Chapter 13/14/20 Flashcards
Physiology of Training
Three principles of training
- Overload
- Reversibility
- Specificity
Principles of training
Overload
what is it, what is it dependent on, too much?
Increased capacity of system in response to training above the level to which it is accustomed
* Dependent on intensity duration and frequency
* Too much leads to overtraining or overreaching
Describe the graph of acute overloading/overeaching showing performance vs. time
Principles of training
Reversibility
when training stopes, the training effect is quickly lsot
Describe the graph of reversibility (measure of fitness vs. time) in respect to detraining and overtraining
Principles of training
Specificity
training effect is specific to…
Training effect is specific to:
* Muscle fibers recruited during exercise (depends on type of exercise you’re doing)
* Type of contraction (eccentric, concentric, isometric)
* Energy system involved (aerobic vs. anaerobic)
Example of specificity for VO2max in sport-specific activities vs. treadmill
VO2 max of rowers,
cyclists, and cross-country skiers was
tested: uphill running on a treadmill
and during their sport-specific activity.
VO2 max attained by all athletes
during their sport-specific activity was
as high (or higher) than those values
obtained on a treadmill.
Training causes specific adaptations
Influence of sex on % strength improvement
men and women respond similarly to training programs
- exercise prescriptions should be individualized but % improvements are similar
Influence of initial fitness level on VO2max improvements
% improvements based on fitness
magnitude of training improvement is always greater in individuals with lower initial fitness (more room to improve)
* 50% increase in VO2max in sedentary adults
* 10-20% improvement in normal, active subjects
* 3-5% improvement in trained athletes
Influence of genetics on VO2max improvements (twin study)
genetics plays important role in how an individual responds to training (but does not account for 100% of improvement)
twin study - similarities but improvment in VO2max varied from 0-40%
Does genotype affect training-induced changes in VO2max
yes lots of variation between genotypes
High responders vs low responders
High responders (genotype E): ideal genetic makeup required for champion endurance athletes
* high untrained VO2max
* larger heart, lungs, or taller
Low responders (genotype A): limited exercise training response
* low untrained VO2max
What area of exercise improvement does genetics mainly determine
anaerobic capacity = more genetically determined than aerobic capacity
* training only improves anaerobic by a small degree
* Dependent largely on fast (IIx) fibers = determined early in development
Labratory tests to quantify endurance exercise potential
3 pillars of performance
- VO2max: how big is the engine
- Economy: how efficiently you use oxygen
- Lactate threshold/ventilatory threshold: how close to VO2max can i sustain for long periods of time
adaptations in muscle
repeated excitation/contraction of muscle fibers during endurance training stimulates changes in structure and function such as changes to
- muscle fiber type
- capillary density
- myoglobin content
- mitochondrial function
- mitochondrial oxidative enzymes
Edurance training effect on muscle fiber type
Fast-to-slow shift
* reduction in cross-sectional area of fast fibers, increase in slow fibers
* Magnitude of change determined by duration of training, type of training, and genetic
Effect of endurance training on capillary density
increased # of capillaries surrounding muscle fibers = more diffused blood thats able to move slower
* enhanced diffusion of oxygen
* Improved removal of waste
Effect of endurance training on myoglobin content
increases muscle myoglobin content by 75-80%
* More myoglobin = more O2 delivery to mitochondria
* Helps support oxidative metabolism after training
Time course of training adaptations in mitochondria
muscle mitochondria adapt quickly to training - double within 5 weeks
Effect of endurance training on mitochondrial volume and turnover
increases the volume of both subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria in muscle fibers
* improved oxidative capacity (shared load) and ability to utilize fat as fuel (multiple working at the same time to create same amount of ATP while preserving glycogen stores)
increases mitochondria turnover (breaking down of damaged mitochondria and replacement with healthy)
* this is termed mitophagy (recycling mitocondria)
significance of increased mitochondrial volume
in terms of ADP and oxidative phsophorylation
increased mitochondria volume =
* greater capacity for oxidative phosphorylation
* decreases cytosolic [ADP] due to increased ADP transporters in mitochondria membrane resulting in less lactate and H+ formation and less PC depletion
utilizing more areas of mitochondria for same amount of energy
Explain why endurance exercise training-reduces the O2 deficit at the onset of work
increases in mitochondria density and volume allows more oxygen consumption = faster rise to steady state
energy cost remains the same, its about how quickly you can generate energy sources
PGC-1a
what activates it, what does it do
secondary signaling molecule that increases with endurance training
* acts on all three adaptations: fast-to-slow fiber type shift (increased protein synthesis), mitochondrial biogenesis, and synthesis of antioxidant enzymes
* low muscle glycogen activates PGC-1a
Is low muscle glycogen a positive influence on endurance training-induced adaptations?
yes, because it activates PGC-1a which promotes adaptations protein synthesis and mitochondria formation
two approaches to lowering muscle glycogen for endurance training adaptations
- Restrict dietary carbohydrates: may cause fatigue and limit training
- Train twice per day (every other day): second training session with lower muscle glycogen
Effect of exercise duration on muscle fuel source
as duration increases, we shift from carbohydrate to fat utilization (due to decrease in muscle glycogen stores - rely on fats instead)
Effect of endurance training on muscle fuel source & how this appears on a graph of duration vs. relative fat oxidation
endurance trained athletes use more fat and less CHO than non-athletes during prolonged exercise at the same intensity
up/leftward shift
how endurance training alters substrate utilization during prolonged exercise.
describe the diagram
increased mitochondria and capillary density will increase FFA utilization and spare plasma glucos
how endurance training improves acid-base balance during exercise
increase in mitochondria ultimately decreases lactate and H+ formation to maintain blood pH
Effect of endurance training on lactate threshold
in the trained state, one can exercise at a higher percentage of one’s VO2max before lactate begins to accumulate
shifts to the right
Cardiovascular adaptations to training include:
list them all out
- maximal endurance capacity (VO2max)
- Cardiac output
- Heart size
- Heart rate (resting, submax, max, recovery)
- Stroke volume
- Blood volume
- Arterial-venous oxygen (a-vO2) difference
typical VO2 max values:
* untrained women
* untrained men
* female athletes
* male athletes
- untrained women: 32-44 (average 38)
- untrained men: 36-52 (average 44)
- female athletes: 49-61(average 55)
- male athletes: 57-85 - large range (average 71)
Describe intensity, duration, and frequency effects on VO2max and risks
explain graph
Most important factor in improving VO2max
intensity (not duration)
recommended intensity for greatest improvement in VO2max
~80% VO2max
What can we measure to prescribe exercise intensity and duration
exercise heart rate can be used to estimate an athlete’s relative training intensity and duration
Calculation of VO2max (equation)
VO2 max = HR max x SV max x max (a-vO2) diff
Effect of training on cardiac ouput
cardiac output increases
endurance training on heart size
to match increased work demand, cardiac muscle mass (cardiac tissue) increases and ventricular volume increases
Note: we don’t always see increase in chamber wall thickness in trained athletes - ventricular dimension can increase (eccentric hypertrophy) = decrease in thickness
Overall there is still an increase in total ventricular mass in these situations
endurance training on resting heart rate vs. submamx HR vs. maxHR
Resting HR: decreases maredly as a result of endurance training (mainly due to increased SV)
- can be as low as 30-40 bpm in highly conditioned endurance athletes
Submax HR: decreases - lower HR at any given absolute exercise intensity
MaxHR: remains unchanges (or slight decrease)
Larger SV requires slower HR for optimal filling
Endurance training on recovery HR
HR returns to baseline much quicker after exercise
The increase in VO2max during training depends on what three factors/adaptations (Fick equation)
- Are they all of equal importance?
- Do they all increase?
Since HRmax stays constant or decreases, increases in VO2max depend on adaptations in SVmax and maximal (a-vO2) difference
Which part of the Fick Equation causes improvements in VO2max during short duration training vs. longer duration training
Short duration training (4 months): increase in SV is dominant factor in increasing VO2max
Longer duration training (28 months): both SV and a-vO2 increase to improve VO2max
Factors that increase stroke volume with training
Factors effecting stroke volume
How does endurance training affect blood volume
Endurance training increases total blood volume (larger effect at higher training intensities)
* increased plasma volume
* increased volume of red blood cells
* **decreases **hematocrit **
This is what leads to an increase in end-diastolic volume (preload) and ultimatly stroke volume
factors effecting stroke volume
how does endurance training effect ventricular filling
improved ventricular filling due to bradycardia
Does SV plateau in elite endurance atheletes
stroke volume may not plateau due to:
* improved ventricular filling
* increase in EDV and SV at high HR
Two main factors that increase a-vO2 difference
- increased muscle blood flow due to decreased SNS vasoconstriction
- Improved ability of the muscle to extract oxygen from the blood due to increased capillary density (slows blood) and increased mitochondrial number
Explain the factors causing increased VO2max with endurance training
whole diagram
Does respiratory function limit performance
Respiratory system function does not usually limit
performance because ventilation can be increased
to a much greater extent than cardiovascular
function
Which training adaptation is a potential mechanism that would explain an increase in VO2max
a. increases in catecholamine concentration that stimulate the blood vessels supplying the working muscles
b. decreased capillary and mitochondrial density
c. increased maximal heart rate after years of training
d. isovolumetric relaxation volume that shifts to the right on a pressure volume loop
e. none of these statements increase VO2max
e. none of these statements increase VO2max
- catecholamines would cause vasoconstriction = less blood flow
- not a good thing, we want opposite
- HRmax does not increase
- shifting end-systolic volume to the right = decreased SV
Does training cause adaptations to lung structure and function at rest
No effect on anatomy (lung structure and function at rest)
However, the respiratory system does undergo specific adaptations to endurance training to maximize its efficiency
adaptation
How is pulmonary ventilation effected by exercise
- ventilation is lower during submax exercise following training
- Maximal pulmonary ventilation is substantially increased
- one can exercise at a higher intensity before ventilatory threshold occurs
Sex and training differences in maximal pulmonary ventilation
- Trained males and females have higher Vemax than untrained of the same sex
- Males have higher Vemax due to larger lungs
- all decline with age due to decline of functionality
Detraining on VO2max
The intital decrease in VO2max (12 days) is due to:
Later decrease is due to:
Initial: decrease in SVmax since its easily regulated
* HR and a-vO2diff remain same or increased
Later: decrease in (a-vO2)max
* decrease in mitochondria (constantly recycled so we just dont build more)
* no change in capillary density
Detraining on VO2max
How quickly do we lose mitochondrial adaptations; can they be gained back quickly?
mitochondrial adaptations lost quickly (even after one week of detraining)
* requires 3-4 weeks of retraining to regain mitochondrial adaptations
Lack of transfer of a training effect
No transfer effect in endurance training - If I train one leg, theres no ability to transfer that to the other leg, I would need to restart that training after switching to the other leg
- responses of cardiovascular, pulmonary, and sympathetic nervous systems are more dependent on the trained state of the muscles involved in the activity than on some specific adaptations in those systems
Muscular strength
maximal force a muscle or muscle group can generate
* 1 repetition maximum (1-RM)
Muscular endurance
ability to make repeated contractions against a submaximal load
two types of strength training
- high-resistance training (6 to 10 reps till fatigue) - results in strength increases
- low-resistance training (35 to 40 reps till fatigue) - results in endurance
is there a transfer effect with resistance training
unlike endurance training, when one arm is exposed to resistance training, a portion of the training is “transferred” to the other arm
* Because of neuromodulation
These adaptations are responsible for early gains in strength (initial 8-20 wks) from resistance training
Neural adaptations
NOT due to hypertrophy
Neural adaptations from resistance training
Increased neural drive
* Increased number motor units recruited
* Increased firing rate of motor units
* Increased motor unit synchronization
* Improved neural transmission across neuromuscular junction.
Describe neural and muscular adaptations to resistance training - timeline of what’s causing strength gains (graph)
Resistance training-induced changes in muscle size
fiber hypertrophy and fiber hyperplasia in humans
Hyperplasia: increase in muscle fiber number
* dont think this happens in humans (unsure tho)
Hypertrophy: increases in cross-sectional area of muscle fibers (adding sarcomeres in parallel)
* Due to increased muscle proteins (actin and myosin)
dominant factor in resistance training-induced increases in muscle mass
hypertrophy
Resistance training effect on muscle fiber type & size
fast-to-slow shift (from IIx to IIa)
* 5-11% change following 20 weeks of training
Both fiber types will increase, but there’s a bigger increase in type IIa
Increase in cross-sectional area of muscle fibers (no change in the actual number of fibers) and increased number of myonuclei (helps further protein synthesis and increase area)
Why is there a shift from IIx to IIa with resistance training
even though IIx generate more force, IIa has a better oxidative capacity (supplying more ATP to muscles especially over time)
Signaling molecule that causes muscle hypertrophy with resistance training
Resistance training will cause mTOR protein activation which increase protein synthesis = muscle hypertrophy (stacking more proteins on the outside/making it bigger)
effect of ingesting protein on protein synthesis
Ingesting protein increases rate of protein
synthesis post-training.
– For both endurance and resistance training.
Plan protein intake around workouts.
Genetic influence on hypertrophy
80% of differences in muscle mass between individuasl is due to genetic variation
the decrease in… and increase in… is what causes muscle atrophy due to inactivity
decrease in protein synthesis and increased in protein breakdow
* muscle takes a lot of energy to sustain
How does strength and muscle fiber size change with detraining
endurance vs resistance?
muscle atrophy and loss of strength
* slower strength post resistance training than endurance
Why is recovery of dynamic strength loss (with retraining) relatively rapid (within 6 weeks)
myonuclei stay on the outside
Is concurrent strength and endurance training beneficial
no, combined strength and endurance training may limit strength gains vs. strength training alone
* this depens on training state, volume & frequency of training
3 mechanism that limit strength gains with concurrent strength/endurance training
- Neural factors: enduced fatigue in neurons/impaired motor unit recruitment (limited evidence)
- Overtraining (no direct evidence)
- Depressed protein synthesis: endurance training cell signaling can interfere with protein synthesis via inhibiton of mTOR by activation of AMPK - stimulated during exercise (strongest evidence)
common training mistakes
non-sport specific training, over-training, not tapering
Periodized Training Program
model that varies the training load over time to acheive acute overload and some overeaching while avoiding overtraining
“ten percent rule” for training load
increase intensity or duration less than or equal to 10% per week - do not increase by more than 10%
Model of the continuum of training stages
symptoms of overtraining
decrease in performance, loss of body weight, chronic fatigue, increased sickness, psychological staleness, elevated HR & blood lactate levels during exercise
HR response to overtraining
HR increases closer to untrained HR
With prolonged overeaching, quick recovery does not occur and overtraining syndrome develops
Right before this occurs, quick recovery is still possible by doing what
tapering
What is tapering and what does it allow
- 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
all about glycogen stores!!
