Chapter 13,14,20 Flashcards
What are the three principles of training
- overload
- reversibility
- specificity
explain overload in training
overload: need to stress body - adaptation
* increased capacity of a system in response to training above the level to which it is accustomed — intensity, duration, frequency
* too much leads to overtaining or overreaching
** if negative on the slope it is overload and positive slope is recovery – over time leads to improvement ** - slide 4
explain what reversibility is in training
when training is stopped – the training effect is quickly lost
- if you stop exercise or have overtraining fitness decreases
Overtraining is what
too much stress
* cant get to origional fitness
* downward trend
explain specificity in training
training effect is specific to:
* muscle fibers recruited during exercise
* type of contraction (eccentric, concentric, isometric)
* energy system involved (aerobic vs. anaerobic)
explain the influence of sex on training
men and women respond similarly to training programs
* exercise prescriptions should be individualized – strength or % improvement is similar
Explain the influence of initial fitness level
training improvement is always greater in individuals with lower initial fitness
- 50% increase in VO2 max in sedentary adults
- 10-20% improvement in normal, active subjects
- 3-5% improvement in trained athletes
Why are there no large improvements in trained individuals in fitness
- dont have unlimited capacity to grow blood volume
- only increase up to certain point
- similar to mitochondrial amount when you reach the “cap”
how does genetics play a role in how an individual responds to training
while there is a similar response in twins the improvement in VO2 max varied from 0-40%
What is the best way to determine the role of genetics in exercise
TWIN studies
Explain genotype E to how genetics influences VO2 max in training
- High responders (genotype e) == have ideal genetic makeup required for champion endurance athletes
– possess a realtively high untrained VO2max (80-90% w/o any endurance training)
Explain genotype A to how genetics influences VO2 max in training
- low responseres (genotype a) == possess a relatively low untrained VO2max
– often exhibit limited exercise training response (ie. McArdle’s disease = prevent exercise)
is anaerobic or aerobic capacity more geneticlally determined
anaerobic training is more genetically determined than aerobic capacity
- training can only improve anaerobic performance to a small degree
- dependent largely on fast (IIx fibers)
- determined early in development
What 4 labratory tests are used to quantify endurance exercise portal
- blood lactate
- expired ventilation (VT/LT)
- economy
- VO2 max
What adaptations occur in the muscle and how do they occur
stimulus repeated excitation and contraction of muscle fibers during endurance training stimulates changes in their structure and function
What 4 adaptations occur in the muscle during endurance training
- muscle fiber type
- capillary density
- myoglobin content
- mitochondrial function
explain the shift in muscle fiber types with exercise
fast-to-slow shift in muscle fiber type
* reduction in (cross sectional area of) fast fibers and increase in (cross sectional area of slow fibers) number of slow fibers
what is the magnitude of fiber type deterined by
- magnitude of fiber type change determined by duration, type of training and genetics
What is capillary density
blood vessel density surrounding muscle fibers
With an increased number of capillaries surrounding muscle fibers what 2 things improve
- enhanced diffusion of oxygen –> want blood moving as slowly as possible (high density) to diffuse more O2
- improved removal of wastes
What happens to the myoglobin conent with endurance training
endurance training increases muscle myogloin by 75-80% –> maximize oxidative metabolism
With more myoglobin content with endurance training what is its effect
supports muscle’s increased capacity for oxidative metabolism after training
what is the timeline for muscle mitochondria to adapt to training
muscle mitochondria adapts quickly to training
* doubles within 5 weeks of training
how is mitochondrial volume effected by exercise and what are the effects on both SS and IMF mitochondria
training increases volume of both subsarcolemmal and intermyofibrillar mitochondria in muscle fibers
Due to the volume increase in mitochondria with training what are the three physiological responses
- improved oxidative capacity and ability ot utilize fat as fuel
- intreases mitochondrial turnover ( breakdown of damaged mitochondria and replace with healthy mitochondria –> increase mitochondria work at the same time so they are able to preserve glycogen stroes and increase fat usage
- breakdown damaged mitochondria
what is mitophagy
breakdown of damaged mitochondria (recycle mitochondria)
What are the two places of significance of increased mitochondrial volume
- increase mitochondrial volume = greater capacity for oxidative phosphorylation
- increase mitochondrial volume and decreases cytosolic [ADP] due to more ADP transporters in mitochondrial membrane
what is the effect of an increase mitochondrial volume and decreases cytosolic [ADP] due to more ADP transporters in mitochondrial membrane
- less lactate and H+ formation
- less PC depletion
(instead of using the same areas within the mitochondria b/c mitochondria is larger it can pass through different areas giving the same energy
endurance training does what to the O2 deficit at the onset of work
with endurance training there is a faster rise in O2 uptake (less O2 deficit) which results in less lactate formation and less PC depletion –> reach steady state faster
If you are exercising at a constant work rate and you do the same work rate before and after training what happens to the O2 consumption
the O2 consumption doesnt change at that given rate
why is there very little impact on O2 consumption with endurance training
*
because the energy cost is still there but just how fast can generate energy from the oxidative sources is different
what two things contribute to exercise-induced adaptation to endurance training
primary and secondary signaling molecules
what molecule acts on all three adaptations: fast-to-slow fiber type shift, mitochondrial biogenesis, synthesis of antioxidant enxymes
PGC-1alpha
Low muscle glycogen is what type of influence on endurane training - induced adaptations
positive influence
* promotes increased protein synthesis and mitochondria formation due to higher activation of PGC-1apha
What are the two approaches to change CHO availability and endurance training adaptations
- restrict dietary carbohydrates = may cuase fatigue and limit training – not stress other places in body
- train twice per day (every other day) = second training session with lower muscle glycogen
what is the effect of endurance trained athletes on muscle fuel source
endurane trained athletes use more fat and less CHO than less trained during prolonged exercise and same intensity
How does endurance training effect capillaries
more endurance training –> increased capillary density –> slower blood flow in the muscle and increased FFA transporters –> increased uptake of FFA –> increase FFA utilization –>
- increased beta oxidation enzymes and carnitine transferase
- spare plasma glucose
endurance training promotes utilization of FFA during exercise – b/c upregulation of enzymes in FFA transport – transport FFA across cell membrane into muscle fiber
carnitine essential for transport FFA across mitochondria membrane – where beta oxidation occur – endurance training increases carnitine transferase – ensure efficient delivery of FFA to site of beta oxidation
How does endurance training effect mitochondria
more endurance training –> increased mitochondrial number –> increased beta oxidation enzymes and carnitine transferase
how does endurance exercise training improve acid-base balance
increase mitochondria –> increase FFA oxidation and decreased PFK activity –> decreased pyruvate formation - (increased H4 form of LDH)-> decreased lactate and H+ formation –> blood pH maintained
increase mitochondria –> increase mitochondrial uptake of pyruvate and NADH –> decreased lactate and H+ formation –> blood pH maintained
decreased need for glycolysis –> less H+ and pyruvate formed –> less change in blood pH
what does H4 form of LDH do
encourage lactate to pyruvate
- decrease lactate and maintain pH
What happens to the lactate threshold in trained individuals
trained == shift right and LT at higher VO2 max
What are the 7 cardiovascular adaptations to training
- maximal endurance capacity (VO2 max)
- cardiac output
- heart size
- heart rate (resting, submax, max, recovery)
- SV
- blood volume
- a-v O2 difference
can you imporve VO2 max with 12 mo. of endurance training
- to improve VO2 max you must exercise close to or b/t LT
explain the realationship between intensity and duration and frequence of exercise and VO2max and the risks
- As you increase VO2 max and incraese frequency and duration the risk of orthopedic problems and cardiac complications increases exponentially from 80-100 Vo2 max and 4-5 days of frequency
- as you increase VO2 max, frequency and duration there are large improvements in VO2 max but plateaus once you reach 80% of VO2 max
there is an optimal training intensity, frequency and duration that is between 60-80 VO2max, 3-4 days/wk, and 20-30 min/day
at what exercise intensity shows the greatest improvement in VO2 max
at about 80% VO2 max greatest improvement
- reduce frequency and duration to get best rance
What is the most important factor in improving VO2 max
training intensity
What can be used as an estimate of an athletes relative training intensity
measurement of exercise HR
What is the equation for calculating VO2 max
VO2max = (HR max * SVmax) * max (a-v) O2 difference
HR * SV = Q
What happens to cardiac output with training
untrained = plateau at about 20 L/min
trained = plateau at 27 L/min
more Q after training
How is heart size adapted based on demand
with an increased work demand –> cardiac muscle mass and ventricular volume increase in endurance training
- increase ventricle radius and increase hypertrophy of L ventricle
what happens to the wall thickness in a heart with endurance training
eccentric hypertrophy = increase in chamber wall thickness - aoverall total ventricular mass
what happens to resting HR due to indurance training
decrease in resting HR = can be as slow as 30-40 bpm in high conditioned athletes
Aerobic training results in what with heart rate
results in lower HR at any given absolute exercise intensity
What happens to HRmax with aerobic training
remains relatively unchanged (or maybe slight decrease)
why does HR decrease post-training
decrease HR b/c you get the same amount of blood out as pretraining
and you have an increase in SV = long filling time = decrease HR b/c better optimal for more trained individuals
what happens to recover heart rate pre vs post training
after endurance training HR returns to resting level much more quickly after an exercise bout than it does before training
smaller EPOC
increases in VO2 max depend on what adaptations (factors)
adaptations in SV max and max (a-v) O2 difference
- HR max either stays the same or decreases so not factored in
Explain the improvements in VO2 max with short and long duration training
- short duration (4mo) = incrase in SV and is dominant factor in increase VO2 max
- longer duration (28 mo) = both SV and a-v O2 incrase to improve VO2 max
how is stroke volume different in pretrianing vs. posttraining
both plateau but for trained individuals plateau at a higher workload
What factors increase SV
- increase in end diastolic volume (“preload”)
- increase contractility
- decrease total peripheral resistance (“afterload”)
What 3 factors increase end diastolic volume (preload)
- increase in plasma volume
- increase in filling time and veous return
- increase in ventricular volume
How does endurance training effect blood volume? If it does how does it effect the three parts of blood
- increases total blood volume = effect larger at higher training intensities –> b/c sweat more dont want to have a decrease in SV which could decrease Q
- increase plasma volume, increase of RBCs, decrease hematocrit (pseudoanemia) –> RBC dont decrease only difference b/t plasma and hematocrit increase
why do endurance athletes have an increased SV at rest
becuase they have improved ventricular filling due to bradycardia
Why do you want more blood volume during exercise
b/c dont want a large drop in SV with a greater duration exercise
Why might SV not plateau in elite endurance athletes
b/c they have
- improved ventricular filling
- increase in end diastolic volume and SV at a higher HR
–> plateau at a slower rate than trained and untrained
What is (a-v) O2 difference
the amount of O2 delievered to the dissues at it goes from the arteries to the veins
endurance athletes have the greatest (a-v) O2 difference == uptake the most oxygen for muscles
What two factors cause an increase in (a-v) O2 difference
- increased muscle blood flow –> cuases decreased SNS vasoconstriction and the same workload
—> plasma norepi and epi decrease with more weeks of training because now not as much of a stress response so dont need as much catecholamines
- improved ability of the muscle to extract oxygen from the blood
- increased capillary density == slow blood flow through muscle
- increased mitochondrial number == increase energy = diffusion gradient = incrase O2 delivered and increase change in O2 (from myoglobin to hemoglobin)
What Factors cause increase in Vo2max starting with decreased SNS activity to working muscle
if you increase SNS = vasoconstrict blood vessel going to muscle
decrease SNS activity to working muscle –> decrease afterload
- increase preload and decrease afterload –> increase SV –> increase max cardiac output –> increase vO2max
decrease SNS activity to working muscle –> incrase muscle blood flow
- increase muscle blood flow and increase capillaries and mitochondria –> increase (a-v) O2 difference –> increase VO2max
Which training adaptation is a potential mechanism that would explain an increase in VO2 max
a) increases in catecholamine concentration that stimulate the blood vessels supplying the working muscles
b) decreased capillary and mitochondrial density
c) increased max HR after yars of training
d) isovolumetric relaxation volume that shifts to the right on a pressure loop
e) none of these statements increase VO2 max
answer: E
- a – if increase catecholamine = increase vasoconstriction = decrease blood flow and decrease VO2 max
- b – want increase capillary and mitocondrial density
- c – high HR = low SV == increased training has lowered HRmax
does respiratory function limit performance and why
no does NOT limit performance b/c ventilation cna be increased to much greater extent than cardiovascular function
- no effect on lung structure and function at rest
How is pulmonary ventilation changed in trained and untrained individuals
- ventilation is during submaximal exercise following training
- maximal pulmonary ventilation is substatially increased
— able to sustain max ventilation
— trained has lower VO2 per Ve
Explain the training differences between sexes that are trained vs untrained
- males have highest capacity b/c larger lungs and larger capacity
What happens to VO2max and cardiovascular variables with detraining
- initial decrease in VO2 max (12 ddays) due to decrease SV max –> b/c easiest to regulate
–> HR and a-v O2 difference remain the same or increased
- later decrease due to decreased (a-v) O2 difference
–> decreased mitochondria, and no change in capillary density
What is effected with detrianing in VO2 max and cardiovascular variables
HRmax doesnt change – everything else decreases
explain the change of mitochondria with detraining
- mitochondrial adaptations lost quickly with detraining
- requires 3-4 wks. of retraining to regain mitochondrial adaptations
– long period to build mitochondrial density –> 1 wk w/ no movement =spike downward mitochondrial density
The responses of the cardiovascular, pulmonary and SNS are more dependent on what and less dependent on what
the trained state of the muscles involved in the activity and less dependent on some specific adaptations in those systems
what is the result of training one leg and its effects on the other leg
there is no ability to transfer training to the other leg
What is muscular strength
max force a muscle or muscle group can generate
1 repetition maximum (1-RPM)
what is muscular endurance
- ability to make repeated contractions against submaximal load over time
explain what strength training
- high-resistance (that is 6-10 reps till fatigue) –> results in strength increases
- low-resistance training (35-40 reps till fatigue) –> results in increases in endurance
when one arm is exposed to resistance training what happens to the strength and transferring
- a portion of the training is “transferred” to the other arm
What adaptations is responsible for early gains in strength
neural adaptations
- initial 8-20 weeks –> more motor units recruited
What 4 improvements come with increased neural drive
- increased number motor units recruited
- increased firing rate of motor units
- increased momtor unit synchronization
- imporved neural transmission across neuromuscular junction
What are the two adaptations that occur with resistance training-induced changes
- increased neural drive
- changes in rate of agonist and antagonist activation
What specific changes in rate of agonist/antagonist activation occur with reistance trainging
- golgi tendon organ and muscle spindles are effected
- untrained = activation of triceps w/ bicep
- trained = use mostly bicep with less tricep with training
with resistance training what is being effected
your strength increases
neural adaptations plateau when?
after past most training studies and goes into most serious strength trainers
when does hypertrophy take over compared to neural
hypertrophy takes over once neural plateaus
* increase exponentially when neural begin to plateau
What happens to strenth and how is it related to hypertrophy
strength plateaus over time but only can increase with steriods past plateu
- strength is related to the plateau in of hypertrophy
what is hyperplasia
- increase in muscle fiber number
- unclear if hyperplasia occurs in humans
what is hypertrophy
- incrase in cross-sectional area of muscle fibers == adding scarcomeres in parallel = increase crossbridges = increase force production
- hypertrophy is likely dominant factor in resistance training-induced increase in muscle mass
- hypertrophy due to increased muscle proteins (actin and myosin)
why would muscle fiber types “shift” from type IIx muscle fibers to type IIa during strength training
IIx = generate most force –shift–> IIa = better oxidative capacity (supply more ATP to muscles over time – less fatigue)
Explain the shift in fiber type during resistance training
fast to slow shift in fiber type
* from type IIx to IIa
* 5-11% change following 20 wks of training
** mean % of IIx fibers decreased significantly but the mean percentage of type IIa fibers increased)
What does mTOR activation do with signaling to lead to resistance training induced muscle hypertrophy
MTOR activation causes protein synthesis which causes muscle hypertrophy
Ingesting protin does what to the rate of protein synthesis in post training? what type of athletes does this apply to
increases rate of protein synthesis post-training
* for both endurance and resistance training
Is it important to plan protein intake around workouts
yes, both protein amount and timing
Resistance training results in what change in the muscle fibers
results in parallel increase in muscle fiber cross-sectional area and increased numbers of nuclei
what does increased number of myonuclei do to help the muscle during resistane training
help synthesis of protein molecules and increase cross sectional area
What is the genetic influence on the magnitude of resistance training-induced hypertrophy
about 80% of the differences in muscle mass b/t individuals is due to genetic variation
- non responder, moderate-responder, high responder
inactivity-induced muscle atrophy ocurs when
due to decreased protein synthesis and increased protein breakdown
- inactive muscle = protein synthesis decrease, protein degradation increase
- active muscle = protein synthesis increases and decrease protein degradation
what happens to the muscle with cessation of resistance training
results in muscle atrophy and loss of strength
* compared to endurance training, rate of detraining (strength loss) is slower
* recovery of dynamic strength loss can occur rapidly (w/i 6 wks) w/ retrining because of myonuclei
what allows the mucle to recover after detraining
myonuclei
what muscle fiber is more resistant to detraining and most resistant
- type 1 is resistant to detraining
- type IIx most likely to decline but comes back with retraining
what happens with combined strength and endurance training
may limit strength gains vs training alone
* strength and endurance begins to increase but over many weeks stength decreases
What are the three mechanisms for the impairment of strength development
- neural factors – tiring yourself out -> less firing rate, muscle connection
- overtraining – if you do high strength and high endurance training == cannot maintain same overtraining
- depressed protein synthesis
explain how neural factors can impair strength training
- impared motor unit recruitment: tiring yourself out
explain how overtraining factors can impair strength training
- it does not impair strength training but cannot train at same overtraining intensity
explain how depressed protein synthesis factors can impair strength training
- endurance training cell signaling can interfere with protien synthesis
- via inhibition of mTOR by activation of AMPK
what is AMPK (relates w/ mTOR)
AMP activated kinase – excreted with exercise
inhibits protein synthesis
* inhibits mTOR = inhibit protein synthesis
explain the pathway of resistance training and why concurent training reduces strength gains
resistance training –> mechanoreceptor activation increases –> mTOR activated –> protein synthesis –> muscle hypertrophy
b/c AMPK excreted w/ exercise can inhibit mTOR increase reducing strength gains
explain the pathway of endurance training and why concurent training reduces strength gains
endurance training –> increase AMPK ( inhibit mTOR) –> PGC-1alpha increase –> mitochondrial biogenesis
what is the best training system for concurrent strength and endurance training
- perform strength and endurance training on alternate days for optimal strength gains = maintain strength gains (in off season) dont need high amounts
- athletes whose sport need max strength should avoid concurrent training
- performance of combined strength- and endurance-training does NOT impair training-induced increase in endurance
What is the structure of a traditional periodized training program
model varies training load over time to achieve acute overload and some overreaching while avoiding overtraining
* 10% rule for increasing training load == increase intensity or duration < or equal to 10% per week
** some reaching overload but back off and allow recovery**
explain the results of undertraining
minor physiological adaptations and no change in performance
explain the results of undertraining
positive physiological adaptations and minor improvements in performance
explain the results of overreaching
- optimal physiological adaptation == small downcycle
optimal physiological adaptations and performance
explain the results of overtraining
physiological maladaptations, performance decrements, and overtraining syndrome
what is included (what type of training) in the zone of enhanced performance in competition and training
acute overload and overreaching
what are the 6 common symptoms of overtraining
- decrease in performance
- loss of body weight
- increased number of infections
- chronic fatigue
- psychological staleness
- elevated HR and blood lactate levels during exercise
** takes years to recover possibly**
explain the HR response during running
before training HR higher than overtraining and much higher than just normal training
- HR decreases a lot with training but can inrease a small amount with overtrianing
explain how normal periodizaiton of training compares to overreaching training
- overall with normal periodization of training and adequate recover performance increases exponentially
- with overreaching training and not enough recovery for the training that is taking place there is downward trend to overtrained syndrom
** quick recovery possible by tapering**
what is tapering
short term reduction in training load prior to competition
* allows muscles to resynthesist (most important) glycogen and heal from training-induced damange
* improves performance in both strength and endurance events
Explain what happens to glycogen stores during heavy training and competition at the end
- as training increases the glycogen stores continue to decrease and cannot get back to origional values because not given enough time to recover with high intensity exercsie
- At competition glycogen stores are at a low and therefore not perform as well
Explain what happens to glycogen stores during tapering and then at the end comptetition
- when tapering for multiple days the training volume is decreased and therefore the muscle glycogen stores and be built up and recoer
- on day of competition will be at a high to be able to produce the best results for competition
Explain the effects on concurrent strength and endurance training on individuals who are strength athletes vs. endurance athletes
strength athletes: combining of strength and endurance training impairs strength increase for strength athletes
endurance athletes: combining of strength and endurance training does NOT impair training-induced increases in endurance
