in the SHR-O group, when compared with the WKY or SHR-S groups, but those were not changed in the SHR-OT group. The protein level of the angiotensin II type I receptor (AT1R) was increased in the SHR-S group, but did not further change those in the SHR-O group, whereas those were decreased in the SHR-OT group. The inflammatory-related protein levels of TNF-α, p-NFκB, COX-2, iNOS and IL-6, as well as the fibrotic-related protein levels of TGF-β, p-Smad2/3, CTGF, tPA, MMP9 and Collagen I were increased in the SHR-S group and increased further in the SHR-O group, whereas those were decreased in the SHR-OT group. The coexistence of hypertension and ovariectomy additively increased cardiac inflammatory and fibrotic pathways partially through hypertension-enhanced AT1R and ovariectomy-depressed estrogen receptors. Exercise training appeared to suppress hypertensive ovariectomized heart-induced inflammatory and fibrotic pathways possibly through decreasing AT1R, but not through estrogen receptors.Reduced paraspinal muscle size and flattening of spinal curvatures have been documented after spaceflight. Assessment of trunk adaptations to hypogravity can contribute to develop specific countermeasures. In this study, parabolic flights were used to investigate spinal curvature and muscle responses to hypogravity. Zolinza Data from five trials at 0.25g, 0.50g and 0.75g were recorded from six participants, positioned in a kneeling-seated position. During the first two trials, participants maintained a normal, upright posture. In the last three trials, small-amplitude perturbations were delivered in the anterior direction at the T10 level. Spinal curvature was estimated using motion capture cameras. Trunk displacement and contact force between the actuator and participant were recorded. Muscle activity responses were collected using intramuscular electromyography (iEMG) of the deep and superficial lumbar multifidus, iliocostalis lumborum, longissimus thoracis, quadratus lumborum, transversus abdominis, obliquus internus and obliquus externus muscles. The root mean square iEMG and the average spinal angles were calculated. Trunk admittance and muscle responses to perturbations were calculated as closed-loop frequency response functions. Compared with 0.75g, 0.25g resulted in lower activation of the longissimus thoracis (P=0.002); lower responses of the superficial multifidus at low frequencies (P=0.043); lower responses of the superficial multifidus (P=0.029) and iliocostalis lumborum (P=0.043); lower trunk admittance (P=0.037) at intermediate frequencies; and stronger responses of the transversus abdominis at higher frequencies (p=0.032). These findings indicate that exposure to hypogravity reduces trunk admittance, partially compensated by weaker stabilizing contributions of the paraspinal muscles and coinciding with an apparent increase of the deep abdominal muscle activity.The heart and lungs are anatomically coupled through the pulmonary circulation and coexist within the sealed thoracic cavity, making the function of these systems highly interdependent. Understanding of the complex mechanical interactions between cardiac and pulmonary systems has evolved over the last century to appreciate that changes in respiratory mechanics significantly impact pulmonary hemodynamics, ventricular filling and ejection. Furthermore, given that the left and right heart share a common septum and are surrounded by the non-distensible pericardium, direct ventricular interaction is an important mediator of both diastolic and systolic performance. While it is generally considered that cardiopulmonary interaction in healthy individuals at rest minimally affects hemodynamics, the significance during exercise is less clear. Adverse heart-lung interaction in respiratory disease is of growing interest as it may contribute to the pathogenesis of comorbid cardiovascular dysfunction and exercise intolerance in these patients.