Huffkelly3405

Corticospinal excitability and inhibition were not found to be different between UNIL and BIL conditions, in line with maximal voluntary activation.Blood supply is essential for osteogenesis, yet its relationship to load-related increases in bone mass is poorly defined. Herein, we aim to investigate the link between load-induced osteogenesis and the blood supply (bone perfusion and vascular porosity) using an established osteogenic non-invasive model of axial loading. Accordingly, 12N mechanical loads were applied to the right tibiae of six male C57BL6 mice at 10-12 weeks of age, 3 times/week for two weeks. Skeletal perfusion was measured acutely (post-loading) and chronically in loaded and contralateral, non-loaded hindlimbs by Laser Doppler imaging. Vascular and lacunar porosity of the cortical bone and tibia load-related changes in trabecular and cortical bone were measured by nanoCT and micro-CT, respectively. We found that the mean skeletal perfusion (loaded non-loaded limb ratio) increased by 56% immediately following the first loading episode (versus baseline, P less then 0.01) and a similar increase was observed after all loading episodes demonstrating that these acute responses were conserved for 2 weeks of loading. Loading failed however to engender any significant chronic changes in mean perfusion between the beginning and the end of the experiment. In contrast, two weeks of loading engendered increased vascular canal number in the tibial cortical compartment (midshaft) and, as expected, also increased trabecular and cortical bone volumes and modified tibial architecture in the loaded limb. Our results indicate that each episode of loading both generates acute enhancement in skeletal blood perfusion and also stimulates chronic vascular architectural changes in the bone cortices which coincide with load-induced increases in bone mass.This study was designed to investigate extrinsic tongue muscle activity in response to bronchopulmonary C-fiber activation following mid-cervical spinal contusion in the rat. Esophageal pressure and electromyogram of the extrinsic tongue muscles (genioglossus and hyoglossus) were monitored before and after inhalation of capsaicin (25 and 100 µg/ml) at the acute (three days), subchronic (12-16 days) and chronic (52-65 days) injured stages following unilateral mid-cervical spinal contusion. Three days after injury, the pre-inspiratory burst amplitude of the extrinsic tongue muscle during at baseline was significantly greater in mid-cervical spinal contused animals than in sham animals. At this time, capsaicin induced a significant reduction in both pre-inspiratory and inspiratory activity of the extrinsic tongue muscle in sham but not contused animals at the acute stage. selleck inhibitor During the chronic injured stage, capsaicin at 100 µg/ml induced stronger suppression of pre-inspiratory genioglossus muscle activity in the contused than in sham animals. These results demonstrated that cervical spinal cord injury alters upper airway motor outputs and their reflex modulation by bronchopulmonary C-fibers. The compensatory increase in respiratory activity of the extrinsic tongue muscle early after cervical spinal cord injury may help to maintain upper airway patency. However, under the condition of chronic cervical spinal cord injury, the increased suppression of genioglossus muscle activity by bronchopulmonary C-fiber activation may increase the risk of airway obstruction following chronic cervical spinal cord injury.The diaphragm is the primary muscle which generates the negative intra-thoracic pressure to drive inspiratory airflow. The diaphragm consists of two parts - the costal and crural portions - with different roles during inspiration in animals, particularly when the stimulus to breathe is increased. In this study, the neural drive to the costal and crural portions of the diaphragm was assessed in 9 healthy participants (8 male, aged 32 ± 13 years (mean ± SD)). Inspiratory electromyographic activity (EMG) was recorded from the costal diaphragm using an intramuscular electrode and from the crural diaphragm with a multi-pair gastro-oesophageal catheter. Participants performed voluntary augmented breaths at 120%, 140% and 160% of their tidal volume and also underwent progressive hypercapnia to induce involuntary breathing. Irrespective of the task, the increase in crural activity (normalized to quiet breathing) was only ~60% of the increase in costal activity (slope 0.56 ± 0.30; P less then 0.001). The onset and peak timing of EMG activity was similar for the costal and crural diaphragm during quiet breathing. Thus, when stimulated by either a voluntary or involuntary drive to breathe above tidal volume, the neural drive to the diaphragm is greater to the costal than crural portion.Patients with mild chronic obstructive pulmonary disease (COPD) demonstrate resting pulmonary vascular dysfunction as well as a blunted pulmonary diffusing capacity (DLCO) and pulmonary capillary blood volume (VC) response to exercise. The transition from the upright to supine position increases central blood volume and perfusion pressure, which may overcome microvascular dysfunction in an otherwise intact alveolar-capillary interface. The present study examined whether the supine position normalized DLCO and VC responses to exercise in mild COPD. Sixteen mild COPD participants and thirteen age-, gender- and height-matched controls completed DLCO maneuvers at rest and during exercise in the upright and supine position. The multiple FIO2-DLCO method was used to determine DLCO, VC, and membrane diffusion capacity (DM). All three variables were adjusted for alveolar volume (DLCOAdj, VCAdj, and DMAdj). The supine position reduced alveolar volume similarly in both groups, but oxygen consumption and cardiac output were unaffected. DLCOAdj, DMAdj, and VCAdj were all lower in COPD. These same variables all increased with upright and supine exercise in both groups. DLCOAdj was unaffected by the supine position. VCAdj increased in the supine position similarly in both groups. DMAdj was reduced in the supine position in both groups. While the supine position increased exercise VCAdj in COPD, the increase was of similar magnitude to healthy controls; therefore, exercise VC remained blunted in COPD. The persistent reduction in exercise DLCO and VC when supine suggests that pulmonary vascular destruction is a contributing factor to the blunted DLCO and VC response to exercise in mild COPD.