Despite the complex loading mechanics of the triceps surae MTU, not all loading is detrimental to tendon health. While extrinsic factors contributing to tendon damage appear to be primarily attributable to submaximal cyclic loading, such as those induced by running and other training-related factors [88], targeted tendon loading of adequate magnitude can induce positive changes in tendon morphological, material, and mechanical properties [29,32]. Specifically, mechanotransduction details the body’s ability to translate mechanical loading into structural tissue change via cellular responses [89].

Mechanosensitive cells are responsive to tension, compression, and shear [90]. Loading magnitude [29,32], and perhaps more precisely strain [42,43,44], appears to modulate mechanotransduction in the healthy Achilles tendon. Specifically, strain magnitude, frequency, rate, and duration influence tenocyte biochemical processes [91,92,93] and gene expression [94,95]. For adequately long intervention durations (generally 12 weeks [36]) loads of greater than 70% of maximum voluntary contraction (MVC) [29,32] or strains of 4.5–6.5% [42,43,44] may deliver the appropriate loading-induced tendon stimulus to initiate mechanotransduction pathways; however, the relationship of tendon force and resulting strain can vary substantially between individuals [96,97]. Additionally, strain calculated as the displacement of the gastrocnemius medialis myotendinous junction from its resting length may differ from strain calculated as the change in length of the free tendon, which is more compliant [98,99], and perhaps where the majority of strain occurs. Theoretically, only looking at strain across the free tendon could change the ‘optimal’ adaptation threshold of 4.5–6.5% strain [42,43,44] typically arising from loading programs of greater than 70% of MVC [29,32].

Although the metabolic activity of tendon is low and the structure is typically static, loading-induced stimuli may trigger mechanotransduction and anabolic signaling pathways in the tendon [3]. In particular, the upregulation of insulin-like growth factor (IGF-I), among other growth factors, influences cellular proliferation and matrix remodeling [89,100,101]. Positive matrix remodeling appears to be largely attributable to a net synthesis of type I collagen, thereby making the tendon more load-resistant, though components of the ECM—proteoglycans, glycosaminoglycans, and cross-links—are also influenced by mechanical loading and contribute to macroscopic tendon behaviour through their actions on collagen fibrils [49,100]. Mechanically, longitudinal stiffness (resistance to deformation) increases [29,32,102], and strain for a given tendon force decreases [43,103] in response to increased loading in vivo. Material properties increasing in response to increased loading in vivo include modulus [29,32,102]. Morphologically, tendon CSA increases in response to increased loading in vivo [29,32,102], though limited evidence suggests that transient fluid redistribution may mask this in the short-term [51,104]. Additionally, loading-induced changes may differ along the Achilles tendon as the regional variation in load management [98,105,106] may preferentially activate mechanotransductive pathways leading to region-specific tendon hypertrophy [43,44]. Though still an area of exploration, the opposite could also be the case in that the non-uniform stress distribution within the Achilles tendon could contribute to the location of abnormalities associated with AT [107]. Moreover, while the tendon changes/adaptations described above are primarily related to resistance training, it appears that other types of mechanical loading, such as cyclic loading (e.g., running), can also induce adaptation in the healthy Achilles tendon [108,109]; however, conflicting evidence suggests that some other types of mechanical loading, such as plyometric exercises, may or may not adapt the Achilles tendon in a similar fashion [110,111,112,113,114,115].

The pathogenesis of tendinopathy appears multifaceted, which has given rise to various pathophysiological theories [36]. Current rhetoric suggests that initial cyclic overloading of the tendon leads to degeneration and disorganization of healthy collagen, which triggers an acute inflammatory response [36,87,101]. If the cyclic overloading is continued without intervention, the tendon pathology worsens through a positive feedback loop of injury to both the original and poor-quality repair tissue, inflammation, and failed repair. Macroscopically, evidence suggests that AT increases tendon CSA [116,117,118] and longitudinal strain [116,117,118], and decreases modulus [116,119], transverse strain [120], longitudinal stiffness [116,118,119], and transverse stiffness [121] in vivo. Taken together, these changes lead to functional deficits across the strength spectrum potentially increasing risk of AT recurrence [122,123,124].

Therapeutic exercise remains one of if not the most effective non-surgical approach for managing AT [1,2]. The suggested mechanism of action is generally considered to be restoration of tendon material, mechanical, and morphological properties similarly to healthy tendon remodeling [36,37,41], thereby improving functional strength [33]. Macroscopically, evidence suggests that targeted mechanical loading decreases tendon thickness [125] and volume [126]; however, there is a paucity of evidence underpinning the restoration of tendinopathic tissue capacity, with most studies focusing on functional and acute analgesic effects [36]. Evidence suggests that abnormal structure (i.e., hypoechoic areas and irregular structure) may normalize in some individuals following a 12-week eccentric exercise protocol [125,127], though the time needed for such changes to occur may vary [38]. Additionally, Cook and colleagues [128] posit that exercise-based adaptation may build capacity in the area of aligned fibrillar structure instead of acting on the area of abnormal structure. Nonetheless, evidence suggests that structural changes do not entirely explain clinical outcomes [129,130]. Building on this idea, O’Neill, Watson, and Barry [37] highlight that tendon structure is not observed to significantly change over the typical intervention period. The authors further suggest that changes in neuromuscular output may explain clinical benefit, and that training should focus on increasing stiffness of the triceps surae MTU, increasing strength, and shifting the length-tension curve of the triceps surae muscles through sarcomerogenesis. Although still an area of exploration, it appears that therapeutic exercise for AT should focus on improving the mechanical and material properties of the entire MTU thereby simultaneously building strength capacity and neuromuscular control [131].