Chapter 10: Tissue Response to Injury

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Chapter 10Tissue Response to Injury
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Inflammatory Response

• Acute Inflammation
• Short onset and duration
• Change in hemodynamics, production of exudate,
  granular leukocytes
• Chronic Inflammation
• Long onset and duration
• Presence of non-granular leukocytes and extensive
  scar tissue

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Cardinal Signs of Inflammation

• Rubor (redness)
• Tumor (swelling)
• Color (heat)
• Dolor (pain)
• Functio laesa (loss of function)

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Phases of the Inflammatory Response

• (3 separate phases)
• 1. Acute phase
• 2. Repair phase
• 3. Remodeling phase

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Phase I Acute Phase

• Initial reaction to an injury occurring 3 hours
  to 4 days following injury
• Goal
• Protect
• Localize
• Decrease injurious agents
• Prepare for healing and repair
• Caused by trauma, chemical agents, thermal
  extremes, pathogenic organisms

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• External and internal injury result in tissue
  death and cell death
• Decreased oxygen to area increases cell death
• Phagocytosis will add to cell death due to excess
  digestive enzymes
• Rest, ice, compression elevation are critical
  to limiting cell death

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• First hour
• Vasoconstriction and coagulation occur to seal
  blood vessels and chemical mediators are released
• Immediately followed by vasodilation or blood
  vessel
• Second hour
• Vasodilation decreases blood flow, increased
  blood viscosity resulting in edema (swelling)

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• Second hour (continued)
• Exudate increases (high concentration of RBCs)
  due to increased vessel permeability
• Permeability changes generally occur in capillary
  and venules
• Margination occurs causing leukocytes to fill the
  area and line endothelial walls
• Through diapedesis and chemotaxis leukocytes move
  to injured area

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• Cellular response
• Mast cells (connective tissue cells) and
  leukocytes (basophils, monocytes, neutrophils)
  enter area
• Mast cells with heparin and histamine serve as
  first line of defense
• Basophils provide anticoagulant
• Neutrophils and monocytes are responsible for
  small and large particles undergoing phagocytosis
  - ingestion of debris and bacteria

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• Cellular mediation
• Histamine provided by platelets, mast cells and
  basophils to enhance permeability and arterial
  dilation
• Serotonin provides for vasoconstriction
• Bradykinin is a plasma protease that enhance
  permeability and causes pain.
• Heparin is provided by mast cells and basophils
  to prevent coagulation
• Leukotrienes and prostaglandins are located in
  cell membranes and develop through the
  arachadonic acid cascade
• Leukotrienes alter permeability
• Prostaglandin add and inhibit inflammation

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• Complimentary systems
• Enzymatic proteins that destroy bacteria and
  other cells through their impact on cell lysis
• Bleeding and exudate
• Amount dependent on damage
• Initial stage thromboplastin is formed
• Second stage Prothrombin is converted to
  thrombin due to interaction with thromboplastin
• Third stage thrombin changes from soluble
  fibrinogen to insoluble fibrin coagulating into a
  network localizing the injury

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Phase II Repair Phase

• Phase will extent from 48 hours to 6 weeks
  following cleaning of fibrin clot, erythrocytes,
  and debris
• Repaired through 3 phases
• Resolution (little tissue damage and normal
  restoration)
• Restoration (if resolution is delayed)
• Regeneration (replacement of tissue by same
  tissue)

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• Scar formation
• Less viable than normal tissue, may compromise
  healing
• Firm, inelastic mass devoid of capillary
  circulation
• Develops from exudate with high protein and
  debris levels resulting in granulation tissue
• Invaded by fibroblasts and and collagen forming a
  dense scar and while normally requiring 3-14
  weeks may require 6 months to contract

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• Primary healing (healing by first intention)
• Closely approximated edges with little
  granulation tissue production
• Secondary healing (heal by secondary intention)
• Gapping, tissue loss, and development of
  extensive granulation tissue
• Common in external lacerations and internal
  musculoskeletal injuries

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• Regeneration
• Related to health, nutrition and tissue type
• Dependent on levels of
• debris (phagocytosis)
• endothelial production (hypoxia and macrophages
  stimulate capillary buds)
• production of fibroblasts (revascularization
  allows for enhanced fibroblast activity and
  collagen production which is tied to Vitamin C,
  lactic acid, and oxygen

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Phase III Remodeling

• Overlaps repair and regeneration
• First 3-6 weeks involves laying down of collagen
  and strengthening of fibers
• 3 months to 2 years allowed for enhanced scar
  tissue strength
• Balance must be maintained between synthesis and
  lysis
• Take into consideration forces applied and
  immobilization/mobilization time frames relative
  to tissue and healing time

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Chronic Inflammation

• Result of failed acute inflammation resolution
  within one month termed subacute inflammation
• Inflammation lasting months/years termed chronic
• Results from repeated microtrauma and overuse
• Proliferation of connective tissue and tissue
  degeneration

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Characteristics of Chronic Inflammation

• Proliferation of connective tissue and tissue
  degeneration
• Presence of lymphocytes, plasma cell,
  macrophages(monocytes) in contrast to neutrophils
  (during acute conditions)
• Major chemicals include
• Kinins (bradykinin) - responsible for
  vasodilation, permeability and pain
• Prostaglandin - responsible for vasodilation but
  can be inhibited with aspirin and NSAIDs

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Factors That Impede Healing

• Extent of injury
• Edema
• Hemorrhage
• Poor Vascular Supply
• Separation of Tissue
• Muscle Spasm
• Atrophy

• Corticosteroids
• Keloids and Hypertrophic Scars
• Infection
• Humidity, Climate, Oxygen Tension
• Health, Age, and Nutrition

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Soft Tissue Healing

• Cell structure/function
• All organisms composed of cells
• Properties of soft tissue derived from structure
  and function of cells
• Cells consist of nucleus surrounded by cytoplasm
  and encapsulated by phospholipid cell membrane
• Nucleus contains chromosomes (DNA)
• Functional elements of cells (organelles) include
  mitochondria, ribosomes, endoplasmic reticulum,
  Golgi apparatus centrioles

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Tissues of the Body

• Bone - not classified as soft tissue
• 4 types of soft tissue
• Epithelial tissue
• Skin, vessel organ linings
• Connective tissue
• Tendons, ligaments, cartilage, fat, blood, and
  bone
• Muscle tissue
• Skeletal, smooth, cardiac muscle
• Nerve tissue
• Brain, spinal cord nerves

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Soft Tissue Adaptations

• Metaplasia - transformation of tissue from one
  type to another that is not normal for
  that tissue
• Dysplasia - abnormal development of tissue
• Hyperplasia- excessive proliferation of normal
  cells in normal tissue arrangement
• Atrophy- a decrease in the size of tissue due to
  cell death and re-absorption or
  decreased cell proliferation
• Hypertrophy - an increase in the size of tissue
  without necessarily changing the number
  of cells

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Cartilage Healing

• Limited capacity to heal
• Little or no direct blood supply
• Chrondrocyte and matrix disruption result in
  variable healing
• Articular cartilage that fails to clot and has no
  perichondrium heals very slowly
• If area involves subchondral bone (enhanced blood
  supply) granulation tissue is present and healing
  proceeds normally

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Ligament Healing

• Follows similar healing course as vascular tissue
• Proper care will result in acute, repair, and
  remodeling phases in same time required by other
  vascular tissue
• Repair phase will involve random laying down of
  collagen which, as scar forms, will mature and
  realign in reaction to joint stresses and strain
• Full healing may require 12 months

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Skeletal Muscle Healing

• Skeletal muscle cannot undergo mitotic activity
  to replace injured cells
• New myofibril regeneration is minimal
• Healing and repair follow the same course as
  other soft tissues developing tensile strength
  (Wolffs Law)

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Nerve Healing

• Cannot regenerate after injury
• Regeneration can take place within a nerve fiber
• Proximity of injury to nerve cell makes
  regeneration more difficult
• For regeneration, optimal environment is required
• Rate of healing occurs at 3-4 mm per day
• Injured central nervous system nerves do not heal
  as well as peripheral nerves

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Modifying Soft-Tissue Healing

• Varying issues exist for all soft tissues
  relative to healing (cartilage, muscle, nerves)
• Blood supply and nutrients is necessary for all
  healing
• Healing in older athletes or those with poor
  diets may take longer
• Certain organic disorders (blood conditions) may
  slow or inhibit the healing process

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Management Concepts

• Drug utilization
• Anitprostaglandin agents used to combat
  inflammation
• Non-steroidal anti-inflammatory agents (NSAIDs)
• Medications will work to decrease vasodilatation
  and capillary permeability

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• Therapeutic Modalities
• Thermal agents are utilized
• Heat stimulates acute inflammation (but works as
  a depressant in chronic conditions)
• Cold is utilized as an inhibitor
• Electrical modalities
• Treatment of inflammation
• Ultrasound, microwave, electrical stimulation
  (includes transcutaneous electrical muscle
  stimulation and electrical muscle stimulation

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• Therapeutic Exercise
• Major aim involves pain free movement, full
  strength power, and full extensibility of
  associated muscles
• Immobilization, while sometimes necessary, can
  have a negative impact on an injury
• Adverse biochemical changes can occur in collagen
• Early mobilization (that is controlled) may
  enhance healing

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Fracture Healing

• Potential serious bone fractures are part of
  athletics
• Time is necessary for proper bone union to occur
  and is often out of the control of a physician
• Conservative treatment will be necessary for
  adequate healing to occur

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• Bone undergoes constant remodeling through
  osteocyte activity
• Osteocytes cellular component of bone
• Osteoblasts are responsible for bone formation
  while osteoclasts resorb bone
• Cambium (periosteum)
• A fibrous covering involved in bone healing
• Vascular and very dense
• Inner cambium
• less vascular and more cellular.
• Provides attachments for muscle, ligaments and
  tendons

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Acute Fracture of Bone

• Follows same three phases of soft tissue healing
• Less complex process
• Acute fractures have 5 stages
• Hematoma formation
• Cellular proliferation
• Callus formation
• Ossification
• Remodeling

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Hematoma Formation

• Trauma to the periosteum and surrounding soft
  tissue occurs due to the initial bone trauma
• During the first 48 hours a hematoma within the
  medullary cavity and the surrounding tissue
  develops
• Blood supply is disrupted by clotting vessels and
  cellular debris
• Dead bone results in an inflammatory response
  (vasodilation, exudate cell migration)

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Cellular Formation

• Granulation forms constructing fibrous union
  between fractured ends
• Capillary buds allow endosteal cells influx from
  cambium layer
• Cells evolve from fibrous callus to cartilage, to
  woven bone
• High oxygen tension fibrous tissue
• Low oxygen tension cartilage tissue
• Bone growth will occur with optimal oxygen
  tension and compression

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Callus Formation

• Soft callus is a random network of woven bone
• Osteoblasts fill the internal and external
  calluses to immobilize the site
• Calluses are formed by bone fragments that bridge
  the fracture gap
• The internal callus creates a rigid
  immobilization early

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• Hard callus formation occurs after 3-4 weeks and
  lasts 3-4 months
• Hard callus is a gradual connection of bone
  filaments to the woven bone
• Less than ideal immobilization produces a
  cartilagenous union instead of a bony union

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Ossification

• Adequate immobilization and compression will
  result in new Haversian systems developing
• Haversian canals allow for the laying down of
  primary bone
• Ossification is complete when bone has been laid
  down and the excess callus has been resorbed by
  osteoclasts.

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Remodeling

• Occurs following callus resorption and trabecular
  bone is laid along lines of stress
• Bioelectric stimulation plays a major role in
  completing the remodeling process
• Osteoblasts are attracted to the electronegative
  (concave/compression) side
• Osteoclasts are attracted to the electropositive
  (convex/tension) side
• The process is complete when the original shape
  is achieved or the structure can withstand
  imposed stresses

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Acute Fracture Management

• Must be appropriately immobilized, until X-rays
  reveal the presence of a hard callus
• Fractures can limit participation for weeks or
  months
• A clinician must be certain that the following
  areas do not interfere with healing
• Poor blood supply
• Poor immobilization
• Infection

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• Poor blood supply
• Bone may die and union/healing will not occur
  (avascular necrosis)
• Common sites include
• Head of femur, navicular of the wrist, talus, and
  isolated bone fragments
• Relatively rare in healthy, young athletes except
  in navicular of the wrist
• Poor immobilization
• Result of poor casting allowing for motion
  between bone parts
• May prevent proper union or result in bony
  deformity

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• Infection
• May interfere with normal healing, particularly
  with compound fractures
• Severe streptococcal and staphylococcal
  infections
• Modern antibiotics has reduced the risk of
  infections
• Closed fractures are not immune to infections
  within the body or blood
• If soft tissue alters bone positioning, surgery
  may be required to ensure proper union

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Healing of Stress Fractures

• Result of cyclic forces, axial compression or
  tension from muscle pulling
• Electrical potential of bone changes relative to
  stress (compression, tension, or torsional)
• Constant stress axially or through muscle
  activity can impact bone resorption, leading to
  microfracture

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• If osteoclastic activity is not in balance with
  oesteoblastic activity bone becomes more
  susceptible to fractures
• To treat stress fractures a balance between
  osteoblast and osteoclast activity must be
  restored
• Early recognition is necessary to prevent
  complete cortical fractures
• Decreased activity and elimination of factors
  causing excess stress will be necessary to allow
  for appropriate bone remodeling

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Pain

• Major indicator of injury
• Pain is individual and subjective
• Factors involved in pain
• Anatomical structures
• Physiological reactions
• Psychological, social, cultural and cognitive
  factors

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Nociception

• Pain receptors -free nerve endings sensitive to
  extreme mechanical, thermal and chemical energy
• Located in meninges, periosteum, skin, teeth, and
  some organs
• Pain information transmitted to spinal cord via
  myelinated C fibers and A delta fibers
• Nociceptor stimulation results in release of
  substance P

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• Signal travels along afferent nerves to the
  spinal cord
• A delta fiber (fast) transmit information to the
  thalamus concerning location of pain and
  perception of pain being sharp, bright or
  stabbing
• C fibers (slower conduction velocity) deal with
  diffused, dull, aching and unpleasant pain
• C fibers signal also passed to limbic cortex
  providing emotional component to pain
• Nociceptive stimuli is at or close to an
  intensity which would result in tissue injury

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Endogenous Analgesics

• Nervous system is electrochemical in nature
• Chemicals called neurotransmitters are released
  by presynaptic cell
• Two types mediate pain
• Endorphins
• Seretonin
• Neurotransmitters release stimulated by noxious
  stimuli- resulting in activation of pain
  inhibition transmission

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• Stimulation of periaqueductal gray matter (PGA)
  and raphe nucleus of pons and medulla cause
  analgesia
• Analgesia is the result of opioids release
• Morphine like substance manufactured in the PGA
  and CNS
• Endorphins and enkephalins
• Other pain modulators
• Norepinephrine (noradrenergic
• Seretonin also will serve as neuromodulator

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Pain Categories

• Pain sources
• Fast versus slow pain
• Acute versus chronic
• Projected or referred pain

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• Pain sources
• Cutaneous, deep somatic, visceral and psychogenic
• Cutaneous pain is sharp, bright and burning with
  fast and slow onset
• Deep somatic pain originates in tendons, muscles,
  joints, periosteum and blood vessels
• Visceral pain begins in organs and is diffused at
  first and may become localized
• Psychogenic pain is felt by the individual but is
  emotional rather than physical

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• Fast versus Slow Pain
• Fast pain localized and carried through A-delta
  axons
• Slow pain is perceived as aching, throbbing, or
  burning (transmitted through C fibers)
• Acute versus Chronic Pain
• Acute pain is less than six months in duration
• Chronic pain last longer than six months
• Chronic pain classified by IASP as pain
  continuing beyond normal healing time

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• Projected (Referred) Pain
• Pain which occurs away from actual site of
  injury/irritation
• Unique to each individual and case
• May elicit motor and/or sensory response
• A-alpha fibers are sensitive to pressure and can
  produce paresthesia
• Three types of referred pain include myofascial,
  sclerotomic, and dermatomic

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• Myofascial Pain
• Trigger points or small hyperirritable areas
  within muscle resulting in bombardment of CNS
• Acute and chronic pain can be associated with
  myofascial points
• Often described as fibrositis, myositis, myalgia,
  myofasciitis and muscular strain
• Two types of trigger points (active and latent)
• Active points cause obvious complaint
• Latent points are dormant potentially causing
  loss of ROM

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• Trigger points do not follow patterns
• Trigger point area referred to as reference zone
  which may or may not be proximal to the point of
  irritation
• Sclerotomic and dermatomic pain
• Deep pain with slow or fast characteristics
• May originate from sclerotomic, myotomic or
  dermatomic nerve irritation/injury
• Sclerotomic pain transmitted by C fibers causing
  deep aching and poorly localized pain
• Can be projected to multiple areas of brain
  causing depression, anxiety, fear or anger

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• Autonomic changes result (vasomotor control, BP
  and sweating
• Dermatomic pain (irritation of A-delta fibers) is
  sharp and localized
• Projects to the thalamus and cortex directly

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• Gate Theory
• Area in dorsal horn of spinal cord causes
  inhibition of pain impulses ascending to cortex
• T-cells will transmit signals to brain
• Substantia gelatinosa functions as gate
  determining if stimulus sent to T-cells
• Pain stimuli exceeding threshold results in pain
  perception
• Stimulation of large fast nerves can block signal
  of small pain fiber input
• Rationale for TENS, accupressure/puncture,
  thermal agents and chemical skin irritants

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Central Biasing Theory
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Release of B-Endorphins
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Variation of Pain Sensitivity

• Hyperesthesia, paresthia or analgesia
• Pain modulation
• Mixture of physical and psychological factors
• Pain management is a challenge to treat
• Generally acute pain management in athletic
  training setting

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• Pain assessment
• Self report is the best reflection of pain and
  discomfort
• Assessment techniques include
• visual analog scales (0-10, marked no pain to
  severe pain)
• verbal descriptor scales (marked none, slight,
  moderate, and severe)
• Pain Treatment
• Must break pain-spasm-hypoxia-pain cycle through
  treatment
• Agents used heat/cold, electrical
  stimulation-induced analgesia, pharmacological
  agents

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• Heat/Cold
• Heat increases circulation, blood vessel
  dilation, reduces nociception and ischemia caused
  by muscle spasm
• Cold applied for vasoconstriction and prevention
  of extravasation of blood into tissue
• Pain reduced through decrease in swelling and
  spasm
• Induced analgesia
• Utilize electrical modalities to reduce pain
• TENS and acupuncture commonly used to target Gate
  Theory

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• Pharmacological Agents
• Oral, injectable medications
• Commonly analgesics and anti-inflammatory agents

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Psychological Aspects of Pain

• Pain can be subjective and psychological
• Pain thresholds vary per individual
• Pain is often worse at night due to solitude and
  absence of external distractions
• Personality differences can also have an impact
• A number of theories relative to pain exist and
  it physiological and psychological components
• Athlete, through conditioning are often able to
  endure pain and block sensations of minor injuries