Time course for strength and muscle thickness changes following upper and lower body resistance training in men and women

 The purpose of this study was to investigate the time course of skeletal muscle adaptations resulting from high-intensity, upper and lower body dynamic resistance training (WT). A group of 17 men and 20 women were recruited for WT, and 6 men and 7 women served as a control group. The WT group performed six dynamic resistance exercises to fatigue using 8–12 repetition maximum (RM). The subjects trained 3 days a week for 12 weeks. One-RM knee extension (KE) and chest press (CP) exercises were measured at baseline and at weeks 2, 4, 6, 8, and 12 for the WT group. Muscle thickness (MTH) was measured by ultrasound at eight anatomical sites. One-RM CP and KE strength had increased significantly at week 4 for the female WT group. For the men in the WT group, 1 RM had increased significantly at week 2 for KE and at week 6 for CP. The mean relative increases in KE and CP strength were 19% and 19% for the men and 19% and 27% for the women, respectively, after 12 weeks of WT. Resistance training elicited a significant increase in MTH of the chest and triceps muscles at week 6 in both sexes. There were non-significant trends for increases in quadriceps MTH for the WT groups. The relative increases in upper and lower body MTH were 12%–21% and 7%–9% in the men and 10%–31% and 7%–8% in the women respectively, after 12 weeks of WT. These results would suggest that increases in MTH in the upper body are greater and occur earlier compared to the lower extremity, during the first 12 weeks of a total body WT programme. The time-course and proportions of the increase in strength and MTH were similar for both the men and the women. Accepted: 6 September 1999     

Short-term and long-term stimulation of Na+−H+ exchange in cortical brush-border membranes during compensatory growth of the rat kidney

The effect of unilateral nephrectomy on Na⁺–H⁺ exchange in rat renal cortical brush-border membrane vesicles (BBMV) was studied by the method of acridine orange fluorescence quenching. The exchanger activity in BBMV from remnant kidney increased rapidly by 70–75% within first 30 min following uninephrectomy. Only a slight further increase was found in later stages of renal growth, i.e. 30 min to 7 days following uninephrectomy. The changes in antiporter activity were restricted toV _max, whereas theK _m for Na⁺ was similar in control and compensatory growing kidney. The increase of Na⁺–H⁺ exchange at 15 min was not affected by actinomycin D in vivo, whereas the increase at 48 h was completely abolished indicating that protein synthesis could be involved in the late, but not in the initial stimulation of renal Na⁺–H⁺ exchange. The late, but not the initial stimulations of Na⁺–H⁺ exchange were associated with elevated activities of cortical (Na⁺+K⁺)-ATPase indicating that changes in antiporter activity precede those in the (Na⁺+K⁺)-pump. The early stimulation of Na⁺–H⁺ exchange in BBMV in one kidney was induced also by the occlusion of blood flow through the contralateral kidney for 15 min, without removing it. Thirty min after the occlusion was removed and the reflow established, the Na⁺–H⁺ exchange in BBMV from the intact kidney decreased to the control values. The observed modulations in renal Na⁺–H⁺ exchanger may be regulated by phosphorylation-dephosphorylation events. In support, the concentration of a well known protein kinase C activator, 1,2-diacylglycerol, in the cortical tissue of the remnant kidney increased up to 100% within 5 min following unilateral nephrectomy and preceded the increase in Na⁺–H⁺ exchange. The early stimulation of Na⁺–H⁺ exchange may be a trigger in initiating the kidney growth.     

溶酶体在实验性心肌肥大过程中的作用

本实验用大鼠主动脉结扎的心肌肥大模型,结合电镜酶细胞化学技术,观察心肌肥大发展过程中溶酶体的变化。结果表明:心肌肥大发展时,溶酶体参与心肌细胞改建;到心肌肥大后期,出现大量自噬现象,造成心肌不可逆损伤。     

Growth resistance-sized arteries in response to bladder hypertrophy in the rat: time-course,DNA-synthesis and LDH-isoform pattern

Bladder growth was induced by partial urethral obstruction. Bladder hypertrophy was evident at 53 h after obstruction and continued over a 6 weeks period. Small bladder arteries were taken from fixed anatomical locations of the bladder circulation, mounted in a small vessel myograph and the optimal diameter for maximal isometric force development was determined (L_max, K⁺=125 mm stimulation). Bladder hypertrophy was associated with an enlarged L_max from 53 h onward (compared with sham-operated controls) and L_max continued to increase until 10 days after urethral obstruction. Between 10 days and 6 weeks no further increase of the diameter was observed. Increased diameters in vitro were accompanied by a transiently increased [³H]Thymidine uptake in the small arteries which peaked at 53 h after obstruction but was still above background at 10 days. At this time point, small arterial growth was associated with a significant relative increase in the M isoform of LDH as determined with agarose electrophoresis on tissue homogenates. Thus organ growth induced small vessel growth in the rat is characterized by a rapid onset, increased but transient DNA-turnover and LDH-isoform changes. The latter mimic changes seen in other types of smooth muscle growth.     

Energy turnover and lactate dehydrogenase activity in detrusor smooth muscle from rats with streptozotocin-induced diabetes

Force generation and tissue glucose metabolism were measured in the urinary bladder smooth muscle from rats with streptozotocin-induced diabetes (7–8 wk duration). Bladder wet wt was almost 4–fold higher in the diabetic animals compared with the untreated controls. Morphological analysis showed that the growth was associated with hypertrophy of the smooth muscle component in the bladder wall. Force generation of isolated bladder strip preparations was measured in vitro at different ambient oxygen tensions. Activation of intramural nerves, with electrical field stimulation, induced contractions that were unaffected by reduction of oxygen tension down to Po₂ 100 mmHg for both control and diabetic muscle strips. At zero Po₂ force was reduced by approximately 10–20% in both groups. High-K⁺ solution induced ‘tonic’ contractions that were slightly more inhibited by lowering Po₂. At intermediate Po₂ (between 100 and 20 mmHg) the diabetic muscle gave slightly higher force. At zero Po₂ no significant difference could be detected between strips from control and diabetic animals. Oxygen consumption and lactate production in the preparations were determined at a Po₂ of 290 mmHg and related to the volume of smooth muscle. At zero Po₂ lactate formation increased 3- to 4-fold. The metabolic tension cost was lower at zero Po₂ No differences in basal and contraction related metabolic rates could be detected between the two groups under normoxic and anoxic conditions. The maximal activity of lactate dehydrogenase (LDH) determined in tissue sampIes was about 2-fold higher in the diabetic bladder muscle. This increased enzymatic activity could thus not be correlated with any altered metabolic properties of the smooth muscle in the urinary bladder from diabetic rats.     

Histological appearances of the long saphenous vein

The long saphenous vein is frequently used as a graft in both coronary artery and femoro-distal bypass surgery. The histological changes which are seen after implantation into the arterial system have been well documented in the past, but little attention has been focused on the histological appearances of the donor long saphenous vein prior to grafting. In this study, samples of the long saphenous vein in excess of that required for bypass have been examined. In none of the veins did the histological appearances conform to the described normal. All showed evidence of intimal fibrosis which contained elastic tissue and enmeshed smooth muscle cells. The longitudinal and circular muscle layers showed evidence of muscle cell hypertrophy with increase in intervening connective tissue. Elsewhere, similar histological changes have been attributed to 'arterialization'. This study shows that many of the changes are present prior to grafting and may be important in graft failure.     

Hypothalamic laterality in regulating gonadotropic function: unilateral hypothalamic lesion and ovarian compensatory hypertrophy

Regardless of the side of hemiovariectomy, unilateral lesion placed in the right-side medial anterior hypothalamus suppressed ovarian compensatory hypertrophy, but the lesion made in the left side failed to suppress it. This suggests the presence of a hypothalamic laterality in regulating gonadotropin secretion.     

不同年龄高血压大鼠心肌中MKP-1的表达及对心肌肥厚的影响

目的：研究不同年龄的自发性高血压大鼠（SHR）和Wistar Kyoto大鼠（WKY）心室肌组织中丝裂原活化蛋白激酶（MAPK）及其磷酸酶（MKP-1）的表达以及与心肌肥厚的关系。方法： 用左心室重量与体重的比值作为心肌肥大指数并以此指标反映心肌肥厚；分别用Western blotting方法和RT-PCR法半定量测定心室肌组织中磷酸化细胞外信号调节激酶（p-ERK）的蛋白表达和MKP-1 mRNA的含量。结果： （1）SHR的血压自8周龄起明显高于WKY（P<0.01），心肌肥大指数明显大于WKY（P<0.05），ERK和MKP-1的表达均比WKY高（P<0.05）；（2）SHR的血压随年龄增长而升高（P<0.05），至14周趋于稳定，心肌肥大指数则在24周时出现激增（P<0.01）；（3）p-ERK随年龄增长呈递增趋势，而MKP-1呈递减趋势，且与心肌肥大指数和ERK的表达呈负相关（P<0.01）。结论： MKP-1在高血压大鼠随年龄和血压增加的心肌肥厚过程中起重要作用，其表达逐渐下降可能是导致ERK激活增加，进而引起心肌细胞肥大的重要原因。     

Positive correlation between aortic valve pressure gradient and mitochondrial respiratory chain capacity in hypertrophied human left ventricle

Summary The effect of chronic left ventricular pressure overload on the activities of mitochondrial respiratory chain enzymes was investigated in myocardial biopsies from the left ventricular apex of 13 patients undergoing aortic valve replacement for aortic valve stenosis. Transvalvular pressure gradients measured by left-sided heart catheterization ranged from 52 to 100 mmHg. The specific activity of mitochondrial respiratory chain enzyme complexes I + III (antimycin A sensitive NADH cytochrome c oxidoreductase) and the myocardial concentrations of coenzyme Q₁₀ (CoQ₁₀) increased significantly (P < 0.05) with increasing aortic valve pressure gradient. In contrast, the specific activities of complex IV (cytochrome c oxidase), succinate dehydrogenase, and citrate synthase, a mitochondrial matrix enzyme, showed no significant correlation with the pressure gradient. Since (CoQ₁₀) is the rate-limiting compound of the activity of complexes 1+111 but not of cytochrome c oxidase, succinate dehydrogenase, or citrate synthase, these data suggest that the increase in the activity of complexes I+III is due to the increase in (CoQ₁₀) content.Abbreviations CoQ coenzyme Q - CoQ₉ coenzyme Q₉ - CoQ₁₀ coenzyme Q₁₀ - SDH succinate dehydrogenase - NCP noncollagen protein