On Physical Therapy residency programs

The topic of physical therapy residencies came up on a DPT student facebook page and I decided to share a brief article I wrote for the Wisconsin Physical Therapy Association’s student corner. Enjoy and comment.

Residency education in any section whether it be orthopedics, cardiopulmonary, sports, neuro, etc offers a competitive edge to clinicians, particularly entry level DPTs. Fast tracking to specialization, direct mentoring, opportunities for research, teaching responsibilities are not typically offered in most places of employment (especially to new grads) and rarely if ever provided in combination. Additionally in certain areas of practice (pediatrics, cardiopulmonary, women’s health and clinical electrophysiology) it is rather difficult to obtain the necessary hours needed to sit for board specialization. For those sections residency training is almost necessary to practice.

That being said if you are unsure after graduating as to what sort of clinician you aspire to become or what area you want to practice in, I would caution against pursuing a residency. As with a residency you are in effect “building on” clinical skills and knowledge more so than “building up”. The extent of that will vary from program to program and amongst sections but in general I feel that is the case; and as sparse as the spots are nationally, they very well should be. Residency training is not mandatory and neither is specialization, although that hopefully may change. So as with anything in life if you are uncertain, avoid making a rash decision and wait. Along those lines if you do decide after graduating and passing the NPTE that you do not wish to pursue a residency immediately, I would strongly recommend limiting that waiting period to 3 years post graduation. By that time you should have your own identity as a clinician, earned at least your first promotion and possibly been a clinical instructor. Instead I would then consider sitting for whichever board specialization you desire as an independent.

In choosing a residency I feel that the best programs are affiliated with a DPT program or a university. Private clinics lack the opportunities for research, teaching and collaboration with other providers that all university based programs offer. Again the importance of this varies between residents but I feel that a program should offer more than just mentoring. A residency should offer pathways to different aspects of the field and develop a therapist into a leader in their section not solely a “clinical expert”. Again this is my opinion alone, talk to other residents in order to gain as many perspectives as possible which will help you make the best choice for YOU. Ultimately it’s your professional life, goals and aspirations.

The Oxygen Delivery Problem

For those working in acute or cardiopulmonary sections of physical therapy you may have considered this:

“If a patient has a low oxygen saturation and they respond to supplemental oxygen why don’t we just put them on a non rebreather mask non-stop? It would surely provide them with enough oxygen that they would never desaturate”.

A non-rebreather mask (NRB)

A non-rebreather mask (NRB)

For starters a non rebreather mask (NRB) is an oxygen delivery device that provides patients with a fraction of inspired oxygen (FiO2) of 100% and is used on patients in critical conditions such as ARDS . Normally the air we inspire is a mixture of gases, mainly nitrogen (78%), and the FiO2 is 21%. The amount of both gases in this mixture is important physiologically for a number of reasons. Due to the increased affinity of hemoglobin for oxygen at the alveolar level due to the Haldane effect (also see Bohr effect transport of O2 to working tissue) oxygen is preferentially absorbed over other gases and nitrogen remains in the lungs which help maintain the inflation of the alveolar sacs. If one were to increase the percentage of inspired O2, over a period of time there would be less nitrogen available to maintain the patency of alveoli. Due to the physiological principles described above this would eventually result in alveolar collapse or the technical term “absorption atelectasis

Secondly, increased blood levels of O2 can suppress the ventillatory drive, especially in patients with Chronic Obstructive Pulmonary Disease (COPD) who demonstrate CO2 retention(1-2). CO2 retention, defined as increased blood gas values of CO2, can occur in patients with severe COPD (1). The mechanisms for this physiological process are still not completely understood. Carbon dioxide values, in a normal functioning system, regulates the drive to breath, via central and peripheral chemoreceptors (3). In patients with CO2 retention this mechanism is altered and their body responds to circulating levels of oxygen; lower levels of O2 facilitates breathing and higher amounts suppress (1-3). Therefore increasing the amount of delivered oxygen to a patient with this condition could possibly result in apnea.

Hyperoxia (higher than normal levels of oxygen) has also been shown have other systemic effects on the body (4-7). In the peripheral vasculature, hyperoxia causes vasoconstriction. The amounts of vasoconstriction and blood flow reduction varies in body area as the coronary arteries and brachial arteries demonstrate markedly reduced blood flow when exposed to hyperoxic states, the reduction in the cerebral arteries appears to be less (5-7). In addition to the vasoactive effects, hyperoxia can also lead to an increase in reactive oxygen species which can lead to oxidative stress and damage tissue (7).

Rarely does one chemical, tissue or system act completely in isolation. Your body is not a petri dish and we do not operate in a vacuum. The effects from something seemingly innocuous to one organ system may result in deleterious effects to another. Just because the reaction in a cell to a given amount of substance is beneficial is does not always mean that more of that chemical is always good. Human physiology is a story, with many subplots and characters with an exer-expanding number of volumes as we learn more about the body.

1 Kim S et al, Oxygen Therapy in Chronic Obstructive Pulmonary Disease Proc Am Thorac Soc. May 1, 2008; 5(4): 513–518. source 

2 Gorini M et al, Breathing pattern and carbon dioxide retention in severe chronic obstructive pulmonary disease Thorax 1996;51:677-683 source 

3 Jones and Barlett Learning LLC 2014, Regulation of Ventilation pgs 4-14, source 

4 Dean J et al, Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neurons, J Appl Physiol 96:784-791, 2004 source 

5 Farguhar H et al, Systematic review of studies of the effect of hyperoxia on coronary blood flow, Am Heart J. 2009 Sep;158(3):371-7 source 

6 Xu F et al, Effect of hypoxia and hyperoxia on cerebral blood flow, blood oxygenation, and oxidative metabolism. J Cereb Blood Flow Metab. 2012 Oct;32(10):1909-18. source 

7 Rossi P and Boussuges A, Hyperoxia-induced arterial compliance decrease in healthy man, Clin Physiol Funct Imaging. 2005 Jan;25(1):10-5 source.

Pediatric Exercise Testing


In the adult population, when a patient sustains a cardiovascular insult requiring surgery or some other form of medical therapy and quite often the patient is referred to cardiac rehabilitation. With increased survival rates following cardiac surgery(1) cardiac rehab is an important component to the overall recovery of the patient by safely returning them to their prior level of function it has also been shown to reduce morbidity, readmission rates and cost (1). An important component to the evaluation process for cardiac rehabilitation is the results from exercise testing. Testing is either performed by a cardiologist before referral or in the outpatient clinic by a physical therapist or exercise physiologist. For adults there are a litany of standardized testing protocols and procedures available to the clinician to use dependent on the case. After finishing a clinical at a Pediatric Trauma 1 hospital where I spent an extensive amount of time treating children with cardiovascular pathologies I began to ask what is the most valid and reliable measure to use for a pediatric population? Similar to adults, pediatric cardiac procedures have improved and patients are living longer(1,2,3). Due to this increased survival rate it would be beneficial to examine the most appropriate functional capacity or exercise test for pediatric patients as the goal of allowing the patient to perform activities at their highest level of functional independence is similar but the hemodynamic response to exercise, gait mechanics, respiratory mechanics are different from adults and amongst different ages of children.  From what I gathered from staff members is that many are not sure either. This post will evaluate  two of the most commonly used exercise tests for pediatrics patients, the Bruce Protocol and 6 minute walk test. The benefits and limitations will be provided for each test as well as a summary and recommendation for clinical implementation.

Bruce Protocol 

The Bruce Protocol is a progressive graded treadmill test. The standard protocol consists of  7 stages, each lasting three minutes. The test can last up to 10 stages though most patients don’t surpass stage 6. The test starts with having the patient walk at 1.7 mph (2.7 km) up a 10% incline and after each 3 minute stage both the treadmill speed and incline are increased according to the protocol (Figure 1). Heart rate, EKG and Respiratory rate are constantly assessed, rate of perceived exhaustion (RPE) is taken every minute, blood pressure is taken after each stage. The patient’s VO2max is then determined either by using a regression plot based on the stage the patient completed (if the test was not a true max test), vitals response and body-weight or gas exchange analysis (Figure 2) (if available at the facility).

Figure 1.

Standard Bruce protocol

Standard Bruce protocol

Figure 2.

treadmill test

A patient performing the Bruce Protocol

Benefits of Bruce Protocol for Pediatric Patient 

The Bruce provide a more accurate assessment of cardiovascular system’s function, more specific information on what caused the termination of the test, a more accurate estimation of VO2max and constant monitoring of vitals. The test has had gone through countless meta-analyses and systematic reviews examining it’s validity and reliability amongst other measures; established norms have been developed for healthy pediatric populations (4,5).

Limitations of Bruce Protocol for a pediatric patient

The Bruce protocol has some practical disadvantages. For well trained children, the walking speed at the first 4 stages of the Bruce protocol are too slow, additionally the 3 minute duration of each stage is too long which may lead to boredom (5). The most appropriate running speeds for well trained children occur during stages when the elevation is high >18% grade (5,6). Thus the most velocity appropriate stages of the Bruce Protocol occur at relatively steep grades which encourages subjects to hold onto the handrails, thereby affecting the oxygen cost of exercise significantly. Several studies have demonstrated that usage of handrail support increases treadmill time (TT) (7,8), with the largest significant difference occurring when the front handrail is used (7), even  support is limited to 2 fingers it is enough to create a small but statistically significant increase in TT in some patients (7,8). There are separate regression tables and values for handrail usage (7,8). For younger or more limited children, the increase in work increments between successive stages may be too great, resulting in the tendency for subjects to quit during the first minute of a new 3-minute stage (7)

6 minute walk test (6MWT)

The 6 minute walk test (6MWT) is a non graded constant load, constant intensity exercise test used to assess the submaximal level of functional capacity. The test is relatively simple in that it only requires a 100-ft hallway (Figure 3) and no exercise equipment or advanced training to administer it. This test measures the distance that a patient can quickly walk on a flat, hard surface in a period of 6 minutes. It evaluates the global and integrated responses of all the systems involved during exercise, including the pulmonary and cardiovascular systems, systemic circulation, peripheral circulation, blood, neuromuscular units, and muscle metabolism (9,10,11).

Figure 3.

6 minute walk

6MWT course

Benefits of the 6 minute walk test for a pediatric patient

6 minute walk test for children has excellent test-retest re- liability (ICC = 0.94) and moderate yet statistically significant, correlation between 6-minute walk distance (6MWD) and V02 (10) have been reported (r = 0.44-0.73, P < .0001). The 6MWT provides information that may be a better index of the patient’s ability to perform daily activities than is peak oxygen uptake as most activities of daily living are performed at submaximal levels of exertion (12)

Limitations of the 6 minute walk test for a pediatric patient

The 6MWT does not determine peak oxygen uptake as it is by design a submaximal test. It does not provide specific information on the function of each of the different organs and systems involved in exercise or the mechanism of exercise limitation, as is possible with maximal cardiopulmonary exercise testing (9,10,11).Patients who become fatigued are in fact allowed to take a rest break . Some authors argue that the results from a 6MWT should not be used to supplant a formal exercise test (such as the Bruce) however some studies suggest that it is a reliable measure of functional capacity (9-11).  A systematic review evaluating the effectiveness of the 6MWT in pediatric populations published  Physical Therapy and found that there was a large variation in test procedures among the included studies, and only 1 study followed all ATS guidelines (10). In addition to that  having a child “walk as fast as they can without running” is a potential problem in regards to compliance due to patient understanding. That may result in skewed data and other statistical or methodological issues.

Discussion and Summary

The Bruce does provide a more accurate assessment of the cardiovascular system’s function however the testing conditions are not reflective of normal daily physical activity. Due to the lack of instrumentation required, the usage of more normal gait conditions and since most activities of daily living are performed at submaximal levels of exertion the 6MWT appears to the more valid test to assess tolerance to functional activity for this patient population. Although Bruce is more a specific test for cardiovascular function the 6MWT is more valid for assessing tolerance to functional activity. More research is needed to examine the cause for the inconsistencies in administration of the 6MWT.

Cardiac Rehabilitation  in the pediatric population is greatly underutilized, and though clinical research on this aspect of therapy is promising it has been limited (2).  However, a systematic review by Tikkaken et al in 2011 found that the “benefits [of cardiac rehab cardiac rehabilitation in children with congenital heart disease] have been observed in many studies, and no adverse events have been reported”. This is encouraging however with any intervention more evidence needs to emerge to support its implementation.

Works Cited

1) Arena, R Et al Cardiac Rehabilitation Attendance and Outcomes in Coronary Artery Disease Patients, Circulation. July 9, 2012;

2) Tikkanen A et el, Paediatric cardiac rehabilitation in congenital heart disease: a systematic review, Cardiology in the Young (2012), 22, 241–250

3) Algra S et al, Improving surgical outcome following the Norwood procedure, Neth Heart J (2011) 19:369–372.

4) Connor J et al, Clinical Outcomes and Secondary Diagnoses for Infants Born With Hypoplastic Left Heart Syndrome, Pediatrics Vol. 114 No. 2 August 2004

5) van der Cammen-van Zijp, M et al, Exercise testing of pre-school children using the Bruce treadmill protocol: new reference values, Eur J Appl Physiol (2010) 108:393–399

6) Cumming, G et al, Bruce Treadmill Test in Children: Normal Values In a Clinic Population, The American Journal of Cardiology (1978) Volume 41 pg 69-76

7)Berling J et al, The Effect of Handrail Support on Oxygen Uptake During Steady-State Treadmill Exercise, Journal of Cardiopulmonary Rehabilitation 2006;26:391/394

8)Manfre M et al, The effect of limited handrail support on total treadmill time and the prediction of vo2 max, Clinical Cardiology Volume 17, Issue 8, pages 445–450, August 1994

9) ATS Statement: Guidelines for the Six-Minute Walk Test; Am J Respir Crit Care Med Vol 166. pp 111–117, 2002

10) Bartels, B et al, The Six-Minute Walk Test in Chronic Pediatric Conditions: A Systematic Review of Measurement Properties, Physical Therapy. 2013; 93:529-541.

11)Lammers A, et al, Comparison of 6-min walk test distance and cardiopulmonary exercise test performance in children with pulmonary hypertension

12) Geiger R et al, Six-Minute Walk Test in Children and Adolescents, J Pediatr 2007;150:395-9

Shone’s Disease a rare congenital heart syndrome

Shone’ Syndrome

  • A rare congenital heart disease described by Shone in 1963
  • Manifests as decreased left ventricular output
  • There are two types of Shone’s syndrome: complete and incomplete Shone’s syndrome.
  • In the complete form of Shone’s syndrome, all four of the lesions will be present.

In the incomplete form, two or three lesions will be present (more common)

Supravalvular mitral membrane (SVMM): Typically the first abnormality to develop. An abnormal ridge of connective tissue on the atrial side of the mitral valve. Often the supravalvular ring may encroach on the orifice of the mitral valve leaflets and restricts their movements. While a supravalvular mitral ring may allow normal haemodynamic flow from the left atrium to the left ventricle, it often causes an obstruction of the mitral valve inflow(cite). Mitral supravalvular ring is associated with other defects in almost 90% of cases

Valvular Mitral Valve stenosis due to a parachute mitral valve: The mitral valve chordae insert into one papillary muscle. In parachute-like asymmetric mitral valve, most or all chordal attachments are to one papillary muscl. This abnormal attachment of the chordae tendonae results in stenosis of the mitral valve since the valves are held in close proximity.

Subaortic stenosis (membranous or muscular): is a fixed form of anatomic obstruction to outlet of blood across the left ventricular outflow tract. There are four basic anatomic variants which are as follows: (1) a thin discrete membrane consisting of endocardial fold and fibrous tissue, (2) a fibromuscular ridge consisting of a thickened membrane with a muscular base at the crest of the interventricular septum, (3) a diffuse, fibromuscular, tunnel-like narrowing of the LVOT, and (4) accessory or anomalous mitral valve tissue.

Aortic Coarctation: Coarctation of the aorta is a narrowing of the aorta most commonly found just distal to the origin of the left subclavian artery. Since the narrowing occurs distal to the L subclavian artery symptoms typically are manifested in the lower extremities such as cramps, cold feet and decreased ability to perform exercise. Aortic coarctation occurs in 20–59% of cases with mitral valve anomalies

Here is an illustration of the pathology:


Associated Pathologies
Heart failure, pulmonary hypertension, pulmonary edema, right ventricular hypertrophy, Left ventricular hypoplasia, pneumonia and cor pulmonale.

Diagnostic Imaging:
Echocardiogram, Pulmonary Artery catherization, MRI, chest radiograph, heart auscultation, EKG

Clinical Exam/Findings:
Loud S2, cold feet, bilateral rales/crackles. Orthopnea, diastolic murmur, atrial fibrillation, low cardiac output,

If detected early surgery can be performed to correct the defects and is typically done in stages, which reduce dysfunctions. The longer the patient goes untreated and the more elevated pulmonary artery pressure increases the more worse the outcome.


A happy patient post surgery 🙂

Differential Diagnosis:
Tetraology of Fallot, Cor triastrium sinister, patent ductus arteriousum, bicuspid aortic valve

Works Cited

  1. Iwata Y, Imai Y, Shin’oka T, Kurosawa H. Subaortic stenosis associated with systolic anterior motion. Heart Vessels. Nov 2008;23(6):436-9.
  2. Morris et al, CT and MR Imaging of the Mitral Valve: Radiologic-Pathologic Correlation, RadioGraphics, October 2010; 30, 1603-1620.
  3. Otto CM, Bonow RO. Valvular heart disease. In: Libby P, Bonow RO, Mann DL, Zipes DP, editors. , eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine 8th ed.Philadelphia, PA: WB Saunders; 2007:1625-1712
  4. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation 2008;118:e523-e661.
  5. Serra W*, Testa P and Ardissino P Mitral supravalvular ring: a case report, Cardiovascular Ultrasound 2005, 3:19
  6. Popescu BA, Jurcut R, Serban M, Parascan L, Ginghina C. Shone’s syndrome diagnosed with echocardiography and confirmed at pathology, Eur J Echocardiogr. 2008 Nov;9(6):865-7
  7. Board, A.D.A.M. Editorial. Coarctation of the Aorta. U.S. National Library of Medicine, 18 Jan. 0001. Web. 08 Mar. 2013.
  8. Brauner R A, Laks H, Drinkwater DC Jr, Scholl F, McCaffery S. Multiple left heart obstructions (Shone’s anomaly) with mitral valve involvement: long-term surgical outcome. Ann Thorac Surg 1997;64:721-9

Caffeine For Strength Training: A Review and Opinion

Much has been researched on the beneficial effects of caffeine for endurance/aerobic training. There are too many articles supporting these claims to make listing them reasonable. There is a reason why the IOC, NCAA and USTAF have strict restrictions and blood testing protocols for caffeine; it simply works. The rationale behind this is that caffeine helps facilitate free-fatty acid metabolism preferentially over glycogen and other carbohydrate homologs in the body. Fat generates a higher yield of ATP with a subsequent lower production of lactate, which is needed in long duration aerobic exercises. In addition to these metabolic effects research has shown caffeine to provide a temporary analgesic effect, which is extremely beneficial to endurance athletes during the final legs of their races when they are pushing themselves and likely utilizing anaerobic systems which can be painful. Cyclists have realized this analgesic effect for years as they used to fill their water bottles during races with flat cola. in addition to these effects, caffeine is a brochiodilator and also allows the diaphragm to contract more forcefully this is why pulmonary therapists administer caffeine to patients prior to treatment.

In a review published by McCormack and Hoffman in this July’s Journal of Strength and conditioning they highlight the potential benefits caffeine may provide for power and strength training. The mechanisms they attribute to the positive effects caffeine may provide are neuromuscular and central nervous system mediated. The CNS effects are founded under caffeine’s stimulant properties by blocking adenosine receptors which alters the perception of fatigue, improves focus and reaction time. Due to these effects, caffeine has been used as an alternative to amphetamines in USAF pilots flying repeated missions who require the mental acuity and sustained reaction time to complete a tactical flight operation.

The neuromuscular effect is mediated by enhanced excitation-contraction coupling through the Treppe effect. The treppe effect improves neuromuscular transmission by increasing the mobilization of intracellular calcium ions from the sarcoplasmic reticulum which is required in for the cross bridging between actin and myosin heads which produce a muscle contractions. Caffeine is also thought to enhance the kinetics of glycolytic regulatory enzymes, which are active in strength training activities, such as phosphorylase. The results of these metabolic and neuromuscular effects appear to allow the muscle to not only produce a more forceful contraction but also increase the number of repetitions per set. There have also been studies that have found caffeine if ingested acutely after a bout of exercise, (in the highlighted study’s case it was short duration high intensity intense cycling) recovery had improved as compared to a placebo on a quadriceps strength test.

Though the authors did report evidence that caffeine ingestion may be beneficial for strength and power training it appears though that the results are inconclusive as to whether or not caffeine in isolation results in these effects. The majority of these studies administered caffeine in the form of an energy drink or some sort of caffeine-proprietary nutrient concoction. The most common additives are taurine, beta-alanine, creatine and other amino acids; all of these supplements have shown to improve recovery and endurance to varying degrees. There also appears to be a dosage effect as well as most of the studies that resulted in improvements administered caffeine at the dosage of 5-6mg/kg body weight. Which if you consider that per 8oz of liquid redbull contains 80mg, coffee contains 110-150mg, and cola contains 30-40mg; so you may have to consume a considerable amount to get these effects much more than most have ever consumed.

Although these results are encouraging for the usage of caffeine for strength training purposes, in my professional opinion I would tread with caution. Caffeine can be rather dangerous to someone if administered in these high dosages without proper cardiovascular testing. Caffeine is sympathomimetic drug, which means it provides effects similar to those caused by the sympathetic nervous system which will increase HR, BP and blood flow to the skeletal muscle, amongst other effects. If someone who had an undiagnosed problem or defect were to ingest caffeine with these recommended dosage rate serious problems could occur. So it would be best to consult your physician before initiating a dosage regimen and have a physical therapist monitor you the first few times you exercise to monitor for deleterious effects/changes. Secondly, though the authors sited evidence of improved strength and power upon further review of the literature a lot of the studies they cited had subjects exercise to exhaustion or tested them on isokinetic strength tests. Tests to exhaustion are not a reliable or valid measure of strength or power and isokinetic testing does not assess the patient in functional movement pattern or at an angular velocity consistent with normal movement. In summary the evidence isn’t that strong to suggest direct strength and power gains but it may improve both factors in an indirect way, which I will elaborate on.

As most people in the field of sport performance and nutrition know most of the focus for supplementation is focused around recovery. Caffeine does directly improve recovery probably due to the increased, cardiac output and perfusion to the skeletal muscle. These cardiovascular effects will help remove metabolic waste products away from the muscles to the liver and help bring nutrients to the muscle. The authors however did not mention the benefit of caffeine as a moderate bronchodilator on training. If the bronchioles are more dilated it will improve ventilation to help buffer out the drop in ph due the shift in the strong ion difference following an acute bout of exercise. Similar to other supplements caffeine does show to improve the amount of repetitions a person can perform due to the previously mentioned improved blood flow and analgesic effect. If someone can decrease the soreness they feel during a max lift or increase the amount of repetitions they can perform, strength will improve over time.

In short caffeine like many other supplements helps you work out longer through it’s metabolic, cardiovascular, neuromuscular and central nervous system effects. It helps improve muscle metabolism by improving blood flow to the muscle, ventilation, focus and decreases pain. Dosage should be close to 5-6mg per kg body weight and administered 45min prior to exercise or immediately after.

Thanks for reading!

Here is a link to the article


Jump training and knee valgus angle: A review and opinion

ACL injuries and other such knee ligamentous pathologies are by far some of the more common and more devastating injuries in sports. Each year 2,220 ACLs are expected to be torn just in female college athletes alone with basketball players having the highest percentage. Some people attribute this preponderance of injury in women to a number of factors including narrowness of the intercondlylar groove of the knee, strength, flexibility and endurance. However, the current literature seems to consider jump landing strategies as function of neuromuscular control to possess the strongest causal link. This idea is reasonable as the mechanism of injury for ACL tears are deceleration/change of direction non-contact injuries with the foot planted. Thus if an athlete lacks control at the knee each time he/she lands the force from impact would be placed passive structures since the active structures don’t fire correctly thus potentiating the risk of injury to ligaments etc.

Due to this knowledge jumping programs focusing on correcting the valgus angle or frontal plane strategies have been initiated. These programs have had success but what researchers, therapists and coaches have trouble with is finding a way to fit these jumping programs into existing strength and conditioning programs. Most studies for valgus prevention utilize programs that last 6-8 weeks and each session can last 20min-1hr, which in the realm of athletics is too long to add to what typically is a very tightly scheduled regimen and programs that long may present problems with compliance . What Lee Herrington’s study examined was whether or not a program in 4 weeks, 2 times a week, for 20min per session could result in the same benefits of the longer jumping programs.

The study took place in Manchester, UK and the subjects were 15 female collegiate basketball players with no history of ACL or other such knee pathology. He evaluated knee “function” through three measures; 1) knee valgus upon landing from a depth jump to simulate a player landing from grabbing a rebound or finishing a shot, this was done via a digital video recording 2) He had the players run from half court to the foul line and shoot a jump shot, this was done to evaluate the players in a functional movement pattern specific to their sport and since the players would more likely concentrate on making the shot it than jump “correctly” which would expose their more normal jumping and landing strategies. Again the valgus angle was recorded via a digital video recording 3) The players were tested on lower extremity power by having them perform a cross over jump test. The test required the players to jump on one leg on diagonals across a line three times with the goal of traveling the farthest possible with 3 reps/jumps.

All subjects were evaluated on all 3 measures at pretest and then initiated a jumping program where they were first educated on how to land correctly with the knees in line in a “sagittal plane strategy” and performed all exercises with close monitoring for form. The program consisted of various plyometric and agility exercises with some basic strength components as well. All subjects completed between 10 to 12 sessions and were all instructed not to perform additional training on the day of each session. The researchers evaluated the test retest reliability for each measure on 5 players independent to the study to evaluate for error and all were found to have high reliability and very small amounts of difference between measure for each recording. The minimal statistical change for the depth jump was 1.2deg, 2.2deg for the jump shot, and 79cm for the cross jump test.

Upon post-test the results were quite impressive. The valgus angle during the depth jump on average decreased by 9.3deg on the left and 12.3deg on the right; the the jump shot valgus angle on average decreased by 4.3deg on the left 4.5deg on the right; for the cross jump test the left improved by 111cm and the right improved by 110cm. All of these results were significant to a p level of 0.05.

Though the subject size was relatively small and this was only tested on women it is not completely generalizable but for the athletic female population this is very applicable. And again other studies that had similar programs but were longer in duration produced benefits of similar magnitudes which suggests that these results are reasonable. The fact that this duration is effective also falls inline with accepted contemporary theories on strength training in that the early gains (under 6-8weeks) in strength and function are more based on neuromuscular adaptations rather than muscle hypertrophy. One must also consider again that since this study was done in a much shorter amount of time future programs like this should have less of a problem with patient compliance. In the future I would like to see a study that evaluates the results of a jump training program conducted in 4 weeks and evaluate the valgus angle 4 weeks after completion of the program to asses the retention of these skills and compare those to a training program under a longer treatment duration. A study analyzing the trend in valgus angle decreases after a 4 week program that continues to 8 weeks would be useful as well to see if the benefits constantly improve with training or if they plateau and to see if the problem lies within motor control vs muscle girth/weakness.

From a clinical aspect these results have huge ramifications for our profession. Injury prevention and performance are two avenues where therapists have the best skill set to make the highest impact. These results can be used as a selling point to coaches because not only do programs such as this prevent injury they have also demonstrated improved performance in relatively a short amount of time. Personally I would like more research to be conducted to further justify this compressed training schedule and programs for other joints such as the shoulder, back and hip. The more we can demonstrate the benefits of preventative interventions the more likely insurance will cover it especially if we can reduce risk with less cost per patient. This will not only provide more avenues for business but it will help our patients in the long run. Research drives reimbursement from insurance and reimbursement drives practice.

I have always stood by the belief that its cheaper and more efficient to prevent a problem than to fix it. Think about it, if you maintain your car and check the oil regularly and brake fluid it will cost you substantially less than paying for it when one of those components fails or in the worst case you have an accident. The same can be said about the human body, if you maintain the body and keep it healthy you can prevent tissue failure and prevent serious injury.

Included are some images of the results on pre and post test. More images to follow.

here is a link to the article


Have a great day!


Adverse Cardiometabolic responses to exercise: A review and opinion

On May 30th 2012 the New York times published an article (http://well.blogs.nytimes.com/2012/05/30/can-exercise-be-bad-for-you/) on a study by Bouchard et al (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0037887) which had discovered significant cardiometabolic adverse reactions in patients following exercise interventions. This report combined the findings of 6 studies and had a total of 1,687 subjects of various levels of health, risk factors, gender and age. These findings were quite profound in that currently exercise particularly aerobic exercise is recommended for patients to prevent or reduce the risk of cardiovascular pathologies. There have been numerous studies that support these claims; all one would have to do is search “exercise and cardiac benefits” to PubMed or even google and a plethora of articles in respectable journals would appear. It must be noted that the overwhelming majority of the interventions evaluated were endurance exercise, only two of the studies evaluated had subjects perform resistance exercise and of those two only one of the studies’ data was used in this report.

The authors of this study are all well known and reputable and after reading the article myself I feel that their findings are solid. They effectively controlled for error in measurement by only classifying AR to be greater than 2  standard deviations from the average to even be considered ‘significant”. Their statistical analyses also controlled for bias due to duration, gender and other variables. Their population pool was enormous and quite variable and the dosage of exercise was considerably mixed which made these findings very generalizable.

With all this being said I would agree with the authors in that stating though these findings do suggest that their may be a “statistically significant” percentage of people who experienced a deleterious effect from exercise, about 10% on average, one must must also realize that close to 90% of people did have positive benefit. When you take a step back and re-review these findings you realize that these findings are not that surprising. Any intervention there is always a chance for negative effects. Look at all of the drug therapies that are currently implemented, almost all could cause an adverse effect in a given patient. We are all very similar but we are all different at the cellular level and molecular level. If we were to abandon every intervention because 10% of the population have a negative side-effect we wouldn’t have that many left. The beauty of the healthcare system is that we have such variability in the way we can intervene with patients and treat pathologies. When the standard doesn’t work you try something else. The same should be said for exercise as well.

As a future physical therapist I feel that this issue is something that we can get involved in. By that I mean what the authors suggested in their discussion which is that there is a 20-30% genetic link for some of these ARs. This finding suggests the need for blood work and pre-screening of patient before and exercise plan is ever administered especially to “at risk” patients. The most effective and efficient way to pre-screen someone for exercise is to administer a stress test which physical therapists are now doing more often with the progression of cardiac rehab. We have a chance to really get involve in this and I hope more research is done in the future in evaluating the ability of a stress test’s and concurrent blood work data at predicting ARs for patients. Too often exercise is prescribed capriciously with out considering that you may hurt your patient if you aren’t careful and treat the intervention as a medicine.

I would also like future research to look at the combination of resistance exercise and aerobic on metabolic risk factors. This study only had one group that did both and they had ARs but less in total, they also had one of the smaller sample sizes and were not American.

That’s enough from me take a look at the article and leave your comments below. Time to play cricket followed by watching the UFC fights.

Cheers guys