Effect of the ovarian hormones on GLUT4 expression and contraction-stimulated glucose uptake

This study examined the roles of the female sex steroids, 17beta-estradiol (E(2)) and progesterone (Prog), on glucose uptake and GLUT4 protein expression. Female Sprague-Dawley rats were either sham operated (C) or ovariectomized and treated with placebo (O), E(2) (E), Prog (P), or both hormones at physiological doses (P + E) or the same dose of Prog with a high dose of E(2) (P + HiE) via timed-release pellets inserted at the time of surgery, 15 days before metabolic testing. On the morning of day 15, animals received a 300-microCi injection (ip) of 2-deoxy-[(14)C]glucose and then either exercised on a motorized treadmill for 30 min at 0.35 m/s or remained sedentary in their cages for the same period. Basal glucose uptake was not different between the treatment groups in either the red or white quadriceps. However, glucose uptake was decreased (P < 0.05) in O, P, and P + E rats during exercise in the red quadriceps compared with C rats, whereas E and P + HiE treatment restored glucose uptake. Glycogen content in skeletal muscle followed similar trends, with no differences seen in resting animals. Postexercise red quadriceps glycogen levels were higher (P < 0.05) in the E and P + HiE rats compared with O and P. Treatment of ovariectomized rats with progesterone (P rats) decreased (P < 0.05) GLUT4 content in the red quadriceps by 21% compared with C rats. These data demonstrate that estrogen-deficient animals have a decreased ability for contraction-stimulated glucose uptake and increased glycogen use during aerobic exercise. However, changes in contraction-stimulated glucose uptake could not be explained by altered transporter protein content, since the absence of E(2) had no effect on GLUT4 protein.     

Effects of estradiol and progesterone on body composition, protein synthesis, and lipoprotein lipase in rats

Prior studies suggest that estradiol and progesterone regulate body composition in growing female rats. Because these studies did not consider the confounding effect of changes in food intake, it remains unclear whether ovarian hormones regulate body composition independently of their effects on food intake. We utilized a pair-feeding paradigm to examine the effects of these hormones on body composition. In addition, skeletal muscle protein fractional synthesis rate and adipose tissue lipoprotein lipase activity were measured to examine pathways of substrate deposition into fat and fat-free tissue. Female Sprague-Dawley rats [pubertal: 7-8 wk old; 190 +/- 0.5 (SE) g] were separated into four groups: 1) sham-operated (S; n = 8), 2) ovariectomized plus placebo (OVX; n = 8), 3) ovariectomized plus estradiol (OVX+E; n = 8), and 4) ovariectomized plus progesterone (OVX+P; n = 8). All ovariectomized groups were pair-fed to the S group. Body composition was measured using total body electrical conductivity. The relative increase in fat-free mass was greater (P < 0.01) in the OVX group (31 +/- 2%) than in the S (17 +/- 2%), OVX+E (18 +/- 2%), and OVX+P (22 +/- 2%) groups. The fractional synthetic rates of gastrocnemius muscle protein paralleled changes in fat-free mass: OVX had a higher (P < 0.05) synthesis rate (21 +/- 3%/day) than S (12 +/- 2%/day), OVX+E (11 +/- 2%/day), and OVX+P (8 +/- 1%/day) groups. Body fat increased in the S group (31 +/- 7%; P < 0.01), whereas the OVX groups lost fat (OVX: -10 +/- 7%; OVX+E: -15 +/- 7%; OVX+P: -13 +/- 7%). No differences in lipoprotein lipase were found. Our results suggest that estradiol and progesterone may regulate the growth of fat and fat-free tissues in female rats. Moreover, ovarian hormones may influence skeletal muscle growth through their effects on skeletal muscle protein synthesis.     

Decreased serum leptin and muscle oxidative enzyme activity with a dietary loss of intra-abdominal fat in rats

The purpose of the present study was to investigate the relationship among intra-abdominal adipose storage, adaptation in the serum leptin concentration and skeletal muscle enzyme activity after a 4-week energy restriction (ER). Thirty-one male Wistar rats were divided into 40% energy restricted (n=24) or ad libitum-fed control (CL) rats (n=7). The energy-restricted rats were grouped into the most fat (MF, n=7), medium (n 10) and the least fat (LF, n=7) by their intra-abdominal fat pads mass (epididymal, mesenteric, and perirenal) after ER. A superficial portion of M. gastrocnemius tissue obtained before and after the diet period were analyzed to determine the activities of hexokinase (HK), beta-hydroxyacyl CoA dehydrogenase (beta-HAD) and citrate synthase (CS). Blood samples were also collected for a serum leptin assay. At the baseline, no difference was found in either the leptin concentration or the enzyme activities among LF, MF and CL. The serum leptin concentration was positively correlated with the muscle activities of beta-HAD and CS, while it negatively correlated with HK/beta-HAD. After ER, the activities of HK, beta-HAD and CS were all significantly lower in LF than in CL. Among the energy-restricted rats, the intra-abdominal fat pad weight, leptin concentration and the activities of beta-HAD, CS, beta-HAD/CS all significantly correlated with one another. The changes in leptin and the activity of beta-HAD were also positively correlated. These findings indicate that parallel decreases in the serum leptin and skeletal muscle enzyme activities with the energy restriction-induced intra-abdominal adipose reduction, thus may suggest the leptin to have a regulative effect on the muscle enzyme activity during ER.     

Estradiol-induced progesterone receptor synthesis in normal and diabetic ovariectomized rat uterus

Estrogen stimulation of progesterone-receptor (Prog R.) synthesis is an important parameter of the sex hormones activity at the uterine level. Experimental diabetes in the rat has been shown to perturb protein synthesis in some tissues and to reduce, under certain circumstances, estrogen and androgen activity on their respective target tissues. The present work tended to evaluate the effect of streptozotocin diabetes on estradiol (E2) stimulation of Prog. R and on Prog R. kinetics in the rat uterus. Two groups of diabetic rats were primed for three consecutive days with 5 microg. E2 s.c. (EP). One group received an acute i.p. injection of progesterone (P), 1 h before sacrifice (Inj), the other group did not (n Inj). Two other groups, not primed with E2 (nEP) were similarly injected or not with P. Four groups of non diabetic animals served as controls. Estrogen priming induced a 20-25% increase in DNA content, both in controls and in diabetics. Protein content was also increased to almost the same extent in diabetics and controls; protein concentration remained however slightly lower in cytosol of EP diabetics as compared to controls. Prog R. increased about 7-fold in cytosol and 4-5-fold in nuclei of EP control and diabetic groups. Cytosol to nuclei ratios of Prog R. decreased similarly in Inj. EP diabetics and controls, compared to the corresponding n Inj. groups. It is concluded that estrogen priming stimulated Prog R., total protein and DNA synthesis to the same extent in diabetic as in control rats Prog R. kinetics was unaltered in diabetics. This finding might be relevant to situations like early pregnancy, when Prog R. levels change rapidly and specifically in relation with the time and the site of implantation.     

Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress

Physical exercise exacerbates the cytotoxic effects of statins in skeletal muscle. Mitochondrial impairments may play an important role in the development of muscular symptoms following statin treatment. Our objective was to characterize mitochondrial function and reactive oxygen species (ROS) production in skeletal muscle after exhaustive exercise in atorvastatin-treated rats. The animals were divided into four groups: resting control (CONT; n = 8) and exercise rats (CONT+EXE; n = 8) as well as resting (ATO; n = 10) and exercise (ATO+EXE; n = 8) rats that were treated with atorvastatin (10 mg·kg(-1)·day(-1) for 2 wk). Exhaustive exercise showed that the distance that was covered by treated animals was reduced (P < 0.05). Using dihydroethidium staining, we showed that the ROS level was increased by 60% in the plantaris muscle of ATO compared with CONT rats and was highly increased in ATO+EXE (226%) compared with that in CONT+EXE rats. The maximal mitochondrial respiration (V(max)) was decreased in ATO rats compared with that in CONT rats (P < 0.01). In CONT+EXE rats, V(max) significantly increased compared with those in CONT rats (P < 0.05). V(max) was significantly lower in ATO+EXE rats (-39%) compared with that in CONT+EXE rats (P < 0.001). The distance that was covered by rats significantly correlated with V(max) (r = 0.62, P < 0.01). The glycogen content was decreased in ATO, CONT+EXE, and ATO+EXE rats compared with that in CONT rats (P < 0.05). GLUT-4 mRNA expression was higher after exhaustive exercise in CONT+EXE rats compared with the other groups (P < 0.05). Our results show that exhaustive exercise exacerbated metabolic perturbations and ROS production in skeletal muscle, which may reduce the exercise capacity and promote the muscular symptoms in sedentary atorvastatin-treated animals.     

Prolonged exercise to fatigue in humans impairs skeletal muscle Na+-K+-ATPase activity, sarcoplasmic reticulum Ca2+ release, and Ca2+ uptake.

Prolonged exhaustive submaximal exercise in humans induces marked metabolic changes, but little is known about effects on muscle Na+-K+-ATPase activity and sarcoplasmic reticulum Ca2+ regulation. We therefore investigated whether these processes were impaired during cycling exercise at 74.3 +/- 1.2% maximal O2 uptake (mean +/- SE) continued until fatigue in eight healthy subjects (maximal O2 uptake of 3.93 +/- 0.69 l/min). A vastus lateralis muscle biopsy was taken at rest, at 10 and 45 min of exercise, and at fatigue. Muscle was analyzed for in vitro Na+-K+-ATPase activity [maximal K+-stimulated 3-O-methylfluorescein phosphatase (3-O-MFPase) activity], Na+-K+-ATPase content ([3H]ouabain binding sites), sarcoplasmic reticulum Ca2+ release rate induced by 4 chloro-m-cresol, and Ca2+ uptake rate. Cycling time to fatigue was 72.18 +/- 6.46 min. Muscle 3-O-MFPase activity (nmol.min(-1).g protein(-1)) fell from rest by 6.6 +/- 2.1% at 10 min (P <0.05), by 10.7 +/- 2.3% at 45 min (P <0.01), and by 12.6 +/- 1.6% at fatigue (P <0.01), whereas 3[H]ouabain binding site content was unchanged. Ca2+ release (mmol.min(-1).g protein(-1)) declined from rest by 10.0 +/- 3.8% at 45 min (P <0.05) and by 17.9 +/- 4.1% at fatigue (P < 0.01), whereas Ca2+ uptake rate fell from rest by 23.8 +/- 12.2% at fatigue (P=0.05). However, the decline in muscle 3-O-MFPase activity, Ca2+ uptake, and Ca2+ release were variable and not significantly correlated with time to fatigue. Thus prolonged exhaustive exercise impaired each of the maximal in vitro Na+-K+-ATPase activity, Ca2+ release, and Ca2+ uptake rates. This suggests that acutely downregulated muscle Na+, K+, and Ca2+ transport processes may be important factors in fatigue during prolonged exercise in humans.     

The effects of training in hyperoxia vs. normoxia on skeletal muscle enzyme activities and exercise performance.

Inspiring a hyperoxic (H) gas permits subjects to exercise at higher power outputs while training, but there is controversy as to whether this improves skeletal muscle oxidative capacity, maximal O(2) consumption (Vo(2 max)), and endurance performance to a greater extent than training in normoxia (N). To determine whether the higher power output during H training leads to a greater increase in these parameters, nine recreationally active subjects were randomly assigned in a single-blind fashion to train in H (60% O(2)) or N for 6 wk (3 sessions/wk of 10 x 4 min at 90% Vo(2 max)). Training heart rate (HR) was maintained during the study by increasing power output. After at least 6 wk of detraining, a second 6-wk training protocol was completed with the other breathing condition. Vo(2 max) and cycle time to exhaustion at 90% of pretraining Vo(2 max) were tested in room air pre- and posttraining. Muscle biopsies were sampled pre- and posttraining for citrate synthase (CS), beta-hydroxyacyl-coenzyme A dehydrogenase (beta-HAD), and mitochondrial aspartate aminotransferase (m-AsAT) activity measurements. Training power outputs were 8% higher (17 W) in H vs. N. However, both conditions produced similar improvements in Vo(2 max) (11-12%); time to exhaustion (approximately 100%); and CS (H, 30%; N, 32%), beta-HAD (H, 23%; N, 21%), and m-AsAT (H, 21%; N, 26%) activities. We conclude that the additional training stimulus provided by training in H was not sufficient to produce greater increases in the aerobic capacity of skeletal muscle and whole body Vo(2 max) and exercise performance compared with training in N.     

Myofibril ATPase activity of cardiac and skeletal muscle of exhaustively exercised rats

The activation characteristics of Mg-ATP and Ca2+ on cardiac and skeletal muscle myofibril ATPase activity were studied in rats following a run to exhaustion. In addition, the effect of varying ionic strength was determined on skeletal muscle from exhausted animals. The exhausted group (E) ran at a speed of 25 m min-1 with an 8% incline. Myofibril ATPase activities for control (C) and E were determined with 1, 3 and 5 mM Mg-ATP and 1 and 10 microM Ca2+ at pH 7.0 and 30 degrees C. For control skeletal muscle, at 1 and 10 microM Ca2+, there was an increase in ATPase activity from 1 to 5 mM Mg-ATP (P less than 0.05). For E animals the myofibril ATPase activities at 10 microM Ca2+ and all Mg-ATP concentrations were similar to C (P greater than 0.05). At 1.0 microM Ca2+ and all Mg-ATP concentrations were similar to C (P greater than 0.05). At 1.0 microM Ca2+ the activities at 3 and 5 mM Mg-ATP were greater for the E animals (P less than 0.05). Increasing KCl concentrations resulted in greater inhibition for E animals. With cardiac muscle, the myofibril ATPase activities at 1.0 microM free Ca2+ were lower for E at all Mg-ATP levels (P less than 0.05). In contrast, at 10 microM Ca2+, the E group exhibited an elevated myofibril ATPase activity. The results indicate that Mg-ATP and Ca2+ activation of cardiac and skeletal muscle myofibril ATPase is altered with exhaustive exercise.     

Ischemia-induced structural change in SR Ca2+-ATPase is associated with reduced enzyme activity in rat muscle

In this study, we employed an in vivo model of prolonged ischemia in rat skeletal muscle to investigate the hypothesis that structural modifications to the sarcoplasmic reticulum (SR) Ca2+-ATPase can explain the alterations in Ca2+-ATPase activity that occur with ischemia. To induce total ischemia, a tourniquet was placed around the upper hindlimb in 27 female Sprague-Dawley rats weighing 256 +/- 6.7 g (mean +/- SE) and was inflated to 350 mmHg for 4 h. The contralateral limb served as control (C) to the ischemic limb (I), and the limbs of animals killed immediately after anesthetization served as a double control (CC). Mixed gastrocnemius and tibialis anterior muscles were sampled and used for SR vesicle preparation. Maximal Ca2+-ATPase activity (micromol x g protein(-1) x min(-1)) of C (15,802 +/- 1,246) and I (11,609 +/- 1,029) was 90 and 73% (P < 0.05) of CC (17,562 +/- 1,682), respectively. No differences were found between groups in either the Hill coefficient or the free Ca2+ at half-maximal activity. The fluorescent probes, FITC and N-cyclohexyl-N'-(dimethylamino-alpha-naphthyl) carbodiimide, used to assess structural alterations in the regions of the ATP binding site and the Ca2+ binding sites of the Ca2+-ATPase, respectively, indicated a 26% reduction (P < 0.05) in FITC binding capacity (absolute units) in I (0.22 +/- 0.01) compared with CC (0.29 +/- 0.02) and C (0.29 +/- 0.03). Our results suggest that the reduction in maximal SR Ca2+-ATPase activity in SR vesicles with ischemia is related to structural modification in the region of the nucleotide binding domain by mechanisms that are as yet unclear.     

Progesterone increases skeletal muscle mitochondrial H2O2 emission in nonmenopausal women

The luteal phase of the female menstrual cycle is associated with both 1) elevated serum progesterone (P4) and estradiol (E2), and 2) reduced insulin sensitivity. Recently, we demonstrated a link between skeletal muscle mitochondrial H(2)O(2) emission (mE(H2O2)) and insulin resistance. To determine whether serum levels of P4 and/or E(2) are related to mitochondrial function, mE(H2O2) and respiratory O(2) flux (Jo(2)) were measured in permeabilized myofibers from insulin-sensitive (IS, n = 24) and -resistant (IR, n = 8) nonmenopausal women (IR = HOMA-IR > 3.6). Succinate-supported mE(H2O2) was more than 50% greater in the IR vs. IS women (P < 0.05). Interestingly, serum P4 correlated positively with succinate-supported mE(H2O2) (r = 0. 53, P < 0.01). To determine whether P4 or E2 directly affect mitochondrial function, saponin-permeabilized vastus lateralis myofibers biopsied from five nonmenopausal women in the early follicular phase were incubated in P4 (60 nM), E2 (1.4 nM), or both. P4 alone inhibited state 3 Jo(2), supported by multisubstrate combination (P < 0.01). However, E2 alone or in combination with P4 had no effect on Jo(2). In contrast, during state 4 respiration, supported by succinate and glycerophosphate, mE(H2O2) was increased with P4 alone or in combination with E2 (P < 0.01). The results suggest that 1) P4 increases mE(H2O2) with or without E2; 2) P4 alone inhibits Jo(2) but not when E2 is present; and 3) P4 is related to the mE(H2O2) previously linked to skeletal muscle insulin resistance.     

Explosive-strength training improves 5-km running time by improving running economy and muscle power.

To investigate the effects of simultaneous explosive-strength and endurance training on physical performance characteristics, 10 experimental (E) and 8 control (C) endurance athletes trained for 9 wk. The total training volume was kept the same in both groups, but 32% of training in E and 3% in C was replaced by explosive-type strength training. A 5-km time trial (5K), running economy (RE), maximal 20-m speed (V20 m), and 5-jump (5J) tests were measured on a track. Maximal anaerobic (MART) and aerobic treadmill running tests were used to determine maximal velocity in the MART (VMART) and maximal oxygen uptake (VO2 max). The 5K time, RE, and VMART improved (P < 0.05) in E, but no changes were observed in C. V20 m and 5J increased in E (P < 0.01) and decreased in C (P < 0.05). VO2 max increased in C (P < 0.05), but no changes were observed in E. In the pooled data, the changes in the 5K velocity during 9 wk of training correlated (P < 0.05) with the changes in RE [O2 uptake (r = -0.54)] and VMART (r = 0.55). In conclusion, the present simultaneous explosive-strength and endurance training improved the 5K time in well-trained endurance athletes without changes in their VO2 max. This improvement was due to improved neuromuscular characteristics that were transferred into improved VMART and running economy.     

Interstitial fluid pressure, composition of interstitium, and interstitial exclusion of albumin in hypothyroid rats

Lack of thyroid hormones may affect the composition and structure of the interstitium. Hypothyrosis was induced in rats by thyroidectomy 4-12 wk before the experiments. In hypothyroid rats (n = 16), interstitial fluid pressure measured with micropipettes in hindlimb skin and muscle averaged +0.1 +/- 0.2 and +0.5 +/- 0.2 mmHg, respectively, with corresponding pressures in control rats (n = 16) of -1.5 +/- 0.1 (P < 0.001) and -0.8 +/- 0.1 mmHg (P < 0.001). Interstitial fluid volume, measured as the difference between the distribution volumes of (51)Cr-EDTA and (125)I-labeled BSA, was similar or lower in skin and higher in hypothyroid muscle. Total protein and albumin concentration in plasma and interstitial fluid (isolated from implanted wicks) was lower in hypothyroid compared with control rats. Hyaluronan content (n = 9) in rat hindlimb skin was 2.05 +/- 0.15 and 1.92 +/- 0.09 mg/g dry wt (P > 0.05) in hypothyroid and control rats, respectively, with corresponding content in hindlimb skeletal muscle of 0.35 +/- 0.07 and 0.23 +/- 0. 01 mg/g dry wt (P < 0.01). Interstitial exclusion of albumin in skin and muscle was measured after (125)I-labeled rat serum albumin infusion for 120-168 h with an implanted osmotic pump. Relative excluded volume for albumin (V(e)/V(i)) was calculated as 1 - V(a)/V(i), and averaged 28 and 28% in hindlimb muscle (P > 0.05), 44 and 45% in hindlimb skin (P > 0.05), and 19 and 32% in back skin (P < 0.05) in hypothyroid and control rats, respectively. Albumin mass was higher in back skin in spite of a lower interstitial fluid albumin concentration, a finding explained by a reduced V(e)/V(i) in back skin in hypothyroid rats. These experiments suggest that lack of thyroid hormones in rats changes the interstitial matrix again leading to reduced interstitial compliance and changes in the transcapillary fluid balance.     

Impaired cardiac reserve and severely diminished skeletal muscle O₂ utilization mediate exercise intolerance in Barth syndrome

Barth syndrome (BTHS) is a mitochondrial myopathy characterized by reports of exercise intolerance. We sought to determine if 1) BTHS leads to abnormalities of skeletal muscle O(2) extraction/utilization and 2) exercise intolerance in BTHS is related to impaired O(2) extraction/utilization, impaired cardiac function, or both. Participants with BTHS (age: 17 ± 5 yr, n = 15) and control participants (age: 13 ± 4 yr, n = 9) underwent graded exercise testing on a cycle ergometer with continuous ECG and metabolic measurements. Echocardiography was performed at rest and at peak exercise. Near-infrared spectroscopy of the vastus lateralis muscle was continuously recorded for measurements of skeletal muscle O(2) extraction. Adjusting for age, peak O(2) consumption (16.5 ± 4.0 vs. 39.5 ± 12.3 ml·kg(-1)·min(-1), P < 0.001) and peak work rate (58 ± 19 vs. 166 ± 60 W, P < 0.001) were significantly lower in BTHS than control participants. The percent increase from rest to peak exercise in ejection fraction (BTHS: 3 ± 10 vs. control: 19 ± 4%, P < 0.01) was blunted in BTHS compared with control participants. The muscle tissue O(2) saturation change from rest to peak exercise was paradoxically opposite (BTHS: 8 ± 16 vs. control: -5 ± 9, P < 0.01), and the deoxyhemoglobin change was blunted (BTHS: 0 ± 12 vs. control: 10 ± 8, P < 0.09) in BTHS compared with control participants, indicating impaired skeletal muscle extraction in BTHS. In conclusion, severe exercise intolerance in BTHS is due to both cardiac and skeletal muscle impairments that are consistent with cardiac and skeletal mitochondrial myopathy. These findings provide further insight to the pathophysiology of BTHS.     

肾上腺髓质素对大鼠损伤性心肌肌浆网功能的改善

通过观察下述五个指标,评价肾上腺髓质素(adrenomedullin,Adm)对大鼠损伤性心肌肌浆网功能的改善程度左心室压力最大变化速率(±dp/dtmax)、肌浆网钙摄取和释放及钙泵活性.皮下注射异丙肾上腺素(isoproterenol,ISO,69μmol/kg体重)制备大鼠心肌损伤坏死模型.摘取心脏后用Adm灌流,观察左心室压力最大变化速率(±dp/dtmax);制备并提纯心肌肌浆网(sarcoplasmicreticulum,SR)膜,测定SRCa2+摄取和释放速率、SR钙泵活性和钙通道蛋白～3H-ryanodine受体的最大结合量.结果发现,5×10-5mol/LAdm灌流能使ISO损伤的大鼠心脏左室±dp/dtmax分别增加16.9%(2?135±281vs1?980±302)和29.2%(1?375±267vs1?064±355,均P<0.05);SRCa2+摄取和释放率分别增加23.0%(15.0±1.4vs12.2±1.2)和43.5%(6.6±1.0vs4.6±0.6,均P<0.01);SRCa2+-ATPase活性和～3H-ryanodine受体最大结合量(Bmax)分别增加24.2%(P<0.01)和42.2%(P<0.05).提示Adm对ISO诱导的大鼠心肌损伤具有保护作用,其机制可能与Adm增加SRCa2+-ATPase活性、增加～3H-ryanodine所致SRCa2+摄取和释放升高有关.外源性给予Adm对损伤心肌可能具有临床治疗作用.     

Influence of acute maximal exercise on lecithin:cholesterol acyltransferase activity in healthy adults of differing aerobic performance

To document the possible influence of a single episode of maximal aerobic stress on the serum lecithin:cholesterol acyltransferase (LCAT) activity in subjects with differing histories of training, two groups of healthy male adults [controls (C), n = 18, 28.6 years, SD 5.2, 50.1 ml.kg-1.min-1 maximal O2 uptake (VO2max), SD 5.3; endurance trained athletes (T), n = 18, 31.4 years, SD 8.8, 65.0 ml.kg-1.min-1 VO2max, SD 2.8] were examined in a maximal aerobic stress test. In addition to the routine assessment of lipid status, LCAT activity was measured immediately before and after exercise. At rest nearly identical LCAT activity values were found in both groups: C 64.4 nmol.ml-1.h-1, SD 16.7 vs T 65.0 nmol.ml-1.h-1, SD 20.9. The post-exercise LCAT values induced by the maximal stress test increased significantly to (C) 95.7 nmol.ml-1.h-1, SD 23.5, +48.6%, P less than 0.001; (T) 83.5 nmol.ml-1.h-1, SD 24.3, +29.1%, P less than 0.01. Neither the pre nor the postexercise individual LCAT activity values showed any significant correlation to the corresponding data on physical performance.     

Effect of progesterone and/or estradiol-17beta on sperm penetration in vitro of bovine oocytes

The effect of progesterone (P4) and estradiol-17beta (E2) on sperm penetration was evaluated by in vitro fertilization technique. When spermatozoa were treated with modified Tyrode's medium (mTALP) alone, mTALP + 1.0 microg/ml heparin (H), mTALP + 0.1 microg/ml P4, mTALP + 0.1 microg/ml E2, or mTALP + 0.1 microg/ml P4 + 0. 1 microg/ml E2, the percentages of penetrated oocytes were 11% (8/74), 94% (54/60), 19% (12/64), 10% (6/63) and 13% (8/62), respectively. The penetration rates by spermatozoa treated with H, H + P4, H + E2 and H + P4 + E2 were 94% (118/125), 100% (138/138), 95% (129/136), and 94% (100/106), respectively. However, the oocyte penetration rates significantly increased (P < 0.01) 4, 5 and 6 h after insemination, respectively, when the spermatozoa were treated with H + P4, H + E2 and H + P4 + E2 compared with that of the control (H). Cleavage rates also increased significantly (P < 0.01) 24 and 30 h following insemination, respectively, when spermatozoa were treated with H + P4, H + E2 and H + P4 + E2 compared with that of H. Nevertheless, There was no difference in the production of > or = 32 cell stage embryos among the 4 treatments (19% = 28/149, 18% = 32/176, 18% = 23/128 and 22% = 26/120, respectively). These results indicate that the time course of capacitated sperm penetration was accelerated by progesterone and estradiol-17beta but it did not affect subsequent early embryonic development.     

Pulmonary gas exchange during exercise in highly trained cyclists with arterial hypoxemia.

The causes of exercise-induced hypoxemia (EIH) remain unclear. We studied the mechanisms of EIH in highly trained cyclists. Five subjects had no significant change from resting arterial PO(2) (Pa(O(2)); 92.1 +/- 2.6 Torr) during maximal exercise (C), and seven subjects (E) had a >10-Torr reduction in Pa(O(2)) (81.7 +/- 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2% O(2)). During normoxia at 90% peak O(2) consumption, Pa(O(2)) was lower in E compared with C (87 +/- 4 vs. 97 +/- 6 Torr, P < 0.001) and alveolar-to-arterial O(2) tension difference (A-aDO(2)) was greater (33 +/- 4 vs. 23 +/- 1 Torr, P < 0. 001). Diffusion limitation accounted for 23 (E) and 13 Torr (C) of the A-aDO(2) (P < 0.01). There were no significant differences between groups in arterial PCO(2) (Pa(CO(2))) or ventilation-perfusion (VA/Q) inequality as measured by the log SD of the perfusion distribution (logSD(Q)). Stepwise multiple linear regression revealed that lung O(2) diffusing capacity (DL(O(2))), logSD(Q), and Pa(CO(2)) each accounted for approximately 30% of the variance in Pa(O(2)) (r = 0.95, P < 0.001). These data suggest that EIH has a multifactorial etiology related to DL(O(2)), VA/Q inequality, and ventilation.     

Thyroid hormone regulation of MHC isoform composition and myofibrillar ATPase activity in rat skeletal muscles.

Myosin heavy chain (MHC) isoform composition and Ca2+ Mg2+ dependent ATPase activity were determined in myofibrils prepared from skeletal muscles (diaphragm, soleus, plantaris and tibialis anterior) of euthyroid (C), hypothyroid (Tx) and hyperthyroid (T3) rats. Direct comparison between T3 and Tx gave an indication of the maximal effect of thyroid hormones. Significant differences in MHC-1 and MHC-2B proportions and in ATPase activity were found in all muscles. The difference in MHC-2A/X proportion was significant only in soleus, diaphragm and plantaris. When T3 and C were compared, significant variations in MHC isoform composition were found only in plantaris and diaphragm. The comparison between Tx and C showed significant differences in MHC isoform distribution and in ATPase activity in most muscles. The differences in ATPase activity among muscles and among thyroid states were consistent with those in MHC isoform distribution. From the correlations between ATPase activity and MHC isoform distribution the enzymatic activities of individual MHC isoforms were calculated. The results indicate that MHC isoform distribution is controlled by thyroid state in all skeletal muscles and that changes in MHC isoforms distribution are accompanied by proportional changes in ATPase activity.