Inhibition by a Capsaicin Antagonist (Capsazepine) of Capsaicin-induced Swimming Capacity Increase in Mice

We investigated the endurance swimming capacity of mice injected with CAP antagonist (capsazepine). The increase of endurance swimming capacity by the administration of CAP was significantly suppressed by the injection of capsazepine. At the same time, serum adrenaline secretion, which was induced by CAP, was depressed by capsazepine. These findings suggested that the increase in endurance swimming capacity by CAP was mediated by the CAP receptor.     

Capsiate, a nonpungent capsaicin analog, increases endurance swimming capacity of mice by stimulation of vanilloid receptors

We investigated the effect of capsiate, a nonpungent natural capsaicin analog, on the swimming capacity of mice in an adjustable-current water pool. Male BALB/c mice orally given capsiate (10 mg/kg) were able to keep swimming longer before exhaustion than the control mice. After 30 min of swimming, the residual glycogen in the gastrocnemius muscle was higher, the serum free fatty acid concentration tended to be higher, and the serum lactic acid concentration was significantly lower in the capsiate-administered mice. The value for the respiratory exchange ratio of the capsiate group was significantly lower during both resting and treadmill running. These physiological differences were abolished by administering the vanilloid receptor antagonist, capsazepin (0.17 mmol/kg, i.p.). The mice were not averse to the capsiate solution during a 4-h two-bottle choice test. These results suggest that the oral administration of capsiate enhanced fat oxidation and spared carbohydrate utilization, and consequently increased the endurance swimming capacity of the mice via stimulation of their vanilloid receptors. Practical application of capsiate is expected.     

水流速度对黑鲷和美国红鱼续航游泳能力及生理代谢的影响

为了确保黑鲷(Acanthopagrus schlegeli)和美国红鱼(Sciaenops ocellatus)在开放海域的养殖产量和鱼类养殖福利,在20℃下,对体长差异性不显著(P>0.05)的两种鱼进行续航游泳能力测试。首先,确定不同流速下的耐力游泳时间,然后选择耐力游泳时间为150min时的速度进行续航游泳实验。其中黑鲷和美国红鱼分别被迫以3.15和4.32 BL/s的恒定游泳速度,进行0、30min、60min、90min、120min和150min的测试,解剖鱼获得肌肉、血液和肝脏,测定样品在6个时间点的代谢物浓度,每个时间点保证3组有效数据。对0和150min的实验组对比,结果显示,两种鱼肝糖原、背肌乳酸和血糖浓度差异显著(P<0.05),肌肉糖原浓度差异不显著(P>0.05)。双变量相关分析显示,随着疲劳程度增加,肝糖原浓度下降,背肌乳酸和血糖上升。灰度关联分析和主成分分析显示,血糖和肝糖原浓度是影响疲劳的主要因素,但黑鲷相比美国红鱼,其浓度变化范围更大。综上:(1)美国红鱼比黑鲷拥有更强的游泳能力,而且黑鲷和美国红鱼不适合养殖在流速超过3.15和4....     

Enhancement of exercise endurance capacity by fermented deer antler in BALB/c mice

To investigate the activity of fermented deer antler on exercise endurance capacity, we evaluated endurance capacity in five-week-old male BALB/c mice by administering the fermented deer antler extract (FA) or the non-fermented deer antler extract (NFA) and then subjected the mice to exercise in the form of swimming. The mice administered 500?mg/kg/day of FA showed a significant increase in swimming time compared with mice administered placebo (16.55?min vs. 21.64?min, P?<?0.05). Serum lactate dehydrogenase (LDH), the marker of the liver and muscle damage, was significantly lower in FA groups. However, NFA groups did not show significantly different swimming time or serum LDH from that of the control group. Moreover, the FA-500 group had significantly higher hepatic superoxide dismutase (SOD) activity after forced swimming than the control and NFA groups (P?<?0.05). These findings suggest that fermentation may increase the exercise endurance capacity of the deer antler.     

Serotonin enhances beta-endorphin secretion to lower plasma glucose in streptozotocin-induced diabetic rats

Although serotonin, serotonin uptake inhibitors and serotonin precursors (including tryptophan or 5-hydroxytryptophan) are known to have hypoglycemic action in rodents or human, it is not clear whether serotonin has hypoglycemic effect in streptozotocin-induced diabetic rats (STZ-diabetic rats). The aim of this study was to investigate the action of serotonin in regulating the plasma glucose STZ-diabetic rats. Plasma glucose, insulin, beta-endorphin and adrenaline were assessed after intraperitoneal administration of serotonin. Serotonin produced hypoglycemic effects without altering plasma insulin and adrenaline levels but increasing beta-endorphin level in STZ-diabetic rats. The glycogen content in soleus muscle was increased at 90 min after application of serotonin (0.3 mg/kg) in STZ-diabetic rats. Dihydroergotamine (non-selective 5-HT receptor blocker) and pimozide (5-HT(7) receptor blocker) abolished the hypoglycemic effect of serotonin in STZ-diabetic rats. Serotonin-induced hypoglycemic effect in association with the increase of beta-endorphin release was abolished in bilaterally adrenalectomized STZ-diabetic rats. In isolated adrenal gland of STZ-diabetic rats, the increase of beta-endorphin secretion in response to serotonin was reduced by either dihydroergotamine or pimozide. Pretreatment with naloxone (1.0 mg/kg, i.p.) prevented serotonin-induced plasma glucose lowering effect in STZ-diabetic rats. The results demonstrated that serotonin may activate 5-HT(7) receptor on rat adrenal gland to enhance of beta-endorphin secretion, which then stimulates the opioid receptor to increase peripheral glucose utilization, resulting in decreased plasma glucose levels in STZ-diabetic rats.     

Stress-Related Changes in Cerebral Catecholamine and Indoleamine Metabolism: Lack of Effect of Adrenalectomy and Corticosterone

The concentrations of catecholamine and indoleamine metabolites were measured in intact and adrenalectomized mice to determine whether adrenal hormones mediate or modulate the stress-induced responses. Thirty minutes of footshock resulted in significant increases of the ratios of the dopamine (DA) catabolite, dihydroxyphenylacetic acid (DOPAC), to DA in prefrontal cortex, nucleus accumbens, striatum, hypothalamus, and brainstem, and of homovanillic (HVA)/DA ratios in nucleus accumbens, striatum, amygdala, and hypothalamus. Ratios of 3-methoxy-4-hydroxyphenylethyleneglycol to norepinephrine (NE) were also increased in prefrontal cortex, nucleus accumbens, septum, amygdala, hypothalamus, hippocampus, and brainstem. The concentration of NE was decreased in amygdala. 5-Hydroxyindoleacetic acid (5-HIAA)/5-hydroxytryptamine (5-HT, serotonin) ratios and free tryptophan were also increased in every brain region. Very similar data were obtained from mice restrained for 30 min. Adrenalectomy resulted in increased HVA/DA ratios in prefrontal cortex and striatum, and 5-HIAA/5-HT in septum. The stress-related changes were largely similar in adrenalectomized mice. Significant interactions between adrenalectomy and footshock treatment occurred in prefrontal cortical DOPAC/DA and hypothalamic NE which was depleted only in adrenalectomized mice, suggesting tendencies for these measures to be more responsive in adrenalectomized mice. Corticosterone administration (0.5-2.0 mg/kg s.c.) which resulted in plasma concentrations in the physiological range did not alter the concentrations of the cerebral metabolites measured in any region. We conclude that adrenal hormones do not mediate cerebral catecholamine or indoleamine metabolism in stress, although adrenalectomy may affect HVA and 5-HIAA metabolism, and there was a tendency for catecholamines to be more sensitive to stress in adrenalectomized animals.     

秋葵籽油对高强度运动所致肝损伤的保护作用

本研究考察了秋葵籽油对高强度运动所致肝损伤的保护作用及机制。研究显示,对昆明小鼠灌胃不同剂量(10 mg/kg,20 mg/kg和50 mg/kg)的秋葵籽油4周后,秋葵籽油以剂量依赖性方式提高了小鼠的力竭游泳时间(p<0.05)。秋葵籽油降低了小鼠血清乳酸和尿素氮水平,并升高了血清游离脂肪酸和肝糖原水平(p<0.05)。秋葵籽油以剂量依赖性方式提高了小鼠肝脏组织中SOD、CAT和GSH-Px活性,并抑制了MDA的合成(p<0.05)。秋葵籽油抑制了力竭游泳诱导的小鼠血清CK、AST和ALT水平及肝脏组织NO水平的升高(p<0.05)。此外,苏木精和伊红(HE)染色证实了秋葵籽油减轻了力竭游泳诱导的肝脏病理改变。因此,本研究初步结论表明,在高强度运动过程中,秋葵籽油可通过抑制乳酸和尿素氮的积累、增加脂肪动员、降低糖原消耗、减弱氧化应激损伤等多种途径来对肝脏发挥保护作用。     

The role of adrenal corticosteroids in induction of micronuclei by morphine.

It has previously been shown that morphine can increase the frequency of micronucleated splenocytes when administered to mice, but not when cells are exposed to the opiate in vitro. Morphine treatment is also known to increase circulating levels of glucocorticosteroids, which have been reported to produce genetic damage in vivo and in vitro. In order to determine whether adrenal hormones might mediate the genotoxic effects of morphine, adrenalectomized and sham-operated mice were treated with morphine sulfate. In sham-operated animals administration of morphine produced a dose-related increase in the frequency of micronucleated cells, whereas adrenalectomy abolished the effect. When plasma from morphine-treated mice was used to supplement growth medium of untreated splenocytes, the frequency of micronucleated cells increased, an effect partially blocked by the steroid antagonist RU 486. The N-methylmorphine, which does not stimulate the release of corticosterone from adrenal glands, induced micronuclei formation in splenocytes, and administration of metyrapone, an inhibitor of corticosterone biosynthesis, blocked the morphine-induced increase in corticosterone secretion, but had no effect on the frequency of micronuclei formation. These results indicate that basal levels of glucocorticosteroids are required for induction of micronuclei by morphine in murine splenocytes, but activation of the hypothalamo-pituitary-adrenal (HPA) axis by morphine does not contribute to the observed response.     

Pituitary adenylate cyclase activating polypeptide provokes cultured rat chromaffin cells to secrete adrenaline.

Pituitary adenylate cyclase activating polypeptide (PACAP) provoked the rat chromaffin cells to secrete adrenaline. Within 20 min, the amount of adrenaline secreted by PACAP (10(-8) M) was as much as that caused by acetylcholine (10(-4) M). PACAP, but not acetylcholine, induced a long-term (over 120 min) increase in secretion of adrenaline. PACAP also activated adenylate cyclase and elevated cytosolic Ca2+ concentration. Furthermore, we found immunoreactive PACAP and PACAP binding sites in the rat adrenal medulla. These results suggest that PACAP has an important role in stimulating secretion of adrenaline in the adrenal medulla.     

Acetic acid enhances endurance capacity of exercise-trained mice by increasing skeletal muscle oxidative properties

Acetic acid has been shown to promote glycogen replenishment in skeletal muscle during exercise training. In this study, we investigated the effects of acetic acid on endurance capacity and muscle oxidative metabolism in the exercise training using in vivo mice model. In exercised mice, acetic acid induced a significant increase in endurance capacity accompanying a reduction in visceral adipose depots. Serum levels of non-esterified fatty acid and urea nitrogen were significantly lower in acetic acid-fed mice in the exercised mice. Importantly, in the mice, acetic acid significantly increased the muscle expression of key enzymes involved in fatty acid oxidation and glycolytic-to-oxidative fiber-type transformation. Taken together, these findings suggest that acetic acid improves endurance exercise capacity by promoting muscle oxidative properties, in part through the AMPK-mediated fatty acid oxidation and provide an important basis for the application of acetic acid as a major component of novel ergogenic aids.     

Enhancement of swimming endurance in mice by highly branched cyclic dextrin

We investigated the ergogenic effect in mice of administering highly branched cyclic dextrin (HBCD), a new type of glucose polymer, on the swimming endurance in an adjustable-current swimming pool. Male Std ddY mice were administered a HBCD, a glucose solution or water via a stomach sonde 10 min before, 10 min after or 30 min after beginning swimming exercise, and were then obliged to swim in the pool. The total swimming period until exhaustion, an index of the swimming endurance, was measured. An ergogenic effect of HBCD was observed at a dose of 500 mg/kg of body weight, whereas it had no effect at a dose of 166 mg/kg of body wt (p < 0.05). The mice administered with the HBCD solution 10 min after starting the exercise were able to swim significantly longer (p < 0.05) than the mice who had ingested water or the glucose solution. The rise in mean blood glucose level in the mice administered with HBCD, which was measured 20 min after starting swimming, was significantly lower (p < 0.05) than that in the mice administered with glucose, although it was significantly higher (p < 0.05) than that in the mice administered with water. The mean blood insulin rise in the mice given HBCD was significantly lower (p < 0.05) than that in the mice given glucose. The mice administered with HBCD 30 min after starting the exercise swam significantly longer (p < 0.05) than the mice who had ingested water, although the enhancement of swimming time was similar to that of the glucose-ingesting mice. The gastric emptying rate of the HBCD solution was significantly faster (p < 0.05) than that of the glucose solution. However, this glucose polymer must have spent more time being absorbed because it has to be hydrolyzed before absorption, reflecting a lower and possibly longer-lasting blood glucose level. We conclude that the prolongation of swimming endurance in mice administered with HBCD depended on its rapid and longer-lasting ability for supplying glucose with a lower postprandial blood insulin response, leading to a delayed onset of fatigue.     

The effect of 4-aminopyrazolo (3,4-d) pyrimidine (4-APP) on some parameters of carbohydrate metabolism in the rat

The study was designed to evaluate some parameters of carbohydrate metabolism in the rat as influenced by 4-APP, an adenine analogue. Adult female rats were injected with 1 mg 4-APP/100 g body weight/day for 3 days. 4-APP evoked a marked enlargement of the liver with lipid droplets accumulation in hepatocytes. This was accompanied by a marked lowering of the liver glycogen content. Within 3 days 4-APP did not change serum glucose, insulin and free fatty acid concentration. Serum glycogenolytic activity studied in an in vitro system showed 7 times as high glucose releasing ability in 4-APP treated rats as that of the serum of control animals. 4-APP resulted also in a marked enlargement of the adrenal medulla and lowered adrenaline and noradrenaline concentrations in the gland. The possibility of an activation of glycogenolysis in the liver of 4-APP treated rats has been discussed.     

Effect of the exercise-induced increase in glucocorticoids on endurance in the rat

To investigate the effect of the increase in glucocorticoids during exercise on endurance, rats were either sham operated (SO) or adrenalectomized. All adrenalectomized rats were given a subcutaneously implanted corticosterone pellet at the time of adrenalectomy. Adrenalectomized rats were injected with corticosterone (ADX Cort) or corn oil (ADX) 5 min before exercise. Rats were killed at rest or after running on a treadmill (21 m/min, 15% grade) until exhaustion. SO rats ran 138 +/- 6 min compared with 114 +/- 9 min for ADX Cort and 89 +/- 8 min for ADX. All differences in run times were significant (P less than 0.05). Corticosterone levels were similar in exhausted SO and ADX Cort groups. ADX exhausted rats had corticosterone levels similar to resting values in SO and ADX rats. Inhibition of the rise in glucocorticoids during exercise had no effect on liver glycogen, liver adenosine 3',5'-cyclic monophosphate, plasma insulin, blood glucose, lactate, glycerol, or 3-hydroxybutyrate, plasma norepinephrine, or red quadriceps and soleus glycogen. Plasma free fatty acids were significantly depressed at exhaustion in ADX rats compared with SO. These data show that glucocorticoids exert effects within the time frame of a prolonged exercise bout and play a role in increasing endurance.     

FT-IR spectrometry analysis of plasma fatty acyl moieties selective mobilization during endurance exercise

This study was designed to describe changes in plasma fatty acyl moieties during a 2-h endurance exercise. Sixteen endurance-trained subjects cycled 2 h at 55% of maximal power output and capillary blood was sampled every 15 min. Fourier-transform infrared (FT-IR) spectrometry was used to determine correlated changes between plasma fatty acyl moieties (FAM) structural characteristics and metabolic parameters (oxygen consumption, respiratory exchange ratio, glucose, lactate, TG, glycerol, and albumin). Opposite changes were found between carbohydrate and fatty acid metabolism during the second hour of exercise, i.e., a decrease of glucose and lactate concentrations while albumin, FAM, and TG increased. For fatty acid metabolism, FAM and TG did not showed the same pattern of changes at the end of exercise, i.e., TG remained constant after 90 min while FAM continued to increase. This late FAM concentration increase was correlated to the changes in albumin concentration and the nu C=C-H/nu(as) CH3 and nu(as) CH2/nu(as) CH3 ratios. These ratios clearly showed that FAM unsaturation increased while chain length decreased. It was hypothesized that PUFA from TG adipose lipolysis ketone bodies (beta-hydroxybutyric acid) from liver may have been released in higher amounts as glycogen stores became depleted after 90 min of exercise.     

大豆卵磷脂对小鼠的抗疲劳和抗氧化作用研究

目的：研究大豆卵磷脂的抗疲劳及抗氧化作用。方法：小鼠经口给予大豆卵磷脂30天后,采用负重游泳实验,观察记录小鼠游泳死亡时间;检测血清尿素氮、肝糖原;测定血清和肝匀浆超氧化物歧化酶（SOD）活性、谷胱甘肽过氧化物酶（GSH—Px）活力、丙二醛（MDA）含量。结果：给予大豆卵磷脂后,与对照组相比,实验组小鼠负重游泳时间明显延长,肝糖原消耗量减少,降低运动后血清尿素氮水平（P〈0．05）;升高小鼠血清和肝匀浆SOD活性及GSH-Px活力,降低MDA的含量（P〈0．05）。结论：大豆卵磷脂具有抗疲劳和抗氧化作用。     

Purification and characterization of ascamycin-hydrolysing aminopeptidase from Xanthomonas citri.

Intact obese rats were hyperinsulinaemic, had higher rates of whole-body fatty acid synthesis, higher activities of hepatic acetyl-CoA carboxylase and tyrosine aminotransferase and a higher hepatic glycogen concentration than intact lean animals. Adrenalectomy abolished all these factors of the obese phenotype. Treatment of adrenalectomized rats with corticosterone for 24 h increased the rate of whole-body fatty acid synthesis to the same extent in both phenotypes, but caused a larger increase in glycogen concentration, tyrosine aminotransferase activity and plasma insulin concentration in obese rats.     

Influence of glucocorticoids on the secretion of pancreatic juice in the rat

The influence of adrenalectomy and hydrocortisone treatment on the exocrine pancreatic secretion has been studied in anaesthetized rats. In the adrenalectomized animals Na+ administered in the saline solution provided for drinking was able to maintain standard sodium levels in serum. In these animals an increase of Na+ secretion in pancreatic juice was observed. Furthermore, the osmotic effect created by the increase in Na+ would account for the increase in pancreatic flow. In these adrenalectomized rats, an increase in K+ output is observed, which can be explained by the high K+ concentrations in serum. Likewise adrenalectomy decreased pancreatic enzyme secretion and produced a loss in weight of the organ that is accounted for by a lack of glucocorticoids. Hydrocortisone administration did not affect neither the secretion nor the weight of the pancreas of the control rats but the hormone proved to be effective in adrenalectomized rats producing a pancreatic secretion close to normal, balancing the secretory rate of water, Na+ and K+, completely restoring total protein secretion and the weight of the pancreas but amylase secretion in part only. It is therefore concluded that the weight of the pancreas and its exocrine secretion are clearly influenced by adrenalectomy and by substitution therapy with hydrocortisone. The administration of this hormone (25 mg.kg-1.day-1 along 6 days) did not affect intact animals.     

Metabolic and endocrine responses to prolonged exercise in rats under beta 2-adrenergic blockade

The respective roles of allosteric regulators and catecholamines in the control of muscle glycogen breakdown during exercise remain a matter of controversy. This study was designed to reassess the role of the sympathoadrenal system during prolonged exercise in rats. Animals were studied at rest or after treadmill exercise (28 m.min-1; 8% slope) to exhaustion in a control situation or following administration of a specific beta 2-adrenergic receptor antagonist (ICI 118,551, 1 mg.kg-1, i.v.). Running times to exhaustion were 54 and 36 min in control and treated rats, respectively. For the purpose of comparison, another group of control rats was studied after a 36-min exercise bout. The reduction in endurance in treated rats was associated with an impairment in glycogen utilization, as measured by muscle glycogen stores, in soleus muscle but not in superficial vastus lateralis or gastrocnemius lateralis muscles. Utilization of liver glycogen stores was similar in the two groups of animals, but plasma glucose (7 vs. 13 mM) and lactate (4 vs. 7 mM) levels were significantly lower in rats under beta-blockade than in control rats run for 36 min. Plasma free fatty acid and glycerol concentrations were not significantly different between groups. On the other hand, plasma epinephrine concentration was significantly higher in treated rats (13 vs. 5 mM), which might reflect a compensatory increase in adrenal activity. These results suggest that glycogen breakdown during prolonged exercise is under the control of the sympathoadrenal system in predominantly slow-twitch but not in predominantly fast-twitch muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Progeny of high muscling sires have reduced muscle response to adrenaline in sheep

This study investigated the impact of variation in Australian sheep breeding values (ASBVs) for yearling eye muscle depth (YEMD) within Merino and Poll Dorset sires on intermediary metabolism of progeny. Specifically, the change in the blood concentrations of lactate, non-esterified fatty acids (NEFA) and glucose in response to administration of an exogenous dose of adrenaline was studied. The experiment used 20 Merino and Merino cross Poll Dorset mixed sex sheep. The sires were selected across a range of YEMD ASBVs. The sheep were fitted with indwelling jugular catheters and administered seven levels of adrenaline over a period of 4 days at 4 months of age (0.1, 0.2, 0.4, 0.6, 0.9, 1.2 and 1.6 μg/kg liveweight (LW)) and 16 months of age (0.1, 0.2, 0.6, 1.2, 1.8, 2.4 and 3.0 μg/kg LW). A total of 16 blood samples were collected between -30 min and 130 min relative to administration of the adrenaline challenge and were later measured for the plasma concentrations of lactate, NEFA and glucose. These data were then used to calculate the time to maximum substrate concentration, the maximum concentration and the area under curve (AUC) between 0 and 10 min, thus reflecting the substrate's response to exogenous adrenaline. Selection for muscling led to decreased muscle response due to adrenaline, as indicated by lower maximum concentrations and AUC for lactate. The muscles' response to adrenaline was more prominent at 16 months of age than at 4 months of age. Thus, animals selected for increased muscling have lower levels of glycogenolysis in situations where endogenous adrenaline levels are increased like pre-slaughter. This may minimise the risk of poor meat quality in these animals, as they will express higher muscle concentrations of glycogen at slaughter. Adipose tissue was more sensitive to adrenaline in young lambs from high YEMD sires. This shows that high muscled growing lambs utilise their adipose tissue deposits in times of stress to produce energy. This may explain the phenotypic leanness of these animals. Blood glucose levels that are indicative of liver response to adrenaline decreased with selection for muscling. This response may indicate a potential limiting of glucose that is available within animals selected for muscling, leanness and growth for brain function.     

Effect of exercise and adrenal insufficiency on urea production in rats

Experiments on Wistar rats were designed to study the effect of exercise on urea production in the liver of intact and adrenalectomized rats. The urea production rate was assessed by the¹⁴C-urea content in liver tissue after administration of NaH¹⁴CO₃. In intact rats swimming caused increases in¹⁴C-urea content in the liver compared to the resting concentrations in intact control rats: by 45% after 30 min of swimming carrying an additional load of 10% body mass by, 35% after 3 h of swimming without an additional load and by 103% after 10 h of swimming. Concentrations of urea in liver and blood were elevated simultaneously. The specific activity of¹⁴C-urea did not change significantly as a result of the exercise performed. In adrenalectomized rats the basal rate of urea production was reduced by an insignificant amount, but swimming for 3 h resulted in a decrease in liver¹⁴C-urea (by 24%). The results confirmed the exercise-induced increase in urea production and indicated as essential role for adrenal hormones in this response.