Alguma relação entre exercício [fitness] e tireoide Ɂ
A relação viciosa entre exercício extenuante [anaeróbico] e hipotireoidismo
[Imagem: lifehacker.ru]
Mais de uma vez, o fisiologista PhD R. Peat sugeriu a cautela que se deve ter, na escolha do exercício, para evitar criar ou agravar um estado de hipotireoidismo.
Ao mesmo tempo, foi ele um dos pioneiros em denunciar a falsa nomenclatura utilizada nas academias de fitness de chamar um exercício que produz ácido lático de “aeróbico”. Exercício anaeróbico é o que produz claramente ácido lático.
E os exercícios usualmente praticados naqueles ambientes são extenuantes, de longa duração e, portanto, logo após os primeiros minutos deveriam ser mais corretamente chamados de “anaeróbicos”, que é o que eles são, com sua copiosa produção do tóxico lactato.
Muitas dietas chamadas “saudáveis” são ricas em feijões, amidos, óleos vegetais de sementes, nozes, cereais e folhas e, são recomendadas junto com exercício anaeróbicos, compõem um combo [“dieta saudável” + exercício] que, dentro de determinado espaço de tempo, ajudarão a construir certas doenças crônico-degenerativas. A asma, por exemplo, é mais comum em atletas do que na população em geral, já foi feita estatística comparativa.
Seria mais acertado conceber um exercício adequado, que seja principalmente aeróbico, concêntrico, aliado a caminhadas na natureza, lúdicas, tranquilas e evitar alimentos antitireoidianos, para ser alcançar a almejada boa saúde.
“Além do jejum ou da deficiência crônica de proteína, dentre as causas comuns de hipotireoidismo encontram-se estresse excessivo de exercício ´aeróbico´[isto é, anaeróbico], e dietas contendo feijões, lentilhas, nozes, óleos insaturados [incluindo caroteno] e brocoli, couve-flor, couve e mostarda mal cozidos.
Muita gente que possui consciência de saúde, termina construindo seu hipotireoidismo através de um programa sinérgico de hortaliças mal cozidas, feijões em vez de proteína animal, óleos em vez da manteiga, caroteno em lugar da vitamina A e exercícios de tirar o fôlego em vez de uma vida estimulante” [R. Peat].
Portanto, para R. Peat, existe uma relação viciosa entre o tipo mais comum de exercício [extenuante, anaeróbico] e o desenvolvimento do hipotireoidismo.
Quando os doutores defendem aquele tipo de exercício ao mesmo tempo em que enaltecem um batimento cardíaco lento, não percebem que se o atleta chegar àquele pulso lento – cantado em prosa e verso pela medicina oficial – ele terá ganho, provavelmente, um hipotireoidismo ou hipometabolismo. Pulso lento, de 60-70, para R. Peat, não é sinal de saúde [o sangue estará irrigando os sistemas e enviando nutrientes com menos eficiência do que o pulso saudável, fisiológico, mais rápido].
E se aquela pessoa já era portadora de hipotireoidismo, o exercício chamado aeróbico será um fator de agravamento, não de promoção da saúde. Mesmo que se sintam - quando indagadas -, muito bem com o exercício, com o corpo aquecido, ativo, interpretando, dessa forma, o bem-estar real gerado pelo exercício de forma unilateral e parcial.
“Um batimento cardíaco lento sugere fortemente hipotireoidismo. Pessoas com hipotireoidismo, que certamente produzem ácido lático mesmo em repouso, são especialmente susceptíveis aos efeitos daninhos do chamado exercício ´aeróbico´.
O bom efeito que algumas pessoas dizem que sentem com o exercício é provavelmente resultado do aumento da temperatura corporal; um banho quente faria a mesma coisa para essas pessoas com baixa temperatura corporal” [R. Peat].
E essas coisas só pioram quando as pessoas são orientadas a combinar jejum com exercício. Jejum aumenta o cortisol e certamente aumenta a absorção de endotoxinas intestinais previamente acumuladas no trato digestivo grosso. O exercício irá se somar a esse processo estressante.
“Estresse incidental do tipo exercício extenuante combinado com jejum [a exemplo de correr ou trabalhar fisicamente antes de ter o breakfast] não apenas diretamente dispara a produção de lactato e de amônia, mas provavelmente aumenta a absorção de endotoxinas bacterianas do intestino. Endotoxina é um estressor universal e crônico. Aumenta lactato e óxido nítrico, intoxicando a respiração mitocondrial, precipitando a secreção de hormônios adaptativos do estresse” [R. Peat].
Mas, em especial exercício extenuante, anaeróbico, cria condições para supressão da tireoide, derrubada dos hormônios tireoidianos.
Alguns dos trabalhos citados abaixo, na bibliografia – mesmo com as limitações de design de boa parte deles - mostram essa inibição tireoidiana como produto direto daquele tipo de exercício.
Uma experiência foi feita com praticantes de tae-kwon-do e outro grupo de sedentários durante quatro semanas. E mostrou que “treinamento até a exaustão provoca redução na atividade do hormônio tireoidiano tanto nos sedentários quanto nos esportistas. E a suplementação de magnésio preveniu redução da atividade hormonal tireoidiana tanto em sedentários quanto nos esportistas” [K].
Experiência com exercícios de alta intensidade em humanos mostrou que houve “supressão da conversão periférica de T4 em T3, implicando em um longo período de recuperação para que os níveis hormonais voltassem ao normal” [L].
Mostrou que exercício não evitou dramática desaceleração do metabolismo em repouso [M].
“Achados do nosso estudo demonstraram que exercício de exaustão levou a uma significante inibição de hormônios tireoidianos e de testosterona” em animais, e que doses fisiológicas de zinco podem beneficiar a performance” [I].
Agora, em outro tipo de experiência, com homens sedentários, os resultados indicaram que “exercício diminui hormônios tireoidianos e testosterona e que suplementação com zinco evita tal redução” [J].
Outra pesquisa, em animais, mostrou que há mudanças nos efeitos periféricos dos hormônios tireoidianos durante treinamento físico [B].
Estudos mostraram queda de T4 e T3 em períodos de treinamento físico [F] em humanos.
Outro dado. “A presente pesquisa em humanos demonstrou que a função tireoidiana é fortemente afetada por exercício físico prolongado em um balanço negativo energético, no qual a privação de sono não possui influência significativa” [A]
Esse balanço negativo, lado a lado com inibição tireoidiana, tem tudo a ver com o fato de infertilidade, baixa libido e outros problemas ligados ao excesso de estrogênio aparecem muito em mulheres atletas.
Trabalho de pesquisa em mulheres atletas destacou que “distúrbios menstruais sutis que afetam a maior parte das mulheres e atletas fisicamente ativas incluem defeitos na fase luteal. Desordens na fase luteal, caracterizados por insuficiente maturação do endométrio, como resultado de produção inadequada de progesterona [P4] e fases luteais curtas, estão associadas com infertilidade e abortos espontâneos habituais. Em atletas recreacionais, a prevalência e incidência de insuficiências na fase luteal-folicular e de ciclos menstruais anovulatórios é de 48% e 79% respectivamente” [G].
“Mulheres com perturbação na fase luteal do ciclo, exibem alterações hormonais consistentes com um estado hipometabólico que é similar ao observado em atletas amenorreicas e outros estados de privação de energia” [H].
“Treinamento atlético sabidamente torna o pulso mais lento. Cortisona, produzida pelo estresse, inibe a glândula tireoide. [Quando a tireoide é lenta, menos oxigênio é necessário, portanto essa é uma adaptação útil para aumentar a resistência]. Agora se sabe que tais mudanças hormonais produzem esterilidade tanto em homens como em mulheres” [R. Peat].
Sempre que a tireoide for impactada é previsível que isso impactará outros hormônios, especialmente produzindo elevação do estrogênio. Tanto em mulheres quanto em homens.
“Alem de causar estresse, níveis de estrogênio são aumentados pelo estresse. Por exemplo, um corredor do sexo masculino terá seu estrogênio dobrado depois de uma corrida. Homens e mulheres que são hospitalizados por conta de doenças graves, tipicamente possuem níveis de estrogênio grandemente aumentados.
O papel do estrogênio na doença termina em um círculo vicioso no qual o estrogênio diminui a capacidade da pessoa de tolerar o estresse, e isso raramente é levado em conta” [R. Peat].
O lúdico e o prazeiroso podem ser parte integrante do exercício, com ganhos para a saúde. Por exemplo, “embora a corrida tenha se tornado popular para a prevenção da doença cardiovascular, frequentemente os especialistas trabalham na base de quantas milhas uma pessoa tem que correr para queimar uma libra de gordura. No entanto, na Rússia, fisiologistas sempre lembram de considerar o cérebro nos seus cálculos; e ocorre que uma caminhada através de arredores prazeirosos e interessantes, consome mais energia do que um exercício custoso e mais entediante. Um cérebro ativo consome tremenda quantidade de combustível” [R. Peat].
De toda forma, o mantra médico de que exercício é essencial para a boa saúde necessita urgentemente de uma reavaliação de conteúdo. A começar pela redefinição oficial do que é o exercício chamado aeróbico, do que é o exercício concêntrico [o mais saudável] e, definitivamente, do papel nefasto do ácido lático, da amônia, dos hormônios do estresse para a boa saúde.
De tal forma que quando a pessoa planeje seu exercício não caia na vala comum de destruir a sua saúde justamente quando está se empenhando em construí-la.
GM Fontes, Brasília, 28-3-24
As informações aqui presentes não pretendem servir para uso diagnóstico, prescrição médica, tratamento, prevenção ou mitigação de qualquer doença humana. Não pretendem substituir a consulta ao profissional médico ou servir como recomendação para qualquer plano de tratamento. Trata-se de informações com fins estritamente educativos. Nenhuma das notas aqui presentes, neste blog, conseguirá atingir o contexto específico do paciente singular, nem doses, modo de usar etc. Este trabalho compete ao paciente com seu médico. Isso significa que nenhuma dessas notas - necessariamente parciais - substitui essa relação.
Referências __________________
[A] OPSTAD P K, FALCH D, 1984. The thyroid function in young men during prolonged exercise and the effect of energy and sleep deprivation. Clin Endocrinol (Oxf). 1984 Jun;20(6):657-69.
Thyroid function has been investigated in 24 young military cadets participating in a 5 d ranger training course with heavy physical exercise, calorie deficiency and deprivation of sleep. The cadets were divided into three groups, each differing in the amount of sleep and food consumption. The serum levels of thyroid hormones (T4, FT4, T3, rT3) and TBG showed a biphasic pattern during the course. Initially there was an increased secretion concomitant with an increased deiodination of T4 to T3 and rT3 mainly due to physical exercise. When the activities lasted for several days without sufficient food supply the thyroid secretion decreased simultaneously with an alteration of the peripheral conversion of T4 to rT3 instead of T3. A significant correlation was found between the changes in total and free thyroxine (r = 0.9) and between the increase in rT3 and decrease in T3 (r = 0.6). TSH decreased during the first day of activities and remained low throughout the course. The TSH response to TRH stimulation was greatly reduced during the course due to physical exercise and calorie deficiency. The present investigation demonstrates that the thyroid function is strongly affected by prolonged physical exercise and a negative energy balance, whereas sleep deprivation does not have any significant influence. The results indicate that the alteration observed is not regulated just by the hypothalamo-pituitary-thyroid-axis alone.
[B] WIRTH A HOLM G LINDSTEDT G, 1981. Thyroid hormones and lipolysis in physically trained rats. Metabolism. 1981 Mar;30(3):237-41.
In rats a single bout of exercise resulted in increased triiodothyronine (T3), thyroxine (T4), and triiodothyronine/reverse triiodothyronine (T3/rT3) ratio 20 hr after exercise. The effect of norepinephrine on lipolysis in vitro was potentiated. In trained rats no changes were found in T4, T3, or rT3 concentrations. The T3/rT3 ratio as well as basal and stimulated TSH concentrations decreased in comparison with sedentary, freely eating rats. Moderate food restriction to produce a body weight similar to that of trained animals caused no changes in T4, T3, or rT3 concentrations but caused a decrease in T3/rT3 and in TSH levels. Training and moderate food restriction groups were not different. T3 in vitro caused a potentiation of catecholamine induced lipolysis in trained and food-restricted animals. With aging the serum concentration of T3 decreased and that of rT3 increased. Acute and chronic exercise both exert an effect on peripheral hormonal responses of lipolysis, while they have different and opposite effects on thyroid hormone concentrations. Physical training seems to have effects in this regard similar to those of moderate energy intake restriction. The results suggest that changes in peripheral effects of thyroid hormones during training should attract more attention.
[C] ROSOLOWSKA-HUSZCZ, 1998. The effect of exercise training intensity on thyroid activity at rest. J Physiol Pharmacol. 1998 Sep;49(3):457-66.
The influence of exercise training intensity on thyroid activity at rest was studied in male Wistar rats, weighting 114 g +/- 24 (mean +/- SD) at the beginning of the experiment. Animals were assigned to the following groups: untrained controls and rats trained on a treadmill at the speed of 20 m/min over a 5-week period with different intensities: 2 x 60 min weekly, 4 x 60 min, 6 x 20 min, 6 x 40 min and 6 x 60 min weekly. Thyroid peroxidase (TPO) and hepatic iodothyronine 5′-monodeiodinase (5’DI) activities as well as plasma thyroxine (T4), 3,3’5-triiodothyronine (T3) and 3,3′.5′-triiodothyronine (rT3) concentrations were determined. Training intensity was found to influence parameters under investigation. TPO activity was decreased in groups trained 240 min (4 x 60 min and 6 x 40 min) and 360 min (6 x 60 min) weekly in comparison to control, untrained group. Furthermore, a drop in T4 plasma concentration in all trained groups and a decrease in T3 plasma concentration in groups exercising for 120 min (2 x 60 min and 6 x 20 min) weekly, as compared to control, untrained rats, was found. Hepatic 5’DI activity and rT3 plasma concentration were not affected by training. Thus, exercise training in rats seems to elicit the fall in TPO activity and T4 plasma concentration at rest but without changing hepatic 5’DI activity and rT3 plasma concentrations. A decline in T3 plasma concentration, observed in rats trained with the lowest exercise intensities, could be regarded as transitional effect in adaptation to chronic exercise”.
[D] BAYLOR L S HACKNEY A C, 2003. Resting thyroid and leptin hormone changes in women following intense, prolonged exercise training. Eur J Appl Physiol. 2003 Jan;88(4-5):480-4. Epub 2002 Nov 22.
“This study examined whether free (f) triidothyronine (T3), f thyroxine (T4), thyroid stimulating hormone (TSH), and leptin concentrations at rest changed in response to 20 weeks of exercise-training. Two groups of women were recruited for participation in the study, collegiate athletes ( n=17) and sedentary controls (n=4). Exercise training consisted of daily athletic activity such as rowing, running, and weight lifting. Subjects were initially grouped into rowers and controls. However, earlier suggested criteria were further used to categorize hormone changes (percentages) in the subjects into (+) responders (increases), (-) responders (decreases), or non-responders (no changes). The fT3 results of the rowers revealed two distinct categories of responses, (-) responder (all decreases; n=10) and non-responder (no change; n=7) rowers. In the responders fT3 concentration decreased (P<0.05) from baseline (BL) during an intense training period [(mean SEM) at 5 weeks by -28.2 (6.2)% and at 10 weeks by -24.9 (7.9)%], then returned towards BL levels (20 weeks compared to BL, P>0.05). Similar changes (P<0.05), at comparable times, were noted for leptin and TSH concentrations in the (-) responder rowers. The non-responder rowers and control subjects displayed no significant (P>0.05) hormone changes over the 20 weeks. The hormone changes observed in the (-) responder rowers were not significantly (P>0.05) correlated with changes in body composition or hydration status during the study. The mechanism for the hormone changes in the (-) responder rowers is unclear. We speculate the decrease in concentrations of TSH and fT3 could be attributable to a lower hypothalamic-pituitary signaling action, and this is related to the decreased leptin concentrations, and could represent a possible means of energy conservation in these exercising women”.
[E] BOYDEN T W PAMENTER R W, 1984. Thyroidal changes associated with endurance training in women. Med Sci Sports Exerc. 1984 Jun;16(3):243-6.
“The associations between endurance training, body composition, and the pituitary-thyroid axis were studied in 17 healthy, young women. Body composition and plasma concentrations of T4, T3, rT3, resin T3 uptake, TSH, and TRH-stimulated TSH were examined at baseline and after each subject’s weekly distance had increased 48 km (delta 48) and 80 km (delta 80) above baseline. Total body weight did not change at delta 48 or delta 80. Mean (+/- SE) lean weight in kg increased from 42.9 +/- 1.2 at baseline to 44.8 +/- 1.2 at delta 80 (P = 0.002). We have reported previously that at delta 48 the subjects had evidence of mild thyroidal impairment, which consisted of decreased T3 and rT3, and an exaggerated TSH response to TRH. With more prolonged training (delta 48 to delta 80) there were significant increases in T4, rT3, and unstimulated TSH, while the ratios of T4/rT3 and T3/rT3 and the TSH response to TRH decreased significantly. Some of the thyroidal changes that occurred between delta 48 and delta 80 are similar to those seen in other stressful non-thyroidal conditions”.
[F] PAKARINEN A HAKKINEN K, 1991. Serum thyroid hormones, thyrotropin and thyroxine binding globulin in elite athletes during very intense strength training of one week. J Sports Med Phys Fitness. 1991 Jun;31(2):142-6.
“The effects of a one-week very intense strength training period on maximal strength and pituitary-thyroid function were investigated in eight elite male weight lifters. No statistically significant changes occurred in the maximal isometric leg extension force of the test subjects. Decreased serum concentrations of thyrotropin (TSH), thyroxine (T4) and triiodothyronine (T3) were found during the training period, but no statistically significant changes occurred in the levels of free thyroxine (fT4), reverse T3 (rT3) and thyroxine binding globulin (TBG). The results suggest that the training stress affects at the hypophyseal and/or hypothalamic level decreasing the secretion of TSH, which leads to slightly decreased function of the thyroid gland”.
[G] DE SOUZA M J, 2003. Menstrual disturbances in athletes: a focus on luteal phase defects. Med Sci Sports Exerc. 2003 Sep;35(9):1553-63.
“Subtle menstrual disturbances that affect the largest proportion of physically active women and athletes include luteal phase defects (LPD). Disorders of the luteal phase, characterized by poor endometrial maturation as a result of inadequate progesterone (P4) production and short luteal phases, are associated with infertility and habitual spontaneous abortions. In recreational athletes, the 3-month sample prevalence and incidence rate of LPD and anovulatory menstrual cycles is 48% and 79%, respectively. A high proportion of active women present with LPD cycles in an intermittent and inconsistent manner. These LPD cycles are characterized by reduced follicle-stimulating hormone (FSH) during the luteal-follicular transition, a somewhat blunted luteinizing hormone surge, decreased early follicular phase estradiol excretion, and decreased luteal phase P4 excretion both with and without a shortened luteal phase. LPD cycles in active women are associated with a metabolic hormone profile indicative of a hypometabolic state that is similar to that observed in amenorrheic athletes but not as comprehensive or severe. These metabolic alterations include decreased serum total triiodothyronine (T3), leptin, and insulin levels. Bone mineral density in these women is apparently not reduced, provided an adequate estradiol environment is maintained despite decreased P4. The high prevalence of LPD warrants further investigation to assess health risks and preventive strategies”.
[H] DE SOUZA M J HEEST van, J, DEMERS L M , 2003. Luteal phase deficiency in recreational runners: evidence for a hypometabolic state. J Clin Endocrinol Metab. 2003 Jan;88(1):337-46.
“Exercising women with amenorrhea exhibit a hypometabolic state. The purpose of this study was to evaluate the relationship of luteal phase deficient (LPD) menstrual cycles to metabolic hormones, including thyroid, insulin, human GH (hGH), leptin, and IGF-I and its binding protein levels in recreational runners. Menstrual cycle status was determined for three consecutive cycles in sedentary and moderately active women. Menstrual status was defined as ovulatory or LPD. Subjects were either sedentary (n = 10) or moderately active (n = 20) and were matched for age (27.7 +/- 1.2 yr), body mass (60.2 +/- 3.3 kg), menstrual cycle length (28.4 +/- 0.9 d), and reproductive age (14.4 +/- 1.2 yr). Daily urine samples for the determination of estrone conjugates, pregnanediol 3-glucuronide, and urinary levels of LH were collected. Blood was collected on a single day during the follicular phase (d 2-6) of each menstrual cycle for analysis of TSH, insulin, total T3, total T4, free T4, leptin, hGH, IGF-I, and IGF binding protein (IGFBP)-1 and IGFBP-3. Among the 10 sedentary subjects, 28 of 31 menstrual cycles were categorized as ovulatory (SedOvul). Among the 20 exercising subjects, 24 menstrual cycles were included in the ovulatory category (ExOvul), and 21 menstrual cycles were included in the LPD category (ExLPD). TSH, total T4, and free T4 levels were not significantly different among the three categories of cycles. Total T3 was suppressed (P = 0.035) in the ExLPD (1.63 +/- 0.07 nmol/liter) and the ExOvul categories of cycles (1.75 +/- 0.8 nmol/liter) compared with the SedOvul category of cycles (2.15 +/- 0.1 nmol/liter). Leptin levels were lower (P < 0.001) in both the ExOvul (5.2 +/- 0.4 microg/liter) and the ExLPD categories of cycles (5.1 +/- 0.4 microg/liter) when compared with the SedOvul category of cycles (13.7 +/- 1.7 microg/liter). Insulin was lower (P = 0.009) only in the ExLPD category of cycles (31.9 +/- 2.8 pmol/liter) compared with the SedOvul (60.4 +/- 8.3 pmol/liter) and ExOvul (61.8 +/- 10.4 pmol/liter) categories of cycles. IGF-I, IGFBP-1, IGFBP-3, IGF-I/IGFBP-1, IGF-I/IGFBP-3, and hGH were comparable among the different categories of cycles. These data suggest that exercising women with LPD menstrual cycles exhibit hormonal alterations consistent with a hypometabolic state that is similar to that observed in amenorrheic athletes and other energy-deprived states, although not as comprehensive. These alterations may represent a metabolic adaptation to an intermittent short-term negative energy balance”.
[I] KILIC M BALTACI A K GUNAY M, 2006. The effect of exhaustion exercise on thyroid hormones and testosterone levels of elite athletes receiving oral zinc. Neuro Endocrinol Lett. 2006 Feb-Apr;27(1-2):247-52.
“OBJECTIVES: The present study aims to investigate how exhaustion exercise affects thyroid hormones and testosterone levels in elite athletes who are supplemented with oral zinc sulfate for 4 weeks.
METHODS: The study included 10 male wrestlers, who had been licensed wrestlers for at least 6 years. Mean age of the wrestlers who volunteered in the study was 18.70 +/- 2.4 years. All subjects were supplemented with oral zinc sulfate (3 mg/kg/day) for 4 weeks in addition to their normal diet. Thyroid hormone and testosterone levels of all subjects were determined as resting and exhaustion before and after zinc supplementation.
RESULTS: Resting TT3, TT4, FT3, FT4 and TSH levels of subjects were higher than the parameters measured after exhaustion exercise before zinc supplementation (p<0.05). Both resting and exhaustion TT3, TT4 and FT3 values after 4-week zinc supplementation were found significantly higher than both of the parameters (resting and exhaustion) measured before zinc supplementation (p<0.05). Resting total testosterone and free testosterone levels before zinc supplementation were significantly higher than exhaustion levels before zinc supplementation (p<0.05). Both resting and exhaustion total and free testosterone levels following 4-week zinc supplementation were found significantly higher than the levels (both resting and exhaustion) measured before zinc supplementation (p<0.05). CONCLUSION:Findings of our study demonstrate that exhaustion exercise led to a significant inhibition of both thyroid hormones and testosterone concentrations, but that 4-week zinc supplementation prevented this inhibition in wrestlers. In conclusion, physiological doses of zinc administration may benefit performance”.
[J] KILIC M, 2007. Effect of fatiguing bicycle exercise on thyroid hormone and testosterone levels in sedentary males supplemented with oral zinc. Neuro Endocrinol Lett. 2007 Oct;28(5):681-5. “OBJECTIVE: The aim of this study was to determine how exercise affects thyroid hormones and testosterone levels in sedentary men receiving oral zinc for 4 weeks.
METHODS: The study included 10 volunteers (mean age, 19.47+/-1.7 years) who did not exercise. All subjects received supplements of oral zinc sulfate (3 mg/kg/day) for 4 weeks and their normal diets. The thyroid hormone and testosterone levels of all subjects were determined at rest and after bicycle exercise before and after zinc supplementation.
RESULTS: TT3, TT4, FT3, and total and free testosterone levels decreased after exercise compared to resting levels before supplementation (p<0.01). Both the resting and fatigue hormone values were higher after 4 weeks of supplementation than the resting and fatigue values before supplementation (p<0.05). CONCLUSION: The results indicate that exercise decreases thyroid hormones and testosterone in sedentary men; however, zinc supplementation prevents this decrease. Administration of a physiologic dose of zinc can be beneficial to performance”.
[K] CINAR V, 2007. The effects of magnesium supplementation on thyroid hormones of sedentars and Tae-Kwon-Do sportsperson at resting and exhaustion. Neuro Endocrinol Lett. 2007 Oct;28(5):708-12. “The effect of magnesium on thyroid hormones of sedentars and sportsperson in Tae-Kwon-Do, has been investigated in a 4-weeks training program. Group 1 consisted of sedentars receiving 10 mg/kg/day Mg for 4 weeks. Group 2 consisted of subjects receiving magnesium (Mg) supplement and practicing Tae-Kwon-Do for 90-120 min/day, for five days a week. Group 3 consisted of subjects practicing Tae-Kwon-Do but receiving Mg supplements. TSH levels increased with training and Mg supplementation (p<0.05). Mg increased FT3 values. (p<0.05). TT3 values of groups reduced in all groups (p<005). After supplementation, group 1 had higher TT4 values than groups 1 and 3 and the group 2 had higher TT4 values than the third group (p<005). Results of this research show that training until exhaustion causes reduction in thyroid hormone activity in sedentars and sportsperson. It has been established that Mg supplementation however, prevents reduction in thyroid hormone activity in sedentars and sportsperson”.
[L] HACKNEY A C KALLMAN A HOSICK K P, 2012. Thyroid hormonal responses to intensive interval versus steady-state endurance exercise sessions. Hormones (Athens). 2012 Jan-Mar;11(1):54-60. “OBJECTIVE: To compare the thyroid hormonal responses to high-intensity interval exercise (IE) and steady-state endurance exercise (SEE) in highly trained males (n=15).
DESIGN: The IE session consisted of repeated periods of 90-seconds treadmill running at 100-110% VO(2max) and 90-seconds active recovery at 40% VO(2max) for 42-47 minutes. The SEE session was a 45-minute run at 60-65% VO(2max). Total work output was equal for each session. A 45-minute supine rest control session (CON) was also performed. Pre-session (PRE), immediate post-session (POST), and 12-hours post-session (12POST) blood samples were collected and used to determine free (f) T₄, fT₃, reverse (r) T₃, and cortisol levels.
RESULTS: All PRE hormone levels were within clinical norms and did not differ significantly between sessions. All POST IE and SEE hormone levels were significantly elevated compared to POST CON (p<0.001). At 12POST, no significant differences between CON and SEE hormonal levels were observed; however, fT₃ was significantly reduced and rT3 was significantly elevated in 12POST IE compared to 12POST SEE and CON (p=0.022). For IE, at 12POST a negative correlation (r(s) = -0.70, p<0.004) was found between fT₃ and rT₃. Also, for IE, a positive correlation (r(s) = 0.74, p<0.002) between cortisol POST and rT₃ 12POST was noted, and a negative correlation (r(s) = -0.72, p<0.003) between cortisol POST and fT₃ 12POST. CONCLUSION: IE results in a suppressed peripheral conversion of T₄ to T₃ implying that a longer recovery period is necessary for hormonal levels to return to normal following IE compared to SEE. These findings are useful in the implementation of training regimens relative to recovery needs and prevention of over-reaching-overtraining”.
[M] JOHANNSEN D L KNUTH N D, 2012. Metabolic slowing with massive weight loss despite preservation of fat-free mass. J Clin Endocrinol Metab. 2012 Jul;97(7):2489-96. doi: 10.1210/jc.2012-1444. Epub 2012 Apr 24.
“CONTEXT: An important goal during weight loss is to maximize fat loss while preserving metabolically active fat-free mass (FFM). Massive weight loss typically results in substantial loss of FFM potentially slowing metabolic rate.
OBJECTIVE: Our objective was to determine whether a weight loss program consisting of diet restriction and vigorous exercise helped to preserve FFM and maintain resting metabolic rate (RMR).
PARTICIPANTS AND INTERVENTION: We measured body composition by dual-energy x-ray absorptiometry, RMR by indirect calorimetry, and total energy expenditure by doubly labeled water at baseline (n = 16), wk 6 (n = 11), and wk 30 (n = 16).
RESULTS: At baseline, participants were severely obese (× ± SD; body mass index 49.4 ± 9.4 kg/m(2)) with 49 ± 5% body fat. At wk 30, more than one third of initial body weight was lost (-38 ± 9%) and consisted of 17 ± 8% from FFM and 83 ± 8% from fat. RMR declined out of proportion to the decrease in body mass, demonstrating a substantial metabolic adaptation (-244 ± 231 and -504 ± 171 kcal/d at wk 6 and 30, respectively, P < 0.01). Energy expenditure attributed to physical activity increased by 10.2 ± 5.1 kcal/kg.d at wk 6 and 6.0 ± 4.1 kcal/kg.d at wk 30 (P < 0.001 vs. zero). CONCLUSIONS: Despite relative preservation of FFM, exercise did not prevent dramatic slowing of resting metabolism out of proportion to weight loss. This metabolic adaptation may persist during weight maintenance and predispose to weight regain unless high levels of physical activity or caloric restriction are maintained”. Mostrou que exercício não evitou dramática desaceleração do metabolismo em repouso [M].
[N] LOUCKS A B CALLISTER R, 1993. Induction and prevention of low-T3 syndrome in exercising women. Am J Physiol. 1993 May;264(5 Pt 2):R924-30.
“To investigate the influence of exercise on thyroid metabolism, 46 healthy young regularly menstruating sedentary women were randomly assigned to a 3 x 2 experimental design of aerobic exercise and energy availability treatments. Energy availability was defined as dietary energy intake minus energy expenditure during exercise. After 4 days of treatments, low energy availability (8 vs. 30 kcal.kg body wt-1.day-1) had reduced 3,5,3′-triiodothyronine (T3) by 15% and free T3 (fT3) by 18% and had increased thyroxine (T4) by 7% and reverse T3 (rT3) by 24% (all P < 0.01), whereas free T4 (fT4) was unchanged (P = 0.08). Exercise quantity (0 vs. 1,300 kcal/day) and intensity (40 vs. 70% of aerobic capacity) did not affect any thyroid hormone (all P > 0.10). That is, low-T3 syndrome was induced by the energy cost of exercise and was prevented in exercising women by increasing dietary energy intake. Selective observation of low-T3 syndrome in amenorrheic and not in regularly menstruating athletes suggests that exercise may compromise the availability of energy for reproductive function in humans. If so, athletic amenorrhea might be prevented or reversed through dietary reform without reducing exercise quantity or intensity”.
[O] Exercise and effect on thyroid hormone, By Team FPS – April 23, 2012. Disponível em: https://www.functionalps.com/blog/2012/04/23/exercise-and-effect-on-thyroid-hormone/
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