Chapter 5

Hormonal Responses to Exercise

EXERCISE PHYSIOLOGYTheory and Application to Fitness and Performance,

6th edition

Scott K. Powers & Edward T. Howley

Neuroendocrinology

• Neuroendocrine system– 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

• 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)

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 cells)• Promotes the storage of glucose, amino acids, and

fats

– Glucagon (from cells)• Promotes the mobilization of fatty acids and glucose

– Somatostatin (from cells)• Controls rate of entry of nutrients into the circulation

– Digestive enzymes and bicarbonate • Into the small intestine

Testes and Ovaries• Testosterone

– 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 -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 (-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– 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