Treatment Protocols have changed significantly when it comes to sports Injuries even though the injuries themselves have remained unchanged in medical textbooks for many years.
Most of the advances in treatment have come about from research lead by exercise physiologists and specialists who monitor and test our elite athletes and of course lets not forget the sharp learning curve provided by good old fashion trial and error.
It wasn’t that long ago a patient booked for knee surgery would be in a cast and asked to rest as much as possible. Medical specialist began to realise that the cast would accelerate atrophy (muscle wasting) of the leg muscles making postoperative recovery a long and unnecessary drawn out.
Nowadays the complete opposite occurs. Instead of resting and immobilising the injured segment, the patient is given a carefully considered treatment plan combined with prescribed rehabilitation exercises, pre and post-operatively.
There are a number of important factors to be considered before any treatment or rehabilitation program is given to minimise aggravation of the healing structures. A poor and inexperienced approach could set back recovery significantly, or worse, contribute to further damage to the recovering tissues.
Our physiotherapists have years of experience treating injuries. They have seen just about every combination of sports injury and treat many elite athletes.
Treating any injury whether it is sports related, work related or just plain bad luck does not change the rehab rules. Each injury is categorised in different phases with goals and criteria to progress through each different phase.
All our rehabilitation exercises are based on best current practices that are evidence-based. Our Physiotherapists clearly set out what type of exercises are appropriate for the current injury level, how many reps, at what intensity and how many times in the day these exercises should be completed.
Combine this approach with his proven treatment protocols gives our patients the best results.
In nearly all cases, treatment is accompanied by a customised exercise rehab program to accelerate recovery and enhance positive long lasting results.
Does running accelerate the development of osteoarthritis?
There are so many misconceptions about running and how bad it can be for your joints. You may have heard many friends and family members comment on this and they may have even tried to convince you to stop running and go swimming instead. Here is what the scientific research tells us so far:
Osteoarthritis (OA) is a musculoskeletal condition that involves degeneration of the joints and impact during weightbearing exercise such as running and may contribute to joint loads. There is very little evidence however, that running causes OA in the knees or hips. One study reported in 1985 by Sohn and Micheli compared incidence of hip and knee pain and surgery over 25 years in 504 former cross-country runners. Only 0.8% of the runners needed surgery for OA in this time and the researchers concluded that moderate running (25.4 miles/week on average) was not associated with increased incidence of OA.
In another smaller study of 35 older runners and 38 controls with a mean age of 63 years, researchers looked at progression of OA over 5 years in the hands, lumbar spine and knees (Lane et al. 1993) . They used questionnaires and x-rays as measurement tools. In a span of 5 years, both groups had some participants who developed OA- but found that running did not increase the rate of OA in the knees. They reported that the 12% risk of developing knee OA in their group could be attributed to aging and not to running. In 2008, a group of researchers reported results from a longitudinal study in which 45 long distance runners and 53 non-runners were followed for 21 years. Assessment of their knee X-Rays, revealed that runners did not have a higher risk of developing OA than the non-running control group. They did note however, that the subjects with worse OA on x-ray also had higher BMI (Body Mass Index) and some early arthritic change in their knees at the outset of the study.
Is it better to walk than to run?
It is a common belief that it must be better to walk than to run to protect your joints. In a recent study comparing the effects of running and walking on the development of OA and hip replacement risk, the incidence of hip OA was 2.6% in the running group, compared with 4.7% in the walking group (Williams et al 2013). The percentage of walkers who eventually required a hip replacement was 0.7%, while in the running group, it was lower at 0.3%. Although the incidence is small, the authors suggest the chance of runners developing OA of the hip is less than walkers.
In the same study, Williams and colleagues reinforced that running actually helped keep middle-age weight gain down. As excess weight may correlate with increased risk of developing OA, running may reduce the risks of OA. The relationship between bodyweight and knee OA has been well-established in scientific studies, so running for fitness and keeping your weight under control is much less likely to wear out your knees than being inactive and carrying excess weight.
Is there a limit?
Recent studies have shown that we should be doing 30 minutes of moderate exercise daily to prevent cardiovascular disease and diabetes. But with running, researchers still have not established the exact dosage of runners that has optimal health effects. Hansen and colleagues’ review of the evidence to date reported that the current literature is inconclusive about the possible relationship about running volume and development of OA but suggested that physiotherapists can help runners by correcting gait abnormalities, treating injuries appropriately and encouraging them to keep the BMI down.
We still do not know how much is “too much” for our joints. However, we do know that with age, we expect degenerative changes to occur in the joints whether we run or not. Osteoarthritis is just as common as getting grey hair. The important thing is that we keep the joints as happy and healthy as possible.
How do you start running?
If you are not a runner and would like to start running, walking would be a good way to start and then work your way up to short running intervals and then longer intervals as you improve your fitness and allow time for your body to adapt. Therefore, running in general is not bad for the joints. It does not seem to increase our risk of developing OA in the hips and knees. But the way you run, the way you train and how fast you change your running frequency and distance may play a role in future injuries of the joints.
Tendinopathy TOP TEN By Jill Cook PhD
Tendon pain and dysfunction are the presenting clinical features of tendinopathy. Research has investigated many treatment options, but consistent, positive, clinical outcomes remain elusive. We know that treatment should be active (eg, exercise-based), and that a consistent and ongoing investment in rehabilitation is required. It is important to maximise this investment by understanding (and conveying to patients) treatments that do not help. The following 10 points high- light treatment approaches to avoid as they do not improve lower limb tendinopathy.
1. Don’t rest completely.
Rest decreases the load tolerance of tendon, and complete rest decreases tendon stiffness within 2 weeks.1 It also decreases strength and power in the muscle attached to the tendon and the function of the kinetic chain,2 and likely changes the motor cortex, leaving the person less able to tolerate load at multiple levels. Treatment should initially reduce painful, high tendon load (point 2) and intro- duce beneficial loads (eg, isometrics3). Once pain is low and stable (consistent on a loading test each day), load can be increased slowly to improve the capacity of the tendon.4
2. Don’t prescribe incorrect exercise.
Understanding load is essential for correct exercise prescription. High tendon load occurs when it is used like a spring, such as in jumping, changing direction and sprinting.5 Tendon springs must be loaded quickly to be effective, so slow exercises even with weights are not high tendon load and can be used early in rehabilitation. However, exercising at a longer muscle tendon length can compress the tendon at its insertion.6 This adds substantial load and should be avoided, even slowly, early in rehabilitation.
3. Don’t rely on passive treatments.
Passive treatments are not helpful in the long term as they promote the patient as a passive recipient of care and do not increase the load tolerance of tendon.Treatments like electrotherapy and ice temporarily ameliorate pain only for it to return when the tendon is loaded.7
4. Avoid injection therapies.
Injections of substances into a tendon have been shown to be no more effective than placebo in good clinical trials.8 Clinicians who support injection therapies incorrectly suggest they will return a pathological tendon to normal. There is little need to intervene in the pathology as
there is evidence that the tendonadapts to the pathology and has plenty of tendon tissue capable of tolerating high load.9 Injections may change pain in the short term as they may affect the nerves, but should only be considered if the tendon has not responded to a good exercise-based programme.
5. Don’t ignore tendon pain. Pain usually increases 24 hours afterexcess tendon load. An increase in pain of 2 or more (out of 10) on a daily loading test should initiate a reduction in the aspects of training that are overloading the tendon (point 2). The overload is likely to be due to excessive spring-like movements such as jumping, running and changing direction.
6. Don’t stretch the tendon.
Aside from the load on a tendon in sport, there are compressive loads on the bone-tendon junction when it is at its longest length. Stretching only serves to add compressive loads that are detrimental to the tendon.10
7. Don’t use friction massage.
A painful tendon is overloaded and irritated (reactive tendon pathology). Massaging or frictioning the tendon can increase pain and will not help pathology.7 An effect on local nerves may reduce pain in the short term only for it to return with high tendon loads.
8. Don’t use tendon images for diagnosis, prognosis or as an outcome measure.
Abnormal tendon images (ultrasound and MRI) in isolation do not support a diagnosis of tendon pain as asymptom- atic pathology is prevalent. There are also no aspects of imaging, such as vascu- larity and ‘tears’, that allow a clinician to determine outcome.11 Pathology on imaging is usually very stable and does not change with treatment and reductionin pain, so images are not a good outcome measure.12
9. Don’t be worried about rupture.
Pain is protective as it causes unloading of a tendon. In fact most people who rupture a tendon have never had pain and do not present clinically, despite the tendon having substantial pathology.13
10. Don’t rush rehabilitation.
Tendon needs time to build its strength and capacity. So does the muscle, the kinetic chain and the brain. Although this can be a substantial time (3 months or more), the long-term outcomes are good if the correct rehabilitation is completed.14
The above 10 treatment approaches take valuable resources and focus away from the best treatment for tendon pain—exer- cise-based rehabilitation. A progressive programme that starts with a muscle strength programme and then progresses through to more spring-like exercises and including endurance aspects will load the tendon correctly and give the best long- term results.
People who exercise have better mental fitness, and a new imaging study from UC Davis Health System shows why. Intense exercise increases levels of two common neurotransmitters — glutamate and gamma-aminobutyric acid, or GABA — that are responsible for chemical messaging within the brain.
Published in this week’s issue of The Journal of Neuroscience, the finding offers new insights into brain metabolism and why exercise could become an important part of treating depression and other neuropsychiatric disorders linked with deficiencies in neurotransmitters, which drive communications between the brain cells that regulate physical and emotional health.
“Major depressive disorder is often characterized by depleted glutamate and GABA, which return to normal when mental health is restored,” said study lead author Richard Maddock, professor in the Department of Psychiatry and Behavioral Sciences. “Our study shows that exercise activates the metabolic pathway that replenishes these neurotransmitters.”
The research also helps solve a persistent question about the brain, an energy-intensive organ that consumes a lot of fuel in the form of glucose and other carbohydrates during exercise. What does it do with that extra fuel?
“From a metabolic standpoint, vigorous exercise is the most demanding activity the brain encounters, much more intense than calculus or chess, but nobody knows what happens with all that energy,” Maddock said. “Apparently, one of the things it’s doing is making more neurotransmitters.”
The striking change in how the brain uses fuel during exercise has largely been overlooked in brain health research. While the new findings account for a small part of the brain’s energy consumption during exercise, they are an important step toward understanding the complexity of brain metabolism. The research also hints at the negative impact sedentary lifestyles might have on brain function, along with the role the brain might play in athletic endurance.
“It is not clear what causes people to ‘hit the wall’ or get suddenly fatigued when exercising,” Maddock said. “We often think of this point in terms of muscles being depleted of oxygen and energy molecules. But part of it may be that the brain has reached its limit.”
To understand how exercise affects the brain, the team studied 38 healthy volunteers. Participants exercised on a stationary bicycle, reaching around 85 percent of their predicted maximum heart rate. To measure glutamate and GABA, the researchers conducted a series of imaging studies using a powerful 3-tesla MRI to detect nuclear magnetic resonance spectra, which can identify several compounds based on the magnetic behavior of hydrogen atoms in molecules.
The researchers measured GABA and glutamate levels in two different parts of the brain immediately before and after three vigorous exercise sessions lasting between eight and 20 minutes, and made similar measurements for a control group that did not exercise. Glutamate or GABA levels increased in the participants who exercised, but not among the non-exercisers. Significant increases were found in the visual cortex, which processes visual information, and the anterior cingulate cortex, which helps regulate heart rate, some cognitive functions and emotion. While these gains trailed off over time, there was some evidence of longer-lasting effects.
“There was a correlation between the resting levels of glutamate in the brain and how much people exercised during the preceding week,” Maddock said. “It’s preliminary information, but it’s very encouraging.”
These findings point to the possibility that exercise could be used as an alternative therapy for depression. This could be especially important for patients under age 25, who sometimes have more side effects from selective serotonin reuptake inhibitors (SSRIs), anti-depressant medications that adjust neurotransmitter levels.
For follow-up studies, Maddock and the team hope to test whether a less-intense activity, such as walking, offers similar brain benefits. They would also like to use their exercise-plus-imaging method on a study of patients with depression to determine the types of exercise that offer the greatest benefit.
“We are offering another view on why regular physical activity may be important to prevent or treat depression,” Maddock said. “Not every depressed person who exercises will improve, but many will. It’s possible that we can help identify the patients who would most benefit from an exercise prescription.”