Diese Präsentation wurde erfolgreich gemeldet.
Wir verwenden Ihre LinkedIn Profilangaben und Informationen zu Ihren Aktivitäten, um Anzeigen zu personalisieren und Ihnen relevantere Inhalte anzuzeigen. Sie können Ihre Anzeigeneinstellungen jederzeit ändern.

Hormonal response to exersize

103 Aufrufe

Veröffentlicht am


Veröffentlicht in: Gesundheit & Medizin
  • Als Erste(r) kommentieren

Hormonal response to exersize

  1. 1.  Introduction  Hormones: Regulation and Action  Hypothalamus and the  Pituitary Gland  Thyroid Gland  Parathyroid Gland  Adrenal Gland  Pancreas  Ovaries and Testes  Neuroendocrinology  Blood Hormone  Concentration  Hormone-Receptor  Interaction  Neuroendocrine aspects of overtraining  Hormonal Control of Substrate Mobilization During Exercise  Muscle-Glycogen  Utilization  Blood Glucose  Homeostasis During  Exercise  Hormone-Substrate  Interaction  Conclusions and clinical relevance References
  2. 2.  HORMNAL RESPONSE Hormonal stimuli refers to the release of a hormone in response to another hormone.  A number of endocrine glands release hormones when stimulated by hormones released by other endocrine glands.  For example, the hypothalamus produces hormones that stimulate the anterior portion of the pituitary gland
  3. 3.  Hormones are necessary to help the body make acute and chronic adaptations to exercise  Acute exercise:- single bout of exercise  Exercise training or the “chronic exercise” intervention can be defined as a repeated amount of bouts of exercise during a short or long-term period of time) are necessary to help the body make acute and chronic adaptations to exercise  single bout of exercise  training or the “ ” intervention can be defined as a repeated amount of bouts of exercise during a short or long-term period of time)
  4. 4.   It is, however, a very varied and complex physiological stimulus .  .  With the increasing popularity of exercise training for the maintainence of good health and even the treatment of existing diseases, . 
  5. 5.
  6. 6.
  7. 7.  or expressed as a percentage (measured directly or calculated) of the individual subject’s maximum work capacity.  Work capacity, in turn, may be expressed as either maximum tolerated work load in the particular experimental system or as the measured maximum aerobic capacity (V02 max)  When assessing hormonal responses to training reference should be made to the relative intensity of the exercise stimulus, expressed as VO2max ~ rather than absolute work load, and this is indicated as appropriate 
  8. 8.  Most exercise studies conclude that both high intensity and endurance exercises cause an increase in plasma ACTH ( Adreno cortico tropic hormone ) and cortisol in humans  However, the exercise-induced plasma cortisol increase may not be directly related to the exercise-induced ACTH increase,because both hormones show a different exercise related response.  ACTH increases curvilinear with exercise intensity, while cortisol increases more with increasing exercise duration.  A significant increase in plasma cortisol concentration was found following exercise. 
  9. 9.  However, there was no relationship with relative work intensity or blood lactate concentration.  The suggestion was made that the exercise test was too short (total time test270 s) to induce a consequent increase in cortisol concentration  In general, for humans  High intensity exercise results in a 2-3 fold increase in cortisol,  Peaking usually 15-30 minutes after exercise, And  Returning to pre-exercise levels within the hour  Endurance exercise usually requires duration of exercise of more than 20 minutes with  
  10. 10.  High intensity exercise results in an increase in ACTH, usually peaking the end of exercise and returning to baseline within 60-120 minutes  Prolonged sub maximal exercise or endurance exercise shows a later peak in plasma cortisol and a slower return to pre-exercise levels than high intensity exercise  Several factors influence the exercise-induced cortisol response EXAMPLE  Circadian rhythm,  Multiple exercise bouts  High intensity versus  Prolonged sub maximal exercise  Nutrition  Training. 
  11. 11.  A significant stimulatory effect of exercise on Cortisol levels  Only in the afternoon and  Not in the early morning or during the night after performing  Low intensity exercise (3h at 40-60% V02max  However, the intensity of exercise might have been too low to induce a good response inthis study. 
  12. 12.  Repeated bouts of high-intensity endurance exercise  2 bouts of 65 min 70% V02 max, 3h rest in between) resulted in increased plasma concentrations of ACTH and cortisol during exercise and early recovery  Two bouts of high intensive exercise with a 4h rest period in between showed an exaggerated response for ACTH and cortis after the second bout  In addition, the first bout of exercise was not able to induce an increase in cortisol concentration 
  13. 13.  Two bouts of moderate intensity exercise (30 min 50% V02 max, 45 minrest in between) did not change the cortisol response to the second bout of exercise  Four bouts of moderate intensity (30 min, 50% V02 max, 30min rest) progressively increased concentrations of cortisol throughout the series of exercise bouts  However, cortisol concentrations were still augmented during the rests in the last study, which may partly account for the progressive increase
  14. 14. Cortisol response after the second bout of exercise(50% V02 max, 90-min, 3-h rest) in men and an increased cortisol response in women  Comparison to other experiments is difficult, because the athlete's plasma glucose was maintained at euglycaemia during the experiment by glucose infusions  
  15. 15.  Some studies investigated the HPA axis during Long-term recovery after exercise  Studied the cortisol response after an incremental exercise test till exhaustion and during a recovery period of 32 hours in 4 geldings  A significant increase of mean plasma cortisol concentration after exercise was found, followed by a significant decrease 4-8 hours post exercise and a significant increase 20-24 hours post exercise compared to basal levels, the same alterations found in men 
  16. 16.  Most studies find elevated ACTH levels at rest intrained subjects versus untrained subjects  Mostly, basal cortisol levels are not elevated, which might indicate that the adrenal gland is less sensitive to ACTH due to training decreased pituitary sensitivity to gluco- corticoids in endurance-trained men (50-70 km running per wk, completed marathon in less than 3h30min) compared to sedentary  men ( < lh physical activity per week) 
  17. 17.  At rest, 3 out of 9 endurance-trained men responded with an increase in ACTH and cortisol after administration of CRH while at the mean time dexa-methason was given to suppress endogenous cortisol secretion  The sedentary group as well as 5 out of 9 endurance-trained athletes did not respond to an injection with oCRH  Basal cortisol and ACTH levels were not significantly different between both groups
  18. 18.  Only the highly trained runners showed basal elevated levels for ACTH and cortisol and a blunted response of ACTH and cortisol to administration of oCRH  Some researchers tried to evaluate prolonged periods of training by determination of the ratio of catabolic to anabolic hormones using cortisol as catabolic hormone and sex steroids or IGF-I as anabolic hormone  However, based on the current literature it is difficult to conclude whether any androgen to cortisol ratio is a useful indicator of training status in endurance athletes 
  19. 19. The responses of ACTH and cortisol reflect the stress impact of the current training load on the body, but it does not necessarily indicate overtraining. 
  20. 20. Hormones are secreted from Endocrine glands  – Hypothalamus and pituitary glands  – Thyroid and parathyroid glands  – Adrenal glands  – Pancreas  – Testes and ovaries 
  21. 21. Hypothalamus Controls secretions from pituitary gland  • Anterior Pituitary Gland –Adrenocorticotropic hormone (ACTH) – Follicle-stimulating hormone (FSH) – Luteinizing hormone (LH) – Melanocyte-stimulating hormone (MSH) – Thyroid-stimulating hormone (TSH) – Growth hormone (GH) – Prolactin  • Posterior Pituitary Gland – Oxytocin – Antidiuretic hormone (ADH) 
  22. 22.  Stimulates release of hormones from Anterior pituitary gland – Releasing hormones or factors  Provides hormones for release from Posterior pituitary gland 
  23. 23.  While it’s very small, the hypothalamus plays a crucial role in many important functions, including:-  Releasing hormones  Regulating body temperature  Maintaining daily physiological cycles  Controlling appetite  Managing of sexual behavior  Regulating emotional responses 
  24. 24.  • Adrenocorticotropic hormone (ACTH) – Stimulates cortisol release from adrenal glands  • Follicle-stimulating hormone (FSH)  • Luteinizing hormone (LH) – Stimulates production of testosterone and estrogen  • Melanocyte-stimulating hormone (MSH)  • Thyroid-stimulating hormone (TSH) – Controls thyroid hormone release from thyroid gland  • Prolactin  • Growth hormone (GH) 
  25. 25.  Some of the most important hormones produced in the anterior region include:  Corticotropin-releasing hormone (CRH)  CRH is involved in the body’s response to both physical and emotional stress.  It signals the pituitary gland to produce a hormone called adreno-corticotropic hormone (ACTH)  ACTH triggers the production of cortisol, an important stress hormone.  Thyrotropin-releasing hormone (TRH). TRH production stimulates the pituitary gland to produce thyroid-stimulating hormone (TSH). TSH plays an important role in the function of many body parts, such as the heart, gastrointestinal tract, and muscles. 
  26. 26.  Gonadotropin-releasing hormone (GnRH):- GnRH production causes the pituitary gland to produce important reproductive hormones, such as follicle- stimulating hormone (FSH) and luteinizing hormone (LH). They act on the ovaries or testes to stimulate sex hormone production, and egg and sperm maturity  Oxytocin.:-This hormone controls many important behaviors and emotions, such as sexual arousal, trust, recognition, and maternal behavior. It’s also involved in some functions of the reproductive system, such as childbirth and lactation. which stimulates uterine contractions during labour and milk secretion during breastfeeding. 
  27. 27.  Vasopressin:- Also called antidiuretic hormone (ADH), this hormone regulates water levels in the body. When vasopressin is released, it signals the kidneys to absorb water.  Somatostatin:- Somatostatin works to stop the pituitary gland from releasing certain hormones, including growth hormones and thyroid-stimulating hormones  Growth hormone, which regulates growth, metabolism and body composition  The anterior region of the hypothalamus also helps regulate body temperature through sweat. It also maintains circadian rhythms. These are physical and behavioral changes that occur on a daily cycle. For example, being awake during the day and sleeping at nighttime is a circadian rhythm related to the presence or absence of light.  
  28. 28. – IGF-1 in muscle responsible for muscle growth  – Amino acid uptake and protein synthesis – Long bone growth -Reduces the use of plasma glucose -Increases gluconeogenesis -Mobilizes fatty acids from adipose tissue 
  29. 29.
  30. 30. – Used to treat childhood dwarfism – Also used by athletes and elderly  – Protein synthesis is collagen, not contractile protein 
  31. 31.  
  32. 32.
  33. 33.
  34. 34.
  35. 35.  – Establishment of metabolic rate  – Permissive hormones  Permit full effect of other hormones – Regulation of plasma Ca+2 Blocks release from bone, stimulates excretion by kidneys – Primary hormone in plasma Ca+2 regulation Stimulates release from bone, stimulates reabsorption by  kidneys 
  36. 36.  Some of the important functions of the thyroid hormones include-  :-Neural growth and differentiation  :-Myocardial contractility :-Regulation of bone formation and resorption,  :- Development and function of brown and white adipose tissue  :-Cholesterol metabolism and synthesis  :- In-utero they are important for fetal growth and differentiation 
  37. 37.  – Primary hormone in plasma Ca+2 regulation  – Stimulates reabsorption of Ca+2 by kidneys  Ca+2 absorption from GI tract 
  38. 38.  The four parathyroid glands make more or less parathyroid hormone (PTH) in response to the level of calcium in the blood. .  Increased PTH causes the body to put more calcium into the blood.  Increased PTH causes the bones to release their calcium into the blood.
  39. 39. – Epinephrine (E) and norepinephrine (NE) Fast-acting hormones Part of “fight or flight” response – Bind to adrenergic receptors Alpha ( ) Beta ( ) – Effects depend on hormone used and receptor type
  40. 40.         
  41. 41.  Epinephrine and norepinephrine bind to - and  -adrenergic receptors and bring about changes in
  42. 42.  Secretes steroid hormones – Derived from cholesterol  • Mineralcorticoids – Aldosterone – Maintenance of plasma Na+ and K+  • Glucocorticoids – Cortisol – Regulation of plasma glucose  • Sex steroids – Androgens and estrogens – Support prepubescent growth
  43. 43.  The adrenal cortex secretes  Aldosterone (mineralcorticoid)  Cortisol (glucocorticoid)  Estrogens and androgens (sex steroids).  Aldosterone regulates Na+ reabsorption and K+ balance.  Aldosterone secretion increases with strenuous exercise, driven by the renin-angiotensin system  . • Regulation of blood volume and blood pressure  – Part of renin-angiotensin-aldosterone system  – All three hormones increase during exercise  • Stimulated by:  – Increased K+ concentration  – Decreased plasma volume
  44. 44.  Exercise, to ensure that fuel (glucose and free fatty acids) is available, and to make amino acids available for tissue repair.
  45. 45.  – Promotes protein breakdown for gluconeogenesis – Stimulates FFA mobilization – Stimulates glucose synthesis – Blocks uptake of glucose into cells  Promotes the use of free fatty acids as fuel   – Stress, via ACTH  Part of General Adaptation Syndrome  – Exercise
  46. 46. Functions in the body It is hormone Released in response to stress and low blood-glucose concentration. Human endocrine system
  47. 47.  – Leptin  Influences appetite through the hypothalamus  Enhances insulin sensitivity and fatty acid oxidation  – Adiponectin  Increases insulin sensitivity and fatty acid oxidation   – Higher leptin levels and lower adiponectin  – Leads to type 2 diabetes and low-grade  inflammation
  48. 48.  > • Secretes: 1:– Insulin (from cells) Promotes the storage of glucose, amino acids, and fats Lack of insulin is called diabetes mellitus 2:– Glucagon (from cells) Promotes the mobilization of fatty acids and glucose 3:– Somatostatin (from cells) Controls rate of entry of nutrients into the circulation 4:– Digestive enzymes and bicarbonate Into the small intestine
  49. 49.  by the Cells of the islets of Langerhans in the pancreas and promotes the storage of glucose, amino acids, and fats. by the Cells of the islets of Langerhans in the pancreas and promotes the mobilization of glucose and fats.
  50. 50. – Released from testes – Anabolic steroid Promotes tissue (muscle) building Performance enhancement – Androgenic steroid Promotes masculine characteristics – Released from ovaries – Establish and maintain reproductive function – Levels vary throughout the menstrual cycle
  51. 51. is a steroid hormone that helps control and guide female sexual development.  Estrogen is responsible for stimulating the development of female secondary sex characteristics.  We know that secondary sex characteristics are defined as characteristics specific to females or males, but not directly related to reproduction.  Therefore, in a female, we see estrogen helps with such things as development of the breasts, widening of the hips, and the growth of body hair.  Estrogen works in harmony with , which is a steroid hormone that acts to prepare the uterus to receive the fertilized egg and maintain pregnancy.  While it is correct to say that progesterone is secreted by the ovaries, it's more correct to say that it is a hormone produced by the corpus luteum of the ovaries.  The corpus luteum is a structure that develops in an  ovary after the egg has been discharged.
  52. 52. is a sex hormone that plays important roles in the body  In men, it’s thought to regulate sex drive (libido), bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm.  A small amount of circulating testosterone is converted to estradiol, a form of estrogen and establish and maintain reproductive function and determine secondary sex characteristics  Chronic exercise (training) can decrease testosterone levels in males and estrogen levels in females.  The latter adaptation has potentially negative consequences related to osteoporosis.
  53. 53.  Muscle mass – In contrast to real-world reports “Subjects” used 10 to 100 times the recommended dosage  • Also associated with negative side effects – Revert to normal after discontinuation  • Widespread use has led to testing of competitive athletes • Most users are not competitive athletes – Take more than one steroid in megadoses
  54. 54. – High-intensity exercise results in greater and more rapid glycogen depletion - High-intensity exercise results in greater increases in plasma epinephrin Hormonal Control of Substrate Mobilization During Exercise
  55. 55. Hormonal Control of Substrate Mobilization During Exercise
  56. 56. Plasma Ep Hormonal Control of Substrate Mobilization During Exercise TIME (MIN)
  57. 57. – Epinephrine-cyclic AMP Via -adrenergic receptors – Ca+2-calmodulin Enhanced during exercise due to Ca+2 release from sarcoplasmic reticulum – Propranolol ( -receptor blocker) has no effect on muscle glycogen utilization Hormonal Control of Substrate Mobilization During Exercise
  58. 58. Hormonal Control of Substrate Mobilization During Exercise
  59. 59. Hormonal Control of Substrate Mobilization During Exercise
  60. 60.  Glycogen breakdown to glucose in muscle is under the dual control of epinephrine-cyclic AMP and Ca+2- calmodulin  The latter’s role is enhanced during exercise due to the increase in Ca+2 from the sarcoplasmic reticulum
  61. 61. – Mobilization of glucose from liver glycogen stores – Mobilization of FFA from adipose tissue Spares blood glucose – Gluconeogenesis from amino acids, lactic acid, and glycerol – Blocking the entry of glucose into cells Forces use of FFA as a fuel – Permissive or slow-acting – Fast-acting Hormonal Control of Substrate Mobilization During Exercise
  62. 62.  – T3 enhances effect of epinephrine to mobilize free fatty acids from adipose tissue  Hormonal Control of Substrate Mobilization During Exercise
  63. 63.  – Stimulate FFA mobilization from adipose tissue – Enhance gluconeogenesis in the liver – Decrease the rate of glucose utilization by cells – Decrease during low-intensity exercise – Increase during high-intensity exercise Above ~60% VO2 max  Hormonal Control of Substrate Mobilization During Exercise
  64. 64. Hormonal Control of Substrate Mobilization During Exercise
  65. 65. Hormonal Control of Substrate Mobilization During Exercise
  66. 66.  – Supports the action of cortisol Decreases glucose uptake by tissues Increases free fatty acid mobilization Enhances gluconeogenesis in the liver – Increase in plasma GH with increased intensity – Greater response in trained runners Hormonal Control of Substrate Mobilization During Exercise
  67. 67. Hormonal Control of Substrate Mobilization During Exercise
  68. 68. Hormonal Control of Substrate Mobilization During Exercise
  69. 69. Hormonal Control of Substrate Mobilization During Exercise
  70. 70.  – Muscle glycogen mobilization – Increasing liver glucose mobilization – Increasing FFA mobilization – Interfere with glucose uptake – Also related to increased heart rate and blood pressure during exercise Hormonal Control of Substrate Mobilization During Exercise
  71. 71. Hormonal Control of Substrate Mobilization During Exercise
  72. 72. Hormonal Control of Substrate Mobilization During Exercise
  73. 73. Hormonal Control of Substrate Mobilization During Exercise
  74. 74.  – Uptake and storage of glucose and FFA  – Plasma concentration decreases during exercise  – Decreased insulin response following training  – Mobilization of glucose and FFA fuels  – Plasma concentration increases during exercise  – Decreased response following training Hormonal Control of Substrate Mobilization During Exercise
  75. 75. Hormonal Control of Substrate Mobilization During Exercise
  76. 76. Hormonal Control of Substrate Mobilization During Exercise
  77. 77. Hormonal Control of Substrate Mobilization During Exercise
  78. 78. Hormonal Control of Substrate Mobilization During Exercise
  79. 79. Hormonal Control of Substrate Mobilization During Exercise
  80. 80. Hormonal Control of Substrate Mobilization During Exercise
  81. 81.  Hormonal Control of Substrate Mobilization During Exercise
  82. 82.  Glucose is taken up seven to twenty times faster during exercise than at rest—even with the decrease in plasma insulin  The increases in intracellular Ca+2 and other factors are associated with an increase in the number of glucose transporters that increase the membrane transport of glucose Training causes a reduction in E, NE, glucagon, and insulin responses to exercise
  83. 83.   – This occurs in spite of persisting hormonal  stimulation for FFA mobilization  – High levels of lactic acid  Promotes resynthesis of triglycerides  – Elevated H+ concentration inhibits HSL  – Inadequate blood flow to adipose tissue  – Insufficient albumin to transport FFA in plasma Hormonal Control of Substrate Mobilization During Exercise
  84. 84. Hormonal Control of Substrate Mobilization During Exercise
  85. 85. Hormonal Control of Substrate Mobilization During Exercise
  86. 86.  (a) the higher H+ concentration inhibiting hormone sensitive lipase  (b) the high levels of lactate during heavy exercise promoting the resynthesis of triglycerides  (c) an inadequate blood flow to adipose tissue, or  (d) insufficient albumin needed to transport the FFA  in the plasma Hormonal Control of Substrate Mobilization During Exercise
  87. 87. – Endocrine system releases hormones – Nervous system uses neurotransmitter
  88. 88. Neuro-endocrinology
  89. 89. – Release hormones directly into the blood
  90. 90.  – Alter the activity of tissues that possess receptors to which the hormone can bind  – Several classes based on chemical makeup  Amino acid derivatives  Peptides/protein  Steroids
  91. 91. Neuro-endocrinology
  92. 92. – Rate of secretion of hormone from endocrine gland Magnitude of input Stimulatory versus inhibitory input – Rate of metabolism or excretion of hormone At the receptor and by the liver and kidneys – Quantity of transport protein Steroid hormones – Changes in plasma volume
  93. 93. Neuro-endocrinology
  94. 94. – Concentration of the hormone – Number of receptors on the cell – Affinity of the receptor for the hormone – Decrease in receptor number in response to high concentration of hormone – Increase in receptor number in response to low concentration of hormone Neuro-endocrinology
  95. 95. – Insulin – Steroid hormones – Cyclic AMP – Ca+2 – Inositol triphosphate – Diacylglycerol – Insulin and growth hormone Neuro-endocrinology
  96. 96. Hormones activate target cells by diffusing through the plasma membrane of the target cells (lipid-soluble hormones) to bind a receptor protein within the cytoplasm of the cell, or by binding a specific receptor protein in the cell membrane of the target cell (water-soluble proteins).
  97. 97. Neuro-endocrinology
  98. 98. Neuro-endocrinology
  99. 99. Neuro-endocrinology
  100. 100. Neuro-endocrinology
  101. 101.  The hormone-receptor interaction triggers events at the cell; changing the concentration of the hormone, the number of receptors on the cell, or the affinity of the receptor for the hormone will all influence the magnitude of the effect  Hormones bring about their effects by modifying membrane transport, activating/suppressing genes to alter protein synthesis, and activating second messengers (cyclic AMP, Ca++, inositol triphosphate, and diacylglycerol) Neuro-endocrinology