Transcript Limits of Human Performance

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
Training effects on autonomic
nervous system
• 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
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
• 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
Glucocorticoids
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
Exercise responses
• What do these
responses tell
us?
• Why measure
– Lactate?
– Lactate
threshold?
– Oxygen deficit?
– Oxygen debt?
• Quantify
exercise
intensity
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
Lactate
concentration
• Blood lactate increases
during exercise above
lactate threshold (>4550% 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
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
– C 3 H 5 O3 + H +
3H2O
protein
protein
bicarbonate
glycogen
glycogen
bicarbonate
3CO2 +
• Lactate may also be
– Incorporated into
Bicarbonate
– Converted to glycogen
– Converted to glucose
– Incorporated into proteins
protein
bicarbonate
Expired
CO2
Expired
CO2
Expired
CO2
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
2
– Clearance (2)
– Rate of appearance (3)
• Note how trained lactate
concentration is lower
due to reduced rate of
appearance and increased
clearance rate
3
1
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 (ATPPCr 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
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
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”