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Biomedical subjects

J L Andersen

Publications and source records attributed to J L Andersen.

At least 19 recordsLinked to original sources
PubMed2005

ATR and GADD45alpha mediate HIV-1 Vpr-induced apoptosis.

The human immunodeficiency virus type-1 (HIV-1) accessory gene vpr encodes a conserved 96-amino-acid protein that is necessary and sufficient for the HIV-1-induced block of cellular proliferation. Expression of vpr in CD4+ lymphocytes results in G2 arrest, followed by apoptosis. In a previous study, we identified the ataxia telangiectasia-mutated (ATM) and Rad3-related protein (ATR) as a cellular factor that mediates Vpr-induced cell cycle arrest. In the present study, we report that the breast cancer-associated protein-1 (BRCA1), a known target of ATR, is activated in the presence of Vpr. In addition, the gene encoding the growth arrest and DNA damage-45 protein alpha (GADD45alpha), a known transcriptional target of BRCA1, is upregulated by Vpr in an ATR-dependent manner. We demonstrate that RNAi-mediated silencing of either ATR or GADD45alpha leads to nearly complete suppression of the proapoptotic effect of Vpr. Our results support a model in which Vpr-induced apoptosis is mediated via ATR phosphorylation of BRCA1, and consequent upregulation of GADD45alpha.

Apoptosis↗
PubMed2005

Saline-induced natriuresis and renal blood flow in conscious dogs: effects of sodium infusion rate and concentration.

AIM: This study focused on static and dynamic changes in total renal blood flow (RBF) during volume expansion and tested whether a change in RBF characteristics is a necessary effector mechanism in saline-induced natriuresis. METHODS: The aortic flow subtraction technique was used to measure RBF continuously. Identical amounts of NaCl (2.4 mmol kg(-1)) were given as slow isotonic (Iso, 120 min), slow hypertonic (Hyper, 120 min), and rapid isotonic loads (IsoRapid, 30 min). RESULTS: During Iso and IsoRapid, arterial blood pressure increased slightly (6-7 mmHg), and during Hyper it remained unchanged. Iso and Hyper increased sodium excretion (4 +/- 1 to 57 +/- 27 and 10 +/- 4 to 79 +/- 28 micromol min(-1), respectively) and decreased plasma renin activity (by 38% and 29%), angiotensin II (by 56% and 58%) and aldosterone (by 47% and 65%), while RBF remained unchanged. IsoRapid caused a similar increase in sodium excretion (to 72 +/- 19 micromol min(-1)), a similar decrease in renin system activity, but a 15% elevation of RBF (282 +/- 22 to 324 +/- 35 mL min(-1)). Selected frequency domain parameters of RBF autoregulation did not change in response to any load. CONCLUSIONS: In response to slow saline loading simulating daily sodium intake, the rate of sodium excretion may increase 10-20-fold without any change in mean arterial blood pressure or in RBF. Regulatory responses to changes in total body NaCl levels appears, therefore, to be mediated primarily by neurohumoral mechanisms and may occur independent of changes in arterial pressure or RBF.

Aldosterone↗
PubMed2005

Effects of power training on muscle structure and neuromuscular performance.

The present study examines changes in muscle structure and neuromuscular performance induced by 15 weeks of power training with explosive muscle actions. Twenty-three subjects, including 10 controls, volunteered for the study. Muscle biopsies were obtained from the gastrocnemius muscle before and after the training period, while maximal voluntary isometric contractions (MVC) and drop jump tests were performed once every fifth week. No statistically significant improvements in MVC of the knee extensor (KE) and plantarflexor muscles were observed during the training period. However, the maximal rate of force development (RFD) of KE increased from 18,836+/-4282 to 25,443+/-8897 N (P<0.05) during the first 10 weeks of training. In addition, vertical jump height (vertical rise of the center of body mass) in the drop jump test increased significantly (P<0.01). Simultaneously, explosive force production of KE muscles measured as knee moment and power increased significantly; however, there was no significant change (P>0.05) in muscle activity (electromyography) of KE. The mean percentage for myosin heavy chain and titin isoforms, muscle fiber-type distributions and areas were unchanged. The enhanced performance in jumping as a result of power training can be explained, in part, by some modification in the joint control strategy and/or increased RFD capabilities of the KE.

Adult↗
PubMed2004

Protein synthesis rates in human muscles: neither anatomical location nor fibre-type composition are major determinants.

In many animals the rate of protein synthesis is higher in slow-twitch, oxidative than fast-twitch, glycolytic muscles. To discover if muscles in the human body also show such differences, we measured [13C]leucine incorporation into proteins of anatomically distinct muscles of markedly different fibre-type composition (vastus lateralis, triceps, soleus) after an overnight fast and during infusion of a mixed amino acid solution (75 mg amino acids kg(-1) h(-1)) in nine healthy, young men. Type-1 fibres contributed 83 +/- 4% (mean +/-s.e.m.) of total fibres in soleus, 59 +/- 3% in vastus lateralis and 22 +/- 2% in triceps. The basal myofibrillar and sarcoplasmic protein fractional synthetic rates (FSR, % h(-1)) were 0.034 +/- 0.001 and 0.064 +/- 0.001 (soleus), 0.031 +/- 0.001 and 0.060 +/- 0.001 (vastus), and 0.027 +/- 0.001 and 0.055 +/- 0.001 (triceps). During amino acid infusion, myofibrillar protein FSR increased to 3-fold, and sarcoplasmic to 2-fold basal values (P < 0.001). The differences between muscles, although significant statistically (triceps versus soleus and vastus lateralis, P < 0.05), were within approximately 15%, biologically probably insignificant. The rates of collagen synthesis were not affected by amino acid infusion and varied by < 5% between muscles and experimental conditions.

Adult↗
PubMed2003

The effect of recombinant human growth hormone and resistance training on IGF-I mRNA expression in the muscles of elderly men.

The expression of two isoforms of insulin-like growth factor-I (IGF-I): mechano growth factor (MGF) and IGF-IEa were studied in muscle in response to growth hormone (GH) administration with and without resistance training in healthy elderly men. A third isoform, IGF-IEb was also investigated in response to resistance training only. The subjects (age 74 +/- 1 years, mean +/- S.E.M) were assigned to either resistance training with placebo, resistance training combined with GH administration or GH administration alone. Real-time quantitative RT-PCR was used to determine mRNA levels in biopsies from the vastus lateralis muscle at baseline, after 5 and 12 weeks in the three groups. GH administration did not change MGF mRNA at 5 weeks, but significantly increased IGF-IEa mRNA (237%). After 12 weeks, MGF mRNA was significantly increased (80%) compared to baseline. Five weeks of resistance training significantly increased the mRNA expression of MGF (163%), IGF-IEa (68%) and IGF-IEb (75%). No further changes were observed after 12 weeks. However, after 5 weeks of training combined with GH treatment, MGF mRNA increased significantly (456%) and IGF-IEa mRNA by (167%). No further significant changes were noted at 12 weeks. The data suggest that when mechanical loading in the form of resistance training is combined with GH, MGF mRNA levels are enhanced. This may reflect an overall up-regulation of transcription of the IGF-I gene prior to splicing.

Aged↗
PubMed2003

Effects of power training on mechanical efficiency in jumping.

The present study investigates the effects of power training on mechanical efficiency (ME) in jumping. Twenty-three subjects, including ten controls, volunteered for the study. The experimental group trained twice a week for 15 weeks performing various jumping exercises such as drop jumps, hurdle jumps, hopping and bouncing. In the maximal jumping test, the take-off velocity increased from 2.56 (0.24) m.s(-1) to 2.77 (0.18) m.s(-1) ( P<0.05). In the submaximal jumping of 50% of the maximum, energy expenditure decreased from 660 (110) to 502 (68) J.kg(-1).min(-1) ( P<0.001) while, simultaneously, ME increased from 37.2 (8.4)% to 47.4 (8.2)% ( P<0.001). Some muscle enzyme activities of the gastrocnemius muscle increased during the training period: citrate synthase from 35 (8) to 39 (7) micromol.g(-1) dry mass.min(-1) ( P<0.05) and beta-hydroxyacyl CoA dehydrogenase from 21 (4) to 23 (5) micromol.g(-1) dry mass.min(-1) ( P<0.05), whereas no significant changes were observed in phosphofructokinase and lactate dehydrogenase. In the control group, no changes in ME or in enzyme activities were observed. In conclusion, the enhanced performance capability of 8% in maximal jumping as a result of power training was characterized by decreased energy expenditure of 24%. Thus, the increased neuromuscular performance, joint control strategy, and intermuscular coordination (primary factors), together with improved aerobic capacity (secondary factor), may result in reduced oxygen demands and increased ME.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2003

Resistance training and insulin action in humans: effects of de-training.

Aerobic endurance training increases insulin action in skeletal muscle, but the effect of resistance training has not been well described. Controversy exists about whether the effect of resistance training is merely due to an increase in muscle mass. We studied the effect of cessation of resistance training in young, healthy subjects by taking muscle biopsies and measuring insulin-mediated whole body and leg glucose uptake rates after 90 days of heavy resistance training (T) and again after 90 days of de-training (dT). Data on leg glucose uptake were expressed relative to accurate measures of leg muscle mass by MRI scanning. Muscle strength (239 +/- 43 vs. 208 +/- 33 N m), quadriceps area (8463 +/- 453 vs. 7763 +/- 329 mm2) and glycogen content (458 +/- 22 vs. 400 +/- 26 mmol (kg dry weight muscle)(-1)) decreased, while myosin heavy chain isoform IIX increased 4-fold in dT vs. T, respectively (all P < 0.05). GLUT4 mRNA levels and enzyme activities and mRNA levels of glycolytic, lipolytic and glyconeogenic enzymes did not change with de-training. Likewise, capillary density did not change. Whole body glucose uptake decreased 11 % and leg glucose uptake decreased from 75 +/- 11 (T) to 50 +/- 6 (dT) nmol min(-1) (mm muscle)(-2) (P < 0.05) at maximal insulin, the latter decrease being due to decreased arterio-femoral venous glucose extraction. The decrease was mainly due to reduced non-oxidative glucose disposal. We have thus shown that 90 days after the termination of heavy resistance training, insulin-mediated glucose uptake rates per unit of skeletal muscle have decreased significantly.

Adult↗
PubMed2002

Muscle fibre type, efficiency, and mechanical optima affect freely chosen pedal rate during cycling.

UNLABELLED: This study investigated the variation in freely chosen pedal rate between subjects and its possible dependence on percentage myosin heavy chain I (%MHC I) in m. vastus lateralis, maximum leg strength and power, as well as efficiency. Additionally, the hypothesis was tested that a positive correlation exists between percentage MHC I and efficiency at pre-set pedal rates but not at freely chosen pedal rate. Twenty males performed cycling at low and high submaximal power output ( approximately 40 and 70% of the power output at which maximum oxygen uptake (VO(2max)) was attained at 80 r.p.m.) with freely chosen and pre-set pedal rates (61, 88, and 115 r.p.m.). Percentage MHC I as well as leg strength and power were determined. Freely chosen pedal rate varied considerably between subjects: 56-88 r.p.m. at low and 61-102 r.p.m. at high submaximal power output. This variation was only partly explained by percentage MHC I (21-97%) as well as by leg strength and power. Interestingly, %MHC I correlated significantly with the pedal rate at which maximum peak crank power occurred (r = -0.81). As hypothesized, %MHC I and efficiency were unrelated at freely chosen pedal rate, which was in contrast to a significant correlation found at pre-set pedal rates (r = 0.61 and r = 0.57 at low and high power output, respectively). CONCLUSIONS: Subjects with high percentage MHC I chose high pedal rates close to the pedal rates at which maximum peak crank power occurred, while subjects with low percentage MHC I tended to choose lower pedal rates, favouring high efficiency. Nevertheless, the considerable variation in freely chosen pedal rate between subjects was neither fully accounted for by percentage MHC I nor by leg strength and power. Previously recognized relationships between percentage Type I ( approximately %MHC I) and efficiency as well as between pedal rate and efficiency were confirmed for pre-set pedal rates, but for freely chosen pedal rate, these variables were unrelated.

Adolescent↗
PubMed2002

Aortic blood flow subtraction: an alternative method for measuring total renal blood flow in conscious dogs.

We have measured total renal blood flow (TRBF) as the difference between signals from ultrasound flow probes implanted around the aorta above and below the renal arteries. The repeatability of the method was investigated by repeated, continuous infusions of angiotensin II and endothelin-1 seven times over 8 wk in the same dog. Angiotensin II decreased TRBF (350 +/- 16 to 299 +/- 15 ml/min), an effect completely blocked by candesartan (TRBF 377 +/- 17 ml/min). Subsequent endothelin-1 infusion reduced TRBF to 268 +/- 20 ml/min. Bilateral carotid occlusion (8 sessions in 3 dogs) increased arterial blood pressure by 49% and decreased TRBF by 12%, providing an increase in renal vascular resistance of 69%. Dynamic analysis showed autoregulation of renal blood flow in the frequency range <0.06-0.07 Hz, with a peak in the transfer function at 0.03 Hz. It is concluded that continuous measurement of TRBF by aortic blood flow subtraction is a practical and reliable method that allows direct comparison of excretory function and renal blood flow from two kidneys. The method also allows direct comparison between TRBF and flow in the caudal aorta.

Angiotensin II↗
PubMed2001

Timing of postexercise protein intake is important for muscle hypertrophy with resistance training in elderly humans.

1. Age-associated loss of skeletal muscle mass and strength can partly be counteracted by resistance training, causing a net synthesis of muscular proteins. Protein synthesis is influenced synergistically by postexercise amino acid supplementation, but the importance of the timing of protein intake remains unresolved. 2. The study investigated the importance of immediate (P0) or delayed (P2) intake of an oral protein supplement upon muscle hypertrophy and strength over a period of resistance training in elderly males. 3. Thirteen men (age, 74 +/- 1 years; body mass index (BMI), 25 +/- 1 kg m(-2) (means +/- S.E.M.)) completed a 12 week resistance training programme (3 times per week) receiving oral protein in liquid form (10 g protein, 7 g carbohydrate, 3 g fat) immediately after (P0) or 2 h after (P2) each training session. Muscle hypertrophy was evaluated by magnetic resonance imaging (MRI) and from muscle biopsies and muscle strength was determined using dynamic and isokinetic strength measurements. Body composition was determined from dual-energy X-ray absorptiometry (DEXA) and food records were obtained over 4 days. The plasma insulin response to protein supplementation was also determined. 4. In response to training, the cross-sectional area of m. quadriceps femoris (54.6 +/- 0.5 to 58.3 +/- 0.5 cm(2)) and mean fibre area (4047 +/- 320 to 5019 +/- 615 microm(2)) increased in the P0 group, whereas no significant increase was observed in P2. For P0 both dynamic and isokinetic strength increased, by 46 and 15 %, respectively (P < 0.05), whereas P2 only improved in dynamic strength, by 36 % (P < 0.05). No differences in glucose or insulin response were observed between protein intake at 0 and 2 h postexercise. 5. We conclude that early intake of an oral protein supplement after resistance training is important for the development of hypertrophy in skeletal muscle of elderly men in response to resistance training.

Aged↗
PubMed2001

A mechanism for increased contractile strength of human pennate muscle in response to strength training: changes in muscle architecture.

1. In human pennate muscle, changes in anatomical cross-sectional area (CSA) or volume caused by training or inactivity may not necessarily reflect the change in physiological CSA, and thereby in maximal contractile force, since a simultaneous change in muscle fibre pennation angle could also occur. 2. Eleven male subjects undertook 14 weeks of heavy-resistance strength training of the lower limb muscles. Before and after training anatomical CSA and volume of the human quadriceps femoris muscle were assessed by use of magnetic resonance imaging (MRI), muscle fibre pennation angle (theta(p)) was measured in the vastus lateralis (VL) by use of ultrasonography, and muscle fibre CSA (CSA(fibre)) was obtained by needle biopsy sampling in VL. 3. Anatomical muscle CSA and volume increased with training from 77.5 +/- 3.0 to 85.0 +/- 2.7 cm(2) and 1676 +/- 63 to 1841 +/- 57 cm(3), respectively (+/- S.E.M.). Furthermore, VL pennation angle increased from 8.0 +/- 0.4 to 10.7 +/- 0.6 deg and CSA(fibre) increased from 3754 +/- 271 to 4238 +/- 202 microm (2). Isometric quadriceps strength increased from 282.6 +/- 11.7 to 327.0 +/- 12.4 N m. 4. A positive relationship was observed between theta(p) and quadriceps volume prior to training (r = 0.622). Multifactor regression analysis revealed a stronger relationship when theta(p) and CSA(fibre) were combined (R = 0.728). Post-training increases in CSA(fibre) were related to the increase in quadriceps volume (r = 0.749). 5. Myosin heavy chain (MHC) isoform distribution (type I and II) remained unaltered with training. 6. VL muscle fibre pennation angle was observed to increase in response to resistance training. This allowed single muscle fibre CSA and maximal contractile strength to increase more (+16 %) than anatomical muscle CSA and volume (+10 %). 7. Collectively, the present data suggest that the morphology, architecture and contractile capacity of human pennate muscle are interrelated, in vivo. This interaction seems to include the specific adaptation responses evoked by intensive resistance training.

Adult↗
PubMed2001

Caspase 3 expression correlates with skeletal muscle apoptosis in Duchenne and facioscapulo human muscular dystrophy. A potential target for pharmacological treatment?

Apoptosis was detected in different muscular diseases, including severe dystrophin deficiency, but apoptotic mechanisms are not completely described in adult skeletal muscle. Studying patients affected by Duchenne muscular dystrophy (DMD) and by facio-scapulo-humeral dystrophy (FSHD) we showed an increase of apoptotic myonuclei, bax, and bcl-2-positive myofibers. Positive correlation was detected between apoptotic nuclei and bax expression (p < 0.01). Expression of caspases was analyzed by RNase protection. Caspase transcript was not detected in normal skeletal muscles. DMD muscles expressed caspase 8, 3, 5, 2, 7 and Granzyme B mRNAs. Low levels of caspase 6, 3, and Granzyme B transcripts were detected in FSHD patients. Tissue levels of caspase 3 protein significantly correlated with apoptotic myonuclei (p < 0.05) and with bax expression (p < 0.01). In all DMD cases the activity of caspase 3 was increased, while the FSHD samples were heterogeneous. These data indicate that human skeletal muscle fibers. during the dystrophic process, modulate the expression of caspases and that caspase 3 is involved in myofiber cell death. opening new perspective in the pharmacological treatments of muscular dystrophies, such as the use of caspase inhibitors.

Adolescent↗
PubMed2000

Myosin heavy chain IIX overshoot in human skeletal muscle.

The distribution of myosin heavy chain (MHC) isoforms, fiber type composition, and fiber size of the vastus lateralis muscle were analyzed by sodium dodecylsulfate polymerase gel electrophoresis (SDS-PAGE), ATPase histochemistry, and immunocytochemistry in a group of adult sedentary men before and after 3 months of heavy-load resistance training and, subsequently, after 3 months of detraining. Following the period of resistance training, MHC IIX content decreased from 9.3 +/- 2.1% to 2.0 +/- 0.8% (P < 0.01), with a corresponding increase in MHC IIA (42.4 +/- 3.9% vs. 49.6 +/- 4.0% [P < 0.05]). Following detraining the amount of MHC IIX reached values that were higher than before and after resistance training (17.2 +/- 3.2% [P < 0.01]). Changes in fiber type composition resembled the changes observed in MHC isoform content. Significant hypertrophy was observed for the type II fibers after resistance training. Maximal isometric quadriceps strength increased after resistance training, but returned to pretraining levels after detraining. The present results suggest that heavy-load resistance training decreases the amount of MHC IIX while reciprocally increasing MHC IIA content. Furthermore, detraining following heavy-load resistance training seems to evoke an overshoot in the amount of MHC IIX to values markedly higher than those observed prior to resistance training.

Adenosine Triphosphatases↗
PubMed2000

Antagonist muscle coactivation during isokinetic knee extension.

The aim of the present study was to quantify the amount of antagonist coactivation and the resultant moment of force generated by the hamstring muscles during maximal quadriceps contraction in slow isokinetic knee extension. The net joint moment at the knee joint and electromyographic (EMG) signals of the vastus medialis, vastus lateralis, rectus femoris muscles (quadriceps) and the biceps femoris caput longum and semitendinosus muscles (hamstrings) were obtained in 16 male subjects during maximal isokinetic knee joint extension (KinCom, ROM 90-10 degrees, 30 degrees x s(-1)). Two types of extension were performed: [1] maximal concentric quadriceps contractions and [2] maximal eccentric hamstring contractions Hamstring antagonist EMG in [1] were converted into antagonist moment based on the EMG-moment relationships determined in [2] and vice versa. Since antagonist muscle coactivation was present in both [1] and [2] a set of related equations was constructed to yield the moment/EMG relationships for the hamstring and quadriceps muscles, respectively. The equations were solved separately for every 0.05 degrees knee joint angle in the 90-10 degrees range of excursion (0 degrees = full extension) ensuring that the specificity of muscle length and internal muscle lever arms were incorporated into the moment/EMG relationships established. Substantial hamstring coactivation was observed during quadriceps agonist contraction. This resulted in a constant level of antagonist hamstring moment of about 30 Nm throughout the range of motion. In the range of 30-10 degrees from full knee extension this antagonist hamstring moment corresponded to 30-75% of the measured knee extensor moment. The level of antagonist coactivation was 3-fold higher for the lateral (Bfcl) compared to medial (ST) hamstring muscles The amount of EMG crosstalk between agonist-antagonist muscle pairs was negligible (Rxy2<0.02-0.06). The present data show that substantial antagonist coactivation of the hamstring muscles may be present during slow isokinetic knee extension. In consequence substantial antagonist flexor moments are generated. The antagonist hamstring moments potentially counteract the anterior tibial shear and excessive internal tibial rotation induced by the contractile forces of the quadriceps near full knee extension. In doing so the hamstring coactivation is suggested to assist the mechanical and neurosensory functions of the anterior cruciate ligament (ACL).

Adult↗
PubMed2000

Hormonal regulation of renal sodium and water excretion during normotensive sodium loading in conscious dogs.

Saline was infused intravenously for 90 min to normal, sodium-replete conscious dogs at three different rates (6, 20, and 30 micromol x kg(-1) x min(-1)) as hypertonic solutions (HyperLoad-6, HyperLoad-20, and HyperLoad-30, respectively) or as isotonic solutions (IsoLoad-6, IsoLoad-20, and IsoLoad-30, respectively). Mean arterial blood pressure did not change with any infusion of 6 or 20 micromol x kg(-1) x min(-1). During HyperLoad-6, plasma vasopressin increased by 30%, although the increase in plasma osmolality (1.0 mosmol/kg) was insignificant. During HyperLoad-20, plasma ANG II decreased from 14+/-2 to 7+/-2 pg/ml and sodium excretion increased markedly (2.3+/-0.8 to 19+/-8 micromol/min), whereas glomerular filtration rate (GFR) remained constant. IsoLoad-20 decreased plasma ANG II similarly (13+/-3 to 7+/-1 pg/ml) concomitant with an increase in GFR and a smaller increase in sodium excretion (1.9+/-1.0 to 11+/-6 micromol/min). HyperLoad-30 and IsoLoad-30 increased mean arterial blood pressure by 6-7 mm Hg and decreased plasma ANG II to approximately 6 pg/ml, whereas sodium excretion increased to approximately 60 micromol/min. The data demonstrate that, during slow sodium loading, the rate of excretion of sodium may increase 10-fold without changes in mean arterial blood pressure and GFR and suggest that the increase may be mediated by a decrease in plasma ANG II. Furthermore, the vasopressin system may respond to changes in plasma osmolality undetectable by conventional osmometry.

Angiotensin II↗
PubMed2000

Volume expansion natriuresis during servo control of systemic blood pressure in conscious dogs.

The importance of arterial blood pressure (BP) and ANG II for the renal natriuretic response (NaEx) to volume expansion (3.5% body wt) was investigated during converting enzyme blockade (enalaprilate, 2 mg/kg). In separate experiments, BP was clamped either 30 mm Hg above or a few millimeters mercury below baseline by servo-controlled infusion of ANG II or sodium nitroprusside, respectively, so that volume expansion did not change BP. Enalapril decreased BP by 8 mm Hg. Without clamping, volume expansion returned BP to that of preenalapril control and increased NaEx 10-fold (40+/-10 to 377+/-69 micromol/min). During high pressure clamping (133+/-2 mm Hg), peak NaEx after volume expansion was 6% of control experiments. During low pressure clamping, NaEx was 68% of control experiments (45+/-15 to 256+/-64 micromol/min). The results show that 1) in absence of ANG II, volume expansion elicited pronounced natriuresis without increases in BP beyond baseline, 2) in the presence of hypertensive amounts of ANG II, the volume expansion-induced natriuresis was almost eliminated, and 3) nitroprusside prevented the increase in BP but not sodium excretion during volume expansion. ANG II appears to dominate the control of NaEx; however, when absent, volume expansion may still induce marked natriuresis even at constant BP, possibly via nitric oxide-mediated mechanisms.

Angiotensin II↗
PubMed2000

Enhanced sarcoplasmic reticulum Ca(2+) release following intermittent sprint training.

To evaluate the effect of intermittent sprint training on sarcoplasmic reticulum (SR) function, nine young men performed a 5 wk high-intensity intermittent bicycle training, and six served as controls. SR function was evaluated from resting vastus lateralis muscle biopsies, before and after the training period. Intermittent sprint performance (ten 8-s all-out periods alternating with 32-s recovery) was enhanced 12% (P < 0.01) after training. The 5-wk sprint training induced a significantly higher (P < 0.05) peak rate of AgNO(3)-stimulated Ca(2+) release from 709 (range 560-877; before) to 774 (596-977) arbitrary units Ca(2+). g protein(-1). min(-1) (after). The relative SR density of functional ryanodine receptors (RyR) remained unchanged after training; there was, however, a 48% (P < 0.05) increase in total number of RyR. No significant differences in Ca(2+) uptake rate and Ca(2+)-ATPase capacity were observed following the training, despite that the relative density of Ca(2+)-ATPase isoforms SERCA1 and SERCA2 had increased 41% and 55%, respectively (P < 0.05). These data suggest that high-intensity training induces an enhanced peak SR Ca(2+) release, due to an enhanced total volume of SR, whereas SR Ca(2+) sequestration function is not altered.

Adenosine Triphosphatases↗