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 (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

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% 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

Lactate concentration

Net Lactate release

• 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

Fate of lactate after exercise

Expired CO2

Expired CO2 Expired

CO2

bicarbonate

bicarbonate

bicarbonate

glycogen

glycogen

proteinprotein

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 Vo2max)

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• Oxygen deficit

– Difference between O2 demand and O2 consumption

• O2 demand = ATP requirement

• O2 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 O2 requirement is not known

– Component of fatigue

“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)

EPOC

• 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

STILL above resting

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

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 Ca2+

• Energy dependent

– Ca2+ 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”