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30. 11. 2012.

What to eat night before competition?

One of the questions that troubles many athletes in team sports and individual sports is what to eat night before competition. Team pasta dinners are still pretty popular, and the idea of "carbo-loading" before a competition or race is still considered by most people to be a good idea. The theory behind carbo-loading is to eat a high carbohydrate meal (usually pasta) the night before a race or competition, so that you will have extra energy (in the form of sugar in your body) for the next day.

During exercise, your body does use stored sugar for energy. Any food that is broken down into sugar can be stored for energy. Sugar, in the form of glycogen and glucose is stored in three places - your muscles, liver, and blood, with your muscles storing the highest amount. Unfortunately, these three systems do not have an unlimited capacity. Once your glycogen and glucose stores are full, no further amount of ingested sugar can be saved. Additional ingested sugar will actually be stored as fat, which is the main theory behind using low carbohydrate diets to trigger weight loss.

With the rise in popularity of ultra, endurance events such as marathons, triathlons and bike races, there has been a lot of research on the performance effects of high carbohydrate diets. Research out of the Department of Physiology at the University of Cape Town Medical School in South Africa, studied the effects of carbo-loading before a one hour cycling time trial. The study showed no performance increase in the tested subjects, and also showed that after the event was complete there was still a reserve of carbohydrate in the subjects’ muscles. This would indicate that muscle glycogen stores are not a determining factor of fatigue in a race of this duration. Additional research out of the Department of Biology at The University of Colorado showed that when subjects participated in a 45-minute bout of exercise at 85% of maximal effort, a high versus low carbohydrate diet had no effect on performance when the low carbohydrate diet had a sufficient amount of total calories.

So what about taking in carbs during long bouts of exercise or between multiple games in one day? Muscle glycogen stores take too long to restore during exercise, but ingested carbohydrate can boost blood glucose very quickly. This is why many serious endurance athletes fuel up with carbohydrate during their races or long training sessions, usually with drinks or sports gels. Research from The Australian Institute of Sport in Canberra showed that while carbo-loading had no effect on performance during a 100 kilometer cycling time trial, boosting blood glucose during exercise with ingested carbs did offset any depletion of stored muscle and liver glycogen.

So the night before a game or race, stick to a balanced meal with plenty of lean protein and vegetables that are high in fiber, and anti-oxidants. If you are an endurance athlete looking for a performance edge, try eating a higher fat diet for a couple of months while training for a big race. Your body will get better at using fat for energy during exercise, and when you go back to eating more carbs, you’ll be able to better utilize both types of stored energy.

If you have done intolerance(test to the food which best suits you), stick to that plan. YOU have YOUR favourite food, your organism knows which food is the best for you. Be aware that carbohydrate overeating can give you benefits, but not in unlimited amounts. And be aware of following concept, the best time for eating:
-          monosaccharides – 10-20 minutes before race
-          carbohydrates(fruit and vegetables - disaccharides) – 40 – 80 minutes before race
-          complex carbohydrates – 80 – 120 minutes before race
-          light meat meal – 180 minutes before race
-          heavy meal – 240 – 360 minutes before race


23. 11. 2012.

Nutritional myths - protein


Nutritional Myths: Protein!

When it comes to the topic of sports nutrition there are many myths and fallacies that float around like some specter in the shadows. They pop up when you least expect them and throw a monkey wrench into the best laid plans of the hard training athlete trying to make some headway. Of all the myths that surface from time to time, the protein myth seems to be the most deep rooted and pervasive. It just won't go away. The problem is, exactly who, or which group, is perpetuating the "myth" cant be easily identified. You see, the conservative nutritional/medical community thinks it is the bodybuilders who perpetuate the myth that athletes need more protein and we of the bodybuilding community think it is them (the mainstream nutritional community) that is perpetuating the myth that athletes don't need additional protein! Who is right?

The conservative medical/nutritional community is an odd group. They make up the rules as they go along and maintain what I refer to as the "nutritional double standard." If for example you speak about taking in additional vitamin C to possibly prevent cancer, heart disease, colds, and other afflictions, they will come back with "there is still not enough data to support the use of vitamin C as a preventative measure for these diseases," when in fact there are literary hundreds of studies showing the many benefits of this vitamin for the prevention and treatment of said diseases.

And of course, if you tell them you are on a high protein diet because you are an athlete they will tell you, "oh you don't want to do that, you don't need it and it will lead to kidney disease" without a single decent study to back up their claim! You see they too are susceptible to the skulking myth specter that spreads lies and confusion. In this article I want to address once and for all (hopefully) the protein myth as it applies to what the average person is told when they tell their doctor or some anemic "all you need are the RDAs" spouting nutritionist that he or she is following a high protein diet.

Myth #1 "Athletes don't need extra protein"

I figured we should start this myth destroying article off with the most annoying myth first. Lord, when will this one go away? Now the average reader person is probably thinking "who in the world still believes that ridiculous statement?" The answer is a great deal of people, even well educated medical professionals and scientists who should know better, still believe this to be true. Don't forget, the high carb, low fat, low protein diet recommendations are alive and well with the average nutritionist, doctor, and of course the "don't confuse us with the facts" media following close behind.

For the past half century or so scientists using crude methods and poor study design with sedentary people have held firm to the belief that bodybuilders, strength athletes of various types, runners, and other highly active people did not require any more protein than Mr. Potato Head.....err, I mean the average couch potato. However, In the past few decades researchers using better study designs and methods with real live athletes have come to a different conclusion altogether, a conclusion hard training bodybuilders have known for years. The fact that active people do indeed require far more protein than the RDA to keep from losing hard earned muscle tissue when dieting or increasing muscle tissue during the off season.

In a recent review paper on the subject one of the top researchers in the field (Dr. Peter Lemon) states "...These data suggest that the RDA for those engaged in regular endurance exercise should be about 1.2-1.4 grams of protein/kilogram of body mass (150%-175% of the current RDA) and 1.7 - 1.8 grams of protein/kilogram of body mass per day (212%-225% of the current RDA) for strength exercisers."

Another group of researchers in the field of protein metabolism have come to similar conclusions repeatedly. They found that strength training athletes eating approximately the RDA/RNI for protein showed a decreased whole body protein synthesis (losing muscle jack!) on a protein intake of 0.86 grams per kilogram of bodyweight. They came to an almost identical conclusion as that of Dr. Lemon in recommending at least 1.76g per kilogram of bodyweight per day for strength training athletes for staying in positive nitrogen balance/increases in whole body protein synthesis.

This same group found in later research that endurance athletes also need far more protein than the RDA/RNI and that men catabolize (break down) more protein than women during endurance exercise.

They concluded "In summary, protein requirements for athletes performing strength training are greater than sedentary individuals and are above the current Canadian and US recommended daily protein intake requirements for young healthy males." All I can say to that is, no sh%# Sherlock?!

Now my intention of presenting the above quotes from the current research is not necessarily to convince the average athlete that they need more protein than Joe shmoe couch potato, but rather to bring to the readers attention some of the figures presented by this current research. How does this information relate to the eating habits of the average athlete and the advice that has been found in the lay bodybuilding literature years before this research ever existed? With some variation, the most common advice on protein intakes that could be-and can be- found in the bodybuilding magazines by the various writers, coaches, bodybuilders, etc., is one gram of protein per pound of body weight per day.

So for a 200 pound guy that would be 200 grams of protein per day. No sweat. So how does this advice fair with the above current research findings? Well let's see. Being scientists like to work in kilograms (don't ask me why) we have to do some converting. A kilogram weighs 2.2lbs. So, 200 divided by 2.2 gives us 90.9. Multiply that times 1.8 (the high end of Dr. Lemon's research) and you get 163.6 grams of protein per day. What about the nutritionists, doctors, and others who call(ed) us "protein pushers" all the while recommending the RDA as being adequate for athletes?

Lets see. The current RDA is 0.8 grams of protein per kilogram of bodyweight: 200 divided by 2.2 x 0.8 = 73 grams of protein per day for a 200lb person. So who was closer, the bodybuilders or the arm chair scientists? Well lets see! 200g (what bodybuilders have recommended for a 200lb athlete) - 163g ( the high end of the current research recommendations for a 200lb person) = 37 grams (the difference between what bodybuilders think they should eat and the current research).

How do the RDA pushers fair? Hey, if they get to call us "protein pushers" than we get to call them "RDA pushers!" Anyway, 163g - 73g = (drum role) 90 grams! So it would appear that the bodybuilding community has been a great deal more accurate about the protein needs of strength athletes than the average nutritionist and I don't think this comes as any surprise to any of us. So should the average bodybuilder reduce his protein intake a bit from this data? No, and I will explain why. As with vitamins and other nutrients, you identify what looks to be the precise amount of the compound needed for the effect you want (in this case positive nitrogen balance, increased protein synthesis, etc) and add a margin of safety to account for the biochemical individuality of different people, the fact that there are low grade protein sources the person might be eating, and other variables.

So the current recommendation by the majority of bodybuilders, writers, coaches, and others of one gram per pound of bodyweight does a good job of taking into account the current research and adding a margin of safety. One things for sure, a little too much protein is far less detrimental to the athletes goal(s) of increasing muscle mass than too little protein, and this makes the RDA pushers advice just that much more.... moronic, for lack of a better word.

There are a few other points I think are important to look at when we recommend additional protein in the diet of athletes, especially strength training athletes. In the off season, the strength training athletes needs not only adequate protein but adequate calories. Assuming our friend (the 200lb bodybuilder) wants to eat approximately 3500 calories a day, how is he supposed to split his calories up? Again, this is where the bodybuilding community and the conservative nutritional/medical community are going to have a parting of the ways... again. The conservative types would say "that's an easy one, just tell the bodybuilder he should make up the majority of his calories from carbohydrates."

Now lets assume the bodybuilder does not want to eat so many carbs. Now the high carb issue is an entirely different fight and article, so I am just not going to go into great depth on the topic here. Suffice it to say, anyone who regularly reads articles, books, etc, >from people such as Dan Duchaine, Dr. Mauro Dipasquale, Barry Sears PhD, Udo Erasmus PhD, yours truly, and others know why the high carb diet bites the big one for losing fat and gaining muscle (In fact, there is recent research that suggests that carbohydrate restriction, not calorie restriction per se, is what's responsible for mobilizing fat stores). So for arguments sake and lack of space, let's just assume our 200lb bodybuilder friend does not want to eat a high carb diet for his own reasons, whatever they may be.

What else can he eat? He is only left with fat and protein. If he splits up his diet into say 30% protein, 30 % fat, and 40% carbs, he will be eating 1050 calories as protein (3500x30% = 1050) and 262.5g of protein a day (1050 divided by 4 = 262.5). So what we have is an amount (262.5g) that meets the current research, has an added margin of safety, and an added component for energy/calorie needs of people who don't want to follow a high carb diet, hich is a large percentage of the bodybuilding/strength training community. here are other reasons for a high protein intake such as hormonal effects (i.e. effects on IGF-1, GH, thyroid ), thermic effects, etc., but I think I have made the appropriate point. So is there a time when the bodybuilder might want to go even higher in his percent of calories >from protein than 30%? Sure, when he is dieting.

It is well established that carbs are "protein sparing" and so more protein is required as percent of calories when one reduces calories. Also, dieting is a time that preserving lean mass (muscle) is at a premium. Finally, as calories decrease the quality and quantity of protein in the diet is the most important variable for maintaining muscle tissue (as it applies to nutritional factors), and of course protein is the least likely nutrient to be converted to bodyfat. In my view, the above information bodes well for the high protein diet. If you tell the average RDA pusher you are eating 40% protein while on a diet, they will tell you that 40% is far too much protein. But is it? Say our 200lb friend has reduced his calories to 2000 in attempt to reduce his bodyfat for a competition, summer time at the beach, or what ever. Lets do the math. 40% x 2000 = 800 calories from protein or 200g (800 divided by 4). So as you can see, he is actually eating less protein per day than in the off season but is still in the range of the current research with the margin of safety/current bodybuilding recommendations intact.

Bottom line? High protein diets are far better for reducing bodyfat, increasing muscle mass, and helping the hard training bodybuilder achieve his (or her!) goals, and it is obvious that endurance athletes will also benefit from diets higher in protein than the worthless and outdated RDAs.

Myth #2 "High protein diets are bad for you"
So the average person reads the above information on the protein needs and benefits of a high protein diet but remembers in the back of their mind another myth about high protein intakes. "I thought high protein diets are bad for the kidneys and will give you osteoporosis! " they exclaim with conviction and indignation. So what are the medical facts behind these claims and why do so many people, including some medical professionals and nutritionists, still believe it?

For starters, the negative health claims of the high protein diet on kidney function is based on information gathered from people who have preexisting kidney problems. You see one of the jobs of the kidneys is the excretion of urea (generally a non toxic compound) that is formed from ammonia (a very toxic compound) which comes from the protein in our diets. People with serious kidney problems have trouble excreting the urea placing more stress on the kidneys and so the logic goes that a high protein diet must be hard on the kidneys for healthy athletes also.

Now for the medical and scientific facts. There is not a single scientific study published in a reputable peer - reviewed journal using healthy adults with normal kidney function that has shown any kidney dysfunction what so ever from a high protein diet. Not one of the studies done with healthy athletes that I mentioned above, or other research I have read, has shown any kidney abnormalities at all. Furthermore, animals studies done using high protein diets also fail to show any kidney dysfunction in healthy animals.

Now don't forget, in the real world, where millions of athletes have been following high protein diets for decades, there has never been a case of kidney failure in a healthy athlete that was determined to have been caused solely by a high protein diet. If the high protein diet was indeed putting undo stress on our kidneys, we would have seen many cases of kidney abnormalities, but we don't nor will we. From a personal perspective as a trainer for many top athletes from various sports, I have known bodybuilders eating considerably more than the above research recommends (above 600 grams a day) who showed no kidney dysfunction or kidney problems and I personally read the damn blood tests! Bottom line? 1-1.5 grams or protein per pound of bodyweight will have absolutely no ill effects on the kidney function of a healthy athlete, period. Now of course too much of anything can be harmful and I suppose it's possible a healthy person could eat enough protein over a long enough period of time to effect kidney function, but it is very unlikely and has yet to be shown in the scientific literature in healthy athletes.

So what about the osteoporosis claim? That's a bit more complicated but the conclusion is the same. The pathology of osteoporosis involves a combination of many risk factors and physiological variables such as macro nutrient intakes (carbs, proteins, fats), micro nutrient intakes (vitamins, minerals, etc), hormonal profiles, lack of exercise, gender, family history, and a few others. The theory is that high protein intakes raise the acidity of the blood and the body must use minerals from bone stores to "buffer" the blood and bring the blood acidity down, thus depleting one's bones of minerals. Even if there was a clear link between a high protein diet and osteoporosis in all populations (and there is not) athletes have few of the above risk factors as they tend to get plenty of exercise, calories, minerals, vitamins, and have positive hormonal profiles. Fact of the matter is, studies have shown athletes to have denser bones than sedentary people, there are millions of athletes who follow high protein diets without any signs of premature bone loss, and we don't have ex athletes who are now older with higher rates of osteoporosis.

In fact, one recent study showed women receiving extra protein from a protein supplement had increased bone density over a group not getting the extra protein! The researchers theorized this was due to an increase in IGF-1 levels which are known to be involved in bone growth. Would I recommend a super high protein diet to some sedentary post menopausal woman? Probably not, but we are not talking about her, we are talking about athletes. Bottom line? A high protein diet does not lead to osteoporosis in healthy athletes with very few risk factors for this affliction, especially in the ranges of protein intake that have been discussed throughout this article.

Myth #3 "All proteins are created equal"
How many times have you heard or read this ridiculous statement? Yes, in a sedentary couch potato who does not care that his butt is the same shape as the cushion he is sitting on, protein quality is of little concern. However, research has shown repeatedly that different proteins have various functional properties that athletes can take advantage of. For example, whey protein concentrate (WPC) has been shown to improve immunity to a variety of challenges and intense exercise has been shown to compromise certain parts of the immune response. WPC is also exceptionally high in the branch chain amino acids which are the amino acids that are oxidized during exercise and have been found to have many benefits to athletes. We also know soy has many uses for athletes.

Anyway, I could go on all day about the various functional properties of different proteins but there is no need. The fact is that science is rapidly discovering that proteins with different amino acid ratios (and various constituents found within the various protein foods) have very different effects on the human body and it is these functional properties that bodybuilders and other athletes can use to their advantage. Bottom line? Let the people who believe that all proteins are created equal continue to eat their low grade proteins and get nowhere while you laugh all the way to a muscular, healthy, low fat body!

Over the years the above myths have been floating around for so long they have just been accepted as true, even though there is little to no research to prove it and a whole bunch of research that disproves it! I hope this article has been helpful in clearing up some of the confusion for people over the myths surrounding protein and athletes. Of course now I still have to address even tougher myths such as "all fats make you fat and are bad for you," "supplements are a waste of time," and my personal favorite, "a calorie is a calorie." The next time someone gives you a hard time about your high protein intake, copy the latest study on the topic and give it to em. If that does not work, role up the largest bodybuilding magazine you can find and hit them over the head with it!

Article References:
1 Lemon, PW, "Is increased dietary protein necessary or beneficial for individuals with a physically active life style?" Nutr. Rev. 54:S169-175, 1996.

2 Lemon, PW, "Do athletes need more dietary protein and amino acids?" International J. Sports Nutri. S39-61, 1995.

3 Tarnopolsky, MA, "Evaluation of protein requirements for trained strength athletes." J. Applied. Phys. 73(5): 1986-1995, 1992

4 Phillips, SM, "Gender differences in leucine kinetics and nitrogen balance in endurance athletes." J. Applied Phys. 75(5): 2134-2141, 1993.

5 Tarnopolsky, MA, 1992.

6 Carroll, RM, "Effects of energy compared with carbohydrate restriction on the lipolytic response to epinephrine." Am. J. Clin. Nutri. 62:757-760, 1996.

7 Bounus, G., Gold, P. "The biological activity of undenatured whey proteins: role of glutathione." Clin. Invest. Med. 14:4, 296-309, 1991

8 Bounus, G. "Dietary whey protein inhibits the development of dimethylhydrazine induced malignancy." Clin. Invest. Med. 12: 213-217, 1988

22. 11. 2012.

Elbow joint - part I


The elbow joint is the intermediate joint of the upper limb, being between the arm and the forearm. It can be considered to be subservient to the hand in the sense that it enables the hand and fingers to be properly placed in space. The elbow joint is responsible for shortening and lengthening the upper limb; the ability to carry food to the mouth is due to flexion at the elbow. If situations arise in which the hand and forearm are not able to move, then the arm and trunk can move towards the hand.
The elbow joint is a synovial joint of the hinge variety, and shares, with the superior radioulnar joint, the same joint capsule. The superior radioulnar joint has no function at the elbow and plays no part in its movements. The elbow joint shows the fundamental characteristics of all hinge joints. The articular surfaces are reciprocally shaped; it has strong collateral ligaments with the forearm muscles grouped at the sides of the joint where they do not interfere with movement.

When viewed laterally, the distal end of the humerus bulges anteriorly and inferiorly at an angle of 45° so that the trochlea lies anterior to the axis of the shaft(a). In a similar way the trochlear notch of the ulna projects anteriorly and superiorly at an angle of 45°, and so lies anterior to the axis of the shaft of the ulna(a). The projection of these two articular surfaces facilitates and promotes a large range of flexion at the elbow. It delays contact between the two bones, in addition to which there is still a space between them to accommodate the musculature until the bones are almost parallel. Without these two features, particularly the first, flexion beyond 90° would be severely limited.
In spite of the anterior projections of the humerus and ulna the long axes of the two bones coincide when viewed laterally. However, when seen from the front, the ulnar axis deviates laterally from that of the humerus(b). This deviation is referred to as the carrying angle, and is said to be approximately 10° to 15° in men and 20° to 25° in women. Normally, the transverse axis of the elbow joint bisects this angle so that when the elbow is acutely flexed the forearm overlies the arm, and tha hand covers the shoulder joint. If, however, the bisected parts of the carrying angle are not equal then the hand will be lateral to the shoulder( A < B, figure b) or medial to the shoulder(A > B, figure b) on acute flexion at the joint.

The transverse axis of the elbow joint runs from inferior posteromedially to superior anterolaterally passing approximately through the middle of the trochlea. Because of this slight obliquity there has been some debate as to whether the joint exhibits a pure hinge movement, especially as this axis also oscillates slightly. However, for practical purposes it can be considered as a pure hinge joint.

Articular surfaces

Three bones are involved in the articulation at the elbow joint; these are the distal end of the humerus, and the proximal ends of the radius and ulna. The distal end of the humerus shows two joined articular regions: the grooved trochlea medially and the rounded capitulum laterally, being separated by a groove of variable depth(a). The whole of this composite surface is covered by a continuous layer of hyaline cartilage. The trochlea articulates with the trochlear notch of the ulna, while the capitulum articulates with the cupped head of the radius. Both of these latter surfaces are also covered with hyaline cartilage.

Trochlea of the humerus

The pulley-shaped trochlea with its groove presents a concave surface in the frontal plane and is convex sagitally. It forms almost a complete circle, being separated by a thin wall of bone, which itself may be perforated, so that 320° to 330° of the surface is cartilage covered(a, b). The medial free border of the trochlea is not circular but describes part of a helix with a slant directed radially. The groove of the trochlea is limited medially by a sharp and prominent ridge and laterally by a lower and blunter ridge which blends with the articular surface of the capitulum(a). The tilt of the trochlea partly accounts for the carrying angle of the elbow.
Although the groove of the trochlea appears to lie in the sagittal plane it does in fact run obliquely. This obliquity shows individual variation; however the most common form is with the anterior part of the groove being vertical and the posterior part running obliquely distally and laterally. As a whole the groove runs in a spiral around the axis of the bone(c). Occasionally, the groove runs obliquely proximally and laterally at the front and distally and laterally at the back, and so as a whole forms a true spiral around the axis of the bone(c). Finally, and rarely, the groove may run obliquely proximally and medially anteriorly, and distally and laterally posteriorly, so that as a whole it forms a circle(c). The functional significance of these variations in the angulation of the trochlea is minimal. The only observable differences are in the degree of the carrying angle and the relative positions of the arm and forearm in acute flexion at the elbow.
Immediately above the trochlea anteriorly is the concave coronoid fossa(a), which receives the coronoid process of the ulna during flexion. Posteriorly, in a similar position, is the olecranon fossa which receives the olecranon process during extension(b). If these two fossae are particularly deep the intervening thin plate of bone may be perforated allowing them to communicate with each other. 


The capitulum is not a complete sphere but a hemisphere on the anterior and inferior surface of the humerus(a). It does not extend posteriorly like the trochlea. Although described as hemispherical, its radius of curvature is not constant, increasing slightly from proximally to distally. The cartilage covering the capitulum is thickest in its central region, and may be as much as 5mm thick. The medial border of the capitulum is truncated forming the capitulotrochlear groove. Above the capitulum anteriorly is the radial fossa which receives the rim of the head of the radius during flexion(a).

Trochlear notch of the ulna

The proximal end of the ulna has the deep trochlear notch which articulates with the trochlea(a, b). It has a rounded, curved longitudinal ridge extending from the tip of the olecranon process superiorly to the tip of the coronoid process inferiorly. The ridge snugly fits the groove of the trochlea, on either side of which is a concave surface for the lips of the trochlea. The cartilage of the trochlear notch is interrupted by a transverse line across its deepest part, providing two separate surfaces, one on the olecranon and the other on the coronoid process.
The obliquity of the shaft of the ulna to the ridge accounts for the majority of the carrying angle.

Head of the radius

The superior surface of the head of the radius is concave for articulation with the capitulum, with the raised margin articulating with the capitulotrochlear groove(c,d). The cartilage of this surface is continuous with that around the sides of the head: it is thickest in the middle of concavity.
Because of the articulations between the radius and ulna, their proximal surfaces may be considered as constituting a single articular surface. However, because of the movements between these two bones, they do not maintain the same relative positions with respect to the humerus, nor does the radius always maintain contact with the humerus.
As indicated previously, the articular surface of the trochlea has an angular value of 330°, while that of the capitulum is 180°(a, b). The angular values of the articular surfaces of the ulna and radius are much smaller, leaving a large portion of the humeral surfaces exposed at all positions of the joint. The angular value of the trochlear notch is 190°, while that of the head of the radius is only 40°. The difference in angular values between corresponding parts of the elbow is therefore 140°,  a value very close to the range of flexion – extension possible at the joint.

Joint capsule and synovial membrane

A fibrous capsule completely encloses the elbow joint and also surrounds the superior radioulnar joint. It has no openings in it, but slight pouching of the synovial membrane may occur beneath the edge of the capsule in one or two areas.
Anteriorly the capsule arises from the medial epicondyle away from the articular surface of the trochlea. It arches upwards and laterally attaching to the margins of the coronoid and radial fossae, and to the articular margin of the capitulum as it reaches the lateral epicondyle. Posteriorly, the capsule follows the lateral margins of the capitulum and arches upwards around the olecranon fossa, returning to the medial epicondyle some distance from the edge of the trochlear surface.


Distally the capsule attaches to the margins of the trochlear notch around the olecranon and coronoid processes. As the capsule reaches the region of the radial notch it passes on to and attaches to the annular ligament of the radius. Medially and laterally it blends with the collateral ligaments of the joint. It should be remembered that the joint capsule has no direct attachment to the radius. If this were the case, then the movements possible between the radius and ulna would be severely limited.
Because it blends with the collateral ligaments at the sides, the capsule is strengthened in these regions; however, it is relatively weak in front and behind. Anteriorly the capsule consists mainly of longitudinal fibres running from above the coronoid and radial fossae on the humerus to the anterior border of the coronoid process and front of the annular ligament(a). Among these longitudinal fibres are some bundles which run obliquely and transversely(a). Consequently, this part of the capsule is thicker in its middle region than at the sides; a feature which has led to it being referred to as the capsular ligament. Some of the deep fibres of brachialis insert into the front of the capsule as the muscle passes anteriorly across the joint. This attachment serves to pull the capsule and underlying synovial membrane upwards when the joint is flexed, thereby preventing them becoming trapped between the two moving bones.
The posterior part of the capsule is thin and membranous, being composed mainly of transverse fibres extending loosely between the margins of the olecranon and the edges of the olecranon fossa. A few fibres stretch across the fossa as a transverse band with a free upper border, which does not reach as high as the upper margin of the fossa, without attaching to the olecranon(b). Posteriorly the capsule also passes laterally from the lateral epicondyle to the posterior border of the radial notch and the posterior part of the annular ligament. The weakest part of the capsule posteriorly is in the midline of the joint. However, here it is attached to the tendon of triceps which supports it, and performs a similar function to the deep part of brachialis in extension at the joint.  

Synovial membrane

The synovial membrane of the joint is extensive attaching to the articular margins of the humerus and ulna. It lines the joint capsule and is reflected onto the humerus to cover the coronoid and radial fossae anteriorly and the olecranon fossa posteriorly. Distally it is prolonged onto the upper part of the deep surface of the annular ligament. The membrane is continued into the superior radioulnar articulation covering the lower part of the annular ligament, and is then reflected onto the neck of the radius. Below the lower border of the annular ligament, the membrane emerges as a redundant fold to give freedom of movement to the head of the radius(a). This downward reflection is supported by a few loose fibres which pass from the lower border of the annular ligament to the neck of the radius. The quadrate ligament supports the synovial membrane as it passes from the medial side of the neck of the radius to the lower border of the radial notch, so preventing its herniation between the anterior and posterior free edges of the annular ligament.
Various synovial folds project onto the processes of the joint between the edges of the articular surfaces. An especially constant fold is one which forms almost a complete ring overlying the periphery of the head of the radius, projecting onto the crevice between it and the capitulum. Slight pouching of the synovial membrane may occur below the lower borders of the annular ligament and the transverse band of the ulnar collateral ligament; and above the transverse capsular fibres across the upper part of the olecranon fossa(b).
Well – marked extrasynovial fat pads lie adjacent to the articular fossae. In extension of the joint, they fill the radial and coronoid fossae, and in flexion the olecranon fossa. They are displaced when the appropriate parts of the ulna or radius occupy the fossae.


The collateral ligaments are strong triangular bands which blend with the sides of the joint capsule. They are placed so that they lie across the axis of movement in all positions of the joint. Consequently, they are relatively tense in all positions of flexion and extension, and impose strict limitations on abduction and adduction movements and axial rotation.


Ulnar collateral ligament

The ulnar collateral ligament fans out from the medial epicondyle and has thick anterior and posterior bands united by a thinner intermediate portion(a). The anterior band passes from the front of the medial epicondyle to the medial edge of the coronoid process. It is intimately associated with the common tendon of the superficial forearm flexor muscles, giving rise to some of the fibres of flexor digitorum superficialis. The posterior band runs from the back of the medial epicondyle to the medial edge of the olecranon. The apex of the thinner intermediate part of the ligament is attached to the undersurface of the medial epicondyle, while its base is attached to the transverse band stretched between the attachments of the anterior and posterior bands to the coronoid process and olecranon(a). The synovial membrane tends to protrude below the free edge of the transverse ligament during movement at the joint. The intermediate grooved part of the ligament is crossed by the ulnar nerve as it passes behind the medial epicondyle to gain access to the forearm.

Radial collateral ligament

The radial collateral ligament is a strong, triangular band attaching above to a depression on the anteroinferior aspect of the lateral epicondyle deep to the overlying common extensor tendon(b). Below, the ligament blends with the annular ligament of the radius, the slightly thicker anterior and posterior margins passing forwards and backwards to attach to the margins of the radial notch on the ulna(b). The ligament is less distinct than the ulnar collateral.

14. 11. 2012.

Shoulder joint - part III



The architecture of the shoulder joint gives it a greater range of movement than at any other joint within the body. Its ball and socket shape means that movement can take place around an infinite number of axes intersecting at the centre of the head of the humerus. For descriptive purposes, the movements of which the shoulder joint is capable are flexion and extension, abduction and adduction, and medial and lateral rotation. However, the axes about which they occur have to be carefully defined as the plane of the glenoid fossa does not coincide with one of the cardinal planes of the body, but is inclined approximately 45° to both of the frontal and sagittal planes. It is thus possible to define two sets of axes about which movements occur, one with respect to the cardinal planes of the body(a) and the other with respect to the plane of the glenoid fossa(b). If the cardinal planes are used, flexion and extension occur about a transverse axis, abduction and adduction occur about an anteroposterior axis, and medial and lateral rotation occur about the longitudinal axis of the humerus, passing between the centre of the head and the centre of the capitulum(a). If, however, the plane of the scapula is used to determine these various axes, then flexion and extension take place about an axis perpendicular to the plane of the fossa, abduction and adduction about an axis parallel  to the plane of the fossa, with medial and lateral rotation occurring about the same axis as previously(b). While the presentation of these two sets of axes may seem initially confusing, the importance of those related to the plane of the glenoid fossa is that in the treatment of certain injuries of the shoulder, the position of the joint which will cause the greatest relief will be when the capsule is not put under tension, that is when the joint is abducted to 90° in the plane of the glenoid fossa. 

Irrespective of the orientation of these axes, the incongruity of the joint surfaces means that all movements, except axial rotation, are a combination of gliding and rolling of the articular surfaces against each other. However, unlike the knee, it is not possible to define the extent of each type of motion within each of the various movements. Although the range of movement at the shoulder joint is relatively large, the mobility of the upper limb against the trunk is increased by movements of the pectoral girdle. Indeed, the movements of flexion and extension, and abduction and adduction, may be considered to be always accompanied by scapular and clavicular movements, except perhaps for the initial stages. Shoulder joint movement is more concerned with bringing the arm to the horizontal position, while pectoral girdle movements, principally those of the scapula, are more concerned in bringing the arm into a vertical position.
The association of shoulder and pectoral girdle movement also increases the power of the movement. The rotator cuff muscles, being attached blose to the axes of movement, have a poor mechanical advantage compared with muscles acting on the scapula, which are generally more powerful as well as having considerable leverage. In patients with fused or fixed shoulder joints a large degree of upper limb mobility with respect to the trunk is still possible because of pectoral girdle movements.
In the following account shoulder joint movements are considered initially with respect to the plane of the glenoid fossa.

Flexion and extension

Flexion and extension occur about an axis perpendicular to the plane of the glenoid fossa, so that in flexion the arm moves forwards and medially at an angle of approximately 45° to the sagittal plane(a). In extension it is carried backwards and laterally(a). The range of flexion is approximately 110° and that of extension 70°. Both of these ranges may be extended by movements of the pectoral girdle so that flexion of the upper limb with respect to the trunk reaches 180° and extension just exceeds 90°. Extension is limited by the greater tubercle of the humerus coming into contact with the coracoacromial arch.
Flexion is produced by the anterior fibres of deltoid, clavicular head of pectoralis major, coracobrachialis and biceps. Passive extension from the flexion position is essentially due to the eccentric contraction of the above muscles. Beyond the neutral position, however, extension is produced by the posterior fibres of deltoid, teres major and latissimus dorsi; to these may be added the long head of triceps and the sternal fibres of pectoralis major when active extension is performed from a flexed position.

Abduction and adduction

Abduction and adduction occur about an oblique horizontal axis in the same plane as the glenoid fossa. In abduction the arm moves anterolaterally away from the trunk(b). The total range of movement at the shoulder joint is 120°; however only the first 25° occurs without concomitant rotation of the scapula, so that between 30° and 180° scapula rotation augments shoulder abduction in the ratio of 1:2.
The terminal part of shoulder joint abduction is accompanied by lateral rotation of the humerus. This occurs not to prevent bony interlocking between the greater tubercle and the acromion, but to provide further articular surface on the head of the humerus for the glenoid fossa. Abduction of the medially rotated humerus is limited by tension in the posterior capsule and the lateral rotators.
Adduction beyond the neutral position of the joint is not possible because of the presence of the trunk. Abduction is initiated by supraspinatus which, although nowhere near as strong as deltoid, is better placed to act on the humerus. With the arm hanging at the side the fibres of deltoid, especially the middle fibres, run almost parallel to the humerus, so that on contraction they pull the humerus upwards. Once the arm has been pulled away from the side then deltoid takes over and continues the movement. Supraspinatus is required for the first 20° of abduction. If deltoid is paralysed, supraspinatus is not functioning, deltoid cannot initiate abduction. A passive abduction of some 20°, or learning to the affected side so that the limb hangs away from the body, will enable deltoid to continue the movement. In some circumstances biceps may be re-educated to take over the initiating role of a paralysed supraspinatus. As abduction proceeds, teres major and minor hold the head of the humerus down against the pull of the deltoid. Together with subscapularis and infraspinatus, teres minor and major stabilize the humeral head against the glenoid fossa.
Lateral rotation of the scapula accompanying abduction of the humerus is produced by the force-couple of the lower part of serratus anterior, acting on the inferior angle of the scapula, and the upper fibres of trapezius pulling on the acromion process.
Adduction is produced by the eccentric contraction of serratus anterior, trapezius, deltoid and supraspinatus, under the action of gravity. If adduction is resisted then a forceful movement is produced by pectoralis major, teres major, latissimus dorsi and coracobrachialis.

Medial and lateral rotation

Rotation takes place about the longitudinal axis through the humerus as described earlier. In lateral rotation, it is the anterior surface of the humerus which is turned laterally(c). It is produced It is produced by infraspinatus, teres minor and the posterior fibrs of deltoid, and has a maximum range of 80°. Medial rotation causes the anterior surface of the humerus to be turned medially(c). The maximum range of medial rotation in excess of 90°; however to reach this value the forearm has to be pulled behind the trunk, otherwise contact between the trunk and forearm limits the movements when the elbow is flexed. Medial rotation is produced by subscapularis, pectoralis major, latissimus dorsi, teres major and the anterior fibres of deltoid. The combined range of rotation varies with the position of the arm, being greatest when the arm is by the side, decreasing to 90° with the arm horizontal, and being negligible as the arm approaches the vertical.
Rotation is limited by the extent of the articular surfaces, and tension in the appropriate part of the joint capsule and opposing musculature. Furthermore, it is the movement most commonly affected by pathology or injury to the shoulder joint. When assessing the range of rotation possible at the joint, the elbow must be flexed so as to exclude the possibility of any pronatory or supinatory action of the forearm.

Movements of the shoulder joint with respect to the cardinal planes of the body

Although movements of the shoulder joint have been considered with respect to the plane of the glenoid fossa, it is often more convenient to test the range of movement possible with respect to the cardinal planes of the body.
Movements of the arm about a transverse axis through the humeral head produce what are termed “flexion” and “extension”. Strictly speaking these movements are a combination of flexion and abduction, and extension and adduction – the degree of each component depending on the orientation of the scapula on the chest wall. The forward “flexion” movement has a range of 180° with scapula rotation. “Adduction” is the combined movement of adduction and flexion.
Again the movement is limited by the trunk so that adduction beyond the neutral position of the joint is not possible. However, with protraction of the pectoral girdle some 30° of “adduction” is possible as the arm is brought across the front of the chest. Similarly, retraction of the pectoral girdle allows a minimal amount of “adduction” to occur behind the back.
Although the terminology used to describe these various movements of the arm at the shoulder joint is of little practical significance, it is important to understand the context in which it is being used. It is also important to be fully aware of which movements are being tested when asking individuals to perform certain actions. Two simple activities that demonstrate the mobility of the shoulder joint and pectoral girdle are  - combing the hair and putting a coat on jacket.
With respect to the cardinal planes when the arm is flexed at 45° and abducted 60° and neither medially nor laterally rotated, it is said to be in the position of function of the shoulder. This corresponds to the position of equilibrium of the short scapular muscles; hence its use when immobilizing fractures of the humeral shaft.

Accessory movements

When the subject is lying supping the muscles around the shoulder are relatively relaxed. In this position the relative laxity of the ligaments and joint capsule allow an appreciable range of accessory movements. By placing the hand high up in the axilla and applying a lateral force to the upper medial aspect of the arm, the head of the humerus can be lifted away from the glenoid fossa by as much as 1cm.
Proximal and distal gliding movements of the head of the humerus against the glenoid fossa can be produced by forces applied along the shaft of the humerus. Similarly, anterior and posterior gliding movements can be produced by applying pressure in an appropriate direction, to the region of the surgical neck.


The line of the shoulder joint cannot be directly palpated due to the mass of muscles surrounding it. However, the surface projection of the joint line can be estimated first by identifying the surface projection of the midpoint of the joint. This latter point is approximately 1cm lateral to the apex of the coracoid process. A vertical line, slightly concave laterally, through this point gives an indication of the joint line.


The rotator cuff muscles are active during abduction and lateral rotation, providing stability at the shoulder joint. However, they are probably also involved in the pathogenesis of dislocation of the shoulder. In any equilibrium analysis of the joint certain assumptions have to be made. The following is based on an account given by Morrey and Chao(1981). The assumptions these authors made were:
  1. that each muscle contributing to the equilibrium acts with a force proportional to its cross-sectional area, this being 6.2kg/cm2;
  2. that each muscle is equally active;
  3. that the active muscle contracts along a straight line connecting the centres of its two areas of attachment.

While none of these assumptions is necessarily true, they do provide a framework within which to work. When the unloaded arm is laterally rotated and abducted to 90° there is a compressive force of approximately 70kg between the articular surfaces, and anterior and inferior shear forces of 12kg and 14kg respectively. These forces are produced by muscles actively resisting the weight of the arm; the resultant force is directed 12° anteriorly with a magnitude of 72kg.
If, as well as being abducted and laterally rotated, the arm is also extended by 30° and loaded so that the muscles are contracting maximally, then the magnitude of the various forces across the joint increase dramatically. The compressive force across the joint is now of the order of 210kg, while the anterior and inferior shear forces have increased to 42kg and 58kg respectively. The resultant force is now directed 36° anteriorly and has a magnitude of 222kg. To prevent anterior dislocation occurring, the shearing forces must be balanced by the joint capsule and its associated ligaments, because the glenoid fossa is too shallow to provide much constraint. As the tensile strength of the capsule and ligaments is of the order of 50kg, an imbalance of forces may occur leading to dislocation at the joint. Once the anterior part of the capsule has been torn then less force is required for subsequent dislocations to occur.
The above force analysis is comparable to the situation when an individual slips when walking on ice and puts out his or her hand and arm to break a backward fall.

Velocity of movement

With the shoulder joint being extremely mobile, some of its movements are performed at fairly high velocities. In many instances, for example when studying natural or artificial joints and their lubrication, a knowledge of the sliding velocities at the articulating surfaces is of importance.
Using cine film techniques and by suitable trigonometric relationships the maximum sliding velocities at the shoulder joint in various common activities have been determined. These are for hanging clothes 100 mm/s, sweeping 34 mm/s, arm swing during walking 30 mm/s, eating 13 mm/s and dressing 25 mm/s. Obviously in activities requiring a fast and forceful movement at the shoulder, such as the tennis serve, then the sliding velocities will be much greater. The demands made upon the lubricating fluid and articular surfaces in such situations are high. It is not surprising therefore that sometimes the system breaks down and some form of joint trauma results.

Shoulder joint replacement

Replacement of a damaged or arthritic humeral head offers the immediate relief of pain. However, an intact rotator cuff and a normal glenoid fossa are prerequisites for this type of replacement. The replacement, when used following a severe fracture of the humeral head, should be done as soon as possible, and certainly not later than four weeks following the injury, because of the extensive development of scar tissue and the subsequent limitation of motion.
Total shoulder implants have proved to be more successful than replacement of the humeral head alone. If the rotator cuff is deficient then a restrained shoulder implant will give stability as well as relief of pain. It is not uncommon for the ball and socket of the joint to be reversed, so that the socket is now on the humerus and the ball on the scapula.

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