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Antoin Alexander Maj USAF MC Adapted from Dr. Terry Adirim.

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Presentation on theme: "Antoin Alexander Maj USAF MC Adapted from Dr. Terry Adirim."— Presentation transcript:

1 Antoin Alexander Maj USAF MC Adapted from Dr. Terry Adirim

2 Overview General Differences Injury Patterns Menstrual Cycle Female Athlete Triad

3 General Differences FemalesMales Prepubertal CapabilitiesEqual Growth Spurt 1113 Maximum Height16-1720-21 Weight DifferenceMinus 11-14 kg  Bone and muscle mass Body Fat26%14% Body ShapeWide HipsWide Shoulders LimbsShorterLonger StrengthEqual relative to lean mass Muscle Hypertrophy  Due to testosterone

4 General Differences FemalesMales Upper Extremity Strength40-75% of men Lower Extremity Strength60-80% of men Average VO2 MaxMinus 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 %

5 Injury Patterns Common injuries in women/girls include: Anterior cruciate ligament (ACL) injuries Patellofemoral pain syndrome Stress fractures

6 ACL Injuries Women have an increased predisposition to ACL injury Many theories, but no one proven definitive cause

7 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

8 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

9 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

10 Patellofemoral Pain Syndrome Probably more than one etiology Chondromalacia Malalignment of patella

11 Patellofemoral Pain Syndrome Causes of PFPS Anatomical Larger “Q” angle Leads to abnormal tracking of the patella

12 Patellofemoral Pain Syndrome Other causes Muscle imbalances Foot type (either pes planus or pes cavus) Shoes Overuse

13 Stress Fractures Chronic, overuse injury Most common in weight bearing bones Feet, tibia, femoral neck Seen commonly in Female Athlete Triad

14 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

15 Menstrual Cycle 1 2 3 4 5 6 7 8 9

16 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

17 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%

18 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

19 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

20 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

21 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

22 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

23 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

24 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

25 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

26 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

27 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

28 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

29 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

30 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

31 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

32 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

33 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

34 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

35 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

36 Questions ?

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