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Principles of Training. OverloadStimulus beyond what tissue is accustomedIntensity, duration, frequency of trainingSpecificityMuscle fiber type(s) recruitedPrincipal energy system involved (aerobic v. anaerobic)Velocity of contraction (Vmax)Type of contraction (concentric, eccentric, isometr
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1. Physiology of Training Powers CH 13
2. Principles of Training Overload
Stimulus beyond what tissue is accustomed
Intensity, duration, frequency of training
Specificity
Muscle fiber type(s) recruited
Principal energy system involved (aerobic v. anaerobic)
Velocity of contraction (Vmax)
Type of contraction (concentric, eccentric, isometric)
Specific Adaptations = “Training Effect”
Aerobic training = capillary and mitochondrial adaptations
Power training = increase in contractile proteins
3. Cardio-Respiratory Adaptations
4. Endurance Training and VO2 Max Programs that enhance VO2 Max:
Involve large muscle mass / dynamic exercise (running, cycling, swimming, XC skiing)
20-60 min. per session
3-5x per week
Intensity @ 50 – 85% VO2 Max
Capacity for improvement:
Large genetic component (differences in mitochondrial DNA explain much of individual differences in VO2 Max)
Largest gains experienced by those with low initial values
5. VO2 Max and Cardiac Output Increases in VO2 Max with endurance training:
50% of increase due to SV
50% of increase due to O2 extraction (A-VO2 diff)
Greater capillary density and increased # of mitochondria in trained muscle ( maximal ex. ventilation)
Increase in Max HR has less influence on VO2 Max
6. Influences on Stroke Volume Influences on increased EDV:
Increased ventricular size
Increased venous return (“preload”)
Increased myocardial contractility
Decreased peripheral resistance to blood flow out of heart (“afterload”)
With endurance training: peripheral resistance = CO
(arterial BP remains unchanged)
7. Detraining and VO2 Max Weeks 1 and 2
Decrease in SV due to decrease in plasma volume
Weeks 3 – 7
Decrease in A-VO2 difference (due to decrease in # of mitochondria more than decrease in capillary density)
Mitochondria number doubles in muscle cell after 5 weeks of training
1 week of inactivity (detraining) = loss of 50% of that gained in 5 weeks of training
3-4 weeks of retraining needed to reach former levels
8. Biochemical Adaptations and O2 Deficit ATP converted to ADP + P allows x-bridges to form
ADP concentration in cell cytoplasm is stimulus for ATP-producing systems to kick in:
Phosphagen system (initially)
Glycolysis
Mitochondrial oxidative phosphorylation (provides ATP aerobically in Steady State exercise)
Endurance Training Effect
Increases in mitochondria #, oxidative enzymes, and # of capillaries in muscle fiber (“shared” chore of ATP production)
9. Biochemical Adaptations and O2 Deficit More mitochondria = “shared” chore in ATP production
Less change required in ADP concentration to stimulate mitochondria to take up O2 (fewer mitochondria to do work requires higher ADP concentration to stimulate mitochondria)
Since less change in ADP concentration is needed to stimulate mitochondria to work, rising ADP levels at onset of work will cause earlier activation of oxidative phosphorylation
This causes faster rise in O2 uptake curve at exercise onset and shorter time to steady state VO2 – resulting in lower O2 deficit, less creatine phosphate depletion, and less lactate and H+ formation.
Mitochondria = money
ADP concentration = hunger
…Think about the price of a snack – either I am very hungry (high adp concentration) or I have plenty of money (increased mitochondria #), but if I am not that hungry and short on $$, I’ll wait to find it cheaper somewhere else (glycolysis or phosphagen systems) however, they are fatigable and are like driving around looking for cheaper snacks and spending all of your money in gas trying to find a better price.Mitochondria = money
ADP concentration = hunger
…Think about the price of a snack – either I am very hungry (high adp concentration) or I have plenty of money (increased mitochondria #), but if I am not that hungry and short on $$, I’ll wait to find it cheaper somewhere else (glycolysis or phosphagen systems) however, they are fatigable and are like driving around looking for cheaper snacks and spending all of your money in gas trying to find a better price.
10. Biochemical Adaptations and Plasma Glucose Concentrations Combination of increased capillary density and # of mitochondria per muscle fiber enhances:
Transport of FFA into muscle
Transport of FFA from cytoplasm into mitochondria
Greater activity of enzyme carnitine transferase
Mitochondrial oxidation of FFA
Increased rate of formation of acetyl CoA from FFA for oxidation in Krebs Cycle
11. Biochemical Adaptations, Blood pH and Lactate Removal Mitochondrial adaptations result in:
Smaller O2 deficit due to more rapid increase in O2 uptake at onset of work
Increase in fat metabolism (muscle glycogen / blood glucose sparing)
Reduction in lactate and H+ formation
Increase in lactate removal
12. Bone and Connective Tissue Adaptations
13. Bone Adaptation Mechanical loading stimulus affecting bone growth:
Magnitude of load (greater intensity = greater stimulus for bone growth)
Rate of loading (higher rates of contraction / high-power activities = greater stimulus)
Direction of forces (alteration of normal bone loading pattern = greater stimulus)
Types of loading:
Compression
Tension
Shear
Bending
Torsion
14. Forces Acting on Bone / Joint Bones accustomed to normal forces (force parallel to long axis) and handles rapid rate of loading due to brittle nature of cortex
Cortical bone can withstand high levels of weight bearing or muscle tension in the longitudinal direction before failure (Fx)
15. Forces Acting on Bone Trabecular (spongy) bone
Scaffolding arrangement
Bone weight reduction
Adaptive to multi-directional stress
16. Bone Integrity Bone is adaptive material sensitive to disuse, immobilization, vigorous activity
Wolff’s Law – change in bone’s internal architecture in response to loading
Bone resorption – osteoclasts
Bone deposition - osteoblasts
17. Physical Activity and Bone Remodeling Cyclic loading
MES ( ~ 1/10 force required to Fx bone)
Increase in appositional (x-sectional) growth
Wolff’s Law
SAID principle
Sharpey’s fibers (kinetic chain)
18. Ligaments and Tendons Connect bone-to-bone (L) or muscle-to-bone (T)
Viscoelastic
Collagen and elastin fibers
Tensile strength related to x-sectional area
Become stiffer with cyclic loading
Fail under rapid stretch
19. Articular cartilage High water content
Stiff but compressible shock absorption
Lubricates joint surfaces via secretion of synovial fluid
20. Joint Degeneration Degenerative Joint Disease
Avascular Necrosis
21. Muscular Adaptations
22. Muscular Adaptations Muscle strength
Maximal force a muscle (group) can generate (1RM)
Power
F x D / t (W/t)
Muscle endurance
Repeated contractions against submaximal load
23. Muscular Adaptations to Resistance Training Hypertrophy
Increase in synthesis of contractile proteins w/in myofibril
Increase in # of myofibrils w/in ms fiber (new myofilaments added to external layers of myofibril – Hyperplasia??)
Increase in x-sectional area of ms fiber = increase in force development
Fiber-type Response
Greater increases in size of Type II (fast twitch) fibers
# of fast twitch fibers relative to slow twitch may indicate ultimate potential for hypertrophy
Neural Adaptations
Primary catalyst for strength gains early (1st month) resistance training
Detraining
Strength decreases occur at faster rate than muscle atrophy
Decreases in 1st month of detraining connected w/ loss of neural adapt.
24. Muscular Adaptations to Endurance Training Fiber-type Response
Selective recruitment of Type I (slow twitch) fibers (sustain low intensity / high volume exercise)
Conversion of Type IIx to Type IIa (glyc-oxidative) to enhance endurance)
Increased training intensity causes increase in fast twitch fiber recruitment
Hypertrophy
Less capacity for hypertrophy in slow twitch fibers principally recruited for endurance events
Energy Production
Increase in mitochondria size and #
Increased myoglobin levels for O2 transport w/in cell??
25. Muscular Adaptations Concurrent performance of intense endurance and resistance training can result in decreased strength gains
Concurrent resistance (strength) training does not hinder (and may enhance) endurance capacity
Anaerobic training may = enhanced aerobic performance
Aerobic training does not = enhanced anaerobic performance
26. Hormonal Adaptations
27. Hormonal Interactions with Muscle Hormonal mechanisms mediate changes in the metabolic and cellular processes of muscle as a result of resistance training
Muscle Remodeling:
Disruption / damage of muscle fibers
Inflammatory response
Hormonal interactions
New protein synthesis (contractile and non-contractile proteins)
28. Adaptations to Resistance Training Increase in muscle contractile proteins (A & M)
Synthesis of non-contractile proteins (laid down 1st to provide structural integrity and orientation of contractile elements within sarcomere)
Protein metabolism
Type II fibers depend on dramatic increase in protein synthesis to maintain hypertrophy
Type I fibers depend on protein degradation reduction