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A1 band - warm-up, recovery, cool-down sets
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Data Source: Zamparo P, Bonifazi M (2013). Bioenergetics of cycling sports activities in water.

Coded for Swimming Science by Cameron Yick

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Does Low Back Pain Resolve Itself?

Take Home Points for Does Low Back Pain Resolve Itself?
  1. Yes, low back pain typically resolves itself, yet underlying issues persist likely increasing the risk of re-injury.
Low back pain (LBP) is extremely common in the general and athletic population and swimmers
even have a higher risk of low back degeneration. Despite this frequency, no resolutions exist for eradicating pain. Luckily, most cases of LBP are acute and remiss over a month. This brevity in symptoms leads many not to seek treatment. However, resolution of pain, without treatment, may but a person at risk for a recurrent injury, as the recurrent rate of low back pain is extremely high.

This situation puts everyone in a bind, as everyone thinks they can wait out pain and get better. However, is waiting out the pain and having it resolve on it's own the best option? Sure, low back pain gets better in most people without any treatment, but is this passive treatment worth the risk of having a higher risk of recurrence?

Does Low Back Pain Resolve Itself?

Butler (2012) recruited fifty-four subjects without LBP and 33 people with a previous low back injury (LBI). In this study, electromyography of the core musculature and motion analysis was taken during the following task: 

“Subjects stood at a table (adjusted to standing elbow height) and performed three trials of lifting and replacing a 2.9 kg load using both hands in two reach conditions while minimizing trunk and pelvis motion. Subjects were required to move the load 4–5 cm off the table in a controlled manner and lower within a standardized 3-s count. An event marker identified lift, transition and lowering phases. Only the lift phase was examined given similar patterns were found for the two other phases. If trunk or pelvis motion was visible during the trial or upon review if the any of the three angular displacement traces exceeded 3, the trial was repeated (Butler 2012).”

The results showed a slight difference between the control and LBI, as the LBI group was slightly older and had a higher body mass index (BMI). Moreover, different movement patterns during the above tasks were noted between both groups. The LBI group also had higher muscle activation for the all the muscles except the external oblique, which showed decreased activation. 

Why is it Different?

All joints have passive structures (ie bones) and active structures (ie muscles). The higher muscular activation in the LBI group may be from a decrease in passive stability, requiring an increase in activity stability. Though high activation is assumed a good thing for stability, it may lead to increased fatigue and increased injury risk. This increases stiffness (stability) could also be a compensatory pattern for an underlying injury. A decrease in the external oblique activation may inhibit force distribution and overall core stability, as one muscle not working properly is theoretically disrupts stability according renowned spinal biomechanist Stuart McGill. 

These “scores indicates that the LBI group included individuals with inhibited as well as enhanced activation in local muscles, suggesting that there are potential subgroups. This may have implications for therapeutic interventions in that those with enhanced local activity may not benefit from therapies that focus on selectively activating deep muscles. Thus our results provide evidence of local muscle alterations although it is the first time that these impairments are reported during a functional but highly controlled task in those recovered from an episode of LBI (Butler 2012)”.

In summary, Butler concluded: “specifically, an overall increase in activity of abdominals and back extensors, increased agonist–antagonist co-activation strategy, reduced posterior oblique fiber activation and impaired local muscle responses to increased demand was found in the LBI

Practical Implications

Swimmers often have low back pain which symptoms quickly resolve. However, this study suggests underlying motor programming and impaired muscle activation exist after the resolution of symptoms. This makes it essential to seek rehabilitation or at least work on improving these imbalances, preventing a relapse. 

For some examples of core training, check out the COR Low Back Solution.

For more examples, consider purchasing Dryland for Swimmers.

  1. Butler HL, Hubley-Kozey CL, Kozey JW. Changes in electromyographic activity of trunk muscles within the sub-acute phase for individuals deemed recovered from a low back injury. J Electromyogr Kinesiol. 2012 Nov 28. doi:pii: S1050-6411(12)00195-2. 10.1016/j.jelekin.2012.10.012. [Epub ahead of print]
By Dr. G. John Mullen received his Doctorate in Physical Therapy from the University of Southern California and a Bachelor of Science of Health from Purdue University where he swam collegiately. He is the owner of COR, Strength Coach Consultant, Creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Thoracic Outlet Syndrome: What it is, How to Spot it, a Case Report, and Prevention!

Take Home Points on Thoracic Outlet Syndrome: What it is, How to Spot it, a Case Report, and Prevention!:
  1. Thoracic outlet syndrome is a narrowing between your collarbone and first rib, putting pressure on your neurovascular structures.
  2. There are many neurovascular impairments at the shoulder.
  3. Monitor shoulder pain, symptoms, and alter sensation closely, and adjust prevention programs and biomechanics for greatest improvement.
Though shoulder impingement is the most common form of shoulder injury in swimmers, other cases of shoulder pain exist. These other syndromes impact other tissues, typically the nerual, arterial or vascular. Although these shoulder conditions are not well known, they still occur in overhead athletes. Asymptomatic pitchers even have impaired blood flow on their throwing side, a potential risk factor for Thoracic Outlet Syndrome (TOS). Some of these issues are treated conservatively, while others require surgery.

Types of Thoracic Outlet Syndrome

Knowing what occurs and the symptoms of tissues other than the muscular system is beneficial for a coach and rehabilitation staff. Here are some examples:
  1. Nerogenic Thoracic Outlet Syndrome: Compromising the brachial plexus. Symptoms are pain, numbness, tingling, and weakness. 
  2. Vascular Thoracic Outlet Syndrome: Compromising the venous or arterial system. The typical presentation includes pain, numbness, tingling, weakness, and/or the presence of vascular compromise. Venous TOS is more common than arterial TOS and is characterized by swelling and cyanosis, pain, and a heavy feeling. 
  3. Paget-Schroetter Syndrome: A thrombosis of the subclavian vein.

Clinical Tests for Thoracic Outlet Syndrome in Swimmers

There are manual and diagnostic test for identifying vascular compromise. Sadeghi-Azandaryani (2009) notes:

"Sensitivity of clinical tests was acceptable overall (mean 72%). The EAST test showed the highest sensitivity with 98%, followed by the Adson (sensitivity: 92%) and Eden tests (sensitivity: 92%). In contrast, the sensitivity of the Hoffmann test (47%) was low. Nevertheless, a positive EAST, Eden, Adson, Green-stone or Adson test was not associated with a poorer outcome (p≥0.05).

Systolic blood pressure was measured before and after exercise. Mean systolic blood pressure of the afflicted side in the group of patients with good or fair outcome (85.9% of all patients) showed an average systolic blood pressure of 123.1 ± 12.5 mmHg before exercise and 108.9 ± 12.8 mmHg after exercise (average decrease: 16.2 ± 9.6 mmHg). A decrease in blood pressure of more than 25 mmHg could not be found in this group. In the group of patients with a poor outcome, the systolic blood pressure before exercise was 140.6 ± 24.6 mmHg and 106.7 ± 21.8 mmHg after exercise (average decrease: 35.0 ± 14.1 mmHg). Statistical analyses showed that a distinct decrease in blood pressure after exercises was associated with a poorer outcome (p = 0.0027)."

Here are some of the most common tests:
  1. Roo's test: The patient stands and abducts shoulders to 90 degrees, externally rotates the shoulders, and flexes the elbows to 90 degrees. The patient then opens and closes the hand slowly for three minutes. The test is positive if the patient is unable to complete the test or experiences heaviness, numbness, tingling or pain.
  2. Adson's test: The examiner locates the radial pulse while arm is held in extension, external rotation and slight abduction. The patient is instructed to take a deep breath and turn head toward the test arm while extending the neck. If there is compression, the radial pulse will be diminished or absent. The goal of this test is to tense the anterior and middle scalenes.
  3. Costoclavicular test: The examiner palpates the radial pulse and then draws the patient's shoulder down and back. If the pulse disappears, the test is positive. The goal of this test is to provide compression of the costoclavicular space.
  4. Halstead maneuver: The examiner palpates the radial pulse and applies downward traction on the test extremity while the patient's neck is hyperextended and rotated to the opposite side. Absence of the pulse indicates a positive test.6
  5.  Wright test (hyperabduction test): The examiner palpates the radial pulse and hyperabducts the arm so the hand is brought overhead with the elbow and arm in the coronal plane. The patient takes a deep breath and may rotate or extend the neck for additional effect.
  6. Allen maneuver: The examiner palpates the radial pulse while positioning the shoulder in external rotation and horizontal abduction. The patient then rotates the head away from the test side.
Diagnostic tests also include a Doppler arteriography testing of the vascular system. If the compromise is neurogenic, nerve stimulation is sometimes used for diagnosis.

Example Swimmer with Paget-Schroetter Syndrome

The patient was a 21-year-old male swimmer who noticed swelling and pain in his non-dominant arm. The patient was advised to ice and rest his shoulder. Then, ten days after the initial heaviness, the symptoms returned and the patient was advised to seek emergency care where a Doppler venous ultrasound could be performed. The results were negative. The patient demonstrated a cease of the radial pulse, swelling, and limb cyanosis with the Wright’s hyperabduction test. He also presented with ⅘ strength on the affected side, but 5/5 strength on the non-affected side. Despite a negative Doppler venous ultrasound, the vascular surgeon suggested a venogram, since a Doppler venous ultrasound is best used as a screening tool, not for diagnostics, since it has difficulty specifically measuring the subclavian vein due to the bony structures. The venogram showed a major block of the subclavian vein, venous stenosis, and concomitant thrombosis.

The patient was then administration heparin and a tissue plasminogen activator (tPA) over a three day period in order to achieve thrombolysis.This improved the thrombus by 70%, indicating 30% of the vein had undergone permanent thrombosis. The patient was then prescribed coumadin and Lovenox as a blood thinner. Electromyography (EMG) was also performed to rule-out a neurogenic case of TOS, which demonstrated no muscle membrane instability.

The swimmer returned to the pool with great success (winning the conference in the 100 and 200 breast), then received a resection of the first rib. After the surgery, the patient complained of pain medial to the shoulder blade and demonstrated shoulder-blade winning. Manual muscle tests were performed again and noted 5/5 strength in all muscles. Fine-wire EMG was conducted again and showed normal signs of all muscles except the serratus anterior which demonstrated signs of denervation (likely due to surgical complications to the long thoracic nerve).

Despite the findings of the serratus anterior, the patient started a physical therapy program and home program which resulted in improved EMG readings for the serratus anterior, three months postoperatively.

Thoracic Outlet Syndrome Swimming Prevention Techniques

Steady Streamline:

If the arms move excessively during streamline, the upper arm and neural structures are stressed. Maintain a stable arm position during all streamline, especially dolphin kicking.

Flatter Butterfly:

Some swimmers (like Michael Phelps) press their chest down as they enter their arms in butterfly, delaying their pull. This creates a position with the arm above the chest, stretching and stretching the brachial plexus (all the nerves and vascular areas).  Try starting the pull earlier, not allowing a position of arms higher than the chest. 

Deep catch:

Many swimmers have a "catch-up" style stroke. Unfortunately, this increases stress at the shoulder joint and vascular system. If working on less stress, have the swimmer have a deeper catch as the enter the water.

Neutral Hand Entry:

Entering without hand entry is paramount for all shoulder prevention, as excessive internal rotation increases shoulder stress.

Shallow Backstroke Catch:

Entering with a deep catch in backstroke stresses and strains the neurovascular structures in the front of the shoulder...no good! Instead, have a wider, more shallow catch, similar to Missy Franklin's technique. 

Thoracic Outlet Syndrome Dryland Techniques

Foam Roll Thoracic Spine:

SMR Scalenes:

SMR Pectoralis:

Nerve Mobility:

First Rib Mobilization: 

Anterior Neck Strengthening:

Scapular Strengthening:

Summary on Thoracic Outlet Syndrome for Swimmers

Some cases of TOS require drastic treatment, like surgery (first rib resection). Instead of dealing with potential surgery, keep a close eye on TOS symptoms and begin early with treatment and technique modifications at the first instance of symptoms. 

These are only some technique modifications and treatments, as each person is individual and different stroke biomechanics and rehabilitation/prevention programs are necessary for each person. Moreover, just because some swimmers perform with techniques which increase shoulder stress, doesn't necessarily result in TOS or injury. Therefore, if you are suffering from TOS, see a rehabilitation specialist for guidance and individualization.

If looking for more injury prevention techniques, consider purchasing the COR Swimmer's Shoulder System.

  1. Nitz AJ, Nitz JA. Vascular thoracic outlet in a competitive swimmer: a case report. Int J Sports Phys Ther. 2013 Feb;8(1):74-9. 
  2. M Sadeghi-Azandaryani, D B├╝rklein, A Ozimek, C Geiger, N Mendl, B Steckmeier, J Heyn Thoracic outlet syndrome: do we have clinical tests as predictors for the outcome after surgery?Eur J Med Res. 2009; 14(10): 443–446. Published online 2009 September 28. doi: 10.1186/2047-783X-14-10-443
By Dr. G. John Mullen received his Doctorate in Physical Therapy from the University of Southern California and a Bachelor of Science of Health from Purdue University where he swam collegiately. He is the owner of COR, Strength Coach Consultant, Creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Do Growth Spurts Increase Injury Risk?

Take Home Points on Do Growth Spurts Increase Injury Risk?
  1. It seems the injury rate increases during growth spurts, but research is very limited. 
Growing pains are common in children, yet the cause and treatment of growing pains are not well known. Some hypothesize growing pains occur from muscles pulling on bones creating discomfort. Others believe increase in bone size simply increases discomfort from an increase in mechanical pressure. 

Growing pains are one type of "injury" during growth spurts. Specific adolescent injuries also exists, which I commonly see for Physical Therapy

Adolescent Injuries

  1. Osgood-Schlatter's Disease: is a painful swelling of the bump on the upper part of the shinbone, just below the knee. This bump is called the anterior tibial tubercle. It is believed to occur in active children who's patella tendon pulls on the tibial tubercle. 
  2. Sever's Disease: inflammation of the growth plate in the heel of growing children, typically adolescents. The condition presents as pain in the heel and is caused by repetitive stress to the heel and is thus particularly common in active children. It usually resolves once the bone has completed growth or activity is lessened.
  3. These are just a few common musculoskeletal injuries effecting children. Many other injuries can occur during growth spurts and parents for decades believe children have a higher injury risk during a growth spurt. Combine this injury risk with chronic poor posture from computers/electronics and early sports specialization and you've got a high injury risk for child...scary!

Growth Spurts and Injuries

Now, before we jump to conclusions about the injury incidence and growth spurts, we should consult
the limited literature:

Yukutake (2014) had 654 baseball players aged 6-12 years, all male, complete an original questionnaire that included items assessing demographic data, developmental factors (increase in height and increase in weight over the preceding 12 months), and baseball related factors. Multiple regression analysis was used to identify the risk factors for elbow pain during the 12 months prior to the study.

The data collected for 392 players without omissions or blank answers were submitted to statistical analysis. The results found that 19.1% of Little League baseball players had experienced elbow pain in the 12 months leading up to the study. The analysis revealed that height and increase in height were risk factors that increased the risk of elbow pain after adjustment for demographic data, developmental data, and baseball related factors.

Wild (2012) looked at ACL injury rates in adolescent boys and girls, noting girls have a higher ACL injury rate from:
  1. The effects of changes in estrogen levels on the metabolic and mechanical properties of the ACL
  2. Changes in musculoskeletal structure and function that occur during puberty, including changes in knee laxity, and lower limb flexibility and strength. 
  3. How these hormonal and musculoskeletal changes impact upon the landing technique displayed by pubescent girls.With limited research, limited conclusions are possible. 
However, the risk of injury increases during periods of growth. Unfortunately, recommendations now are purely theoretical. Some would suggest decreasing activity during maturation, but these are the peak years of motor learning. Instead, decreasing training volume and varying activities may be the best solution. This website has brought up the idea of a "swim stroke count", similar to a pitch for baseball. However, swim stroke counts may not be effective nor practical as many other factors influence musculosketetal stress on maturing bodies. Looks like we need more research on maturing athletic children!

  1. Yukutake T, Nagai K, Yamada M, Aoyama T. Risk factors for elbow pain in Little League baseball players: a cross-sectional study focusing on anthropometric characteristics. J Sports Med Phys Fitness. 2014 Apr 9.
  2. Wild CY, Steele JR, Munro BJ. Why do girls sustain more anterior cruciate ligament injuries than boys?: a review of the changes in estrogen and musculoskeletal structure and function during puberty. Sports Med. 2012 Sep 1;42(9):733-49. doi: 10.2165/11632800-000000000-00000. Review.
By Dr. G. John Mullen received his Doctorate in Physical Therapy from the University of Southern California and a Bachelor of Science of Health from Purdue University where he swam collegiately. He is the owner of COR, Strength Coach Consultant, Creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Are Ice and NSAIDs Beneficial for Recovery?

Take Home Points on Are Ice and NSAIDs Beneficial for Recovery?
  • Ice helps decrease pain, but does increase muscle damage.
  • NSAIDs restore function, but improve bone, but not soft tissue healing.
The use of non-steroid anti-inflammatory drugs (NSAIDs) and ice are common staples in
sports medicine. Yet, the use of these modalities has recently received resistance from some online experts (Kelly Starrett, Dr. Gabe Mirkin). Despite this criticism, these modalities are still frequently used, sometimes ad libium. Now, before I make a notion on these modalities, it is important to understand the injury process, below is an exert from the COR Swimmer's Shoulder System.

Everyone is familiar with inflammation. The inflammatory process occurs within seconds of every injury, but can linger for weeks or months with bad injuries or poor management.

Inflammation is stemmed by the infiltration of cells, entitled neutrophils, during the first 6-24 hours; they are replaced by other cells (monocytes) in 24-48 hours. These cells will try to attack the inflammation and remove injurious agents. Phagocytosis is involved in the process of engulfing foreign particles and releasing the enzymes of neutrophils and macrophages which are responsible for eliminating the injurious agents. These are two major benefits derived by the accumulation of leukocytes at the inflammatory site.

Chronic inflammation is a different warrior. The key player is another type of cell, the macrophage. Macrophages are large cells that can remain for weeks to months, perpetuating injuries.

The classic signs and symptoms of inflammation are swelling, redness, throbbing, radiating heat, and constant pain. These pains especially occur when you wake up in the morning and last between thirty and sixty minutes. Also, just because you had the initial injury four months ago doesn’t mean inflammation has resolved or hasn’t returned, so pay closer attention to the signs and symptoms as opposed to the duration.

Once again, the inflammtory process initiates every injury. This process is beneficial in restoring the body, but does decrease strength. This decrease in strength is why many seek improvement [well and the pain]. This has resulted in the use of the two most common modalities NSAIDs and ice. Unfortunately, these two modalities may prevent the normal physiological reaction of an injury. This impairment is thought to alter long-term improvement. However, many people take NSAIDs and ice for short-term gains. If someone needs improvement, for a quick return to the pool, then NSAIDs and ice are beneficial. However, the use of these modalities likely decreases long-term recovery, perhaps increasing the risk of re-injury. Unfortunately, most of this research is based on rodents, not humans and as I've mentioned before, rodents have different inflammatory processes! This makes the research nontransferable to humans ... oh well! Nonetheless, lets look at the research we have!

NSAIDs on Healing

The authors reviewed the effectiveness of NSAIDS and selective (COX-2 inhibitors) NSAIDS on soft tissue and bone healing. A total of 44 articles reviewed (9 on soft tissue and 35 on bone healing). Thirty-nine of these articles were on animals and 5 on humans.

No humans studies have been done on humans assessing the interaction between NSAIDS and soft tissue healing. Of the studies reviewed, there is a controversy between the administration of selective and non-selective NSAIDS after surgery, as many studies suggest detrimental effects on bone and soft tissue healing. However, the literature on this subject in humans is minimal.

It appears inflammation mediated by prostaglandins is necessary to improve bone healing. However, in soft tissue injury, growth factors are more important and prostaglandins less involved. This suggest NAIDS are likely beneficial in soft tissue, but potentially not bone healing.

Improving inflammation is necessary to decrease symptoms, however the use of NAIDS during bone repair may impair recovery, therefore only use NSAIDs in soft tissue injuries. However, more human clinical trials are necessary before a definitive answer is possible.

NSAIDs on Gut Bacteria

One potential hazardous result of NSAID consumption is the potential loss of integrity of bacteria, making the gut permeable to harmful substance.

Nine male trained cyclists underwent small intestine lining permeability in four different conditions (Van Wijck 2012):

1) during and after cycling after intake of ibuprofen

2) during and after cycling without ibuprofen

3) rest with prior intake of ibuprofen

4) rest with prior ibuprofen intake

The small intestinal lining was evaluated by providing the subjects a sugary drink, then assessing the amount of human intestinal fatty acid binding protein (I-FABP).

The ibuprofen conditions took 400 mg of ibuprofen the night before and 1-hour prior to cycling on a fasted stomach. The cyclist performed roughly 90 minutes of cycling at moderate/hard cycling.

In both exercise conditions, the I-FABP levels gradually increased with cycling. However, cycling with ibuprofen ingestion resulted in even high levels of I-FABP.

These results show cycling alone increases both gastroduodenal and small intestinal permeability. This difference increased with ibuprofen intake. This is thought to be from splanchic hypoperfusion, reducing the blood to the gut and including injury to the enterocytes. One of the major pathways suspected for GI damage is:

“to be involved is the inhibition of COX isotypes 1 and 2, resulting in local inflammation and vascular dysregulation, ultimately reducing perfusion and promoting mucosal integrity loss within the splanchnic area (Van Wijck 2012)”.

Unless ergogenic benefits from NSAIDs exists, swimmers should not use these medications prior to exercise. Moreover, inflammation may yield greater results in endurance sports. One flaw with the study is the fact the athletes were fasted while taking NSAIDs. However, one note is the athletes were fasted during this test, this may have increased the intestinal lining to susceptibility.

For rehabilitation, NSAIDs may still be beneficial, but at this time it is not certain if the benefits outweigh the risks.

Ice and Muscle Damage Healing

Eleven male college baseball players underwent two trials: sham application and topical cooling. Each trial was used five sessions of 15-min cold pack application to the exercised muscles 0 hours, 3 hours, 24 hours, 48 hours, and 72 hours after eccentric exercise training.

The eccentric training protocol consisted of 6 sets of 5 eccentric contractions with 2 min rest between sets at 85% of their maximal strength. Muscle hemodynamics (hemoglobin most notably), inflammatory cytokines (multiple interleukins), muscle damage markers (Creatine kinase), visual analog scale (VAS), and muscle isometric strength.

After topical cooling, rapid and sustained elevations in total hemoglobin and tissue oxygen saturation were noted. Also, creatine kinase was noted in both trials, but was elevated after topical cooling. Inflammatory markers were not changed following cooling. VAS was not different between groups, however topical cooling significantly increased rating of fatigue post-exercise. No significant differences were noted in strength between groups.

Increased muscle damage, most notably the creatine kinase increase, was apparent in the topical cooling group. This is thought to occur from the rapid deviation in blood supply to the muscle.

Using ice after practice improves muscular soreness, but appears to increase muscle damage due to rapid changes in ischemia. Therefore, unless injured topical cooling should be avoided.

Ice and Blood Flow

Nineteen subjects participated in this single-blinded, where the clinician was blinded. There was no history of lower extremity injuries for the past 6 injuries. Each participant visited the laboratory four separate times where baselines were measured at the first two visits, then the next two visits a trial of ice (750-g of crushed ice placed on the medial gastrocnemius) and a control trial.

“There was a significant correlation (r = 0.49) between subcutaneous tissue thickness and change in intramuscular temperature immediately after treatment (P = 0.05) for the cryotherapy condition. Significant correlations were also found for change in temperature during the rewarming period and change in blood volume at rewarming (r = 0.53, P = 0.033) and change in blood flow at rewarming (r = 0.56, P = 0.025) for cryotherapy (Selkow 2012)”.

Microvascular perfusion of the gastrocnemius did not decrease from baseline with cyrotherapy was applied, despite the decrease in subcutaneous temperature. The result was different than past studies, as many think cryotherapy decreases blood flow. This may be from no alterations noted in the microvascular.

In the healthy population, cryotherapy appears not to alter blood-flow. Therefore, benefits and risks associated with cryotherapy application for inflammation may be negligible. However, next research must look at inflammation specifically. Until then, the effects of ice for injuries seem purely for slowing nerve conduction to gate pain.

NSAIDs or Corticosteroids for Recovery

Zheng (2014) performed a systematic review of all the high-quality studies comparing NSAIDs and corticosteroid injections, a total of ten full articles. Overall, 267 patients were analyzed and of the six studies two focuses on rotator cuff tendonitis patients, two on shoulder impingement syndrome, one studied frozen shoulder of diabetes and the other investigated shoulder pain.

Of these studies, NSAIDs and corticosteroids did not have a significant difference in pain improvement. Corticosteroids were significantly better for remission of symptoms. Five of the studies reported range of active shoulder abduction and note NSAIDs did not significantly improve the active shoulder abduction compared to corticosteroids. The studies assessed were 4 – 6 weeks in length.

Compared to NSAIDs, corticosteroid injections provide faster relief. However, comparisons of other therapies and conjunctions of therapy are needed, as well as longer study periods and follow-ups.

My Recommendations

If you are injured, stop exercising. If the pain is non-stop, see a rehabilitation specialist like a physical therapist. At this time, apply ice, as it does reduce pain and doesn't seem to alter blood flow. However, apply the ice for a short period, as it may increase muscular damage. I suggest applying the ice for up to 10 minutes and remove it for 20 minutes. Only ice immediately after the injury, ~6 hours after the injury. If you are competing at a meet and must perform, NSAIDs can help decrease pain and restore function. However, if you are not in a rush for return, try not to ice and consider compression instead. Compression helps naturally clear the fluid from the joint, facilitating recovery. When you are able to move comfortably without pain, do so. Movement also helps move fluid out of the joint and restore function. However, do not move into pain, as this can alter movement patterns and impair function. 

Try and prevent using NSAIDs, unless unrelenting pain exists and the injury appears muscular. If recovering from an injury, a corticosteroid injection is likely better than just NSAIDs, but remember other rehabilitation is needed. 

We have much more research needed on the subject, but it isn't clear that ice and NSAIDs are a “no brainer”. Until more research is performed, I'll continue the suggestions I've made for years, if you're in no rush, let the inflammation naturally make it's way throughout the body, giving yourself rest and compression for improvement. Once you're able to move naturally do so! However, if you are in a rush, like at a big competition and need to get in the pool, NSAIDs and ice can help!


By Dr. G. John Mullen received his Doctorate in Physical Therapy from the University of Southern California and a Bachelor of Science of Health from Purdue University where he swam collegiately. He is the owner of COR, Strength Coach Consultant, Creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Inflammation in Sports

Inflammation in sports is a baffling subject. Some view inflammation as beneficial, while others consider it detrimental. This subject is confusing as inflammation occurs in seemingly two different scenarios. For example, how can inflammation after exercise be beneficial, where inflammation about injury is harmful if both are the same process?

This article tackles the difference between inflammation after injury and exercise while providing a practice approach for using common anti-inflammatory medication.

Spotting Inflammation
There are five attributes to inflammation in sports:
  • Redness, swelling, heat, pain, loss of function
Moreover, pain all the time (not only during movement) and pain in the morning are typical signs of inflammation. Increased joint fluid increases pressure on pain receptors (nocioceptors), causing pain all the time. If pain is worse in the morning, it is likely inflammation surrounds the joint, as muscle contractions did not pump the fluid away from the joint during sleep. This increased fluid increases the pressure on pain receptors increasing pain during the morning.

Exercise Induced Inflammation
Many feel inflammation in sports help long-term strength gains as inflammation repairs damaged muscle fibers following exertion. Mishra in 1995, determined supplementing a strength training group with anti-inflammatory medication had an acute increase in strength, compared to the control group. This increase persisted at 7 days, but at 28 days the medication group experienced a step back, as their maximal muscle tension dropped by about 1/3 of their maximum tension.

It appears anti-inflammatory medication resolves acute exercise induced inflammation resulting in increased strength, as it would allow them to recover and be stronger, as they less sore from the muscle fibers being destructed during the exercise.

However, the mechanism which NSAIDs improve acute performance has not been justified:
“anti-inflammatory doses of ibuprofen reduced CK activity but not the neutrophil response or other indirect markers of muscle injury during recovery from eccentric arm exercise (Pizza 1999).”

After training Gulick performed an analysis of many types of treatment and concluded:

“none of the treatments were effective in abating the signs and symptoms of DOMS. In fact, the NSAID and A. montana treatments appeared to impede recovery of muscle function (Gulick 1996).”

Therefore, it seems NSAIDs improve acute strength with NSAID, but it seems to prevent overall recovery of muscle and strength gains.

This is perhaps from NSAIDs masking the amount of damage during exercise, allowing the body to do more damage without allowing proper recovery time. Don't beat yourself while you're down!

No study has directly studied NSAIDs on in-water strength, but one could guess NSAIDs would impair in-water strength development. This loss of strength impairs swimming progress as in water strength (especially of the upper body) correlates with speed (Hsu 2000).

Injury Induced Inflammation
After any musculoskeletal injury inflammation occurs. This process increases the volume of fluid in an unwanted area. When too much fluid is in a confined area, the amount of mechanical pressure increases. This mechanical pressure presses on nocioceptors and causes pain. Pain inhibits strength and athletic performance, therefore resolving this mechanical pressure is mandatory to move the injury from inflammation to remodeling.

The best method to improve this is with homeopathic and over-the counter medication. Combining Ginsenosides and Large volumes of NSAIDs helps inflammation by helping the medication reach 'titer level' or the minimum effective level (Read more about tips to improve shoulder inflammation) (note: take with food and watch stomach irritation).
Once the inflammation subsides, discontinuing the anti-inflammatories is essential for improving strength (see below).

If you are looking for short-term improvement whether you are at a competition or injured, NSAIDs acutely improve strength. However, if you’re seeking long-term strength gains, do not use NSAIDs to trick the body into working harder or not letting inflammation to aide full repair and remodeling, essentials for muscle strength.

Last Point
Lastly, the chronic use NSAIDs appears damaging to tendons.

In rats, Dimmen 2009 determined:
“We found a significantly lower tensile strength in rats given both parecoxib and indomethacin (anti-inflammatory medications) compared to the control group. Stiffness in the healing tendons was significantly lower in the parecoxib group compared to both the placebo and the indomethacin groups. The transverse and sagittal diameters of the tendons were reduced in both the parecoxib and indomethacin groups. Both parecoxib and indomethacin impaired tendon healing; the negative effect was most pronounced with parecoxib (Dimmen 2009).”

This has not been proven in humans, but is worrisome nonetheless.
Make sure you are not abusing NSAIDs and use them properly, as overuse is damaging and reckless. Follow these simple guidelines:
  • Only take NSAIDs after an acute musculoskeletal injury
  • Discontinue intake after inflammation resolves
  • Do not take NSAIDs after exercise unless at a competition, where performance not strength gains are most important
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  3. Dimmen S, Engebretsen L, Nordsletten L, Madsen JE. Negative effects of parecoxib and indomethacin on tendon healing: an experimental study in rats. Knee Surg Sports Traumatol Arthrosc. 2009 Jul;17(7):835-9. Epub 2009 Mar 19.
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By G. John Mullen founder of the Center of Optimal Restoration, head strength coach at Santa Clara Swim Club, creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.