Runner’s knee, defined as anterior knee pain, is prevalent in athletes. Fortunately, there are several effective strategies for reducing the pain and eliminating the source of the problem.
Runner’s knee is defined as anterior knee pain that is exacerbated by physical activity. Aside from the pain, other symptoms include swelling and reduced patellar mobility. As its name suggests, runner’s knee is common in runners, but it is also prevalent in the general population; runner’s knee is responsible for up to 25% of all knee injuries. Interestingly, runner’s knee is two times more prevalent in females than their male counterparts. The formal medical term for runner’s knee is patellofemoral pain syndrome. A comprehensive review of patellofemoral pain syndrome and other knee injuries was published in a primary care journal last year (Meniscal, Plica, Patellar and Patellofemoral Injuries of the Knee, 2013. Morelli V and Braxton TM).
Runner’s knee is caused by a variety of related factors that ultimately result in patellar misalignment, friction and/or inflammation. The patella, also known as the kneecap, is a small triangular bone at the knee joint. When the muscles that hold the patella in place become imbalanced, the patella may track laterally. The muscle pull on the patella may become imbalanced due to tightness, weakness or strength. When the patella tracks out of place, the patella grinds into cartilage on the femur producing the inflammation and pain characteristic of runner’s knee. Additional causes of runner’s knee may include flat feet, which causes stress on the achilles tendon that gets transmitted up to the knee, or a direct blow to the knee.
Runner’s knee, once contracted, requires treatment. One study found that 94% of patients with untreated runners knee were unable to alleviate symptoms after 4 years, and the symptoms were still present in 25% of patients 20 years later. Many of the treatments are easy to follow remedies prescribed on WebMD. Some methods of reducing the inflammation include icing the knee, elevating the knee, compressing the knee and taking anti-inflammatory pain killers. Furthermore, resting the knee would alleviate friction and, if prolonged, possible reduce the muscle imbalance. These solutions would relieve the pain and inflammation symptoms of runner’s knee. However, these would be quick-fixes and not necessarily solutions for the source of the problem: patellar misalignment.
There are several non-operative treatments for runner’s knee that have been found to have long term success. For athlete’s who are flat footed, a treatment is using arch support to help ease the strain on the achilles tendon. Foot orthotics was found by one study to significantly improve 80% of patients with runner’s knee. Stretching can reduce muscle tightness and balance out the forces pulling on the patella. Focus on the iliotibial band (commonly referred to as the IT band), which runs laterally from the hip to the knee. A stretch for the IT band can be seen in the figure on the right. Taping methods can help realign the patella and relieve pressure on the femur cartilage. One study found Kinesio taping to be ineffective, while McConnell taping was effective in 66% of patients, particularly those with a low BMI. Knee braces and sleeves have been shown to be effective strategies of eliminating runner’s knee. Finally, physical therapy has been found by some studies to reduce pain up to 90%. These treatments, both individually and combined with one another, have been found to significantly improve most patients with runner’s knee. Nonetheless, surgery may be required as a last resort. Surgical treatments for runner’s knee remove damaged cartilage on the femur.
Runner’s knee will persist for years if left untreated. However, there are several easy remedies that can both remove the pain and realign the patella (the source of runner’s knee). Just like tomorrow’s workout, runner’s knee is manageable!
Researchers show that aging muscle satellite cells undergo an irreversible transition from quiescence to senescence leading to impaired muscle fiber regeneration observed in elderly patients. The molecule responsible is tumor-supressing protein p16INK4a.
One of muscles’s greatest strengths is its response to injury. Muscle tissue uses many injuries as an opportunity to make itself stronger. Many athletes, for example, take advantage of this phenomenon when training. Repeated injury to the muscle fibers during training causes the fibers to regrow and repair themselves so that the muscle as a whole is strengthened. Satellite cells attached to the muscle fibers play a fundamental role in this process because they act as stem cells producing new muscle fibers when the muscle is damaged.
Satellite cells are normally in a reversible quiescent state, meaning they have exited the cell cycle into G0 phase where they are not actively dividing. Damage to the muscle fiber causes to the satellite cell to reenter the cell cycle and produce new muscle progenitors cells, which eventually generate mature muscle fibers. The satellite cells continue to produce new muscle fibers until the muscle is repaired. However, when this system fails it leads to muscle deterioration (or atrophy). Severe muscle deterioration to the point of dysfunction is called sarcopenia and commonly seen in people of old age or with the disease progeria. The figure below illustrates the process of muscle generation in healthy patients and patients with sarcopenia.
The muscle fails to regenerate after the satellite cells enter a senescent state. In a senescent state the satellite cell is incapable of reentering the cell cycle and spawning new stem cells. A new study published last month in Nature has found a molecule that may be responsible for driving the satellite cell into a senescent state (Geriatric muscle stem cells switch reversible quiescence into senescence, 2014. Pedro Sousa-Victor, et al.).
Increased expression of tumor-supressor molecule p16INK4a was found in the senescent satellite cells of both progeria and geriatric mice models. To further demonstrate its ability to cause sarcopenia, researchers silenced the expression of p16INK4a using short hairpin RNA. Nearly 30% of geriatric satellite cells in culture were activated following p16INK4a silencing compared to less than 15% of cultured geriatric satellite cells without p16INK4a silencing. When young cultured satellite cells were treated with p16INK4a their regeneration activity dramatically decreased. These findings were confirmed in humans with muscle biopsies of geriatric patients with sarcopenia and young adults. The elderly patient biopsies had significantly higher levels of p16INK4a expression compared to young adults of average age 25. It appears that the increased p16INK4a expression drives the satellite cells into the senescent state by hindering the phosphorylation of restinoblastoma. The inactivation of restinoblastoma irreversibly arrests the satellite cell in the G0 phase of the cell cycle.
This study poses many further questions. Would it be possible to use p16INK4a silencing as a therapy for progeria and geriatric muscle sarcopenia? The experiments done in cultured mice satellite cells are encouraging, but whether it would carry over to humans remains to be seen. Furthermore, what causes p16INK4a expression to increase? The authors suggest that one possibility is simply the same genomic decay that is responsible for most cancers. Could reduced physical activity play a role? If so, this would be one more biological phenomenon that follows the “use it or lose it” principle.
A study finds that low cardiovascular fitness and cognitive performance at age 18 is a risk factor for early-onset dementia and mild cognitive impairment later in life.
Early-onset dementia is rare: just 6-10 people out of a population of 10,000 will be diagnosed with early-onset dementia. However, over 35 million people worldwide are currently living with some form of dementia. Understanding early-onset dementia can help researchers pinpoint risk factors that lead to dementia in general. Early-onset dementia is defined as dementia diagnosed before the age of 65. Dementia is not one disease, but rather an assortment of diseases that lead to brain and memory deterioration. Although Alzheimer’s Disease is one of the chief causes of dementia, it is responsible for less than 0.1% of early-onset cases of dementia. A massive longitudinal study published earlier this month in the journal Brain finds two predictors of early-onset dementia: low cognitive performance and low cardiovascular fitness (Cardiovascular and cognitive fitness at age 18 and risk of early-onset dementia, 2014. Nyberg J, et al.).
The study utilized over one million Swedish males who were required to register for the military from 1968 to 2005. When the participants registered at age 18, they were required to take a cardiovascular fitness test as well as a cognitive performance test. The cardiovascular fitness test was performed on a cycle ergometer. The cognitive performance test measured ability in logical, verbal, visuospatial and technical cognition. The cognitive and cardiovascular tests were divided into tertiles: low, medium and high. For the purposes of this study, poor or low performance is defined by being in the lower third.
The researchers found that low cardiovascular fitness and poor performance on the cognitive tests at age 18 led to an increase risk of developing mild cognitive impairment and early-onset dementia. The hazard ratio of low cardiovascular fitness was 2.49 for early-onset dementia and 3.57 for mild cognitive impairment. The hazard ratio of low cognitive performance was 4.11 for early-onset dementia and 3.23 for mild cognitive impairment. Poor performance in both the cardiovascular fitness test and the cognitive performance test generated a hazard ratio of 7.34 for early-onset dementia and a hazard ratio of 8.44 for mild cognitive impairment. It should be noted that hazard ratios measure the amount of people who contract a disease over time, not the the total number of people who contract a disease after x years.
While a 7-fold increase in prevalence of early-onset dementia seems alarming for those who score in the lower third of cardiovascular fitness and cognitive performance, the prevalence of these neurodegenerative diseases is still very small. Although the researchers acknowledge that low cognitive performance may play some role in mediating poor cardiovascular fitness, the significance of cardiovascular fitness held up across a number of confounding factors such as socioeconomic status.
The study authors point to specific neurotropic factors such as brain-derived neurotropic factor (BDNF) and insulin-like growth factor 1 (IGF-1) as potential mediators of cardiovascular fitness on early-onset dementia and mild cognitive impairment. These factors are produced with exercise and increase neuroplasticity in the brain.
This study shows a link between poor cardiovascular fitness and cognitive performance and the diseases associated with mild cognitive impairment and early-onset dementia, but more work must be done to determine the biological mechanism for this correlation.