Nutrition Tips for the Teenage Athlete

nutrition for student athletes

By Tara Hackney, PT, DPT, OCS, KTTP for Athletico Physical Therapy

During the school year it is common for teenage athletes to find their schedules jammed packed with class, homework, practice and competition. When students are this busy, eating can be overlooked. Sometimes meals are skipped or home-cooked meals are substituted for fast food while running from one practice to another. Proper nutrition is important as the food we eat becomes the fuel for our bodies.

Athletes have unique needs compared to their less active peers. Athletes need more calories each day for proper performance and teenage athletes also need to meet their body’s growing requirements. Teenage athletes may need 2,000-5,000 total calories per day depending on how active they are. A well balanced diet of protein, fats, carbohydrates, vitamins and minerals, as well as proper hydration, will ensure a teenage athlete will meet their body’s energy demands.

What Can Happen if Athletes Don’t Have Proper Nutrition?

  • Less likely to achieve peak performance
  • May breakdown rather than build up muscles
  • May not be as fast or strong
  • May not maintain their weight
  • In extreme conditions, athletes can be at increased risk for fractures or growth problems

Healthy Eating Tips for Teen Athletes:

  1. Eat a meal with protein and carbohydrates 2-4 hours before practice or competition.
    -Examples: turkey or chicken sandwich, milk and cereal, pasta with tomato sauce
  2. If you don’t have time for a full meal, eat a snack if less than 2 hours before your practice or competition.
    – Examples: melons, cherries, low fat yogurt, bagel, carrots, crackers
  3. Consider not eating anything 1 hour before practice as digestion takes energy and leaving food in your stomach can make you feel bloated or cause abdominal cramping
  4. Sugary snacks and drinks can give you a quick burst of energy but also lead to a “crash” before the end of practice.
    – Sugary snacks and drinks also do not provide proper nutrients
  5. Your body needs fats for energy and to function properly. However, since fats can also slow down digestion, it is best to avoid a high fat meal too close to practice or competition.
  6. Although fast food is easy to grab and go, it has a lot of excess “empty” calories that don’t necessarily provide proper nutrition.
    – There are ways to make fast food a “better” option, such as grilled chicken, eliminating the bun, and being careful of extra add-on items like cheese, bacon, etc.
  7. Water is important to stay hydrated, including replacing what is lost as we perspire during exercise.
    – Athletes benefit from drinking water before, after and during practice (every 15-20 minutes during practice)
  8. Sports drinks can be beneficial when exercising for more than 60-90 minutes in hot weather.
  9. Avoid energy drinks before exercise. They contain caffeine, a diuretic, which can contribute to dehydration.

If you would like to learn more from an Athletico physical therapist, please use the button below to request an appointment!

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The Power of Simulated Altitude Training for Athletes at all levels

Dr. Gregory Nicholson and Steve Kashul talk with Sharone Aharone about the power of simulated altitude training for pro athletes and well as weekend warriors. Sharone is a USA Triathlon Level III Elite coach and the Owner/Head Coach of Well-Fit Performance in Chicago Illinois.

Well-Fit Training Center is Chicago’s oldest and most widely known provider of Multi-sport coaching and personal training. Well-Fit was founded by Sharone Aharon, a former special forces commander and a secret service agent, in 1998 and operated on a “consulting” basis. The mission is to help people and coaches of all ages and abilities discover their inner potential and perform at their personal best. 

Sharone’s competitive and coaching history expands more than 30 years. Starting in 1988, Sharone has competed in some of the first triathlon races in Israel.  To date, he has competed in dozens of running events, qualified for the Boston Marathon, completed seven Ironman distance races, including three Ironman World Championships in Kona, Hawaii.

Sports Medicine Weekly on 670 The Score

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Off-season training for Amateur Golfers

Image result for off season golf workout program

Dr. Nikhil Verma from Midwest Orthopaedics at Rush and Steve Kashul talk with James Standhardt about workout programs for amateur golfers leading into the off-season.

James graduated from the Professional Golf Management program at Ferris StateJames Standhardt University and acquired his PGA membership in 2006. He has been teaching at GOLFTEC for 11 years in the Naperville learning center and is the Director of Instruction.

He has received the Outstanding Achievement Award for Instruction from 2011-2016.

Sports Medicine Weekly on 670 The Score

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How Exercise Might “Clean” the Alzheimer’s Brain

How Exercise Might "Clean" the Alzheimer's Brain

For the 50 million individuals worldwide ailing from Alzheimer’s disease, the announcements by pharmaceutical giants earlier this year that they will end research on therapeutics were devastating. The news is even more devastating considering projections that 100 million more people will be diagnosed with Alzheimer’s disease across the globe by 2050, all potentially without a medical means to better their quality of life.

As it happens, though, the pursuit of a therapeutic has been given a lifeline. New research shows that physical exercise can “clean up” the hostile environments in the brains of Alzheimer’s mice, allowing new nerve cells in the hippocampus, the brain structure involved in memory and learning, to enable cognitive improvements, such as learning and memory. These findings imply that pharmacological agents that enrich the hippocampal environment to boost cell growth and survival might be effective to recuperate brain health and function in human Alzheimer’s disease patients.

The brain of an individual with Alzheimer’s disease is a harsh place filled with buildups of harmful nerve cell junk—amyloid plaques and neurofibrillary tangles—and dramatic loss of nerve cells and connections that occur with severe cognitive decline, such as memory loss. Targeting and disrupting this harmful junk, specifically amyloid plaques, to restore brain function has been the basis of many failed clinical trials. This futility has led to a re-evaluation of the amyloid hypothesis—the central dogma for Alzheimer’s disease pathology based on the toxic accumulation of amyloid plaques.

At the same time, there have been traces of evidence for exercise playing a preventative role in Alzheimer’s disease, but exactly how this occurs and how to take advantage of it therapeutically has remained elusive. Exercise has been shown to create biochemical changes that fertilize the brain’s environment to mend nerve cell health. Additionally, exercise induces restorative changes relevant to Alzheimer’s disease pathology with improved nerve cell growth and connectivity in the hippocampus, a process called adult hippocampal neurogenesis. For these reasons, the authors Choi et al. explored whether exercise-induced effects and hippocampal nerve cell growth could be utilized for therapeutic purposes in Alzheimer’s disease to restore brain function.

The researchers found that exercised animals from a mouse model of Alzheimer’s had greatly enhanced memory compared to sedentary ones due to improved adult hippocampal neurogenesis and a rise in amounts of a specific molecule that promotes brain cell growth called BDNF.  Importantly, they could recover brain function, specifically memory, in mice with Alzheimer’s disease but without exercise by increasing hippocampal cell growth and BDNF levels using a combination of genetic—injecting a virus—and pharmacological means. On the other hand, blocking hippocampal neurogenesis early in Alzheimer’s worsened nerve cell health later in stages, leading to degeneration of the hippocampus and, subsequently, memory function. This provides preclinical proof of concept that a combination of drugs that increase adult hippocampal neurogenesis and BDNF levels could be disease-modifying or prevent Alzheimer’s disease altogether.

With this work, things don’t look promising for the amyloid hypothesis—that Alzheimer’s disease is caused by the deposition of amyloid plaques. In this study, it was shown that eliminating amyloid plaques were not to necessary to ameliorate memory defects, which is consistent with evidence that plaques can also be found in the brains of healthy individuals. On the contrary, we may be looking at a new and improved fundamental theory for Alzheimer’s disease based on promoting a healthier brain environment and adult hippocampal neurogenesis.

However, this inspiring news should be taken with an important caution—mouse models of Alzheimer’s are notorious for failing to translate into humans such that treatments that have worked to remedy mice have failed for humans. Besides, even if these findings translate into humans, it may apply to a fraction of Alzheimer’s individuals with relevant genetic components to the mouse model utilized. Future studies will need to replicate these results in mouse models emulating the range of known Alzheimer’s disease genetic milieus and, more importantly, prove its medical relevance to human disease.

Before translating these findings into human patients, there remains significant research to establish that a medication or drug could mimic the effects of exercise—exercise mimetics—by “cleaning up” the brain with BDNF and stimulating neurogenesis to combat Alzheimer’s disease. Currently, the method for administering BDNF to animals in the lab—by direct injection into the brain—is not ideal for use in people, and a hippocampal neurogenesis stimulating compound remains elusive.

Future attempts to generate pharmacological means to imitate and heighten the benefits of exercise—exercise mimetics—to increase adult hippocampal neurogenesis in addition to BDNF may someday provide an effective means of improving cognition in people with Alzheimer’s disease. Moreover, increasing neurogenesis in the earliest stages of the disease may protect against neuronal cell death later in the disease, providing a potentially powerful disease-modifying treatment strategy.

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