Rate-responsive pacing with a pacemaker that detects respiratory rate (Biorate): clinical advantages and complications

The respiratory-dependent pacemaker (RDP3 or MB-1, Biorate, Biotec International, S.p.A., Bologna, Italy) detects the respiratory rate by measuring thoracic impedance using a subcutaneous auxiliary lead. The sensed respiratory rate is used to determine the pacing rate response. This pacemaker had been implanted in 9 patients with a mean age of 58 (range 42-69) years. During symptom-limited treadmill exercise, rate-modulated pacing resulted in a significant increase in pacing rate (mean +/- SD, 124 +/- 10 vs. 71 +/- 3 beats/min p less than 0.001) and exercise capacity (343 +/- 147 vs. 463 +/- 120 s, p less than 0.05) compared to those achieved with constant rate ventricular pacing. Brief treadmill exercise tests showed appropriate rate response to increased walking speed and gradient. However, rate response was modified by arm swinging-induced motion artefact which affected the measured "impedance." Complications observed on follow-up included perforation of the auxiliary lead in 2 patients and symptomatic myopotential interference in 3 patients with the RDP3 pacemaker, all of whom required unit replacement. It is concluded that although the respiratory-dependent pacemaker can confer physiological benefit in patients with bradycardia, myopotential interference (largely overcome by the new version MB-1 with programmable sensitivity) and the auxiliary lead can be problematic in some patients.     

Determination of left ventricular wall thickness and muscle mass by intravenous digital subtractionangiocardiography: validation of the method

Left ventricular (LV) wall thickness and muscle mass are importantmeasures of LV hypertrophy. In 24 patients LV end-diastolicwall thickness and muscle mass were determined (two observers)by digital subtraction angiocardiography (DSA) and conventionalLV angiocardiography (LVA). Wall thickness was determined overthe anterolateral wall of the left ventricle according to thetechnique of Rackley (method 1) or by planimetry (method 2).Seventeen patients were studied at rest and seven during dynamicexercise. Wall thickness correlated well between LVA and DSA;the best correlations were obtained by a combined subtractionmode using either method 1 or 2 (method 1, r0–80; method2,r0. 75). The standard error of estimate of the mean (SEE) wasslightly lower for method 2 ( 10%) than for method 1 ( 13%).DSA significantly overestimated wall thickness by 5–7%with method 1 and underestimated by 12–14% with method2. Muscle mass correlated well between LVA and DSA; the SEEwas 15% for method 1 and 12% for method 2. Overestimation ofmuscle mass by DSA was 7–11% with method 1 and underestimationwas 13–15% with method 2.It is concluded that LV wallthickness can be determined accurately by DSA with an SEE rangingbetween 10 and 13%. Determination of LV muscle mass is slightlyless accurate and the SEE is slightly larger ranging between13 to 17%. With method 1, wall thickness and muscle mass wereover estimated and with method 2 underestimated.     

过量运动对健康大鼠肾脏结构与功能的影响

目的：观察过量运动对健康大鼠肾脏结构与功能的影响并探讨其可能机制。方法：将30只健康Sprauge-Dawley(SD)大鼠按照随机数字表随机分为安静对照组和过量运动组,每组15只。安静对照组在鼠笼内安静饲养,过量运动组进行16周高强度跑台力竭运动。实验后,测定24 h尿蛋白（UP）、血尿素氮（BUN）和血清肌酐（SCr）含量评价肾功能;分别行HE、Masson染色观察肾脏组织病理学改变,同时获取肾小球和肾小管损伤评分以及纤维化指数（FI）;免疫印迹测定转化生长因子-β1(TGF-β1)、基质金属蛋白酶-9(MMP-9)、α-平滑肌肌动蛋白（α-SMA）和E-钙黏蛋白（E-CA）蛋白表达量。结果：与安静对照组比较,过量运动组肾脏结构异常,肾小球损伤评分、肾小管损伤评分、FI、UP、BUN和SCr增加（t分别为-6.895、-7.365、-9.234、-4.964、-7.753、-16.444,均P<0.05）,MMP-9蛋白表达下调（t=5.077,P<0.05）,而TGF-β1、α-SMA和E-CA蛋白表达差异无统计学意义（t分别为-1.801、-1.129、1.585,...     

综合矫正训练方案联合中药熏蒸治疗上交叉综合征疗效观察

<正>上交叉综合征(upper crossed syndrome,UCS)是指因上半身长期处于不良姿势,造成相关肌群功能失衡,进而引起颈肩背部疼痛不适、胸闷、睡眠障碍等一系列不良症状的一种亚健康状态^[1]。UCS常见的体态是圆肩、驼背、头前倾^[2]。目前临床上主要通过纠正局部的肌肉失衡来治疗UCS,常用的方法有运动疗法、肌肉能量技术、针灸和推拿等^[3]。     

Cardiovascular responses in paraplegic subjects during arm exercise

Summary The purpose of this study was to examine cardiovascular responses during arm exercise in paraplegics compared to a well-matched control group. A group of 11 male paraplegics (P) with complete spinal cord-lesions between T6 and T12 and 11 male control subjects (C), matched for physical activity, sport participation and age performed maximal arm-cranking exercise and submaximal exercise at 20%, 40% and 6070 of the maximal load for each individual. Cardiac output (Q _c) was determined by the CO₂ rebreathing method. Maximal oxygen uptake was significantly lower and maximal heart rate (f _c) was sigificantly higher in P compared to C. At the same oxygen uptakes no significant differences were observed inQ _c between P and C; however, stroke volume (SV) was significantly lower andf _c significantly higher in P than in C. The lower SV in P could be explained by an impaired redistribution of blood and, therefore, a reduced ventricular filling pressure, due to pooling of venous blood caused by inactivity of the skeletal muscle pump in the legs and lack of sympathetic vasoconstriction below the lesion. In conclusion, in P maximal performance appears to have been limited by a smaller active muscle mass and a lower SV despite the higher _c,max. During submaximal exercise, however, this lower SV was compensated for by a higherf _c and, thus at the same submaximal oxygen uptake,Q _c was similar to that in the control group.     

Role of nitric oxide in skeletal muscle: synthesis,distribution and functional importance

Over the last two decades, nitric oxide (NO) has been established as a novel mediator of biological processes, ranging from vascular control to long-term memory, from tissue inflammation to penile erection. This paper reviews recent research which shows that NO and its derivatives also are synthesized within skeletal muscle and that NO derivatives influence various aspects of muscle function. Individual muscle fibres express one or both of the constitutive NO synthase (NOS) isoforms. Type I (neuronal) NOS is localized to the sarcolemma of fast fibres; type III (endothelial) NOS is associated with mitochondria. Isolated skeletal muscle produces NO at low rates under resting conditions and at higher rates during repetitive contraction. NO appears to mediate cell–cell interactions in muscle, including vasodilation and inhibition of leucocyte adhesion. NO also acts directly on muscle fibres to alter cell function. Muscle metabolism appears to be NO-sensitive at several sites, including glucose uptake, glycolysis, mitochondrial oxygen consumption and creatine kinase activity. NO also modulates muscle contraction, inhibiting force output by altering excitation–contraction coupling. The mechanisms of NO action are likely to include direct effects on redox-sensitive regulatory proteins, interaction with endogenous reactive oxygen species, and activation of second messengers such as cyclic guanosine monophosphate (cGMP). In conclusion, research published over the past few years makes it clear that skeletal muscle produces NO and that endogenous NO modulates muscle function. Much remains to be learned, however, about the physiological importance of NO actions and about their underlying mechanisms.     

Low plasma glutamine in combination with high glutamate levels indicate risk for loss of body cell mass in healthy individuals: the effect of N-acetyl-cysteine

Skeletal muscle catabolism, low plasma glutamine, and high venous glutamate levels are common among patients with cancer or human immunodeficiency virus infection. In addition, a high glycolytic activity is commonly found in muscle tissue of cachectic cancer patients, suggesting insufficient mitochondrial energy metabolism. We therefore investigated (a) whether an anaerobic physical exercise program causes similar changes in plasma amino acid levels, and (b) whether low plasma glutamine or high glutamate levels are risk factors for loss of body cell mass (BCM) in healthy human subjects, i.e., in the absence of a tumor or virus infection. Longitudinal measurements from healthy subjects over longer periods suggest that the age-related loss of BCM occur mainly during episodes with high venous glutamate levels, indicative of decreased muscular transport activity for glutamate. A significant increase in venous glutamate levels from 25 to about 40 M was seen after a program of anaerobic physical exercise. This was associated with changes in T lymphocyte numbers. Under these conditions persons with low baseline levels of plasma glutamine, arginine, and cystine levels also showed a loss of BCM. This loss of BCM was correlated not only with the amino acid levels at baseline examination, but also with an increase in plasma glutamine, arginine, and cystine levels during the observation period, suggesting that a loss of BCM in healthy individuals terminates itself by adjusting these amino acids to higher levels that stabilize BCM. To test a possible regulatory role of cysteine in this context we determined the effect of N-acetyl-cysteine on BCM in a group of subjects with relatively low glutamine levels. The placebo group of this study showed a loss of BCM and an increase in body fat, suggesting that body protein had been converted into other forms of chemical energy. The decrease in mean BCM/body fat ratios was prevented by N-acetyl-cysteine, indicating that cysteine indeed plays a regulatory role in the physiological control of BCM.Abbreviations BCM Body cell mass - HIV Human immunodeficiency virus type 1 - NAC N-Acetyl-cysteine     

Effect of different types of high carbohydrate diets on glycogen metabolism in liver and skeletal muscle of endurance-trained rats

Male Wistar rats were fed ad libitum four different diets containing fructose, sucrose, maltodextrins or starch as the source of carbohydrate (CH). One group was subjected to moderate physical training on a motor-driven treadmill for 10 weeks (trained rats). A second group received no training and acted as a control (sedentary rats). Glycogen metabolism was studied in the liver and skeletal muscle of these animals. In the sedentary rats, liver glycogen concentrations increased by 60%–90% with the administration of simple CH diets compared with complex CH diets, whereas skeletal muscle glycogen stores were not significantly affected by the diet. Physical training induced a marked decrease in the glycogen content in liver (20%–30% of the sedentary rats) and skeletal muscle (50%–80% of the sedentary rats) in animals fed simple (but not complex) CH diets. In liver this was accompanied by a two-fold increase of triacylglycerol concentrations. Compared with simple CH diets, complex CH feeding increased by 50%–150% glycogen synthase (GS) activity in liver, whereas only a slight increase in GS activity was observed in skeletal muscle. In all the animal groups, a direct relationship existed between tissue glucose 6-phosphate concentration and glycogen content (r = 0.9911 in liver, r = 0.7177 in skeletal muscle). In contrast, no relationship was evident between glycogen concentrations and either glycogen phosphorylase activity or adenosine 5-monophosphate tissue concentration. The results from this study thus suggest that for trained rats diets containing complex CH (compared with diets containing simple CH) improve the glycogenic capacity of liver and skeletal muscle, thus enabling the adequate regeneration of glycogen stores in these two tissues.     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Summary Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O₂ consumption (% O_2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol ·1^–1 (Th_an =83.6% O_2max, SD 8.9). Time-dependent changes in blood lactate concentration ([la_b]) during exercise occurred in two phases: the oxygen uptake ( O₂) transient phase (from 0 to 4 min) and the O₂ steady-state phase (4–30 min). During the transient phase, [la_b] increased markedly (l.30 mmol · l ^–1 · min ^–1, SD 0.13). During the steady-state phase, [la_b] increased slightly (0.02 mmol · 1^–1 · min^–1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [la_b] in half of the subjects. Following hyperlacticaemia (8.8 mmol -l^–1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% O_2max), [la_b] decreased during the O₂ transient (–0.118 mmol · 1^–1 · min^–1, SD 0.209) and steady-state (–0.088 mmol · 1^–1 · min ^–1, SD 0.103) phases of 30 min exercise (91.4% O_2max, SD 4.8). In conclusion, it was not possible from the Th_an to determine the maximal [la_b] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the O₂ transient phase of exercise performed at an intensity above the Th_an. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [la_b] during the O₂ steady state was also affected.     

Potentiation and restitution of heart muscle contraction in rats adapted to exercise

The original amplitude of contraction of strips of myocardium determined the inotropic response to paired stimulation. The higher the initial amplitude, the lower the degree of potentiation and the higher the degree of restitution of contraction. For equal amplitude, the degree of potentiation of myocardial contraction of exercise-adapted rats was greater and the degree of restitution smaller than in the control. These changes probably reflect changes in the ion transport system of the myocardial cells.Presented by Academician of the Academy of Medical Sciences of the USSR A. M. Chernukh.Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 7, pp. 780–782, July, 1976.