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Chapter 5 Î Hormonal Responses to Exercise Objectives 1. Describe the concept of hormone-receptor interaction. 2. Identify the four factors influencing the concentration of a hormone in the bld. 3. Describe the mechanism by which steroid hormones act on cells. 4. Describe the “2nd messenger” hypothesis of hormone action. 5. Describe the role of hypothalamus-releasing factors in the control of hormone secretion from the anterior pituitary gland. Objectives 6. Describe the relationship of the hypothalamus to the secretion of hormones from the posterior pituitary gland. 7. Identify the site of release, stimulus for release, & the predominant action of the following hormones: epinephrine, norepinephrine, glucagon, insulin, cortisol, aldosterone, thyroxine, growth hormone, estrogen, & testosterone. 8. Discuss the use of testosterone (an anabolic steroid) & growth hormone on muscle growth & their potential side effects. 1 Objectives 9. Contrast the role of plasma catecholamines w/ intracellular factors in the mobilization of muscle glycogen during exercise. 10. Briefly discuss the following four mechanisms by which bld glu homeostasis is maintained: mobilizing glu from liver glycogen stores, mobilizing plasma FFAs from adipose tissue, synthesizing glu from AAs & glycerol in the liver, & blocking glu entry into cells. Objectives 11. Describe the Δs in the hormones insulin, glucagon, cortisol, growth hormone, epinephrine, & norepinephrine during graded & prolonged exercise & discuss how those Δs influence the four ou mechanisms ec a s s used to maintain a ta the t e [b [bld d glu]. g u] 12. Describe the effect of changing hormone & substrate levels in the bld on the mobilization of FFAs from adipose tissue. Neuroendocrinology Neuroendocrinology • Neuroendocrine system • Endocrine glands • Hormones 2 Neuroendocrinology [Bld Hormone] Neuroendocrinology Factors That Influence the Secretion of Hormones Figure 5.1 Neuroendocrinology Hormone-Receptor Interactions 3 Neuroendocrinology Mechanisms of Hormone Action Neuroendocrinology Mechanism of Steroid Hormone Action Figure 5.2 Neuroendocrinology Cyclic AMP “2nd Messenger” Mechanism Figure 5.3 4 Neuroendocrinology Calcium & Phospholipase C 2nd Messenger Mechanisms Figure 5.4 Neuroendocrinology Insulin Receptor Figure 5.5 Neuroendocrinology In Summary The hormone-receptor interaction triggers events at the cell; changing the concentration of the hormone, the number of receptors on the cell, or the affinity of the receptor for the hormone will all influence the magnitude of the effect. Hormones bring about their effects by modifying mb transport, activating/suppressing genes to alter pro synthesis, & activating 2nd messengers (cyclic AMP, Ca++, inositol triphosphate, & diacylglycerol). 5 Hormones: Regulation & Action Hypothalamus & Pituitary Gland • Hypothalamus – Controls secretions from pituitary gland • Anterior Pituitary Gland – Adrenocorticotropic hormone (ACTH) – Follicle-stimulating 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) Hypothalamus • Stimulates release of hormones from anterior pituitary gland – Releasing hormones or factors p • Provides hormones for release from posterior pituitary gland 6 Anterior Pituitary Gland • Adrenocorticotropic hormone (ACTH) – Stimulates cortisol release form adrenal glands • Follicle-stimulating hormone (FSH) • Luteinizing hormone (LH) – Stimulates production of testosterone & estrogen • Melanocyte-stimulating hormone (MSH) • Thyroid-stimulating hormone (TSH) – Controls thyroid hormone release from thyroid gland • Prolactin • Growth hormone (GH) Growth Hormone Influences on Growth Hormone Release Figure 5.6 7 A Closer Look 5.1 Growth Hormone & Performance In Summary The hypothalamus controls the activity of both the anterior pituitary & posterior pituitary glands. GH is released from the anterior pituitary gland & is essential for normal growth. GH ↑s during exercise to mobilize FFAs from adipose tissue & to aid in the maintenance of bld glu. Posterior Pituitary Gland 8 Δ in Plasma [ADH] during Exercise Figure 5.7 Thyroid Gland • Stimulated by TSH • Triiodothyronine (T3) & thyroxine (T4) – Establishment of metabolic rate – Permissive hormones Permit full effect of other hormones • Calcitonin – Regulation of plasma Ca+2 Blocks release from bone, stimulates excretion by kidneys • Parathyroid Hormone – 1° hormone in plasma Ca+2 regulation Stimulates release from bone, stimulates reabsorption by kidneys In Summary Thyroid hormones T3 & T4 are important for maintaining the metabolic rate & allowing other hormones to bring about their full effect. 9 Parathyroid Gland • Parathyroid hormone – 1° hormone in plasma Ca+2 regulation – Stimulates Ca+2 release from bone – Stimulates reabsorption of Ca+2 by kidneys – Converts vitamin D3 into a hormone that ↑ Ca+2 absorption from GI tract Adrenal Medulla Effects of E &N 10 In Summary The adrenal medulla secretes the catecholamines epinephrine (E) & norepinephrine (NE). E is the adrenal medulla’s 1° secretion (80%), while NE is primarily secreted from the adrenergic neurons of the sympathetic nervous system. t Epinephrine & norepinephrine bind to α- & β-adrenergic receptors &bring about Δs in cellular activity (e.g., ↑d HR, mobilization of FAs from adipose tissue) via 2nd messengers. Adrenal Cortex • Secretes steroid hormones – Derived from cholesterol • Mineralcorticoids – Aldosterone – Maintenance of plasma Na+ &K+ • Glucocorticoids – Cortisol – Regulation of plasma glu • Sex steroids – Androgens & estrogens – Support prepubescent growth Aldosterone • Control of Na+ reabsorption & K+ secretion – Na+/H2O balance • Regulation of bld volume &bld pressure – Part of renin renin-angiotensin-aldosterone angiotensin aldosterone system – All three hormones ↑ during exercise • Stimulated by: – ↑d [K+] – ↓d plasma volume 11 Δ in Renin, Angiotensin II, &Aldosterone during Exercise Figure 5.8 Cortisol Control of Cortisol Secretion Figure 5.9 12 In Summary The adrenal cortex secretes aldosterone (mineralcorticoid), cortisol (glucocorticoid), &estrogens &androgens (sex steroids). Aldosterone regulates Na+ &K+ balance. Aldosterone secretion ↑s w/ strenuous exercise, driven by the reninangiotensin system. Cortisol responds to a variety of stressors, including exercise, to ensure that fuel (glu &FFAs) is available, &to make AAs available for tissue repair. A Closer Look 5.2 Adipose Tissue Is an Endocrine Organ Pancreas 13 In Summary Insulin is secreted by the β cells of the islets of Langerhans in the pancreas &promotes the storage of glu, AAs, &fats. Glucagon is secreted by the α cells of the islets of Langerhans in the pancreas &promotes the mobilization of glu &fats. Testes &Ovaries • Testosterone – Released from testes – Anabolic steroid Promotes tissue (muscle) building Performance P f enhancement h t – Androgenic steroid Promotes masculine characteristics • Estrogen &Progesterone – Released from ovaries – Establish &maintain reproductive function – Levels vary throughout the menstrual cycle Control of Testosterone Secretion Figure 5.10 14 Control of Estrogen Secretion Figure 5.11 Δ in FSH, LH, Progesterone, & Estradiol during Exercise Figure 5.12 A Closer Look 5.3 Anabolic Steroids &Performance 15 In Summary Testosterone & estrogen establish &maintain reproductive function & determine secondary sex characteristics. Chronic exercise (training) can ↓ testosterone levels in males & estrogen levels in females. The latter adaptation has potentially negative consequences related to osteoporosis. Hormonal Control of Substrate Mobilization During Exercise Muscle Glycogen Utilization Glycogen Depletion during Exercise Figure 5.13 16 Plasma [EPI] during Exercise Figure 5.14 Hormonal Control of Substrate Mobilization During Exercise Control of Muscle Glycogen Utilization Δs in Muscle Glycogen Before & After Propranolol Administration Figure 5.15 17 Control of Glycogenolysis Figure 5.16 In Summary Glycogen breakdown to glu in muscle is under the dual control of epinephrine-cyclic AMP &Ca+2-calmodulin. The latter’s role is enhanced during exercise due to the ↑ in Ca+2 from the sarcoplasmic reticulum. In this way, the d li delivery off ffuell ((glu) l ) parallels ll l th the activation ti ti off contraction. Hormonal Control of Substrate Mobilization During Exercise Bld Glu Homeostasis during Exercise 18 Hormonal Control of Substrate Mobilization During Exercise Thyroid Hormones Hormonal Control of Substrate Mobilization During Exercise Cortisol Hormonal Control of Substrate Mobilization During Exercise Role of Cortisol in the Maintenance of bld glu Figure 5.17 19 Hormonal Control of Substrate Mobilization During Exercise Δs in Plasma Cortisol during Exercise Figure 5.18 Hormonal Control of Substrate Mobilization During Exercise Growth Hormone Hormonal Control of Substrate Mobilization During Exercise Role of Growth Hormone in the Maintenance of Plasma glu Figure 5.19 20 Hormonal Control of Substrate Mobilization During Exercise Δs in Plasma Growth Hormone during Exercise Figure 5.20 Hormonal Control of Substrate Mobilization During Exercise In Summary The hormones thyroxine, cortisol, & growth hormone act in a permissive manner to support the actions of other hormones during exercise. Growth hormone & cortisol also provide a “slow-acting” effect on CHO & fat metabolism during exercise. Hormonal Control of Substrate Mobilization During Exercise Epinephrine & Norepinephrine 21 Hormonal Control of Substrate Mobilization During Exercise Role of Catecholamines in Substrate Mobilization Figure 5.21 Hormonal Control of Substrate Mobilization During Exercise Δ in Plasma E & NE during Exercise Figure 5.22 Hormonal Control of Substrate Mobilization During Exercise Plasma Catecholamines Responses to Exercise following Training Figure 5.23 22 Hormonal Control of Substrate Mobilization During Exercise Fast-Acting Hormones Hormonal Control of Substrate Mobilization During Exercise Effects of Insulin & Glucagon Figure 5.24 Hormonal Control of Substrate Mobilization During Exercise Δs in Plasma Insulin during Exercise Figure 5.25 23 Hormonal Control of Substrate Mobilization During Exercise Δs in Plasma Glucagon during Exercise Figure 5.26 Hormonal Control of Substrate Mobilization During Exercise Effect of E & N on Insulin & Glucagon Secretion Figure 5.27 Hormonal Control of Substrate Mobilization During Exercise Effect of the SNS on Substrate Mobilization Figure 5.28 24 Hormonal Control of Substrate Mobilization During Exercise Summary of the Hormonal Responses to Exercise Figure 5.29 Hormonal Control of Substrate Mobilization During Exercise In Summary Plasma glu is maintained during exercise by ↑ng liver glycogen mobilization, using more plasma FFA, ↑ng gluconeogenesis, & ↓ng glu uptake by tissues. The ↓ in plasma insulin & the ↑ in plasma E, NE, GH, glucagon, & cortisol ti l d during i exercise i control t l th these mechanisms h i tto maintain the [glu]. Hormonal Control of Substrate Mobilization During Exercise In Summary glu is taken up 7-to 20-times faster during exercise than at rest—even w/ the ↓ in plasma insulin. The ↑s in intracellular Ca+2 & other factors are associated w/ an ↑ in the number of glu transporters that ↑ the mb transport of g o glu. u Training causes a reduction in E, NE, glucagon, & insulin responses to exercise. 25 Hormonal Control of Substrate Mobilization During Exercise Hormone-Substrate Interaction Hormonal Control of Substrate Mobilization During Exercise Δs in Plasma FFA Due to Lactic Acid Figure 5.30 Hormonal Control of Substrate Mobilization During Exercise Effect of Lactic Acid on FFA Mobilization Figure 5.30 26 Hormonal Control of Substrate Mobilization During Exercise In Summary The plasma [FFA] ↓s during heavy exercise even though the adipose cell is stimulated by a variety of hormones to ↑ triglyceride breakdown to FFA & glycerol. This may be due to: (a) the higher [H+] inhibiting hormone sensitive se s e lipase, pase, (b) the e high g levels e es o of lactate ac a e du during g heavy exercise promoting the resynthesis of triglycerides, (c) an inadequate bld flow to adipose tissue, or (d) insufficient albumin needed to transport the FFA in the plasma. Study Questions 1. Draw & label a diagram of a negative feedback mechanism for hormonal control using cortisol as an example. 2. List the factors that can influence the [bld] of a hormone. 3. Discuss the use of testosterone & growth hormone as aids to ↑ muscle size &strength, &discuss the potential long-term consequences of such use. 4. List each endocrine gland, the hormones(s) secreted from that gland, & its (their) action(s). 5. Describe the two mechanisms by which muscle glycogen is broken down to glu (glycogenolysis) for use in glycolysis. Which one is activated at the same time as muscle contraction? Study Questions 6. Identify the four mechanisms involved in maintaining the bld [glu]. 7. Draw a summary graph of the Δs in the following hormones w/ exercise of increasing intensity or duration: epinephrine, norepinephrine cortisol growth hormone, norepinephrine, hormone insulin, insulin & glucagon. 8. What is the effect of training on the responses of epinephrine, norepinephrine, & glucagon to the same exercise task? 9. Briefly explain how glu can be taken into the muscle at a high rate during exercise when plasma insulin is reduced. Include the role of glu transporters. 27 Study Questions 10. Explain how FFA mobilization from the adipose cell ↓s during maximal work in spite of the cell being stimulated by all the hormones to break down triglycerides. 11. Discuss the effect of glu ingestion on the mobilization of FFAs during exercise exercise. 28