Physiology Training Flashcards
Overload
Training effect occurs when a system is exercised at a level beyond which it is normally accustomed with respect to intensity, duration, and frequency
Specificity
Muscle adapts specifically to the type of activity
Mitochondrial and capillary adaptations to
endurance training
Contractile protein adaptations to
resistance training
Training effect is specific to
- Energy System (aerobic vs. anaerobic)
- Muscle Fibers involved
- Type of contraction (eccentric, concentric, isometric)
- Velocity of contraction
Reversibility
Gains are lost fairly quickly when overload is removed
Endurance Training to increase VO2max
- Large muscle groups, dynamic activity
- 20 -60 min 3-5 times/week at 50-85% VO2 max
- HIIT, 30 sec-3min intervals at greater than or equal to 85% VO2 max or 75-175% PPO interspersed with rest or low intensity intervals for recovery, 20-25 min, 6 sessions over a 2 week period is an example HIIT program.
Expected increases in VO2 max with endurance training
- Average = 15-20%
- 2-% in those with high initial VO2 mac - requires an intensity of > 70% VO2 max
- Up to 50% in those with low initial VO2 max - initial training intensity of 40-50% VO2 max
Genetic Predisposition and endurance training
Accounts for about 50% of VO2 max and is a prerequisite for bery high VO2 max
The HERITAGE Family Study
Designd to study the role of genotype in cardiovascular, metabolic, and hormonal responses to exercise and training
Results of the Heritage Family Study
- Heritability of VO2 max is 50%
- Large variaton in change in VO2 max with training (20 week endurance training program)
2a. average improvement is 15-20%
2b. Ranged fro no improvement to 50% increase
2c. heritability of change in VO2 max is 47%
3 21 genes play a role rleated to adaptations and improvements in VO2 max with training
Fick Equation
VO2max = HR max x SV max x (a-vO2) max
Stroke Volume
EDV-ESV or Preload x Contractility x afterload
Differences in VO2 max in different populations is primarily due to
differences in SV max
Improvements in VO2 max
- Overall 40% increase in SV and a-vO2
- Shorter duration training (4 months) - SV increase is greater than the increase in a-vO2
- Longer duration training (28 months) - increase in a-vO2 is greater than the increase in stroke volume
Increase maximal stroke volume by
increasing preload, decreasing afterload and increasing contractility
Increased preload (EDV) due to
increased plasma volume, increases venous return and increases ventricular volume
Decreased afterload (TPR) due to
decreased arterial constriction and increased maximal muscle blood flow with no change in MAP
Increase in contractility is due to
upregulated calcium release and uptake in myocardium
Changes to stroke volume occur rapidly - within six days of training
- 11% increase in plasma volume
2, 7% increase in VO2 max - 10% increase in stroke volume
A-VO2 difference occur because of an
increase in muscle blood flow and an improved ability of the muscle to extract oxygen from the blood
Muscle blood flow increases because if a
decreases in SNS vasoconstriction to trained muscle
Improved ability of the muscle to extract oxygen from the blood occurs because of an
increase in capillary density, and an increase in mitochondrial number
An increase in capillary density occurs because of
decreased diffusion distance to the mitochondria slow blood flow through the muscle to allow more time for O2 diffusion from capillary to muscle fiber.
The ability to perform prolonged, submaximal work is dependent on
the maintenance of homeostasis during the activity
endurance training causes
- More rapid transition from rest to steady state
- Reduced resilance on glycogen stores from liver and muscle
- CVS and thermoregulatory adaptations.
- Improved neural and or hormonal receptor function likely precedes biochemical adaptations in skeletal muscle
- Structural and biochemical changes in muscle
Structural and biochemical changes in muscle with endurance training
- Increased type 1 fiber percentage
- Increased mitochondria
- Increased ability to metabolize fat for fuel
- Increased muscle anti-oxidant capacity
- Increased capillary density
Endurance training causes a shift in muscle fiber types from -
fast to slow shift in muscle fiber types with a
- reduction in fast myosin
- increase in slow myosin
- extent of change determined by duration of training and genetics
Endurance training causes an increase number of
capillaries with enhanced diffusion of oxygen and increased removal of waste
Endurance training increases _______ content in skeletal muscle
Mitochondria
2 sub populations of mitochondria in the muscle
subsarcolemmal and intermyofibrillar
Subsarcolemmal Mitochondria
Located below the sarcolemma
Intermyofibrillar Mitochondria
are located around the contractile proteins 80% of total mitochondria making up the larger population
Mitochondrial content increases quickly depending on
intensity and duration of training - you can see an icnrease of 50-100% within the first 6 weeks
Mitochondrial content changes result in
increased endurance performance due to changes in muscle metabolism
Intracellular signaling and Inhibition of Protein Synthesis
Signaling pathways during concurrent resistance and endurance training.
AMPK activation causes
inhibition of mTOR via TSC1/2
AMPK activation supresses
resistance training induced protein synthesis
Mechanisms of Impairment of Strength Development
- Neural Factors
- Low Muscle Glycogen Content
- Overtraining
- Depressed protein synthesis
Neural Factors that impair strength development
Impaired motor unit recruitment and force productions - limited evidence
Low muscle glycogen content impairs strength development by
Due to successive bouts of endurance exercise - low glycogen content can therefore reduce the intensity at which you can perform subsequent resistance training sessions which would decrease the ability to adapt and gain strength
Overtraining
Imbalance between training and recovery
There is no direct evidence that
overtraining occurs when combining strength training with endurance training
Depressed protein synthesis impairs strength development by
endurance training adaptations (from AMPK signaling and increases in mitochondrial biogenesis) interferes with protein synthesis.
TSC1/2
tuberous sclerosis complex 1/2
Concurrent Strength and Endurance Training causes a potential for interference of adaptation
- Endurance training increases mitochondrial proteins
- Strength training increases contractile proteins
- Depends on intensity, volume, and frequency of training
Studied report that combining Strength and endurance training impairs
Strength gains overall - it depends on intensity, volume and frequency of training
31% decrease in strength after
30 weeks but very little atrophy during this time
Loss in strength during detraining is mostly related to
the neural component
Rapid gains in strength and fiber cross- sectional area with just 6 weeks of
retraining back to pre-training levels or better
Detraining results in a slow decrease in
Strength
31% decrease in strength following 30 weeks detraining associated with small changes in fiber size due primarily to nervous system changes
Small changes in fiber types with detraining
type 1 fiber size -2%
type 2a fiber size - 10%
type 2x fiber size - 14%
Retraining results in rapid regain of strength and muscle size
with in 6 weeks after resuming training can maintain strength with reduced training for up to 12 weeks
Resistance training induced fiber hypertrophy results in a
parallel increase in myonuclei, myofibrillar proteins, and fiber cross sectional area (CSA)
Both primary and secondary signals are involved in muscle adaptations to
resistance exercise
Increases in protein synthesis are primarily due to an increase in the
amount of protein synthesized per molecule of mRNA rather than an increase in total mRNA
resistance exercise promotes muscle
protein synthesis by improving translational efficiency
Primary signal to stimulate muscle protein synthesis
is the increase in muscle stretch or force
Secondary signal s to stimulate muscle protein synthesis
increased IGF-1, Increased Akt, increased mTOR
A single bout can increase protein synthesis 50-100%
Responses to resistance training induced signaling events
muscle hypertrophy- and increased number of myonuclei in each new growing fiber
Increased number of myonuclei in each new growing fiber
Arise from satellite cell (type of stem cell b/w sarcolemma and outer layer of connective tissue. Required for continued muscle adaptations and muscle growth
Muscle hypertrophy in resistance training
- Increased cross-sectional area of fibers
- Hypertrophy occurs when protein synthesis is greater than the rate of protein break down.
- All essential amino acids must be present for protein synthesis to occur.
Resistance training improves muscle
antioxidant enzyme activity
Resistance training improves
antioxidant capacity - 100% increase in two antioxidant enzyme which should protect the muscle against oxidative damage associated with exercise induced production of free radicals - limited evidemce of long term benefits of this exists.
Can resistance training improve muscle oxidative capacity and increase capillary number?
Conflicting results of studies
- Some studies show a decrease or no change in mitochondrial content others show a small increase
- Some show a small increase in capillary number while others show a small decrease.
Reason for conflicting results in the studies of whether resistance training improve muscle oxidative capacity and increase capillary number
Different frequency and duration of training and long term high volume training can improve oxidative capacity of muscle.
Resistance training induced changes in the muscle fiber types
- Fast to slow shift in fiber type from type 2x to 2a with a 5-11% decrease in type IIx fibers with a corresponding increase in type IIa fibers following 20 weeks
- No increase in percentage of type 1 fibers
- Lesser extent of fiber type shift than endurance training
Resistance training induced changes in the skeletal muscle size
Hyperplasia and hypertrophy
Hyperplasia and resistance training
- increase in muscle fiber number
- Mixed evidence in human studies
- 90-95% muscle enlargement due to hypertrophy
Hypertrophy and resistance training
- A gradual process that can take months to see changes in general
- High-Intensity resistance training can elicit changes in muscle size by 3 weeks.
- Enlargement of both type 1 and 2 fibers - greater degree of hypertrophy in type II fibers
- Increase in myofibrillar proteins (increase in actin and myosin filaments occurs
An increase in [ADP] at the onset of exercise stimulates
mitochondrial ATP producing systems to meet the ATP demands of the cross bridges via the ATP-PC system, Glycolysis, and oxidative phosphorylation.
Increased mitochondrial number following training
- Lowers [ADP]
- ATP production is now shared among more mitochondria meaning the rate of ADP transportation into the mitochondria is faster
- The concentration of ADP in the cytosol increases only half as much because of the additional mitochondria present to take up the ADP to create ATP
Oxygen deficits following training is
Lower because it is the same VO2 at a lower [ADP] (less reliant on anaerobic respiration) and the energy requirement can be met by the aerobic ATP system at the onset of exercise.
There is a faster rise in the VO2 curve and steady state is reached earlier
The oxygen debt following training is lower resulting in
- Less lactate and H+ formation
2. Less PC depletion and less stimulation of glycolysis
After training mitochondria
Doubles and therefore the rate of ADP transportation doubles. The ADP concentration only doubles half as much because of the extra mitochondria available to take up the ADP. The load is shared
Citrate Synthase
Market of mitochondrial oxidative capacity
Effects of exercise intensity on mitochondrial adaptations
55%, 65% or 75% VO2 max leads to increased CS in oxidative type IIa fibers with all training intensities
Effects of duration on mitochondrial adaptations
- 30, 60, or 90 minutes
- No difference btw duration on CS activity in IIa fibers
3.
Increase in IIx fiber CS activity with
Higher intensity and longer duration training
Type IIa activity changes independently of
Intensity and duration
Training causes a huge change in muscle metabolism by
Increasing the utilization of fat and sparing of plasma glucose, muscle and liver glycogen stores. These changes are due to improvements in
- Transport of FFA into the muscle
- Transport of FFA from the cytoplasm to the mitochondria
- Mitochondrial FFA oxidation
Transport of FFA into the Muscle
- increased capillary density (slow rate of blood flow past the cell membrane allows for more time for FFA to be transported into the blood.)
- increased fatty acid binding protein and fatty acid translocation
- 50% of lipid is oxidized from intramuscular fat
- plasma FFA provides the other 50%
- plasma FFA must be transported by carrier molecules across cell membrane to the cytoplasm and then to the mitochondria before oxidation can occur
Transport of FFA from the cytoplasm to the mitochondria
- Increased number of mitochondria and surface area of the mitochondria
- Higher level of CPT-1 and FAT lead to faster rates of FFA transfer from cytoplasm to mitochondria
Mitochondrial Oxidation of FFA
- Increased Enzymes of Bets Oxidation
- Increased rate of acetyl CoA formation from FFA (citrate is the first molecule formed in the TCA cycle)
- High citrate levels inhibit PFK and glycolysis - I.e. Carbohydrate metabolism
Increased mitochondria and capillary density
Increase rate of FFA utilization which preserves plasma glucose
Free radicals are produced by
Contracting muscles
Two groups of antioxidants
Endogenous and exogenous
Exogenous antioxidants
Are derived from the diet and can neutralize free radicals
Endogenous Antioxidants
Protects against oxidative damage and radical mediated muscle fatigue
They are produced by cells in the body
Training increases
Endogenous antioxidant in skeletal muscles
Exercise training improves
Acid base balance during exercise
Lactate production during exercise occurs when
There is an accumulation of pyruvate and NADH in the cytoplasm
Training adaptations for acid base balance
- Increased mitochondrial number
- Increased NADH shuttle
- Change in LDH type
Increased mitochondrial number
- Less carbohydrate utilized = less pyruvate formed
- Pyruvate that is formed is more likely to be taken up by the increase in mitochondria for the Krebs cycle rather than being converted to lactate in cytoplasm
Increased NADH shuttles from cytoplasm to mitochondria
- NADH formed from glycolysis shuttled to mitochondria faster
- Less NADH available for lactic acid and H+ formation
Changes in LDH types (5 different forms/ isoenzymes exist)
M4–)M3H–)M2H2–)MH3–)H4
Heart form from H4 has a lower affinity for pyruvate so there is less lactic acid formation
Endurance and resistance exercise increase specific muscle proteins
- Exercise stress stimulates cell signaling pathways in skeletal muscle that activate transcription
- Gene activation results in transcription of mRNA
Process of training induced muscle adaptation
- Muscle contraction activates primary and secondary messengers
- Results in expression of genes and synthesis of proteins peaks in 4-8 hours and is back to base line on 24 hours
Neural adaptations are responsible for early gains in strength (initial 8-20 weeks)
Adaptations include
- increased ability to recruit motor units
- Altered motor neuron firing rates
- Enhanced motor unit synchronization
- Removal of neural inhibition
Decline in strength after age
50
Due to loss of muscle mass loss of both type 1 and 2 with atrophy of type 2 fibers and loss of intramuscular fat and connective tissues. Loss of motor units lead to loss in muscle fibers and reorganization of motor units also associated with NSAID use.
Progressive resistance training causes
- Muscle hypertrophy and strength gains
2. Important for activities of daily living, balance and reduced risk for falls.
Basic Principles and Terms of Strength Training
Muscular strength and endurance
Muscle strength
Maximal force of a muscle or muscle group can generate through the full range of motion
1-repetition maximum
The max load you can do once
Muscular endurance
Ability to make repeated contractions against a submaximal load
Responses to strength training
- Percent gain inversely proportional to initial strength - genetic limitation
- High resistance training results in gain of strengths 2-10 RPM
- Low resistance training results in gains in endurance +20 RPM
Muscle mitochondria
Adapt quickly to training - double within 5 weeks of training
Mitochondrial adaptations are lost quickly with
Detraining - loss of 50% of gains within first week majority lost within two weeks
Requires 3-4 weeks of retraining to
Regain mitochondrial adaptations
Detraining and VO2 max
- Rapid decrease in VO2 max
- Decreases in SV
- Decrease in maximal a-vO2 difference
3a. Decrease in mitochondria
3b. Decrease oxidative capacity of muscle
3c. Decrease type IIa fibers and increase in type IIx fibers - Initial decrease during the first 12 days is due to SV decrease and then it’s due to decrease in A-V O2
Central Control
Cardiorespiratory - increase Ve, HR and decreased blood flow to the kidney and liver
Motor unit recruitment - VO2 increase
Signals come from the motor cortex, cerebellum and basal ganglia
Peripheral Control
Spinal Cord to
Cardiorespiratory control center - HR, Ve, increase and Blood flow to the kidney and liver decrease
Working muscle - group 3 and 4 fibers via temperature, tension, and local factor increases
Peripheral feedback from working muscles
Group 3 and 4 nerve fibers which are responsive to temperature, tension, and local fibers and feed into cardiovascular control centers an increase their rate of firing in proportion to the metabolic demand
Central Command encompasses higher brain centers
Motor cortex, basal ganglia and cerebellum
- Recruitment of muscle fibers
- Stimulates cardiorespiratory control centers
Following endurance training the concentration of local factors
Do not increase as much leading to less chemo input to cardiorespiratory centers in addition tension is maintained causing less SNS output less HR and Ve increase
Biochemical adaptations to training influence the physiological response to submaximal exercise by affecting
- SNS decrease and care holding decrease
- HR decrease
- Ventilation decrease
Due to reduction in feedback from muscle chemoreceptors and reduced number of motor unit recruitments
Primary signals of endurance exercise excite secondary signals downstream such as
Increased primary signals
Increase
Calcium
AMP:ATP ratio
Free radicals
Activate downstream secondary signals
Increase Calcinuerin CaMPK AMPK P38 NFkB PGC 1-a
Responses to signaling during endurance training
- Fast to slow twitch fiber types
- Mitochondrial biogenesis
- Antioxidant enzyme synthesis
AMPK
Stimulate glucose uptake, fatty acid oxidation, and mitochondrial biogenesis
Activated due to muscle fiber phosphate energy changes
P38
Stimulates by endurance exercise induced changes induced production of free radicals once activated it causes mitochondrial biogenesis by stimulating PGC-1a
PGC-1a
Increases in capillaries fast to slow muscle fiber type shift, mitochondria, antioxidant enzymes
Activated by P38, and AMPK, and CaMK
CaMK
Signaled upstream by cytosolic calcium levels
Contributes to the activation of PGC-1a
Calcineurin
Fiber growth
Fast to slow fiber type shift
Activated by cytosolic calcium
IGF-1, Akt, mTOR
Muscle growth from resistance training activated by contractile activity
NFkB
Activated by free radicals which promotes expression of antioxidant enzymes in skeletal muscles
Primary signals
Lead to protein synthesis response depends on
Resistance vs. endurance training
Intensity vs. duration
4 primary signals
- Muscle stretch
- Increased cellular calcium
- Elevated free radicals from activate skeletal muscle
- Muscle fibers phosphate/energy levels
