Injury to the core region of energy-storing tendons is a frequent occurrence in both human and equine athletes, the incidence of which increases with age. Such energy-storing tendons include the human Achilles tendon (AT) and the equine superficial digital flexor tendon (SDFT). By definition, energy-storing tendons experience high strains during high-speed athletic activity. In contrast, anatomically opposing tendons (“positional” tendons), such as the common digital extensor tendon (CDET) in the horse and extensor digitorum longus tendon in man act only to transmit muscular force and rarely suffer exercise–induced injury. Functional adaptation of muscle and bone in response to exercise is well – documented, but there has been no convincing evidence to suggest that the energy-storing tendons in adults have the ability to adapt to exercise. We hypothesised that adaptive increases in tenocyte cellularity would occur in the energy-storing and positional tendons of young horses subjected to three specific exercise regimens. Samples were taken from midmeta-carpal regions of the SDFT (periphery and core) and CDET of young Thoroughbred horses from the following groups. Group 1: 6 horses exercised on a high-speed treadmill for 18 months from 21.3 months of age (SD 1.1) with 6 age-matched controls that underwent walking exercise only (long-term); Group 2: 6 horses exercised on a high-speed treadmill for 18 weeks from 19.4 months of age (SD 0.6) with 6 age-matched controls that underwent walking exercise only (short-term) and Group 3: 6 horses trained on pasture in New Zealand for 18 months beginning at 7–10 days of age, with 6 age-matched controls kept at pasture with no additional enforced exercise (Global Equine Research Alliance). Tenocyte nuclei were counted and measured in digital images from histological sections stained with haematoxylin and eosin, by computerised image analysis. Tenocyte densities (per mm2) for exercised and control groups for each study were evaluated using paired t-tests. Tenocyte density was significantly higher in the CDET of exercised horses in Group 3 (mean ± SD =260.4 ± 23.4) compared with the non – exercised controls (mean ± SD =226.9 ± 23.8) (p < 0.01). There was no such difference in the SDFT (core or periphery). There was also no significant exercise-related difference in tenocyte density in either the SDFT (core or periphery) or CDET for Groups 1 or 2. No previous data is available on the effect of exercise on tenocyte populations in equine tendons. The lack of other adaptive changes in previous studies of mature equine tendons had raised the question as to whether immature tendons would be more able to adapt to mechanical stimuli. In this study we were able to show that beginning training of horses shortly after birth (Group 3) stimulated an adaptive response by tenocytes in the positional CDET but not the SDFT. The inability of energy-storing tendons to show functional adaptation to exercise in immature or mature animals may explain the high incidence of strain-induced injury. Understanding the pathway by which exercise-related increases in tenocyte densities occur in immature positional but not energy-storing tendons may increase our understanding of the pathogenesis of strain-induced tendon injury.