ORTHOPEDICS I Module No.

SPORTS MEDICINE 5
Dr. Jesse Noel Conjares 17 JAN 2018

LEGEND
Lecture Powerpoint, Audio, Handouts, Upper batch trans, Transer’s
note, Textbook

I. PARTS OF THE MUSCLE

1. Sarcomere
2. Myofilaments
3. Myofibril
4. Muscle Fiber
5. Muscle Fasciculus
II. PHYSIOLOGY AND BIOCHEMISTRY OF MUSCLE CONTRACTION
1. generation of nerve action potential
2. release of neurotransmitter
3. generation of muscle action potential
4. release of calcium ions and propagation
5. troponin-tropomyosin-actin changes
6. use of ATP
7. muscle contraction
8. return to resting state

I (light band)- actin

A (dark band)- actin+myosin
Z disc- attaches myofibrils to each other across muscle fiber

Transcribed by: Kathryn Bernabdon, Arwan Heussaff Checked by: Ange Encina Page 1 of 10
 ORTHOPEDICS I SPORTS MEDICINE Module 3, Lecture #5

Physio Throwback: MUSCLE CONTRACTION Glycogen-Lactate System

 As the duration of exercise progresses, the glycogen-lactate

system starts to be utilized. Lactate is produced as by-product
as glucose from glycogen is used in the absence of oxygen. It
predominates during intermediate duration and intensity
activities.
 Glucose produced by breaking down liver and muscle
glycogen
 Glycolysis breaks down glucose into pyruvic acid producing
ATP and NADH (net 2 ATP produced)
 In the mitochondria and the presence of oxygen, pyruvic
acid goes thru the krebs’ cycle and the electron transport
chain to produce more ATP (longer process) (34 ATP)
 Otherwise (in the cytosol and no oxygen), pyruvic acid is
reversibly converted to lactate to use up NADH (and produce
NAD+ needed for glycolysis to proceed)
 ATP produced in this manner is inefficient and is enough to
sustain contraction for a few minutes only
CORI cycle: Lactate exits the cell (e.g. muscle, rbc, brain,
gut) then later recovered by others (e.g. kidney, liver, heart),
and converted to pyruvic acid when oxygen present and
energy demand low for
o aerobic metabolism (krebs’ cycle),
o glucose production (gluconeogenesis) or
o glycogen storage depending on the body’s need
 Normal blood lactate is balanced at <2mmol/L
III. ATP  If energy demand high and oxygen still low, blood lactate
 ATP is needed for muscle contraction accumulates.
 ATP required to make the myosin “let go” of the actin by
effecting a decrease in affinity  Kapag walang oxygen hindi siya magtutuloy sa Kreb’s cycle
 ATP hydrolase activity at the myosin head “cocks up the  Pyruvate is converted to lactate to produce the NAD+ which is need
myosin head” making it ready for binding for glycolysis to push through.
 ATP needed by the calcium pump to remove calcium from the  Pag walang ginagawa walang heat or use of energy the demand for
sarcoplasmic reticulum ATP is low pyruvic acid undergoes aerobic metabolism glucose
 ATP needed by the Na-K pump to maintain the resting reduction and glycogen storage.
potential along the muscle cell membrane  Pag kailangan ng ATP at walang oxygen ang ginagawa nya ay
 ATP in muscle is enough for muscle contraction for 3 secs yung pyruvate-lactate system.
only.
 Sources of ATP
Dependent on type of exercise:
o Creatine phosphate
o Glycogen-lactic acid system
o Aerobic metabolism

SOURCES OF ATP
CREATINE PHOSPHATE SYSTEM

 This is the initial ATP source of muscle contraction. It

predominates during short duration high intensity activities
 High energy phosphate bond between creatine and a
phosphate radical produces 10,300 calories per mole
 Muscle cells contain up to 4x more creatine phosphate
than ATP
 Creatine phosphate reversibly combines with ADP to form
ATP
 Enough to sustain muscle contraction up to 8-10 sec (e.g.
• Glycolysis Produces: ADP, H+, Pi, water, NADH, ATP,
100m dash)
pyruvic acid
• Glycolysis Needs: Glucose, ATP, NAD+, Pi
• Lactate production Produces: Lactate, NAD+
• Lactate production Uses: NADH, H+

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 ORTHOPEDICS I SPORTS MEDICINE
IV. LACTATE AND MUSCLE SORENESS
 Maximum onset 1-3 days after exercise
 Post-exercise muscle soreness (PEMS) is experienced even
at low blood lactate levels.
 Serum levels of creatine phosphokinase (CPK), lactate
dehydrogenase (LDH) and myoglobin and urinary
hydroxyproline are increased in patients with PEMS.
 CPK, LDH are intracellular enzymes. Increased
blood levels indicate muscle damage.
 Urinary hydroxyproline indicates connective tissue
damage
 It is more of direct damage to the muscle fibers, mostly
microscopic, which causes the soreness.
 Before ang akala nila yung muscle soreness is because of LACTIC
ACID, but few recent studies showed that the cause of muscle
soreness is not because of accumulation of lactic acid.
 After 1-2 days of exercise you will experience muscle soreness you
called it POST EXERCISE MUSCLE SORENESS.
 And these people who experience muscle soreness lactic acid is
measured mababa siya.
 Meaning muscle soreness can be experience without the presence
of lactic acid in the blood.
 In PEMS there’s actual damage hindi man gross but microscopically
at the biochemical level.
 Intracellular enzymes escape from inside the cell to outside the cell.
 IT IS NOT actually the lactic acid but the destruction of your muscle
and connective tissue that causes the soreness after exercise.
V. LACTATE AND ACIDOSIS
 Byproduct of glycolysis is H+
 Increased anaerobic metabolism for energy production,
increases both lactate and H+
 If sustained, increases in H+ overwhelms buffer systems,
metabolic acidosis ensues. Inc lactate does not cause the
acidosis. It is the increase in H+
 Usually seen in diseased states where there is tissue
hypoperfusion, ischemia among others
 Inc lactate and blood ph, more of a sign than the cause of
symptoms
 Pag may metabolic acidosis after exercise is due to hypoperfusion
lack of oxygen sa tissue or predominance of anaerobic state.
VI. AEROBIC METABOLISM
 If exercise duration continues, energy production shifts into
the mitochondrion to a more efficient system utilizing oxygen.
 Pyruvic acid from glucose enters the krebs cycle-electron
transport chain system
 Fats and protein may likewise be utilized once glycogen
stores are used up (usually at about 1-2 hrs of cycling or
halfway thru a marathon
Transcribed By: Kathryn Bernabdon, Arwan Heussaff
Module 3, Lecture #5
VII. EXERCISE
A. EXERCISE
 The 3 separate systems work simultaneously during exercise
 Preference for 1 system dependent on exercise duration and
intensity
 Short duration, high intensity: creatine P, glucose, lactate
 Intermediate duration, mid to high intensity: anaerobic
metabolism
 Longer duration, lower intensity: aerobic metabolism
 There are three separate systems, that works during exercise.
 First is the Short Duration High Intensity (Creatine Phosphate)
 Second is the Intermediate Duration, Mid-High Intensity
(Anaerobic Metabolism)
 Third is the Lower Duration, High Intensity / Endurance (Aerobic
Metabolism)
B. RECOVERY AFTER EXERCISE
 After termination of exercise:
o Increased respiration, increases oxygen delivery to
tissues
o Lactate is removed and converted to glucose and
used or stored as glycogen via CORI cycle
o Muscle glycogen is replenished mainly via a high
carbohydrate diet and may take a few days
 High carbohydrate diet 3-5 days before marathon, to replenish
glycogen storage
 You do not exercise everyday, hindi pwede maipon ang exercise at
pahinga, because sa exercise there is muscle damage, no time to
heal, magkakaroon ng overuse syndrome, like tendinitis.
 Remember sa exercise there is tissue damage, hindi man gross but
it is micrscopically
C. TRAINING FOR ENDURANCE
 Refers to training to increase energy production from aerobic
metabolism (increase in oxidative capacity)
 Increases muscle ability to preferentially use fat over glucose
 Gradual and discontinuous regimen allowing rest days (light
training) between intense work-outs to permit physiologic
adaptations to occur
o Increased capillary blood flow to muscles
o Increased mitochondrial density
o Allows replenishment of glycogen stores
o Healing of muscle damage
 Trains you for aerobic metabolism
D. COMBINATION TRAINING
 Most of the time endurance training is combined with strength
training in a regular exercise regimen to achieve the benefits
of both types of exercise
 Endurance (distance) training- to improve aerobic capacity
and fat utilization, as well as faster recovery times from
intense exertion
 Speed training (sprints)- to acclimatize the body to
increases in lactate and develop its capacity for its removal
 This is the ideal, this long duration, low intensity exercises.
 You train your body to favor the aerobic metabolism
 Combine it with your low carbohydrate diet para yung fat ang
mautilize
E. TAPERING
 Allows the body to recover from training regimen and be
ready for competition
 Varies from sport-to-sport
 Muscle glycogen needs 2-3 days to reach max storage levels
 Adaptive increases in mitochondrial levels decay in 1-2 weeks
of lay-off
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 ORTHOPEDICS I SPORTS MEDICINE Module 3, Lecture #5

VIII. DIFFERENT MUSCLE FIBER TYPES Flexibility training

 Each muscle has a combination of fast and slow-twitch
muscle fibers. Specific muscles may have predominance of  Mainly composed of stretching exercises (both generic and sports-
one type over the other. specific) that aim to maximize joint range-of-motion reducing the
risk for muscle, tendon and ligament injury.
 SLOW (type I, aerobic, red)
o Used for prolonged muscle activity  Several types:
o Smaller fiber diameter o Active static stretching
o High capillary and mitochondrial density for aerobic  Static active stretching- using active muscle
metabolism contraction (agonist) to stretch its antagonist muscle and
o Higher myoglobin content for increased oxygen holding the stretch for 30 secs, develops active flexibility
capacity giving the red appearance o In taekwondo, holding the leg up so the foot is at
o Longer duration sports activity. Endurance activity the level of an opponent’s head and holding that
 FAST (type II, glycogen-dependent, white) position.
o Repeated kicking the foot up to the same level is
o Bursts of strong contractions of limited duration
dynamic stretching
o Larger diameter for greater contraction strength
o Have extensive sarcoplasmic reticula for rapid release of
calcium ions
o Contain more glycolytic enzymes
o Lower capillary and mitochondrial density
o Lower myoglobin content
o These are the target muscle fibers by sprinters, power
lifters. Short duration sports athletes.
F. TYPES OF EXERCISE

Strength Training

 Stressing a muscle with progressive resistance such that

only a few reps are possible before failure
 High intensity exercises lasting less than a minute
 Dependent on the anaerobic pathway (Creatine Phosphate
and glycogen systems) o Passive static stretching
 Strength of contraction largely dependent on muscle size  Static passive stretching- limb is stretched slowly and held at an
 Power determined by strength, distance it contracts and no. end position by using an external force (chair or a trainer) for about
of times it contracts per min 30 secs, no active muscle contraction
o At normal resting length, maximal overlap between  Best at increasing joint range of motion over time for
contractile proteins. In a contracted or stretched athletes away from competition
state, contraction weakens  Traditionally, included in warm-ups prior to competition
o Power is highest in the 1st few secs then halves by  Recent evidence shows if done immediately before
the 1st minute and tapers by 30 min exercise detrimental to power, balance, reaction time
 Results in
o Muscle hypertrophy (inc in size and number of
muscle fibers esp type II) and increased number of
available fibers for contraction
o Improved motor unit recruitment and increased
number of active fibers contracting (from 60% to
90%)
o A 60-80% increase in components of the creatine Dynamic stretching- uses speed and active muscle contraction to
phosphate system stretch, includes exaggerated movements which may be sports-specific,
o A 50% increase in stored glycogen reduces muscle tightness, increases blood flow to muscles
o A 50-100% increase in stored triglycerides o Walking lunges, exaggerated kicking, exaggerated
 Atrophy is quick to set in once resistance is removed. arm circumduction
Endurance Training o Recommended before actual competition as part of
 Stressing muscle with lower resistance and higher number of warm-up
repetitions before failure
 Increasing the ability to utilize oxidative processes for energy
production
 Includes improvement of the respiratory and cardiovascular
system to increase oxygen delivery
 Increases capillary and mitochondrial density of muscles
 If duration is sustained, fats are utilized as energy sources
 A gradual and discontinuous endurance training regimen
which allows rest days (light training) between intense work-
outs is important to permit physiologic adaptations to occur
like:
o Increased capillary blood flow to muscles Other definitions:
o Increased mitochondrial density
 Isotonic- muscle shortening against a constant load Lifting 10lbs
o Allowing time for replenishment of glycogen stores
o Healing of muscle damage (which causes muscle dumbbell-biceps
soreness)  Isometric- muscle contraction without shortening
 Regular endurance training results in  Isokinetic- muscle contraction maintained at the same speed by
1. Increases in the ability to utilize aerobic processes for adjusting the load Increase the load but same repetition and
energy production. timeframe
2. In improvement of the respiratory and cardiovascular
 Concentric- muscle contraction with shortening Normal muscle
system to increase oxygen delivery.
3. Increases in the capillary and mitochondrial density of activity, origin and insertion come close together
muscles.  Eccentric- muscle contraction with lengthening elbow flexion-when
4. Fats being utilized as energy sources, if duration is you shorten your biceps your triceps also contracts (it lengthens) to
sustained. prevent sudden movement

 Endurance training is a fat burning exercise

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 ORTHOPEDICS I SPORTS MEDICINE Module 3, Lecture #5

Performance-enhancing drugs IX. COMMON SPORTS INJURIES

Substances used by athletes to improve performance in sports
(ergogenic aids) pwedeng bawal, pwedeng hindi  Head and spine injuries
Several groups of substances:
 Rotator cuff disease
Drugs that increase muscle mass
 Tennis elbow
1. Testosterone and its analogues (anabolic steroids)
 ACL tears
2. Beta 2 agonists
 Stress fractures
3. Human growth hormone
 Heat injuries
A. MUSCLE INJURIES

Muscle strain

 Anatomic disruption usually at the

musculotendinous junction from an excessive
tensile force
 Results from a significant eccentric contraction
 Common in 2-joint muscles of the lower extremity
(hamstrings, rectus femoris, gastrocnemius)
because of a longer musculotendinous junction
 3 phases of healing: inflammatory, protein
synthesis, maturation

 Damage to the muscle fibers

 Muscles are damage by pulling apart of the muscle fibers
 Can be microscopic
 Can be grossly, napunit na talaga

Contusion

 Blunt injury to the muscle with hematoma formation

 If severe, bone may deposit in the hematoma
(myositis ossificans)
 Resting the muscle in its normal length prevents
shortening, stiffness which delays recovery
 Direct blow to the muscle

Laceration

 Results from penetrating trauma

 Myoblasts from surrounding area form new muscle
cells and fibers
See Appendix for bigger picture  If gap is big, connective tissue proliferates and may
 Stimulants - increase alertness and decrease fatigue interfere with muscle function later
1. Caffeine  There is penetrating trauma with a sharp object
2. Amphetamines
 Diuretics - cause water loss for immediate weight-loss (in Atrophy
sports with weight classes)
 Beta-blockers - block adrenergic effects of stress like anxiety  Loss of muscle mass with a decrease in size of
and tremors (e.g. shooting, archery) fibers
 Usually results from immobilization
 Analgesics - increase pain threshold
 Joint should be immobilized with muscles in slight
 Sedatives, alcohol, marijuana - anxiolytic and reduces
tension to minimize atrophy
tremors
 Erythropoietin and blood doping - increases aerobic
capacity B. TENDON INJURIES
 Masking drugs - substances with no performance-enhancing
Acute onset
effect but masks the presence of other drugs like
epitestosterone, diuretics like ethacrynic acid, and probenecid  Lacerations, contusions, tears, avulsions
 Very common is the blunt trauma Achilles Tendon Rupture,
 Tears are common sa weekend warriors, yung hindi nagttraining
Supplements
biglang naglaro
 These are substances taken in addition to food.
 Some have actual benefits especially in medical and surgical  Avulsions, trauma from sudden explosive movements, like crossfit
conditions where there is impairment in the absorption of
nutrition. Longer onset
 Examples include may be due to systemic disorders also
o branched chain amino acids (BCAA) o Tendonitis - overuse syndrome with injury to collagen fibrils,
o chondroitin and glucosamine sulfate tendon matrix and microvasculature, with pain and inflammation
o creatine
o Results from the inability of the reparative process to
o glutamine
o hydroxymethyl butyrate (HMB) balance the microtrauma from repetitive activity
o De quervain’s tenosynovitis, trigger finger
See o Histologic appearance: angiofibroblastic hyperplasia
Appendix o Tendinosis - a more chronic degeneration of the tendon
for bigger substance without histologic or clinical signs of inflammation
picture o Central necrosis with mucoid degeneration with
proliferation of fibroblasts, new capillaries, decrease in
no. and a more disorganized orientation of collagen
fibrils
o May be painless but puts the tendon at risk of failure
o Example: rotator cuff disease (tendonitis-tendinosis
cycle), tennis elbow

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 ORTHOPEDICS I SPORTS MEDICINE
 Kapag ang inflammation ay long standing na, nagkakaroon ng
calcification/calcium deposition, the tendon will become
heterogenous, magiging weak na siya, dun sa site na weak yung
napuputol.
 Management
 Rest – pain goes away at rest
 Anti-inflammatory medications
 Steroids
C. ROTATOR CUFF DISEASE
 The Rotator cuff (your SSIT muscles) covers the superior surface
of the humeral head. Supraspinatus, Subscapularis,
Infraspinatus and Teres Minor. When it pulls, the head goes into
the socket.
 You can rehabilitate the shoulder to increase stability. You
strengthen the rotator cuff but of course only up to a certain extent.
You cannot rehab ligaments. Ligaments kapag napunit, hihintayin
mo lang mag-heal.
 Rotator Cuff Disease, may acute onset and may chronic. Both
manifest pain and impaired tears in the rotator cuff. Most commonly
impaired is the SUPRASPINATUS muscle. What does it do? It
abducts (first 15 degrees of abduction). All of these will cause
limitation of motion. Painful on ABDUCTION of the shoulder
 FROZEN SHOULDER – a description of the condition of the
shoulder na ‘hindi mo magalaw’… frozen. May be due to several
case. Pwedeng may rupture, inflammation, tear etc.
 Long standing inflammation will cause calcium deposit-radio
opaque
 Usual diagnosis on x-ray- Calcific tendonitis
 Treatment: REST- mainstay on particular tendon, ANTI-
INFLAMMATORY MEDICATION, STERIODS
D. TENNIS ELBOW
 Lateral epicondylitis
o Overuse of wrist extensors usually seen in racket
sports and throwing, use of wrist swinging tools,
sweeping
o Pain and/or tenderness on the lateral elbow esp on
resisted wrist extension (Cozen’s test)
 Problem dito is overuse and inflammation
 Management
 Rest – what I do is casting, above elbow, kasi you have to
remove the use
 Medicine – bigyan mo ng steroids
Transcribed By: Kathryn Bernabdon, Arwan Heussaff
Module 3, Lecture #5
E. GOLFER’S ELBOW
 Medial epicondylitis
o Overuse syndrome
o Pain and/or tenderness over the medial elbow esp on
resisted wrist flexion
o Flexor-pronator group stabilize the elbow vs. valgus
stress
 Management
 Rest – pain goes away at rest
 Anti-inflammatory medications
 Steroids
 Apply heat or cold? Answer: There’s no rule. Basta kung ano
yung nagbebenefit sa patient. Huwag niyo lang ipapahilot.
F. LIGAMENT INJURY
 Sprains account to up to 45% of all musculoskeletal injuries.
 Ligaments are static joint stabilizers while allowing joint
motion together with muscle, tendon, bone and cartilage.
 Injury to one without adequate healing may cause
degeneration in the other stabilizers resulting in arthroses.
 Intrasubstance tears of extra-articular ligaments heal better
than intra-articular ligaments.
 3 phases of healing: inflammatory, repair (within 3 days up to
several weeks), remodelling (after several weeks up to
several months)
 Minimally vascular, may contain nerve endings for pain and
proprioception.
 Short term immobilization for pain control followed by early
mobilization optimizes recovery. Others require
reconstruction.
 Examples: distal radio-ulnar joint, wrist, ankle sprains, ACL,
MCL
 You need to rest it. If its severe you can repair
 There are ligament injuries na cannot be repaired kaya
reconstruction na
 No excercises to strengthen ligaments.
 Management
 Short term immobilization
ACL INJURY
 Indirect injury from a non-contact pivoting motion common
in high demand sport as soccer, basketball and football
 More than half associated with injuries to articular cartilage,
meniscus, collateral ligaments – unhappy triad, ACL, MCL
tyaka medial meniscus tear
 Higher incidence in females: smaller ligaments, increased
general ligament laxity, increased knee laxity, increased
valgus knee loading when landing
 History of a popping sound followed by pain, swelling,
limitation of motion, joint line tenderness and limp
 X-rays needed asap to rule out fractures
 Diagnosis can be mainly from clinical and functional
evaluation, more conclusive after a few days when pain and
swelling subside
 Lachman test is the most sensitive
 MRI not needed for a diagnosis
 Treatment dependent on patient’s needs. E.g. Young active
patients will require reconstruction to return to sports.
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 ORTHOPEDICS I SPORTS MEDICINE Module 3, Lecture #5

 Reconstruction using grafts to serve as tissue scaffolds on

which new ligament tissue have been shown to fully replace
by 9 mos

 Do physical exam once the pain and swelling subsided

 ACL ay hindi narerepair, always reconstuction, maghaharvest ka
from other parts of the body or you can use allograft.

G. HEAD INJURY

 Concussion (old term) or traumatic brain injury (new term) is

the most common sports head injury.
 3 grades: I mild, II moderate, III severe
o Has specific criteria* and guidelines for return to
play
o *Mild: no loss of consciousness, transient
confusion, symptoms resolve in 15min
o Moderate: no loss of consciousness, transient
confusion, symptoms last >15min
o Severe: any loss of consciousness
 Examples of post-concussion symptoms, depression,
dizziness, sleep, fatigue, headache, personality changes,
disorientation, nausea, nervousness, numbness, poor
balance, poor concentration, ringing in the ears, seeing stars,
sensitive to noise and light, vomiting, having a blank stare,
emotionally labile when questioned repeatedly
 Head injury return to play guidelines

i. Medial Tibial Stress Syndrome

 A lesser entity but in the same family as stress fractures of

the lower extremity
 Also known as “shin splints”
 Has similar causes as stress fractures of the tibia- “doing too
much, too soon”
 Caused by tears in the proximal attachment to bone of the big
muscles of the leg (e.g. gastroc-soleus complex)
 Athlete experiences intense pain at the area of tear
 Managed with rest, pain relief modalities, activity and
equipment modification
See appendix for bigger picture
H.. STRESS FRACTURES

 Fractures resulting from inability of bone to remodel after

excessive repetitive loading without rest stimulating
osteoclastic activity > osteoblastic activity.
After a history of an increase in training duration and intensity over a
short period of time. (e.g. from training team to varsity, from high school
to college level)
 >90% occur in the lower extremity
 Running is the most common activity leading to a stress
fracture.
 Poor footwear and training surface play a role. (e.g. athletic
shoes > 6 months, concrete vs grass)

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 ORTHOPEDICS I SPORTS MEDICINE Module 3, Lecture #5

J. Heat Related Injuries  Significant declines in aerobic fitness after 2 weeks of no

 Heat cramps- painful muscle spasms after vigorous exercise
in extreme heat
o symptoms: flushed, moist skin, mild fever
 Heat exhaustion- results from excessive water and salt loss
from sweating and inadequate hydration
o symptoms: muscle cramps, pale, moist skin,
usually has a fever over 39º C, nausea, vomiting,
diarrhea, headache, fatigue, weakness, anxiety,
and dizziness
 Heat stroke- when the body’s thermoregulating system has
been overwhelmed by excessive heat
o symptoms: warm, dry skin, high fever, usually over
40º C, rapid heart rate, loss of appetite, nausea,
vomiting, headache, fatigue, confusion, agitation,
lethargy, stupor, seizures, coma, and death
o Treatment:
o Removal to a cool place
o Adequate replacement of water and
electrolytes
o Try to cool patient with ice under armpits
and groin, removal of excessive clothing,
drenching of skin with water
training have been observed.
 max heart rate (age-related formula): 220-age
 Online search: HRmax = 205.8 − (0.685 × age) +/- 6 bpm
 The most common cause of sudden cardiac death in young
athletes is hypertrophic cardiomyopathy.
 Increase glycogen stores prior to competition by decreasing
activity and loading with carbohydrates x 2-3 days prior.
 Weight reduction by fluid and food restriction is not
recommended.
REFERENCES
Lecture notes
Powerpoint presentation
Handouts
Upper batch trans 2017-2018

X. THE FEMALE ATHLETE

 Anatomic differences VS Males:
 Shorter in stature and lower body mass
 Narrower shoulders and shorter humerii (less
powerful throws)
 Shorter femora (more stable with a lower center of
gravity)
 Wider pelvis and greater genu valga (larger Q angle,
pull of quadriceps on patella more angular, unequal
loading across the patello-femoral joint)
 Lower bone density (osteoporosis)
 More body fat (more buoyant in water sports)
 More lax ligaments (more prone to joint instability,
subluxations and dislocations)
 Smaller thoracic cage (lower vital capacity, smaller
tidal volumes, increased respiratory rates)
 Smaller heart (30% less cardiac output)
 Problem triad (1992): amenorrhea, osteoporosis, anorexia
o Diagnosis of one component should lead to ruling out
the other
o Anorexia develops as loss of body fat and weight loss is
seen to enhance performance and appearance
o Energy expenditure exceeds energy intake leading to
energy depletion and alteration of the hypothalamus-
pituitary-ovarian system causing menstrual irregularity
o Estrogen lack leads to bone demineralization and
secondary osteoporosis
o Treatment geared at maintaining proper nutrition and
altering training to fit the athlete.
o Pharmacologic intervention is done to supplement
recovery of menses and preserve bone mass.
o Education and support systems are also strengthened.

XI. ATHLETES AND TRAINING

 Each muscle has both fast and slow twitch fibers. Distribution
of fast and slow twitch fibers are genetically determined.
 Training can selectively improve the fibers. Endurance
athletes have a higher percentage of slow twitch fibers.
Strength athletes have more fast twitch fibers.
 Endurance training: decreased loads, more repetitions
 inc efficiency of slow twitch fibers
 Inc mitochondrial and capillary density
 Inc oxidative capacity
 Strength training: increasing loads, less reps
o Inc number and cross-sectional area of fast twitch fibers
(hypertrophy)
 Aerobic training for healthy adults at least 3x a week for 20-
60min at 60-90% of max heart rate* lowers incidence of back
injury.
 Target training heart rate (for safety): 50-75% of max heart
rate

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 ORTHOPEDICS I Module No. 3

SPORTS MEDICINE 5
Dr. Jesse Noel Conjares 17 JAN 2018
Appendix

Transcribed by: Kathryn Bernabdon, Arwan Heussaff Checked by: Ange Encina Page 9 of 10
 ORTHOPEDICS I SPORTS MEDICINE Module 3, Lecture #5

Transcribed By: Kathryn Bernabdon, Arwan Heussaff Checked by: Ange Encina Page 10 of 10