Autonomic nervous system

Intro Autonomic nervous system (ANS) –Sympathetic nervous system (SNS) Fight or flight –Major nerve: Sympathetic chain »Major neurotransmitters: Epi, NE »Bind to: α and β receptors –Parasympathetic nervous system (PNS) Rest and digest –Major nerve: Vagus »Major neurotransmitter: Ach »Binds to: Cholinergic receptors

SNS PNS Sympathetic chain Cranial nerve X (Vagus n.)

Autonomic response to exercise Epi, NE increase exponentially with ex intensity Effects: –BP increase –Vasoconstriction –Increased cardiac output –HR increase –Activates glycolysis/lipolysis

Submaximal exercise –Reduced catecholamine response Reduced HR Reduced blood pressure response Reduced lactate? Altered fuel use? Training effects on autonomic nervous system

Maximal exercise –Maximal adrenergic activity is increased with training Effects –Increased maximal hepatic glucose production Also –Helps defend blood pressure –Helps maintain cardiac output Training effects on autonomic nervous system Trained

Hormonal response to exercise

Growth hormone Polypeptide hormone –anterior pituitary gland Regulates –Growth (Anabolic) »Stimulates protein synthesis –Cell reproduction –Metabolism »Potent stimulator of lipolysis Endocrine gland –Releases hormones into the blood Released during –Fasting –Exercise –Sleep Neuro-endocrine integration –Hypothalamic-pituitary axis Hypothalamus regulates output from anterior Pituitary –Growth hormone releasing factor (GHRF)

Growth hormone response during exercise Lag of ~ 15 minutes before GH increases Proposed metabolic effects of GH –Increases growth of all tissues –Increases lipolysis –Promotes gluconeogenesis –Reduces hepatic glucose uptake

Cortisol and the pituitary-adrenal axis Cortisol –Steroid hormone Cholesterol –Glucocorticoid Promotes glucose production –Stimulates AA release from muscle (catabolic) –stimulates gluconeogenesis Hypothalamus –Releases corticotrophin releasing factor (CRF) Anterior Pituitary –Adrenocorticotrophin (ACTH) Adrenal cortex –cortisol Anterior pituitary

Glucocorticoids Glucocorticoid –Cortisol/cortisone Help to regulate blood glucose Released during prolonged, exhaustive exercise Mineralcorticoid –Aldosterone Released from adrenal cortex Works with renin/angiotensin system Electrolyte homeostasis –Reabsorption of water and sodium, excretion of potassium

Cortisol Note how cortisol changes throughout the day –also, rises to highest level at the end of exercise –Influenced by intensity and duration of exercise

Thyroid hormone Triiodothyronine (T 3 ) and thyroxine (T 4 ) T 3 greatest biological activity Thyroid stimulating hormone (TSH; anterior pituitary) stimulates thyroid to release thyroxine Cells convert T 4 to T 3 Stimulates metabolism “permissive” effect –Enhances the effects of other hormones –Perhaps through adenylate cyclase/cAMP effect

Metabolic response to exercise

What do these responses tell us? Why measure –Lactate? –Lactate threshold? –Oxygen deficit? –Oxygen debt? Quantify exercise intensity Exercise responses

Exercise metabolism Oyxgen consumption –Principle measure of exercise intensity –Increases linearly with intensity Blood lactate –Easy to measure –Fair index of intensity

Lactate issues Blood lactate –Balance between rate of appearance (Ra) and disappearance (Rd) –Lactate used by other tissues as an energy source –Level in blood Balance between Ra/Rd Determined by fiber type and oxidative capacity of tissue

Muscle: Consumer of lactate Blood lactate increases during exercise above lactate threshold (>45- 50% Vo 2 max) –Release from tissue (muscle) greater than uptake (less active tissues) –Release from muscle is quite high initially, then falls –Some subjects actually switch to net uptake Lactate concentration Net Lactate release

Following exercise blood lactate levels fall The vast majority of the Carbon from lactate (C 3 H 5 O 3 ) shows up as expired CO 2 –Oxidized –C 3 H 5 O 3 + H + 3CO 2 + 3H 2 O Lactate may also be –Incorporated into Bicarbonate –Converted to glycogen –Converted to glucose –Incorporated into proteins Fate of lactate after exercise Expired CO 2 bicarbonate glycogen protein

Lactate turnover during exercise Turnover –Balance between production and removal Rest –Balance between production and removal Blood lactate low Exercise –Production greater than removal at all intensities above lactate threshold (45-50% of Vo 2 max)

Lactate turnover Blood concentration (1) is dependent upon the balance between –Clearance (2) –Rate of appearance (3) Note how trained lactate concentration is lower due to reduced rate of appearance and increased clearance rate 1 2 3

Endurance exercise and lactate Turnover –Measure used when metabolite is infused –Turnover is then based on infusion rate/amount in blood Greater clearance from blood necessitates greater infusion rate to maintain a certain level Lactate turnover is increased with endurance training Metabolic clearance –Measure of rate of disappearance from blood –Also increased with endurance training

Causes of the Lactate Threshold Lactate threshold –Point where blood lactate starts to accumulate in the blood –Balance between Ra and Rd changes –MCR reaches a maximum –Greater recruitment of fast-twitch fibers –SNS? Shunts blood flow away from inactive tissues May reduce uptake

Oxygen deficit –Difference between O 2 demand and O 2 consumption O 2 demand = ATP requirement O 2 consumption = mitochondrial ATP production –Energy deficit supplemented by ATP-PCr and anaerobic metabolism –Typically used during >LT to maximal work –Tough to determine during “supra-maximal” exercise, where the O 2 requirement is not known –Component of fatigue

“Oxygen debt” O 2 consumption should fall back to resting levels immediately once the exercise ceases –This DOES NOT happen –Originally thought that O 2 debt equal to the O 2 deficit Extra O 2 consumption during recovery to “pay back” the debt Thought to be completely due to non-aerobic metabolism (ATP- PCr and anaerobic metabolism) Currently: Known that other factors help determine the size of the oxygen debt –Name changed to Excess post exercise oxygen consumption (EPOC)

EPOC O 2 consumption follows exponential decrease to resting levels Time course can be quite prolonged (vs short time course of O 2 deficit) Temperature, catecholamines and pH impact EPOC, but have little or no effect on O 2 deficit So, some of the EPOC is due to oxidation of lactate/regeneration of glycogen and PCr but not a 1:1 relationship STILL above resting

EPOC Causes of excess post exercise VO 2 –Temperature Heat production and muscle temperature increase dramatically during exercise –Muscle temperature can get as high as 40°C High temperature can “loosen” the coupling between oxidation and phosphorylation

EPOC and mitochondrial uncoupling Fatty acids and ions –Fatty acids may be involved in “uncoupling” of oxidative and phosphorylation brown adipose tissue of rats So, heat is produced, but ATP is not –May also impact the permeability of Na + and K + across the mitochondrial memebranes This “linkage” is affected

EPOC and mitochondrial uncoupling Calcium Increases oxygen consumption –Mitochondria sequester Ca 2+ Energy dependent –Ca 2+ uncouples oxidation and phosphorylation

EPOC and mitochondrial uncoupling Epinephrine and Nor-epinephrine –Take some time to be cleared from the blood following exercise pH –Inhibits PCr recovery –May make mitochondrial membrane “leakier”