Ergogenic aids and the athlete

In the complex world of sports, today, many athletes and coaches are in a continuous search “how to gain a competitive advantage to improve athletic performance.” The slightest improvement in athletic performance often means the difference between “the thrill of victory and the agony of defeat.”

Coaches as well as athletes utilize special aids to enhance the athletic performance known as ergogenic aids. An ergogenic aid is any agent, substitute or technique that improves physical performance through its particular effect on human body. The term ergogenic aids also refers to any substance, process or procedure that may enhance the performance through improvement of strength, speed, response time or endurance of the athlete.

The use of doping substances in many sports and on all continents has become a major public health issue. The problem of drug abuse in sports first was tackled by the international sports authorities, in the form of the International Olympic Committee (IOC), during the 1960s. An official definition of doping first was given by the IOC in 1964 and the first programs of antidoping tests were activated by the IOC and its newborn Medical Commission in 1967. The global and universal characteristics of doping led to the formation in 1999 of the World Anti-Doping Agency (WADA), a unique collaboration between sports and governments. WADA is founded on equal partnership between public authorities and Olympic sport. Since then, as mandated by the World Anti Doping Code, the WADA has been responsible for the upgrade and publication of the list of “Prohibited substances and practices”. The 2014 list of Prohibited substances is now available at http://www.wada-ama.org/en/Science-Medicine/Prohibited-List 

Classification of performance-enhancing aids:

• Acceptable practices or substances. 
• Questionable or potentially harmful practices and substances. 
• Illegal practices and substances.

Acceptable practices or substances:

• amino acids, protiens
• sports drinks
• vitamin E
• relaxation techniques
• carbohydrate approaches (loading,feeding, replenishment)
• water (prehydration, hydration, rehydration)
• minerals and liquid food suppliments
• psychological approaches.

Questionable or potentially harmful practices and substances:

• caffeine
• alcohol
• nicotine- tobacco, Heroin
• oxygen utilization (before, during and after performance)
• marijuana, bee pollen, bicarbonate ingestion

Illegal practices and substances:

• anabolic-androgenic steroids
• diuretics, 
• amphetamines, cocaine
• blood doping (RBC reinfusion)
• beta blockers
• human growth hormone

Rationale for use of performance-enhancing aids: Use or Abuse?

• greater success and potential in sports.
• accessibility of and exposure to ergogenic aids.
• peer pressure and peer acceptance.
• pressure by coach, trainer, or physician.
• legality of substance or technique.
• shortcut to goal attainment.
• ease of administration.
• lack of fear of potential adverse health effect.
• performance stress relief.

references:

• Zachazewski , J.E.: Athletic Injuries and Rehabilitation. W.B. Saunders Company
• Drug Abuse in Sports, Utox Update 2002, volume 4, number 1.
• Catlin D. H. Medicine and science in the fight against doping in sport. J Intern Med 2008; 264: 99–114.

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           a POWER POINT PRESENTATION ON

   Periarthritis shoulder

Introduction

ÒPA is a condition characterized by pain & progressive limitation of GH movements.

ÒIt is the initial manifestation of ongoing pathology which usually culminates in frozen shoulder.

ÒDuplay in 1872 referred the condition as humerocapsular Periarthritis.

ÒCodman in 1934 coined the term ‘Frozen shoulder’ – painful loss of motion with normal radiographic studies.

ÒIn 1946, Naviaser ,named the condition ‘adhesive capsulitis’ based on his work & radiographic appearance.

ÒIn 1949, Simmonds, proposed that rotator cuff inflammation preceds PA shoulder.

ÒIn 1973, Macnab illustrated that degenerative changes in supraspinatus, leads to an autoimmune reaction, produces diffuse capsulitis.    

ÒPA shoulder/ frozen shoulder –

ÉPrimary adhesive capsulitis

ÉSecondary adhesive capsulitis / acquired shoulder stiffness.

ÒUncommon in athletes, may occur due to prolonged immobilization.

 

Etiology
ÒExact cause is unknown.
ÒCertain factors considered to contribute to development of PA are:

ÉPain

ÉDisuse / immobilization

É& periarthritic personality.

Pathoanatomy
ÒThickening & contracture of joint capsule with obliteration of inferior recess.
Òcollagen band bridging across recesses, random collagen production.
ÒAcquired cases reflects the underlying causes :

ÉSurgery

ÉTrauma

ÉOther pathological conditions like insulin dependent diabetes, reflex sympathetic dystrophy, etc.

Clinical presentation:

PRIMARY ADHESIVE CAPSULITIS

ÒInsidious and idiopathic

ÒUsually older than 40 yr. of age.

ÒHigher incidence in females.

ÒHistory of progressive shoulder stiffness associated with diffuse pain

Òadhesive capsulitis is classically characterized by three stages:

ÉInitial/ freezing phase

ÉSecond / frozen phase

ÉFinal/ thawing phase

( Reeves B:The natural history of the frozen shoulder syndrome. Scand J Rheumatol 4;193,1975) 

ÒInitial/ freezing phase

ÉOnset of diffuse, aching pain in the shoulder.

ÉPhase can last for 2 to 9 months.

ÉPatient position the arm in abduction & internal rotation.

ÉAssociated with acute inflammatory synovitis.

ÒSecond / frozen phase

ÉPain at rest usually diminishes .

ÉADLs becomes severely restricted according to capsular pattern.

ÉSevere pain occurs attempted motion.

ÉThis stiffening phase can last for 4 to 12 months.

ÉGH motion lost under anesthesia.

ÉHypervascular proliferative synovitis & Capsular fibrosis

ÒFinal/ thawing phase

ÉOccurs with slow recovery of motion.

ÉGradual resumption of ADLs

ÉThis phase can last for 6 months to 2 years.

ÉThe capsule is now very scarred, thick, fibrotic, & hypovascular.

SECONDARY OR ACQUIRED SHOULDER STIFFNESS

ÒThis condition is associated with a known predisposing condition of the shoulder

ÒPatient with acquired stiff shoulder have much clearer & concise history.

ÒLoss of external rotation, abduction & flexion.

ÒRadiographs are helpful in acquired cases.

Differential diagnosis

ÒPartial rupture of supraspinatus tendon.

ÒSupraspinatus tendinitis.

ÒBrachial neuritis.

ÒOA of the AC joint.

ÒTuberculous arthritis of shoulder

Treatment : 

PHYSIOTHERAPY  Treatment

ÒPhase 1: weeks 0-8

ÉRelieve pain

ÉRestore motion

ÐExercises

×AROM

×AAROM

×PROM

ÉHome exercise program should be instituted from beginning.

ÒPhase 2: Weeks 8-16

ÉContinue the treatment program of phase 1 &

ÉExercises for strengthening of rotator cuff & scapular stabilizers.

ÐClosed chain isometric strengthening

ÐOpen chain strengthening

ÐLight isotonic dumbbell exercise

ÒPhase 3: Months 4 & beyond

ÉThere should be resolution of pain & significant functional recovery of shoulder motion.

ÉHome exercise program should be continued.

ÒMaximum improvement may be achieved 6-9 months after treatment initiation.

Surgical treatment

ÒSurgical intervention may be indicated, if no improvement is seen after 3 months of management:

ÉClosed manipulation under anesthesia

ÉArthroscopic capsular release.

ÉOpen release.

Postop. management

ÒShould begin on the day of surgery.
ÒTherapy should begun with ROM exercises.
ÒTherapy should consist a stretching program in all planes.
ÒOnce pain free arc is regained, a strengthening
program may be added.

references:

ÒHunter James M: Rehabilitation of the hand & upper extremity. 5th Ed.

ÒBrotzman S Brent: Clinical orthopedic rehabilitation.2nd Ed.

ÒDonatelli Robert A: Physical Therapy of Shoulder.2nd Ed.

ÒCyriax J: text book of orthopedic medicine volume 1. 8th Ed.

ÒSolomon L: Apley’s system of orthopedics & fractures. 8th Ed

ÒReid David C: Sports injury Assessment & rehabilition

ÒMaitland GD: Peripheral Manipulation. 2nd Ed.

ÒSimonds FA: SHOULDER PAIN With Particular Reference to the “ Frozen” Shoulder . The Journal Of Bone And Joint Surgery 31B:426,1949

ÒNEVIASER JS: ADHESIVE CAPSULITIS OF THE SHOULDER: A Study Pathological Findings in Periarthritis of the Shoulder. J Bone Joint Surg Am. 1945;27:211-222.

ÒManske Robert C: Diagnosis and management of adhesive capsulitis. Curr Rev Musculoskelet Med (2008) 1:180–189

ÒCharnley J: Periarthritis of shoulder

Osteoporosis

Osteoporosis :

      Osteoporosis is a condition in which the bones are weakened due to a decrease in the bone mass that makes up the skeleton. Due to Osteoporosis bones become fragile and more likely to fracture. Usually the bone loses density, which measures the amount of calcium and minerals in the bone.

      Throughout life, bones are continuously remodeled. While a child is growing, the rate of bone formation is greater than the rate of bone breakdown. The skeletal mass continues to increase until ages 20 to 30. After that, the rates of formation and breakdown of bone mass are equal until ages 40 to 50. Then, re-absorption begins to exceed formation, and the total bone mass slowly decreases.

Causes, incidence, and risk factors: 

      Osteoporosis is the most common type of bone disease. Because of osteoporosis about half of all women over the age of 50 will have a fracture of the hip, wrist, or vertebra (bone of the spine) during their lifetime. Bone is living tissue. Existing bone is constantly being replaced by new bone. Osteoporosis occurs when the body fails to form enough new bone, when too much existing bone is reabsorbed by the body, or both. Calcium is one of the important minerals needed for bones to form. If you do not get enough calcium and vitamin D, or your body does not absorb enough calcium from your diet, your bones may become brittle and more likely to fracture. Sometimes bone loss occurs without any cause.  Sometimes the tendency to have bone loss and thin bones is passed down through families. 

      A drop in estrogen in women at the time of menopause and a drop in testosterone in men is a leading cause of bone loss. Over time, men are apt to lose 25% and women 35% of their bone mass. But we have to consider that men tend to have denser bones than women anyway, and their testosterone (male sex hormone) level generally does not begin to decline significantly until after age 65. In contrast, the estrogen (female sex hormone) level in women begins to decline at about age 45. Because sex hormones play an important role in maintaining bone strength, this difference means that women are more likely than men to suffer fractures, involving especially the hip, vertebrae, long bones, and pelvis. Although osteoporosis may at times be the result of various disease processes, it is essentially a disease of aging.
     

Other risk factors include: 

• Absence of menstrual periods (amenorrhea) for long periods of time. 
• A family history of osteoporosis. 
• Drinking a large amount of alcohol.
• Low body weight.
• Smoking.

 Symptoms:

      There are no symptoms in the early stages of osteoporosis. Many times, people will have a fracture before learning that they have the disease. Pain almost anywhere in the spine can be caused by fractures of the bones of the spine. These are called compression fractures. They often occur without an injury. The pain occurs suddenly or slowly over time. There can be a loss of height (as much as 6 inches) over time. A stooped posture or kyphosis (also called a dowager's hump) may develop. 

Diagnosis:

      Baseline laboratory studies include the following: 

• Complete blood count: May reveal anemia or raise suspicion of alcoholism. 
• Serum chemistry levels: Usually normal in persons with primary osteoporosis. • Serum iron and ferritin levels: Helpful when malabsorption or hemochromatosis is suspected. 
• Liver function tests: Elevations may indicate alcoholism.
• Thyroid-stimulating hormone level: Thyroid dysfunction has been associated with osteoporosis.
• 25-Hydroxy vitamin D level: Vitamin D insufficiency can predispose to osteoporosis. 

      Bone mineral density (BMD) measurement: It is recommended in the following patients: 

• Women aged 65 years or older and men aged 70 years or older, regardless of clinical risk factors.
• Younger postmenopausal women and men aged 50-70 years with clinical risk factors for fracture.
• Women in menopausal transition with a specific risk factor associated with increased risk for fracture (ie, low body weight, prior low-trauma fracture, use of a high-risk medication).
• Adults with fragility fractures.
• Adults who have a condition associated with low bone mass or bone loss (eg, rheumatoid arthritis)/
• Adults who take a medication associated with low bone mass or bone loss (eg, glucocorticoids, ≥5 mg of prednisone daily for ≥3 mo).
• Anyone being considered for pharmacologic therapy for osteoporosis.
• Anyone being treated for osteoporosis (to monitor treatment effect).

      Dual-energy x-ray absorptiometry (DXA): 

      It is currently the criterion standard for the evaluation of BMD. Peripheral DXA is used to measure BMD at the wrist; it may be most useful in identifying patients at very low fracture risk who require no further workup. DXA provides the patient’s T-score, which is the BMD value compared with that of control subjects who are at their peak BMD. 

      World Health Organization (WHO) criteria define a normal T-score value as within 1 standard deviation (SD) of the mean BMD value in a healthy young adult. Values lying farther from the mean are stratified as follows: 

• T-score of –1 to –2.5 SD indicates osteopenia.
• T-score of less than –2.5 SD indicates osteoporosis.
• T-score of less than –2.5 SD with fragility fracture(s) indicates severe osteoporosis.

      DXA also provides the patient’s Z-score, which reflects a value compared with that of persons matched for age and sex. Z-scores adjusted for ethnicity or race should be used in the following patients:

• Premenopausal women. 
• Men younger than 50 years. 
• Children.

      Z-score values of –2.0 SD or lower are defined as "below the expected range for age" and those above –2.0 SD as "within the expected range for age." The diagnosis of osteoporosis in these groups should not be based on densitometric criteria alone.

 

Plain radiography features and recommendations are as follows:

• Obtain radiographs of the affected area in symptomatic patients
• Lateral spine radiography can be performed in asymptomatic patients in whom a vertebral fracture is suspected; a scoliosis series is useful for detecting occult vertebral fractures 
• Radiographic findings can suggest the presence of osteopenia, or bone loss, but cannot be used to diagnose osteoporosis 
• Radiographs may also show other conditions, such as osteoarthritis, disk disease, or spondylolisthesis.

Management:

Treatment for osteoporosis may involve:

• Lifestyle changes, such as diet and exercise.
• Taking calcium and vitamin D 
• Using medicines

Medicines are used to strengthen bones when:

• Osteoporosis has been diagnosed by a bone density study, whether or not you have a fracture.
• A bone fracture has occurred and a bone density test shows that you have thin bones, but not osteoporosis.

Medicines used to treat osteoporosis: 

      The National Osteoporosis Foundation (NOF) recommends that pharmacologic therapy should be reserved for postmenopausal women and men aged 50 years or older who present with the following: 

• A hip or vertebral fracture (vertebral fractures may be clinical or morphometric [ie, identified on a radiograph alone])
• T-score of –2.5 or less at the femoral neck or spine after appropriate evaluation to exclude secondary causes  
• Low bone mass (T-score between –1.0 and –2.5 at the femoral neck or spine) and a 10-year probability of a hip fracture of 3% or greater or a 10-year probability of a major osteoporosis-related fracture of 20% or greater based on the US-adapted World Health Organization algorithm.

      Guidelines from the American Association of Clinical Endocrinologists include the following recommendations for choosing drugs to treat osteoporosis:

• First-line agents: Alendronate, risedronate, zoledronic acid, denosumab
• Second-line agent: Ibandronat.
• Second- or third-line agent: Raloxifene 
• Last-line agent: Calcitonin 
• Treatment for patients with very high fracture risk or in whom bisphosphonate therapy has failed: teriparatide

• Bisphosphonates (the main drugs used to prevent and treat osteoporosis in postmenopausal women)

Exercise plays a key role in preserving bone density : 

      In older adults some of the exercises recommended to reduce the chance of a fracture include:

• Weight-bearing exercises -- walking, jogging, playing tennis, dancing.
• Free weights, weight machines, stretch bands
• Balance exercises -- tai chi, yoga 
• Rowing machines.

     Avoid any exercise that presents a risk of falling. Also, do not do high-impact exercises that can cause fractures in older adults.

     Your body needs calcium and vitamin D to keep your bones strong. Vitamin D helps your body absorb calcium.

• The U.S. National Institutes of Health recommend a calcium intake of 1,200–1,500 mg per day during puberty.
• Adults under age 50 should have 1,000 mg of calcium and 400 - 800 IU of vitamin D daily. 
• Women ages 51 to 70 should have 1,200 mg of calcium and 400 - 800 IU of vitamin D a day; 
• Men ages 51 to 70 need 1,000 mg of calcium and 400 - 800 IU of vitamin D a day. 
• Adults over age 70 should get 1,200 mg of calcium and 800 IU of vitamin D daily.

      Follow a diet that provides the proper amount of calcium and vitamin D.

Stop unhealthy habits:

• Quit smoking, if you smoke.
• Limit your alcohol intake. Too much alcohol can damage your bones. This puts you at risk of falling and breaking a bone.

It is important to prevent falls. The following are suggestions on how to do this:

• Do not take sedating medicines, which can make you drowsy and unsteady. If you must take them, be extra careful when you are up and about. For example, hold on to countertops or sturdy furniture to avoid falling.
• Remove household hazards, such as throw rugs, to reduce the risk of falls. 
• Leave lights on at night so you can see better when walking around your house. 
• Install and use safety grab bars in the bathroom. 
• Make sure your vision is good. Have your eyes checked once or twice a year by an eye doctor. 
• Wear shoes that fit well and that have heels. This includes slippers. Slippers that do not have heels can cause you to trip and fall. 
• Do not walk outdoors alone on icy days.

Prognosis:

      The prognosis for osteoporosis is good if bone loss is detected in the early phases and proper intervention is undertaken. Patients can increase BMD and decrease fracture risk with the appropriate anti-osteoporotic medication. In addition, patients can decrease their risk of falls by participating in a multifaceted approach that includes rehabilitation and environmental modifications. Worsening of medical status can be prevented by providing appropriate pain management and, if indicated, orthotic devices.

      Osteoporosis can cause a person to become disabled from weakened bones. Hip fractures are one of the main reasons people are admitted to nursing homes. Calcium is important for building and maintaining healthy bone. A small daily amount of vitamin D is also necessary to absorb calcium from the digestive tract. Exposure to sunlight is required to allow skin to synthesize vitamin D. Following a healthy, well-balanced diet can help you get these and other important nutrients. Postmenopausal women should have an evaluation of their bone density.

The Aging Athlete

Life Sp­­­­an:

The human organism has a fixed life span. This genetically determined, species-specific constant is best as a fixed number of normal cell replications. Once this normal number of cell cycles reached, abnormal changes within the cell occur with increasing frequency. Further the amount of time between cell division increases.

Life Expectancy:

            Life expectancy connotes a far different concept. It deals more closely with the influence of environmental factors on the organism. Hostile environmental factors diminish life expectancy whereas a conductive environment allows life expectancy to genetically approach the determined life span. As the life expectancy approaches life span in our society, quality of life issues become increasingly important. It is with these issues that the physical caring for the aging athlete must contend.

Aging Process:

Skeletal changes-   

The aging process is associated with predictable physiologic and biomechanical changes:   

• Decrease in bone mass.

• Decrease in cortical thickness.

• Increase in cross sectional diameter.

A decrease in bone mass can be measured in the normal human female by the time she reaches her mid-forties. Similarly, normal males show a measurable decrease in bone mass by the time they reach their fifties.

Factors that stimulates bone resorption & bone loss:

•         low serum calcium

•         high serum phosphate

•         inactivity (leads to disuse atrophy)

•         acidosis

•         steroids

The physiologic activity of bone throughout life is subject to a variety of imbalances. As a general rule, the normal aging process of males relates to a decrease in formation of bone in latter decades of life. Women, however, are subject to increased resorption of bone, particularly in the years surrounding menopause.

Factors that slow bone resorption & bone loss:

•         estrogen

•         alkalosis

•         high ratio of serum calcium to phosphorus

•         increased activity level

•         high clcium intake

Minimum adult requirement for dietary calcium:

·         Premenopausal women – 1000 mg/day

·         Postmenopausal women – 1500 mg/day

·         Lactating women – 2000 mg/day

·         Men – 1000 mg/day

To a certain extent, loss of bone mass is reversible. An increase in the level of activity, medication and dietary correction stimulates a measurable increase in bone mass in all age group.

Soft tissue changes:

            At all ages myotendinous junction is the weakest link in the muscle tendon unit and in its attachment to bone. Although the muscle tissue remains relatively homogenous and fails at an unpredictable location. “Disuse atrophy” diminishes the efficiency of the myotendinous unit and contributes to a loss of stiffness and to a decreased load to failure.

Physiological changes in Aging muscle:

·         A loss of motor units.

·         Decrease in number of muscle fibres.

·         Decrease in speed of contraction.

·         Increase in reflex time.

·         Slower relaxation phase of contraction.

·         Increased average collagen fibril size in tendon.

·         Increased insoluble collagen content and collagen cross linking in tendon (causes increased stiffness of the aging tendon).

·         Decreased tendon water, chondroitin sulphate and hyaluronic acid content.

·         Decreased capillary density.

Healing response:

            Vascular insufficiency, diabetes and a variety of other disease process results in delayed healing. The literature describing age related changes in skeletal and soft tissues has at least one major flaw. All studies even those that stratify patients according to age, fail to differentiate activity levels.