Division I College Football Lift Schedule 2008 University of Delaware

Trevor Mooney Here is the actual lifting schedule at the University of Delaware during the 2008 season. During the seasons I played at Washington State, the lifting and conditioning was nearly identical.

In-Season Workouts (Real Sample Weekly Workout Routine)

***In Comparison to Post-Season Workout, the Repititions and Lifts are consistent, because of the
maintanance lifting of the season

Weightlifting Philosophy and Mentality Advice

Saturday- Gameday

Sunday- After Game Lift

1) Warm Up
2) Squats 4x 8 Repititions 50% (of Max)
3) Pull Ups 4×6 Body Weight
4) Close Grip Barbell Bench 4×6 (185, 225 lbs) Light Enough To Get Soreness Out
5) Shoulder Complex 3×6 (5/10 lbs)Bent Over Flys, Side Raises, Front Raises, Hi-Rows, Bicep to Military)
6) Quad/ Hamstring Machines 3×12 Light
7)Abs Isometric and Isokinetic Abs and Back ~Roughly 10 min. straight
8 ) Conditioning: 12×100 yard Striders 75% of Maximum Speed

Monday- Mandatory Off Day by NCAA (Still have film and rehab if needed)

Tuesday Lift (1 day of practice during the week)

1) Warmup
2) 5 Minutes of Jump Rope (Several Different Exercises)
3) Hang Cleans 4×4 75-85% (of Max)
4) 1 Legged Body Weight Squats 2×6 Body Weight (2 Sets on Each Leg)
5) Barbell Bench 8 @65%, 8 @ 70%, 6 @ 75%, 6 @ 80%
6) Barbell Skull Crushers 3×12 85-135 lbs
7) Dumbbell Incline 3×6 (75-110 lb DBs depending on strength)
8 ) Shoulder Complex 3×6 15-30 lb DBs depending on strength (Look above for the exercises)
9) Abs Isometric and Isokinetic Abs and Back ~Roughly 10 min. straight

Film and Practice after Class

Wednesday (2nd Day of Practice)
No Lift, but additional conditioning after practice

Thursday (3rd Day of Practice)
1) Warmup
2) 5 Minutes of Jump Rope (Various Exercises)
3) Push Jerk 3×6 (Relatively Heavy 185-225 lbs depending on strength)
4) Barbell Shrugs 3×12 (275-425 depending on strength)
5) One-Foot Lunges 3×6 with 135-225 depending on strength
6) Pull Ups 3×8 Body Weight or with weight vest
7) Machine Pull Downs 3×12 Heavy depending on the strength
8 ) Biceps 3×12 (Various Exercises)
9) Hamstrings/ Quads Machines 3×12
10) Abs Isometric and Isokinetic Abs and Back ~Roughly 10 min. straight

Friday (Walk-thrus and final preparations) No Lift or Significant Conditioning

Off-Season Workouts (December-April)
***The Week Schedule given here is a sample; the repititions weights and percentages follow a Russian
Periodization scale (Which will be briefly explained in furture articles)
***Lifting during spring ball resembles in-season lifts

Winter Conditioning
Monday Lift

1) Warm Up
2) Push Jerk 3×6 (Relatively Heavy 185-225 lbs depending on strength)
3) BB Bench 10@55%, 8@60%, 6@70%, 6@80%, 4@90% (Repititions change significantly thru weeks)”
4) DB Incline 3×8 75-115 lb DBs depending on strength
5) Shoulder Complex 3×6 15-30 lb DBs (Exercises listed above)
6) DB Skull Crushers 3×6 35- 65 lb DBs depending on strength
7) Machine Pushdown 3×12 weight dependent on strength
8 ) Abs Isometric and Isokinetic Abs and Back ~Roughly 10 min. straight
9) Conditioning: Jump Rope ~5 minutes, hurdle work (hip flexibility), Speed Ladder ~7 minutes

Tuesday Lift

1) Warm Up
2) Hang Clean 4×4 (Heavy)
3) One Legged Barbell Squat 3×6 135-225 lbs depending on strength
4) Pull Ups 4×8 Body Weight/ Weight Vest
5) DB Rows 4×8 Heavy 80-130 lbs depending on strength
6) Pull Down Machine 4×8 weight depends on strength
7) Hamstring/ Quad machines 3×12
8 ) Biceps 3×8 various exercises
9) Abs Isometric and Isokinetic Abs and Back ~Roughly 10 min. straight
Conditioning: Coach’s Circuit (Brutal Agility and Speed Circuit ~Roughly 90 minutes)

Wednesday- No Lift or Conditioning

Thursday Lift
1) Warm Up
2) Clean Jerk 3×6 (heavy but with speed 185-305 lbs)
3) 1 Legged Body Weight Squats 2×6 Body Weight (2 Sets on Each Leg)
4) Close Grip Bench 4×8 weight depends on strength (185-265)
5) Barbell Skull Crushers 3×12 weight depends on strength (85-135)
6) DB Incline 8, 8, 6, 6 weight depends on strength
7) Tricep Pushdown Machine 3×12
8 ) Shoulder Complex 3×6 15-30 lb DBs depends on strength
9)Abs Isometric and Isokinetic Abs and Back ~Roughly 10 min. straight
Conditioning: Coach’s Circuit (Brutal Agility and Speed Circuit ~Roughly 90 minutes)

Friday Lift
1) Warm Up
2) Barbell Squat 10, 8, 8, 6, 6, 4 (Weights change through the weeks)”
3) Shrugs 3×12 275-405 lbs depends on strength
4) Walking Lunges 3×16 Steps 55-80 lb DBs depends on strength
5) Pull Ups 3×8 Body Weight/ Weighted Vest
6) DB Rows 3×8 DB Rows 80-130lb DBs depends on strength
7) Machine Pull Downs 3×12
8 ) Biceps 3×12 Various Exercises
Conditioning: 1000 Steps Stairmaster (100% Sprints Roughly 6-8 minutes will burn like hell after squating)
or (if injured) 20x 30 seconds bike sprints (Level 12-15) with 15 second rests

***During Spring Ball (April and May) workouts are similar to in-season lifts
***During Summer (May, June, July) workouts are similar to winter lifts and conditioning
***Pre-Season (August Two-a-Days) workouts are similar to in-season lifts


Head Trauma in the NFL

A thesis on hidden dangers lurking behind America’s favorite game

In June of 2007 a leading forensic pathologist named Bennet Omalu scrutinized two brains exhibiting similar damage. When examined under a microscope, the damage to both brains was extensive, including neurofibrillary tangles, plaques and severe scar tissue. It was determined that the pathology of the brains was comparable to what would be present in an eight-five year old with beginning stages of Alzheimer’s disease. But to the contrary, the brains were those of two recently deceased football players who were both in their mid-forties and retired. Their names were Andre Waters and Justin Strzelczyk (Farrey, “Pathologist Says Walters’ Brain Tissue had Deteriorated” 1). The damage to the brain tissue was not caused by natural aging, but due to the debilitating nature of years of professional football.

Football has permeated our culture with unrivaled magnitude. From an analogy in a presidential speech to Saturdays and Sundays solely dedicated to the sport, football is an American obsession. The same violence and pain that both players and fans thrive off of delivers devastating effects to a person’s body. Today’s game witnesses hits that measure upwards of 120 G’s (Farrey, “The Case for HGH” 2). That amount of force is equivalent to a severe car crash. In a game that has evolved from a relatively unknown sport to a multi-billion dollar business, motivation to succeed in this competitive and aggressive environment has led to bigger, stronger and faster athletes. These elements increase the force behind collisions and the severity of head injuries in football. With the deaths of four former NFL athletes who displayed similar neurological symptoms, irrational behavior and brain damage, the issue has become a focus of the media.

The impact of some hits has the force as a severe car wreck.

Researchers believe there is a link between brain damage and multiple concussions which athletes receive playing football. Even with the mounting evidence in favor of long-lasting brain damage due to concussions, the NFL is still skeptical about the validity of the claims made by outside researchers. To better understand the ongoing debate about the head trauma issue, it is important to understand the physiology and damage caused by traumatic head injuries, including concussions and pituitary damage. The short and long-term effects of damage to the brain have recently become a significant issue in the media. Over the past decade the NFL has been diverting the issue, but now with new leadership time may see change.

Each year nearly three hundred thousand sports-related head injuries occur in the United States (Guskiewicz et al., “Cumulative Effects Associated with Recurrent Concussion in Collegiate Football” 2553). The most common type of sports injury to the head is known as Mild Traumatic Brain Injury or MTBI for short. This encompasses all concussive type injuries, and many use the term interchangeably for concussion.

In contact sports such as football, basketball, soccer, baseball and boxing, moderate to high amounts of concussions may occur during play. The rate of reported concussions in the NFL tends to be nearly double that of reported concussions in high school football. This is of significance in that it indicates the difference in speed of the game at the professional level. According to one study, twenty-five percent of all football players report suffering three or more concussions in a season (Nowinski 10). In contrast, a study endorsed by the NFL stated that only four percent of high school players suffer from a concussion during the course of a season. In reality as many as ninety percent of concussions go unreported (Nowinski 33). One of the big discrepancies of the NFL-endorsed study and many other studies is that the information stems from trainers who can only report on concussions that players admitted to sustaining. At all levels, participants tend to ignore symptoms such as “seeing stars” or “having their bell rung” for various reasons, including the heat of battle and being ignorant of the true symptoms of a concussion.

Though concussions have been identified for thousands of years, people are still unaware of what concussions actually are. A concussion is not defined as an actual physical injury, but by loss of brain function induced by physical trauma (Nowinski 25). The NFL defines a concussion as a “traumatically induced alteration of awareness or consciousness, including but not limited to a loss of consciousness, a sensation of being dazed or stunned and by symptoms commonly associated with post—concussion syndrome, including loss of balance, headaches, amnesia, sleep disturbances, vertigo, and hearing loss.” Some common signs of a concussion are confusion, amnesia, headache and irritability (Nowinski 124).

In fact “seeing stars” is a mild form of a concussion. The frightening truth is that according to one study ninety-two percent of players and coaches believe that a “bell ringer” is a different injury than a concussion (Nowinski 32). No wonder so many concussions are going undetected! In my own career, I have never been “diagnosed” with a concussion, but I know of at least six or seven times in which I have become dazed and confused following a hit. It is an all too familiar story for many others. Study after study has shown that repeated concussions can put a person at greater risk for developing serious disorders such as dementia, Alzheimer’s disease or Parkinson’s disease. Links have been found that determined neurological illness is proportionate to how many concussions a person has sustained (Nowinski 9).

Sudden accelerations, decelerations and blows to the head cause concussions. The fluid surrounding the brain, called cerebrospinal fluid, acts as a cushion and protects the brain from light trauma. More severe forces will cause injury however. The wave of energy from the impact “passes through the brain tissue and can crush, stretch, and shear brain cells and the nerve fibers connecting them that are also known as axons” in a process known as the neurometabolic cascade of concussion (Nowinski 27). The rotational forces of a concussion cause dysfunction over a widespread area of the brain, most affecting midbrain structures such as Substaintia Negra, Ventral Tegmental Area (VTA) and diencephalons (Jorge et al. 44).

Immediately following a concussion many changes in the brain neurochemistry occur. First is the impairment of neurotransmission. Neurons inability to communicate with one another lead to difficulty in tasks such coordination and memory recall. More specifically loss of the regulation of ions that are released in the synaptic channels results in less efficient neurotransmitter release. The disorganization of the neurotransmission creates wasted energy expenditure for cellular metabolism in the brain.

Decreased blood flow lasts for approximately seven to ten days, the period of time in which the brain is most susceptible to re-injury. Consequently second degree or Type II concussions, the most common form of reported concussions, require at least one week of abstinence from a sport. Eventually the ions of the brain become balanced and blood flow returns to normal.

Animal studies have revealed that numerous neurons can die with even a slight change in blood flow (Guskiewicz et al., “Cumulative Effects Associated with Recurrent Concussion in Collegiate Football” 2551). After concussions there is a noticeable spike in blood glucose levels in the brain. Because of a lack of blood flow the brain goes through anaerobic respiration, leaving a byproduct that tends to be lactic acid (Chen et al. 84). A build up of lactic acid can cause additional damage to the brain. While our current understanding is that mild concussion does not cause brain cell death, it can cause the deterioration of the fatty covering of brain cells known as myelin, resulting in less efficient and slowed transmission (Nowinski 44).

The unique symptoms of each concussion can be related to the affected brain areas. Certain symptoms such as headache, nausea and incoordination can be attributed to dysfunction of the brainstem. Other symptoms such as confusion, amnesia and disorientation can be attributed to dysfunction of the frontal lobe and more specifically the cerebral cortex (Nowinski 35). Symptoms such as irritability, fatigue and sleep disturbance may be delayed in onset. What makes concussions difficult to evaluate is that many areas of the brain may be affected, but symptoms manifest at different stages. One doctor explains, “With brain injury, after the initial injury, the damage is not done –after the initial injury, it can continue. That’s what is so challenging about these injuries” (Nowinski 31).Concussions are the most common of MTBI. The Cantu grading system continues to be the gold standard for assessing concussions. Concussions are graded by severity. The mildest form of concussion, grade I, has symptoms of post-traumatic amnesia of less than thirty minutes and no loss of consciousness (Burke 2). Usually a player can return to a game or activity after a fifteen-minute rest.

The Cantu Guidelines separates concussions into three separate grades.

A grade II concussion is the most common concussion witnessed by trainers. It has symptoms of amnesia lasting thirty minutes to twenty-four hours and a loss of consciousness for less than five minutes. A grade II concussion is more dangerous and requires at least one week of rest. A grade III concussion is the most severe form with symptoms of amnesia for over twenty-four hours and a loss of consciousness of over five minutes. A player could be restricted from the sport for several weeks in order to prevent serious brain injury. For each of the three cases the treatment plan is quite simple. The athlete needs to get adequate sleep and refrain from physical activity for the allotted time needed to recover.

Trainers have used the Cantu Grading System for over twenty years, but more personal concussion assessments based on computer tests are becoming increasingly popular (Oelke). The idea of grading concussions is losing steam. Although widely used, many doctors, including Dr.Cantu, are beginning to support the notion of not grading concussions until symptoms have disappeared. This will allow for a more accurate assessment of the injury (Nowinski 138).

The trainers and team physicians are responsible for determining when a player seems fit to return to play. If someone is allowed to compete too early or is forced back into play too soon, the athlete is at risk for a devastating injury called second-impact syndrome. Permanent damage or even death can result from the condition (Burke 3). Christopher Nowinski, author of Head Games: Football’s Concussion Crisis, explains, “a football concussion, although it may not cause bleeding and rarely requires an ambulance, is at least as significant as that concussion that was sustained in a car accident, if not more so, because the athlete is more likely to experience secondary impacts.” (64) For example, in a 2007 New York Times article, Ted Johnson, a former Patriots linebacker, stated he was not given enough time to recover from a 2002 concussion. Against the team trainer’s advice, Bill Belichick ordered him to play through the concussion. Within minutes Johnson had a subsequent concussion. Over the next three years Johnson sustained several more concussions and now has bouts of severe depression that he attributes to his days of playing football. Even though an anecdotal story, this sequence of events is only too familiar throughout the NFL (Keating, “NFL Retools Approach to Concussion Research” 2).

The long-term effects of concussions have been thrown into the spotlight by the recent deaths of the retired football athletes. Termed “post-concussion syndrome,” the symptoms that are experienced long after the initial effects of the injury have subsided include episodes of dizziness, fatigue, headaches, irritability and depression. These symptoms may take weeks to resolve or may be permanent and last a lifetime. Damage from concussions can cause psychiatric disorders and loss of long-term memory. Depression is one of the most significant and emotionally debilitating effects of a concussion. Injuries occurring early in adulthood can lead to symptoms of major and minor depression lasting indefinitely (Holsinger et al. 18).

MTBIs consistently are associated with damage to the prefrontal cortex and basal ganglia. In teenagers this area of the brain is especially vulnerable when a concussion occurs, because the frontal lobe has not fully developed. In cases of concussive injury, a middle schooler’s brain may take nearly three times as long to recover from injury as an adult’s (Nowinski 45). The prefrontal cortex of the frontal lobe is responsible for decision-making and reasoning. Those with major depression consistently have “significantly reduced left prefrontal gray matter volume”(Jorge et al. 45). Imaging studies have described the association between prefrontal damage and Major Depression Disorder (Chen et al. 86). Damage to the prefrontal cortex can leave a person feeling “mentally-clouded.” The basal ganglia is used in motor control. When this area is injured fine motor movement can be affected.

MTBI’s and concussions can create cerebral atrophy in the temporal and parietal lobes, in addition to the frontal lobe, creating a significant reduction in brain mass (Guskiewicz et al., “Association between Recurrent Concussion and Late-Life Coginitive Impairment in Retired Professional Football Players” 4). The average brain could lose as much as one-third of its mass; losing 400 grams from the original 1200 grams of brain mass.

Damage to brain structures due to MTBIs can increase the likelihood of developing Parkinson’s disease, Alzheimers disease or dementia pugilistica. Genetic susceptibility also seems to be a factor as to whether these amnesia-related diseases develop. Former football player, Justin Strzelczyk, was diagnosed with dementia pugilistica. This a disorder that is characterized by scarring of brain tissue and neurofibrillary tangles throughout the cerebrum and cerebellum. As its name implies, boxing is notorious for this serious disorder and has nearly been outlawed several times because of the brain damage the sport can cause. This disease is also common in wrestlers who have suffered multiple concussions. Interestingly enough dementia pugilistica tends to onset twelve years to sixteen years after the beginning of a boxer’s career (Guskiewicz et al., “Association between Recurrent Concussion and Late-Life Coginitive Impairment in Retired Professional Football Players” 3). This time period is similar to that of many football players who begin displaying symptoms of the disease when in their late thirties and early forties. Symptoms of the disease include memory problems, dementia and lack of coordination. Further damage caused by amyloid proteins, the plaques and vascular degeneration can lead to Alzheimer’s disease. Alzheimer’s disease is a more advanced form of dementia pugilistica. The difference is that in the case of dementia pugilistica the plaques and scarring occur predominantly near the surface of the brain. In Alzheimer’s disease, the plaque is present in deeper layers of the brain. NFL veterans have a thirty-seven percent greater chance of developing Alzheimer’s disease than the average person (Nowinski 65). A former NFL football player, Andre Waters’ brain had deteriorated to the onset of Alzheimer’s, unthinkable for a man of forty-four years of age (Keating, “Concussions Research Remains Question for NFL” 1).

Additional damage can affect structures such as the substantia negra, ventral tegmental area (VTA), and hippocampus. The substantia negra is responsible for the production of dopamine and is involved in movement. Damage to this critical midbrain structure has been linked to Parkinson’s disease. People who have suffered moderate to severe head trauma are eleven times more likely to develop Parkinson’s disease (“Mayo Clinic Researchers Discover Significant Link Between Head Injury and Parkinson’s Disease” 1). A notable example of head trauma and the development of Parkinson’s disease is Muhammad Ali. The VTA is the brain’s reward center. Dopamine is also released there. Once damaged, incidents of depression are quite common. Thehippocampus is needed for long-term memory formation. Studies have demonstrated links between damage to this area of the brain with emotional outbursts and irrational behavior (Guskiewicz et al., “Association between Recurrent Concussion and Late-Life Coginitive Impairment in Retired Professional Football Players” 6).

Andre Waters and football Hall of Famer, Mike Webster, displayed similar deterioration of brain tissue. Both had the alerting amyloid plaques that are eerily reminiscent of those of the elderly diagnosed with Alzheimer’s disease. Each player became increasingly erratic with their display of emotion and logically irrational. In 1991, while still playing in the NFL, Andre Waters attempted suicide by ingesting rat poison and cold medications (Omalu et al., “Chronic Traumatic Encephalopathy in a National Football League Player: Part II” 1088). Even after years of psychotherapy, Waters made several suicide attempts. In more recent years, consumed with suicidal thoughts, he continued his self-destructive behavior. In 2007 he succeeded in committing suicide by ingesting antifreeze.

Mike Webster struggled with his psychological well being in his later years. He was unemployed, drowning in debt and occasionally homeless. A physician diagnosed him as having dementia pugilista. Mike Webster fought severe depression and succumbed to heart failure in 2002 at the age of 50 (Omalu et al., “Chronic Traumatic Encephalopathy in a National Football League Player” 130). Interestingly enough the physician wrote “chronic concussive brain injury” on his death certificate; indicating that his brain injuries had contributed to Webster’s death (Nowinski 73). Justin Strzelczyk did not have as extensive of brain damage as did Mike Webster, but he exhibited signs of irrational behavior and reckless driving that led to his death in 2004. He was in a head on collision with a semi-tractor trailer.

The most recent case in the media of irrational behavior leading to death involves the murder suicide of wrestler Chris Benoit. The acrobatic moves of professional wrestlers cause much stress to the athletes’ bodies, especially to the neck and head. Benoit even had to undergo fusion of vertebrae in his neck in 2001 (Keating, “Head-Trauma Researchers Want to Study Benoit’s Brain” 2). In the months leading up to the wrestler’s death, his behavior became increasingly odd. For example a neighbor stated that he walked around his property with a rosary around his neck. Chris’s father, Michael Benoit replied to this with, “That would have been completely out of character. He was not religious.”(Keating, “Study Suggests Brain Damage May Have Affected Benoit” 2) After murdering is wife and son, Chris Benoit placed a bible by each of their sides shortly before taking his own life. The irrational behavior is a result of altered brain chemistry. There is another piece to the puzzle left after a MTBI. Not only is the brain affected by traumatic brain injury, but the pituitary gland, which is vital to proper endocrine system function, is also affected.

After MTBI’s occur, medical staff consistently analyze symptoms of concussions. The function of the pituitary gland is almost always overlooked. Neuroendocrine dysfunction following traumatic brain injury is under-diagnosed, under-treated and may adversely affect the rate of recovery (Kelly et al. 934). Today at the college and professional levels it is not standard practice to test pituitary function, even though it is critical to homeostasis in the body (Oelke). The pea-sized pituitary gland is vital to a properly functioning endocrine system. Most commonly MTBIs affect the gonadal and growth hormone axes. The gondal axis is responsible for releasing gonadtropins that cause the release of the sex hormones, testosterone and estrogen. The growth hormone axis controls the release of growth hormone. But MTBI’s can also lead to deficiencies of hormones such as Thyroid (T4) and can induce diabetes insipidus (Benvenga, et al. 1357).

The pituitary gland is relatively well protected by the sphenoid bone of the skull, but the stalk of the gland, connecting to the hypothalamus, is susceptible to damage. Case reports of chronic pituitary dysfunction or hypopituitarism exist in which there was spontaneous recovery of the gland, but this does not seem to be the normal pattern for patients (Kelly et al. 932). Generally once the gland is damaged the effects are life lasting.

In the late 1990’s, Dr. Daniel Kelly observed in several patients the classic signs of pituitary failure; depression, fatigue and poor concentration (Lieberman et al. 2753). After publishing his findings in 2000 at least eight subsequent studies have followed in the footsteps of his research. The studies were able to confirm what he suspected, a link between traumatic brain injury and hormonal dysfunction. Deficiencies of growth hormone and testosterone (directly related to gonad hormone release) were most common. Twenty percent of the MTBI patients were deficient in growth hormone and nearly fifteen percent were deficient in testosterone. These are startling numbers for just one trauma. In the context of football MTBIs happen multiple times.

A 2004 Turkish study of boxers found forty-five percent had hypopituitarism Farrey, “The Case for HGH” 2). These numbers are representative of head trauma in the National Football League. A natural decrease of hormonal output occurs as the human body ages. After output peaks in our twenties there is a steady decrease until we are old and gray. Damaging the gland can speed up the aging process exponentially.

Several retirees of the NFL report similar symptoms as those defined by Dr. Kelly. Also signs of decreased human growth hormone (HGH) such as loss of lean muscle, bone density and increases in fat are common. “Retired Jacksonville Jaguars lineman Jeff Novak, who stays in touch with many of his former teammates: ‘I know a lot of guys with several of those symptoms’” (Farrey, “The Case for HGH” 3). It is no wonder that a majority of ex-NFL veterans don’t live to reach the age of sixty-five (Colston 2).

Supplementation of hormones is a reality for many ex-NFL players. Though controversial, hormone therapy has been shown to help offset some of the physical ailments brought about by a TBI and a damaged pituitary gland.

The most effective solution in a doctor’s arsenal against hormonal deficiency is to supplement with artificial ones. Though still considered controversial, some of the retirees are not waiting for the final approval by the medical board. Brad Leggett, a former New Orleans Saint center, has taken HGH prescribed by a doctor. Prior to treatment he was miserable and surviving on painkillers to combat an aching back. Seven years ago he decided to visit an endocrinologist and have his hormone levels checked. He was found to be deficient in testosterone and growth hormone. Since then Leggett has been given supplements of testosterone and growth hormone under the supervision of a doctor. Leggett is a living example of the results, “ ‘the aches and pains I had from playing football, I don’t have anymore’” (Farrey, “The Case for HGH” 2).

Despite the numerous studies and countless anecdotal accounts the NFL continues to deny the existence of a definitive link between mild traumatic brain injuries and long lasting effects (Milhoces 3). The NFL has conducted concussion studies. In a study headed by Dr. Pellman, then chairman of the MTBI committee, results “confirmed” “there was no evidence of worsening injury or chronic cumulative effects of multiple MTBIs in NFL players” (Keating, “See No Evil: The NFL Won’t Face Concussion Facts 2). Dr. Pellman believed that the conflicting results were inaccurate and unscientific, because surveys were used over more scientific methods. The NFL has run its own studies using samples that were not representative. Dr. Pellman authored a recent study that appeared in the prestigious medical journal Neurosurgery. It was severely biased, leaving out hundreds of neurological tests conducted on NFL players. In turn medical reviewers denounced the study, as it seemed “to be at odds with virtually all published studies dealing with concussions” (Nowinski 89).

Wayne Cherbet shortly after receiving a devastating concussion against the New York Giants.

The approach for treating NFL athletes is questionable at best. Today doctors pay for the “right” to treat players making aggressive treatment a much simpler option. Dr. Delaney explains, “At the professional level, if you practiced the most conservative guidelines, you probably wouldn’t be a pro doc very long” (Nowinski 91). Wayne Chrebet of the New York Jets was a victim of overly aggressive care, ironically given by Dr. Pellman. In a game versus the Giants, Chrebet fell to the turf from a hit and was out cold. Once he became conscious, Pellman asked if Chrebet felt well enough to play. Chrebet although dazed answered yes. Controversially Pellman put Chrebet back into the game even though pictures and video had documented that Wayne Chrebet had obviously had a serious concussion (Nowinski 88). Unfortunately for Chrebet additional concussions followed in the next few weeks. He was forced to retire within one year because of “post-concussion syndrome.”

Several outside researchers have attempted to gain cooperation from the NFL. For example Dr. Guskiewicz of North Carolina University applied for funding from the NFL, along with many others. Usually if rejected by an organization, he would receive a multiple page letter explaining how to reapply and improve his chances. The NFL rejected his application but gave no further information on how to resubmit. This is a similar trend for the authors of many other concussion-based studies (Keating, “NFL Retools Approach to Concussion Research” 2).

The NFL continues to justify its practices because if it becomes apparent that the league was placing its employees at risk, it would be a legal and financial nightmare. While doctors, including Dan Kelly, agree hormonal dysfunction testing in NFL players who have had concussions should be implemented, the NFL is far from ready. Today’s court system now looks at head trauma as a disability. Two million dollars was awarded to the Webster family for benefits that were denied him (Farrey, “The Case for HGH” 3). The court agreed that Webster’s brain damage was caused by a long career in the NFL. Many other suits would follow if the NFL acknowledged what a majority of studies suggest.

With a new NFL commissioner, Roger Goodell, comes an opportunity to change how the NFL is perceived when dealing with its players. Next season will be the first in which all thirty-two teams will be required to give baseline concussion tests. A larger empirical NFL concussion study is already underway. Only this time it is using thehelping hand of outside researchers. Could this be a change in the guard? Will the NFL finally give its players the protection they deserve? Only time will tell.

Change is needed. The NFL has left many of its gridiron greats with debilitating injuries and little financial security to show for it. The NFL, the world’s most successful sports league, has one of the worst pension plans. The MLB pays out on average thirty-six thousand dollars per year, nearly three times the amount given out by the NFL (Colston 4). A new program to give in-home care for ex-players has recently been initiated by NFL Players’ Association leader Gene Upshaw. Unfortunately this program can only sustain a small group of a few dozen players. It overlooks the thousands who have similar injuries and disorders.

Neither rule changes nor technology will save players from concussions. The only way to prevent or better treat the injuries is through education. Education can act as a catalyst for change. With a better understanding of concussions and their long-term effects, players will be more likely to speak up. Players must be willing to understand “a successful player has to play through injury but this does not apply to brain injuries” (Nowinski 130). If we want to help players avoid the horrible effects of concussions, our top priority should be to diagnose a greater amount of concussions.

The NFL must take more preventative measures to protect its current players from falling into the same fate as their predecessors. Once the league acknowledges the overwhelming evidence linking TMBIs and deteriorating effects on long-term health, more proactive measures in prevention could be taken. More preventative assessments, including pituitary screening, could greatly reduce the lasting effects of head trauma in the NFL. Merril Hoge, former NFL player and now ESPN analyst was forced to retire due to “post-concussion syndrome” expresses how he believes concussions should be treated, “In order to avoid all the pressures of the game, I still wish there were a guideline implemented in the NFL for when a guy has experienced a certain kind of concussion. For example, if his symptoms are A,B,C, then he has to sit out a week, or two weeks, etc. That would really take the pressures off the medical staff, the player, and the team” (Nowinski 82).

Soon we may even see the supplementation of testosterone and growth hormone, under a doctor’s supervision, as a viable treatment option for athletes with a history of head trauma. It is already a reality in the NFL for a small number of players with testicular disease. Additionally the World Anti-Doping Agency has granted several exemptions for use of HGH and testosterone for those with hypopituitarism (Farrey, “The Case For HGH” 4). Use of these substances could one day help a players’ body better cope with the physical nature of football. Injuries such as those that have afflicted Andre Waters and Justin Strzelczyk could be a worry of the past. America’s ultimate sport obsession could once again be loved for its violence with a clear conscience knowing that its idols will have the medical protection that they deserve.

Written By Trevor Mooney

University of Delaware


Here is Chris Nowinski’s website, an excellent resource for those interested in further reading on the topic


Benvenga, Salvatore, et al. “Hypopituitarism Secondary to Head Trauma.” The Jouranl of Clinical Endocrinology and Metabolism 85.4 (2008): 1353-1361.

Burke III, Charles J. “Sports Injuries: Concussions.” ESPN Network 29 September 2007: 4 pp. 25 March 2008. http://espn.go.com/trainingroom/s/1999/0929/85532.html.

Chen, Jen-Kai, et al. “Neural Substrates of Symptoms of Depression Following Concussion in Male Athletes With Persisting Postconcussion Symptoms.” Arch Gen Psychiatry 65.1 (2008): 81-89.

Colston, Chris. “NFL Retirees Feel Forgotten as Fight for Benefits.” USA Today 25 July 2007: 5 pp. 25 March 2008. http://www.usatoday.com/sports/football/nfl/2007-07-08-sw-retirees_N.htm.

Estes, Susie M., and Randall J Urban. “Hormonal Replacement in Patients with Brain Injury-Induced Hypopituitarism: Who, When, and How to Treat?.” Pituitary 8 (2005): 267-270.

Farrey, Tom. “The Case for HGH.” ESPN Network. 18 January 2007: 4 pp. 25 March 2008. http://sports.espn.com/nfl/new/story?id=2733919.

– – -. “Former Saint Leggett Takes HGH.” ESPN Network. 21 January 2007: 4 pp. 25 March 2008. http://sports.espn.com/nfl/new/story?id=2734254.

– – -. “Pathologist Says Waters’ Brain Tissue Had Deteriorated.” ESPN Network 19 January 2007: 2 pp. 25 March 2008. http://sports.espn.com/nfl/new/story?id=2734941.

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Keating, Peter. “Concussions Research Remains Question for NFL.” ESPN Network. 7 March 2007: 3 pp. 25 March 2008. http://sports.espn.go.com/nfl/columns?id=2790047.

– – -. “Head-Trauma Researchers Want to Study Benoit’s Brain.” ESPN Network. 30 June 2007: 3 pp. 25 March 2008. http://sports.espn.com/nfl/new/story?id=2920925.

– – -. “NFL Retools Approach to Concussion Research.” ESPN Network. 20 April 2007: 3 pp. 25 March 2008. http://sports.espn.go.com/nfl/news/story?id=2844041.

– – -. “See No Evil: The NFL Won’t Face Concussion Facts.” ESPN Network 19 January 2007: 3 pp. 25 March 2008. http://sports.espn.com/nfl/new/story?id=2736505.

– – -. “Study Suggests Brain Damage May Have Affected Benoit.” ESPN Network. 6 September 2007: 3 pp. 25 March 2008. http://sports.espn.com/nfl/new/story?id=3005520.

Kelly, Daniel F., et al. “Neurobehavioral and Quality of Life Changes Associated with Growth Hormone Insufficiency after Complicated Mild, Moderate, or Severe Traumatic Brain Injury.” Journal of Neurotrauma 23.6 (2006): 929-938. Trevor Mooney went to the University of Delaware and Received an Honors Bachelor’s of Science in Economics Degree

Klein, Milton J. “Post Head Injury Endocrine Complications.” eMedicine. 16 March 2006: 20 pp. 25 March 2008. http://www.emedicine.com/pmr/topic109.htm.

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Oelke, Brian. Personal Interview. 6 April 2008.

Omalu, Bennett I, et al. “Chronic Traumatic Encephalopathy in a National Football League Player.” Neurosurgery 57.1 (2005): 128-134.

Omalu, Bennett I, et al. “Chronic Traumatic Encephalopathy in a National Football League Player: Part II.” Neurosurgery 59.5 (2006): 1086-1093.

Schneider, Manfred, Harald J. Schneider, and Gunter K. Stalla. “Anterior Pituitary Hormone Abnormalities following Traumatic Brain Injury.” Journal of Neurotrauma 22.9 (2005): 937-946. Trevor Mooney Tight End University of Delaware 84

Trevor Mooney played at the University of Delaware as a Tight End #84

Trevor Mooney played college football at the University of Delaware as a tight end #84 and was a member of the ESPN Academic All-Region team and ESPN All-American Finalist.