Does endurance running before orchidectomy prevent osteopenia in rats?

This experiment was performed to study the effects on femoral bone of endurance training performed during the 3 months before orchidectomy in rats which were then killed 90 days later. A total of 70 male Wistar rats were used at 8 weeks old. One day 0 of the experiment, 10 rats were killed by cervical dislocation and used as first controls. Among the 60 others, 30 were selected for treadmill running (60% maximal oxygen uptake, 1 h x day(-1), 6 days x week(-1) for 90 days). The 30 other rats remained at rest. On day 90, 10 exercised (IE) and resting (IR) rats were killed and used as intermediary controls. Among the 20 other animals of each group, 10 were surgically castrated (CXE, CXR) or 10 sham-operated (SHE, SHR) and killed on day 180. On day 90 femoral failure load (three-point bending test) was greater in IE than in IR. Simultaneously, the deoxypyridinolinuria was lower in IE than in IR. On day 180, femoral bones were thinner in CXR than in CXE. The lowest values for trabecular bone are in the distal femoral metaphysis were measured in CXE and CXR rats, but the value measured in CXE was no different from that measured in SHR. Simultaneously total femoral bone density was lower in CXR than in SHE, while no difference concerning femoral metaphyseal density was observed between CXE and SHR. These results confirmed that endurance running increased femoral bone growth and modelling and femoral trabecular area, and thereby peak bone mass, in 8-month-old male rats. In resting animals, castrated after the training period, androgen deficiency decreased femoral density, mineral content and trabecular area. This decrease was not observed in castrated but previously exercised rats. Thus, by increasing peak bone mass, it was considered that endurance training may have a preventive effect against orchidectomy-induced bone loss.     

High-impact exercise strengthens bone in osteopenic ovariectomized rats with the same outcome as Sham rats.

The effect of jump exercise on middle-aged osteopenic rats was investigated. Forty-two 9-mo-old female rats were either sham-operated (Sham) or ovariectomized (OVX). Three months after surgery, the rats were divided into the following groups: Sham sedentary, Sham exercised, OVX sedentary, and OVX exercised. Rats in the exercise groups jumped 10 times/day, 5 days/wk, for 8 wk, with a jumping height of 40 cm. Less than 1 min was required for the jump training. After the experiment, the right tibia and femur were dissected, and blood was obtained from each rat. OVX rats were observed to have increased body weights and decreased bone mass in their tibiae and femurs. Jump-exercised rats, on the other hand, had significantly increased tibial bone mass, strength, and cortical areas. The bone mass and strength of OVX exercised rats increased to approximately the same extent as Sham exercised rats, despite estrogen deficiency or osteopenia. Our data suggest that jump exercise has beneficial effects on lower limb bone mass, strength, bone mineral density, and morphometry in middle-aged osteopenic rats, as well as in Sham rats.     

Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise.

This study had the following objectives: 1) to determine whether diabetic rats could increase muscle mass due to a physiological manipulation (chronic resistance exercise), 2) to determine whether exercise training status modifies the effect of the last bout of exercise on elevations in rates of protein synthesis, and 3) to determine whether chronic resistance exercise alters basal glycemia. Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half (P < 0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 +/- 0.003 vs. 0.032 +/- 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 +/- 0.068 vs. 0.53 +/- 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P < 0.05) but not in nondiabetic (0.041 +/- 0.0026 vs. 0.042 +/- 0.003 g/cm for sedentary vs. exercised soleus and 0.72 +/- 0.015 vs. 0.69 +/- 0.013 g/cm for sedentary vs. exercised gastrocnemius-plantaris) rats when muscle weight was expressed relative to tibial length or body weight (data not shown). Another group of diabetic rats that lifted heavier weights showed muscle hypertrophy. Rates of protein synthesis were higher in red gastrocnemius in chronically exercised than in sedentary rats: 155 +/- 11 and 170 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in exercised diabetic and nondiabetic rats vs. 110 +/- 14 and 143 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in sedentary diabetic and nondiabetic rats. These elevations, however, were lower than in acutely exercised (but untrained) rats: 176 +/- 15 and 193 +/- 8 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in diabetic and nondiabetic rats. Finally, chronic exercise training in diabetic rats was associated with reductions in basal glycemia, and such reductions did not occur in sedentary diabetic groups. These data demonstrate that, despite lower circulating insulin concentrations, diabetic rats can increase muscle mass in response to a physiological stimulus.     

Water exercise prevents femur density loss associated with ovariectomy in the retired breeder rat

The effect of non-weight-bearing exercise on skeletal bone remains controversial. The objective of this pilot study was to examine the effects of water exercise training on femur density and serum alkaline phosphatase activity in ovariectomized and sham-operated (ovaries left intact) retired breeder rats. Exercised animals swam at progressively increasing duration from 5 minutes to 75 min.d(-1), 5 d.wk(-1), for a 6-week conditioning period. Exercised rats had greater (p < 0.02) soleus muscle citrate synthase activity than sedentary rats, confirming an aerobic training effect. Femur density (g.cm(-3)) was greater (p < 0.0007) for exercised rats than sedentary rats but lower (p < 0.01) for ovariectomized rats compared to sham rats. Serum alkaline phosphatase activity tended (p < 0.06) to be greater for exercised rats compared to sedentary rats. These results indicate that dynamic water-flotation exercise prevents the femur bone loss associated with ovariectomy in rats. We conclude that this form of exercise could be beneficial in maintaining bone density in hormone-deficient postmenopausal women, especially the elderly who may not be able to perform weight-bearing activities.     

Differential response of rat limb bones to strenuous exercise

We examined the influence of a strenuous exercise regimen on tibial and metatarsal bones to show not only how the geometric, histological, and mechanical properties of immature bone respond to strenuous exercise but also how long bones within the same limb may respond differentially to exercise. Female Sprague-Dawley rats (8 wk old) were divided randomly into two groups: a sedentary control (n = 15) and an exercised group (n = 15). The exercise intensity was 80-90% of maximum oxygen capacity 5 days/wk for 10 wk. Mechanical properties of tibia and second metatarsus (MT) were determined with three-point bending, and contralateral bones were used for geometric and histological analyses. Length and middiaphyseal cross-sectional geometry of the exercised tibiae were significantly less than controls, but material properties were not different. The exercised tibiae had significantly lower structural properties (e.g., loads at the proportional limit and maximum and energy at failure load). The middiaphyseal dorsal cortex of exercised MT was significantly thicker than controls, but tensile stress at the proportional limit and elastic modulus of exercised MT were significantly less than controls. The average number of osteons and osteocytes per unit area of the tibial middiaphysis was significantly greater in the exercised group--especially in lateral and posterior cortices. The number of osteons and osteocytes per unit area in the MT, however, was significantly less in the exercised group. The differential effects of strenuous exercise on tibia and MT suggest that local loading and bone-specific responses have important roles in modulating the response of immature bone to strenuous exercise.     

Swim training prevents hyperglycemia in ZDF rats: mechanisms involved in the partial maintenance of beta-cell function

Exercise improves glucose tolerance in obese rodent models and humans; however, effects with respect to mechanisms of beta-cell compensation remain unexplained. We examined exercise's effects during the progression of hyperglycemia in male Zucker diabetic fatty (ZDF) rats until 19 wk of age. At 6 wk old, rats were assigned to 1) basal--euthanized for baseline values; 2) exercise--swam individually for 1 h/day, 5 days/wk; and 3) controls (n = 8-10/group). Exercise (13 wk) resulted in maintenance of fasted hyperinsulinemia and prevented increases in fed and fasted glucose (P < 0.05) compared with sham-exercised and sedentary controls (P < 0.05). Beta-cell function calculations indicate prolonged beta-cell adaptation in exercised animals alone. During an intraperitoneal glucose tolerance test (IPGTT), exercised rats had lower 2-h glucose (P < 0.05) vs. controls. Area-under-the-curve analyses from baseline for IPGTT glucose and insulin indicate improved glucose tolerance with exercise was associated with increased insulin production and/or secretion. Beta-cell mass increased in exercised vs. basal animals; however, mass expansion was absent at 19 wk in controls (P < 0.05). Hypertrophy and replication contributed to expansion of beta-cell mass; exercised animals had increased beta-cell size and bromodeoxyuridine incorporation rates vs. controls (P < 0.05). The relative area of GLUT2 and protein kinase B was significantly elevated in exercised vs. sedentary controls (P < 0.05). Last, we show formation of ubiquitinated protein aggregates, a response to cellular/oxidative stress, occurred in nonexercised 19 wk-old ZDF rats but not in lean, 6 wk-old basal, or exercised rats. In conclusion, improved beta-cell compensation through increased beta-cell function and mass occurs in exercised but not sedentary ZDF rats and may be in part responsible for improved glucoregulation.     

Treadmill running starting 3 months after orchidectomy restores femoral bone mass in rats

The present study was designed to provide data on the effects on femoral bone of endurance training starting only 3 months after orchidectomy in rats. A total of 70 Wistar male rats were used at 8 weeks of age. On day 0 of the experiment, 10 rats were killed by cervical dislocation to be used as first controls. Among the 60 other animals, half was surgically castrated (CX) or sham operated (SH). On day 90, 10 CX and 10 SH were killed and used as intermediary controls (ICX and ISH). Among the other 20 CX and 20 SH, 10 within each group (CXE, SHE) were selected for treadmill running (60% maximal oxygen uptake, 1 h x day(-1), 5 days x week(-1) for 12 weeks). The 20 other rats were used as sedentary controls (CXR, SHR) and killed (as runners) on day 180. On day 90 femoral bone density (BMD) and mineral content (BMC) were lower in ICX than in ISH. On day 180 total femoral BMD was lower in CXR than in CXE. Simultaneously metaphyseal femoral BMD was lower in CXR than in CXE, SHR or SHE. Furthermore, at that time, no significant difference concerning BMD and BMC was observed between SHR and CXE. This would indicate that treadmill running starting only 3 months after orchidectomy is able to restore BMD and BMC to control values, mainly by inhibiting bone resorption (as shown by decreased urinary deoxypyridinoline excretion in CXE) without decreasing osteoblastic activity (evaluated by plasma osteocalcin concentration).     

Influence of exercise on the immune function of rats of various ages

The purpose of this study was to determine whether exercise could prevent the age-related decline in mitogenesis, which has been well documented in rats, mice, and humans. At 1, 6, 12, and 18 mo of age, male Fischer F344 rats were subjected daily to swimming exercise for 6 mo. At the end of the 6-mo training period, spleen lymphocytes were isolated from the exercised rats and from age-matched sedentary controls. The induction of lymphocyte proliferation was measured with the mitogens concanavalin A (ConA) and lipopolysaccharide (LPS). In addition, the ability of the lymphocytes to produce interleukin 2 (IL 2) in response to ConA induction was measured. ConA- and LPS-induced proliferation decreased 41-63% between 7 and 25 mo of age in both exercised and sedentary control rats. ConA-induced IL 2 production decreased 42 and 62% between 7 and 25 mo of age for exercised and sedentary control rats, respectively. Although the age-related decline in mitogen-induced proliferation and IL 2 production was smaller in exercised rats, this was due to a lower level of mitogenesis and IL 2 production in lymphocytes from young exercised rats. Exercise resulted in a significant decrease (23-32%) in mitogen-induced lymphocyte proliferation and IL-2 production in 7-mo-old exercised rats compared with 7-mo-old sedentary rats. However, in the 18- and 24-mo-old rats, mitogen-induced lymphocyte proliferation and IL 2 production was not significantly different between exercised and sedentary control rats.     

Relationship between exercise-induced changes in serum and hepatic cholesterol metabolism in rats

The purpose of the present study was to determine the effects of exercise training on serum cholesterol level and hepatic cholesterol metabolism in rats. Twenty-four male Wistar strain rats, aged 6 weeks, were assigned to one of three experimental groups; control (n = 8), exercised 20 minutes a day (E20, n = 8), and exercised 60 minutes a day (E60, n = 8). Rats were sacrificed after ten weeks exercise. The levels of serum total cholesterol and HDL-cholesterol in the group E20 and group E60 were lower than that of control, 8% and 24% (p less than 0.01) for the total cholesterol and 10% and 24% (p less than 0.05) for the HDL-cholesterol, respectively. The activity of HMG-CoA reductase in liver microsome was significantly higher in the group E60 than that of control. The hepatic microsomal HMG-CoA reductase activity was negatively related to serum total (r = -0.62, p less than 0.01) and HDL (r = -0.58, p less than 0.01) cholesterol levels. From these results, we concluded that the enhancement of the cholesterol metabolism in the liver by exercise is a major course of the exercise-induced change in serum cholesterol of Wistar rats.     

Bones benefits gained by jump training are preserved after detraining in young and adult rats.

We investigated the osteogenic responses to jump training and subsequent detraining in young and adult male rats to test the following hypotheses: 1) jump training has skeletal benefits; 2) these skeletal benefits are preserved with subsequent detraining throughout bone morphometric changes; and 3) there are no differences between young and adult rats during detraining in terms of the maintenance of exercise-induced changes. Twelve-week-old (young) and 44-wk-old (adult) rats were divided into the following four groups: young-sedentary, young-exercised, adult-sedentary, and adult-exercised. The exercised groups performed jump training (height = 40 cm, 10 jumps/day, 5 days/wk) for 8 wk followed by 24 wk of being sedentary. Tibial bone mineral content and bone mineral density in vivo significantly increased with jump training, and the effects were maintained after detraining in both the young and adult exercised groups, although the benefits of training became somewhat diminished. After 24 wk of detraining, the beneficial effects of training on bone mass and strength were preserved and associated with morphometric changes, such as periosteal perimeter, cortical area, and moment of inertia. There were no significant age-exercise interactions in such parameters, except for the periosteal perimeter. These results suggest that there are few differences in bone accommodation and maintenance by training and detraining between young and adult rats.     

Exercise training and its effects with renal hypertensive rats

The influence of endurance training on functional capacity [maximal O2 consumption (VO2 max)], caudal arterial blood pressure, and myocardial capillary density were investigated in normotensive rats and rats made hypertensive using the two-kidney one-clip approach (Goldblatt's hypertension). Male Sprague-Dawley rats were assigned to sham (N: 120-140 mmHg), moderately hypertensive (MH = 0.30-mm clips, 150-170 mmHg), or severely hypertensive (SH = 0.25-mm clips, 190-230 mmHg) groups. Rats designated to be runners (T) were exercised on a motor-driven treadmill equal to 50-70% of their VO2 max values for 8-12 wk. Compared with their nontrained (NT) controls, training was associated with significantly higher VO2 max values (12-15%) and muscle cytochrome-c oxidase activities (33-78%). Resting systolic blood pressure was not significantly changed in the N-and MH-T subgroups; however, it was 20-30 mmHg higher in the SH-T subgroup. Mean absolute heart weight for only the N-T group was significantly heavier than their NT controls. However, the mean predicted heart weights (heart wt = 0.639 X body wt of N-NT + 0.001 g) of the two SH groups were significantly higher than expected. The SH-T group had a lower (11%) subepicardial capillary density mean than its NT control and significantly fewer capillaries in the subendocardial region than the other five subgroups. It was concluded that moderate exercise training appeared to be detrimental to rats with severe hypertension because it increased resting blood pressure and decreased myocardial capillary density, even though it improved their functioning capacity.     

Increased nitric oxide is one of the causes of changes of iron metabolism in strenuously exercised rats

This study was carried out to investigate the possible role of increased nitric oxide (NO) production in the development of the low iron status in strenuously exercised rats. Female Sprague-Dawley rats were randomly assigned to four groups: sedentary (S1), sedentary + nitro-L-arginine methyl ester (L-NAME; S2), exercise (E1), and exercise + L-NAME (E2). Animals in the E1 and E2 groups swam for 2 h/day for 3 mo. L-NAME in the drinking water (1 mg/ml) was administrated to rats in the S2 and E2 groups for the same period. At the end of third month, hematological indexes and nitrite and nitrate (NOx) contents in the plasma and non-heme iron and NOx levels in the liver, spleen, and bone marrow cells were measured. Three months of exercise induced a significant increase in NOx content and a decrease in iron level both in plasma and tissues. Treatment with L-NAME, an inhibitor of NO synthase (NOS), led to a significant decrease in NOx and an increase in iron level both in plasma and tissues in the exercised rats. The E2 group had a significantly lower NOx content as well as a higher iron level both in plasma and tissues than the E1 group. However, the iron contents in the plasma and tissues of the E2 group were still significantly lower than those found in S1. No difference was found in NOx levels between E2 and S1. These findings showed that exercise was associated with elevation in NOx and reduction in iron in plasma and the tissues. Treatment with L-NAME was able to completely inhibit the effect of exercise on NOx as well as partly recover the decreased iron contents in plasma and tissues resulting from exercise. This suggests that the increased production of NO might be one of the causes of the lower iron status in exercised rats.     

Plasma nitric oxide and iron concentrations in exercised rats are negatively correlated

The aim of this study was to investigate the effect of strenuous exercise on plasma nitric oxide and iron (PI) concentrations in rats. The rats were divided into six groups: 3, 6 and 12 months of the exercise (swimming) groups and their corresponding controls. At the end of experimental periods, blood samples were collected to measure plasma NOx (nitrate and nitrite) and iron concentrations and other hematological indices. The correlative analysis of plasma NOx with PI in the exercised and the control rats was performed. The results showed that plasma NOx concentration was significantly greater and PI lower in the 3, 6, and 12 months of the exercise groups compared to their sedentary controls (p < 0.01). However, the duration of strenuous exercise had no significant effect on plasma NOx or PI contents. A negative correlation between plasma NOx and PI levels was found in all three exercise groups (r = -0.750, -0.578, and -0.808 and p < 0.01, 0.05, 0.01 respectively), but not in the sedentary control groups. These results imply that strenuous exercise may lead to an increase in plasma NOx concentration as well as a low iron level. They also suggest the possibility that the increased NO production might be associated with the development of the lower iron status in exercise.     

Influence of 4-week and 8-week exercise training on the pharmacokinetics and pharmacodynamics of intravenous and oral azosemide in rats

Cytochrome P450 expression was determined in the livers of control, 4-week exercised (4WE) and 8-week exercised (8WE) rats. Even though the 4-week and 8-week exercise training caused 53 and 25% increases, respectively, in total cytochrome P450 contents in the liver, exercise training did not cause any changes in the levels of P450 1A2 (which primarily metabolizes azosemide), 2E1 and 3A23 in the liver, as assessed by both Western and Northern blot analyses. Also, exercise training failed to alter the activity of NADPH-dependent cytochrome P450 reductase. The plasma concentrations of norepinephrine and epinephrine were significantly (2 to 3 folds) higher in 4WE rats than in controls, presumably due to physical stress, but the catecholamine levels in 8 WE rats returned to control levels. After intravenous administration (10 mg/kg of azosemide), the amount of unchanged azosemide excreted in 8-h urine (Ae(Azo, 0-8 h)) was significantly greater (46% increase) in 4WE rats than that in control rats. This resulted in a significantly faster (82% increase) renal clearance of azosemide. However, the nonrenal clearances were not significantly different between control and 4WE rats. The significantly greater Ae(Azo, 0-8 h) in 4WE rats was mainly due to a significant increase in intrinsic active secretion of azosemide in renal tubules and not due to a decrease in the metabolism of azosemide. After oral administration (20 mg/kg), Ae(Azo, 0-8 h) was also significantly greater (264%) in 4WE rats and this again was due to a significant increase in intrinsic active renal secretion of azosemide and not due to an increase in gastrointestinal absorption. After both intravenous and oral administration, the 8-h urine output was not significantly different between control and 4WE rats although Ae(Azo, 0-8 h) increased significantly in 4WE rats. This could be due to the fact that the urine output reached a plateau at 10 mg/kg after intravenous administration and 20 mg/kg after oral administration of azosemide to rats and possibly due to increase in plasma antidiuretic hormone levels and aldosterone production in 4WE rats.     

Skeletal effects of zinc deficiency in growing rats.

There is ample evidence that zinc plays an important role in bone metabolism and zinc deficiency has been implicated as a risk factor in the development of osteoporosis. It was the aim of the present study to investigate the skeletal effects of alimentary zinc deficiency in growing rats using quantitative bone histomorphometry. Twenty-four male Sprague Dawley rats with a mean initial body weight of 101 +/- 2 g were allocated in two groups of 12 rats each and had free access to a semi-synthetic, casein-based, zinc-deficient diet (0.76 mg zinc/kg) or to the same diet supplemented with 60 mg zinc per kg. All rats were sacrificed 42 days after the start of the experiment and the right distal femur was removed for bone histomorphometry. Relative to controls (+Zn), the zinc-deficient rats (-Zn) had a significantly lower body weight and about an 80% reduction in plasma and femur zinc concentration. The histomorphometric evaluation of the distal femoral metaphysis showed that zinc deficiency led to a 45% reduction (p < 0.01) in cancellous bone mass and to a deterioration of trabecular bone architecture, with fewer and thinner trabeculae. The osteopenia in -Zn rats was accompanied by significant reductions in osteoid perimeter (-31%, p < 0.05), osteoblast perimeter (-30%, p < 0.05), and osteoclast number (-38%, p < 0.01) relative to +Zn controls. We conclude that zinc deficiency induced low turnover osteopenia in femoral cancellous bone of growing rats. These results support the hypothesis that zinc deficiency during growth may impair the accumulation of maximal bone mass in humans; additionally, they suggest that zinc deficiency may play a role as a risk factor in the pathogenesis of osteoporosis.     

Skeletal sensitivity to dietary calcium deficiency is increased in the female compared with the male rat

We investigated potential sex differences in bone resorption and the conservation of whole body bone mass in 24-week-old Sprague-Dawley rats maintained on a 1.0% calcium diet and then fed diets containing 0.02, 0.5, 1.0, or 1.75% calcium for 31 days. Lowering dietary calcium from 1.00% to 0.02% doubled whole skeleton bone resorption (urinary 3H-tetracycline loss). Female rats were more sensitive to calcium stress, exhibiting the maximal resorptive response when fed the 0.5% calcium diet, whereas the 0.02% calcium diet was required to elicit this response in males. Despite the evidence of increased bone resorption, whole skeleton mass was unchanged in females and was significantly increased in males, indicating that switching to even the 0.02% calcium diet did not result in an overt loss of total body bone mass. Compared with controls, the skeleton mass of females (97+/-1.4%) maintained on the 0.02% calcium diet was significantly lower than males (107+/-2.4%), again suggesting a greater impact of calcium deficiency in females. The calculation of the average percentage growth of selected individual bones in male rats indicated a proportional increase in bone mass between the axial and appendicular skeleton of approximately +4% and +18% in animals maintained on 0.02 and 1.75% diets, respectively. By comparison, female rats consuming the 0.02% calcium diet showed an average 14% loss in axial bone and 7.5% gain in appendicular bone mass. The results indicate increased sensitivity to dietary calcium deficiency in female rats which involves a significant loss in axial bone mass not observed in male rats maintained under similar dietary conditions.     

Time course changes in IGFBP-1 after treadmill exercise and postexercise food intake in rats

Prolonged exercise increases circulating insulin-like growth factor binding protein-1 (IGFBP-1) in humans and animals, but its physiological significance is unknown. This study examined 1) time-course changes in plasma IGFBP-1 and hepatic IGFBP-1 mRNA expression after exercise, 2) changes in IGFBP-1 in relation to plasma glucose, insulin, and IGF-I, and 3) the impact of feeding a postexercise meal on the IGFBP-1 response. Food-deprived male rats were vigorously run on a treadmill and compared with nonexercised controls at 15 min and 1, 4, 8, and 12 h after exercise. Circulating insulin concentrations in exercised rats were lower than in controls at 15 min and 1 h, whereas plasma glucose and IGF-I remained unaffected. Circulating and hepatic expression of IGFBP-1 was markedly increased above that of controls at 15 min, 1 h, and 12 h. In a separate experiment, one-half of the exercised animals received a nutritionally complete meal immediately after the experimental run. The meal elevated plasma insulin and glucose concentrations at 15 min and 1 h. Despite this change in nutritional status, serum IGFBP-1 concentrations and hepatic IGFBP-1 abundance remained elevated at 15 min and 1 h. These results demonstrate that the IGFBP-1 response to a single bout of treadmill exercise is short in duration and independent of insulin, glucose, and amino acid availability.     

Exercise decreases cytosolic aconitase activity in the liver, spleen, and bone marrow in rats

Effects of strenuous exercise on cytosolic aconitase activity (CAA) were investigated in this study. Female Sprague-Dawley rats were randomly assigned to four groups: S1 (Sedentary), S2 (Sedentary + L-NAME [N-nitro-l-arginine methyl ester]), E1 (Exercise), and E2 (Exercise + L-NAME). Rats in the E1 and E2 groups swam for 2 h/day for 3 months. L-NAME (an inhibitor of NOS) in drinking water (1 mg/ml) was administered to rats in the S2 and E2 groups for the same period. At the end of the third month, the CAA in the liver, spleen, and bone marrow cells was measured. In the exercise group (E1), CAA in the liver, spleen, and bone marrow cells was 19.99 +/- 1.49, 1.61 +/- 0.13, and 0.59 +/- 0.09 mU/mg protein, respectively. These values were significantly lower than the corresponding sedentary values in the S1 group (33.96 +/- 1.38, 3.96 +/- 0.19, and 3.20 +/- 0.18 mU/mg protein) (P < 0.01, 0.001, and 0.001, respectively). The treatment of L-NAME led to a significant increase in tissue CAA in the sedentary rats (S2). Also, the significantly higher CAA in the liver, spleen, and bone marrow cells was found in the exercised rats treated with L-NAME (E2) (29.50 +/- 1.27, 2.89 +/- 0.25, and 1.34 +/- 0.20 mU/mg) than without L-NAME (E1) (P < 0.01, 0.01, 0.05, respectively). However, the values in the E2 group were still significantly lower than those in the S1 group (P < 0.05, 0.01, and 0.001, respectively). This indicates that L-NAME treatment can partly recover the decreased CA in tissues in the exercised rats. These results provide evidence for the existence of the increased activity of IRP1 (iron regulatory protein 1) that is probably induced by the increased nitric oxide production in the strenuously exercised rats.     

Changes in membrane fluidity and lipid peroxidation of skeletal muscle mitochondria after exhausting exercise in rats

We studied the effects of exhausting exercise and exercise training on skeletal muscle mitochondrial membrane fluidity and lipid peroxidation in rats. The first part of the study involved 60 untrained rats divided into six equal groups. Of the total number 10 rats were sedentary and acted as controls. The remaining 50 rats exercised to exhaustion and were sacrificed at 0-h, 24-h, 48-h, 72-h, and 96-h post-exercise. The second part of the study involved 40 rats which were divided into four equal groups. Of these 10 rats were sedentary and acted as controls. The remaining 30 rats underwent 8 weeks of exercise training. They were then subjected to a single period of exhausting exercise and were sacrificed at 0-h, 24-h and 48-h post-exercise. Membrane fluidity was measured using the fluorescence polarization method. Lipid peroxidation was estimated by determining the thiobarbituric acid-reactive substances (TBARS) in mitochondria. In the untrained rats, mitochondrial fluorescence polarization and TBARS contents were significantly increased post-exercise compared with the sedentary controls (P < 0.05). They did not return to near control levels until 96 h and 48 h, respectively. In the trained rats, fluorescence polarization was raised compared with the sedentary controls but this was significantly lower than those measured at the same times of the untrained group post-exercise (P < 0.05). Exhausting exercise decreased membrane fluidity and increased lipid peroxidation in rat skeletal muscle mitochondria. These effects were relieved to some extent by exercise training.