Autonomic nervous system

1. Autonomic nervous system

2. 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

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

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

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

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

7. Hormonal response to exercise

8. 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)

9. 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

10. 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

11. 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

12. 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

13. Thyroid hormone • Triiodothyronine (T3) and thyroxine (T4) • T3 greatest biological activity • Thyroid stimulating hormone (TSH; anterior pituitary) stimulates thyroid to release thyroxine • Cells convert T4 to T3 • Stimulates metabolism • “permissive” effect • Enhances the effects of other hormones • Perhaps through adenylate cyclase/cAMP effect

14. Metabolic response to exercise

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

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

17. 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

18. Muscle: Consumer of lactate Lactate concentration • Blood lactate increases during exercise above lactate threshold (>45-50% Vo2max) • 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 Net Lactate release

19. Fate of lactate after exercise • Following exercise blood lactate levels fall • The vast majority of the Carbon from lactate (C3H5O3) shows up as expired CO2 • Oxidized • C3H5O3 + H+ 3CO2 + 3H2O • Lactate may also be • Incorporated into Bicarbonate • Converted to glycogen • Converted to glucose • Incorporated into proteins protein protein bicarbonate glycogen protein glycogen bicarbonate bicarbonate Expired CO2 Expired CO2 Expired CO2

20. 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 Vo2max)

21. 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 2 3 1

22. 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

23. 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

24. Oxygen deficit • Oxygen deficit • Difference between O2 demand and O2 consumption • O2 demand = ATP requirement • O2consumption = 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 O2 requirement is not known • Component of fatigue

25. “Oxygen debt” • O2 consumption should fall back to resting levels immediately once the exercise ceases • This DOES NOT happen • Originally thought that O2 debt equal to the O2 deficit • Extra O2 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)

26. EPOC STILL above resting • O2 consumption follows exponential decrease to resting levels • Time course can be quite prolonged (vs short time course of O2 deficit) • Temperature, catecholamines and pH impact EPOC, but have little or no effect on O2 deficit • So, some of the EPOC is due to oxidation of lactate/regeneration of glycogen and PCr but not a 1:1 relationship

27. EPOC • Causes of excess post exercise VO2 • 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

28. 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

29. EPOC and mitochondrial uncoupling • Calcium • Increases oxygen consumption • Mitochondria sequester Ca2+ • Energy dependent • Ca2+ uncouples oxidation and phosphorylation

30. 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”