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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise intolerance is a problem in renal failure. Stationary cycle training during hemodialysis treatment is recommended as safe, effective, and practical, but requires compensations for both exercise and acute changes in uremia. Eight patients pedalled for 5 minutes, at 60% of VO2peak, at 0, 1, 2, and 3 hours of a hemodialysis treatment. Fluid removed, blood pressure, cardiac output, heart rate, O2 uptake, hematocrit, and arterial O2 content were measured. Mean arterial blood pressure, systemic vascular resistance, stroke volume, (a-v)O2 difference, and mixed-venous O2 content were calculated. Fluid removed was 1,356 mL/hr (P < 0.002 for each hour), but with no significant cardiovascular effects during the first 2 hours. At 3 hours, decreasing cardiac output, stroke volume, and mean arterial pressure all reached significance at rest (P < 0.05), and five of eight patients could not exercise. We conclude that the cardiovascular exercise response is superimposed on hemodynamic effects of dialysis and is adequately stable during the first 2 hours of treatment. After 2 hours, cardiovascular decompensation may preclude exercise.
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PMID:Cardiovascular response to submaximal stationary cycling during hemodialysis. 953 Nov 79

Exercise intolerance in persons with paraplegia (PARAS) is thought to be secondary to insufficient venous return and a subnormal cardiac output at a given oxygen uptake. However, these issues have not been resolved fully. This study utilized lower-body positive pressure (LBPP) as an intervention during arm crank exercise in PARAS in order to examine this issue. Endurance-trained (TP, n = 7) and untrained PARAS (UP, n = 10) with complete lesions between T6 and T12, and a control group consisting of sedentary able-bodied subjects (SAB, n = 10) were tested. UP and TP subjects demonstrated a diminished cardiac output (via CO2 rebreathing) during exercise compared to SAB subjects. Peak oxygen uptake (O2peak) remained unchanged for all groups following LBPP. LBPP resulted in a significant decrease in heart rate (HR) in UP and TP (P < 0.05), but not SAB subjects. LBPP produced an insignificant increase in cardiac output (Q) and stroke volume (SV). The significant decrease in HR in both PARA groups may indicate a modest hemodynamic benefit of LBPP at higher work rates where circulatory sufficiency may be most compromised. We conclude that PARAS possess a diminished cardiac output during exercise compared to the able-bodied, and LBPP fails to ameliorate significantly their exercise response irrespective of the conditioning level. These results support previous observations of a lower cardiac output during exercise in PARAS, but indicate that lower-limb blood pooling may not be a primary limitation to arm exercise in paraplegia.
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PMID:The effect of lower body positive pressure on the cardiovascular response to exercise in sedentary and endurance-trained persons with paraplegia. 969 13

Exercise intolerance and heart failure with preserved ejection fraction are common in females. Recently, arterial stiffness has been suggested to be a significant contributor in the development of heart failure. How gender difference affects arterial stiffening and its response to exercise is not well known. We hypothesized that arterial elastance index during exercise would be more abnormal in females with hypertension than males. Arterial elastance index was estimated as arterial end systolic pressure/stroke volume controlled for body surface area and was measured at rest and during graded supine bicycle exercise (25 watts, 3-minute increments) in 298 patients with hypertension (149 males; 149 females; mean age, 59). The subjects were divided into 2 groups by gender. Exercise duration was significantly shorter in females compared to males (692+/-222 versus 483+/-128 seconds, P<0.001). Although arterial elastance index at baseline was significantly higher in males, the magnitude of increase was steeper in females with the magnitude of change at 75 W of exercise being significantly higher in females compared to males (0.69+/-0.83 versus 0.43+/-0.69, P=0.018). Arterial elastance index at each stage of exercise up to 75 W was independently associated with decreased exercise duration. In conclusion, despite lower arterial elastance index at rest, the increase during exercise was steeper in women with hypertension, suggesting a gender-related difference in dynamic arterial stiffness. The arterial elastance index during exercise was significantly associated with exercise duration in patients with hypertension.
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PMID:Gender-related difference in arterial elastance during exercise in patients with hypertension. 1825 19

We report a 35-year-old woman presenting a stroke-like episode with transitory aphasia followed by generalized tonic-clonic seizures. She had severe hearing loss and suffered from frequent episodes of migraine. Although a brain MRI disclosed a T2-hyperintense lesion in the left parietal lobe, she had hardly any long-term sequela. Exercise intolerance, myalgias and limb-girdle muscle weakness indicated a slowly progressive myopathy. Extra-neurological features included short stature, and secondary amenorrhea with low gonadotropin levels, indicating secondary hypogonadism. However, she had three mutation-free, healthy children by ovarian stimulation. A muscle biopsy showed ragged-red, cytochrome c oxidase-negative fibers, and an isolated defect of cytochrome c oxidase activity in muscle mitochondria. Sequence analysis of muscle mtDNA revealed a previously unreported heteroplasmic m.6597C>A transversion in the MTCOI gene, encoding subunit I of cytochrome c oxidase, corresponding to p.Q232K aminoacid change. Analysis on transmitochondrial cybrids demonstrated that the mutation is indeed associated with COX deficiency, i.e. pathogenic.
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PMID:MELAS-like encephalomyopathy caused by a new pathogenic mutation in the mitochondrial DNA encoded cytochrome c oxidase subunit I. 2283 41