Test 4 study guide thingy Flashcards
what is signal transduction?
-ligand receptor interaction causes a response in the target cell called signal transduction
what controls the effectiveness and concentration of a hormone? does this change during exercise?
- the number of receptors available for binding
2. blood hormone concentration
blood hormone concentration determined by
- rate of secretion from the endocrine gland
- rate of metabolism or excretion of hormone
- quantity of transport protein
- changes in plasma volume
what happens to plasma volume during exercise?
during exercise, plasma volume decreases which causes a slight increase in hormone concentration in plamsa
what are the three effects elicited by a hormone receptor interaction?
- alter membrane transport
- stimulate DNA to increase proteins synthesis
- activates second messengers (cyclic AMP and CA++)
are steroid hormones lipophobic or lipophilic, and what does this mean with respect to carrier molecules?
steroid hormones cross the cell membrane very easily, meaning they are lipophilic. The carrier moleucles don’t have to increase intracellular concentration of ions or substrates
what are some examples of second messengers?
phosphorylase hormone sensitive lipase g protein diacylglycerol inositol triphosphate cyclic AMP Ca++
what are the main endocrine systems we described in class?
- hypothalamus
- posterior pituitary
- anterior pituitary
- thyroid
- adrenal glands
- pancrease
- testes
- adipose tissue
- skeletal muscle
hypothalamus
regulator of the pituitary
-influence by + and - input
anterior pituitary gland
- true endocrine gland
- secretes growth hormone which aids in the maintenance of blood glucose
posterior pituitary gland
- secretes ADH (vasopressin) and oxytocin
- it reduces water loss
- stimulated by high plasma osmolality and low plasma volume due to sweating, and exercise
thyroid
T3 and T4 maintain metabolic rate
- T4:T3 is 20:1
- T4 can be converted into T3
- increases metabolic rate
- The thyroid gland is very slow
- secretes calcitonin and pTH
what is the actual % of people with hypothyroid?
3-4%
calcitonin
regulates Ca++
adrenal gland
secrete 80% epinephrine and 20% norepinephrine
-it increases HR, glycogenolysis, lipolysis, and BP
where is growth hormone secreted from? what does it do?
- secreted from the anterior pituitary gland
- stimulates protein synthesis and long bone growth
- mobilized free fatty acid from adipose tissue
- aids in the maintenance of blood glucose
- growth hormone increases during exercise*
what is ADH and how does its concentration change during exercise?
ADH = antidiuretic hormone
- reduces water loss to maintain plasma volume
- stimulated by high plasma osmolality and low plasma volume due to sweating and exercise
- * ADH increases at 60% VO2 max***`
what does the adrenal medulla secrete? are these agents slow or fast acting?
- adrenal medulla secretes epinephrine and norepinephrine
- they are fast acting due to the fight or flight response
- it increases HR, glycogenolysis, lipolysis, and BP
what does the adrenal cortex secrete?
mineralcorticoids (aldosterone) glucocorticoids (cortisol) sex steroids (androgens and estrogens)
what stimulates the release of aldosterone? What is the aldosterone response to exercise?
the adrenal cortex secretes mineral corticoids (aldosterone)
- plasma k+ is the direct controller as well as Ang II (increased k+ induce secretion of aldosterone)
- little exercise: little change in aldo and renin and Ang II
- heavy exercise: (>50% VO2 max) parallel increases in aldo, renin and Ang II
- as plasma K+ increases aldosterone does as well
what stimulates the secretion of cortisol?
stimulated by exercise and long term fasting (to maintain plasma glucose)
how is the regulation of muscle glycogen utilization altered with exercise?
high intensity and duration exercise results in a more rapid glycogen depletion
- not greater but faster
- the heavier the exercise, the faster the glycogen is depleted
- * greater at 90 min @ 75% VO2 max than 30 min at 90% VO2 max*
during exercise what are permissive hormones
- they are helper and facilitator hormones
- without T3, epinephrine has little effect on FFA mobilization from adipose tissue, so T3 is a permissive hormone
does plasma growth hormone change with increasing exercise intensity?
as intensity increases, so does the levels of plasma growth hormone
-maximal work is >25x resting value (more sensitive with aerobic training)
does endurance training alter plasma norepinephrine or epinephrine levels to a fixed workload?
endurance training causes a rapid decrease In plasma NE and E to a fixed workload. YES.
what happens to FFA mobilization in light/moderate exercise versus heavy/sever exercise?
FFA mobilization decreases during heavy exercise
- doesn’t decrease in light/moderate exercise
- possibly because of high levels of lactic acid, elevated H+, or inadequate blood flow
what is the tolerated variation in core temperature and what effects does getting near temperature thresholds have on the body?
normal core: 37 C
too hot: 45 C or 113 F this may denature proteins and enzymes and lead to death
too cold: 34 C or 93.2 F: this may cause slowed metabolism and arrythmias
what are the mechanisms of involuntary heat production?
- shivering
- action of hormones :T3 and catacholamines
what are the predominant mechanisms in which we lose heat at rest? Does the contribution from these mechanisms change during exercise?
Radiation-
conduction
convection
evaporation
radiation
transfer of heat via infared rays
- no physical contact between surfaces
- 60% heat loss at rest
conduction
heat loss due to contact with another surface
convection
form of conductive heat loss
-heat transferred to air or water
evaporation
- heat transferre via water (sweat) on skin surface.
- depends on temp and relative humidity
- 25% heat loss at rest
- maximal sweat rate: 1.5 L/hr. After acclamation, 3.5 L/hr. Cooling power: 600 calories/L
What is the bodies thermostat in response to heat?
the hypothalamus is the body’s thermostat
- anterior pituitary increases core temp, sweating, increased blood flow
- posterior pituitary: cold exposure, heat production, shivering, decrease skin blood flow
anterior hypothalamus
works with heat exposure
-increased core temp, sweating, increase skin blood flow (vasodilation)
posterior hypothalamus
cold exposure, heat production (shivering), non shivering thermogenesis (T3 and catacholamines), decrease skin blood flow (vasoconstriction)
during a heat stress, how does the body attempt to regulate temperature? how can the effects of trying to regulate core temperature in a hot environment impact exercise?
Heat load: vasodilation and sweating
cold: shivering, vasoconstriction, catecholamine release and thyroxin release
-in a hot environment exercise could have impaired performance, and hyperthermia. Earlier onset of muscle fatigue
how can exercising in a hot/humid environment effect the onset of fatigue or impair performance?
there is an earlier onset of fatigue by -reduced mental drive, -reduced muscle blood flow during high intensity exercise, -accelerated glycogen metabolism,
- accelerate production of free radicals
- useless water loss
- higher core temp and sweat rate
How does the body acclimate to heat, and is this a slow (months) or a fast (days) response?
- adaptions occur within 7-14 days
- 10-12% increase in plasma voume
- increased sweat rate (can double)
- decreases salt loss in sweat
- increase in the synthesis of heat shock proteins (induced by increased temp- they are protective proteins)
with decreasing barometric pressure, what happens to the composition of air? in other words, what happens to the fraction (%) and density of O2, N2, CO2, etc. with increasing altitude?
less molecules as altitude increases, but same % of O2 N2 Ar CO2. the % do not change
compare and contrast heart rate, cardiac output, and ventilation at a fixed submaximal exercise load being performed at sea level Vs. high altitude (>4000 meters)
High altitude: decrease in VO2 max due to decrease in arterial PO2.
- Q decreases as well
- HR increases
- less O2 in blood , so ventilation increases
during increasing altitude the inspired pressure of oxygen decreases. for the pormula provided for PiO2 what variables are changing?
PiO2= (Pbar- 47 mmhg) * .2093
- dry gas pressure (Pbar) is changing
- P bar decreases at altitude
how does the body combat the reduced PiO2 in order to elevatee alveolar PO2?
***hyperventilation increases O2 levels
what is the normal arterial pressure of O2 (PaO2) at sea level?
100 mmHg
does the oxygen-dissociation curve shift with altitude?
it will shift to the LEFT. hyperventilation decreases CO2 in the blood
How does the body adapt to high altitude?
the body produces more RBC with carry O2
- people who grew up in high altitude have COMPLETE ADAPTATATION in aO2 content and VO2
- 6 g more hemoglobin in high altitude
contractile protein adaptations happen in
resistance training
mitochondrial and capillary adaptations happen in
endurance training
cross sectional study
the largest difference between ATH and NA is stroke volume
longitudinal study
studies show significant increases in aVO2 difference
how much does average VO2 max increase as a result of endurance training
15-20%
genetic predisposition accounts for _____% of ones VO2 max value
40-60%
factors influencing SV with training
increased preload
decreased afterload
increased contractility
in a 6 day training program (2 hr/day @ 65% of VO
2 max) resulted in a ___% increase in VO2 max due to:
7% increase due to:
11% increase In plasma volume
10% increase In SV
the initial changes in VO2 have been attributed to :
stroke volume
the initial decrease in VO2 max is ___% within how many days
- initial decrease is 8% within 12 days
- decreases 20% within 84 days
decrease in stroke volume max is due to:
rapid loss of plasma volume
the INITIAL metabolic adaptations to endurance training are likely _____
neural hormonal receptor changes
endurance training increases mitochondrial content in the muscle by how much
- increases quickly with in the first 5 days
- can increase 50-100% in the first 6 weeks
- mitochondrial content doubles within 5 to 6 weeks of training
what happens to mitochondrial adaptations with detraining?
- about 50% of the increase in mitochondrial content is lost after 1 week of detraining
- majority of adaptations lost within 2 weeks of detraining
to increase the CS activity in type IIx fibers with higher intensity, longer duration training to:
increase the oxidative capacity of those fiber types
ADP stimulates :
mitochondrial ATP production
why does exercise challenge homeostasis?
has to regulate temp, maintain PCO2 and PO2 levels
- maintain MAP via vasodilation of muscle
- glucose uptake increases
- and pH decreases
what are the three principles of training and examples for each?
overload: system is exercise at a level beyone which is accustomed
ex: sprinter runs marathon
specificity: training is specific to muscles involved, fiber type, energy system, velocity of contraction and type of contraction
ex: jumps to increase height
reversibility: gains are quickly lost when overload is removed
ex: don’t exercise you lose what you gained
to improve ones VO2 max roughly what duration and intensities are required? is the latter different if you are sedentary or exercise trained?
- training increases VO2 max
- 20-60 min
- 3-5 x per week at 50-85% VO2 max
- a trained individual needs >70% VO2 max
- a sedentary individual needs 40-50% VO2 max
what are the range of VO2 max values measured in athletes? healthy individuals? and those with cardiovascular pulmonary disease.
athlete: 84 l/min
healthy individual: 45 l/min
cardiovascular/pulmonary disease: 13-22 L/min
** a trained individual can only increase VO2 by 2-3% but sedentary can increases as high as 50% although genetics mainly determines VO2**
what is the main variable from the fick equation that is responsible for large difference in VO2 max in different populations (from cross-sectional studies)
Fick equation: Q x (avo2)
- avo2 difference shows a significant increase in VO2 max across different populations, HOWEVER THE LARGES DIFFERENCE ARE DUE TO STROKE VOLUME
how does exercise training effect cardiac output, and what are the underlying mechanisms?
exercise training INCREASES CARDIAC OUTPUT (HR decreases while SV increases)
how can avo2 difference change with long term aerobic exercise training? TEST QUESTION
the avo2 difference is due to increased O2 extraction from the blood, but is not due to an increase In arterial PO2 content with training
can endurance training shift muscle fiber type?
yes. endurance training makes type I med: type IIa , fast: type IIx
how does endurance training effect mitochondrial content in muscle?
with more endurance training, mitochondrial content will INCREASE QUICKLY within the first 5 days
-50-100% within the first 6 weeks
how does endurance training affect the O2 deficit?
reduces the O2 deficit
- less lactate and H+ formation, les PCr depletion
- less disruption of homeostasis
what is the rate limiting enzyme in glycolysis?
PFK
free radicals are produced by:
contracting muscles
free radicals can :
disturb cellular homeostasis
- damage muscle contractile proteins
- contribute to muscle fatigue during prolonged endurance events
training increases _____ antioxidants
exogenous
- this means training protects against oxidative damage and fatigue
after endurance training what happens to pyruvate formation?
decreased pyruvate formation
-decreased PFK= decreased glycolysis= less pyruvate= less lactate
percent gains are ____ proportional to initial strength
inversely
majority of strength gains are due to
neural adaptations
what are the neural adaptations?
increased ability to recruit motor units
- altered motor neuron firing rates
- enhanced motor unit synchronization
- removal of neural inhibition
true or false: WITH RESISTANCE TRAINING if one arm is trained then the contralateral side received strength gains also
TRUE
hyperplasia
increase in muscle fiber number
** there is not conclusive evidence that hyperplasia happens in humans*
true or false: hyperplasia contributes to strength gains
FALSE: hyperplasia does not contribute to strength gains
detraining:
-31% decrease in strength following 30 weeks detraining
retraining
- results in rapid regain of strength and muscle size
- within 6 weeks after resuming training muscle was gained back (muscle memory?)
force is dependent on the ____ of a muscle fiber
CSA
true or false: you lose the number of nuclei within the muscle with detraining
FALSE you do not lose the number of nuclei with in the muscle
upon training, myonuclei fuse by satellite cells
TRUE
there is a decline in strength after age ____.
50
- they start to lose muscle fibers and motor units
sarcopenia
loss of muscle mass
what are the #1 cause of injury in older adults?
falls
true or false: studies report that combining strength and endurance training impairs strength gains
true
mTOR increases what
mTOR increase hypertrophy
true or false: endurance training stops mTOR resulting in lower strength gains
TRUE
true or false: electrical stimulation can produce more tension in the muscle
True
-there is clear evidence of central fatigue is electrical stimulation and force production goes up
the neuromuscular junction is NOT a likely site of fatigue
true
training can increase the NA/K+ pump and may reduce the potential for fatigue via its mechanism
True
ATP falls only to ___% of its pre exercise levels
ATP falls only to 70% of its pre-exercise levels
true or false: DOMS is due to lactic acid buildup.
FALSE
it is due to microscopic muscle tears and inflammation
ergogenic aid
a substance, appliance or procedure that improves performance
