Hormones Pt 2

ACTH Target tissues

1. Adrenal cortex to cause release of cortisol 2. Adipose tissue: stimulates liplysis 3. Liver: stimulate gluconeogensis/glycogenolyis 4. muscle: attenuate glucose uptake -potentiates cortisol by small percent, but not as effective alone -hard to measure, has short half-life

Aldosterone secretion during exercise is stimulated by

1. Decrease in plasma volume (from sweating) wh/ causes . . . 2. Increase in plasma [K+] 3. Increase in SNS activity

How is high glucose uptake achieved during exercise w/ fall of insulin

1. GLUT-4 (activated by muscle contraction) 2. Increased blood flow > increased delivery of glucose

how glucose uptake attenuated

1. decrease insulin removes stimulus to take up glucose into muscle 2. action of counter-regulatory hormones

effector responses homeostatic regulation of plasma osmolality

1. vasoconstriction 2. secretion of aldosterone >>> increases water reabsorption by kidney

Peak of FFA oxidation (i.e. highest contribution to energy expenditure)

50% VO2max -E binds to beta receptors in adipocytes > activate HSL > stimulate lipolysis -above this level, E binds to alpha receptors in adipocytes > inhibit HSL & lipolysis (less FFA delivered to muscle)

Peak of IMTG oxidation (i.e. highest contribution to energy expenditure)

60% VO2max -up to this level, E binds to beta receptors in muscle (wh/ doesn't have alpha receptors) > activates HSL -up to this level, increased [Ca++] > activates HSL

Effectors in homeostatic regulation of plasma osmolality

Adrenal

Control center of plasma glucose homeostatic regulation

Alpha & beta cells of pancreas -if high glucose sensed, increase insulin release, decrease glucagon release

Sensor of Plasma glucose homeostatic regulation

Alpha and beta cells of pancreas (thru GLUT 1 and GLUT 2)

Sensors in homeostatic regulation of blood pressure (5 liters)

Baroreceptors sense dec. BP Kidney sense dec BP, [Na+] Heart senses dec stretch

Effectors in homeostatic regulation of blood pressure

Blood vessels Adrenals Kidney Intestines

Effector responses in regulation of blood pressure

Blood vessels: vasoconstrict Adrenals: secrete aldosterone (acts on kidneys & intestines) Kidney: increase water resorption, activate renin Intestines: increase water absorption

ACE in lungs

Converts angiotensin I to angiotensin II

Hormones that stimulate lipolysis in adipose tissue

Cortisol, GH, E/NE, glucagon (all increase during exercise)

Hormones that attentuate glucose uptake into skeletal muscle

Cortisol, GH, Epi (all increase during exercise)

GH

Direct effects: -increase FFA supply by stimulating Lipolysis in adipose -stimulates Gluconeogenesis & glycogenolysis in liver -attenuates glucose uptake by muscle Indirect (longer term effects) 1. stimulates release of IGF by liver 2. Promotes growth & repair in skeletal muscle

Pancreas

Exocrine role: secretes digestive enzymes & bicarbonate into SI Endocrine role: secretes insulin & glucagon

Counter-regulatory hormones

Glucagon, Cortisol, E/NE & GH Function to decrease risk of hypoglycemia -released anytime blood glucose is threatened (e.g. during exercise, fasting, sleep) -starts when below 80, greater response as gets further from homeostatic levels -increase availability of other fuels (FFA, AA): E/NE, cortisol, GH -stimulate gluconeogenesis: E/NE, Glucagon -attenuate uptake of glucose into cells: E/NE, Cortisol, GH (wh/ favors increase in plasma FFA uptake)

6 g of glucose/hour

How much glucose the adult brain uses Usually only 4.5 g total blood glucose when fasted (900 mg/L x 5 L)

Control center in homeostatic regulation of blood pressure

Hypothalamus Kidney Atria (secretes ANP) >>> increase SNS activity

Hormones that stimulate glucose uptake & inhibit lipolysis

Insulin

signals wh/ stimulate kidney to start RAAS

Low plasma vol Low BP Low plasma Na+ Increase SNS

Osmolality

Measure of how much solute is in plasma (normal = 280-295 mosM/kg) Determined by total level of electrolytes in plasma (primarily Na+) -if high, there is less water than solute -if low, there is more water than solute -regulated more precisely than plasma volume (changes more w/ sweating than PV)

Effector organs in plasma glucose homeostatic regulation

Muscle, fat, liver

Effector responses (if increased insulin, decreased glucagon)

Muscle: increase glucose uptake, decrease lipolyis of IMTG Fat: increase glucose uptake, decrease lipolysis Liver: increase glucose uptake, decrease Hepatic Glucose Output

Thyroid hormone (active form is T3)

No acute effects during exercise Converted at target tissue -inhibited by stress, fasting, illness, cortisol 1. Stimulates basal metabolic rate in muscle & brown adipose tissue 2. Primarily (during exercise), enhances effect of catecholamines (potentiates)

BP drops (during exercise)

Occurs as a result of fluid losses & fluid shifts -in addition to changes in osmolality, will stimulate different response than just this alone

Glucagon

Produced in alpha cells of pancreas in response to low plasma glucose Promotes the mobilization of fatty acids from adipose tissue & glucose from liver; PRIMARY Driver of Gluconeogenesis in liver -stimulates glycogenolysis in liver (not in muscle) -stimulates Lipolysis in adipose tissue (alternate fuel source)

When liver glycogen is full (100, excess CHO)

Production of VLDL

Catecholamine release during exercise

Regulate insulin & glucagon secretion (in addition to plasma glucose) -further increasing glucagon & further suppressing insulin Direct effects: inhibit glucose uptake & stimulate glycogenolysis in muscle Indirect effect: stimulates release of glucagon & inhibits release of insulin

Parathyroid hormone (PTH)

Release stimulated by low serum Ca++ (lower than 9-11 mg/dL) & exercise 1. stimulates release of Ca++ from bones 2. stimulates Ca++ uptake in kidneys (and uptake by intestines via vitamin D effect)

Aldosterone

Released by adrenal cortex -regulates plasma volume and Na/H20 balance by regulating Na+ absorption & K+ secretion at kidney Acts on heart > release ANP Acts on arteries > vasoconstrict > increase BP Acts on kidney > Na & H2O retention > increase BP

ADH/Vasopressin

Released from post. pituitary The water conserving hormone -preserves plasma volume, reduces urine -stimulated by decrease in arterial P Stimulates reabsorption of water in kidneys -same actions as aldosterone

Calcitonin

Released from thyroid gland Stimulated by high serum Ca++ Blocks release of Ca++ from bone: Stimulates calcium storage in bone & secretion at kidneys

Posterior pituitary

Releases hormones when stimulated directly by neurohormones (cells of supraoptic & paraventricular nuclei wh/ travel via axons) -ADH (vasopressin) -oxytocin

Insulin fall during exercise

Removes stimulus to take up glucose into muscle - directly proportional to duration & intensity of exercise

Angiotensin II

Signals adrenals to release aldosterone Also increases: - Na+ retention by kidney (via aldosterone) -water retention by kidney (via Na+ uptake & vasopressin) -salt appetite -drinking -returns BP to normal

Parathyroid gland

Site of calcium regulation -stressed during exercise

Regulation of hepatic glucose output

Stimulated by 1. GLUCAGON: primary driver 2. Direct SNS innervation (breakdown of glycogen) 3. Circulating catecholamines 4. Slower acting hormones (ACTH, GH, cortisol) Ca++ does not play a role here Inhibited by Insulin

Aldosterone secretion

Stimulated by 2 pathways 1. High plasma [K+] sensed by adrenal cortex 2. Renin angiotensin aldosterone system -responds to fall in blood pressure

Insulin

Storage hormone, secreted as soon as excess nutrients sensed Produced in beta cells of pancreas in response to high plasma glucose Promotes the storage of glucose, amino acids & fats -inhibits lipolysis in adipose tissue & glucose release from liver -concentration decreases during exercise

How exercise leads to decrease in plasma vol & increase in plasma [K+]

Sweating Fluid shift Plasma osmolality - regulated much more precisely than plasma volume (changes more w/ sweating)

phosporylase

enzyme that stimulates glycogen breakdown in muscle -stimulated by Epi -inhibited by insulin

4 ways that body can maintain plasma glucose during exercise (because demand from muscles and CNS are greater than supply)

glycogenolysis - obtain glucose from liver Gluconeogenesis - make new glucose Increase reliance on fatty acids (IMTG, FFA) Attenuate glucose uptake into muscle (conserve plasma glucose)

control center in homeostatic regulation of plasma osmolality

hypothalamus >>> increases SNS activity

sensor in homeostatic regulation of plasma osmolality

osmosensors in hypothalamus (high = 325mosM/kg)

When liver glycogen is low (50-79)

promotes synthesis of liver glycogen

Renin

released by kidney Acts on angiotensinogen to convert to angiotensin I

IGF1 (insulin like growth factor)

released by liver 8-30 hrs after GH, potentiates effects of GH (when insulin present) to tissues impacted by exercise -promotes growth & repair of bone & muscle -inhibited by inflammatory cytokines

Increased reliance on fatty acids (IMTG, FFA) during exercise (i.e.Lipolysis)

stimulated by E/NE, glucagon, GH, cortisol inhibited by insulin Fast effects: increase E/NE, increase glucagon, decreased insulin Slow effects (fine tuners): increase GH, increase cortisol

epinephrine

the primary stimulator of glycogen breakdown in muscle 2 effects on CHO in muscle (to preserve plasma glucose for CNS) -attenuates plasma glucose uptake -increases glycogen breakdown INCREASES during exercise