Before the first interventional studies to define exercise regimes for improving bone characteristics were performed in the 1990s, an important step was the finding of differences in bone density between different athletic populations14. This built on prior animal studies and helped to show that exercise may well result in anabolic adaptation of bone. In this vein, the current study builds on prior work in animal, cell and tissue explant models7 and provides the first ever cross-sectional evidence in humans that exercise may well favourably impact the IVD.

Our main finding was that long-distance runners and joggers showed better hydration and glycosaminoglycan levels (higher lumbar IVD T2-times13) than the non-athletic individuals. This is consistent with findings of an anabolic response in the IVD in quadrupedal animals10,11 to running. The finding is also consistent with the notion, developed on the basis of cell, tissue explant and animal models7,15, of a “likely anabolic window” for IVD loading. The effect of running in humans on IVD composition was most obvious in the IVD nucleus where intra-discal pressure increases with applied axial load are constrained by the ring-formed annular fibres16.

Beyond the compositional differences, there was evidence of IVD hypertrophy in the long-distance runners. The height of the IVD relative to that of the vertebral body, which serves as an internal control for body size, was greater in the long-distance runners. This extends on findings17 from monozygotic twins that IVDs were marginally, but not significantly, larger in those twins that were at least 8 kg heavier than their twin pair and presumably experienced greater habitual spinal loading. Hypertrophy of the IVD may well be an adaptation to habitual loading in runners. Similar to hypertrophic responses seen in muscle due to resistance training18, this suggests that tissue adaptation will occur in the IVD with exercise. Overall our findings provide support for the hypothesis that an adaptive, anabolic and hypertrophic response is possible in the human IVD with exercise.

The current study also provides some guidance on what kinds of loading protocols may be better for the IVD. To understand what kinds of physical activity in humans might be the drivers of an anabolic response in the IVD, we examined the physical activity patterns of our collective via objective accelerometry. Total physical activity levels were not related to positive adaptations in the IVD, rather accelerations in a specific range. The strongest association to higher IVD T2-times were seen between 0.44 and 0.59 g mean amplitude deviation. This fits with the idea from animal, tissue and cell models7 of a “likely anabolic window” for the IVD. To better understand what kinds of activities generate these acceleration magnitudes, we collected additional accelerometry data under different conditions. Walking or slow running at 2 m/s fell inside this range with slower walking falling below this range. Fast running and high-impact jumping activities were above this range. This is in line with the notion that high-impact loading is considered7,19 to be detrimental to the IVD and vertebral end-plate. Dynamic IVD loading of 0.2–0.8 MPa, generating intra-discal pressures of approximately 0.3–1.2 MPa, is thought7 to be an optimal loading magnitude for the IVD. Based upon data on in vivo intradiscal pressures8, activities such as walking and running, but not lifting a 20 kg load or lying down, fall into this loading magnitude window. This corresponds well to our observations here of the impact of exercise in athletes. We also noted that sedentary activities were unrelated to IVD characteristics. In light of prior work, the results of our study suggest that, in comparison to other locomotor activity, fast walking or slow running may provide the strongest anabolic stimulus for adaptation in the IVD in humans.

Whilst the long-distance running group showed consistently better IVD properties than the jogging group, there were no statistically significant differences between the two. Also, there was no relationship between the IVD characteristics and physical activity in the 0.7 to 0.9 g MAD range where the physical activity associated with running was most evident (Supplementary Figure 1). This indicates a ceiling effect of exercise for the IVD was approached for both volume of upright axial spine loading and intensity. A ceiling effect in relation to exercise has been observed for muscle hypertrophy20 and bone adaptation to exercise21. It is possible that high volume or intensity running is not required for a beneficial adaptation in the IVD.

In the wider population, it is the lower lumbar IVDs that are most commonly affected by degeneration22. Furthermore, repetitive loading of the spine is considered23 to be a contributory factor to the development of IVD degeneration. Despite repetitive loading of the spine during running, the exercise groups of the current study did not show any detrimental effects at these lower lumbar segments. In contrast, the long-distance runners and joggers showed evidence of better IVD hydration and glycosaminoglycan content in the lower lumbar spine than those that did not perform sport. Furthermore, the evidence for IVD hypertrophy subsequent to habitual running was strongest at the lower lumbar levels. Our data show that repetitive axial loading of the spine under body weight during running in otherwise healthy people may well be beneficial for the lower lumbar IVDs.

It is important to consider some of the limitations of the current study. We performed a cross-sectional study as a first step to examine whether certain types of exercise might be beneficial for the IVD in humans. In this design it is not possible to completely rule out other confounding factors. We showed, for example, that lumbar muscle size was similar in all groups and this indicates that muscle adaptation per se is not the likely cause of differences in IVD characteristics in our populations. However, we cannot rule out other factors such as differences in muscle function, differences in nutrition, systemic hormonal (e.g. growth factors, cytokines, stress hormones) differences, or other indirect effects. To definitively determine that the mechanical loading from specific exercise forms result in positive adaptations in the IVD, to determine mechanisms of action, and delineate exercise guidelines for strengthening the IVD, randomised controlled exercise trials are necessary.

That an optimal loading level and pattern for the IVD exists makes sense from a tissue homeostatis perspective. Given that tissues such as bone21 and muscle18 have optimal loading conditions for an anabolic response, for the IVD we should expect it to be no different. Our findings support the perspective that, when loaded appropriately, anabolic IVD adaptation can occur in humans and that this can occur on time frame for it to be meaningful within the human lifespan.

Evidence that the IVD will respond anabolically in humans to certain types of loading may have public health implications. Spinal pain consistently presents one of the greatest costs to developed societies for disability and lost productivity, including when increased death rates in other diseases are accounted for24. IVD degeneration and herniation is one important contributing factor to spinal pain. Similar to understanding the impact of specific exercise in other disease constellations, for example in type II diabetes25, knowing that the IVD can respond to certain kinds of loading, and understanding what kinds of loading are optimal, will result in better exercise guidelines for the prevention and management of spinal pain.