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ORIGINAL ARTICLE
Year : 2012  |  Volume : 9  |  Issue : 3  |  Page : 88-92

Effects of submaximal aerobic exercise on thyroid hormones in hypoxic conditions in trained young men


1 Department of Exercise Physiology, Islamic Azad University, Central Tehran Branch, Tehran, Iran
2 Department of Clinical, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran
3 Department of Biostatistics, National Public Health Management Center and Department of Statistics and Epidemiology, Tabriz University of Medical Sciences, Tabriz, Iran

Date of Web Publication11-Aug-2012

Correspondence Address:
Suzan Sanavi
Akhavan Center, Monyrieh squ, Valiye-Asr Ave, 1113813111
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-0354.99651

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  Abstract 

Background: There are many conflicting opinions regarding the effects of hypoxia on thyroid hormones in different situations. This study evaluates the effect of exercise-induced hypoxia on thyroid hormones and thyroid-stimulating hormone (TSH) in trained young men. Materials and Methods: The participants consisted of 17 healthy men, aged 20-24 years, with mean maximal oxygen uptake and body mass index of 48.6 ± 3.96 ml/kg/min and 21.6 ± 0.91 kg/m 2 , respectively. They did 30-min running on treadmill, at the intensity of 70% of maximal heart rate, in normoxia and three different levels of simulated hypoxic conditions at 2750, 3250, and 3750 m heights. The sessions were interspaced with 72-hour resting breaks. Blood samples for hormonal assays were obtained before exercise and at 0 h and 1 h after exercise. Results: Data analysis, using mixed models, showed no statistically significant hormonal difference among the hypoxic conditions (P > 0.05) except increased thyroxin levels following exercise in all sessions , which were significant only in normoxia and 2750 m height (P < 0.05), without any significant changes in serum triiodotyronine and TSH. Conclusion: With respect to different reports surrounding the effects of high-altitude-induced hypoxia on pituitary-thyroid axis (including stimulatory, inhibitory, or changeless effects), this study revealed only significant increased thyroxin level at 1200 (normoxia) and 2750 m heights, following exercise. These contradictory findings may be attributed to the degree of prescribed hypoxia, planning of natural or simulated height, activity level and type, and study duration. However, for a precise conclusion, further research is recommended.

Keywords: Aerobic activity, height, hypoxia, thyroid hormones


How to cite this article:
Peeri M, Kohanpour MA, Sanavi S, Pazukian M, Jafarabadi MA, Mirsepasi M. Effects of submaximal aerobic exercise on thyroid hormones in hypoxic conditions in trained young men. Thyroid Res Pract 2012;9:88-92

How to cite this URL:
Peeri M, Kohanpour MA, Sanavi S, Pazukian M, Jafarabadi MA, Mirsepasi M. Effects of submaximal aerobic exercise on thyroid hormones in hypoxic conditions in trained young men. Thyroid Res Pract [serial online] 2012 [cited 2020 Oct 24];9:88-92. Available from: https://www.thetrp.net/text.asp?2012/9/3/88/99651


  Introduction Top


High altitude, elevation above 3000 m from sea level, causes physiological and biochemical changes in most individuals. However, there is controversy in definite description of high altitude. [1],[2] High-altitude-induced hypoxia can influence various hormonal responses including pituitary and thyroid hormones, although its role is not well understood. There are two main thyroid hormones, thyroxin (T 4 ) and triiodotyronine (T 3 ), which increase the rate of metabolism with different severity. Thyroid gland function is regulated by pituitary thyroid-stimulating hormone (TSH). These hormones play a critical role in cell differentiation during development and help maintain thermogenic and metabolic homeostasis in the adult. Although TSH is the dominant hormonal regulator of thyroid gland function, a variety of physiological and environmental factors such as exercise and hypoxia can influence thyroid hormone synthesis, through the hypothalamic thyrotropin-releasing hormone (TRH). It seems that implementation of the simulated heights by commercial devices, as a popular approach, results in further improvement in aerobic capacity of individuals for training purposes. However, because of increased physiological stress in these situations (physical activity in hypoxic conditions), the individual's ability to maintain hormonal balance may change. [3],[4] For instance, while the basal metabolic rate increases about 10-17% in high elevations, [5],[6] severe hypoxia can surprisingly reduce thyroid gland function in rats. Indeed, there has been a lot of controversy surrounding the effects of hypoxia on thyroid hormones so that either stimulatory [7],[8],[9] or inhibitory effects have been reported. [10],[11] This study evaluates the effects of submaximal aerobic activity on thyroid hormones and TSH in different hypoxic conditions in trained young men.


  Materials and Methods Top


Subjects

Following announcing call among university students in Tehran and clearly defining the study purposes, out of 23 volunteers 17 eligible (based on medical history, physical examination and laboratory records in a questionnaire) healthy men (non smoker and non alcoholic) were registered for the study. They were trained young (20-24 years) males who had regular physical training of 6.0 ± 0.55 h/week, during prior 2 years.

Exercise program

At first, aerobic power of the participants was measured, using Bruce test on treadmill, [12] and 5 days later they met in the first exercise session. Exercise protocol consisted of four sessions of 30-min running on treadmill at the intensity of 70% of age-predicted maximal heart rate (APMHR) in normoxia, at 1200 m height above sea level, in Tehran [fraction of inspired oxygen (FiO 2 ) of 0.21] and three different levels of simulated normobaric hypoxic conditions (2 of 0.15, 0.14, and 0.13 equivalent to 2750, 3250, and 3750 m heights, provided by an Australia made high-altitude simulator device the "Go2Altitude® Hypoxicator"). [12] Indeed, the hypoxic environment was created by reducing the O 2 concentration of inspired air using a commercially available device through inhalation. Maximal heart rate (MHR) was calculated by the following equation: 208 − (0.7 × age).[13] The sessions were interfered with 72-hour resting periods, and to avoid misleading results, the order of sessions was chosen on a random basis. The participants were asked to avoid caffeine intake at nights before sampling days. Each session was started and finished in a definite time which was similar for each participant during the study. All protocols were approved by the Graduate Council of Faculty of Physical Education and Sport Sciences of Islamic Azad University.

Blood sampling and hormone analysis

Venous blood samples from antecubital vein in the sitting position were taken before, immediately (0 h) and 1 hour after each exercise session. Serum T 4, T 3 , and TSH levels were measured for each participant by a chemiluminescence method using Chinese kits "Autobio" with a sensitivity of 1 mcg/dL, 0.5 ng/mL, and 0.25 mIU/mL, respectively.

Statistical analysis

All analyses were performed using the SPSS v.16 statistical software (SPSS Inc., Chicago, IL). Quantitative variables were presented as mean ± standard deviation (SD). The normality of the study variables was determined by one-sample Kolmogorov-Smirnov test. In addition, skewness and kurtosis measures have been used to confirm the results of the test due to low number of samples, since in this case the KS test tends toward rejecting the null hypothesis of normal distribution. Absolute values less than 2 and 3, respectively, for skewness and kurtosis were considered as normality. For TSH and T 3 , the normality of data was rejected and hence logarithmic transformations were applied on the data. Linear mixed model analyses were used to assess the effect of repeated measurements within four sessions of exercises. Repeated measures within session constructed the covariance structure in these analyses. Based on Akaike's Information Criterion, the first-order autoregressive as the optimal covariance structure was determined. Restricted maximum likelihood procedure was used to fit the model. To address the hypotheses of the study, several analyses were performed for each dependent variable. In significant cases, the results of mixed models were followed by Sidak post hoc test (adjusted for pairwise comparisons). P-values less than 0.05 were considered as significant.


  Results Top


Physical characteristics of the participants have been summarized in [Table 1]. [Table 2], [Table 3] and [Table 4] show the mean values of serum T 4 , T 3 , and TSH levels in pre- and post-exercise (at 0 h and 1 hour) stages.
Table 1: Physical characteristics of the participants

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Table 2: Pre and post-exercise T4 levels (mcg/dL)

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Table 3: Pre and post-exercise T3 levels (ng/mL)

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Table 4: Pre and post-exercise TSH levels (mIU/mL)

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A significant difference was found for T 4 levels within measures totally evaluated in the sessions [F(8,72) = 2.261, P = 0.032]. Moreover, in separate evaluation of measurements, significant differences were observed between normoxia and hypoxia at 2750 m height (both P < 0.05). In addition, the results of the post hoc test showed a significant difference between pre-exercise and 0 h post-exercise stages (P = 0.028 and P = 0.035, respectively) and pre-exercise and 1 h post-exercise stages (P = 0.004 and P = 0.024, respectively). No significant difference was found among four sessions in different stages (all P > 0.05) [Table 2].

No significant difference was observed for T 3 and TSH levels within measures totally evaluated in the sessions [F(8,68) = 1.176, P = 0.327 and F(8,84) = 0.578, P = 0.793, respectively], within measurements in all the four sessions (all P >0.05) and among sessions in different stages (all P >0.05) [Table 3] and [Table 4].


  Discussion Top


The thyroid axis is a classic example of an endocrine feedback loop. Hypothalamic TRH stimulates pituitary production of TSH, which, in turn, stimulates thyroid hormone synthesis and secretion. Thyroid hormone feedback negatively inhibits TRH and TSH production. The "set-point" in this axis is established by TSH. It has been reported that thyroid gland can escape from hypothalamic-pituitary axis and act independently in hypoxic conditions at elevations below 5000 m resulting in normal values of TRH and TSH levels. [14],[15],[16],[17] However, decreased [18],[19] and increased [20],[21],[22] TSH levels have been found in different investigations, particularly at elevations above 5000 m, which can be attributed to the severity and duration of hypoxia. [18],[19] It seems that the matter continues to be a subject of controversy. Similar to the investigation by Richalet et al., [23] our study showed no significant alteration of TSH probably due to the low level of prescribed simulated hypoxia or shortness of training sessions indicating that the hypophyseal response to hypothalamic factors did not appear to be blunted.

Hypoxia, either natural or simulated, can increase thyroid hormones. [14],[15],[16],[17],[24] Several environmental factors may contribute in this effect, particularly with natural hypoxic conditions, such as the cold, humidity, wind speed, the amount of sun light and ultraviolet light, and separation from family. [17] How environmental factors affect the thyroid gland function in humans, at high altitude, is still unknown. However, these factors may explain some disagreements regarding the controversial findings of different studies. Basu et al suggested that high-altitude-induced elevated level of thyroid hormones could be due to increased binding affinity to thyroxin binding globulin, [17] but other investigators did not confirm this finding. [14],[16],[25] Another explanation for increased thyroid hormones at high altitude arise from increasing of basal metabolic rate (BMR) related to physical stress and increased oxygen demand. Thyroid gland in association with adrenal medulla plays an important role in regulation of metabolism resulting in 10-17% increment of BMR. [5],[6],[26],[27] Furthermore, it has been suggested that thyroid hormones may be necessary for erythrocyte 2,3-diphosphoglyceric acid synthesis in hemoglobin-oxygen dissociation process in hypoxic conditions. [28] However, some studies have shown reduced levels of thyroid hormones, at different heights, related to decreasing of iodide binding to serum proteins and decreased iodide uptake as a critical first step in thyroid hormone synthesis. Iodide uptake is mediated by the Na + /I symporter, which is expressed at the basolateral membrane of thyroid follicular cells. Reduction of thyroid hormones may also be attributed to inhibition of iodide trapping; oxidation (organification) and coupling that are catalyzed by thyroid peroxidase or hormone release due to severe hypoxia. It seems that the severity and duration of hypoxia determine the intensity of inhibition of thyroid hormone synthesis. [7],[19],[20],[29],[30],[31],[32] Simonides et al found that hypoxia induced expression of the type 3 deiodinase (D3) gene, an enzyme that inactivates T 3 and prevents activation of the prohormone-thyroxin, by a hypoxia-inducible factor-dependent (HIF-dependent) pathway. [33] Controversy over this issue still continues and needs further investigation. This study revealed increased levels of T 4 following exercise in all sessions, which were significant only in normoxia and 2750 m height, without any significant changes in serum T 3 . Comparing to other studies, [34] our findings may be influenced by the level and nature (simulated) of prescribed hypoxia or height, shortness of training sessions, and intensity or type of exercise program.


  Conclusion Top


Although submaximal aerobic exercise with the intensity of 70% of MHR in normoxic and different simulated hypoxic conditions resulted in no significant changes of thyroid hormones, it may be reasonable to encourage the young athletes using the hypoxia simulating devices (up to simulation of hypoxic condition at 3750 m height) to improve their physical performance.

 
  References Top

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]


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