Please Scroll Down to See Forums Below Arioch - I would love to but we are so damn rural that it took an act of God to get to see this one. He comes from about 3 hours away every other month or so. The next closest would be 8 hours one way and the local docs only refer to this guy. How do I begin to look for somebody qualified 8 hours away?
Chondromalacia of Patella
- Thread starter Temple
- Start date
Arioch
New member
http://www.physsportsmed.com/clinics.htm
http://www.sportsinjuryclinic.net/clinics/indextherapist.php
If you are on a low carb diet, stop.
http://www.sportsinjuryclinic.net/clinics/indextherapist.php
If you are on a low carb diet, stop.
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Temple,
Sorry to hear about the negative Ortho experience. Seems that some ortho's have a demi-god complex and love to condemn us lowly peasants.
I assume that he did a MRI, bone density scan, or scoped you to make his diagnosis? If not, he's a betting man and basing his diagnosis on probabitities. Did he happen to mention what Grade damage was present?
I'll ask our project head again if she has any thoughts or input. (she predicted that you would have probs with most non-sports orthos) If you want, shoot me a hushmail or PM and I'll see if she knows of anyone in sportsmed near you. (I understand 'near' is a relative term.)
No squatting is NOT the end of BBing though. Although not as efficient at working many muscles, lying stiff-legged weighted T's do work without straining knees. And the glucosamine/chondroiton sulfate does help me tremendously. NSAIDs, MSM and SAMe didn't have much effect though.
Whatever you decide to do, I pray the best for you. Believe me, you will quickly learn to compensate and work around the problem areas. I imagine Wilson6 can help with the work-arounds too. But I hear his leg routines may be quite the pain.
Sorry to hear about the negative Ortho experience. Seems that some ortho's have a demi-god complex and love to condemn us lowly peasants.
I assume that he did a MRI, bone density scan, or scoped you to make his diagnosis? If not, he's a betting man and basing his diagnosis on probabitities. Did he happen to mention what Grade damage was present?
I'll ask our project head again if she has any thoughts or input. (she predicted that you would have probs with most non-sports orthos) If you want, shoot me a hushmail or PM and I'll see if she knows of anyone in sportsmed near you. (I understand 'near' is a relative term.)
No squatting is NOT the end of BBing though. Although not as efficient at working many muscles, lying stiff-legged weighted T's do work without straining knees. And the glucosamine/chondroiton sulfate does help me tremendously. NSAIDs, MSM and SAMe didn't have much effect though.
Whatever you decide to do, I pray the best for you. Believe me, you will quickly learn to compensate and work around the problem areas. I imagine Wilson6 can help with the work-arounds too. But I hear his leg routines may be quite the pain.
Arioch and BE - I will email both of you tomorrow, I truly appreciate your help and would love some help from W6 as well.
To answer your questions BE - he did none of the above, spent two seconds looking at my xrays, had me lie on my back and twisted my legs around. Gave me the nice girls don't lift speech and left. I did get a little less than pleasant about half way thru this and it went down hill from there.
To answer your questions BE - he did none of the above, spent two seconds looking at my xrays, had me lie on my back and twisted my legs around. Gave me the nice girls don't lift speech and left. I did get a little less than pleasant about half way thru this and it went down hill from there.
Arioch
New member
FWIW, I have no original cartiliage in my right knee, and most of the cartilage in the left knee has been restructred and/or replaced. Admittedly, my injuries were following an accident, but I do understand.
I still squat, and quite well for an old guy.
Avoid extensions. These eliminate the ability of the hamstring to protect the patella tendon during flexion of the quadriceps through co-contraction.
Do not hack squat, or any style of squatting that does not transfer the load from the knees to the hips. IOW, if you are still going to squat, which you probably should, you will need to experiment with your stance. Not only wider, but play with foot position as well. In my case despite the fact that my feet are twice as wide as my shoulders, my feet are pointing straight forward. This allows me to use my hips even more and my quads less.
Do not front squat, or split squat. When you recover, you can carefully add these back in, but it will take time. A lot of time.
Strengthen the hamstrings. Both aspects. Not just leg curls, but heavy good mornings and SLDL's.
And, like BigEasy, I take both GAG's (glucosamine and chondroitin) as well as MSM. It helps some.
I still squat, and quite well for an old guy.
Avoid extensions. These eliminate the ability of the hamstring to protect the patella tendon during flexion of the quadriceps through co-contraction.
Do not hack squat, or any style of squatting that does not transfer the load from the knees to the hips. IOW, if you are still going to squat, which you probably should, you will need to experiment with your stance. Not only wider, but play with foot position as well. In my case despite the fact that my feet are twice as wide as my shoulders, my feet are pointing straight forward. This allows me to use my hips even more and my quads less.
Do not front squat, or split squat. When you recover, you can carefully add these back in, but it will take time. A lot of time.
Strengthen the hamstrings. Both aspects. Not just leg curls, but heavy good mornings and SLDL's.
And, like BigEasy, I take both GAG's (glucosamine and chondroitin) as well as MSM. It helps some.
I feel ya Temp, that's what the docs claim I have...nothing has helped, I don't go heavy on legs at all...that helps but cardio sessions kill me as well. ...just got done with PT sessions, she was taping my knee, I'm not sure how well that was working since my knees get irritated with those punny exercises, after I stopped it started to feel my knee was confused and started popping over....I have given up on therapy and docs....let me know if you discover something new, supposedly the taping is supposed to help but I didn't like the feeling of my knee popping to the side so I stopped...might try it again...
Arioch
New member
Quick paste job.
More to follow.
Nutrition and Connective Tissue
Calories (1,2,3)
Many studies demonstrate that collagen production is sensitive to changes in short and long-term dietary intake. Within 24 hours of fasting of some animal models, collagen synthesis in articular cartilage decreases to 50% of normal. This reduction declines to 8 - 12% of control levels after 96 hours. Most conditions are not a severe as starvation. However, energy restriction may reduce collagen syntheses depending on duration and degree of food deprivation. Specific effects of malnutrition on connective tissue turnover are dependant on many factors such as exercise activities, injuries, and disease. As well, nutrition restriction effects may be age-related. Youngsters that are still growing are more sensitive to nutritional changes. Replacement of tissue pools of macronutrients requires weeks to months and certainly affects turnover rates of tissue components. Likewise, dietary deficiencies or excess and physical activities influence turnover rates.
Calories provide the body with cellular energy for normal metabolism, building and repairing tissues and stimulate hormonal responses. Individuals with injuries or other trauma should avoid a decrease in calories below maintainence or slightly above, thereby providing the nutrients and energy needed for healing and repair. Considering that connective tissue structures are created from all macronutrients, each are discussed below.
Protein
Severe caloric restriction (1,2,3) is usually accompanied by protein deficiency. The two major sources of protein during times of bulk loss are muscle and connective tissue. Muscle tissue provides a steady source of amino acids for general body needs. Connective tissue is the second source, which is reflective of the relative rate of turnover to muscle tissue. Many studies have demonstrated that a protein deficient diet results in a reduction of growth and development of the organism as well as delay in wound healing and repairs.
All of the essential amino acids are required for systhesis of proteins and other componenets and growth factors in the extracellular matrix. Some studies show that supplementing certain individual amino acids (methionine, lysine, arginine, and proline) to a protein deficient diet may inhibit prolongation of the inflamation phase of connective tissue healing and aid in fiber cross-linking mechanisms during repair.
Although countless studies demonstrate that protein malnutrition is significantly detrimental to normal turnover and healing of connective tissues, most athletes are generally well nourished with protein intake. Unless an individual is presented with severe trauma, surgery, or diabetes, a protein deficit that would negatively effect normal connective tissue metabolism should not be an issue.
Carbohydrates (1,3)
Aside from protein, carbohydrates are a major component of an athlete’s diet and supply quick energy for the body in the form of glucose. Although little information exists on the direct effects of glucose deficiencies on connective tissues, it is well known that glucose is an energy source for several components and growth mediators. Phagocytes and other white cells that mediate the inflammatory process utilize glucose as an energy source. Activity by these cells during the acute and healing phases prepare the tissue for repair after injury. Tissue cells such as fibroblasts and chondroblasts require glucose for synthesis of various macromolecules. Glucose is a building block of glycosaminoglycans and glycoproteins in the ground substance of the matrix. Arguably, hypoglycemia impairs normal cell function and delays wound healing. As well, production and release of several hormones, such as insulin and growth hormone, decline with low levels of plasma glucose further delaying tissue growth and repair.
Conversely, high levels of plasma glucose may also be detrimental. Decreased insulin function may lead to hyperglycemia which also impairs wound healing. High levels of plasma glucose reportedly may inhibit the stimulatory action of ascorbic acid on proteoglycan and collagen production (4). Furthermore, recall that chronic high plasma and tissue glucose levels produce advanced glycation products that affect the physical, chemical, and mechanical properties of collagen and elastin protein. Although associated with aging, this process is prematurely evident in diabetics. Proper glycemic control may delay the onset of complications related to excessive glycation and oxidation stress (5). For diabetics, exogenous insulin may be necessary for glycemic control. Additionally, avoiding a diet with excessive carbohydrate intake may postpone effects of high accumulation of glycation and oxidative products.
Diets low in carbohydrates typically cause body water loss. For athletes, the resultant dehydration may compromise integrity of connective tissues subject to mechanical loading. Considering that many connective tissues such as in articular joints require a relatively high water content for optimal functioning under stress, dehydration may increase incidence of injury or jeopardize healing and repair of injured tissue.
Fats (6,7)
Fats are very calorically dense and provide energy for the body. Furthermore, saturated fats and polyunsaturated fats (PUFAs) are precursors for many hormones such as steroids and prostoglandins. PUFAs are essential constituents of the cell membrane, contributing to their structural and functional integrity. Saturated fats are commonly found in animal foods and in some vegatable plants and have little direct import in the physiology of connective tissue. Therefore, discussion will concentrate on the influences of PUFAs and their influence on injured connective tissue.
The major PUFAs are classified as two types: n-3 and n-6 PUFAs. The n-6 familiy is the major PUFA in cell membranes and is derived from vegetable oils. Low levels of n-3 PUFAs exist in most individual cell membranes because diets are generally low in fish oils which are the source of this PUFA family. PUFAs are precursors for a family of hormones called eicosanoids, which are relased by macrophages and other cells and mediate many cellular functions. These substances have powerful autocrine and paracrine actions. The major role of eicosanoids is in the inflammatory response; therefore, dietary PUFAs may moderate the length of the inflammatory phase.
The n-6 PUFAs are precursors for arachidonic acid and the series 1 and 3 eicosanoids. Eicosapentanoic acid and eicosanoid series 2 are formed from the n-3 PUFAs. Generally, the 1 and 3 eicosanoid series are anti-inflammatory and the series 2 eicosanoids are pro-inflamatory. A relative excess of n-6 PUFAs stimulates production of prostoglandin E2 which may prolong the inflammatory response.
Dietary n-3 PUFAs can replace n-6 PUFAs. Increasing the ratio of dietary n-3:n-6 PUFAs may decrease macrophage prostaglandin E2 and cytokine release, and a balance between the eicosanoids may maintain the repair process with the least amount of inflammation. Although increasing intake of n-3 PUFAs may not impact acute inflammation, such nutritional support quite possibly moderates long-term inflammation related to excessive prostoglandin E2 production and cytokine release from activated marcophages.
References
1. Ruberg RL. Role of nutrition in wound healing. Surg Cl No Am 1984; 4:705-714.
2. Tinker D, Rucker R. Role of selected nutrients in synthesis, accumulation, and chemical modification of connective tissue proteins. Phys Rev 1985; 65:607-657.
3. Berg RA, Kerr JS. Nutritional aspects of collagen metabolism. Annu Rev Nutr 1992; 369-390.
4. Fisher E, McLennan SV, Tada H, et al. Interation of ascorbic acid and glucose on production of collagen and proteoglycan by fibroblasts. Diabetes 1991; 40:371-376.
5. Odetti P, Traverso N, Cosso L, et al. Good glycemic control reduces oxidative stress in diabetes mellitus and ageing. Free Rad Biol Med 1991; 10:339-352.
6. Cerra FB. Nutrient modulation of inflammatory and immune function. Am J Surg 1991; 161:230-234.
7. Bucci LR. Nutrition Applied to Injury Rehabilitation and Sports Medicine. 1995. Human Kinetics Press.
More to follow.
Nutrition and Connective Tissue
Calories (1,2,3)
Many studies demonstrate that collagen production is sensitive to changes in short and long-term dietary intake. Within 24 hours of fasting of some animal models, collagen synthesis in articular cartilage decreases to 50% of normal. This reduction declines to 8 - 12% of control levels after 96 hours. Most conditions are not a severe as starvation. However, energy restriction may reduce collagen syntheses depending on duration and degree of food deprivation. Specific effects of malnutrition on connective tissue turnover are dependant on many factors such as exercise activities, injuries, and disease. As well, nutrition restriction effects may be age-related. Youngsters that are still growing are more sensitive to nutritional changes. Replacement of tissue pools of macronutrients requires weeks to months and certainly affects turnover rates of tissue components. Likewise, dietary deficiencies or excess and physical activities influence turnover rates.
Calories provide the body with cellular energy for normal metabolism, building and repairing tissues and stimulate hormonal responses. Individuals with injuries or other trauma should avoid a decrease in calories below maintainence or slightly above, thereby providing the nutrients and energy needed for healing and repair. Considering that connective tissue structures are created from all macronutrients, each are discussed below.
Protein
Severe caloric restriction (1,2,3) is usually accompanied by protein deficiency. The two major sources of protein during times of bulk loss are muscle and connective tissue. Muscle tissue provides a steady source of amino acids for general body needs. Connective tissue is the second source, which is reflective of the relative rate of turnover to muscle tissue. Many studies have demonstrated that a protein deficient diet results in a reduction of growth and development of the organism as well as delay in wound healing and repairs.
All of the essential amino acids are required for systhesis of proteins and other componenets and growth factors in the extracellular matrix. Some studies show that supplementing certain individual amino acids (methionine, lysine, arginine, and proline) to a protein deficient diet may inhibit prolongation of the inflamation phase of connective tissue healing and aid in fiber cross-linking mechanisms during repair.
Although countless studies demonstrate that protein malnutrition is significantly detrimental to normal turnover and healing of connective tissues, most athletes are generally well nourished with protein intake. Unless an individual is presented with severe trauma, surgery, or diabetes, a protein deficit that would negatively effect normal connective tissue metabolism should not be an issue.
Carbohydrates (1,3)
Aside from protein, carbohydrates are a major component of an athlete’s diet and supply quick energy for the body in the form of glucose. Although little information exists on the direct effects of glucose deficiencies on connective tissues, it is well known that glucose is an energy source for several components and growth mediators. Phagocytes and other white cells that mediate the inflammatory process utilize glucose as an energy source. Activity by these cells during the acute and healing phases prepare the tissue for repair after injury. Tissue cells such as fibroblasts and chondroblasts require glucose for synthesis of various macromolecules. Glucose is a building block of glycosaminoglycans and glycoproteins in the ground substance of the matrix. Arguably, hypoglycemia impairs normal cell function and delays wound healing. As well, production and release of several hormones, such as insulin and growth hormone, decline with low levels of plasma glucose further delaying tissue growth and repair.
Conversely, high levels of plasma glucose may also be detrimental. Decreased insulin function may lead to hyperglycemia which also impairs wound healing. High levels of plasma glucose reportedly may inhibit the stimulatory action of ascorbic acid on proteoglycan and collagen production (4). Furthermore, recall that chronic high plasma and tissue glucose levels produce advanced glycation products that affect the physical, chemical, and mechanical properties of collagen and elastin protein. Although associated with aging, this process is prematurely evident in diabetics. Proper glycemic control may delay the onset of complications related to excessive glycation and oxidation stress (5). For diabetics, exogenous insulin may be necessary for glycemic control. Additionally, avoiding a diet with excessive carbohydrate intake may postpone effects of high accumulation of glycation and oxidative products.
Diets low in carbohydrates typically cause body water loss. For athletes, the resultant dehydration may compromise integrity of connective tissues subject to mechanical loading. Considering that many connective tissues such as in articular joints require a relatively high water content for optimal functioning under stress, dehydration may increase incidence of injury or jeopardize healing and repair of injured tissue.
Fats (6,7)
Fats are very calorically dense and provide energy for the body. Furthermore, saturated fats and polyunsaturated fats (PUFAs) are precursors for many hormones such as steroids and prostoglandins. PUFAs are essential constituents of the cell membrane, contributing to their structural and functional integrity. Saturated fats are commonly found in animal foods and in some vegatable plants and have little direct import in the physiology of connective tissue. Therefore, discussion will concentrate on the influences of PUFAs and their influence on injured connective tissue.
The major PUFAs are classified as two types: n-3 and n-6 PUFAs. The n-6 familiy is the major PUFA in cell membranes and is derived from vegetable oils. Low levels of n-3 PUFAs exist in most individual cell membranes because diets are generally low in fish oils which are the source of this PUFA family. PUFAs are precursors for a family of hormones called eicosanoids, which are relased by macrophages and other cells and mediate many cellular functions. These substances have powerful autocrine and paracrine actions. The major role of eicosanoids is in the inflammatory response; therefore, dietary PUFAs may moderate the length of the inflammatory phase.
The n-6 PUFAs are precursors for arachidonic acid and the series 1 and 3 eicosanoids. Eicosapentanoic acid and eicosanoid series 2 are formed from the n-3 PUFAs. Generally, the 1 and 3 eicosanoid series are anti-inflammatory and the series 2 eicosanoids are pro-inflamatory. A relative excess of n-6 PUFAs stimulates production of prostoglandin E2 which may prolong the inflammatory response.
Dietary n-3 PUFAs can replace n-6 PUFAs. Increasing the ratio of dietary n-3:n-6 PUFAs may decrease macrophage prostaglandin E2 and cytokine release, and a balance between the eicosanoids may maintain the repair process with the least amount of inflammation. Although increasing intake of n-3 PUFAs may not impact acute inflammation, such nutritional support quite possibly moderates long-term inflammation related to excessive prostoglandin E2 production and cytokine release from activated marcophages.
References
1. Ruberg RL. Role of nutrition in wound healing. Surg Cl No Am 1984; 4:705-714.
2. Tinker D, Rucker R. Role of selected nutrients in synthesis, accumulation, and chemical modification of connective tissue proteins. Phys Rev 1985; 65:607-657.
3. Berg RA, Kerr JS. Nutritional aspects of collagen metabolism. Annu Rev Nutr 1992; 369-390.
4. Fisher E, McLennan SV, Tada H, et al. Interation of ascorbic acid and glucose on production of collagen and proteoglycan by fibroblasts. Diabetes 1991; 40:371-376.
5. Odetti P, Traverso N, Cosso L, et al. Good glycemic control reduces oxidative stress in diabetes mellitus and ageing. Free Rad Biol Med 1991; 10:339-352.
6. Cerra FB. Nutrient modulation of inflammatory and immune function. Am J Surg 1991; 161:230-234.
7. Bucci LR. Nutrition Applied to Injury Rehabilitation and Sports Medicine. 1995. Human Kinetics Press.
Arioch
New member
Macronutrients
Macronutrients have many documented roles in cellular function and thus are critical in the wound healing process. Of nearly any population, athletes generally maintain an adequate diet specifically designed to meet the needs of their sport. Most athletes eat a balanced diet that adequately supplies both macro and macronutrients. Therefore, defects in collagen, elastin and proteoglycan metabolism are generally only seen as a result of deficiencies or excess. As well, successful healing of connective tissue injuries will rely on the presence of adequate nutritional stores.
As voiced in the field of protein balance, is a state of “accommodation” of micronutrient intake satisfactory in wound healing? (1,2) The body adjusts to changes within different ranges of a nutrient intake. In relation to protein, Waterlow (2) stated that “some adaptations may be at the expense of full functional ability.” For instance, a child may survive on an undernourished diet, but with a slower rate of growth and develop into a smaller-sized adult with sub-average muscle mass and physical strength. Such an adjustment has been termed “accommodation” rather than full adaptation with no loss of function (1,3). This then poses the question of the need for pharmacological supplementation of macronutrients during wound healing. During wound healing is there a need for higher than normally recommended levels to obtain micronutrient balance?
There are several ways a micronutrient deficiency can manifest: deficiencies caused by dietary intake, diet-gene interactions, and nutrient-drug interactions. The first is self-explanatory. Secondly, a genetic dysfunction may produce a differential response to a diet that is deficient or marginal in a nutrient. Additional, a single or multiple mutant genes may result in expression which resembles a nutrient deficiency or toxicity. These are clinically seen as genetic disorders resulting in abnormal metabolism of macronutrients. Thirdly, some studies suggest that connective tissue defects result from drug interaction with macronutrients.
Vitamins
Vitamin C
Of all the vitamins, ascorbic acid probably has the most influence on connective tissue metabolism and has been the most studied. The roles of AA in connective tissue can be quite complex and varied. Macromolecule turnover is affected by synthesis and intracellular and extracelluar degradation. Important mediators of these two processes are enzymes. Ascorbic acid is a cofactor for many of the enzymatic reactions in synthetic processes. Degradation of collagen outpaces syntheses; new collagen cannot replace losses and results in disease (scurvy).
In connective tissue, AA is involved in several metabolic reactions. Iron is necessary for a variety of enzymatic reactions, and AA protects iron from oxidation. AA preserves the enzyme-iron complex that catalyzes the reaction for intracellular assembly of collagen (6,35,36). Underhydroxylated collagen is unable to fold into a stable triple-helix and therefore is subject to increased intracellular degradation. The turnover rate of collagen is then in negative balance and degradation outpaces the rate of synthesis.
A large focus of research in AA and connective tissue has been related to the pathophysiology of diabetes. Animal and human diabetics appear to be deficient in plasma concentrations of AA which may be connected to associated delays in wound healing by decreased synthesis of collagen and Pgs (33,36). AA is structurally similar to glucose and its cellular uptake is mediated by glucose transport mechanisms. Studies have shown that cellular uptake of AA is inhibited by high extracellular concentrations of glucose (in the presence of as well as the absence of insulin) as seen in diabetes (4,5,33). This inhibition of AA uptake may exacerbate problems associated with AA deficiencies. Ths, increased intake of dietary AA may prevent inhibition induced by high glucose on collagen and proteoglycan syntheses (4,5).
In addition to collagen, the influence of AA extends to proteoglycans (Pgs). AA may serve as a cofactor in sulfation reactions in PGs (4,6,35), However, the exact mechanism of AA influence in GAG metabolism is not yet elucidated.
The most commonly known role of AA is as an antioxidant. Although not clearly demonstrated in the literature, AA may protect macromolecules from damage by free radicals by acting as a scavenger. These deleterious metabolites are highly reactive by-products produced from metabolism of glucose, one of which is free radicals. Thus, some authors postulate that AA deficiency may intensify oxidative damage leading to secondary effects on cellular structures and functions (5,33,36).
Recommendations for dietary intake of AA remain controversial. The increased demand for collagen synthesis in growing or injured individuals, or in diabetics with low plasma levels may require higher intakes of dietary AA. Studies with animals are difficult to extrapolate to humans as species requirement for AA most likely varies (4). As well, alterations in connective tissue by nutrient or other factors such as pharmaceuticals depend on whether they are of short-term or long-term duration. Age, typ of nutritional alteration, and specific tissue are also factors.
The Recommended Daily Allowance (RDA) for vitamin C was determined by the amount necessary to prevent scurvy and the amount where excess is eliminated from the body. The daily amount believed to prevent scurvy in an adult on a diet deficient in vitamin C is 10 mg./day. Considering depletion and turnover rates of whole body AA, the RDA was arbitrarily set at 60 mg./day for an adult male and female. However, by conventional reasoning, if the body requires higher levels of AA due to higher turnover rates, such as in disease or injury, then higher doses may be warranted and tolerated. Some proponents of increased vitamin C dosages use bowel tolerance to determine the maximum therapeutic dose.
Bowel tolerance is a method to determine body tolerance to AA. Theoretically, the sicker the body is, the more AA the body utilizes and can therefore tolerate higher doses. When plasma, intracellular and extracellular compartments are maximized, whole body tolerance is reached. Excess intake results in increased bowel activity. The levels where such symptoms appear vary individually with physiological status. During illness or injury, an individual may tolerate very high doses and experience no diarrhea. After the sickness or injury, the body does not require high doses and tolerance decreases, causing diarrhea. Many proponents claim that doses just below the bowel tolerance are most therapeutic. However, studies with such therapeutic doses have not been performed with human subjects. Nevertheless, research with animal models has shown that such therapeutic doses of AA resulted in reduced symptoms of osteoarthritis. Also, AA supplementation in surgical and non-surgical patients resulted in improved would healing, reduced inflammation and improved recovery.
Vitamin B Complex
The B vitamin complex is a large group of compounds with different structure and biological activity. They are usually found within the same food sources. The primary role of the B vitamins is cellular energy metabolism. Any deficit in cellular energy will have adverse effects on cellular function. Therefore, the B vitamins are essential in connective tissue metabolism.
Many of the B complex serve as cofactors in the process of collagen and elastin cross-linking. Deficiencies in several of the B vitamins influence expression of collagen genes and induce decreased mechanical strength of repaired and remodeled tissue (32,34,35).
Since most B vitamins are found together in similar food groups, deficiencies of one singular vitamin are uncommon. However, deficiencies may exist if overall dietary intake is reduced. A mixture of all B vitamins should adequately provide for daily needs. Since most athletes supplement with a multivitamin product, intakes are generally at or above the RDA.;
Vitamin A
Retinoids are a group of compounds of which some have vitamin A activity and others do not. Vitamin A is often referred to as retinol in much of the literature and will be used interchangeably here. Although carotenoids are commonly mistaken for vitamin A, only a fraction of them have any vitamin A activity. b-Carotene is the most significant because in the body it can be broken down into the two retinol molecules and therefore supply vitamin A when needed. Retinol is stored in the liver and distributed to peripheral tissues by strict regulatory mechanisms and metabolized in several pathways (7).
Retinol is converted to retinoic acid inside cells and both are potent regulators of specific genes, including expression of fibronectin and type I procollagen (32,35). Other metabolites of retinol regulate cell differentiation and are associated with glycosaminoglycan (GAG), glycoprotein and proteoglycan (PG) synthesis. Although still unclear, the role of vitamin A in PG synthesis may be involved in sulfation of GAGs. Tissue from animals deficient in vitamin A typically displays decreased synthesis of highly sulfated GAGs (35).
Few in vivo studies exist documenting specific roles of retinoids in connective tissue, except for those studying wound healing in animal models. That rapidly growing tissues are sensitive to vitamin A deficiency is well known. Deficiency of other nutrients, such as zinc and protein, that assist in the transport and metabolism of retinol may induce deficiency symptoms (8). Therefore, since retinol distribution from the liver is tightly regulated, functional deficiencies may result with normal vitamin A intake and stores. Additionally, extra-physiological doses of vitamin A may counteract the inhibitory effects of systemic corticosteroids on plasma retinol transport (32,34).
Because vitamin A is fat-soluble, toxicity is also a concern in connective tissue metabolism. High levels may inhibit collagen synthesis, as seen in the skin, and increase catabolism of cartilage. This may be concentration dependent since excessively high levels affect ascorbate induced lipid peroxidation, which in turn inhibits AA-induced collagen synthesis (35,36).
Vitamin E
Vitamin E is a group of compounds comprising two major classes: tocopherols and tocotrinols. The basic chemical structure in each class is similar with variations of substituents and confirmation resulting in different relative activity. For a complete discussion, please refer to a text on nutrition or medicinal chemistry. The term Vitamin E is used in this article as a reference primarily to the tocopherols, as they have the greatest activity within the body.
Literature information on the role of vitamin E connective tissue metabolism is controversial. The major function of vitamin E is as an antioxidant and in the maintenance of cell membrane integrity. Its role as an antioxidant is thought to require vitamin C and selenium. Although no specific disease of connective tissue can be attributed to vitamin E deficiency, it is no doubt need for life and cell processes.
Animal model studies have shown that severe deficiency in vitamin E influence collagen cross-linking and an increase in susceptibility of insoluble collagen to degradation by proteinases (35). Conversely, excessive doses of vitamin E elicit effects similar to those of corticosteroids: inhibition of collagen synthesis and wound repair. Rats given supra physiological doses of vitamin E exhibited less tensile strength in skin of healed wounds. Indeed, vitamin E may potentiate adverse effects of corticosteroids (34,35).
Vitamin E has exhibited anti-inflammatory effects in some animal models. As an antioxidant, vitamin E may protect lysosome membranes leading to a decrease in histamine and serotonin from mast cells during inflammation. However, studies show that vitamin E has a preventative role rather than therapeutic. If sufficient vitamin E is present before inflammation response is initiated, the inflammatory phase may be shortened. Apparently, therapeutic administration did not affect duration or progress of the inflammation phase (32). Thus perhaps optimal results may be seen in individuals with degenerative joint conditions or with chronic inflammation.
Minerals
Minerals are required for normal cell function and several serve as cofactors in the many enzymatic processes involved in synthesis of connective tissue macromolecules. Copper and manganese are critical cofactors for collagen and GAG synthesis and metabolism. Some recent research alludes to an increased role of manganese in synthesis of GAGs (10). However, a deficiency in these minerals is extremely rare. Some pharmaceuticals are known to negatively interact with some minerals. Nonetheless, defects in collagen synthesis are generally observed only at the lowest levels of dietary intake of most minerals. An athlete eating a diet with adequate protein and calories is like to have normal levels of minerals.
Clinical evidence is largely lacking for effects of mineral deficiencies on connective tissue except for zinc. This mineral primarily acts as a cofactor in many enzyme systems that regulate cell proliferation and growth and in immune integrity. Diminution of collagen synthesis and strength as well as impaired healing is seen in animal tissues with zinc deficiencies.
Controversy exists in whether supplemental zinc can accelerate healing above the normal rate. Several supplement companies in the sports marketing arena claim that most athletes are deficient in this mineral. However, total body assessment of zinc is not easily obtained and many published studies have erroneously relied on data interpretation from zinc plasma concentrations in humans (8,9,11,32). As well, most studies do not measure plasma concentration versus time to assess fluctuations.
Zinc exists in intracellular and extracellular pools and its exchange in the body is tightly regulated (12). Many factors influence tissue pool concentrations, such as absorption, oral contraceptives, and steroid therapy (11). Nonetheless, a well-nourished athlete with a healthy intake of animal protein, fruit, vegetables and a vitamin/mineral supplement is unlikely to be deficient in zinc. Populations who may exhibit deficiencies are the elderly, those with malabsorption, and lactovegetarians who consume large amounts of foods with phytates.
References
1.Carpenter, KJ. Protein and Energy: A study of changing ideas in nutrition. 1994. Cambridge University. Press.
2. Waterlow JC. Metabolic Adaptation to low intakes of energy and protein. Ann Rev Nutr, 1986; 6:495-526.
3. Scrimshaw, NS and Young VR. Adaptation to low protein and energy intakes. Human Org, 1989; 48:20-30.
4. Fay MJ, Bush MJ, Verlangier AJ. Effects of cytochalasin B on uptake of ascorbic acid and glucose by 3T3 fibroblasts: mechanism of impaired ascorbate transport in diabetes. Life Sciences, 1990, 46:619-624.
5. Okuda Y, Magahama M, Mizutani M, et al. Ascorbic acid prevents the inhibition of DNA synthesis induced by high glucose concentration in cultured human endothelial cells. Diabetes Res, 1991; 18:65-68.
6. Russel JE, Manske PR. Ascorbic acid requirement for optimal flexor tendon repair in vitro. J Orthop Res, 1991; 9:714-719.
7. Foye WO, Lemke TL, Williams DA, eds. In: Priciples of Medicinal Chemistry, fourth ed. 1995. Williams and Wilkins pub.
8. Groff JL, Gropper SS, Hunt SM. In: Advanced Nutrition and Human Metabolism, second ed. 1995. West Publishing Co.
9. Dimitrov NV, MacDonald D, Malovrh MM. Bioavailability of Micronutrients in Humans. J Appl Nutr 1997; 49:56-65.
10. Leach RM. Role of Manganese in mucopolysaccharide metabolism. Fed Proc 1971; 30-991.
11. Milne DB. Assessment of zinc and copper nutritional status in man. Nutr MD 1987; 13:1-2.
12. King MT, King JC, Tamura T, et al. Assessment of zinc status. J Nutr 1990; 120:1474-1479.
32. Bucci LR. Nutrition applied to Injury Rehabilitation and Sports Medicine. 1995. Human Kinetics Press.
33. Fisher E, McLennan SV, Tada H, et al. Interaction of ascorbic acid and glucose on production of collagen and proteoglycan by fibroblasts. Diabetes 1991; 40:371-376.
34. Ruberg RL. Role of Nutrition in wound healing. Surg Cl No Am 1984; 4:705-714.
35. Tinker D, Rucker R. Role of selected nutrients in synthesis, accumulation, and chemical modification of connective tissue proteins. Phys Rev 1985; 65:607-657.
36. Berg RA, Kerr JS. Nutritional aspects of collagen metabolism. Annu Rev Nutr 1992; 369-390.
Macronutrients have many documented roles in cellular function and thus are critical in the wound healing process. Of nearly any population, athletes generally maintain an adequate diet specifically designed to meet the needs of their sport. Most athletes eat a balanced diet that adequately supplies both macro and macronutrients. Therefore, defects in collagen, elastin and proteoglycan metabolism are generally only seen as a result of deficiencies or excess. As well, successful healing of connective tissue injuries will rely on the presence of adequate nutritional stores.
As voiced in the field of protein balance, is a state of “accommodation” of micronutrient intake satisfactory in wound healing? (1,2) The body adjusts to changes within different ranges of a nutrient intake. In relation to protein, Waterlow (2) stated that “some adaptations may be at the expense of full functional ability.” For instance, a child may survive on an undernourished diet, but with a slower rate of growth and develop into a smaller-sized adult with sub-average muscle mass and physical strength. Such an adjustment has been termed “accommodation” rather than full adaptation with no loss of function (1,3). This then poses the question of the need for pharmacological supplementation of macronutrients during wound healing. During wound healing is there a need for higher than normally recommended levels to obtain micronutrient balance?
There are several ways a micronutrient deficiency can manifest: deficiencies caused by dietary intake, diet-gene interactions, and nutrient-drug interactions. The first is self-explanatory. Secondly, a genetic dysfunction may produce a differential response to a diet that is deficient or marginal in a nutrient. Additional, a single or multiple mutant genes may result in expression which resembles a nutrient deficiency or toxicity. These are clinically seen as genetic disorders resulting in abnormal metabolism of macronutrients. Thirdly, some studies suggest that connective tissue defects result from drug interaction with macronutrients.
Vitamins
Vitamin C
Of all the vitamins, ascorbic acid probably has the most influence on connective tissue metabolism and has been the most studied. The roles of AA in connective tissue can be quite complex and varied. Macromolecule turnover is affected by synthesis and intracellular and extracelluar degradation. Important mediators of these two processes are enzymes. Ascorbic acid is a cofactor for many of the enzymatic reactions in synthetic processes. Degradation of collagen outpaces syntheses; new collagen cannot replace losses and results in disease (scurvy).
In connective tissue, AA is involved in several metabolic reactions. Iron is necessary for a variety of enzymatic reactions, and AA protects iron from oxidation. AA preserves the enzyme-iron complex that catalyzes the reaction for intracellular assembly of collagen (6,35,36). Underhydroxylated collagen is unable to fold into a stable triple-helix and therefore is subject to increased intracellular degradation. The turnover rate of collagen is then in negative balance and degradation outpaces the rate of synthesis.
A large focus of research in AA and connective tissue has been related to the pathophysiology of diabetes. Animal and human diabetics appear to be deficient in plasma concentrations of AA which may be connected to associated delays in wound healing by decreased synthesis of collagen and Pgs (33,36). AA is structurally similar to glucose and its cellular uptake is mediated by glucose transport mechanisms. Studies have shown that cellular uptake of AA is inhibited by high extracellular concentrations of glucose (in the presence of as well as the absence of insulin) as seen in diabetes (4,5,33). This inhibition of AA uptake may exacerbate problems associated with AA deficiencies. Ths, increased intake of dietary AA may prevent inhibition induced by high glucose on collagen and proteoglycan syntheses (4,5).
In addition to collagen, the influence of AA extends to proteoglycans (Pgs). AA may serve as a cofactor in sulfation reactions in PGs (4,6,35), However, the exact mechanism of AA influence in GAG metabolism is not yet elucidated.
The most commonly known role of AA is as an antioxidant. Although not clearly demonstrated in the literature, AA may protect macromolecules from damage by free radicals by acting as a scavenger. These deleterious metabolites are highly reactive by-products produced from metabolism of glucose, one of which is free radicals. Thus, some authors postulate that AA deficiency may intensify oxidative damage leading to secondary effects on cellular structures and functions (5,33,36).
Recommendations for dietary intake of AA remain controversial. The increased demand for collagen synthesis in growing or injured individuals, or in diabetics with low plasma levels may require higher intakes of dietary AA. Studies with animals are difficult to extrapolate to humans as species requirement for AA most likely varies (4). As well, alterations in connective tissue by nutrient or other factors such as pharmaceuticals depend on whether they are of short-term or long-term duration. Age, typ of nutritional alteration, and specific tissue are also factors.
The Recommended Daily Allowance (RDA) for vitamin C was determined by the amount necessary to prevent scurvy and the amount where excess is eliminated from the body. The daily amount believed to prevent scurvy in an adult on a diet deficient in vitamin C is 10 mg./day. Considering depletion and turnover rates of whole body AA, the RDA was arbitrarily set at 60 mg./day for an adult male and female. However, by conventional reasoning, if the body requires higher levels of AA due to higher turnover rates, such as in disease or injury, then higher doses may be warranted and tolerated. Some proponents of increased vitamin C dosages use bowel tolerance to determine the maximum therapeutic dose.
Bowel tolerance is a method to determine body tolerance to AA. Theoretically, the sicker the body is, the more AA the body utilizes and can therefore tolerate higher doses. When plasma, intracellular and extracellular compartments are maximized, whole body tolerance is reached. Excess intake results in increased bowel activity. The levels where such symptoms appear vary individually with physiological status. During illness or injury, an individual may tolerate very high doses and experience no diarrhea. After the sickness or injury, the body does not require high doses and tolerance decreases, causing diarrhea. Many proponents claim that doses just below the bowel tolerance are most therapeutic. However, studies with such therapeutic doses have not been performed with human subjects. Nevertheless, research with animal models has shown that such therapeutic doses of AA resulted in reduced symptoms of osteoarthritis. Also, AA supplementation in surgical and non-surgical patients resulted in improved would healing, reduced inflammation and improved recovery.
Vitamin B Complex
The B vitamin complex is a large group of compounds with different structure and biological activity. They are usually found within the same food sources. The primary role of the B vitamins is cellular energy metabolism. Any deficit in cellular energy will have adverse effects on cellular function. Therefore, the B vitamins are essential in connective tissue metabolism.
Many of the B complex serve as cofactors in the process of collagen and elastin cross-linking. Deficiencies in several of the B vitamins influence expression of collagen genes and induce decreased mechanical strength of repaired and remodeled tissue (32,34,35).
Since most B vitamins are found together in similar food groups, deficiencies of one singular vitamin are uncommon. However, deficiencies may exist if overall dietary intake is reduced. A mixture of all B vitamins should adequately provide for daily needs. Since most athletes supplement with a multivitamin product, intakes are generally at or above the RDA.;
Vitamin A
Retinoids are a group of compounds of which some have vitamin A activity and others do not. Vitamin A is often referred to as retinol in much of the literature and will be used interchangeably here. Although carotenoids are commonly mistaken for vitamin A, only a fraction of them have any vitamin A activity. b-Carotene is the most significant because in the body it can be broken down into the two retinol molecules and therefore supply vitamin A when needed. Retinol is stored in the liver and distributed to peripheral tissues by strict regulatory mechanisms and metabolized in several pathways (7).
Retinol is converted to retinoic acid inside cells and both are potent regulators of specific genes, including expression of fibronectin and type I procollagen (32,35). Other metabolites of retinol regulate cell differentiation and are associated with glycosaminoglycan (GAG), glycoprotein and proteoglycan (PG) synthesis. Although still unclear, the role of vitamin A in PG synthesis may be involved in sulfation of GAGs. Tissue from animals deficient in vitamin A typically displays decreased synthesis of highly sulfated GAGs (35).
Few in vivo studies exist documenting specific roles of retinoids in connective tissue, except for those studying wound healing in animal models. That rapidly growing tissues are sensitive to vitamin A deficiency is well known. Deficiency of other nutrients, such as zinc and protein, that assist in the transport and metabolism of retinol may induce deficiency symptoms (8). Therefore, since retinol distribution from the liver is tightly regulated, functional deficiencies may result with normal vitamin A intake and stores. Additionally, extra-physiological doses of vitamin A may counteract the inhibitory effects of systemic corticosteroids on plasma retinol transport (32,34).
Because vitamin A is fat-soluble, toxicity is also a concern in connective tissue metabolism. High levels may inhibit collagen synthesis, as seen in the skin, and increase catabolism of cartilage. This may be concentration dependent since excessively high levels affect ascorbate induced lipid peroxidation, which in turn inhibits AA-induced collagen synthesis (35,36).
Vitamin E
Vitamin E is a group of compounds comprising two major classes: tocopherols and tocotrinols. The basic chemical structure in each class is similar with variations of substituents and confirmation resulting in different relative activity. For a complete discussion, please refer to a text on nutrition or medicinal chemistry. The term Vitamin E is used in this article as a reference primarily to the tocopherols, as they have the greatest activity within the body.
Literature information on the role of vitamin E connective tissue metabolism is controversial. The major function of vitamin E is as an antioxidant and in the maintenance of cell membrane integrity. Its role as an antioxidant is thought to require vitamin C and selenium. Although no specific disease of connective tissue can be attributed to vitamin E deficiency, it is no doubt need for life and cell processes.
Animal model studies have shown that severe deficiency in vitamin E influence collagen cross-linking and an increase in susceptibility of insoluble collagen to degradation by proteinases (35). Conversely, excessive doses of vitamin E elicit effects similar to those of corticosteroids: inhibition of collagen synthesis and wound repair. Rats given supra physiological doses of vitamin E exhibited less tensile strength in skin of healed wounds. Indeed, vitamin E may potentiate adverse effects of corticosteroids (34,35).
Vitamin E has exhibited anti-inflammatory effects in some animal models. As an antioxidant, vitamin E may protect lysosome membranes leading to a decrease in histamine and serotonin from mast cells during inflammation. However, studies show that vitamin E has a preventative role rather than therapeutic. If sufficient vitamin E is present before inflammation response is initiated, the inflammatory phase may be shortened. Apparently, therapeutic administration did not affect duration or progress of the inflammation phase (32). Thus perhaps optimal results may be seen in individuals with degenerative joint conditions or with chronic inflammation.
Minerals
Minerals are required for normal cell function and several serve as cofactors in the many enzymatic processes involved in synthesis of connective tissue macromolecules. Copper and manganese are critical cofactors for collagen and GAG synthesis and metabolism. Some recent research alludes to an increased role of manganese in synthesis of GAGs (10). However, a deficiency in these minerals is extremely rare. Some pharmaceuticals are known to negatively interact with some minerals. Nonetheless, defects in collagen synthesis are generally observed only at the lowest levels of dietary intake of most minerals. An athlete eating a diet with adequate protein and calories is like to have normal levels of minerals.
Clinical evidence is largely lacking for effects of mineral deficiencies on connective tissue except for zinc. This mineral primarily acts as a cofactor in many enzyme systems that regulate cell proliferation and growth and in immune integrity. Diminution of collagen synthesis and strength as well as impaired healing is seen in animal tissues with zinc deficiencies.
Controversy exists in whether supplemental zinc can accelerate healing above the normal rate. Several supplement companies in the sports marketing arena claim that most athletes are deficient in this mineral. However, total body assessment of zinc is not easily obtained and many published studies have erroneously relied on data interpretation from zinc plasma concentrations in humans (8,9,11,32). As well, most studies do not measure plasma concentration versus time to assess fluctuations.
Zinc exists in intracellular and extracellular pools and its exchange in the body is tightly regulated (12). Many factors influence tissue pool concentrations, such as absorption, oral contraceptives, and steroid therapy (11). Nonetheless, a well-nourished athlete with a healthy intake of animal protein, fruit, vegetables and a vitamin/mineral supplement is unlikely to be deficient in zinc. Populations who may exhibit deficiencies are the elderly, those with malabsorption, and lactovegetarians who consume large amounts of foods with phytates.
References
1.Carpenter, KJ. Protein and Energy: A study of changing ideas in nutrition. 1994. Cambridge University. Press.
2. Waterlow JC. Metabolic Adaptation to low intakes of energy and protein. Ann Rev Nutr, 1986; 6:495-526.
3. Scrimshaw, NS and Young VR. Adaptation to low protein and energy intakes. Human Org, 1989; 48:20-30.
4. Fay MJ, Bush MJ, Verlangier AJ. Effects of cytochalasin B on uptake of ascorbic acid and glucose by 3T3 fibroblasts: mechanism of impaired ascorbate transport in diabetes. Life Sciences, 1990, 46:619-624.
5. Okuda Y, Magahama M, Mizutani M, et al. Ascorbic acid prevents the inhibition of DNA synthesis induced by high glucose concentration in cultured human endothelial cells. Diabetes Res, 1991; 18:65-68.
6. Russel JE, Manske PR. Ascorbic acid requirement for optimal flexor tendon repair in vitro. J Orthop Res, 1991; 9:714-719.
7. Foye WO, Lemke TL, Williams DA, eds. In: Priciples of Medicinal Chemistry, fourth ed. 1995. Williams and Wilkins pub.
8. Groff JL, Gropper SS, Hunt SM. In: Advanced Nutrition and Human Metabolism, second ed. 1995. West Publishing Co.
9. Dimitrov NV, MacDonald D, Malovrh MM. Bioavailability of Micronutrients in Humans. J Appl Nutr 1997; 49:56-65.
10. Leach RM. Role of Manganese in mucopolysaccharide metabolism. Fed Proc 1971; 30-991.
11. Milne DB. Assessment of zinc and copper nutritional status in man. Nutr MD 1987; 13:1-2.
12. King MT, King JC, Tamura T, et al. Assessment of zinc status. J Nutr 1990; 120:1474-1479.
32. Bucci LR. Nutrition applied to Injury Rehabilitation and Sports Medicine. 1995. Human Kinetics Press.
33. Fisher E, McLennan SV, Tada H, et al. Interaction of ascorbic acid and glucose on production of collagen and proteoglycan by fibroblasts. Diabetes 1991; 40:371-376.
34. Ruberg RL. Role of Nutrition in wound healing. Surg Cl No Am 1984; 4:705-714.
35. Tinker D, Rucker R. Role of selected nutrients in synthesis, accumulation, and chemical modification of connective tissue proteins. Phys Rev 1985; 65:607-657.
36. Berg RA, Kerr JS. Nutritional aspects of collagen metabolism. Annu Rev Nutr 1992; 369-390.
Arioch - here is where I am at nutrition and supp wise -
2200 cal - 40/40/20 CLEAN
the weak spot is in the fats - tend to forget to take my flax
Bratis Ox 5mg/ed split am/pm
Tylers Liver Detox 2ed
alpha lipoic acid 600 mg ed
glucosamine 3g ed - thought this had the C in it but it doesn't
msm 1000mg ed
saw palmetto 320 mg ed
l glutamine - 5g post workout
2200 cal - 40/40/20 CLEAN
the weak spot is in the fats - tend to forget to take my flax
Bratis Ox 5mg/ed split am/pm
Tylers Liver Detox 2ed
alpha lipoic acid 600 mg ed
glucosamine 3g ed - thought this had the C in it but it doesn't
msm 1000mg ed
saw palmetto 320 mg ed
l glutamine - 5g post workout
