Your tendons are weak. Your genes may explain why.

COL5A1 encodes collagen type V, a critical component of tendon and ligament structure. This collagen type regulates the diameter and organization of collagen fibers in connective tissue. When collagen type V is properly expressed, it creates the right fiber diameter and cross-linking patterns that give tendons tensile strength and elasticity.

The rs12722 T allele variant, present in roughly 30-35% of the population, is associated with higher susceptibility to tendon and ligament injury, particularly in runners and people doing repetitive overhead movements. Carriers of this variant have structurally weaker collagen fibers even at the microscopic level.

If you carry this variant, your tendons are less able to tolerate high loads. You recover more slowly from eccentric exercise (loading on the way down, like running downhill or lowering weight). You may experience tendon pain that seems disproportionate to your training volume. Switching to lower-impact training, progressively loading tendons over longer periods, and ensuring adequate protein and micronutrients becomes essential rather than optional.

COL1A1 encodes collagen type I, the dominant structural protein in tendons, accounting for roughly 85-90% of tendon dry weight. This gene controls how much collagen your body can synthesize in response to load and mechanical signal. Higher COL1A1 expression means faster tendon repair and greater capacity to adapt to training.

Variants affecting COL1A1 expression or stability reduce your tendon’s capacity to build new collagen in response to training stimulus. Even with heavy training stimulus, your body produces less collagen, meaning tendon adaptation happens more slowly and incompletely. This creates a situation where you’re training hard but your tendons aren’t strengthening at the rate they should.

You may find that periods of rest actually help more than continued training. You might notice that your tendons feel stronger after weeks of reduced activity, then weaken again quickly under normal load. Soreness and pain come without corresponding strength gains. Your tendons feel chronically underdeveloped for the sport or activity you’re doing.

The VDR gene encodes the vitamin D receptor, a protein that sits on muscle cells, bone cells, and immune cells. Vitamin D must bind to VDR to activate muscle protein synthesis, regulate calcium handling, and coordinate the muscle-tendon unit during movement and recovery.

VDR variants (particularly the FokI and BsmI polymorphisms) are carried by roughly 30-50% of the population in various combinations. Carriers of certain VDR variants require higher circulating vitamin D levels to achieve the same biological effect, meaning standard vitamin D levels that look normal on a blood test may still be functionally insufficient for your tendon repair and muscle-tendon coordination.

You may experience poor muscle-tendon synchronization during complex movements, leading to compensatory stress on tendons. Muscle soreness lingers longer than expected. Calcium handling may be impaired, affecting muscle contraction quality. Even when your vitamin D blood level is technically adequate, your cells cannot use it efficiently.

SOD2 encodes superoxide dismutase 2, the main antioxidant enzyme inside mitochondria. During exercise, your muscles produce oxidative stress as a byproduct of energy production. SOD2 neutralizes this stress, allowing your muscle cells to adapt and recover properly. Without adequate SOD2 function, oxidative damage accumulates, slowing protein synthesis and tendon healing.

The Val16Ala variant in SOD2, present in roughly 40% of the population as a homozygous variant, impairs the enzyme’s activity and expression. People with this variant experience higher muscle damage during and after exercise, slower oxidative stress clearance, and more pronounced delayed-onset muscle soreness (DOMS). This affects tendons because excess oxidative stress impairs collagen synthesis and increases inflammatory signaling.

Your muscles feel sore longer after training. You may experience DOMS that lasts 4-5 days when others recover in 2-3. Fatigue accumulates across your training week more quickly. Your tendons feel slower to strengthen despite the training stimulus, partly because the oxidative environment is hostile to healing.

IL6 encodes interleukin-6, a cytokine that signals inflammation. IL6 is necessary for initiating the repair response after training and injury. However, sustained elevated IL6 prevents the switch from inflammation to resolution, trapping tissue in an inflammatory state where repair cannot complete.

Variants in the IL6 gene are present in a significant portion of the population and affect how quickly IL6 signaling ramps up and down after exercise. Some genetic variants cause IL6 to remain elevated longer than optimal, extending the inflammatory phase of recovery. This is particularly problematic for tendons, which heal more slowly than muscle and require precise inflammatory timing.

Your tendon pain lingers beyond the acute phase. Soreness that should resolve in a few days persists for weeks. You may notice that anti-inflammatory approaches (NSAIDs, ice) provide only temporary relief because the underlying IL6 signaling isn’t normalizing. Training in a chronically elevated inflammatory state impairs collagen synthesis and increases secondary damage.

TNF encodes tumor necrosis factor alpha, a key inflammatory cytokine. TNF is essential for initiating immune response and triggering adaptation after exercise. However, when TNF remains elevated, it drives muscle protein breakdown, impairs tendon cell function, and shifts the tissue environment toward catabolism rather than repair.

TNF gene variants affect the baseline level of TNF expression and how quickly TNF signaling resolves after exercise stress. Carriers of certain TNF variants have chronically elevated TNF, even at rest, which creates a baseline inflammatory state that tendon healing must fight against. This is cumulative: each training session adds inflammatory stress on top of an already-inflamed baseline.

Your baseline energy level is lower than you’d expect. Tendon pain feels chronic rather than acute, even with adequate rest. Muscle recovery is slower across the board. Your tendons feel perpetually sore or tender, as if they never fully exit the inflammatory phase. This constant low-grade inflammation impairs the precise molecular events needed for quality tendon repair.