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Chapter 5:
Hormonal Responses
to Exercise
EXERCISE PHYSIOLOGY
Theory and Application to Fitness and Performance, 5th edition
Scott K. Powers & Edward T. Howley
Presentation revised and updated by
TK Koesterer, Ph.D., ATC
Humboldt State University
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
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
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
Objectives
• Describe the effect of changing hormone and
substrate levels in the blood on the
mobilitzation of free fatty acids from adipose
tissue
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
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
Control of Hormone Secretion
• Rate of insulin secretion from the pancreas is
dependent on:
– Magnitude of input
– Stimulatory vs. inhibitory
Factors That Influence the
Secretion of Hormones
Fig 5.1
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
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
Mechanism of
Steroid
Hormones
Fig 5.2
Cyclic AMP
“Second
Messenger”
Mechanism
Fig 5.3
Other
“Second
Messenger”
Systems
Fig 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
• Controls activity of the anterior and posterior
pituitary glands
• Influenced by positive and negative input
Positive and
Negative Input
to the
Hypothalamus
Fig 5.6
Anterior Pituitary Gland
Fig 5.5
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
Growth
Hormone
Fig 5.6
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
Change in the Plasma ADH
Concentration During Exercise
Fig 5.7
Thyroid Gland
• Triiodothyronine (T3) & thyroxine (T4)
– 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
Adrenal Medulla
• Secretes Epinephrine and
Norepinephrine
• Increases
–HR, Glycogenolysis, Lypolysis,
Adrenal Cortex
• Mineralcorticoids (aldosterone)
– Maintain plasma Na+ and K+
– Regulation of blood pressure
Change in Mineralcorticoids
During Exercise
Fig 5.8
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
Control of
Cortisol
Secretion
Fig 5.9
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
Testes
• Release testosterone
– Anabolic steroid
• Promotes tissue (muscle) building
• Performance enhancement
– Androgenic steroid
• Promotes masculine characteristics
Control of
Testosterone
Secretion
Fig 5.10
Estrogen
• Establish and maintain reproductive
function
• Levels vary throughout the menstrual
cycle
Control of
Estrogen
Secretion
Fig 5.11
Muscle Glycogen Utilization
• Breakdown of muscle glycogen is under dual
control
– Epinephrine-cyclic AMP
– Ca2+-calmodulin
• Delivery of glucose parallels activation of
muscle contraction
• Glycogenolysis – breakdown of glycogen
Fig 5.16
Control of Glycogenolysis
Glycogenolysis
Fig 5.16
Muscle Glycogen Utilization
• Glycogenolysis is related to exercise intensity
– High-intensity of exercise results in greater
and more rapid glycogen depletion Fig 5.13
• Plasma epinephrine is a powerful simulator of
glycogenolysis
– High-intensity of exercise results in greater
increases in plasma epinephrine Fig 5.14
Glycogen Depletion During
Exercise
Fig 5.13
Plasma Epinephrine
Concentration During Exercise
Fig 5.14
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
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
Cortisol
• Stimulates FFA mobilization from
adipose tissue
• Mobilizes amino acids for
gluconeogenesis
• Blocks entry of glucose into cells
Fig 5.17
Role of Cortisol in the
Maintenance of Blood
Glucose
Fig 5.17
Plasma Cortisol During
Exercise
• At low intensity
– plasma cortisol decreases
• At high intensity
– plasma cortisol increases
Fig 5.18
Changes in Plasma Cortisol
During Exercise
Fig 5.18
Growth Hormone
• Important in the maintenance of plasma
glucose
– Decreases glucose uptake
– Increases FFA mobilization
– Enhances gluconeogenesis
Fig 5.19
Growth Hormone in the
Maintenance of Plasma Glucose
Fig 5.19
Growth Hormone During Exercise:
Effect of Intensity
Fig 5.20
Growth Hormone During Exercise:
Trained vs. Untrained
Fig 5.20
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
Role of Catecholamines in
Substrate Mobilization
Fig 5.21
Epinephrine & Norepinephrine
During Exercise
• Increase linearly during exercise
• Favor the mobilization of FFA and
maintenance of plasma glucose
Fig 5.22
Change in Plasma Catecholamines
During Exercise
Fig 5.22
Epinephrine & Norepinephrine
Following Training
• Decreased plasma levels in response to
exercise bout
• Parallels reduction in glucose mobilization
Fig 5.23
Plasma Catecholamines
During Exercise Following
Training
Fig 5.23
Effects of Insulin & Glucagon
Fig 5.24
Insulin During Exercise
• Plasma insulin decreases during exercise
– Prevents rapid uptake of plasma glucose
– Favors mobilization of liver glucose and
Fig 5.25
lipid FFA
• Trained subjects during exercise
– More rapid decrease in plasma insulin Fig 5.25
– Increase in plasma glucagon
Fig 5.26
Changes in Plasma Insulin
During Exercise
Fig 5.25
Effect of Training on Plasma
Insulin During Exercise
Fig 5.25
Effect of Training on Plasma
Glucagon During Exercise
Fig 5.26
Effect of SNS on Substrate
Mobilization
Fig 5.28
Hormonal Responses to
Exercise
Fig 5.29a
Hormonal Responses to
Exercise
Fig 5.29b
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
Effect of Lactic Acid on FFA
Mobilization
Fig 5.30