Are Ironwomen more prone to Injury?

Women are very quickly becoming the fastest growing segment of endurance athletes. Studies suggest that women utilize less glycogen and more fat than men in long, lower-intensity exercise such as triathlons/ marathons/ pelotons. This makes female athletes particularly well suited for, and may potentially provide an advantage over men in endurance events. Triathletes are vulnerable to the full spectrum of sports injuries that could be sustained from swimming, cycling or running.

Although acute traumatic injuries can occur during an event or training, most triathletes suffer overuse or overtraining injuries.  Looking at the scientific literature in running, we can see that women indeed do, on the whole, get injured more often than men do.  But the difference is not quite as drastic as popular wisdom might hold—a 2002 study of around two thousand patients at a Vancouver, Canada sports injury clinic found that women represented 54% of injuries, with men taking up the other 46%.  Having said that, among some specific injuries, women are at significantly higher risk such as Anterior Cruciate Ligament (ACL) Tears.

Three main differences exist between the male and female athlete: Anatomical, Physiological and Training considerations.

Anatomical Factors

#1 Bones and joints.
Compared with men, women have shorter and smaller limbs relative to body length. In the athletic disciplines where balance control is very important (eg, gymnastics), shorter stature and wider pelvis give women lower center of gravity, which gives them substantial advantage. However, wider pelvis can produce a condition generally known as “knock-knees” which is a result of an increased Q angle. The Q-angle is the angle between a line connecting a point on the front of the hip bone and the center of the kneecap and another connecting the kneecap and a point on the upper shin-bone. This is known to be a predisposing factor for patellofemoral (knee cap joint) problems.

#2 Muscles
During the puberty, however, because of the influence of the testosterone boys accumulate greater muscle mass. In adults, total cross-sectional area of muscles in women is 60%, compared with 80% in men. As a result, maximal strength measures and maximal power measures are reduced. Although it has been shown that when only muscle quality is concerned, male and female muscle is not different. However, the strength and power differences between the sexes are a function of muscle quantity and not only of their quality.

#3 Ligaments and joints
Female athletes have increased general joint laxity than their male counterparts. It can be due to an increased laxity of the ligaments, tendons and the joint capsule itself. In addition, the lower muscle mass may also decrease the restrains of excessive joint movement in females.

Physiological factors

#1 Hormonal Differences

The predominant hormone affecting muscular and bone development in females is oestrogen and testosterone in males. After the stabilization of hormonal levels during the pubertal years, these hormonal differences results in greater gender differences. Proper oestrogen serum levels are also necessary for women to obtain maximum peak bone mass during the second and third decade. There are some studies that show there were more injuries than expected in the ovulatory phase of the cycle. In contrast, significantly fewer injuries occurred in the follicular phase. This is postulated to be due to oestrogen and relaxin’s direct effect on collagen metabolism and behaviour.

Oestrogen levels reach their peak during the follicular phase of the menstrual cycle just before ovulation and remain elevated until just before menstruation.

The effect of oestrogen on bone and ligaments include:

  • Inhibition of bone cells that breakdown bone (osteoclasts)
  • Inhibition of the development of new cells that breakdown bone
  • Promotes the survival of cells that build bone (osteoblasts)
  • Promotes the production of collagen in connective tissue including ligaments

Relaxin is produced during pregnancy; and in non-pregnant females during the luteal phase (2nd half) of the cycle. It peaks within 14 days of ovulation.

Effects of relaxin include:

  • Inhibition of collagen production
  • Promotes collagen breakdown

Taking into account the effect of these hormones, you might expect that women would be more vulnerable to injury pre-menstrually or at the beginning of the period when the ligaments would appear to be at their loosest. However, studies have shown inconclusive results. There are some studies that show there were more injuries than expected in the ovulatory phase of the cycle. In contrast, significantly fewer injuries occurred in the follicular phase. However, some have shown a greater than expected percentage of injury mid cycle where you would expect the tissues to be at their stiffest and thickest.


Training/ Conditioning factors (doll games vs ball games)

Until recent years, males are involved training actively for competitive sports at an early age compared to females. As such they are physically better conditioned to withstand sports injuries. Hence, there was a saying that boys were involved in ball games as compared to girls being involved in doll games at an earlier age. Nevertheless, the combination of the greater susceptibility and a 10-fold increase in the female sports population since the inception of Title IX in the United States has resulted in a dramatic increase in the number of sports injuries in females. Locally, increased emphasis in sports and fitness has also allowed us to witness a large increased in the number of females involved in recreational and competitive sports and consequently an increase in the number of injured females.

Common overuse injuries the ironwoman encounter include

Stress fractures

Stress fractures are relatively common overuse injuries, especially in athletes or military personnel. Although they are not exclusive to female athletes, females in general have a higher incidence of stress fractures and, second, distribution of stress fracture sites seems to differ between genders. Stress fractures result from cumulative repetitive forces insufficient to cause an acute fracture. It has been noted previously that stress fractures occur more frequently in amenorrheic (non-menstruating) than normally-menstruating females. The exact mechanism of the development of stress fractures in amenorrheic women is uncertain and may be partly related to low bone density. Lower-extremity bones are most commonly affected, but stress fractures also occur in non-weight-bearing bones such as upper extremities and ribs. The tibia (lower leg bone) is the most commonly involved site for both men and women, but the fractures of the neck of femur (thigh bone), foot bones, and pelvis are seen more commonly in the female athlete The athlete with stress fracture presents with gradual onset of pain, aggravated by exercise. The hallmark of stress fracture is localized tenderness at the fracture site. The main treatment of stress fractures is rest from the offending athletic activity, a concept known as “relative rest,” and it is usually conducted as a step by step treatment algorithm General conditioning is maintained by exercising other areas of body and partaking alternative training, such as water running, swimming, or cycling. When patients do not respond to conservative treatment, surgical procedure may be advised.

Patellofemoral (knee cap joint) pain syndrome

Patellofemoral pain syndrome (PFPS) is a term used to describe painful but stable patella. It is a very common problem among female runners and cyclists and the increased incidence of PFPS in women compared with male athletes is thought to be related to the anatomical, physiological, biomechanical and conditioning differences between genders. Three major factors contributing to the development of PFPS are lower extremity and patellofemoral malalignment, quadriceps muscle imbalance and/or weakness, and physical overload of patellofemoral joint.  Conservative treatment is effective in most patients. Quadriceps muscle stretches, balanced strengthening, proprioceptive training, hip external rotator strengthening, orthotic devices, and effective bracing will relieve the pain in most of the patients. Only if a comprehensive rehabilitation program of at least 6-month duration fails, surgical treatment should then be considered as the last resort.

Patellar (knee cap) tendinitis – jumper’s knee

Patellar tendinitis (jumper’s knee) is a clinical entity characterized with anterior knee pain and is the most common athletic injury to the knee. Pain is aggravated by excessive strain on the extensor (straightening) system of the knees after numerous jumps or long periods of running. It can also be caused by poor bike fit where the saddle height is too low, resulting a greater knee flexion. Important causative factor was found to be the amount of training (both the amount of time and the amount of mechanical strain placed on the knee) that the athlete habitually carries out. The most common site of tendinitis is around lowest part (inferior pole) of the patella. In very rare cases, continuation of intensive athletic activities, despite the presence of evident symptoms of the disease, leads to a complete rupture of the patellar tendon. Of the numerous treatments available, physiotherapy and correction of technical errors are often efficient.

Iliotibial band friction syndrome

The Ilitotibial band is a thick strip of connective tissue connecting several muscles in the outer thigh to help stabilize the knee. Iliotibial band friction syndrome (ITBFS) is one of the most common overuse injuries in runners. It is caused by many repetitive flexion and extension movements of the knee, during which rubbing of the band against lateral femoral epicondyle (outermost point of the thigh bone at the knee) occurs. Friction occurs near foot strike, predominantly in the foot contact phase, between the back edge of the iliotibial band and the underlying lateral femoral epicondyle. There is a higher incidence of ITBFS in long-distance runners than middle-distance runners and sprinters. The dominant symptom is pain at the lateral side of the knee, aggravated by running. Pain is stinging in nature, and is located around 2 cm above the knee joint line. The treatment is usually non-operative and is based on modification of athletic activity, stretching exercises, and correction of predisposing factors. Again, only in recalcitrant cases of ITBFS, surgery has been advocated.


Swimmer’s Shoulders

Swimmer’s shoulder is a musculoskeletal condition that results in symptoms in the area of the front and outer aspect of the shoulder. The onset of symptoms may be associated with impaired posture, shoulder joint mobility, muscular control, or muscle performance. Additionally, training errors such as overuse, misuse, or abuse may also contribute to this condition. In extreme cases, patients with swimmer’s shoulder may have soft tissue injuries of the rotator cuff, long head of the biceps, or glenoid labrum (shock absorber in the shoulder joint). For competitive swimmers and triathletes, it is important to focus on prevention and early treatment, addressing the impairments associated with this condition, and analyzing training methods and stroke mechanics. Often, a comprehensive rehabilitation program usually includes strengthening of the rotator cuff and scapular stabilizers, stretching anterior chest musculature that may be shortened, and implementing activity modification so the athlete can still participate in the sport. In cases where proper technique and rehabilitation are insufficient, a more thorough consult with the doctor may be required to assess for any significant injuries that may then warrant surgery as the last resort.

In conclusion, female endurance sports have come a long way and regular exercise is very important for obtaining general health, positive lifestyle behavior, and positive self-image, as well as learning such skills as teamwork, commitment, and goal setting. The collective differences in anatomical, physiological and conditioning factors may pose a higher health risk to the female athlete but the gender gap is definitely closing. If the symptoms of overuse injury surfaces and persists during training or competition, early diagnosis and a multidisciplinary approach are the essential aspects of the treatment. With a holistic, intergrated and personalized approach to peak performance, injury prevention and treatment, ironwomen can definitely swim bike run the world.

Weight Loss: The Golden Ticket to Osteoarthritis Prevention

My 8 year old daughter confronted me just a few weeks ago about the miracle creams and pills that the television advertisements are showing for arthritis. “There is no need for any more surgery then.” That led me to wonder: if these supplements and creams are the tickets to osteoarthritis prevention, that is really an excellent quick fix. No need to exercising either since running is terrible to our knees and ankles as the stomping trashes the joints. The marathoners must be destroying their knees! But are the professional runners really getting osteoarthritis early and more frequently then the rest of us?

In a study published when I was still doing 2.4km runs in less then 9.05mins, formerly competitive runners did not have higher rates of arthritis in their hips, knees or ankles when compared to nonrunners. (1)What about the regular recreational runners? A more recent study in the American Journal of Preventative Medicine investigated differences in the progression of knee OA in middle- to older-aged runners compared to healthy non-runners over two decades. No association was found. (2) Medical literature generally does not support the idea that running and exercising contributes to the degeneration of articular cartilage (3).

So what does? Whereas once knee osteoarthritis was considered a ‘wear-and-tear’ condition, it is now recognized that knee osteoarthritis exists in the highly metabolic and inflammatory environments of fat tissue. Chemicals known as cytokines associated with adipose tissue may influence osteoarthritis though direct joint degradation or control of local inflammatory processes. Moreover, obesity loads may be detected by mechanical receptors on cartilage cell surfaces triggering production of such chemicals leading to increased arthritis.

Fat (Adipose) tissue, once considered a passive storage of energy, is now recognized as a highly metabolic endocrine organ with the capacity to secrete such inflammatory chemicals which have been detected in the joint fluid and the blood of patients with osteoarthritis. (4,5) As doctors will tell you, inflammation is an important hallmark of osteoarthritis, and we give you anti-inflammatory medications to help reduce the pain and swelling from osteoarthritis. With the cytokines found in fat tissue being an important part of inflammatory processes, prevention can be done by reducing fat tissue where these nasty chemicals are produced. Voila, the golden ticket!

In addition to the nasty chemicals, being overweight also leads to abnormal loads on the joints. Clinical and animal studies of joint loading have provided evidence that abnormal loads can lead to changes in the composition, structure, and mechanical properties of articular cartilage. 6,7,8 Kind of like a watermelon placed on a grape, I guess you get the picture. But weight is not just the whole picture, loss of muscle mass and strength may reduce the shock-absorbing potential of the joint, thereby causing cartilage damage. 9

Pain is the main reason patients see me when they have osteoarthritis. Obesity has been known to be linked to abnormal glucose homeostasis (control) and insulin resistance in the body. In studies of acute pain in trauma and surgery, there is decreased insulin sensitivity.10 In these same studies of induced acute pain, there were increases in circulating concentrations of hormones associated with altered glucose homeostasis. Because obesity is frequently, though not always, associated with insulin resistance, altered glucose homeostasis has an important role related to chronic pain from the arthritis.

We have been searching for miracle drugs to reverse osteoarthritis for a long time to no avail. Of course, weight management, albeit the Golden Ticket to osteoarthritis prevention, may not be the quick fix everyone is looking for but I guess we can also defer to surgery like a knee replacement or an ankle fusion by Orthopaedic Surgeons like myself. We will always be available to help you with that when it comes to that.


  1. Konradsen L, Hansen EM, Sondergaard L. Long distance running and osteoarthrosis. Am J Sports Med. Jul-Aug 1990;18(4):379-381.
  2. Chakravarty EF, Hubert HB, Lingala VB, Zatarain E, Fries JF. Long distance running and knee osteoarthritis. A prospective study. Am J Prev Med. Aug 2008;35(2):133-138.
  3. Willick SE, Hansen PA. Running and osteoarthritis. Clin Sports Med. Jul 2010;29(3):417-428.
  4. Dumond H, Presle N, Terlain B, et al. Evidence for a key role of leptin in osteoarthritis. Arthritis Rheum 2003; 48:3118–3129.
  5. Chen TH, Chen L, Hsieh MS, et al. Evidence for a protective role for adiponectin in osteoarthritis. Biochimica et Biophysica Acta 2006; 1762:711–718.
  6. Mundermann A, Dyrby CO, Andriacchi TP. Secondary gait changes in patients with medial compartment knee osteoarthritis: increased load at the ankle, knee, and hip during walking. Arthritis Rheum 2005; 52:2835–2844.
  7. Maly MR, Costigan PA, Olney SJ. Contribution of psychosocial and mechanical variables to physical performance measures in knee osteoarthritis. Phys Ther 2005; 85:1318–1328.
  8. Rejeski WJ, Craven T, Ettinger WH Jr, et al. Self-efficacy and pain in disability with osteoarthritis of the knee. J Gerontol B Psychol Sci Soc Sci 1996; 51:24–29.
  9. Bennell KL, Hunt MA, Wrigley TV, et al. Role of muscle in the genesis and management of knee osteoarthritis. Rheum Dis Clin N Am 2008; 34:731–754.
  10. Greisen J, Juhl CB, Grofte T, et al. Acute pain induces insulin resistance in humans. Anesthesiology 2001; 95:578–584.

Bone Loss – Perils of Treating Osteoporosis

Fragility fractures resulting from osteoporosis often require a long recovery period and can result in severe residual pain and immobility. Such fractures in the elderly often represent sentinel events and resulting in significant morbidity and even mortality. The prevention of such fractures involves fall prevention and the proper management of the underlying osteoporotic condition.

Osteoporosis is a systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue. World Health Organisation defines it as a bone mineral density (measured using a dual-energy X-ray absorptiometry scan) of 2.5 standard deviations or more below the young adult mean. Based on this definition, one-third of all adult females can be said to suffer from osteoporosis. One might even consider the onset of menopause as a harbinger for this condition.

The management of osteoporosis is based on 2 main principles: one seeks to attain maximum peak bone mass, even while reducing resorption. Most of our current first-line pharmacological treatments focus on the reduction of resorption. That said, bone is a living structure that has to heal and repair the accumulated damage it acquires. Anti-resorptive medication halts this process, leading to undesirable sequelae such as severe suppression of bone turnover (SSBT) and atypical fractures.

Careful patient selection, introduction of drug holidays, monitoring for signs of SSBT and management of atypical fractures have been undertaken by doctors dealing with osteoporosis with great interest over recent years, though many questions are still unanswered. Newer intramedullary nailing techniques have helped in the management of atypical fractures. In addition, the use of Vitamin D supplements has also played a great role in the management of the disease.

For peak mass and maximal resorption reduction, bone needs to be used and stressed – hence one would not be far off the mark to say: use it or lose it!