1. Chapter 5: Hormonal Responses to Exercise EXERCISE PHYSIOLOGY Theory and Application to Fitness and Performance, 5 th edition Scott K. Powers & Edward T. Howley Presentation revised and updated by TK Koesterer, Ph.D., ATC Humboldt State University

2. Objectives Describe the hormone-receptor interaction Identify 4 factors that influence the contraction of a hormone in the blood Describe how steroid hormones act on cell Describe “second messenger” hormone action Describe the role of hypothalamus-releasing factors in the control of hormone secretion from the anterior and posterior pituitary

3. Objectives Identify the site of release, stimulus for release, and the predominate action of the following hormones: epinephrine, norepinephrine, glucagon, insulin, cortisol, aldosterone, thyroxine, growth hormone, estrogen, and testosterone Discuss the use of anabolic steroid and growth hormone on muscle growth and their potential side effects

4. Objectives Contrast the role of plasma catecholamines with intracellular factors in the mobilization of muscle glycogen during exercise Graphically describe the chagnes in the following hormones during graded and prolonged exercise and discuss how those changes influence the four mechanisms used to maintain the blood glucose concentration: insulin, glucagon, cortisol, gorwth hormone, epinephrine, and horepinephrine

5. Objectives Describe the effect of changing hormone and substrate levels in the blood on the mobilitzation of free fatty acids from adipose tissue

6. Neuroendocrinology Endocrine glands release hormones directly into the blood Hormones alter the activity of tissues that possess receptors to which the hormone can bind The plasma hormone concentration determines the magnitude of the effect at the tissue level

7. Blood Hormone Concentration Determined by: Rate of secretion of hormone from endocrine gland Rate of metabolism or excretion of hormone Quantity of transport protein Changes in plasma volume

8. Control of Hormone Secretion Rate of insulin secretion from the pancreas is dependent on: –Magnitude of input –Stimulatory vs. inhibitory

9. Factors That Influence the Secretion of Hormones Fig 5.1

10. Hormone-Receptor Interactions Trigger events at the cell Magnitude of effect dependent on: –Concentration of the hormone –Number of receptors on the cell –Affinity of the receptor for the hormone

11. Hormone-Receptor Interactions Hormones bring about effects by: –Altering membrane transport –Stimulating DNA to increase protein synthesis –Activating second messengers Cyclic AMP Ca ++ Inositol triphosphate Diacylglycerol

12. Fig 5.2 Mechanism of Steroid Hormones

13. Fig 5.3 Cyclic AMP “Second Messenger” Mechanism

14. Fig 5.4 Other “Second Messenger” Systems

15. Hormones: Regulation and Action Hormones are secreted from endocrine glands –Hypothalamus and pituitary glands –Thyroid and parathyroid glands –Adrenal glands –Pancreas –Testes and Ovaries

16. Hypothalamus Controls activity of the anterior and posterior pituitary glands Influenced by positive and negative input

17. Fig 5.6 Positive and Negative Input to the Hypothalamus

18. Anterior Pituitary Gland Fig 5.5

19. Growth Hormone Secreted from the anterior pituitary gland Essential for normal growth –Stimulates protein synthesis and long bone growth Increases during exercise –Mobilizes fatty acids from adipose tissue –Aids in the maintenance of blood glucose

20. Growth Hormone Fig 5.6

21. Posterior Pituitary Gland Secretes antidiuretic hormone (ADH) or vasopressin Reduces water loss from the body to maintain plasma volume Stimulated by: –High plasma osmolality and low plasma volume due to sweating –Exercise

22. Change in the Plasma ADH Concentration During Exercise Fig 5.7

23. Thyroid Gland Triiodothyronine (T 3 ) & thyroxine (T 4 ) –Important in maintaining metabolic rate and allowing full effect of other hormones Calcitonin –Regulation of plasma Ca ++ Parathyroid Hormone –Also involved in plasma Ca ++ regulation

24. Adrenal Medulla Secretes Epinephrine and Norepinephrine Increases –HR, Glycogenolysis, Lypolysis,

25. Adrenal Cortex Mineralcorticoids (aldosterone) –Maintain plasma Na + and K + – Regulation of blood pressure

26. Change in Mineralcorticoids During Exercise Fig 5.8

27. Adrenal Cortex Glucocorticoids (Cortisol) –Stimulated by exercise and long-term fasting –Promotes the use of free fatty acids as fuel –Stimulates glucose synthesis –Promotes protein breakdown for gluconeogenesis and tissue repair

28. Control of Cortisol Secretion Fig 5.9

29. Pancreas Secretes digestive enzymes and bicarbonate into small intestine Releases –Insulin - Promotes the storage of glucose, amino acids, and fats –Glucagon - Promotes the mobilization of fatty acids and glucose –Somatostatin - Controls rate of entry of nutrients into the circulation

30. Testes Release testosterone –Anabolic steroid Promotes tissue (muscle) building Performance enhancement –Androgenic steroid Promotes masculine characteristics

31. Control of Testosterone Secretion Fig 5.10

32. Estrogen Establish and maintain reproductive function Levels vary throughout the menstrual cycle

33. Control of Estrogen Secretion Fig 5.11

34. Muscle Glycogen Utilization Breakdown of muscle glycogen is under dual control –Epinephrine-cyclic AMP –Ca 2+ -calmodulin Delivery of glucose parallels activation of muscle contraction Glycogenolysis – breakdown of glycogen Fig 5.16

35. Control of Glycogenolysis Fig 5.16 Glycogenolysis

36. Muscle Glycogen Utilization Glycogenolysis is related to exercise intensity –High-intensity of exercise results in greater and more rapid glycogen depletion Plasma epinephrine is a powerful simulator of glycogenolysis –High-intensity of exercise results in greater increases in plasma epinephrine Fig 5.14 Fig 5.13

37. Glycogen Depletion During Exercise Fig 5.13

38. Plasma Epinephrine Concentration During Exercise Fig 5.14

39. Maintenance of Plasma Glucose During Exercise 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

40. Blood Glucose Homeostasis During Exercise Permissive and slow-acting hormones –Thyroxine –Cortisol –Growth hormone Act in a permissive manner to support actions of other hormones

41. Cortisol Stimulates FFA mobilization from adipose tissue Mobilizes amino acids for gluconeogenesis Blocks entry of glucose into cells Fig 5.17

42. Role of Cortisol in the Maintenance of Blood Glucose Fig 5.17

43. Plasma Cortisol During Exercise At low intensity –plasma cortisol decreases At high intensity –plasma cortisol increases Fig 5.18

44. Changes in Plasma Cortisol During Exercise Fig 5.18

45. Growth Hormone Important in the maintenance of plasma glucose –Decreases glucose uptake –Increases FFA mobilization –Enhances gluconeogenesis Fig 5.19

46. Growth Hormone in the Maintenance of Plasma Glucose Fig 5.19

47. Growth Hormone During Exercise: Effect of Intensity Fig 5.20

48. Growth Hormone During Exercise: Trained vs. Untrained Fig 5.20

49. Blood Glucose Homeostasis During Exercise Fast-acting hormones –Norepinephrine and epinephrine –Insulin and glucagon Maintain plasma glucose –Increasing liver glucose mobilization –Increased levels of plasma FFA –Decreasing glucose uptake –Increasing gluconeogenesis Fig 5.21

50. Role of Catecholamines in Substrate Mobilization Fig 5.21

51. Epinephrine & Norepinephrine During Exercise Increase linearly during exercise Favor the mobilization of FFA and maintenance of plasma glucose Fig 5.22

52. Change in Plasma Catecholamines During Exercise Fig 5.22

53. Epinephrine & Norepinephrine Following Training Decreased plasma levels in response to exercise bout Parallels reduction in glucose mobilization Fig 5.23

54. Plasma Catecholamines During Exercise Following Training Fig 5.23

55. Effects of Insulin & Glucagon Fig 5.24

56. Insulin During Exercise Plasma insulin decreases during exercise –Prevents rapid uptake of plasma glucose –Favors mobilization of liver glucose and lipid FFA Trained subjects during exercise – More rapid decrease in plasma insulin –Increase in plasma glucagon Fig 5.25 Fig 5.26 Fig 5.25

57. Changes in Plasma Insulin During Exercise Fig 5.25

58. Effect of Training on Plasma Insulin During Exercise Fig 5.25

59. Effect of Training on Plasma Glucagon During Exercise Fig 5.26

60. Effect of SNS on Substrate Mobilization Fig 5.28

61. Hormonal Responses to Exercise Fig 5.29a

62. Hormonal Responses to Exercise Fig 5.29b

63. Free Fatty Acid Mobilization During Heavy Exercise FFA mobilization decreases during heavy exercise –This occurs in spite of persisting hormonal stimulation for FFA mobilization May be due to high levels of lactic acid –Promotes resynthesis of triglycerides –Inadequate blood flow to adipose tissue –Insufficient transporter for FFA in plasma Fig 5.30

64. Effect of Lactic Acid on FFA Mobilization Fig 5.30