Physical training under the influence of beta blockade in rats: effect on adrenergic responses.

Rats were trained by daily swimming or running exercises with and without daily propranolol injections. Both training methods resulted in cardiac enlargement, but only swimming exercise caused hypertrophy of the brown adipose tissue. These changes were antagonized by beta blockade. The size of the adrenals reflected the stress of the treatments, but other known stress parameters, such as the size of the thymus or sexual organs dit not. Only swimming training without beta blockade sensitized the rats to the calorigenic action of noradrenaline. The cooling rate of the rats in water, when taking into account the insulative capacity of the body, was decreased in swimming-trained as well as in propranolol-treated rats but increased in running-trained rats. The latter two changes may be due to circulatory alterations, while the delayed body cooling in swimming-trained rats probably results from increased heat production capacity. Training-induced resting bradycardia and enhanced tachycardic response to isoprenaline were observable only in the animal groups trained without beta blockade. The pressor response to noradrenaline tended to be higher in the trained groups and the propranolol-treated group than in the controls and was smaller in the animal groups trained under the influence of beta blockade. On the other hand, the hypotonic response to isoprenaline was smaller in the propranolol-treated and running-trained animals. The results emphasize the importance of the sympathetic nervous system in the adaptation of an organism to physical training.     

Is exhaustive training adequate preparation for endurance performance?

Our purpose was to test the significance of exhaustive training in aerobic or endurance capacity. The extent of adaptations to endurance training was evaluated by assessing the increase in physical performance capability and oxidative markers in the organs of rats trained by various exercise programs. Rats were trained by treadmill running 5 days.week-1 at 30 m.min-1 for 8 weeks by one of three protocols: T1-60 min.day-1; T2-120 min.day-1; and T3-120 min.day-1 (3 days.week-1) and to exhaustion (2 days.week-1). Groups T2 and T3 ran for longer than T1 in an endurance exercise test (P less than 0.05), in which the animals ran at 30 m.min-1 to exhaustion; no difference was observed between groups T2 and T3. All 3 trained groups showed a similar increase (20-27%) in the fast-twitch oxidative-glycolytic (FOG) fibers with a concomitant decrease in the fast-twitch glycolytic (FG) fiber population in gastrocnemius (p less than 0.05). The capillary supply in gastrocnemius increased with the duration of exercise (p less than 0.05): no difference was found between groups T2 and T3. Likewise, no distinction was seen between groups T2 and T3 in the increase in succinate dehydrogenase activity in gastrocnemius and the heart. These results suggest that the maximal adaptive response to endurance training does not require daily exhaustive exercise.     

Vasopressin accelerates appetitive discrimination learning and impairs its reversal

Rats were trained in a semi-automated Y maze to find food at the end of the lighted arm. Those treated with 10 μ g lysine vasopressin, 90 min before training learned the response to a $\text{9}\text{10}$ correct choice criterion significantly faster than saline treated animals. There was no difference in rate of forgetting between the treatment groups, as evidenced by a retention test, 3 weeks after training. There was no direct effect of vasopressin on retrieval, since animals treated before the retention test performed at the same level as non treated animals. Finally, vasopressin impaired reversal from light to dark. In a second experiment, the acquisition facilitation seen in Exp. I was replicated, but there was no effect of the treatment on animals trained to dark S_D. However, the impairment seen in Exp. I when vasopressin treated animals, trained to light, were reversed to dark, was replicated in this experiment in animals trained to dark and reversed to light.Previous demonstrations of vasopressin facilitation of learning and memory have, with few exceptions, relied on shock avoidance tasks. The present experiments demonstrate a reliable facilitation of appetitive learning by vasopressin. The fact that vasopressin impairs reversal may be due to an increased tendency to perseverate.     

Exercise training induces glycogen sparing during exercise by old rats

Glycogen utilization during exercise appears to be related to muscle respiratory capacity. Since the decline in hindlimb muscle respiratory capacity that occurs in rats during old age is eliminated when young and old rats undergo an identical exercise training protocol, liver and gastrocnemius glycogen concentrations were determined in identically trained young and old Fischer 344 rats at rest and immediately after a 30-min run requiring approximately 75% of maximal O2 consumption. These values were also compared with untrained age-matched control animals. The animals, which were 10 or 24 mo old after 6 mo of training, were fasted for 24 h before they were killed. Resting gastrocnemius glycogen did not differ among the groups. After 30 min of running, gastrocnemius glycogen was lower in the untrained than the trained groups and was not different between the trained groups. Resting liver glycogen was lower in the old trained group than the untrained groups but not statistically different from the young trained group. The postrun liver glycogen did not differ among the groups. Estimated gastrocnemius and liver glycogen utilization during exercise was decreased in both trained groups compared with untrained age-matched controls. These results indicate that the training-induced glycogen sparing during exercise of the same relative intensity was not diminished with age in identically trained young and old rats.     

Endurance exercise training increases insulin responsiveness in isolated adipocytes through IRS/PI3-kinase/Akt pathway.

Endurance exercise training promotes important metabolic adaptations, and the adipose tissue is particularly affected. The aim of this study was to investigate how endurance exercise training modulates some aspects of insulin action in isolated adipocytes and in intact adipose tissue. Male Wistar rats were submitted to daily treadmill running (1 h/day) for 7 wk. Sedentary age-matched rats were used as controls. Final body weight, body weight gain, and epididymal fat pad weight did not show any statistical differences between groups. Adipocytes from trained rats were smaller than those from sedentary rats (205 +/- 16.8 vs. 286 +/- 26.4 pl; P < 0.05). Trained rats showed decreased plasma glucose (4.9 +/- 0.13 vs. 5.3 +/- 0.07 mM; P < 0.05) and insulin levels (0.24 +/- 0.012 vs. 0.41 +/- 0.049 mM; P < 0.05) and increased insulin-stimulated glucose uptake (23.1 +/- 3.1 vs. 12.1 +/- 2.9 pmol/cm(2); P < 0.05) compared with sedentary rats. The number of insulin receptors and the insulin-induced tyrosine phosphorylation of insulin receptor-beta subunit did not change between groups. Insulin-induced tyrosine phosphorylation insulin receptor substrates (IRS)-1 and -2 increased significantly (1.57- and 2.38-fold, respectively) in trained rats. Insulin-induced IRS-1/phosphatidylinositol 3 (PI3)-kinase (but not IRS-2/PI3-kinase) association and serine Akt phosphorylation also increased (2.06- and 3.15-fold, respectively) after training. The protein content of insulin receptor-beta subunit, IRS-1 and -2, did not differ between groups. Taken together, these data support the hypothesis that the increased adipocyte responsiveness to insulin observed after endurance exercise training is modulated by IRS/PI3-kinase/Akt pathway.     

Physical training under the influence of beta-blockade in rats. II. Effects on vascular reactivity.

Rats were treated by daily swimming or running exercises for 7 weeks. One group of rats was also trained under the influence of propranolol, while another group received daily propranolol injections only. The rat groups trained without beta blockade maintained a higher tail skin temperature when exposed to 5 degrees C after the 7-week training period. This phenomenon was not observable in the animals having received their training under the influence of beta-blockade. Both rat groups trained without beta-blockade showed increased vasodilatatory response to isoprenaline, as judged from a higher elevation of the tail skin temperature in response to the drug. This response was absent in the animal group having performed its training periods under the influence of propranolol. After the injection of phenylephrine the trained rats had a higher tail skin temperature than did the controls or propranolol-treated rats. The present results suggest an elevated sensitivity of beta 2-adrenoceptors and/or decreased sensitivity of alpha-adrenoceptors in trained rats. It is suggested that for the development of these changes repeated activation of the sympathetic nervous system by exercise periods is needed. That is why they are preventable if the training is performed under the influence of beta-blockade.     

Impact of the training program on lipid profile and cardiac health

The aim of this study was to investigate the effects of training programs on serum lipid profile and myocardial oxidative stress. Male Wistar rats (2 mo-old) were divided into three groups (n = 8): sedentary (S), loadless trained (T) and trained-overload 2% body weight (TL). T and TL were trained through swimming for 9 weeks. T and TL rats had increased myocardial lipoperoxide (TBA) and lipid hydroperoxide (HP), whereas HP was higher in TL than in T animals. Superoxide dismutase (SOD) activities were lowest in TL. Myocardial glutathione peroxidase (GSH-Px) was lower in TL than in T and S rats. TL decreased HDL-cholesterol and increased LDL-cholesterol. The serum lactate dehydrogenase and TBA were increased, while SOD and GSH-Px activities were decreased in TL rats. Loadless training was able to improve HDL-cholesterol and to reduce LDL-cholesterol. In conclusion, the loadless training program induced beneficial effects on lipid profile, while overload training induced dyslipidemic profile that was associated with serum oxidative stress. The overload training program was deleterious relative to loadless training program, increasing myocardial oxidative stress.     

Interorgan cooperativity in carnitine metabolism in the trained state

This study was designed to evaluate the effects of chronic exercise training on carnitine acetyl- and palmitoyltransferase activity and the distribution of carnitine forms and concentrations in various organs and tissues of female rats. Sprague-Dawley rats were swim trained 6 days/wk and progressed to 75-min swims twice daily (with 3% of their total body weight attached to the medial portion of the tail) at the end of 5 wk of training. Sedentary (S, n = 12) and trained (T, n = 13) animals were killed by decapitation, and the livers, kidneys, hearts, and several skeletal muscle types were removed and immediately frozen in liquid N2 and/or extracted for enzyme activity assays. Blood was collected and plasma was stored frozen. Samples were assayed for free, acid-soluble, and acid-insoluble carnitine. Free carnitine increased significantly (P less than 0.03) in T hearts. Free carnitine remained unchanged in liver, but short-chain acylcarnitines increased significantly (P less than 0.001). There was a significant (P less than 0.001) reduction in long-chain acylcarnitines in kidney in the trained rats, and plasma short-chain acylcarnitine levels also decreased (P less than 0.001). Several significant changes in carnitine distribution also occurred in the superficial and deep portions of the vastus lateralis and in the mixed gastrocnemius muscles. There was a significant reduction in carnitine acetyltransferase activity with training in both the soleus (P less than 0.02) and superficial gastrocnemius (P less than 0.002) muscles. The deep portion of the gastrocnemius muscle contained significantly higher activity than either the superficial portion or the soleus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolonged decrease of adipocyte size after rosiglitazone treatment in high- and low-fat-fed rats

Objective: The anti‐diabetic thiazolidinediones (TZDs) stimulate adipocyte differentiation and decrease mean adipocyte size. However, whether these smaller, more insulin‐sensitive adipocytes maintain their size after TZD therapy is discontinued has not been studied. Research Methods and Procedures: Adult female Sprague‐Dawley rats were fed a low‐fat (10% fat) diet or, to elevate body weight (BW), a high‐fat (HF) diet (45% fat) for 6 weeks. Rats were initially randomized to groups (n = 12) fed either low‐fat or HF diets, with or without the TZD rosiglitazone (ROSI; 5 mg/kg per day), for 6 weeks. ROSI was then discontinued, and all animals were fed HF for another 6 weeks before sacrifice. Retroperitoneal (RP) adipose tissue morphology was determined from tissue collected by serial biopsies before and after 6 weeks of ROSI treatment and at sacrifice. Results: Measures of BW and adiposity did not differ among groups 6 weeks after stopping ROSI treatment. However, during treatment, ROSI in both diets significantly decreased RP adipocyte size and increased RP DNA content, and these effects continued to be observed after discontinuing treatment. ROSI administration also decreased circulating insulin, leptin, and triglycerides and increased circulating adiponectin levels; however, these effects were reversed on stopping treatment. Discussion: These results demonstrated that TZD‐induced effects on adipocyte size and number were maintained after discontinuing treatment, even with consumption of an obesigenic diet. However, additional studies are needed to determine whether TZD‐treated animals eventually achieve an adipocyte size similar to that of untreated animals at the expense of a higher BW.     

Effects of treatment with coenzyme Q10 on exercised rat aorta

In this study, the effect of long-term supplementation of coenzyme Q10 (CoQ10) on the responses of swim-trained rat aorta was investigated. Twenty-four adult male Wistar rats were divided into four groups: untrained, trained, untrained+CoQ10, and trained+CoQ10 group. In the trained groups rats swam for 60 min/day, five days/week for six weeks. The CoQ10 supplements were administered by intraperitoneal injection at a daily dose of 10 mg·kg-1 of body weight five days/week for six weeks. Swimming of the rats was performed in a container containing tap water. Rats were sacrificed and thoracic aortas were removed for ex vivo analysis after the last swimming session. The aortas were cut into rings 2.5 mm in length. Concentration-response curves for phenylephrine (PHE, 10-9-3×10-4 M) and potassium chloride (KCl, 5-100 mM) were isometrically recorded. The sensitivity and maximal responses to PHE and KCl of aortic rings obtained from trained rats were lower than those of untrained rats. CoQ10 supplementation decreased the responses to both vasoconstrictors in untrained and especially in trained groups. Although neither CoQ10 nor training did affect malondialdehyde (MDA) and protein carbonyl (PC) levels, creatine kinase (CK) activity decreased and superoxide dismutase (SOD) activity increased only with exercise training. Glutathione (GSH) levels increased in CoQ10 supplemented-untrained rats. In conclusion, our results suggest that CoQ10 supplementation may have beneficial effects during exercise.     

Effects of wire-bottom caging on heart rate, activity and body temperature in telemetry-implanted rats

Some experimental procedures are associated with placement of animals in wire-bottom cages. The goal of this study was to evaluate stress-related physiological parameters (heart rate [HR], body temperature [BT], locomotor activity [LA], body weight [BW] and food consumption) in rats under two housing conditions, namely in wire-bottom cages and in bedding-bottom cages. Telemetry devices were surgically implanted in male Sprague-Dawley rats. HR, BT and LA were recorded at 5 min intervals. Analysis under each housing condition was performed from 16:00 to 08:00 h of the following day (4 h light, 12 h dark). During almost all of the light phase, the HR of rats housed in wire-bottom cages remained high (371 ± 35 bpm; mean ± SD; n = 6) and was significantly different from that of rats housed in bedding-bottom cages (340 ± 29 bpm; n = 6; P < 0.001; Student's t-test). In general, BT was similar under the two housing conditions. However, when rats were in wire-bottom cages, BT tended to fluctuate more widely during the dark phase. LA decreased when animals were housed in wire-bottom cages, in particular during the dark phase. Moreover, there was a significant difference with respect to the gain in BW: BW of rats housed in bedding-bottom cages increased 12 ± 2 g, whereas that of rats in wire-bottom cages decreased by 2 ± 3 g (P < 0.001). Our results demonstrate that housing rats in wire-bottom cages overnight leads to immediate alterations of HR, BW and LA, which might be related to a stress response.     

Aerobic training reduces oxidative stress in skeletal muscle of rats exposed to air pollution and supplemented with chromium picolinate

Objective: The purpose of this study was to investigate the effects of chromium picolinate (CrPic) supplementation associated with aerobic exercise using measures of oxidative stress in rats exposed to air pollution.

Methods: Sixty-one male Wistar rats were divided into eight groups: residual oil fly ash (ROFA) exposure and sedentary (ROFA-SED); ROFA exposure, sedentary and supplemented (ROFA-SED-CrPic); ROFA exposure and trained (ROFA-AT); ROFA exposure, supplemented and trained (ROFA-AT-CrPic); sedentary (Sal-SED); sedentary and supplemented (Sal-SED-CrPic); trained (Sal-AT); and supplemented and trained (Sal-AT-CrPic). Rats exposed to ROFA (air pollution) received 50?µg of ROFA daily via intranasal instillation. Supplemented rats received CrPic (1?mg/kg/day) daily by oral gavage. Exercise training was performed on a rat treadmill (5×/week). Oxidative parameters were evaluated at the end of protocols.

Results: Trained groups demonstrated lower gain of body mass (P?P?P?P?=?.0014), although CAT activity did not differ among groups (P?=?.4487).

Conclusion: Air pollution exposure did not lead to alterations in oxidative markers in lungs and heart, and exercise training was responsible for decreasing oxidative stress of the gastrocnemius.     

Secretion and storage of newly synthesized hepatic triacylglycerol fatty acids in vivo in different nutritional states and in diabetes.

Hepatic lipid synthesis was measured in rats in vivo with 3H2O, and the appearance of label in triacylglycerol and its constituent fatty acid and glycerol moieties was determined. In rats treated with Triton WR1339, the amount of newly synthesized fatty acid secreted as very-low-density lipoprotein (VLDL) triacylglycerol was greater during the dark phase of the diurnal cycle than during the light phase (11.3 versus 4.8 mumol of 3H2O/3 h per g of liver respectively). However, the total mass of VLDL triacylglycerol secreted remained constant, as did the amount of label in the secreted triacylglycerol glycerol. Newly synthesized fatty acids comprised only a small proportion of the total VLDL triacylglycerol fatty acids (TGFA) at both times (dark phase, 7.7%; light phase, 2.4%). Starvation for 24 h resulted in a small increase in the secretion of VLDL triacylglycerol. However, the contribution from newly synthesized fatty acids was decreased. Similar effects were observed in streptozotocin-diabetic animals. During the light and dark phases of the cycle, similar quantities of newly synthesized TGFA entered the hepatic cytosol, and these amounts were much smaller than those secreted as VLDL triacylglycerol. The mass of cytosolic triacylglycerol showed a diurnal variation, with a greater concentration during the light phase than in the dark. In diabetes, the mass of triacylglycerol was increased in the cytosol, as was the incorporation of labelled acylglycerol glycerol. Diabetes also abolished the diurnal variation in the quantity of cytosolic triacylglycerol. In each group of animals the specific radioactivity of the microsomal triacylglycerol was similar to that of the respective newly secreted plasma VLDL. The specific radioactivity of the cytosolic triacylglycerol was only 15.8% (dark phase) or 16.8% (light phase) that of the microsomal triacylglycerol. This increased to 35.5% in the starved animals and 40.2% in the diabetic animals.     

Attenuation of exercise-induced heat shock protein 72 expression blunts improvements in whole-body insulin resistance in rats with type 2 diabetes

Heat shock proteins (HSPs) play an important role in insulin resistance and improve the cellular stress response via HSP induction by exercise to treat type 2 diabetes. In this study, the effects of exercise-induced HSP72 expression levels on whole-body insulin resistance in type 2 diabetic rats were investigated. Male 25-week-old Otsuka Long-Evans Tokushima Fatty rats were divided into three groups: sedentary (Sed), trained in a thermal-neutral environment (NTr: 25 °C), and trained in a cold environment (CTr: 4 °C). Exercise training was conducted 5 days/week for 10 weeks. Rectal temperature was measured following each bout of exercise. An intraperitoneal glucose tolerance test (IPGTT) was performed after the training sessions. The serum, gastrocnemius muscle, and liver were sampled 48 h after the final exercise session. HSP72 and heat shock cognate protein 73 expression levels were analyzed by Western blot, and serum total cholesterol, triglyceride (TG), and free fatty acid (FFA) levels were measured. NTr animals exhibited significantly higher body temperatures following exercise, whereas, CTr animals did not. Exercise training increased HSP72 levels in the gastrocnemius muscle and liver, whereas, HSP72 expression was significantly lower in the CTr group than that in the NTr group (p < 0.05). Glucose tolerance improved equally in both trained animals; however, insulin levels during the IPGTT were higher in CTr animals than those in NTr animals (p < 0.05). In addition, the TG and FFA levels decreased significantly only in NTr animals compared with those in Sed animals. These results suggest that attenuation of exercise-induced HSP72 expression partially blunts improvement in whole-body insulin resistance and lipid metabolism in type 2 diabetic rats.     

Muscle respiratory capacity and VO2 max in identically trained young and old rats

Old rats have a decreased hindlimb muscle respiratory capacity and whole-body maximal O2 consumption (VO2 max). The decline in spontaneous physical activity in old rats might contribute to these age-related changes. The magnitude of the age-related decline is not uniform in all skeletal muscle respiratory enzymes, and the decrease in palmitate oxidation is particularly great. This study was designed to determine if young and old rats subjected to the same exercise-training protocol would attain similar values for VO2 max and several markers of muscle respiratory capacity. Four- and 18-mo-old Fischer 344 rats underwent an identical 6-mo program of treadmill running. After training, both age groups had increased VO2 max above sedentary age-matched controls. However, the old trained rats had a lower VO2 max than identically trained young rats. In contrast to VO2 max, the two trained groups attained similar values for gastrocnemius citrate synthase, cytochrome oxidase, 3-hydroxyacyl-CoA dehydrogenase, palmitate oxidation, and total carnitine concentration. Thus, when the young and old rats performed an identical exercise protocol within the capacity of the old animals, differences in skeletal muscle respiratory capacity were eliminated. The dissimilarity in VO2 max between the identically trained groups was apparently caused by age-related differences in factors other than muscle respiratory capacity.     

Hepatic adaptations to iron deficiency and exercise training.

Brooks et al. [Am. J. Physiol. 253 (Endocrinol. Metab. 16): E461-E466, 1987] demonstrated an elevated gluconeogenic rate in resting iron-deficient rats. Because physical exercise also imposes demand on this hepatic function, we hypothesized that exercise training superimposed on iron deficiency would augment the hepatic capacity for amino acid transamination/deamination and pyruvate carboxylation. Sprague-Dawley rats (n = 32) were obtained at weaning (21 days of age) and randomly assigned to iron-sufficient (dietary iron = 60 mg iron/kg diet) or iron-deficient (3 mg iron/kg) dietary groups. Dietary groups were subdivided into sedentary and trained subgroups. Treadmill training was 4 wk in duration, 6 days/wk, 1 h/day, 0% grade. Treadmill speed was initially 26.8 m/min and was decreased to 14.3 m/min over the 4-wk training period. The mild exercise-training regimen did not affect any measured variable in iron-sufficient rats. In contrast, in iron-deficient animals, training increased endurance capacity threefold and reduced blood lactate and the lactate-to-alanine ratio during submaximal exercise by 34 and 27%, respectively. The mitochondrial oxidative capacity of gastrocnemius muscle was increased 46% by training. However, the oxidative capacity of liver was not affected by either iron deficiency or training. Maximal rates of pyruvate carboxylation and glutamine metabolism by isolated liver mitochondria were also evaluated. Iron deficiency and training interacted to increase pyruvate carboxylation by intact mitochondria. Glutamine metabolism was increased roughly threefold by iron deficiency alone, and training amplified this effect to a ninefold increase over iron-sufficient animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endurance exercise training reduces lactate production

In situ muscle stimulation in trained and untrained rats was used to reevaluate whether adaptations induced by endurance exercise training result in decreased lactate production by contracting muscles. The gastrocnemius-plantaris-soleus muscle group was stimulated to perform isotonic contractions. After 3 min of stimulation with 100-ms trains at 50 Hz at 60/min, the increases in lactate concentration in the plantaris, soleus, and fast-twitch red muscle (deep portion of lateral head of gastrocnemius) were only approximately 50% as great in trained as in sedentary rats. In the predominantly fast-twitch white superficial portion of the medial head of the gastrocnemius the increase in lactate concentration was 28% less in the trained than in the sedentary group. The decreases in muscle glycogen concentration seen after 3 min of stimulation at 60 trains/min were smaller in the trained than in the untrained group. The reduction in lactate accumulation that occurred in the different muscles in response to training was roughly proportional to the degree of glycogen sparing. These results show that endurance training induces adaptations that result in a slower production of lactate by muscle during contractile activity.     

Iodoamino acid distribution and weight of the thyroid gland, T4 serum level and T4 metabolism in relation to diet, body fat content and age of rats

Rats were rendered obese by feeding them a fatty diet (HFD, fat: 50% of weight). At the end of the experimental period the animals were divided, also the control rats, which were fed a low-fat diet (LFD, fat: 3% of weight), in light and heavy weight groups. The heavy and obese HFD groups showed, unlike the light LFD-animals, equal absolute but significantly lower relative thyroidal weights. The absolute thyroidal weights of light and heavy animal groups, which received in each case the same diet, were identical, the relative thyroidal weights of the heavy rats on the other hand decreased significantly. The iodoamino acid distribution in the thyroid of rats showed no variation in animals fed various diets and differed in body mass and fat content. The T4 serum levels of the HFD-, in comparison to the LFD-animals increased significantly. Between light and heavy animals in equal diet groups no differences were obtained for the T4 serum values. The serum T3 levels of LFD- and HFD-rats were also equal. The heavy HFD- showed in comparison to the light LFD-animals a significantly lower T4 clearance and in the higher age groups a significantly extended T4 half-life time. The HFD- and LFD-rats with approximately equal body mass and body fat content showed no differences in T4 half-life time and T4 clearance rate depending on diet. A relation between higher body fat content and increased serum T4 levels as a possible adaption to obesity in heavy HFD-rats is discussed. By the comparison of younger and older rats in the most investigated diet and weight groups the older animals showed a decreasing tendency for K and TD/100 g KM and a significant decrease in the clearance rate and in the TD for T4, related to body mass. An influence of diet, body mass or fat content on the decrease of the T4 metabolism of rats with increased age is not evident. The T4 serum levels were not different in dependence on age, but the free T4 serum level was significantly lower in the older rats.     

The effect of anti-hypertensive drug treatment on brown adipocyte diameter and locule distribution in rats

To determine the effects of sympathoplegic anti-hypertensive drug treatment on brown adipose tissue morphology, groups of adult male Wistar-Kyoto (WKY) and spontaneous hypertensive (SHR) rats were orally administered a solution containing 2.3 microM reserpine, 0.5 M hydralazine and 1.68 mM hydrochlorothiazide ad libitum or tap water and brown adipocyte diameter and extent of fat loculization were determined 3 weeks later. Pulse rates of rats were significantly greater in SHR than WKY and were unaffected by treatment, while drug treatment resulted in significant decreases in mean arterial pressure of both groups at the end of the study. Mean adipocyte diameters were smaller in untreated SHR than WKY and drug treatment of both groups was associated with increases in adipocyte diameter and cytological change from physiologically more active to less active cells. These drug-induced alterations in BAT morphology area consistent with decreased sympathetic activity and suggest that thermogenic capacity of brown adipose tissue may be pharmacologically modified, thereby altering an animal's capacity for energy expenditure.