Chapter 13, 14, 20 Flashcards
overload
the need to stress the body in order to create adaptations
increased capacity of a system in response to training above the level to which it is accustomed
what are the 3 key components of overload
intensity
duration
frequency
can you have too much overloading
yes which would lead to overtraining or overreaching
reversibility
when training is stopped, the training gains are lost quickly
specificity: training effect is specific to
muscle fibers recruited during exercise
type of contraction (eccentric or concentric)
energy system involved (aerobic vs anaerobic)
suppose you test the VO2 max of highly trained rowers, cyclists, skiers on uphill running on a treadmill and then during their sport specific activity. What changes in VO2 max would be observed?
VO2 max attained by all athletes during their SPORT specific activity was as high or higher than the values obtained on the treadmill
influence of sex on training
men and women respond similarly to training programs even though exercise training Rx should be personalized
how does fitness level relate to training improvement
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
influence of genetics on training
genetics plays an important role in how people respond to training, however is not the only factor as variability still exists
high responders (genotype E)
individuals with the ideal genetic makeup required for champion endurance athletes
posses a relatively high untrained VO2 max
low responders (genotype A)
possess a relatively low untrained VO2 max
often exhibit limited exercise training response
such as McArdles patients
what is more genetically determined: aerobic or anaerobic capacity
anaerobic capacity is more genetically determined than aerobic capacity
can training improve anaerobic performance
only to a small degree
what anaerobic capacity largely dependent on
fast type IIx fibers which is determined early in development
even if you increase hypertrophy, if you don’t have a lot of these fibers it is hard to increase performance
3 main pillars of performance
VO2 max
economy
LT/VT - how close to VO2 max can I sustain HR for longer
adaptations in muscle as a result of endurance training
repeated excitation and contraction of muscle fibers during endurance training stimulate changes in their structure and function
changes seen in:
muscle fiber type
capillary density
Mb content
mitochondrial function
mitochondrial oxidative enzymes
as a result of endurance training what happens to muscle fiber type
fast to slow shift in muscle fiber type
reduction in the cross sectional area of fast fibers and increase in the number of slow fibers
magnitude of muscle fiber type change is determined by
duration, training, type of training, and genetics
as a result of endurance training what happens to capillary density
increased number of capillaries surrounding muscle fibers leading to enhanced diffusion of O2 (since moving blood as slowly as possible) and the improved removal of wastes
as a result of endurance training, what happens to Mb content
endurance training increases muscle Mb content by 75-80% which supports a muscles increased capacity for oxidative metabolism after training
time course of training mitochondrial changes
muscle mitochondria adapt quickly to training
the # of muscle mitochondria doubles within 5 weeks of training
endurance training effects of mitochondrial volume
endurance training increases the volume of both sarcolemmal (SS) and intermyofibrillar (IMF) mitochondria in muscle fibers
as a result of increased volume of SS and IMF mitochondria, what happens to oxidative capacity
improved oxidative capacity and ability to utilize fat as fuel
share workload across other mitochondria (1 mitochondria- use CHO, 2+ mitochondria, use FATs)
endurance training effects on mitochondrial turnover
increases mitochondrial turnover (which is the breakdown of damaged mitochondria and replacement with healthy mitochondria)
mitophagy
the breakdown of damaged mitochondria
significance of increased mitochondrial volume
increased mitochondrial volume results in greater capacity for oxidative phosphorylation meaning more energy
increased mitochondrial volume also decreases cytosolic [ADP] due to increased ADP transporters in mitochondrial membrane resulting in less lactate and H+ formation and less PC depletion
effects of endurance training on O2 deficit
reduces the O2 deficit at the onset of work
reach steady state faster
faster rise in O2 uptake = less lactate formation and less PC depletion
exercise induced signaling : primary and secondary signaling molecules
primary and secondary signaling molecules contribute to exercise induced adaptation to endurance training
3 primary signals and 6 secondary signals
what is the main secondary signal
PGC-1a
why is low muscle glycogen a positive influence on endurance training induced adaptations
low muscle glycogen activates PGC-1a and promotes increased protein synthesis and mitochondria formation
two approaches to the increase in PGC-1a
1) restrict dietary CHO - but this may cause fatigue and limit training
2) train twice per day (every other day) which should lead to the second training session having lower muscle glycogen
as exercise duration increases what happens to substrate utilization
decrease in CHO and an increase in FAT utilization due to low muscle glycogen stores
endurance trained athletes: substrate utilization
endurance trained athletes use more fat and less CHO than less fit athletes during prolonged exercise at the same intensity
shifts relative fat oxidation graph up and left
training effects on lactate threshold
in a trained state, one can exercise at a higher % of one’s VO2 max before lactate begins to accumulate in the blood
shifts LT to the right
cardiovascular adaptations that occur in response to endurance training
changes in
VO2 max
Q
heart size
HR (resting, submax, max, and recovery)
SV
Blood volume
(a-v)O2 difference
effects of training on VO2 max
VO2 max is increased with 12 months of endurance training
what exercise intensities show the greatest improvement in VO2 max
intensities ~80% VO2 max
what is the most important factor in improving VO2 max?
intensity NOT duration
what can be used as an estimate of an athletes relative training intensity
measurement of exercise HR
calculation of VO2 max
product of max Q and (a-v)O2 difference
VO2 max= HRmax x SVmax x max(a-v)O2 difference
or VO2 max= Qmax x (a-v)O2 difference
effects of training on cardiac output
increases with training
effects of endurance training on heart size
as an adaptation to increased work demand, cardiac muscle mass and ventricular volume increase with endurance training
(increase in chamber radius and left ventricular hypertophy)
effects of endurance training on resting heart rate
decreases markedly as a result of endurance training
can be as low as 30-40 bpm in highly conditioned endurance athletes (bradycardia)
effects of aerobic training on HR
aerobic training results in a lower HR at any given absolute exercise intensity
effects of aerobic training on maxHR
maxHR typically remains relatively unchanged (or may slightly decrease) after training
effects of endurance training on recovery HR
after endurance training, HR returns to resting level much more quickly after an exercise bout than it does before training
increases in VO2 max depend on adaptations in
SV max and max (a-v)O2 difference
not HRmax because it stays the same or decreases
improvements in VO2 max during short duration (4 months) training is due to
increase in SV
the improvements in VO2 max after a longer duration of training (~28 months) is due to
increases in SV and (a-v)O2 difference
effects of endurance training on SV
SV will plateau at a much higher workload if trained
endurance training effects on blood volume
increases total blood volume and this effect is larger at higher training intensities
increase plasma volume, increase volume of RBCs, decrease hematocrit
why is an increase in plasma volume a good thing
prevents decreases in SV due to loss of fluids due to sweat
increase blood volume= increase in SV in longer duration exercises
why is there an increased SV at rest in endurance athletes
improved ventricular filling due to bradycardia
why might SV not plateau in elite athletes
improved ventricular filling
increase in EDV and SV at a high HR
(a-v)O2 difference
amount of O2 delivered as you go from arteries to veins
arteries deliver O2 to capillaries and remaining O2 in veins goes back to the heart
factors increasing (a-v)O2 difference
increased muscle blood flow due to decreases SNS vasoconstriction at the same work load
improved ability of the muscle to extract O2 from the blood
what is involved in the improved ability of muscle to extract O2 from the blood
increased capillary density (slowed blood flow through muscle)
increased mitochondrial number (more O2 molecules dropped off at mitochondria which increases the drive for O2 to be delivered from Hb to Mb)
does the respiratory system limit performance
the respiratory system does NOT limit performance because ventilation can be increased to a much greater extent than cardiovascular function
training effects on lung structure and function
no effect at rest
effects of training on pulmonary ventilation
ventilation is lower during submaximal exercise following training
max pulmonary ventilation is substantially increased
detraining: first 12 days
initial decrease in VO2max due to decrease SV max (12 days)
HR and (a-vO2) difference remained the same or increased
detraining: after 12 days (later effect)
later decrease in VO2 max due to decrease in (a-vO2) max
due to a decrease in mitochondria but no change in capillary density
time course of detraining mitochondrial changes
mitochondrial changes are lost quickly with detraining
requires 3-4 weeks of retraining to regain mitochondrial adaptations
lack of transfer: endurance events
if I train one leg, no ability to transfer training to another leg
muscular strength
maximal force a muscle or muscle group can generate
1 repetition max (1-RM)
muscular endurance
ability to make repeated contractions against a submaximal load
strength training
high resistance training (6-10 reps till fatigue)
low resistance training (35 to 40 reps till fatigue)
high resistance training results in
strength increases
low resistance training results in
endurance
transfer : resistance training
unlike endurance training, when one arm is exposed to resistance training, a portion of the training is “transferred” to the other arm due to neuromodulation that occurs with strength training
what is responsible for early gains in strength due to resistance training
neural adaptations for initial 8-20 weeks
adaptations in initial 8-20 weeks as a result of resistance training
increased neural drive
- increased number of motor units recruited
- increased firing rate of motor units
-increased motor unit synchronization
-improved neural transmission across neuromuscular junction
changes in rate of agonist/antagonist activation
hyperplasia
increase in the number of muscle fibers
does not occur in humans
hypertrophy
increase in cross sectional area of muscle fibers
due to increased muscle proteins (actin and myosin) which increases cross bridges and increases force production
(adding sarcomeres in parallel)
what is the dominant factor in resistance training induced increases in muscle mass
hypertrophy
resistance training effect on muscle fiber type
fast to slow shift in fiber type (from type IIx to IIa) due to increased oxidative capacity which increases ATP available to muscles
5-11% change following 20 weeks of training
mTOR activation
resistance training
downstream effect
activate mTOR
protein synthesis
hypertrophy
**just stacking muscle fibers in parallel and increasing numbers of myonuclei not changing the number of fibers themselves
consequences of ingesting proteins
ingesting proteins increases the rate of protein synthesis post-training for both endurance and resistance training
plan protein intake around workouts (amount and timing)
genetic influence on resistance training induced hypertrophy
approx 80% of differences in muscle mass between individuals is due to genetic variation
why does inactivity induced muscle atrophy occur
due to decreased protein synthesis and increased protein breakdown
cessation of resistance training results in
muscle atrophy and loss of strength
compared to endurance training, the rate of strength loss (detraining) in resistance training is
slower
compared to endurance training, the recovery of dynamic strength loss can occur ___ with resistance retraining
rapidly (within 6 weeks)
what types of training may reduce strength gains
combined strength and endurance training may limit strength gains vs strength training alone
- depends on training state of subject, volume and frequency of training, and integration of methods
- endurance training >3 days/week and 40-40 min/day
why does a combination of endurance and strength training decrease gains
1) neural factors - fatigue
2) overtraining = fatigue
3) depressed protein synthesis
depressed protein synthesis as a result of endurance and strength training together
endurance training interferes with protein synthesis via inhibition of mTOR by activation of AMPK
AMPK activated during exercise which inhibits mTOR which inhibits protein synthesis and muscle hypertrophy decreasing strength
recommendations for concurrent strength and endurance training
- perform strength and endurance training on alternate days for optimal STRENGTH gains
- athletes whose sport requires maximal strength should avoid concurrent training
*the performance of combined strength and endurance training does NOT impair training induced increases in ENDURANCE
periodized training programs
varies the training load over time to achieve acute overload and some overreaching while avoiding overtraining
10% rule for increasing training load
increasing intensity or duration < 10% / week
what indicates optimal psychological adaptations and performance
overreaching
tapering
short term reduction in training load prior to competition
allows muscles to resynthesize glycogen and heal from training induced damage
improves performance in both strength and endurance events (athletes can reduce training load by 60% without a reduction in performance)
