Recent research has shown that sinew (tendons and ligaments) and ECM are not inert structures, but in fact dynamic “smart tissues” that change throughout lifespan as influenced by nearly 1000 genes with many intrinsic and extrinsic factors coming into play. The mechanical superstructure of these tissues develops throughout childhood and adolescence, and this foundation—particularly the tendon core—becomes the basis for connective tissue function as an adult. (Thus the importance of a widely varying youth sport experience that imparts increasing mechanical load on connective tissues throughout the body.)
Among adults morphological and material changes occur much more slowly. Mechanical loading stimulates a small pool of active tenocytes and signals enzymatic cross-linking, which together can significantly modify mechanical properties and positively influence the overall function of the muscle-tendon complex. Increases in cross-sectional area, cross-linking, and hydration protect the tendon during extreme and/or compressive loading, whereas changes in the ECM enhance muscle quality and efficiency (increased rate of force development, reduced ATP cost of movement, and decreased micro-trauma among contractile proteins). Let’s examine more closely the two primary exercise-induced modifications: collagen synthesis and enzymatic cross-linking.
While the adolescent body is prolific at laying down new collagen, turnover of collagen occurs much more slowly in adults. In a similar fashion to hypertrophy of muscle contractile proteins, tendon and ECM degrade slightly as a result of training and then regenerate to regain homeostasis and strengthen slightly during the recovery period (Figure 4). A critical difference between muscle and sinew, however, is the limited blood flow and nutrient supply available to tendons and ligaments. The small pool of active tenocytes (fibroblastic cells which extrude collagen in the peritendinous tissue around the perimeter of fascicles) resulting in slight tendon hypertrophy that is only recognized after months and years of training, whereas well-perfused nutrient-rich muscle recovers and hypertrophies much more quickly.
For the adult climber, then, the road to stronger tendons is slow—but it can be steady with a dedicated schedule of appropriate training and adequate rest. Recovery from an intense workout or climbing day requires 48 to 72 hour (or more) for return to homeostasis. While submaximal climbing and training is possible during this recovery period, frequent back-to-back days of high load and/or high volume training will result in a homeostasis perturbation that may lead to mild reactive tendinopathy (finger, arm or shoulder tendon pain) and, perhaps eventually, an acute tear (e.g. A2 pulley) or tendinosis.
Interestingly, tendon and ECM stiffness change more quickly with significant increase (or decrease) in stiffness in a matter of weeks of training (or inactivity). As described earlier, sinew and ECM are comprised of densely packed collagen fibrils aligned in parallel along the axis of mechanical strain. Stiffness is added to this system via crosslinks which connect collagen molecules and fibrils much like cross-bracing of a wooden truss. Through appropriate training, cross-linking can be increased heading into the competitive or performance season—like tightening the suspension of a sports car, the additional stiffness increases force transfer and performance.
More stiffness (greater elastic modulus) is not always better, however, as injury risk increases when tendon is trained to be stiffer than the muscle is strong. Consequently, elite level performance—and injury avoidance—demands a highly nuanced training cycle that includes distinct and separate training interventions for increasing both strength and stiffness. Moreover, a climber with a mildly painful tendon or more severe chronic tendinosis is best served by training/rehabilitation that reduces stiffness of the musculotendon system, particularly on the muscle end of the tendon (thus, increasing the stiffness gradient across the length of the tendon).
Finally, it’s vital to recognize that there are many confounding factors that affect tendon, ligament, and ECM adaptations and health. As you read the following list, keep in mind that smart training and nutrition can tip the scales in your favor, regardless of any limitations or predispositions.
Age – Collagen synthesis decreases from middle age onward. About the time your skin begins to wrinkle (30s), you can be sure that collagen turnover throughout your body is beginning to wane slowly. Furthermore, non-enzymatic crosslinks (“bad” crosslinks that diminish muscle quality and function) increase with age, especially among those with poor diet and exercise habits or suffering from diabetes and other metabolic diseases.
Sex – High (and changing) estrogen levels among female athletes have benefits and risks. On the plus side, estrogen supports a higher average collagen synthesis rate in women than men. Unfortunately, the brief estrogen spike around day 12 of the menstrual cycle results in a brief, but significant decrease in collagen cross-linking, thus increasing risk of sinew injury. It’s well documented that female soccer players are up to four times more likely to suffer an ACL tear compared to their male counterparts.
Medication – There’s an increased occurrence of tendon rupture among individuals on fluoroquinolone antibiotics, corticosteroid therapy (such as prednisone), and cortisone injections. Also noteworthy is growing evidence that NSAID use (Ibuprofen and such) inhibits some aspects of tendon healing, although the topic has not yet been fully elucidated.
Smoking – Smoking has been shown to decrease synthesis of Type-I and Type-III collagen by 18% and 22%, respectively. Remember, Type-I collagen comprises 80% of the dry weight of tendon!
Nutrition – Consuming the right nutrients at the right time can accelerate collagen synthesis and tissue recovery, reduce joint pain, and increase ECM structure and muscle strength. (In just a moment, you’ll learn more about the advantages of Supercharged Collagen™.)
Genetics – At least a half-dozen genetic variants have been discovered that correlate to soft tissue injury occurrence. Individuals prone to recurrent injury likely possess one or more of these gene polymorphisms. Fortunately, you can exert an influence over your genetic predisposition via training and nutrition interventions (i.e. epigenetics).
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