Exam 2 Flashcards
neuroendocrine system
endocrine system releases hormones into blood to circulate to tissues
the nervous system uses neurotransmitters to relay messages from one nerve to another
types of hormones
amino acid derivatives
peptide/protein
steroids
Insulin
fast acting hormone
uptake and storage of glucose and FFA
insulin during exercise
insulin in plasma concentration decreases during exercise
decreased insulin response following exercise
glucagon
fast acting hormone
mobilization of glucose and FFA fuels
glucagon during exercise
glucagon in plasma concentration increases during exercise
decreased response following training
insulin and glucagon secretion influenced by…
…catecholamines
absorption of a meal (what happens with insulin and glucagon)
increased insulin, decreased glucagon
increased storage of glycogen, fat and protein
decreased plasma glucose, amino acids, and fatty acids
during fasting and exercise (what happens with insulin and glucagon)
decreased insulin, increased glucagon
increased hydrolysis of glycogen, fat, and protein
increased gluconeogenesis
increased plasma glucose, amino acids, and fatty acids
trained vs untrained glucagon concentration
as one gets trained, glucagon concentration no longer increases during exercise because NE and E can mobilize faster
only untrained individuals rely on glucagon and insulin (on top of NE and E)
hormone-substrate interaction
- FFA mobilization dependent on hormone-sensitive lipase (HSL)
- FFA mobilization decreases during heavy exercise
- due to high levels of lactic acid (promotes resynthesis of triglycerides) the more lactic acid in the system the more FFA reduces
- elevated H+ concentration inhibits HSL
- inadequate blood flow to adipose tissue
- insufficient albumin to transport FFA in plasma
2 adjustments of blood flow during exercise
- increased cardiac output
- redistribution of blood flow of inactive organs to active muscle
pulmonary circuit
- right side of heart
- deox blood to lungs via pulmonary arteries
- ox blood to left side of heart via pulmonary veins
systemic circuit
- left side of the heart
- ox blood to body via arteries
- deox blood to right side of heart via veins
pericardium
- rigid sac around heart that keeps it in place and limits expansion
- athletes have expanded pericardium
cardiac muscle vs skeletal muscle (nuclei, energy system, structure)
- cardiac single nucleus in each fiber, skeletal multiple nuclei
- cardiac primarily aerobic, skeletal aerobic and anaerobic
- both striated but cardiac shorter, skeletal longer
Exercise training and the heart
regular exercise reduces incidence of heart attack and improves survival from heart attacks due to accumulation of oxidative stress from exercise developing antioxidant capacity in heart
Systole
- contraction phase
- ejection of blood
Diastole
- relaxation phase
- filling with blood
diastole and systole at rest and exercise
at rest diastole is longer than systole
during exercise both shorten, diastole decreases time a lot more
Pressure changes in diastole
- pressure in ventricles is low, filing with blood from atria
pressure changes in systole
- pressure in ventricles rises, blood ejected in pulmonary and systemic circulation
heart sounds
- first: closing of AV valves
- second: closing of aortic and pulmonary valves
blood pressure expressed as
systolic/ diastolic
120/80
- beginning of Koroskoff sound is systolic, sound disappearing is diastolic
pulse pressure
difference between systolic and diastolic blood pressure
- some people develop isolated systolic hypertension which is increased pulse pressure
mean arterial pressure (MAP)
how much blood flow your tissues are receiving
MAP = DBP + 0.33 (SBP-DBP)
hypertension (threshold, types, risks)
- bp over 130-140/90
- types: primary (essential) hypertension: cause unknown/ stiff blood vessels 90% of cases, secondary hypertension: result of other disease usually kidney
- risk factor for: left ventricular hypertrophy (precursor for heart failure), heart attack, atherosclerosis, kidney damage, stroke
determinants of mean arterial pressure (MAP)
- cardiac output
- total vascular resistance
MAP= cardiac output * total vascular resistance
(like ohms law, voltage=current*resistance)
short term regulation of BP
- use sympathetic nervous system to activate baroreceptors in aorta and carotid arteries
- increase in BP= decreased SNS activity
-decrease in BP= increased SNS activity
long term regulation of BP
- kidneys via control of blood volume
- often with use of diuretics
- reduces blood volume which reduces stroke volume which reduces cardiac output which decreases MAP
Post exercise hypotension
during exercise BP is high and post-exercise it goes below resting BP
indicates how chronic training can reduce your BP (exercise intensity-dependent)
Blood hormone concentration
the effect of a hormone on a tissue is determined by the plasma concentration and number of active receptors
plasma concentration is determined by***
- rate of secretion of hormone from endocrine gland, magnitude of input, stimulatory vs inhibitory input
- rate of metabolism or excretion of hormone, inactivation near the receptor and/or metabolized by the liver and kidneys
- quantity of transport protein, steroid hormones and thyroxine are transported bound to plasma proteins
- change in plasma volume, hormone concentration goes up with less blood volume and vice versa
factors that influence the secretion of insulin
high plasma glucose, high plasma amino acids stimulate pancreatic islet beta cells, insulin is secreted to normalize them
nervous system also impacts insulin secretion
Magnitude of hormone effect depends on
- concentration of hormone (blood volume)
- affinity of receptor for hormone
- number of receptors on the cell
downregulation
decrease in receptor number in response to high concentration of hormone
ex) high cortisol in bloodstream for a period of time leads to decrease in cortisol receptors to prevent cortisol from attacking proteins and tissue
upregulation
increase in receptor number in response to low concentration of hormone
- have not performed exercise in a while, so when you exercise, HR and BP go super high because stress hormone concentrations are low, so receptors are high
Mechanisms of hormone action
- activation of genes to alter protein synthesis (steroid hormones)
- activating second messengers in the cell via G protein (cyclic AMP, Ca++, inositol triphosphate, diacylglycerol)
- altering membrane transport (insulin via tyrosine kinase)
- Mechanism of Steroid Hormone action
steroids rely on transport proteins
1. hormone passes through plasma membrane (made of cholesterol (fat), phospholipid membrane (fat) so it can cross
2. inside target cell, the hormone binds to a receptor protein in the cytoplasm or nucleus
3. hormone-receptor binds to hormone response element on DNA in nucleus, regulating gene transcription
4. creates response (protein synthesis)
- cyclic AMP second messenger mechanism
- some hormones cannot cross cell membranes so they rely on second messengers
1. hormones bind to receptor on cell membrane
2. activate GDP -> GTP -> ATP-> CAMP (cyclic AMP) - cyclic AMP is the second messenger used to deliver action, it goes down biochemical pathways to create cellular response
contraction of the heart depends on…
…electrical stimulation of the myocardium
low resting heart rate can mean
- you are an endurance athlete
or - you have a damaged pacemaker (HR gets lower with each redundant mechanism)
conduction system
- sinoatrial node (SA node)
- atrioventricular node (AV node)
- bundle branches
- Purkinje fibers
ECG and its parts
- records the electrical activity follow
1. P wave (atrial depolarization)
2. QRS complex
(ventricu;ar depolarization and atrial repolarization)
3. T wave (ventricular repolarization) - ECG abnormalities may indicate coronary heart disease
Diagnostic use of ECG during exercise
graded exercise test to evaluate cardiac function to see if coronary arteries are ok
- can be artherosclerosis (plaque in coronary arteries)
-can be ST-segment depression (myocardial ischemia)
cardiac output
amount of blood pumped by the heart each minute
Q=HR * SV
heart rate times stroke volume
stroke volume
amount of blood ejected in each beat
regulation of HR
- Parasympathetic nervous system, slows HR by inhibiting SA and AV node via vagus nerve
- Sympathetic nervous system, increases HR by stimulating SA and AV node via cardiac accelerator nerves
why trained pop. has lower HR
low resting HR due to parasympathetic tone
increase in HR at onset of exercise
- initial increase due to parasympathetic withdrawal until 100 bpm
- sympathetic nervous system takes over after 100 bpm
Beta-blockade and HR
-beta-blockers compete with norepinephrine and epinephrine for beta-adrenergic receptors in the heart
- beta blockers reduce HR which lowers the myocardial oxygen demand
- they lower HR during sub and maximal exercise
beta-blockers prescribed for
patients with coronary artery disease and hyper tension
Heart rate variability
- time between heart beats
- wide variation in HRV is “healthy”, the baroreflex is working detecting change in BP
- low HRV is a predictor of cardiovascular morbidity
- not used often anymore as it doesn’t mean much
Regulation of Stroke Volume
Average aortic blood pressure “afterload”
Strength of the ventricular contraction “contractility”
End-diastolic volume (EDV) “preload”
average aortic blood pressure
“afterload”
pressure the heart must pump against to eject blood (mean arterial pressure)
strength of the ventricular contraction
“contractility”
enhanced by circulating E and NE and by direct sympathetic stimulation of heart
End-diastolic volume (EDV)
“preload”
volume of blood in the ventricles at the end of diastole
frank-starling mechanism
- the more the left ventricle is filled (EDV) the greater the stroke volume
- depends on venous return
venous return increased by
- venoconstriction via SNS (can be exercise induced)
- skeletal muscle pump (skeletal muscle contractions force blood toward heart)
- respiratory pump (changes in thoracic pressure pull blood toward heart)
