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PubMed1983

Mechanisms for decreased exercise capacity after bed rest in normal middle-aged men.

The mechanisms responsible for the decrease in exercise capacity after bed rest were assessed in 12 apparently healthy men aged 50 +/- 4 years who underwent equilibrium gated blood pool scintigraphy during supine and upright multistage bicycle ergometry before and after 10 days of bed rest. After bed rest, echocardiographically measured supine resting left ventricular end-diastolic volume decreased by 16% (p less than 0.05). Peak oxygen uptake during supine effort after bed rest was diminished by 6% (p = not significant [NS]), whereas peak oxygen uptake during upright effort declined by 15% (p less than 0.05). After bed rest, increases in heart rate were also greater during exercise in the upright than in the supine position (p less than 0.05). Values of left ventricular ejection fraction increased normally during both supine and upright effort after bed rest and were higher than corresponding values before bed rest (p less than 0.05). After bed rest, increased left ventricular ejection fraction and heart rate largely compensated for the reduced cardiac volume during supine effort, but these mechanisms were insufficient to maintain oxygen transport capacity at levels during upright effort before bed rest. These results indicate that orthostatically induced cardiac underfilling, not physical deconditioning or left ventricular dysfunction, is the major cause of reduced effort tolerance after 10 days of bed rest in normal middle-aged men.

Bed Rest↗
PubMed2003

The use of actimetry to assess changes to the rest-activity cycle.

The endogenous circadian oscillator (the body clock) is slow to adjust to altered rest-activity patterns. As a result, several negative consequences arise during night work and after time-zone transitions. The process of adjustment can be assessed by measurements of the sleep electroencephalogram (EEG), core temperature or melatonin secretion, for example, but these techniques are very difficult to apply in field studies, and make very great demands upon both experimenters and subjects. We have sought to establish if the activity record, measured conveniently and unobtrusively by a monitor attached to the wrist, can be treated in ways that enable estimates to be made of the disruption caused by changes to the rest-activity cycle, and the process of adjustment to them. In Part A, we describe the calculation and assessment of a series of "activity indices" that measure the overall activity pattern, activity when out of bed or in bed, or the activity in the hours adjacent to going to bed or getting up. The value of the indices was assessed by measuring changes to them in subjects undergoing night work or undergoing time-zone transitions. In both cases, there is a large body of literature describing the changes that would be expected. First, night workers (working 2 to 4 successive night shifts) were investigated during rest days and night shifts. The indices indicated that night work was associated with lower activity when the subjects were out of bed and higher activity when in bed. Some indices also measured when subjects took an afternoon nap before starting a series of night shifts and gave information about the process of adjustment to night work and recovery from it. Second, in studies from travelers crossing six or more time zones to the east or west, the indices indicated that there were changes to the rest-activity cycle immediately after the flights, both in its overall profile and when activity of the subjects in bed or out of bed was considered, and that adjustment took place on subsequent days. By focusing on those indices describing the activity records during the last hour in bed (LHIB) and the first hour out of bed (FHOB), some evidence was found for incomplete adjustment of the body clock, and for differences between westward and eastward flights. In Part B, the battery of indices are applied to the activity records of long-haul pilots, whose activity patterns showed a mixture of effects due to night work and time-zone transitions. Actimetry was performed during the flights themselves and during the layover days (which were either rest or work days). The indices indicated that all pilots had disrupted rest-activity cycles caused by night flights, and that there were added problems for those who had also undergone time-zone transitions. Rest days were valuable for normalizing the activity profile. For those pilots who flew to the west, adjustment was by delay, though not all aspects of the rest-activity cycle adjusted immediately; for those who flew to the east, some attempted to advance their rest-activity cycle while others maintained home-based activity profiles. The indices indicated that the activity profile was disrupted more in those pilots who attempted to advance their rest-activity cycle. We conclude that objective estimates of the disruption caused to the rest-activity cycle and the circadian system can be obtained by suitable analysis of the activity record.

Activity Cycles↗
PubMed1994

Altered autonomic regulation of cardiac function during head-up tilt after 28-day head-down bed-rest with counter-measures.

The effects of 28 days continuous 6 degrees head-down tilt bed-rest on heart rate variability and the slope of the spontaneous arterial baroreflex were evaluated during supine rest and the first 10 min of 60 degrees head-up tilt. Twelve healthy men were assigned to either a no counter-measure (No-CM), or a counter-measure (CM) group so that there was no difference in maximal oxygen uptake. Counter-measures consisted of short-term, high resistance exercise for 6 days per week from days 7-28, and lower body negative pressure (-28 mmHg) for 15 min on days 16, 18, 20 and 22-28. In spite of balanced between-group fitness, mean RR-interval was different between the No-CM and the CM group prior to bed-rest, but neither this nor any other variables showed significant counter-measure by bed-rest interaction effects. Therefore, all data presented are from the main effects of bed-rest or tilt from the analysis of variance. RR-interval was reduced significantly by bed-rest and by tilt (P < 0.0001). Indicators from spectral analysis of heart-rate variability suggested reduced parasympathetic nervous system activity with bed-rest (P < 0.01) and head-up tilt (P < 0.05), and increased sympathetic nervous system activity after bed-rest (P < 0.01). An indicator of complexity of cardiovascular control mechanisms, taken from the slope (beta) of log spectral power vs. log frequency relationship, suggested reduced complexity with bed-rest (P < 0.05) and head-up tilt (P < 0.01). The spontaneous baroreflex slope was reduced significantly by bed-rest (P < 0.03) and by head-up tilt (P < 0.04). Taken together, these data support the concept of altered autonomic nervous system function in the aetiology of cardiovascular deconditioning with bed-rest or space travel; and it would appear that no benefit is derived from these specific counter-measures.

Adult↗
PubMed2004

Effects of 20 days of bed rest on the viscoelastic properties of tendon structures in lower limb muscles.

OBJECTIVES: The purpose of this study was to investigate the effects of 20 days' bed rest on the viscoelastic properties of human tendon structures in knee extensor and plantar flexor muscles in vivo. METHODS: Eight healthy men (age: 24+/-4 years, height: 172+/-9 m, body mass: 69+/-13 kg) carried out a 6 degrees head-down bed rest for 20 days. Before and after bed rest, elongation (L) of the tendon and aponeurosis of vastus lateralis (VL) and medial gastrocnemius muscles (MG) during isometric knee extension and plantar flexion, respectively, were determined using real-time ultrasonic apparatus, while the subjects performed ramp isometric contraction up to the voluntary maximum, followed by ramp relaxation. The relationship between estimated muscle force (Fm) and tendon elongation (L) was fitted to a linear regression, the slope of which was defined as stiffness. The hysteresis was calculated as the ratio of the area within the Fm-L loop to the area beneath the load portion of the curve. RESULTS: L values above 100 N were significantly greater after bed rest for VL, while there were no significant differences in L values between before and after for MG. The stiffness decreased after bed rest for VL (70.3+/-27.4 v 50.1+/-24.8 N/mm, before and after bed rest, respectively; p = 0.003) and MG (29.4+/-7.5 v 25.6+/-7.8 N/mm, before and after bed rest, respectively; p = 0.054). In addition, hysteresis increased after bed rest for VL (16.5+/-7.1% v 28.2+/-12.9%, before and after bed rest, respectively; p = 0.017), but not for MG (17.4+/-4.4% v 17.7+/-6.1%, before and after bed rest, respectively; p = 0.925). CONCLUSIONS: These results suggested that bed rest decreased the stiffness of human tendon structures and increased their hysteresis, and that these changes were found in knee extensors, but not the plantar flexors.

Adult↗
PubMed2004

Reduced baroreflex control of heart period after bed rest is normalized by acute plasma volume restoration.

Adaptation to spaceflight or head-down-tilt bed rest leads to hypovolemia and an apparent abnormality of baroreflex regulation of cardiac period. In a previous study, we demonstrated that both chronic (2 wk) head-down-tilt bed rest and acute induced hypovolemia led to similar impairments in spontaneous baroreflex control of cardiac period, suggesting that a reduction in plasma volume may be responsible for this abnormality after bed rest. Therefore we hypothesized that this reduced "baroreflex function" could be restored by intravenous volume infusion equivalent to the reduction in plasma volume after bed rest. Six healthy subjects underwent 2 wk of -6 degrees head-down bed rest. Beat-by-beat arterial blood pressure and ECG were recorded during 6 min of spontaneous respiration and fixed-rate breathing (0.2 Hz), and transfer function analysis between systolic blood pressure and R-R interval was performed. Plasma volume was measured with Evans blue dye, and cardiac filling pressures were directly measured (Swan-Ganz catheter). After bed rest, studies were repeated before and after plasma volume restoration, with which both plasma volume and left ventricular end-diastolic pressure were restored to pre-bed rest levels by intravenous dextran40 infusion (288 +/- 31 ml). Transfer function gain in the high-frequency range, used as an index of vagally mediated arterial-cardiac baroreflex function, decreased significantly (13.4 +/- 3.1 to 8.1 +/- 2.9 ms/mmHg, P < 0.05) after bed rest. However, reduced transfer function gain was normalized to the pre-bed rest level (12.2 +/- 3.6 ms/mmHg) after precise plasma volume restoration. This result confirms that reductions in plasma volume, rather than a unique autonomic nervous system adaptation to bed rest, are largely responsible for the observed changes in spontaneous arterial-cardiac baroreflex function after bed rest.

Adult↗
PubMed2001

Maximal and submaximal forces of slow fibers in human soleus after bed rest.

The effects of 2 and 4 mo of bed rest, with or without exercise countermeasures, on the contractile properties of slow fibers in the human soleus muscle were examined. Mean fiber diameters were 8 and 36% smaller after 2 and 4 mo of bed rest, respectively, than the pre-bed rest level. Maximum tetanic force (P(o)), maximum activated force (F(max)) per cross-sectional area (CSA), and the common-logarithm value of free Ca(2+) concentration required for half-maximal activation (pCa(50)) also decreased after 2 and 4 mo of bed rest. In contrast, maximum unloaded shortening velocity (V(o)) was increased after 2 and 4 mo of bed rest. After 1 mo of recovery, fiber diameters, P(o), F(max) per CSA (P > 0.05), and pCa(50) were increased and V(o) decreased toward pre-bed rest levels. Effects of knee extension/flexion exercise by wearing an anti-G Penguin suit for 10 h daily, and the effects of loading or unloading of the plantar flexors with (Penguin-1) or without (Penguin-2) placing the elastic loading elements of the suit, respectively, were investigated during ~2 mo of bed rest. In the Penguin-1 group, mean fiber diameter, P(o), F(max) per CSA, V(o), and pCa(50) were similar before and after bed rest. However, the responses of fiber size and contractile properties to bed rest were not prevented in the Penguin-2 group, although the degree of the changes was less than those induced by bed rest without any countermeasure. These results indicate that long-term bed rest results in reductions of fiber size, force-generation capacity, and Ca(2+) sensitivity, and enhancement of shortening velocity in slow fibers of the soleus. The data indicate that continuous mechanical loading on muscle, such as stretching of muscle, is an effective countermeasure for the prevention of muscular adaptations to gravitational unloading.

Adult↗
PubMed2003

Bone resorption is induced on the second day of bed rest: results of a controlled crossover trial.

The aim of the study was to analyze the kinetics of short-term changes in bone turnover. We studied in a randomized crossover design the effects of 6 days of bed rest on eight healthy male subjects (mean body wt: 70.1 +/- 5.7 kg; mean age: 25.5 +/- 2.9 yr). The metabolic ward period was divided into three parts: 4 ambulatory days, 6 days of either bed rest or non-bed rest periods, and 1 recovery day. The diet was identical in both bed rest and non-bed rest phases. Continuous urine collection started on the first day in the metabolic ward to analyze excretion of bone resorption markers, namely C-telopeptide (CTX) and N-telopeptide (NTX), creatinine, urea, and 3-methylhistidine. On the second ambulatory day and on the fifth day of bed rest or during the non-bed rest phase, blood was drawn to analyze bone formation markers and amino acid concentrations. Urinary calcium excretion was increased as early as the first day of bed rest (P < 0.01). CTX and NTX excretion stayed unchanged during the first 24 h of bed rest compared with the non-bed rest period. However, already on the second day, both resorption markers had increased significantly. NTX excretion increased by 28.7 +/- 14.0% (P < 0.01), whereas CTX excretion rose by 17.8 +/- 8.3% (P < 0.001). Creatinine, urea, and 3-methylhistidine excretion did not change. We conclude that 24 h of bed rest are sufficient to induce a significant rise in osteoclast activity in healthy subjects.

Adult↗
PubMed1997

Minimizing fatigue during repetitive jobs: optimal work-rest schedules.

Twenty women were asked to generate forces using a dynamometer that were consistent with one of three different work-rest schedules (a low-, medium-, and high-force schedule). Each work-rest schedule consisted of 6 identical blocks of 10 work-rest cycles. Each of the 10 work-rest cycles lasted 1 min. The first work-rest cycle in each block consisted of a 6-s maximal voluntary contraction and a 54-s rest. The remaining 9 work-rest cycles in each block consisted of a submaximal contraction and a rest period. The desired force of the submaximal contraction, the length of this contraction, and the duration of the rest period remained constant within schedules but varied across schedules. The amount of physiological work was kept constant among schedules. The fatigue that developed in the medium-force schedule was significantly lower than that developed in either the low- or high-force schedule. A model was developed that predicted the amount of fatiguable strength at the beginning and end of each contraction of a work-rest cycle. When fit to the results from the experiment, the model explained 94% of the variance. The model can be used to predict the work-rest schedule that minimizes fatigue in a given repetitive job, thereby potentially increasing productivity and reducing the incidence of cumulative trauma disorders.

Adult↗
PubMed2006

Kinematic, kinetic, and blood lactate profiles of continuous and intraset rest loading schemes.

The purpose of this study was to investigate and compare the acute kinematic, kinetic, and blood lactate responses to continuous and intraset rest loading schemes that differed in terms of rest frequency but not total rest duration. Nine male subjects performed an isoinertial bench press task (6 repetition maximum load) with a continuous, an intraset rest equated by total rest time, volume, and load (ISRV), and an intraset rest equated by total rest time and load (ISRR) loading scheme. The scheme order was assigned in a block-randomized order with a minimum of 48 hours of recovery between testing sessions. Attached to the bar of the Smith machine was a linear position transducer that measured vertical displacement with an accuracy of 0.01 cm. Displacement data was sampled at 1,000 Hz and collected by a laptop computer running custom-built data acquisition software. Finger prick blood lactate samples were taken from the nondominant hand before exercise, immediately after exercise, and 5, 15 and 30 minutes after exercise. Blood glucose samples were taken before exercise only. It was observed that manipulating the rest period, by increasing the frequency but decreasing the length of each rest period, did not significantly influence the kinematics and kinetics associated with resistance training, but did have an effect on the postexercise blood lactate response when the load, rest duration, and training volume were equated (ISRV). This finding may be of practical significance if fatigue is important in strength development or conversely if power training requires minimal fatigue. It was also observed that increasing the frequency of the rest period enabled the subjects to perform a greater number of repetitions (ISRR), resulting in significantly greater kinematics, kinetics, and blood lactate accumulation.

Adult↗
PubMed2005

Bed rest effects on human calf hemodynamics and orthostatic intolerance: a model-based analysis.

INTRODUCTION: Microgravity-induced orthostatic intolerance continues to be a primary problem after space missions. Its etiology remains uncertain despite significant research efforts over the past years. We hypothesized that calf hemodynamic parameters (compliance and resistance) are significantly affected by 14 to 16-d head-down bed rest (simulated microgravity), and their alterations play a role in the pathogenesis of orthostatic intolerance (OI) following bed rest. METHODS: To estimate these parameters, we developed a model-based approach to quantitatively simulate calf vascular response to venous occlusion, which only necessitates measurement of plethysmography data. In this study, plethysmography data were obtained from 29 subjects before and after 14-16 d of head-down bed rest. The subjects also underwent a tilt/stand test before and after bed rest. RESULTS: Statistical analyses demonstrated an increase in calf compliance (1.87 +/- 0.08, mean +/- SE, pre-bed rest; 2.16 +/- 0.10, end-bed rest) but no significant change in vascular resistance following bed rest. Compared with the tilt-intolerant subjects, those who were tilt-tolerant before bed rest had significantly higher calf compliance [2.00 +/- 0.09 (tolerant); 1.58 +/- 0.09 (intolerant)] and higher vascular resistance [7.79 +/- 0.18 (tolerant); 6.91 +/- 0.40 (intolerant)]. After bed rest, no such difference was detected. DISCUSSION: Based on these results, we validated the hypothesis that, instead of causing orthostatic intolerance, higher calf compliance before bed rest leads to recruitment of compensatory mechanisms (validated by the enhanced vascular resistance during venous occlusion) for a better toleration of orthostatic stress. With the absence of orthostatic challenge during bed rest, the difference in calf hemodynamic parameters is attenuated between the tilt-tolerant and tilt-intolerant groups.

Adaptation, Physiological↗
PubMed2006

A brief review: factors affecting the length of the rest interval between resistance exercise sets.

Research has indicated that multiple sets are superior to single sets for maximal strength development. However, whether maximal strength gains are achieved may depend on the ability to sustain a consistent number of repetitions over consecutive sets. A key factor that determines the ability to sustain repetitions is the length of rest interval between sets. The length of the rest interval is commonly prescribed based on the training goal, but may vary based on several other factors. The purpose of this review was to discuss these factors in the context of different training goals. When training for muscular strength, the magnitude of the load lifted is a key determinant of the rest interval prescribed between sets. For loads less than 90% of 1 repetition maximum, 3-5 minutes rest between sets allows for greater strength increases through the maintenance of training intensity. However, when testing for maximal strength, 1-2 minutes rest between sets might be sufficient between repeated attempts. When training for muscular power, a minimum of 3 minutes rest should be prescribed between sets of repeated maximal effort movements (e.g., plyometric jumps). When training for muscular hypertrophy, consecutive sets should be performed prior to when full recovery has taken place. Shorter rest intervals of 30-60 seconds between sets have been associated with higher acute increases in growth hormone, which may contribute to the hypertrophic effect. When training for muscular endurance, an ideal strategy might be to perform resistance exercises in a circuit, with shorter rest intervals (e.g., 30 seconds) between exercises that involve dissimilar muscle groups, and longer rest intervals (e.g., 3 minutes) between exercises that involve similar muscle groups. In summary, the length of the rest interval between sets is only 1 component of a resistance exercise program directed toward different training goals. Prescribing the appropriate rest interval does not ensure a desired outcome if other components such as intensity and volume are not prescribed appropriately.

Exercise↗
PubMed1998

Changes in thyroid hormones and lipids in endurance trained volunteers during acute and rigorous bed rest conditions.

The aim of this study was to evaluate the effect of an acute rigorous bed rest (ABR) (abrupt confinement to a rigorous bed rest regimen) and a rigorous bed rest (RBR) regimen on serum concentrations of thyroid hormones and lipids. The studies were done during seven days of a pre bed rest period and during seven days of an ABR and RBR period. Thirty endurance trained male volunteers aged 22 to 26 years with a peak oxygen uptake of 66.0 mL.min-1.kg-1 and running an average of 14.0 km.day-1 were chosen as subjects. They were divided equally into three groups: (one) ten athletes placed under ambulatory conditions served as ambulatory control subjects (ACS), (two) ten athletes subjected to an acute rigorous bed rest regimen served as acute bed rested subjects (ABRS) and (three) ten athletes submitted to a rigorous bed rest regimen served as rigorous bed rested subjects (RBRS). For the simulation of the effect of ABR the ABRS group was submitted abruptly to a rigorous bed rest regimen. They did not have any prior knowledge of the exact date and time when they would be asked to submit to the RBR. For the simulation of the effect of RBR the RBRS group was subjected to a rigorous bed rest regimen on a predetermined date and time known to them right from the start of the study. During the pre bed rest period and during the ABR and RBR periods serum concentrations of thyroxine (T3), triiodothyronine (T4), thyroid-stimulating hormone (TSH), cholesterol, triglycerides, total protein and albumin were measured. In the ABRS and RBRS groups serum concentrations of T3, T4, TSH, cholesterol, triglycerides, total protein and albumin increased significantly when compared with the ACS group. Serum concentrations of thyroid hormones and lipids in the ABRS group increased much faster and were more pronounced than in the RBRS group. It is concluded that exposure to RBR and, especially, to ABR conditions induces significant increases in serum concentrations of thyroid hormones and lipids. These changes occurred much earlier and were much greater in the ABRS group than in the RBRS group.

Adult↗
PubMed1993

Paradoxical twitch potentiation after rest in cardiac muscle: increased fractional release of SR calcium.

Rest interval dependent changes in contractile force (rest decay and rest potentiation) were studied in rabbit, rat and ferret ventricular muscle and myocytes. The SR Ca content was assessed by rapid cooling contractures or caffeine induced contractures. Intracellular Ca transients, action potentials and Ca current were also recorded. Rest decay of twitches in rabbit ventricle are roughly paralleled by a decline in SR Ca content. Rat ventricle exhibits primarily rest potentiation, which is not necessarily paralleled by an increased SR Ca content. Ferret ventricle exhibits both rest potentiation and rest decay. However, the SR Ca content in ferret appears to decline monotonically throughout the rest. It is demonstrated that the rest potentiation is not due to an increase in Ca current or in action potential duration. We conclude that there is an increase in the fraction of SR Ca content which is released during the time that rest potentiation develops. The differences in post-rest contractile function among different cardiac preparations can be described by a simple unifying mechanistic model. In this model there is an exponential time dependent recovery of the ability of the SR to release Ca (e.g. recovery from inactivation) which can be considered to increase the fraction of SR Ca release in response to activation. This fractional SR Ca release is multiplied by the SR Ca content (which may decline exponentially) to provide a measure of the Ca available for activation of contractile force.

Animals↗
PubMed1995

Value of radionuclide rest and exercise left ventricular ejection fraction in assessing survival of patients after thrombolytic therapy for acute myocardial infarction: results of Thrombolysis in Myocardial Infarction (TIMI) phase II study. The TIMI Study Group.

OBJECTIVES: This study sought to determine the prognostic value of rest and exercise left ventricular ejection fraction in patients receiving thrombolytic therapy as part of the Thrombolysis in Myocardial Infarction (TIMI) trial. BACKGROUND: In the prethrombolytic era, ejection fraction at rest as well as during exercise was an important prognostic index in patients recovering from acute myocardial infarction. The prognostic value of these measurements in the thrombolytic era is not clear. METHODS: As part of the TIMI II protocol, we obtained radionuclide left ventricular ejection fraction at rest and during symptom-limited submaximal supine exercise. Measurements were related to 1-year all-cause as well as cardiac mortality. In addition, the relation between ejection fraction obtained at rest and 1-year cardiac mortality in this study was compared with the relation established previously in the prethrombolytic era by the Multicenter Postinfarction Research Group. RESULTS: A distinct relation was noted between left ventricular ejection fraction at rest and all-cause mortality. The highest mortality rate (9.9%) was noted in patients with an ejection fraction < 30%. Those not undergoing a study had a 1-year mortality rate of 6.2%. Peak exercise ejection fraction provided prognostic information similar to that of rest ejection fraction. Likewise, change in ejection fraction from rest to exercise did not appreciably improve prognostic impact. CONCLUSIONS: Rest left ventricular ejection fraction is an important prognostic index in patients receiving thrombolytic therapy. Peak exercise ejection fraction and the change in ejection fraction from rest to exercise do not provide appreciable prognostic data beyond those obtained at rest. Patients unable to exercise or those not having a rest study have a poor prognosis. When compared with the Multicenter Postinfarction Research Group data, there was strong evidence of a difference in survival in the two studies. At any level of ejection fraction, mortality was lower in TIMI II patients than in patients in the prethrombolytic era.

Aged↗
PubMed1998

Exaggerated blood pressure response to exercise: importance of resting blood pressure.

Normotensive individuals who exhibit an exaggerated blood pressure (BP) response to exercise have an increased risk of future hypertension. However, previous studies failed to control for resting BP despite the fact that an elevated resting BP in the normotensive range is also a strong predictor of future hypertension. Therefore, we determined whether maximal systolic BP is associated with resting BP. Resting BP was measured in 68 healthy normotensive men on three separate days. The subjects then performed a graded, maximal exercise test on a Monark cycle ergometer. Maximal systolic BP was strongly correlated with resting systolic BP (r = 0.64, P < 0.0001). Subjects with elevations in systolic BP during maximal exercise (> 220 mmHg) also had higher (P < 0.005) resting BP than those without (< 220 mmHg). When stepwise regression analyses were performed, systolic BP at rest was a significant independent predictor of maximal systolic BP, explaining over 40% of the variability. These results suggest that exaggerated BP response as a predictor of future hypertension reported in previous studies may be little more than a simple reflection of elevated resting BP. Specifically, these studies should not be interpreted as demonstrating that exercise BP is a better predictor of future hypertension than resting BP alone. In the future, defining the BP 'response' to exercise as a change score (i.e. maximal BP minus resting BP) may be advantageous as it permits the effects of exercise to be examined independently of the level of resting BP.

Adult↗
PubMed2000

The co-repressor mSin3A is a functional component of the REST-CoREST repressor complex.

The repressor REST/NRSF restricts expression of a large set of genes to neurons by suppressing their expression in non-neural tissues. We find that REST repression involves two distinct repressor proteins. One of these, CoREST, interacts with the COOH-terminal repressor domain of REST (Andres, M. E., Burger, C., Peral-Rubio, M. J., Battaglioli, E., Anderson, M. E., Grimes, J., Dallmanm J., Ballas, N. , and Mandel, G. (1999) Proc. Natl. Acad. Sci. U. S. A. 96, 9873-9878). Here we show that the co-repressor mSin3A also interacts with REST. The REST-mSin3A association involves the NH(2)-terminal repressor domain of REST and the paired amphipathic helix 2 domain of mSin3A. REST forms complexes with endogenous mSin3A in mammalian cells, and both mSin3A and CoREST interact with REST in intact mammalian cells. REST repression is blocked in yeast lacking Sin3 and rescued in its presence. In mammalian cells, repression by REST is reduced when binding to mSin3A is inhibited. In mouse embryos, the distribution of mSin3A and REST transcripts is largely coincident. The pattern of CoREST gene expression is more restricted, suggesting that mSin3A is required constitutively for REST repression, whereas CoREST is recruited for more specialized repressor functions.

Animals↗
PubMed1999

Effects of red blood cell transfusion on resting energy expenditure in adolescents with sickle cell anemia.

BACKGROUND: Previous studies indicate that resting energy expenditure is elevated in children with sickle cell anemia, possibly caused in part by hemolysis and increased erythropoietic activity. The purpose of the present investigation was to determine whether erythrocyte transfusion normalizes resting energy expenditure in sickle cell anemia. METHODS: Five adolescents with sickle cell anemia (12-16 years old; 4 boys, 1 girl) were studied before and 1 week after erythrocyte transfusion before elective surgery or at the initial transfusion for growth failure. Resting energy expenditure was measured by indirect calorimetry, and laboratory measures were determined by routine, validated methods. Data comparisons were by nonparametric analysis. RESULTS: After erythrocyte transfusion, total hemoglobin levels increased (difference (D) = 15 g/l; p < 0.05), whereas hemoglobin S (D = -0.36; p < 0.05) and reticulocyte count (D = -0.12; p < 0.05) decreased. Mean pretransfusion resting energy expenditure was elevated to 124% above predicted levels (p < 0.05) and increased further to 134% above prediction (p < 0.05 vs. pretransfusion levels). Plasma triiodothyronine (T3) levels increased (D = 0.17 nmol/l; p < 0.05), reverse T3 (rT3) levels tended to decline (D = -0.04 nmol/l; p = 0.14), and rT3/T3 decreased (D = -0.03; p < 0.05). Plasma insulin-like growth factor-I (IGF-I) levels were low-normal before transfusion and did not change, despite the change in resting energy expenditure. CONCLUSIONS: The results confirm that resting energy expenditure is elevated in patients with sickle cell anemia. However, resting energy expenditure further increased after transfusion, despite decreased erythropoietic activity. A posttransfusion decrease in rT3/T3 may contribute to the increased resting energy expenditure. That there was no change in IGF-I implies that the growth hormone-IGF system is not involved in posttransfusion regulation of resting energy expenditure. Therefore, our data are not consistent with the hypothesis that increased resting energy expenditure in sickle cell anemia is directly related to erythropoietic activity. The mechanisms by which resting energy expenditure increases after transfusion in sickle cell anemia require additional investigation.

Adolescent↗
PubMed2005

Cell type-specific regulation of RE-1 silencing transcription factor (REST) target genes.

RE-1 silencing transcription factor (REST) is a transcriptional repressor that represses neuronal gene transcription in non-neuronal cells. REST target genes are expressed in neurons and in neuroendocrine cells. Here, we show that treatment with the histone deacetylase inhibitor trichostatin A (TSA) or expression of a mutant of REST (DP-REST:ER) that contains a transcriptional activation domain enhanced expression of the REST target genes encoding synaptophysin and secretogranin II in neuronal as well as in neuroendocrine cells. These data indicate that the synaptophysin and secretogranin II genes are similarly regulated in neuronal and neuroendocrine cells. In contrast, expression of the connexin36 gene was inducible by TSA or DP-REST:ER only in pancreatic alpha and beta cells, but not in neuronal and pituitary cells, indicating that transcriptional repression by REST functions in a cell type-specific manner. Expression of the BDNF and GluR2 genes, both described as targets of REST, was not induced by either TSA or expression of DP-REST:ER in neuronal or neuroendocrine cells. Chromatin immunoprecipitation experiments using antibodies directed against methylated histone H3Lys4 or H3Lys9 showed a perfect correlation between expression of REST target genes in different cell types and nucleosomal modifications that distinguish active from inactive genes. We conclude that the cell type-specific microenvironment, in particular the cell type-specific structure of the chromatin, is crucial for the ability of REST to control gene transcription.

Adrenocorticotropic Hormone↗