Artificial gravity with ergometric exercise preserves the cardiac, but not cerebrovascular, functions during 4 days of head-down bed rest

Cardiovascular and musculoskeletal deconditioning occurring in long-term spaceflight requires new strategies to counteract these adverse effects. We previously reported that a short-arm centrifuge produced artificial gravity (AG), together with ergometer, has an approving effect on promoting cardiovascular function. The current study sought to investigate whether the cardiac and cerebrovascular functions were maintained and improved using a strategy of AG combined with exercise training on cardiovascular function during 4-day head-down bed rest (HDBR). Twelve healthy male subjects were assigned to a control group (CONT, n=6) and an AG combined with ergometric exercise training group (CM, n=6). Simultaneously, cardiac pumping and systolic functions, cerebral blood flow were measured before, during, and after HDBR. The results showed that AG combined with ergometric exercise caused an increase trend of number of tolerance, however, there was no significant difference between the two groups. After 4-day HDBR in the CONT group, heart rate increased significantly (59±6 vs 66±7 beats/min), while stroke volume (98±12 vs 68±13 mL) and cardiac output (6±1 vs 4±1 L/min) decreased significantly (p<0.05). All subjects had similar drops on cerebral vascular function. Volume regulating hormone aldosterone increased in both groups (by 119.9% in CONT group and 112.8% in the CM group), but only in the CONT group there were a significant changes (p<0.05). Angiotensin II was significantly increased by 140.5% after 4-day HDBR in the CONT group (p<0.05), while no significant changes were observed in the CM group. These results indicated that artificial gravity with ergometric exercise successfully eliminated changes induced by simulated weightlessness in heart rate, volume regulating hormones, and cardiac pumping function and partially maintained cardiac systolic function. Hence, a daily 1h alternating +1.0 and +2.0 Gz with 40 W exercise training appear to be an effective countermeasure against cardiac deconditioning.     

不同强度的体育运动对糖尿病大鼠骨密度及骨代谢的影响

目的:探讨运动强度对糖尿病大鼠骨密度及骨代谢的影响,为糖尿病骨质疏松的预防和治疗提供实验依据。方法:采用一次性腹腔注射链服佐菌素建立糖尿病大鼠模型,随机分为糖尿病对照组、小强度运动组(10 m/min)、中强度运动组(20 m/min)和高强度运动组(30 m/min)。分别于运动前后测定各组大鼠的血糖、骨密度、血清骨钙素(BGP)、碱性磷酸化酶(AKP)、血钙(S-Ca)及血磷(S-P)含量。结果:运动组大鼠血糖均低于训练前和对照组(P0.05)。小强度运动组和高强度运动组大鼠骨密度低于对照组,中强度运动组大鼠骨密度显著高于对照组、小强度运动组和高强度运动组(P0.05);小强度运动组与高强度运动组大鼠骨密度无显著性差异(P0.05)。运动组大鼠BGP和S-P显著升高,AKP下降,差异具有统计学意义(P0.05)。小强度运动组和高强度运动组大鼠S-Ca无显著变化(P0.05);中强度运动组大鼠S-Ca显著升高,且高于小强度运动组和高强度运动组(P0.05)。结论:运动强度对骨密度和骨代谢有一定影响,采取适当的体育运动可提高血清骨钙素含量,改善骨代谢状况,有利于糖尿病骨质疏松症的预防。     

Inactivity, exercise, and visceral fat. STRRIDE: a randomized, controlled study of exercise intensity and amount.

Despite the importance of randomized, dose-response studies for proper evaluation of effective clinical interventions, there have been no dose-response studies on the effects of exercise amount on abdominal obesity, a major risk factor for metabolic syndrome, diabetes, and cardiovascular disease. One hundred seventy-five sedentary, overweight men and women with mild to moderate dyslipidemia were randomly assigned to participate for 6 mo in a control group or for approximately 8 mo in one of three exercise groups: 1) low amount, moderate intensity, equivalent to walking 12 miles/wk (19.2 km) at 40-55% of peak oxygen consumption; 2) low amount, vigorous intensity, equivalent to jogging 12 miles/wk at 65-80% of peak oxygen consumption; or 3) high amount, vigorous intensity, equivalent to jogging 20 miles/wk (32.0 km). Computed tomography scans were analyzed for abdominal fat. Controls gained visceral fat (8.6 +/- 17.2%; P = 0.001). The equivalent of 11 miles of exercise per week, at either intensity, prevented significant accumulation of visceral fat. The highest amount of exercise resulted in decreased visceral (-6.9 +/- 20.8%; P = 0.038) and subcutaneous (-7.0 +/- 10.8%; P < 0.001) abdominal fat. Significant gains in visceral fat over only 6 mo emphasize the high cost of continued inactivity. A modest exercise program, consistent with recommendations from the Centers for Disease Control/American College of Sports Medicine (CDC/ACSM), prevented significant increases in visceral fat. Importantly, a modest increase over the CDC/ACSM exercise recommendations resulted in significant decreases in visceral, subcutaneous, and total abdominal fat without changes in caloric intake.     

Vascular adaptation to deconditioning and the effect of an exercise countermeasure: results of the Berlin Bed Rest study.

Deconditioning is a risk factor for cardiovascular disease. The physiology of vascular adaptation to deconditioning has not been elucidated. The purpose of the present study was to assess the effects of bed rest deconditioning on vascular dimension and function of leg conduit arteries. In addition, the effectiveness of resistive vibration exercise as a countermeasure for vascular deconditioning during bed rest was evaluated. Sixteen healthy men were randomly assigned to bed rest (BR-Ctrl) or to bed rest with resistive vibration exercise (BR-RVE). Before and after 25 and 52 days of strict horizontal bed rest, arterial diameter, blood flow, flow-mediated dilatation (FMD), and nitroglycerin-mediated dilatation were measured by echo Doppler ultrasound. In the BR-Ctrl group, the diameter of the common femoral artery decreased by 13 +/- 3% after 25 and 17 +/- 1% after 52 days of bed rest (P < 0.001). In the BR-RVE group this decrease in diameter was significantly attenuated (5 +/- 2% after 25 days and 6 +/- 2% after 52 days, P < 0.01 vs. BR-Ctrl). Baseline blood flow did not change after bed rest in either group. After 52 days of bed rest, FMD and nitroglycerin-mediated dilatation of the superficial femoral artery were increased in both groups, possibly by increased nitric oxide sensitivity. In conclusion, bed rest deconditioning is accompanied by a reduction in the diameter of the conduit arteries and by an increased reactivity to nitric oxide. Resistive vibration exercise effectively attenuates the diameter decrease of leg conduit arteries after bed rest.     

Effect of rowing ergometry and oral volume loading on cardiovascular structure and function during bed rest

This study examined the effectiveness of a short-duration but high-intensity exercise countermeasure in combination with a novel oral volume load in preventing bed rest deconditioning and orthostatic intolerance. Bed rest reduces work capacity and orthostatic tolerance due in part to cardiac atrophy and decreased stroke volume. Twenty seven healthy subjects completed 5 wk of -6 degree head down bed rest. Eighteen were randomized to daily rowing ergometry and biweekly strength training while nine remained sedentary. Measurements included cardiac mass, invasive pressure-volume relations, maximal upright exercise capacity, and orthostatic tolerance. Before post-bed rest orthostatic tolerance and exercise testing, nine exercise subjects were given 2 days of fludrocortisone and increased salt. Sedentary bed rest led to cardiac atrophy (125 ± 23 vs. 115 ± 20 g; P < 0.001); however, exercise preserved cardiac mass (128 ± 38 vs. 137 ± 34 g; P = 0.002). Exercise training preserved left ventricular chamber compliance, whereas sedentary bed rest increased stiffness (180 ± 170%, P = 0.032). Orthostatic tolerance was preserved only when exercise was combined with volume loading (-10 ± 22%, P = 0.169) but not with exercise (-14 ± 43%, P = 0.047) or sedentary bed rest (-24 ± 26%, P = 0.035) alone. Rowing and supplemental strength training prevent cardiovascular deconditioning during prolonged bed rest. When combined with an oral volume load, orthostatic tolerance is also preserved. This combined countermeasure may be an ideal strategy for prolonged spaceflight, or patients with orthostatic intolerance.     

Low-magnitude whole body vibration with resistive exercise as a countermeasure against cardiovascular deconditioning after 60 days of head-down bed rest

Whole body vibration with resistive exercise is a promising countermeasure against some weightlessness-induced dysfunctions. Our objective was to study whether the combination of low-magnitude whole body vibration with a resistive exercise can prevent the cardiovascular deconditioning induced by a nonstrict 60-day head-down bed rest (Earth Star International Bed Rest Experiment Project). Fourteen healthy men participated in this study. We recorded electrocardiograms and blood pressure waves by means of a noninvasive beat-by-beat measurement system (Cardiospace, integrated by Centre National d'Etudes Spatiales and Astronaut Center of China) during an orthostatic test (20 min of 75-degree head-up tilt test) before and immediately after bed rest. We estimated heart rate, blood pressure, cardiac output, stroke volume, total peripheral resistance, baroreflex sensitivity, and heart rate variability. Low-magnitude whole body vibration with resistive exercise prevented an increase of the sympathetic index (reflecting the sympathovagal balance of cardiac autonomic control) and limited the decrease of the spontaneous baroreflex sensitivity induced by 60 days of head-down bed rest. However, this countermeasure had very little effect on cardiac hemodynamics and did not improve the orthostatic tolerance. This combined countermeasure did not efficiently prevent orthostatic intolerance but prevents changes in the autonomic nervous system associated with cardiovascular deconditioning. The underlying mechanisms remain hypothetical but might involve cutaneous and muscular mechanoreceptors.     

Role of exercise intensity on GLUT4 content,aerobic fitness and fasting plasma glucose in type 2 diabetic mice

Type 2 diabetes mellitus (T2D) results in several metabolic and cardiovascular dysfunctions, clinically characterized by hyperglycaemia due to lower glucose uptake and oxidation. Physical exercise is an effective intervention for glycaemic control. However, the effects of exercising at different intensities have not yet been addressed. The present study analysed the effects of 8 weeks of training performed at different exercise intensities on type 4 glucose transporters (GLUT4) content and glycaemic control of T2D (ob/ob) and non‐diabetic mice (ob/OB). The animals were divided into six groups, with four groups being subjected either to low‐intensity (ob/obL and ob/OBL: 3% body weight, three times/week/40 min) or high‐intensity (ob/obH and ob/OBH: 6% body weight, three times per week per 20 min) swimming training. An incremental swimming test was performed to measure aerobic fitness. After the training intervention period, glycaemia and the content of GLUT4 were quantified. Although both training intensities were beneficial, the high‐intensity regimen induced a more significant improvement in GLUT4 levels and glycaemic profile compared with sedentary controls (p < 0·05). Only animals in the high‐intensity exercise group improved aerobic fitness. Thus, our study shows that high‐intensity training was more effective for increasing GLUT4 content and glycaemia reduction in insulin‐resistant mice, perhaps because of a higher metabolic demand imposed by this form of exercise. Copyright © 2015 John Wiley & Sons, Ltd.     

The Effect of Exercise on Platelet Aggregability and Lipid Peroxidation

The effects of single bicycle ergometric exercises of a moderate or high intensity on platelet ADP-dependent aggregation, content of malonic dialdehyde (MDA), and activity of catalase were studied in young men with relatively high working capacities. Platelet aggregability either increased or decreased in response to the exercise. Hyperaggregation was recorded in about two-thirds of the subjects and hypoaggregation, in one-third. Changes in the aggregation parameters correlated with their basal values at rest. Muscular activity raised the aggregability of platelets when it was initially low and lowered it when it was initially high. An increased intensity of exercise made these correlations stronger. The exercise-caused changes in the MDA content in platelets also correlated with its basal level. A low MDA content at rest increased, and an initially high MDA content decreased. The response of hypoaggregation was associated with moderate and strong correlations between the basal content of MDA and catalase activity in platelets and the exercise-induced changes in the MDA content and platelet aggregability. It was concluded that a high basal level of MDA in platelets is a factor decreasing platelet aggregability during muscular activity.     

Clinical evaluation of four study protocols with 99mTc-methoxyisobutylisonitrile and SPECT for detecting diseased coronary vessels

Different techniques have been suggested for coronary artery disease (CAD) detection with single-photon emission computed tomography (SPECT) and 99mTc-methoxyisobutylisonitrile (99mTc-MIBI). We evaluated four protocols employing myocardial SPECT with 99mTc-MIBI in separate groups of patients. The first involved stress and rest studies performed on separate days, whereas the other three involved "same day" studies. Group 1 (n = 23) was examined in separate sessions, after ergometric exercise and at rest. Group 2 (n = 24) was first injected after dipyridamole infusion, then injected again at rest after completion of the stress study. Group 3 (n = 24) was first injected at rest and imaged one hour later. Afterwards an ergometric stress was performed, with injection at peak exercise. The inverse sequence was adopted for group 4 (n = 24). All patients underwent coronary angiography. For all groups and vessels, the sensitivity and specificity for diseased coronary artery identification were not statistically different. Studies using the new myocardial perfusion tracer 99mTc-MIBI may therefore be completed on the same day or on separate days according to laboratory and patient needs. Dipyridamole iv infusion proved to be as effective as ergometric exercise for diseased coronary artery identification.     

Blood lipid profile and myocardial superoxide dismutase in swim-trained young and middle-aged rats: comparison between left and right ventricular adaptations to oxidative stress

Region-wise interactive effects of age, swim intensity, and duration on exercise performance in the myocardium and serum lipid profile in young (4 months) and middle-aged (12 months) rats were examined. Animals were allocated to the sedentary control (SE-C) or one of the nine trainee groups. Swim training was for 6 days/week and for 4 weeks at 3 durations (20, 40, and 60 min/day) and intensities (2%, low; 3%, medium; 5%, high). Swim velocity and external work showed an age-related decline with low-intensity of 20 min/day in the middle aged. Reduction in serum cholesterol, low-density lipoproteins (LDLs), and triglycerides were accompanied by elevated levels in high-density lipoprotein in the low-to-moderately trained ones for 20 and 40 min/day. Training at 2%, intensity for 20 min/day was sufficient to alter the blood lipid profile and improve swim performance, and endurance in terms of blood lactate. A concomitant increase in Mn-superoxide dismutase (Mn-SOD) activity and reduced malondialdehyde in the left ventricle (LV) and right ventricle (RV) were evident. Lipofuscin was higher in the LV compared to RV. Our results reflect the minimization of free radical generation through appropriate exercise protocols. Our findings on improved blood lipid profile could be related to lower free radicals, which would otherwise oxidize LDLs. Further, swim training when initiated in the young and middle age for as low as 20 min/day at 2% intensity improves the Mn-SOD in the LV and RV. However, the adaptive response of the LV was weaker when compared to the RV, more so in the middle aged.     

Contribution of social isolation, restraint, and hindlimb unloading to changes in hemodynamic parameters and motion activity in rats

The most accepted animal model for simulation of the physiological and morphological consequences of microgravity on the cardiovascular system is one of head-down hindlimb unloading. Experimental conditions surrounding this model include not only head-down tilting of rats, but also social and restraint stresses that have their own influences on cardiovascular system function. Here, we studied levels of spontaneous locomotor activity, blood pressure, and heart rate during 14 days under the following experimental conditions: cage control, social isolation in standard rat housing, social isolation in special cages for hindlimb unloading, horizontal attachment (restraint), and head-down hindlimb unloading. General activity and hemodynamic parameters were continuously monitored in conscious rats by telemetry. Heart rate and blood pressure were both evaluated during treadmill running to reveal cardiovascular deconditioning development as a result of unloading. The main findings of our work are that: social isolation and restraint induced persistent physical inactivity, while unloading in rats resulted in initial inactivity followed by normalization and increased locomotion after one week. Moreover, 14 days of hindlimb unloading showed significant elevation of blood pressure and slight elevation of heart rate. Hemodynamic changes in isolated and restrained rats largely reproduced the trends observed during unloading. Finally, we detected no augmentation of tachycardia during moderate exercise in rats after 14 days of unloading. Thus, we concluded that both social isolation and restraint, as an integral part of the model conditions, contribute essentially to cardiovascular reactions during head-down hindlimb unloading, compared to the little changes in the hydrostatic gradient.     

Exercise prescription and thrombogenesis

Lifestyle habits, such as exercise, may significantly influence risk of major vascular thrombotic events. The risk of primary cardiac arrest has been shown to transiently increase during vigorous exercise, whereas regular moderate-intensity exercise is associated with an overall reduced risk of cardiovascular diseases. What are the mechanisms underlying these paradoxical effects of vigorous exercise versus exercise training on thrombotic modification? This review analyzes research regarding effects and their underlying mechanisms of acute exercise, endurance training, and deconditioning on platelets, coagulation, and fibrinolysis. Evidence suggests that (i) light, acute exercise ( < or = 49% VO(2 max)) does not affect platelet reactivity and coagulation and increases fibrinolytic activity; (ii) moderate, acute exercise (50 to approximately 74% VO(2 max)) suppresses platelet reactivity and enhances fibrinolysis, which remains unchanged in the coagulation system; and, (iii) strenuous, acute exercise ( > or = 75% VO(2 max)) enhances both platelet reactivity and coagulation, simultaneously promoting fibrinolytic activity. Therefore, moderate exercise is likely a safe and effective exercise dosage for minimizing risk of cardiovascular diseases by inducing beneficial anti-thrombotic changes. Moreover, moderate-intensity exercise training reduces platelet reactivity and enhances fibrinolysis at rest, also attenuating enhanced platelet reactivity and augmenting hyper-fibrinolytic activity during strenuous exercise. However, these favorable effects of exercise training on thrombotic modification return to a pre-training state after a period of deconditioning. These findings can aid in determining appropriate exercise regimes to prevent early thrombotic events and further hinder the cardiovascular disease progression.     

Application of determined NT-proBNP in physical standardized exercise

Natriuretic peptides can be used as markers of heart failure, its severity and also in the differential diagnosis of dyspnea. Moreover, the dynamics of natriuretic peptides in physical standardized exercise may be used in the assessment of latent heart failure. AIM OF THE STUDY: Can determination of NT-proBNP be used in the diagnosis of exercise-induced ischemia or latent heart failure? 18 probands (10 men, 8 women) under study were risk persons with unspecified ECG, without signs of manifest heart failure. They were subjected to ergometric bike exercises up to the subjective maximum, SPECT myocardium with estimated ejection fraction of the left ventricle at peak ergometric exercise. The following parameters were followed-up: a) before ergometric exercise: NT-proBNP, CRP, TNF-alpha, Hb, Htc, lactate b) at subjective maximum: NT-proBNP, Hb, Htc, lactate c) 30 min after stopping the exercise: NT-proBNP d) 60 min after stopping the exercise: NT-proBNP. The volume blood changes were taken into account (estimation from the dynamics of Htc, Hb with calculation of metabolic changes of NT-proBNP). To evaluate the dynamics of NT-proBNP, the group was divided into subgroups according to the results obtained in ergometric exercises. RESULTS: initial values of NT-proBNP within normal limits (< 59 pmol/l, 500 ng/l) in 94%, the submaximal pulse rate was reached in 94%, ischemic changes in ECG were observed in 59%, typical clinical signs of heart ischemia were recorded in 35%. Signs of heart dysfunction according to SPECT were found in 47% and ischemic symptoms were observed in 43%. In general, the plasmatic volume decreased by 24% at maximal exercise. Lactate concentration in the plasma increased in all cases. Conversion of NT-proBNP into volume blood changes revealed that increased NT-proBNP occurred only in 22%. Differences between NT-proBNP before exercises and at maximal exercise prior and after correction into volume blood changes were statistically insignificant. 30 and 60 min after the exercise, no significant differences were found in NT-proBNP concentrations. Dividing into subgroups according to the results of ergometric exercises, showed no significant differences in NT-proBNP concentrations. Dynamics of NT-proBNP changes during and after ergometric exercises cannot be used for the diagnosis of exercise-induced heart failure. The high stability of NT-proBNP related to physical activity was confirmed.     

Salt-loading and simulated microgravity on baroreflex responsiveness in rats

Cardiovascular adaptations observed during exposure to microgravity results in impairment of baroreflex activity partially as a result of fluid and electrolyte shifts. The head-down tilt rat model mimics some of the physiological observations that have been made in astronauts. We examined the effects of salt-loading on baroreflex activity after 7 day simulated microgravity (30 degrees tail-suspension) and the subsequent 6 hr post-suspension in Sprague-Dawley (SD) rats, using low salt (0.3% NaCl) and high salt (8% NaCl) diets. In suspended animals on a low salt diet, the baroreflex response curve was shifted to the left, while the heart rate (HR) range and MAP50 values were reduced compared to their parallel tethered, non-suspended controls. For non-suspended animals, salt-loading shifted the curve to the right with a reduced HR range. In salt-loaded, suspended animals, the curve and its parameters resemble those of non-suspended animals on a low salt diet. In summary, these data have demonstrated that a short-term (seven days) simulated weightlessness may elicit cardiovascular deconditioning in rats after release from the simulation manifested as an altered responsiveness in baroreceptor-heart rate reflex and a lowered blood pressure while the rats are tethered and horizontal. Our results also suggest the counteracting effect of salt loading on cardiovascular deconditioning.     

WISE 2005: chronic bed rest impairs microcirculatory endothelium in women

Sedentary behavior has deleterious effects on the cardiovascular system, including reduced endothelial functions. A 2-mo bed rest study in healthy women [women international space simulation for exploration (WISE) 2005 program] presented a unique opportunity to analyze the specific effects of prolonged inactivity without other vascular risk factors on the endothelium. We investigated endothelial properties before and after 56 days of bed rest in 8 subjects who performed no exercise (control group: No-EX) and in 8 subjects who regularly performed treadmill exercise in a lower body negative pressure chamber as well as resistance exercise (countermeasure group, EX). A functional evaluation of the microcirculation in the skin was assessed with laser Doppler. We studied endothelium-dependent and -independent vasodilation using iontophoresis of acetylcholine and sodium nitroprusside, respectively. We also measured circulating endothelial cells (CECs), an index of endothelial damage. In the No-EX group, endothelium-dependent vasodilation was significantly reduced (35.4 +/- 4.8% vs. 24.1 +/- 3.8%, P < 0.05) by bed rest with a significant increase in the number of CECs (3.6 +/- 1.4 vs. 10.6 +/- 2.7 ml(-1), P < 0.05). In the EX group, endothelium-dependent vasodilation and number of CECs were preserved. Our study shows that in humans prolonged bed rest causes impairment of endothelium-dependent function at the microcirculatory level, along with an increase in circulating endothelial cells. Microcirculatory endothelial dysfunction might participate in cardiovascular deconditioning, as well as in several bed rest-induced pathologies. We therefore conclude that the endothelium should be a target for countermeasures during periods of prolonged deconditioning.     

Effects of Exercise Intensity on Spatial Memory Performance and Hippocampal Synaptic Plasticity in Transient Brain Ischemic Rats

Memory impairment is commonly noted in stroke survivors, and can lead to delay of functional recovery. Exercise has been proved to improve memory in adult healthy subjects. Such beneficial effects are often suggested to relate to hippocampal synaptic plasticity, which is important for memory processing. Previous evidence showed that in normal rats, low intensity exercise can improve synaptic plasticity better than high intensity exercise. However, the effects of exercise intensities on hippocampal synaptic plasticity and spatial memory after brain ischemia remain unclear. In this study, we investigated such effects in brain ischemic rats. The middle cerebral artery occlusion (MCAO) procedure was used to induce brain ischemia. After the MCAO procedure, rats were randomly assigned to sedentary (Sed), low-intensity exercise (Low-Ex), or high-intensity exercise (High-Ex) group. Treadmill training began from the second day post MCAO procedure, 30 min/day for 14 consecutive days for the exercise groups. The Low-Ex group was trained at the speed of 8 m/min, while the High-Ex group at the speed of 20 m/min. The spatial memory, hippocampal brain-derived neurotrophic factor (BDNF), synapsin-I, postsynaptic density protein 95 (PSD-95), and dendritic structures were examined to document the effects. Serum corticosterone level was also quantified as stress marker. Our results showed the Low-Ex group, but not the High-Ex group, demonstrated better spatial memory performance than the Sed group. Dendritic complexity and the levels of BDNF and PSD-95 increased significantly only in the Low-Ex group as compared with the Sed group in bilateral hippocampus. Notably, increased level of corticosterone was found in the High-Ex group, implicating higher stress response. In conclusion, after brain ischemia, low intensity exercise may result in better synaptic plasticity and spatial memory performance than high intensity exercise; therefore, the intensity is suggested to be considered during exercise training.     

Long-term bed rest-induced reductions in stroke volume during rest and exercise: cardiac dysfunction vs. volume depletion.

Long-term head-down-tilt bed rest (HDT) causes cardiovascular deconditioning, attributed to reflex dysfunctions, plasma volume reduction, or cardiac impairments. Our objective with the present study was to evaluate the functional importance and relative contribution of these during rest and exercise in supine and upright postures. We studied six subjects before (baseline), during [days 60 (D60) and 113 (D113)], and after [recovery days 0 (R0), 3 (R3), and 15 (R15)] 120 days of -6 degrees HDT. We determined cardiac output, stroke volume (SV), mean arterial pressure, and heart rate during rest and exercise in supine and upright postures. Cardiac output and SV decreased significantly in all four conditions, but the time courses differed for rest and exercise. Upright resting SV was decreased by 24 +/- 9% at D60 compared with baseline but had recovered already at R3. Supine exercise SV decreased more slowly (by 5 +/- 8% at D60 and by 18 +/- 4% at D113) and recovered more slowly after HDT termination. Steady-state mean arterial pressure showed no changes. Heart rate had increased by 18 +/- 4% at D60 and had recovered partially at R3. Our data indicate that long-term HDT causes both a rapid, preload-dependent reduction in SV, most evident during rest in the upright position, and a more slowly developing cardiac dysfunction, most evident during supine exercise. However, the ability to maintain blood pressure and to perform sustained low levels of dynamic exercise is not influenced by HDT.     

Effects of chronic and acute training on glucocorticoid receptors concentrations in rats

The effects of chronic endurance training and acute exercise on glucocorticoid receptors were investigated in rats. For chronic endurance training, rats were exposed to progressive running training on a motor-driven treadmill for 3, 5 and 7 weeks, twice a day and 6 days a week. The samples were taken, 34-36 hours after the last exercise bout. Some of the 7-week training rats were killed by decapitation 7 days following the last exercise bout. The glucocorticoid receptors in hepatic cytosol in 5-week and 7-week rats decreased as compared to the sedentary control. There was no significant difference between the glucocorticoid receptors in hepatic cytosol in some of the 7-week rats those who had stopped training for 7 days and those in the controls. The chronic endurance training did not lead to change of the apparent dissociation constant (Kd). The changes of glucocorticoid receptors after acute exercise have also been investigated and it showed profound decreases of glucocorticoid receptors in renal and myocardial cytosol in low intensity (swimming without an extra weight for 60 minutes) and high intensity (swimming with a weight equal to 6% of body mass for 60 minutes) training groups. The decreases in glucocorticoid receptors in renal and myocardial cytosol were less prominent after low intensity training. These results demonstrated that both acute exercise training and chronic endurance training could lead to a decrease in glucocorticoid receptors, which was in a training intensity- and training load volume-dependent manner, and the changes in glucocorticoid receptors during exercise training were reversible.     

Work capacity during 30 days of bed rest with isotonic and isokinetic exercise training

The purpose was to test the hypothesis that twice daily, short-term, variable intensity isotonic and intermittent high-intensity isokinetic leg exercise would maintain peak O2 uptake (VO2) and muscular strength and endurance, respectively, at or near ambulatory control levels during 30 days of -6 degrees head-down bed rest (BR) deconditioning. Nineteen men (aged 32-42 yr) were divided into no exercise control (peak VO2 once/wk, n = 5), isokinetic (Lido ergometer, n = 7), and isotonic (Quinton ergometer, n = 7) groups. Exercise training was conducted in the supine position for two 30-min periods/day for 5 days/wk. Isotonic training was at 60-90% of peak VO2, and isokinetic training (knee flexion-extension) was at 100 degrees/s. Mean (+/- SE) changes (P less than 0.05) in peak VO2 (ml.m-1.kg-1) from ambulatory control to BR day 28 were 44 +/- 4 to 36 +/- 3, -18.2% (3.27-2.60 l/m) for no exercise, 39 +/- 4 to 40 +/- 3, +2.6% (3.13-3.14 l/min) for isotonic, and 44 +/- 3 to 40 +/- 2, -9.1% (3.24-2.90 l/min) for isokinetic. There were no significant changes in any groups in leg peak torque (right knee flexion or extension), leg mean total work, arm total peak torque, or arm mean total work. Mean energy costs for the isotonic and isokinetic exercise training were 446 kcal/h (18.8 +/- 1.6 ml.min-1.kg-1) and 214 kcal/h (8.9 +/- 0.5 ml.m-1.kg-1), respectively. Thus near-peak, variable intensity, isotonic leg exercise maintains peak VO2 during 30 days of BR, while this peak, intermittent, isokinetic leg exercise protocol does not.     

Vascular adaptation to 4 wk of deconditioning by unilateral lower limb suspension

Physical inactivity or deconditioning is an independent risk factor for atherosclerosis and cardiovascular disease. In contrast to exercise, the vascular changes that occur as a result of deconditioning have not been characterized. We used 4 wk of unilateral lower limb suspension (ULLS) to study arterial and venous adaptations to deconditioning. In contrast to previous studies, this model is not confounded by denervation or microgravity. Seven healthy subjects participated in the study. Arterial and venous characteristics of the legs were assessed by echo Doppler ultrasound and venous occlusion plethysmography. The diameter of the common and superficial femoral artery decreased by 12% after 4 wk of ULLS. Baseline calf blood flow, as measured by plethysmography, decreased from 2.1 +/- 0.2 to 1.6 +/- 0.2 ml.min(-1).dl tissue(-1). Both arterial diameter and calf blood flow returned to baseline values after 4 wk of recovery. There was no indication of a decrease in flow-mediated dilation of the superficial femoral artery after ULLS deconditioning. This means that functional adaptations to inactivity are not simply the inverse of adaptations to exercise. The venous pressure-volume curve is shifted downward after ULLS, without any effect on compliance. In conclusion, deconditioning by 4 wk of ULLS causes significant changes in both the arterial and the venous system.