chapter 5 hormonal responses to exercise exercise physiology theory and application to fitness and...
TRANSCRIPT
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Chapter 5
Hormonal Responses to Exercise
EXERCISE PHYSIOLOGYTheory and Application to Fitness and Performance,
6th edition
Scott K. Powers & Edward T. Howley
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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
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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
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Factors That Influence the Secretion of Hormones
Figure 5.1
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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
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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
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Mechanism of Steroid Hormone
Action
Figure 5.2
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Cyclic AMP “Second Messenger” Mechanism
Figure 5.3
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Calcium and Phospholipase C Second Messenger Mechanisms
Figure 5.4
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Hormones: Regulation and Action
• Hormones are secreted from endocrine glands– Hypothalamus and pituitary glands– Thyroid and parathyroid glands– Adrenal glands– Pancreas– Testes and Ovaries
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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)
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Hormones Released From the Anterior Pituitary
Gland
Figure 5.5
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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
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The Influence of the Hypothalamus on Growth Hormone Secretion
Figure 5.6
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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
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Change in Plasma ADH Concentration During Exercise
Figure 5.7
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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
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Adrenal Medulla
• Secretes the catecholamines – Epinephrine (E) and norepinephrine (NE)– Bind to adrenergic receptors
• Alpha ()• Beta ()
– Effects depend on hormone used and receptor type
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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
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Change in Renin, Angiotensin II, and Aldosterone During Exercise
Figure 5.8
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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
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Control of Cortisol
Secretion
Figure 5.9
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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
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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
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Control of Testosterone Secretion
Figure 5.10
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Control of Estrogen Secretion
Figure 5.11
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Change in FSH, LH, Progesterone, and
Estradiol During Exercise
Figure 5.12
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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
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Glycogen Depletion During Exercise
Figure 5.13
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Plasma Epinephrine Concentration During Exercise
Figure 5.14
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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
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Control of Glycogenolysis
Figure 5.16
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Changes in Muscle Glycogen Before and After Propranolol Administration
Figure 5.15
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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
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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
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Role of Cortisol in the Maintenance of Blood Glucose
Figure 5.17
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Changes in Plasma Cortisol During Exercise
Figure 5.18
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Role of Growth Hormone in the Maintenance of Plasma Glucose
Figure 5.19
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Changes in Plasma Growth Hormone During Exercise
Figure 5.20
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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
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Role of Catecholamines in Substrate Mobilization
Figure 5.21
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Change in Plasma Epinephrine and Norepinephrine During Exercise
Figure 5.22
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Plasma Catecholamines Responses to Exercise
Following Training
Figure 5.23
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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
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Effects of Insulin and Glucagon
Figure 5.24
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Changes in Plasma Insulin During Exercise
Figure 5.25
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Changes in Plasma Glucagon During Exercise
Figure 5.26
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Effect of Epinephrine and Norepinephrine on Insulin and Glucagon Secretion
Figure 5.27
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Effect of the SNS on Substrate Mobilization
Figure 5.28
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Summary of the Hormonal Responses to Exercise
Figure 5.29
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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
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Changes in Plasma FFA Due to Lactic Acid
Figure 5.30
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Effect of Lactic Acid on FFA Mobilization
Figure 5.30