by Frank Bodnar, DC, MS
Ortho Molecular Products, Inc
In a perfect world we would stay forever young and be able to rebound quickly from biomechanical stress. Have you ever wondered why we begin to slow down? Is it all in our head? Is age ‘just a number’ as they say? After all we’re not completely fragile or helpless. We’ve seen our bodies respond with resilience before. Why now does it seem to take just a little bit longer to recover from the round of golf or weekend 5k run? While we joke about turning 40 and waking up stiff and achy, the truth is aging is a legitimate culprit. Aging is a multi-factorial process that unfortunately makes the glue that holds everything together weaker the older we get.
The process of aging is a universal gradual decline that isn’t naturally pathological but is felt and seen in human performance and injury rates (1). Aging is a highly individual process due to genetic, lifestyle, injury history, past diseases and current co-morbidities. All of these factors can directly affect the individual aging process (2). One of the most common connective tissue injuries to walk into a chiropractor’s office are tendinopathies. The underlying pathology is largely due to the degeneration of the collagen fibers in the tendons of athletes, recreational athletes and those with repetitive tasks at work (3). We know age plays a key role in overuse injuries because studies have shown that older individuals have a greater frequency of tendon injuries than younger individuals, highly suggestive of a more degenerative role rather than an acute tissue injury mechanism (4,5).
The aging of a tendon is a multi-factorial process that can include a variety of cellular and tissue mechanisms. The process of aging includes less vascular supply and degenerative changes of not only the collagen fibers but the non-collagenous matrix components of the tendons as well. These changes result in less collagen fibers that are less compliant, less resilient, less organized, less able to withstand cellular stress, a decreased ability to regenerate and have a much higher risk of failing under physical stress (6-10).
In general, we associate aging with gray hair and wrinkles, but below the surface the cells responsible for producing collagen fibers, material for the extracellular matrix and literally make up the fabric of our tendons are undergoing a multitude of changes. On a cellular level tendon cells responsible for growth and repair, tenoblasts, transform into tenocytes which have less healing and regenerative capabilities (10). This transformation is a hallmark sign of tendon aging and results in the decreased density of tendon cells as well as less basement membrane, which protects and attaches tendons to surrounding tissues (11,12).
With increasing age there is also less metabolic overall metabolic activity of both tenoblasts and tenocytes, which results in a reduced ability of a tendon to repair itself. Tendon blood flow and the number of capillaries decrease with age as well (10). Blood vessels begin to become less elastic, more rigid and provide less arterial blood flow which causes less nutrients and oxygen to be delivered to cells, limiting their ability to repair and thrive (13,14). Inside the tenocytes the rough endoplasmic reticulum begins to decline in its capacity for protein synthesis, and a decrease in the number of mitochondria results in less overall ability to create energy from lipids and carbohydrates. The Krebs cycle, responsible for ATP production, also begins to shift its overall metabolic pathways from less aerobic to more anaerobic, which is highly inefficient, and energy production begins to slow and eventually shut down (10,11,15,16).
Collagen turnover and collagen synthesis both decline with age and tendon cells lose their ability to divide and grow as quickly. As early as our mid-twenties we begin to see a decline in the amount of collagen production, and past forty may see production decline as much as 25%. But even more concerning to the health of a tendon is the decrease in the production of the surrounding extracellular matrix materials. The decline of proteoglycans and glycoproteins, which pull water into connective tissues, declines by about 70% which contributes to age-dependent stiffness and a loss in collagen fiber gliding capacity (1,11). Biological aging results in a decreased thickness, dehydration and ultimately less rebound capability of a tendon under stress and load.
Although we don’t always feel these changes as they occur, we can definitely start to see them. If we were to take a tissue sample and examine it under a microscope, we would see that the aging tendon’s collagen fibers appear less organized, less bundled, and more fragmented. A tendon of an elderly individual appears more like a glob of frayed yarn compared to tendon of a teenager, which appears more like a well-organized cable that is capable of bearing high stress and maintaining tension under stress.
Another tap of the zoom button on our microscope would also reveal that in those 40 and older we would see more tissue samples with an accumulation of lipids, glycosaminoglycans, and calcium deposits. Lipid deposition disrupts the fiber bundles and reduces tendon strength. Areas of reduced blood flow and maximal lipid deposition correlate with classic sites of tendon rupture (21). Sometimes fibrin and evidence of thrombus formation are apparent in surrounding blood vessels as well (10). The most common sites of these changes are in the Achilles, biceps brachii, anterior tibial, quadriceps and patellar tendons (22,23).
The most severe biomechanical change of is decreased tensile strength, or the ability of something to resist being pulled apart (17). This decrease starts with the core protein of tendons, which is collagen. The mechanical property of collagen begins to decline due to an increase in collagen molecule crosslinking which makes the collagen fibrils very stiff and rigid (18). Unfortunately, there is no way to avoid or reverse this process and because of this collagen crosslinking is actually considered the best biomarker of aging. These mechanical adaptations result in a decreased ability to tolerate strain, load, elasticity, and maintain tensile strength (8,19,20). Less stress relaxation, mechanical recovery and creep (20), along with less elastin and proteoglycan matrix (10) make the older tendons weaker and more likely to tear or suffer from overuse injury when stressed and strained (1).
Co-morbidities and Contributing External Factors
Apart from all of the cellular, metabolic, tissue quality and vascular changes of aging there are a multitude of external factors at play that can influence the rate of tendon degeneration that clinicians should be aware of.
Research has shown that diabetes causes premature aging and degeneration. Collagen from 40-year-old diabetic has been found to be comparable to that of those close to 100 years of age (33).
Nutritional deficiencies are also be associated with tendon degeneration. Protein is needed for the necessary amino acids of collagen and other proteins, and carbohydrates for the maintenance of the ground substance. Emerging evidence shows that specific collagen peptides may help with tendon repair as well (24,25), counteracting catabolic effects of tissue damage (25), enhance connective tissue remodeling (26,28) and enhancing clinical outcomes (27-31) especially when paired with specific exercise rehabilitation.
Medications such as corticosteroids and fluoroquinolones are catabolic, especially at high levels and with chronic use because they inhibit the production of new collagen (9,38).
Exercise and physical activity, or the lack of activity also stimulates specific responses in tendons. Exercise appears to have a beneficial effect on aging tendons (10,34), but of course individual caution should be used in terms of exercise type in those prone to tendon injury, or with past injury. Long-term exercise increases the mass, collagen content, cross-sectional area, tensile strength, weight-to-length ratio, and load-to-failure of tendon tissue (10,32,35–37). Exercise could reduce the rate of degeneration but may not completely prevent injury or degeneration. With one of the mechanisms of an aging tendon being poor blood supply a sedentary lifestyle will decrease circulation and result in less nutrients, oxygen and overall cellular health (21).
In clinical practice, providing patients with sound nutritional and exercise advice are key preventative measures that can be taken to prevent age-related tendon degeneration and related symptoms.
Daily stretching, mobility exercises, and compound multi-joint movements will help maintain range of motion and tissue compliance.
Long warm-ups and cooling-down periods should also be part of the routine. The older an individual, the more gradual increase in intensity, shorter duration and less frequent bouts of exercise are recommended.
Movements with strong impact, quick acceleration or quick deceleration movements, like sprinting and jumping should be avoided. Better alternatives would be swimming, rowing, cycling, walking and full body resistance exercises such as squats, deadlifts and presses would also be acceptable.
Finally, as mentioned earlier nutrition also plays a key role in the aging process, and degeneration of tendons. The dietary reference intake (DRI) for an individual should be at least 0.8 g or protein per kilogram of body weight, which amounts to about 56 grams per day of protein for normal tissue repair and maintenance. Following a Mediterranean diet will provide sufficient macro and micronutrients that are not only essential to connective tissue synthesis, but anti-inflammatory (39,40) and demonstrate the ability to limit chronic inflammatory mechanisms (40). In order to maximize tendon strength and tissue healing additional vitamin C and magnesium, along with collagen peptides and mucopolysaccharides should be supplemented during acute injury, tissue regeneration and tissue remodeling as a patient undergoes physical rehab.
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