Sex Differences On The Cardiorespiratory Fitness Response To Treadmill Interval Training In Mice
Kevin Alves BarretoA.B. FrareAna Beatriz S. SousaGuilherme Rodrigues VieiraDaniel MartínEdgard de Melo Keene Von Koenig SoaresF. A. R. NevesAdriana LA PortoSidney Alcântara PereiraLuiz Guilherme Grossi Porto
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Sex steroid hormones are major effectors of the sexual dimorphism in mammals and are suposed to differently impact cardiometabolic responses to exercise training. Testosterone is related to the development of strength and muscle mass while estrogen is believed to associate with endurance capacity. Sex differences on cardiorespiratory fitness (CRF) response to interval training (IT) deserve further evaluation, specially in animal models. PURPOSE: To compare the CRF response to a treadmill interval training protocol in mice of both sexes. METHODS: 26 adult (3-4 months old) C57BL/6 mice were evaluated (14 fem / 12 males). Firstly, all animals were subjected to a 10-day treadmill familiarization step within 2 weeks, 5 days/week, at 25° inclination, having both session duration and speed progressively increased from 5 to 10 min and 5 to 10 m/min), respectively. After familiarization, 3 maximum exercise tests were carried out on a 48 h-interval to assess the average maximum distance and speed reached (MSR). The test consisted of 5-min warm up at 6 m/min followed by incremental speed stages of 2 m/min every 2 min, at 25° inclination. Tests were considered maximum when mice were unable to, or refused to run even with mechanical stimulation. After basal CRF evaluation, mice were separated into exercise (EG–9 fem/7 mal) and control groups (CG-5 fem/9 mal). The EG trained for 4 weeks, starting with a warm-up at 5 m/min and a subsequent IT of 10 bouts of 4 min running at moderate intensity (55–65% MSR), interspersed by 2 min active rest (5 m/min), always at 25°. After training, CRF was assessed as in the pre-training period. Groups were compared before and after training protocol. RESULTS: The IT significantly increased CRF (p < 0.01) in EG. Remarkably, females showed a higher CRF increase (56.3%) than males (43.1%) (p < 0.01). CRF remained unchanged in CGs of both sexes (p > 0.05). CONCLUSION: The 4-week of IT was effective to improve CRF in both sexes but females had a significantly higher improvement compared to males. Our findings suggest that sex differences must be taken into account in animal studies once sex hormonal and/or behavioral differences may significantly impact the training responses in mice. Supported by Fundação de Apoio à Pesquisa do Distrito Federal - FAP DF:0193.001571/2017; KAB is a PIBIC student – FAP DF: 00193.001467/2016.Keywords:
Treadmill
Interval training
Basal (medicine)
Endurance Training
THE CLASSICAL CONCEPT of neuroendocrine control of the pituitary as proposed by Harris stipulates that the endocrine functions of the anterior pituitary are controlled by hypothalamic releasing factors or release-inhibiting factors. It was postulated that these factors are present in hypothalamic neurons which project into the median eminence (ME) of the basal hypothalamus and end in contact with the hypothalamic-hypophyseal portal vessels (1). It has subsequently been shown that growth hormone (GH) secretion is regulated by both stimulatory and inhibitory factors of hypothalamic origin. Like other anterior pituitary hormones, GH is secreted episodically. In all mammalian species so far studied spontaneous episodes of GH secretion occur several times over a 24-h period (2–8). Particularly in the adult male rat there is a striking regularity in the GH pulses which occur at 3- to 4-h intervals and reach levels of several hundred ng/ml.
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Sexual dimorphism
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Eleven boys aged 1-10 years with central precocious puberty were studied. According to the pubertal development six were classified as P2, one as P3 and four as P5. In all cases plasma testosterone levels were definitely elevated (1.7-5.8 ng/ml) when compared with pre-pubertal controls. Peak values after HCG (3 X 1500 units) in four of the boys were in the high adult range. The binding capacity of serum testosterone oestradiol binding globuline (TeBG) ranged between 0.5 and 7.30 microgram/dl. Basal plasma levels of LH and FSH were respectively 2.06 +/- 0.64 and 1.2 +/- 0.25 miu/ml, and peak levels after LHRH (0.1 mg/m2) 13.9 +/- 3.7 and 2.6 +/- 0.43 miu/ml respectively. The data demonstrated a significant increase of plasma testosterone and post LHRH LH peak levels in boys with central precocious puberty when compared with pre-pubertal controls. The patients at stage P2 exhibited high levels of plasma testosterone contrasting with the degree of pubertal maturation, high values of TeBG and low response to LHRH which were in the pre-pubertal range. These findings suggest that the testicular sensitivity to LH increases early in boys with central precocious puberty, while the testosterone responsiveness, both at peripheral and hypothalamic levels, is delayed.
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Microgram
Hypothalamic–pituitary–gonadal axis
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ABSTRACT Administration of a depot testosterone preparation to male and female rats resulted in no change in body or pituitary weight in either sex. Pituitary corticotrophin content was unaltered in male animals but was reduced in females. Adrenal weights and adrenal RNA and DNA contents were decreased in both sexes. Plasma corticosterone concentrations were unaffected in males but were reduced in female rats after stress or corticotrophin injection. Hepatic reduction of ring A in vitro and biological half-life of corticosterone in vivo were unchanged in male animals but impaired in females. Testosterone administration to intact male rats significantly increased adrenal steroidogenesis measured in vitro . A significant decrease in steroid production was found in intact females but increased steroidogenesis was observed in adrenals from testosterone-treated oophorectomized animals. No effect was obtained following addition of testosterone directly in vitro . The data suggest that testosterone leads both to diminution of corticotrophin secretion and enhancement of adrenal steroid secretory capacity. In intact female rats, these effects are complicated by suppression of oestrogen secretion, the effects of which have been reported previously.
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ABSTRACT In the long-term castrated rat the negative feedback effect of testosterone is markedly reduced and the raised levels of plasma LH seen in the castrated animals are not suppressed by physiological concentrations of plasma testosterone. In this study we have measured pituitary gonadotrophin-releasing hormone (GnRH) receptor content as well as plasma and pituitary LH on days 1, 10 and 40 after castration and noted the effect of testosterone replacement on these parameters. We found that the negative feedback effect of physiological concentrations of testosterone on plasma and pituitary LH, pituitary GnRH receptor content and response to exogenous GnRH was attenuated 10 and 40 days after castration. It is suggested that the lack of effect of testosterone in the long-term castrated rat is due to its inability to reduce the pituitary GnRH receptor content. On increasing testosterone to supraphysiological levels, the negative feedback effect was reinstated. We also found that in rats 40 days after castration, physiological and subphysiological concentrations of testosterone significantly increased pituitary GnRH receptor content and this may explain the previous findings that low concentrations of testosterone can enhance the effect of GnRH and increase plasma LH levels. J. Endocr. (1986) 108, 441–449
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Immunoreactive FSH and LH, testosterone and cortisol were measured in venous plasma samples obtained every 4 hr for 24 hr from 8 healthy young men. Subjects were studied on 2 occasions, one week apart, once with and once without dexamethasone treatment, the order randomly assigned. On no treatment, FSH, testosterone and cortisol each showed a diurnal cycle with concurrence of highest mean levels at 8:00 hr and lowest mean levels between 24:00 and 4:00 hr. The relative amplitudes3 of the cycles were: cortisol +102, −83%; testosterone +13, −20%; and FSH +6, −5%. No cycle in LH was demonstrated. Dexamethasone administration resulted in marked suppression of cortisol levels with loss of cyclicity, elevation of LH levels, and no change in over-all levels or cyclicity of FSH and testosterone. The results suggest that FSH and testosterone levels are linked together, but the mechanism is not known. The reason for the elevation of LH levels by dexamethasone is unclear.
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Intact male rats were injected with 50 μg E2B (estradiol benzoate) or with 100 μg E2 (estradiol). Six hours after injection plasma and testicular testosterone levels and production were significantly decreased. Concomitant with this change lowered LH plasma levels could be observed in the estrogentreated animals. Twenty-four hours after injection of 50 μg E2B LH levels, testosterone levels and testicular testosterone production were still reduced, whereas 24 h after E2 administration both testosterone and LH levels had returned to control levels. One and 3 h after injection of 500 ng estradiol, plasma and tissue testosterone levels, as well as testicular testosterone production, were decreased. However, this low dose of E2 also caused a decrease in LH plasma levels. In order to investigate whether estrogens would inhibit testicular testosterone synthesis or release by mechanisms other than inhibition of LH secretion, estrogen or vehicle only were injected into hypophysectomized animals given exogenous LH. No effects of estrogens on testosterone levels or production were observed in such animals. These findings suppport the view that the observed effect of administered estrogens on testosterone production in rat testicular tissue reflect primarily extra-testicular estrogen actions such as the negative feedback effect on LH secretion.
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Abstract. After 5 days of starvation, the body weight of adult male Wistar rats was on the average 34% lower than that of control animals. Luteinizing hormone (LH) and testosterone in plasma were significantly decreased in the starved animals (−95% and −82% on the average). The in vivo response to hCG (10 IU per animal for 3 days) was not diminished in the starved rats. The in vivo stimulation with synthetic LRH (100, 200, 500, 1000 ng/kg body weight iv) caused an increase of LH at all doses. The response however was quantitatively decreased in starved rats. The pituitary content of the LH and the LRH content in the preoptic area and in the hypothalamus were not influenced by starvation; the LRH content, however, was greatly increased in the median eminence (33.2 ± 11.7 versus 15.5 ± 7.1 ng per mg protein). The feedback was studied by castrating the animals and implanting silastic tubes of various sizes which released testosterone. The plasma levels of testosterone were proportional to the length of the capsules used. LH levels increased greatly (> 90 ng/ml) when testosterone levels were lower than 1.80 ng/ml in the control rats. The straved rats tolerated testosterone levels as low as 1.00 ng/ml plasma before LH was elevated. The LRH content in the median eminence increased in starved and control animals when plasma levels of testosterone dropped below 1.80 ng/ml. These data indicate that the increased sensitivity of the testosterone-LH feedback may be caused by an impaired release of LRH from the median eminence.
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ABSTRACT To study the role of testosterone on the regulation of the hypothalamic-pituitary-testicular axis, young intact male Wistar rats were given acute (24 h) or chronic (5 days) subcutaneous treatments of 500 μg testosterone propionate (TP) or vehicle alone. Plasma LH, prolactin and testosterone levels were measured both basally and after administration of LH-releasing hormone (LHRH) or human chorionic gonadotrophin (hCG) by means of specific radioimmunoassay systems using materials supplied by the NIADDK. After acute treatment with TP there was an increase in basal plasma testosterone concentrations and no modification in the hCG response when compared with vehicle-treated animals. No difference could be detected in basal plasma testosterone levels after the chronic treatment, but a significant reduction in the hCG response was observed. Both acute and chronic treatments with TP resulted in a significant decrease of basal plasma LH levels. A reduced LH response to LHRH in acutely treated rats and no response in the chronically treated rats was detected. Plasma prolactin levels showed an increase after both acute and chronic treatments. To evaluate the possible role of the increased plasma prolactin levels on the above modifications during TP treatment, another group of animals was treated with TP and bromocriptine (dopamine agonist) simultaneously to avoid the increase in plasma prolactin levels. In this situation, neither basal plasma LH levels nor the response to LHRH were altered when compared to vehicle-treated rats; a normal testosterone response to hCG stimulation was observed in spite of the high basal plasma testosterone levels. All these observations suggest that increased prolactin levels may exert a modulatory role on the negative feedback effect of testosterone both at the testicular and central levels. J. Endocr. (1985) 105 , 423–427
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We have examined the effect of experimental diabetes on plasma testosterone levels in adult female Sprague-Dawley rats. Within 24 h after the injection of streptozotocin (SZ), plasma testosterone concentrations increased from 46.5 ± 3.16 (mean ± SE) to 270 ± 43.5 ng/dl (P < 0.001), levels observed in normal, reproductively competent male rats. This elevation persisted for the entire 4-week period studied and appeared to be closely correlated with plasma ketone levels (r = 0.895). Animals made diabetic with alloxan had less severe diabetes with minimal ketosis, but still had testosterone levels more than 3 times those of controls. Prevention of diabetes by injection of 3-O-methylglucose before SZ administration abolished the increase in testosterone. Insulin therapy, initiated 16 h after SZ and continued every 4 h for an additional 32 h to maintain normoglycemia, maintained plasma testosterone at normal female levels. The plasma precursor steroids 17-hydroxyprogesterone and androstenedione were elevated (P < 0.001) in diabetic rats; dehydroepiandrosterone (DHEA) was not. Studies were performed to determine the origin of these steroids. When adult rats were ovariectomized 8 days before SZ injection, testosterone was elevated to 180 ± 9 ng/dl 48 h after the onset of diabetes, but to a lesser degree than in intact diabetics. Adrenalectomy 2 days after SZ administration not only prevented the increase in plasma testosterone, but decreased these values compared to those in both unoperated and adrenalectomized controls. When incubated with [3H]DHEA, hepatic cytosol preparations from 5-day-diabetic rats showed a marked increase in the conversion of DHEA to androstenedione and testosterone (P < 0.001) compared to controls. These results indicate that experimental diabetes resulting in ketosis leads to increased plasma testosterone levels in adult female rats. The large elevation in plasma testosterone appears to be mainly of adrenal origin. Increased precursor steroids are present in plasma, and increased peripheral conversion of DHEA to testoserone can be demonstrated in vitro. This elevation of plasma testosterone may account for some of the previously observed abnormalities of reproductive function in the female diabetic rat.
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Abstract. Cryptorchid boys show evident alterations in the fine structure of the testes, although they respond in a normal manner to various tests of endocrine function. On the other hand, there is evidence that glucocorticoids suppress plasma testosterone levels, although the mechanism is unknown. Eight control subjects and 8 bilaterally cryptorchid boys, at Pl stage of sexual maturation, were therefore studied by determining the degree of testosterone suppression induced by glucocorticoids. The subjects were submitted to a short dexamethasone (DXM) suppression (1.5 + 0.5 mg at 20.00 and 24.00 h, respectively) and to a short iv ACTH stimulation (1 U/m 2 body surface). Basal concentrations of cortisol, androstenedione and testosterone were similar in both groups. Cortisol and androstenedione responded to both DXM suppression and ACTH stimulation in an identical manner in the two groups. DXM lowered the basal levels of testosterone by 46.4 ± 5.8% (mean ± se ) in the controls, but only by 6.9 ± 6.6% in the cryptorchid boys ( P < 0.001). ACTH only induced a significant decrease in the controls (from 110.9 ± 18.5 to 61.4 ± 10.9 and 72.3 ± 11.8 pg/ml ( P < 0.025), after respectively 20 and 30 min), while no significant differences were found in the cryptorchid subjects. These data indicate that in bilateral cryptorchidism, plasma T is not affected by exogenous (DXM) or endogenous (cortisol) glucocorticoids.
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