Frenchdrejer6818

This perspectives paper discusses patient-centered care for people living with motor neuron disease. We identify challenges and offer solutions from the patient-centered care literature for this population in frontline care, service delivery, research and health system organization. Examples from Australian and international motor neuron disease care are used to illustrate interrelated issues for practice and policy.We examined the influence of graded cold-water immersion (CWI) on global and regional quadriceps muscle perfusion using positron emission tomography (PET) and [15O]H2O. In thirty healthy males (33±8 yrs; 81±10 kg; 184±5 cm; percentage body fat 13±5%; V̇O2peak 47±8 mL·kg-1·min-1) quadriceps perfusion, thigh and calf cutaneous vascular conductance (CVC), intestinal, muscle and local skin temperatures, thermal comfort, mean arterial pressure and heart rate were assessed prior to and following 10-min of CWI at 8°C, 15°C or 22°C. Global quadriceps perfusion did not change beyond a clinically relevant threshold (0.75 mL∙100g∙min-1) in any condition, and was similar between conditions [range of the differences (95% confidence interval [CI]); 0.1 mL∙100g∙min-1 (-0.9 to 1.2 mL∙100g∙min-1) to 0.9 mL∙100g∙min-1 (-0.2 to 1.9 mL∙100g∙min-1)]. Muscle perfusion was greater in vastus intermedius (VI) compared with vastus lateralis (VL) (2.2 mL∙100g∙min-1; 95%CI 1.5 to 3.0 mL∙100g∙min-1) and rectus femoris (RF) (2.2 mL∙100g∙min-1; 1.4 to 2.9 mL∙100g∙min-1). A clinically relevant increase in VI muscle perfusion after immersion at 8°C and a decrease in RF muscle perfusion at 15°C were observed. A clinically relevant increase in perfusion was observed in the VI in 8°C compared with 22°C water (2.3 mL∙100g∙min-1; 1.1 to 3.5 mL∙100g∙min-1). There were no clinically relevant between-condition differences in thigh CVC. Our findings suggest that CWI (8-22°C) does not reduce global quadriceps muscle perfusion to a clinically relevant extent, however, colder-water (8°C) increases deep muscle perfusion and reduces (15°C) superficial muscle (RF) perfusion in the quadriceps muscle.This study aimed to examine the carotid baroreflex (CBR) control of the central and peripheral hemodynamics after exercise using the neck pressure (NP) and neck suction (NS) technique. Sixteen healthy young male participants (age 27 ± 6 years) were in a supine position for 30 min pre-exercise, followed by 60 min of cycling exercise, and then returned to a supine position for an additional 60 min post-exercise. Both pre- and post-exercise, the CBR-mediated responses of the central and peripheral hemodynamics were evaluated using 5 s periods of NP and NS (-60, -40, or +40 mmHg). As the central hemodynamics measurements, heart rate (HR), mean arterial pressure (MAP), cardiac output, and total vascular conductance were assessed. To determine peripheral circulation, vascular conductance in active and inactive limbs was measured. Eight participants (responder (RE) group) showed substantial post-exercise hypotension (PEH) during recovery from exercise (Δ MAP ~ -5 ± 0.9 mmHg, p less then 0.05). The other eight participants did not display a reduction in MAP after exercise (non-RE group). In the non-RE group, the responsiveness of CBR-mediated changes in HR, MAP, and vascular conductance increased, particularly in response to -40 mmHg NS during post-exercise compared with pre-exercise. However, in the RE group, any alterations in responsiveness to NP and NS were unchanged during PEH compared with pre-exercise. In conclusion, some normotensive individuals do not show PEH because the responsiveness of the CBR in central and peripheral hemodynamics following exercise is augmented, particularly to high blood pressure.We investigated the effects of testosterone replacement therapy (TRT) with and without evoked resistance training (RT) on protein expression of key metabolic and hypertrophy regulators, muscle fiber cross sectional area (CSA) and markers of mitochondrial health after spinal cord injury (SCI). Twenty-two men with chronic motor complete SCI were randomly assigned to either TRT+RT (n = 11) or TRT (n = 11) for 16 weeks. TRT+RT men underwent twice weekly progressive RT using electrical stimulation with ankle weights. TRT was administered via testosterone patches (2-6 mg/day). learn more Muscle biopsies were obtained before and after 16 weeks from the right vastus lateralis. Expression of proteins associated with oxidative muscles and mechanical loading (PGC1α and FAK), muscle hypertrophy (total and phosphorylated AKT, total and phosphorylated mTOR), and cellular metabolism (total and phosphorylated AMPK and GLUT4) were evaluated. Immunohistochemistry analysis was performed to measure fiber CSA, and succinate dehydrogenase (SDH) activity as well as mitochondrial citrate synthase (CS) activity and complex III (CIII)activities. TRT+RT demonstrated a robust 27.5% increase in average fiber CSA compared to -9% decreased following TRT only (P=0.01). GLUT4 protein expression was elevated in the TRT+RT group compared to the TRT only (P=0.005). Total Akt (P=0.06) and phosphorylated AktSer389 (P=0.049) were also elevated in the TRT+RT group. Mitochondrial activity of SDH (P =0.03) and CS (P=0.006) increased in TRT+RT group with no changes in TRT only group. Sixteen weeks of TRT with RT resulted in fiber hypertrophy and beneficial changes in markers of skeletal muscle health and function.The therapeutic effects of heat have been harnessed for centuries to treat skeletal muscle disorders and other pathologies. However, the fundamental mechanisms underlying the well-documented clinical benefits associated with heat therapy (HT) remain poorly defined. Foundational studies in cultured skeletal muscle and endothelial cells as well as in rodents revealed that episodic exposure to heat stress activates a number of intracellular signaling networks and promotes skeletal muscle remodeling. Renewed interest in the physiology of HT in recent years has provided greater understanding of the signals and molecular players involved in the skeletal muscle adaptations to episodic exposures to HT. It is increasingly clear that heat stress promotes signaling mechanisms involved in angiogenesis, muscle hypertrophy, mitochondrial biogenesis and glucose metabolism through not only elevations in tissue temperature but also other perturbations including increased intramyocellular calcium and enhanced energy turnover. The few available translational studies seem to indicate that the earlier observations in rodents also apply to human skeletal muscle.