The Female Athlete

Report
Antoin Alexander
Maj USAF MC
Adapted from Dr. Terry Adirim
Overview
 General Differences
 Injury Patterns
 Menstrual Cycle
 Female Athlete Triad
General Differences
Females
Males
Prepubertal Capabilities
Equal
Equal
Growth Spurt
11
13
Maximum Height
16-17
20-21
Weight Difference
Minus 11-14 kg
 Bone and muscle
mass
Body Fat
26%
14%
Body Shape
Wide Hips
Wide Shoulders
Limbs
Shorter
Longer
Strength
Equal relative to lean mass
Muscle Hypertrophy
 Due to testosterone
General Differences
Females
Males
Upper Extremity Strength
40-75% of men
Lower Extremity Strength
60-80% of men
Average VO2 Max
Minus 40%
VO2 Max vs Lean Body wt
Minus 10%
Cardiac
 Size and output
 Heart rates
Pulm
 Thoracic cage
 Vital Capacity by 10%
Distance Events
 By 5-15 %
Injury Patterns
 Common injuries in women/girls include:
 Anterior cruciate ligament (ACL) injuries
 Patellofemoral pain syndrome
 Stress fractures
ACL Injuries
 Women have an increased predisposition to ACL
injury
 Many theories, but no one proven definitive cause
ACL Injury
 Intrinsic factors:
 Joint laxity
 Hormones
 Limb alignment
 Ligament size
 Intercondylar
notch size
 Extrinsic factors:
 Conditioning
 Experience
 Skill
 Strength
 Muscle
recruitment
patterns
 Landing
techniques
ACL Injury
 Intercondylar notch width well studied
 Some studies have shown differences in size between
the sexes; others have not
 Smaller notch may mean smaller and weaker ACL
 Same size ACL, but smaller notch may cause
impingement on the ligament
ACL Injury
 What to do?
 Teach preventative skills
 Learn how to fall, jump and to cut
 Plyometric training

Reduce landing forces and improve strength ratios
 Increase hamstring activation
Patellofemoral Pain Syndrome
 Probably more than one etiology
 Chondromalacia
 Malalignment of patella
Patellofemoral Pain Syndrome
 Causes of PFPS
 Anatomical


Larger “Q” angle
Leads to abnormal tracking
of the patella
Patellofemoral Pain Syndrome
 Other causes
 Muscle imbalances
 Foot type (either pes planus or pes cavus)
 Shoes
 Overuse
Stress Fractures
 Chronic, overuse injury
 Most common in weight bearing bones
 Feet, tibia, femoral neck
 Seen commonly in Female Athlete Triad
Menstrual Cycle




Average Age Menarche : 12.8 years
Average Cycle Length : 28 days (20-45)
Well-Defined Pattern of hormonal changes
Follicular or Proliferative phase




Menses through Ovulation
FSH causes overies to make estrogen
Follicle Forms and lining proliferates
Follicle ruptures and Ovum formed
 Luteal or secretory phase
 Ovulation through menstruation – 14 days
  Estrogen  LH Surge Ovulation  Estrogen/Progesterone
 If no fertilization  Estrogen/Progesterone  Menstruation
6
3
Menstrual Cycle
9
5
1
2
4
7
8
Menstruation
 Studies fail to show decreased performance
 Luteal Phase  7 beats per minute ≠ Δ in performance
 ? Asthmatics Vulnerable during perimenstrual phase
 Peak expiration flow rates reported  30-40%
 ER visits  4 times
  Progesterone  bronchoconstriction
 ? Performance Impact of increased core temperature
 Unclear impact on ACL injuries, cognition, aerobic
and anaerobic capacity, and performance
Female Athlete Triad
 Definition
ACSM 1992 – Disordered eating, amenorrhea, and
osteoporosis
 Current- Energy Availability, menstrual function, and
bone mineral density interrelationship
 Belief that lower body weight needed for athletic
success and social acceptance
 Prevalence of all components = 1-3%
 Disordered eating 18-25%, Menstrual dysfunction 25%
Energy Availability
Availability = Dietary intake – exercise expenditure
Key dysfunction underlying triad is disordered eating
manifesting as low energy availability
May be inadvertent
DSM-IV eating disorders
Anorexia nervosa
Bulimia Nervosa
Eating Disorders not otherwise specified
Energy Availability
 Affects cascade of metabolic hormones
 Insulin, cortisol, growth hormone, triiodothyronine,
leptin, glucose, fatty acids, ketones
 Leptin regulates basal metabolic rate


Level of 1.85 mg required for normal menstruation
Low levels in athletes with disordered eating and amenorrhea
Energy Availability
 Risk Factors
 Dieting or restrictive eating
 Vegetarianism
 Belief that thinness = social success
 Belief  weight or fat performance
 Perfectionism or obsessive-compulsive traits
 Competitive Nature
 Judging sports, revealing uniforms, weight classification
 Onset sport training early age
 Coaching emphasizing weight and body type
Anorexia Nervosa
 DSM IV Criteria
 Refusal to maintain minimally normal body weight
 Body weight < 85% expected
 Primary amenorrhea by age 16
 Secondary amenorrhea (absent 3 consecutive cycles)
 Restrictive Type
 Not regularly engaged in binge-eating or purging
 Binge-Eating/Purging type
 During Episode person regularly binge-eating/purging
Anorexia Nervosa Complications
 Cardiovascular- mortality 10%
 Hypotension and bradycardia
 Arrhythmias (Look for prolonged QT)
 Cardiomyopathy (from refeeding or ipecac)
 Endocrine
 Amenorrhea with  FSH and LH despite estrogen
 Electrolyte imbalance:  K,Na,Ph,Mg
 Euthyroid sick syndrome:  T3/T4,  reverse T3
 Osteopenia/Osteoporosis
 Hypothermia, Hypoglycemia, Diabetes Insipidus
Anorexia Nervosa Complications
 GI: Constipation, decreased intestinal motility
 Heme: Anemia, leucopenia, thrombocytopenia
 Integument: Dry skin, lanugo,fragile nails
 Neuro: Cerebral atrophy, ventricular enlargement
 Reproductive: Infertility, low birth weight infant
Bulemia Nervosa
 DSM IV Criteria
 Recurrent Binge Eating


> food than most people would eat in a discrete period
Sense of lack of control of eating
 Recurrent inappropriate compensatory behavior
 Binging and Compensation occur twice a week for 3 mo
 Self eval unduly influenced by body shape/weight
 Not exclusively during Anorexia Nervosa Episode
 Purging Type: vomiting, laxatives, diuretics, enemas
 Nonpurging Type: fasting, excessive exercise
Bulemia Nervosa Complications
 Cardiovascular: Arrythmia, hypertension (diet pills)
 Endocrine:
 Menstrual irregularities
 Pseudo-Bartter Syndrome- normotensive hypokalemic
alkalosis
 Hyperchloremic metabolic alkalosis with laxatives
 GI: Enlarged salivary glands, esophageal dysmotility,
postbinge pancreatitis
 Skin: Russell’s Sign- scarring/callous dorsal index/middle
fingers
 Neuro: Cerebral hemorrhage (diet pills)
 Pulm: Pneumomediastinum
Eating Disorder Not Otherwise
Specified
 Meets some or most criteria for Anorexia or Bulemia but
does not meet full criteria for specific disorder





Anorexia with normal menses
Anorexia but despite weight loss normal weight range
Bulimia but < twice a week or 3 months
Purging after small amounts of food
Chewing and spitting out food
Menstrual Disorders
 Delayed Menarche or Primary Amenorrhea
 Age 15 with secondary sex characteristics
 Secondary Amenorrhea
 NOT A NORMAL RESPONSE TO TRAINING
 Luteal phase deficiency
 Prolonged follicular phase but luteal phase < 10 days
 Decreased progesterone and anovulatory cycle
 One study incidence 78% incidence in regularly
menstruating recreational runner vs 9% sedentary
Functional Hypothalamic
Amenorrhea
 Insufficient calories/carbs to brain disrupts GnRH
 Energy conservation  reproductive function
suppression and hypoestrogenism
 Likely to occur if < 30kcal/kg lean body mass per day
 LH pulse disrupted if < 30kcal/kg for 5 days
 Must exclude other causes of amenorrhea
Amenorrhea Evaluation
 History: menstrual, training, diet, drugs, stress, family
 Exam: Turner’s, Cushing’s, hirsutism, fundi, thyroid,
tanner staging, breast exam, pelvic exam
 Labs: HcG, TSH, prolactin, FSH, LH, testosterone,
DHEAS
 Progestin Challenge test
 Estrogen/progesterone challenge test
 Positive = hypothalamic-pituitary axis dysfunction or ovarian
failure
Amenorrhea Treatment
 Increase caloric intake: 25-30 kcal/kg of fat free mass
 Decrease training if needed
 AAP recommends OCP’s if 16 yo or 3 years post
menarche
 Low dose OCP (20 to 35 ug) no associated weight gain
Bone Mineral Density
 Bone Mineral Density used to evaluate bone health
 Should be assessed if
 6 months amenorrhea, oligomenorrhea
 6 months disordered eating
 After stress or low-impact fracture
 BMD loss can be irreversible
 Athletes in weight bearing sports BMD  12-15%
 Hypoestrogenic state  accelerated bone resorption
 Estrogen has a suppressive effect on osteoclasts
Bone Mineral Density Classification
 T-scores
 Average peak adult BMD
 Used in postmenopausal women
 Fracture risk doubles every SD below the mean
 Normal > -1, Osteopenia -1 to -2.5, Osteoporosis < -2.5
 Z-scores
 Mean for chronologic age
 Used in premenopausal women,adolescents, children
 ACSM accounts for 5-15%  in athletes


Low if secondary clinical risk factors and -2 < Z < -1
Osteoporosis if secondary clinical risk factor and Z < -2
Low BMD Treatment
 Initiate within first year of amenorrhea
 Correct energy deficits
 OCP
 Evidence good in perimenopausal
 Evidence fair in hypothalamic oligomenorrheic
premenopausal
Evidence Limited in anorexic and healthy
premenopausal
Consider if over 16 and BMD  despite  nutrition
DO NOT USE < 16 yo : premature growth plate closure
Low BMD Treatment
 Nasal Calcitonin
 Calcium 1500 and Vitamin D 400-1000 IU daily
 Weight bearing exercise and resistance training
 Smoking cessation
 Reduce excessive alcohol intake
 Synthetic human parathyroid hormone
 DO NOT USE Bisphosphonates in premenopausal
women
Summary
 Men and Women are different, but not so different
 Woman have a higher incidence of ACL Injury, PFPS,
and stress fractures
 Menstrual Cycle is an important metabolic factor
 Female Athlete Triad of energy availability, menstrual
function, and BMD interrelationship is important to
consider, prevent, and treat
Questions

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