Research Review: Ulnar and Median Nerve Palsy in Cyclists

Posted on July 31, 2015 by Alynn Kakuk

Ulnar and Median Nerve Palsy in Cyclists

Patterson JM, Jaggars MM, Boyer MI. Ulnar and median nerve palsy in long-distance cyclists. A prospective study. Am J Sports Med. 2003 Jul-Aug;31(4):585-9. PubMed PMID: 12860549. 

http://www.ncbi.nlm.nih.gov/pubmed/?term=12860549

 

Summary:

Prior to this study in 2003, there have been case studies and descriptions of “cyclist palsy” (ulnar nerve compression at Guyon’s canal in cyclist) in medical literature but there has been no research to determine the prevalence of cyclist palsy. The ulnar nerve courses in the medial forearm and gives off the dorsal cutaneous branch of the ulnar nerve prior to travelling through Guyon’s canal, thus the dorsal cutaneous branch of the ulnar nerve is preserved in cyclist palsy. There are several branches of the ulnar nerve in the hand including the motor branch to the hypothenar muscles, deep motor branch of ulnar nerve, and sensory component of the ulnar nerve. Understanding of the complex anatomy of the ulnar nerve provides better localization of nerve lesions. The authors of the study randomly chose 25 riders who were participating in a 600 km bicycle ride to complete a questionnaire and obtained baseline ulnar and median nerve (motor and sensory) function (with extensive motor and sensory testing). After completing the 600 km bicycle ride, the subjects had repeat nerve testing and questionnaires. Subjects were almost equal male:female (13:12), average age 33.7, cycled on average 139 km/week, mostly intermediate level cyclists (13/25), and without systemic illness (HIV/AIDS, diabetes, thyroid disease or neurological). Three riders had symptoms of nerve compression prior to the study (numbness in ulnar nerve distribution in one hand, +Phalen’s in one hand, and numbness in digits 4-5 with elbow provocative testing in three separate subjects). After the 600 kn bicycle ride, 36% of subjects had motor symptoms, 10% had sensory symptoms, and 24% in both motor and sensory symptoms. Only 30% of subjects had neither sensory nor motor symptoms. The authors concluded that there was no difference in symptoms in rider ability or whether mountain or road cyclist when assess motor function. There was however a greater incidence of sensory changes in mountain bikers, which the authors discuss, may be due to less handlebar positions. With fewer positions, riders may not be readjusting hands as frequently causing more compression on nerve.

 

Questions for discussion:

  1. This study suggests that cyclist palsy is very common with 70% of the subjects having either sensory or motor symptoms. This was a very small study with only 25 subjects. Is the prevalence of cyclist palsy in all cyclists? What is the prevalence of cyclist palsy in professional cyclists?
  2. In this study, there was no difference in motor symptoms but there was a difference in sensory symptoms in mountain bikers compared to road cyclist. The authors discuss this could be due less options for hand positioning in mountain bike bars. Would the use of bar ends, togs (http://togs.com/pages/wholesale-usa) or an ergonomical grip (such as http://www.ergon-bike.com/us/en/product/gp1) change the symptoms of nerve compression?
  3. This study was performed over a short time period. How long do subjects have the symptoms of nerve compression and is there any electrodiagnostic evidence of nerve injury.

 

Author: Alexandra Flis, MD

Research Review: Endofibrosis of the Iliac Arteries

Posted on July 22, 2015 by Alynn Kakuk

The Danger of the Drops- A Review of Peach et al. 2011

A Question

Bradley Wiggins broke the world record for longest distance covered on a bicycle in one hour by riding 54.526km on June 7th, 2015. Because 90% of the resistance when biking on a level surface above 12mph comes from air drag and 70% of that drag comes from the rider [1], significant attention was paid to finding the most aerodynamic bike fit possible for Bradley. Among other things, this position included a lot of forward bend and flexion at the hips.

As a bike fitter in Oakland California, I spend a lot more time fitting people to climb hills than to time trial, but I do see a fair number of triathletes for whom the generally level cycling courses make aerodynamics paramount. I've heard that spending a lot of time exercising in this bent over position can cause thickening of the walls of the large arteries in the abdomen.

When I fit someone in an aggressive amount of hip flexion and forward bend, am I putting them at risk for vascular damage? As usual, I turned to the research literature to find the answer.

Some Data

A group of vascular surgeons and sports scientists in the UK and Netherlands published a systematic review on all the research on iliac artery damage during endurance exercise [2]. They found 47 relevant studies, the highest quality studies were case-control studies with no randomized controlled trials found on the topic. Most of the cases they found were of young endurance athletes with exercise induced cramping that didn't improve with physical therapy. What was going on with these athletes? To understand this problem, we'll need to cover a little anatomy first.

Where is the external iliac artery?

The external common iliac arteriers are a pair of large blood vessels that come off the aorta and the external iliac branch supplies fresh oxygenated blood to the legs. All the blood to the quads, lower hamstrings and everything below the knee comes from this artery.

Untitled Image from the Visible Body ipad app

What limits blood flow in the iliac artery in otherwise healthy endurance athletes?

Endofibrosis is a thickening of the inner wall of the blood vessel called the tunica intima. This thickening makes the internal diameter of the blood vessel smaller and thus limits blood flow. The thickening is usally 2-6cm long and 90% occur in the external iliac artery. Most cases (85%) occur on only one side of the body with the left begin more commonly affect than the right (52% to  90% left sided depending on the study).

What causes endofibrosis of the external iliac artery?

Many causes have been proposed, here are the most common

  1. Repetitive stretching and bending of the arteries while exercising in a bent-over position.The problem is most common in speed skaters and endurance cyclists.
  2. Enlargement of the psoas muscle under the external iliac artery.The larger the psoas muscle the more it will push up on the external iliac artery, causing it to bend at a sharper angle. Cyclists with endrofibrosis have been found to have a thigh circumference 3cm larger on the affected side.
  3. Fixation of the psoas muscle.Excessive fascial connetions, scar tissue or even the extra blood vessels the grow into the psoas from training can tether the artery and make it kink.
  4. Unusually long iliac arteries.A longer artery has to kink more to fit in the same space. The length of the artery is most likely genetic.  A very long artery can cause kinking that limits blood flow even without endofibrosis.
  5. Unique systemic factors.Diabetes compromises the vessel walls. Abnormal methionine metabolism has been found in 75% of one cohort of patients with endofibrosis

Untitled2This image from the Visible Body ipad app shows how the external iliac artery makes a sharp turn along the back side of the abdomen before exiting the front of the pelvis.

How Common is Iliac Artery Blood Flow Impairment?

In the general population the condition is very rare, in elite endurance athletes it may be as high as 10-20% although the difficulty in diagnosis make estimates uncertain. A survey of cyclists with the condition found that:

  • All of the cyclists had ridden an average of 9,009-12,427 miles per year (14,500 to 20,000 km/yr) for many years. That's 173 to 239 miles per week year after year.
  • 88% were men, but this may be skewed by the fact that there are more male elite endurance athletes

This rare condition is most common in cyclists but has also been reported in other sports with a bend-over posture such as speed skating, and cross-country skiing, but a few cases have been reported in sports that are more upright such as endurance running, rugby, soccer, and body building.

Am I at risk?

The most common symptom is a cramp and a feeling of swelling, numbness or pain in the buttock, thigh or calf on one side of the body.  The pain may be mild. Professional cyclists Hayden Godfrey described his symptoms of endofibrosis as feeling like his leg was falling asleep and losing power. Because these  symptoms are somewhat vague and tend to go away after exercise and because endurance athletes are accustomed to feeling discomfort in their legs,  people tend to go un-diagnosed for a long time.

Fortunately Schep et al. reviewed the research and found that when all of the following four signs and symptoms  were present, they were able to correctly diagnose iliac endodfibrosis 79% of the time [3].

Four signs and symptoms that leg cramping, swelling, numbness or pain is coming from endofibrosis:

  • The complaint goes away less than 5 minutes after stopping exercise. More than 3 out of the 6 major leg muscles are involved. (sens: 0.97,  spec: 0.29)
  • More than 3 out of the six major muscle of the leg are involved (sens: 0.48, spec: 0.94)
  • Femoral bruit with hip in extension- Abnormal blood vessel sounds found using a stethoscope (sens: 0.36, spec: 0.94)
  • Normal lower back flexibility (sens: 0.91, spec: 0.29)

What is the treatment?

If you are concerned that you may have this condition, schedule an appointment with your doctor to discuss it. Further testing may be warranted such as measuring blood pressure at the arms and ankles immediately after cycling. Treatments vary depending on the cause of the blood flow restriction.

Ankle Brachial Index- Wikipedia Creative Commons

Untitled3Blood pressure is compared between arms to detect arterial blood flow limitations. Wikipedia.

For minor cases in cyclists the following treatments are often sufficient:

  • reducing the hip flexion angle by
    • spending less time in the drops
    • moving the saddle forward
    • raising the handlebars
  • reducing psoas hypertrophy by not pulling up on the pedals
  • reducing riding time

Ryan Cox- Wikipedia creative commons license

More severe cases may require one to give up cycling or undergo surgery to continue cycling.  Many professional cyclists have undergone surgery for arterial endofibrosis and have returned to professional competition without incident. However, Ryan Cox's tragic death on August 1st 2007 at age 28 from endofibrosis surgical complications is a painful reminder of the risks of this condition.

Conclusion

I think it is worth emphasizing that this is a rare condition outside of professional cycling and speed skating. If you are cycling less than 173 miles per week and/or your position is not extremely low (ie your thigh is not hitting your chest) then it seems you have little to worry about. It is the combination of a low position and high mileage that increase the risk for this condition. Elite cyclists and high mileage recreational riders (ie Iron Man triathletes) should take any lower extremity symptoms seriously and seek medical attention as the condition does not improve on its own.

References

  1.  Burke,E. Serious Cycling 2nd ed. Human Kinetics 2002
  2. Peach- Endofibrosis and Kinking of the Iliac Arteries in Athletes- A Systematic Review. 2011
  3. Schep G, Schmikli SL, Bender MH, Mosterd WL, Hammacher ER, Wijn PF. Recognising
    vascular causes of leg complaints in endurance athletes. Part 1: validation
    of a decision algorithm. Int J Sports Med 2002;23(5):313e21
  4. Schep G, Bender MH, Schmikli SL, Mosterd WL, Hammacher ER, Scheltinga M,
    et al. Recognising vascular causes of leg complaints in endurance athletes. Part
    2: the value of patient history, physical examination, cycling exercise test and
    echo-Doppler examination. Int J Sports Med 2002;23(5):322e8

About the Author: Bryan Ausinheiler is a physical therapist, personal trainer and bike fitter with a clinic and studio in Oakland California.

 

Ride the track at MOCC 2015

Posted on July 21, 2015 by Courtney Barnes
Remember to turn left!!!
The Medicine of Cycling Conference is excited to announce the Friday night reception sponsored by USA Cycling  at the 7-Eleven Velodrome in Colorado Springs onAugust 14.  This will be a fun and exciting way to start the conference, mingle with the attendees and USA Cycling staff as well as ride the track.  This is in addition to the USA Cycling sponsored ride in Garden of the Gods on Saturday afternoon as well as the traditional dinner at Marigold.
Register now for the conference. time is running out.  http://www.medicineofcycling.com/conference/

MOCC 2015: Only TWO days left for the early bird registration rate

Posted on July 15, 2015 by Courtney Barnes

With the upcoming Medicine of Cycling Conference only a month away, we are nearing the end of our early bird registration rate will expire on July 18th, only TWO days away.   Register soon to get the reduced rate! http://www.ucsfcme.com/2016/MMJ16002/info.html

Only 1 Week Left to Submit Your Abstracts

Posted on June 3, 2015 by Alynn Kakuk

The Medicine of Cycling Conference is a great venue to share your research and to learn from others' novel findings! We welcome all types of research, as long as it is relevant to cycling medicine or rehabilitation. Please consider sharing your research! For more information regarding abstract submission: http://www.medicineofcycling.com/blog/abstract-submission-deadline-extended/less

Abstract Submission Deadline Extended!

Posted on May 4, 2015 by Alynn Kakuk

Call for Abstracts for 2015 Medicine of Cycling Conference

The deadline for abstract submissions for the 2015 Medicine of Cycling conference in Colorado Springs has been extended to June 10, 2015!  We encourage you and your colleagues to submit your original research for consideration for oral or poster presentations at our annual conference on August 14-16, 2015 in Colorado Springs, CO.

 

We encourage abstract proposals in a variety of areas, however, the abstract must be relevant to cycling medicine.  Both quantitative (including data) and qualitative (program descriptions, educational interventions, etc) are acceptable, but published data cannot be submitted.  Submitted abstracts will be reviewed for relevance and quality, and highly ranked abstracts will be invited to give an oral presentation (limited to 10-minute presentation followed by a 5-minute Q&A).  Some abstracts may be invited to provide a poster presentation.  Research presentations are likely to occur on August 15th.

 

The following prizes will be awarded:

2 Best Student/Resident/Fellow Abstract Award: 2015 waived conference fee

1 Best Professional Abstract: 2015 waived conference fee

The waived conference fee is contingent upon presenting at the conference.

 

Guidelines:

Abstracts must be no longer than 300 words (excluding a single Table or Figure) and should address the following:

  • Objective
  • Methods
  • Results
  • Significance to Cycling Medicine

Please include full author names, degrees and institutional affiliation if applicable.  Authors of accepted abstracts will be asked to disclose potential conflicts of interests.

 

Deadlines:

Abstract Submission Deadline:  June 10th, 2015

Abstract Acceptance/Non-acceptance email notifications: June 30th, 2015

 

Abstracts should be submitted via email to Alynn Kakuk, DPT at alynn@medicineofcycling.com.

Members of the Research Task Force will be involved in the selection process.

 

We look forward to your submissions!

 

Sincerely,

Medicine of Cycling Research Task Force

Research Blog: Exercise Induced Increases in Cell Free DNA

Posted on April 23, 2015 by Alynn Kakuk

Article Review: Exercise-induced increases in cell free DNA in human plasma originate predominantly from cells of the hematopoietic lineage

Tug S, Helmig S, Deichmann ER, Schmeier-Jurchott A, Wagner E, Zimmerman T et al. Exercise-induced increases in cell free DNA in human plasma originate predominantly from cells of the hematopoietic lineage. Exerc Immunol Rev, 2015;21: 164-173.

http://www.medizin.uni-tuebingen.de/transfusionsmedizin/institut/eir/content/2015/164/article.pdf

Article Summary:

The authors utilize sex-mismatched transplantation patients to analyze the origin of cell-free DNA (cfDNA) increases after a treadmill exercise test. During normal physiologic states, roughly 1-50ng of fragmented DNA can be found extracellularly per milliliter of plasma. During exercise, this value increases, upwards of 20-fold. Recently, cfDNA has gained popularity as a biomarker for chromosomal abnormalities during pregnancy, as the fetus and placenta both contribute to cfDNA. It has also been suggested as a biomarker for cancers and autoimmune diseases, as both instances lead to a raise in total cfDNA. While it is known from transfusion studies that under normal conditions, most cfDNA is of hematopoietic origin, there currently is no good method to determine the origin of cfDNA.

Many studies use cfDNA collected from subjects after exercise, since they are able to collect higher quantities. However, since we do not know if the origin of this DNA is the same as at normal conditions, this collection technique could potentially bias cfDNA studies. Tug et al. recruited five female HSCT patients who received from male donors, two male HSCT patients who received from female donors, five females who received a liver transplant from a male donor, and three male and female controls. The researchers collected blood from the antecubital vein before, immediately after, and 90 minutes after an incremental treadmill test, and measured nuclear and Y chromosomal cfDNA via qPCR.

In the male patients with female donors, only +5.5ng/ml and -2.6ng/ml changes were found in Y-chromosomal DNA, suggesting that most of the increase was from the transplanted hematopoietic cells. However, in the five female patients with male donors, the data only accounts for about half of the total cfDNA. They suggest that this could be due to lack of sensitivity of their qPCR assay or that it could reflect the success of grafting. Regardless, while the data support that the rise in cfDNA is likely due to DNA from hematopoietic lineage, it is far from conclusive.

Questions for Discussion:

  1. This study was conducted in accordance with a short incremental treadmill test. While this test has been shown to lead to increases in cfDNA, much larger increases have been identified during endurance exercise such as marathon running and cycling. Will the hematopoietic origin hold true during these endurance events? During marathons, there is evidence of liver and gall bladder damage (Wu 2004), kidney dysfunction (Neyiackas 1981), vascular damage (Fagerhol 2005) and brain damage (Marchi 2003). As novel methods for analyzing cfDNA are developed, it would be interesting to determine whether these systems are contributing to the increase during endurance exercise.
  2. How could the authors have improved their quantification assay? While only accounting for <50% of cfDNA, it is hard to make the claim that most of the cfDNA comes from one lineage. A better assay for copy number variation in Y-chromosomal and nuclear DNA could help to greatly increase sensitivity.
  3. This is an amazing patient cohort for addressing the question of cfDNA origin. What additional types of experiments could be conducted to better address the question? For example, could the study be repeated with strength vs. endurance exercise, as they are suggested to have different mechanisms?

 

Written By: Jason Klein

Reviewed By: Paul Nelson, PT

Research Blog: Strategies for Maintaining Muscle Mass When Injured

Posted on March 14, 2015 by Alynn Kakuk

Article Review:

Strategies to maintain skeletal muscle mass in the injured athlete: Nutritional considerations and exercise mimetics

Benjamin T. Wall, James P. Morton & Luc J. C. van Loon (2015) Strategies to maintain skeletal muscle mass in the injured athlete: Nutritional considerations and exercise mimetics, European Journal of Sport Science, 15:1, 53-62.

http://www.ncbi.nlm.nih.gov/pubmed/25027662 

Article Summary:

Injuries in cycling can be caused by crashes, overuse or from poor bike fit. Regardless of the cause of a severe injury, recovery often involves a period of immobilization and associated muscle disuse, which can result in a rapid muscle loss and reduced functional capacity.

The decline in muscle mass and strength is most profound during the first 1–2 weeks post-injury, when interventions are not conventionally considered a priority for the athlete. The muscle loss is primarily due to a reduction in basal muscle protein synthesis rate and the development of anabolic resistance to dietary protein intake.

Although further work is required to translate research findings directly to managing athlete injuries, the following recommendations are presented for practitioners to limit the loss of muscle after injury in their athletes.

Key nutritional considerations during the period of disuse:

  • Daily protein intake of 1.6–2.5 g per kg of body mass:
    • Ideally through regular (4-6 times daily, every 3-4 hrs) consumption of adequate amounts (20–35 g) of rapidly digested protein sources with a high content of the branched chain amino-acid, leucine (2.5–3 g); and
    • Including dietary protein with breakfast and prior to sleep.
  • Intake of specific nutritional compounds that may also promote the maintenance of muscle protein synthesis rates such as:
    • omega-3 fatty acids, branched chain amino acids (including leucine), creatine, and HMB (a metabolite of leucine).
  • It is challenging for athletes to achieve optimal macronutrient intakes to maintain skeletal muscle mass but prevent any gains in fat mass, due to the reduced energy expenditure during the recovery period.

Additional interventions that can attenuate muscle loss, include:

  • Utilizing neuromuscular electrical stimulation (NMES) to invoke involuntary muscle contractions, which can stimulate muscle protein synthesis rates.
  • Prescribing an exercise stimulus (particularly resistance exercise) for the uninjured muscle groups to minimize or prevent unwanted reductions in regional muscle mass that may result in reduced whole-body muscle mass and affect metabolic function. 

Questions for Discussion:

Recovery from cycling injuries may involve total or partial immobilization. What are the major causes of injury in cyclists that cause total or partial immobilization? What are specific considerations for an injured cyclist during rehabilitation?

NMES represents a practical strategy for maintaining a degree of physical activity during the early stages of recovery from injury. The potential for structured and supervised NMES to maintain muscle protein synthesis rates, metabolic health and muscle mass and function during more prolonged rehabilitation requires future investigation. It would be worthwhile to consider developing optimal parameters for NMES protocols, in terms of duration, stimulation intensity and other specific parameters, for recovery from common cycling injuries.

In addition, although beyond the scope of this article, recent studies have examined the effect of NMES on post-exercise recovery. Future work to develop parameters for NMES could also investigate the potential benefits of NMES and optimal protocols for post-race recovery for cyclists competing in stage races.

The summarized dietary manipulations can help to minimize muscle loss during injury. What are the effects of these manipulations on long-term recovery of muscle mass and strength?

Future studies are warranted to enhance our understanding of how the known acute effects of dietary manipulation impact upon long-term measures of muscle mass, function, rehabilitation time and the duration required to return to competition.

Written By: Felice Beitzel, PhD, LMT

Reviewed By: Alexandra Flis, MD

Research Blog: Aerobic Fitness Variables

Posted on March 2, 2015 by Alynn Kakuk

Article Review: Aerobic fitness variables do not predict the professional career of young cyclists.

Menaspà P1, Sassi A, Impellizzeri FM. Aerobic fitness variables do not predict the professional career of young cyclists. Med Sci Sports Exerc, 2010;42(4):805-12.

http://www.ncbi.nlm.nih.gov/pubmed/19952851

Article Summary:
In sport, organizations look to the junior ranks for new talent. Predicting who will become a successful professional athlete based on their performance in the junior ranks is difficult (e.g. In American football, Tom Brady was a 6th round draft pick and is now considered one of the all time greats). Individual aerobic capacity is thought to be more important in a sport such as cycling, The goal of this study was to determine if aerobic fitness variables derived from traditional VO2 max testing could predict future success as a pro cyclist.

The study used retrospective data (1996-2002) from metabolic testing performed on 309 cyclists ages 17 to 18. Seventy two of the juniors competed for their respective national cycling team. In December 2008, researchers looked at their cycling careers. Cyclists were considered to be a professional cyclist if they had been on a UCI team for at least three years. Further, professional cyclists were subdivided into further categories including lower ranked professionals versus ProTour cyclists and their cycling style (climber versus sprinter versus time trialist).

Overall, none of the six measurements derived from V02 max testing nor any of the anthropometric variables was predictive of either becoming a professional cyclist or success at the professional level. There were some trends noted for some variables that may increase or decrease the odds of success, especially for particular cycling styles. Other factors including economy, anaerobic characteristics, technical ability, tactical skills, mental fatigue, perception of effort and ability to recover are likely all other important variables for excelling at the professional level.

Questions for Discussion

1) I’m assuming this study was done only on male cyclists (it’s not clear in the paper but that’s my inference.). Would these same findings hold true for young female cyclists?

2) The role of doping and performance enhancing drugs is unclear. This paper was published in 2010. At the time, none of the cyclists who went on to pro careers had tested positive for performance enhancing drugs. Now that it’s 2015 and more facts have come out about doping at the professional level during this period, does the study still hold true? Was success as a professional based primarily on the athlete’s decision to use PEDs?

3) The average VO2 max of the juniors tested here was quite high (50th percentile VO2 max was 71.4 and the 10th percentile VO2 max as 62.4- still fairly high). How would this study look if the study was performed on a group of youth cyclists with a wider range of physiologic variables?

4) In light of athlete progression into the pro-tour who have previously tested below 62.4 VO2 max, FTP 60 and 20 mins average, how do we manage testing/quantifying young riders to ensure that ‘the numbers’ are developed alongside attributes such as tactical awareness, determination, ability to suffer and pure grit. More ‘purist’ European teams often quote these as key aspects of selection, often at the expense of watts and VO2 max etc.

Written by: Andy Pasternak, MD, MS

Reviewed by: Graham Theobald, BSc. (Hons), MSST

Research Blog: Biking and Bone Health

Posted on February 9, 2015 by Alynn Kakuk

A RESEARCH REVIEW

Biking and Bone Health: The Facts

 

A QUESTION

The street in front of our house turns sharply and soon my wife and I are punishing the drive train of our tandem up a 12% grade. At a combined weight of 330lbs and a combined continuous rep pull-up max of 35 reps, we clearly aren't your average bike monkeys. Nay, we are the larger, slower moving apes of the cycling world.

A spindly 130lb man flies past us up the hill with a weathered face that could say either 50+ years or 500,000 miles on a bicycle. He is clearly the master of this hill. His chiseled quads don't look weak, but as a physical therapist, I wonder about his bones. I have heard of professional cyclists having low bone density and shattering hips on falls that wouldn’t have broken the average person’s bones. I’ve heard that because of the high cadence even a power output of 300w only produces about 100lb of force per stroke; less bone-stimulating weight bearing force than walking. But what does the research say? Is cycling bad for your bones?

SOME BACKGROUND

Bone is living tissue, it is constantly being broken down and rebuilt, piece by piece. Cells called osteoclasts eat away at the bone and cells called osteoblasts make new bone. Over the course of 7-10 years the entire bone will be replaced. The balance of bone breakdown and bone rebuilding is determined by internal and external factors. Low bone density is called osteopenia, dangerously low bone density is called osteoporosis. Here are some of the most important factors:

Internal:
• Estrogen promotes more bone growth, a drop in estrogen results in a drop in bone density.
• Cortisol results in a reduction in bone growth and thus prolonged cortisol results in lowering bone density. Cortisol is the hormone released when the body is under stress.
• Age: After around age 30, slightly more bone is broken down than rebuilt and bone density declines with age.
• Diet: If one doesn't eat enough calcium (<1000mg/day), or doesn't get enough vitamin-D ( • Genetics: Genetic factors affect

External:
• Repetitive impact such as running or weight lifting breaks down bone, but this same impact signals the osteoblasts to make more bone and they usually end up making more than was damaged. The larger the weight (including the body weight), the more impact and thus the more bone growth.

SOME DATA

To answer my questions about bone density and cycling I searched through google scholar and PubMed until I found a Systematic Review on Cycling and Bone Health published in 2012 by Hugo Olmedillas and his research group in Spain [1]. They group examined all of the recent research and came to these conclusions

It’s True
People who just ride a road bike all the time, really do have worse bone density and it only gets worse with time

• 2/3 of the professional and master adult road cyclists could be classified as osteopenic [2]
• Both in professional and recreational cyclists, bone density has been found to be lower than in the general population [3,4]
• Nichols compared cylists to age-matched non-athletes. The cyclists lost more bone density over the course of the seven year study [4]
• Bone density in competitive cyclists gets worse as the racing season progresses [5]
• Low levels of bone density earlier in life may contribute to dangerously low levels (osteoporosis) later in life [6]

Some impact is better than none
Almost any exercise is better for your bones than just endurance cycling (except maybe swimming)

• Wilks et all found that sprint trained cyclists had higher bone density than endurance trained cyclists [7]
• Mountain bikers have been found to have better bone density than road cyclists. [13]
• Weightlifting builds bone density more than anything else [8].
• Duathletes and Triathletes had higher bone density than those who only did endurance cycling. [1]
• Adolescent runners had better bone density than their peers who were cyclists or non-athletes [9].

Nutrition
You can't just take more calcium. But a greater % of fat in the diet might help.

Calcium is like the bricks, impact is like the blueprints. Send a extra bricks to the construction site but no orders and nothing extra gets built. Except maybe a kidney stone...[10]
• Barry et al. tried to stave off the decline in bone density by giving a group of cyclists extra calcium but although it change their calcium levels after exercise, it didn't improve their bone density [11].
• Brown et al. showed a small uptick in bone density in the group that ate a higher percentage of their diet as fat for 12 weeks, with no difference in body mass or fat between groups [12].
• Although factors such as nutrition and endocrine (ie cortisol levels from the stress of long rides) are beginning to be studied in cyclists, initial results haven't shown levels far enough from normal to explain the low bone density [1].

APPLICATION

Cycling itself doesn't reduce your bone density, it just doesn't do anything to help your bone density, and if cycling is all you are doing then you aren't doing much to help your bone density.

How to help your bone density:
• Adequate nutrition: 1000mg of calcium and 600U of vitamin D. Don’t remove fat from your diet.
• Weight bearing activity. Running, jumping and weight lifting are the most effective.

The catch:
The very same weight bearing exercise that builds bone density can cause fractures in those with very poor bone density when given in excessive doses.

The Solution:
If road cycling has been your exclusive form of exercise for more than a few years I recommend contacting your doctor to get your bone density checked. This is especially important if you have a history of smoking, are Asian or Caucasian, over age 60 and light. Then connect with a physical therapist to get exercises that will safely improve your bone density.

REFERENCES

1. Olmedillas H, Gonzalez-Aguero A, Moreno LA, Casajus JA, Vicente-Rodriquez G. Cycling and Bone Health: A Systematic Review. BMC Medicine. 2012. 10.168
2. Medelli J, Lounana J, Menuet JJ, Shabani M, Cordero-MacIntyre Z: Is osteopenia a health risk in professional cyclists? J Clin Densitom 2009, 12:28-34
3. Nichols JF, Palmer JE, Levy SS: Low bone mineral density in highly trained male master cyclists. Osteoporos Int 2003, 14:644-649.
4. Nichols JF, Rauh MJ: Longitudinal changes in bone mineral density in male master cyclists and nonathletes. J Strength Cond Res 2012, 25:727-734.
5. Barry DW, Kohrt WM: BMD decreases over the course of a year in competitive male cyclists. J Bone Miner Res 2008, 23:484-491.
6. Rizzoli R, Bianchi ML, Garabedian M, McKay HA, Moreno LA: Maximizing bone mineral mass gain during growth for the prevention of fractures in the adolescents and the elderly. Bone 2010, 46:294-305.
7. Wilks DC, Gilliver SF, Rittweger J: Forearm and tibial bone measures of distance- and sprint-trained master cyclists. Med Sci Sports Exerc 2009, 41:566-573.
8. Heinonen A, Oja P, Kannus P, Sievanen H, Manttari A, Vuori I: Bone mineral density of female athletes in different sports. Bone Miner 1993, 23:1-14.
9. Duncan CS, Blimkie CJ, Kemp A, Higgs W, Cowell CT, Woodhead H, Briody JN, Howman-Giles R: Mid-femur geometry and biomechanical properties in 15- to 18-yr-old female athletes. Med Sci Sports Exerc 2002, 34:673-681.
10. Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones.
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Written By: Bryan Ausinheiler, DPT, CSCS

Reviewed By: Alfonso Lopez

About the Author
Bryan Ausinheiler is a Physical Therapist, Personal Trainer and Bike Fitter in Oakland California. Find more of his writing at his blog: posturemovementpain.com Find more about his clinic and fitting studio at bit.ly/ausinheiler