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 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 d 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