Chapter 5 Hormonal Responses to Exercise EXERCISE PHYSIOLOGY Theory and Application to Fitness and Performance, 6th edition Scott K. Powers & Edward T. Howley

Neuroendocrinology Neuroendocrine system Endocrine glands Hormones Endocrine system releases hormones Nervous system uses neurotransmitters Endocrine glands Release hormones directly into the blood Hormones Alter the activity of tissues that possess receptors to which the hormone can bind

Blood Hormone Concentration The free plasma hormone concentration determines the magnitude of the effect at the tissue level Determined by: Rate of secretion of hormone from endocrine gland Magnitude of input Stimulatory vs. 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

Factors That Influence the Secretion of Hormones Figure 5.1

Hormone-Receptor Interactions Hormone affect only tissue with specific receptors Magnitude of effect dependent on: Concentration of the hormone Number of receptors on the cell Affinity of the receptor for the hormone Downregulation Decrease in receptor number in response to high concentration of hormone Upregulation Increase in receptor number in response to low concentration of hormone

Mechanisms of Hormone Action Altering membrane transport Insulin Stimulating DNA to increase protein synthesis Steroid hormones Activating second messengers via G protein Cyclic AMP Ca+2 Inositol triphosphate Diacylglycerol

Mechanism of Steroid Hormone Action Figure 5.2

Cyclic AMP “Second Messenger” Mechanism Figure 5.3

Calcium and Phospholipase C Second Messenger Mechanisms Figure 5.4

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

Hypothalamus and Pituitary Gland 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)

Hormones Released From the Anterior Pituitary Gland Figure 5.5

Growth Hormone Secreted from the anterior pituitary gland Stimulates release of insulin-like growth factors (IGFs) Essential growth of all tissues Amino acid uptake and protein synthesis Long bone growth Spares plasma glucose Reduces the use of plasma glucose Increases gluconeogenesis Mobilizes fatty acids from adipose tissue

The Influence of the Hypothalamus on Growth Hormone Secretion Figure 5.6

Antidiuretic Hormone Reduces water loss from the body to maintain plasma volume Favors the reabsorption of water from the kidney Stimulated by: High plasma osmolality and low plasma volume Due to sweat loss without water replacement

Change in Plasma ADH Concentration During Exercise Figure 5.7

Thyroid Gland Stimulated by TSH Triiodothyronine (T3) and thyroxine (T4) Maintenance of metabolic rate Allowing the full effect of other hormones Calcitonin Regulation of plasma Ca+2 Parathyroid Hormone Primary hormone in plasma Ca+2 regulation

Adrenal Medulla Secretes the catecholamines Epinephrine (E) and norepinephrine (NE) Bind to adrenergic receptors Alpha () Beta () Effects depend on hormone used and receptor type

Adrenal Cortex Aldosterone (mineralcorticoid) Control of Na+ reabsorption and K+ secretion Na+/H2O balance Regulation of blood volume and blood pressure Part of renin-angiotensin-aldosterone system Stimulated by: Increased K+ concentration Decreased plasma volume

Change in Renin, Angiotensin II, and Aldosterone During Exercise Figure 5.8

Adrenal Cortex Cortisol (glucocorticoid) Promotes protein breakdown for gluconeogenesis and tissue repair Stimulates FFA mobilization Stimulates glucose synthesis Blocks uptake of glucose into cells Promotes the use of free fatty acids as fuel Stimulated by: Stress, via ACTH Exercise

Control of Cortisol Secretion Figure 5.9

Pancreas Both exocrine and endocrine functions Secretes: Insulin (from b cells) Promotes the storage of glucose, amino acids, and fats Glucagon (from a cells) Promotes the mobilization of fatty acids and glucose Somatostatin (from d cells) Controls rate of entry of nutrients into the circulation Digestive enzymes and bicarbonate Into the small intestine

Testes and Ovaries Testosterone Estrogen Released from testes Anabolic steroid Promotes tissue (muscle) building Performance enhancement Androgenic steroid Promotes masculine characteristics Estrogen Released from ovaries Establish and maintain reproductive function Levels vary throughout the menstrual cycle

Control of Testosterone Secretion Figure 5.10

Control of Estrogen Secretion Figure 5.11

Change in FSH, LH, Progesterone, and Estradiol During Exercise Figure 5.12

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

Glycogen Depletion During Exercise Figure 5.13

Plasma Epinephrine Concentration During Exercise Figure 5.14

Control of Muscle Glycogen Utilization Breakdown of muscle glycogen is under dual control Epinephrine-cyclic AMP Via b-adrenergic receptors Ca+2-calmodulin Enhanced during exercise due to Ca+2 release from sarcoplasmic reticulum Evidence for role of Ca+2-calmodulin in glycogenolysis Propranolol (b-receptor blocker) has no effect on muscle glycogen utilization

Control of Glycogenolysis Figure 5.16

Changes in Muscle Glycogen Before and After Propranolol Administration Figure 5.15

Blood Glucose Homeostasis During Exercise Plasma glucose maintained through four processes: 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 Controlled by hormones Permissive or slow-acting Fast-acting

Permissive and Slow-Acting Hormones Thyroid hormones Act in a permissive manner to support actions of other hormones Cortisol and growth hormone Stimulate FFA mobilization from adipose tissue Enhance gluconeogenesis in the liver Decrease the rate of glucose utilization by cells

Role of Cortisol in the Maintenance of Blood Glucose Figure 5.17

Changes in Plasma Cortisol During Exercise Figure 5.18

Role of Growth Hormone in the Maintenance of Plasma Glucose Figure 5.19

Changes in Plasma Growth Hormone During Exercise Figure 5.20

Fast-Acting Hormones Epinephrine and norepinephrine Maintain blood glucose during exercise Muscle glycogen mobilization Increasing liver glucose mobilization Increasing FFA mobilization Interfere with glucose uptake Plasma E and NE increase during exercise Decreased plasma E and NE following training

Role of Catecholamines in Substrate Mobilization Figure 5.21

Change in Plasma Epinephrine and Norepinephrine During Exercise Figure 5.22

Plasma Catecholamines Responses to Exercise Following Training Figure 5.23

Fast-Acting Hormones Insulin Glucagon Uptake and storage of glucose and FFA Plasma concentration decreases during exercise Decreased insulin response following training Glucagon Mobilization of glucose and FFA fuels Plasma concentration increases during exercise Decreased response following training Insulin and glucagon secretion influenced by catecholamines

Effects of Insulin and Glucagon Figure 5.24

Changes in Plasma Insulin During Exercise Figure 5.25

Changes in Plasma Glucagon During Exercise Figure 5.26

Effect of Epinephrine and Norepinephrine on Insulin and Glucagon Secretion Figure 5.27

Effect of the SNS on Substrate Mobilization Figure 5.28

Summary of the Hormonal Responses to Exercise Figure 5.29

Hormone-Substrate Interaction 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 albumin to transport FFA in plasma

Changes in Plasma FFA Due to Lactic Acid Figure 5.30

Effect of Lactic Acid on FFA Mobilization Figure 5.30