Physiology of Training

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 _at_ 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

Powers CH 13, Table 13.1 p263
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

Powers CH 13, Figure 13.3, p. 268
Increased plasma volume and total Hb with
endurance training
6
Influences on Stroke Volume
SV EDV - ESV

• 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

Reverse of training effect
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)

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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.

Think about the price of a snack??
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

Powers CH 13, Fig. 13.9, pg 273
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

Powers CH 13, Fig. 13.10, pg 273
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

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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)

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Forces Acting on Bone

• Trabecular (spongy) bone
• Scaffolding arrangement
• Bone weight reduction
• Adaptive to multi-directional stress

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Bone Integrity

• Bone is adaptive material sensitive to disuse,
  immobilization, vigorous activity
• Wolffs Law change in bones internal
  architecture in response to loading
• Bone resorption osteoclasts
• Bone deposition - osteoblasts

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Physical Activity and Bone Remodeling

• Cyclic loading
• MES ( 1/10 force required to Fx bone)
• Increase in appositional (x-sectional) growth
• Wolffs Law
• SAID principle
• Sharpeys fibers (kinetic chain)

Catalyst wt bearing activity / structural lifts
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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

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Articular cartilage

• High water content
• Stiff but compressible shock absorption
• Lubricates joint surfaces via secretion of
  synovial fluid

Lacks its own blood supply Depends on diffusion
of O2 and nutrients from synovial fluid,
therefore, requires joint motion to remain viable
(heals poorly)
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Joint Degeneration

• Degenerative Joint Disease
• Avascular Necrosis

21
Muscular Adaptations
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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

Overload and Specificity??
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.

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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

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Hormonal Adaptations
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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)

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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