Article from 'The Lancet'. A peer reviewed medical journal
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Could sudden increases in physical activity cause degeneration of intervertebral discs?

Michael A Adams PhD, Patricia Dolan PhD. Lancet 1997; 350: 734-735.

Epidemiological studies link high repetitive loading of the lower back with degeneration of intervertebral discs, and experiments on cadaver spines confirm that repetitive mechanical loading can disrupt the lumbar discs in a manner characteristic of "degeneration". But why do living discs not just strengthen in response to this stimulus, as other musculo-skeletal tissues do? Our hypothesis proposes that the low metabolic rate of lumbar discs (the largest avascular structures in the body) prevents them from keeping pace with adaptive remodeling changes in adjacent tissues, so that the large and abrupt increases in a person's level of physical activity may leave the lumbar discs the weak link in a strengthening and heavily loaded spine. Recent laboratory investigations support the hypothesis, but clinical evidence is required to relate recent disc degeneration with recent increases in physical activity, and so to test the hypothesis.

Introduction

Disc degeneration involves structural disruption of the annulus fibrosus and cell-mediated changes throughout the disc and subchondral bone (1). Disruption of the annulus is associated with back pain (2,3) although some other degenerative changes in discs, such as a dehydrated nucleus pulposus, are of little clinical relevance (3,4) and may simply be signs of ageing. From a review of the evidence linking structural disc degeneration with mechanical loading, we develop an hypothesis that degeneration can occur when the rate of accumulating fatigue damage outpaces the adaptive remodeling response of discs.

Mechanical loading and disc degeneration

The least equivocal sign of disc degeneration is a prolapsed disc confirmed at surgery, and the most common risk factor for this is repetitive and high mechanical loading (5). Experiments on cadaver spines have shown how excessive loading applied to apparently normal discs can create radial fissures in the postero-lateral annulus (6), posterior herniation of nucleus pulposus (7), and internal disruption of the annulus (8). There are complex changes in cell biology and tissue composition in degenerated discs, but animal experiments show that these can follow mechanical interventions (9), and they can be explained in terms of disc-cell responses to an altered mechanical environment (10). Biological changes may be consequences rather than causes of structural failure. Genetic predisposition to disc degeneration (11) does not argue against mechanical causes because inheritance may involve small discs and a heavy body.

Fatigue failure

Few patients with disc degeneration recall injuring their backs. However, the high risk associated with repetitive loading (5), suggests that fatigue failure may be more important than trauma. In engineering materials, repetitive loading can cause microdamage to accumulate and lead to gross failure. Fatigue damage accumulates when the cyclic force exceeds a threshold value, which for the annulus fibrosus is approximately 45% of the force required to cause sudden failure (12).The more cycles are applied, the lower the force required for failure.

Adaptive remodeling

In skeletal tissues, the accumulation of microdamage is countered by cells repairing and strengthening the tissue matrix. Cells also respond to increased (deformation) by increasing the stiffness of the matrix; a stiffer matrix deforms less, so deformation returns to normal levels (13). Heavily-loaded vertebrae may develop marginal osteophytes (4), apparently in an attempt to increase their cross-sectional area and reduce stress. These self regulating processes are manifestations of Wolf's Law, which is usually applied to bone but may also be applicable to ligaments (14) and intervertebral discs (15).

Fatigue failure versus adaptive remodeling

All skeletal tissues adapt to increased mechanical demands, but they may not always adapt quickly enough. People who suddenly change to a physically-demanding occupation may subject their skeletons to increased repetitive loading, and cause fatigue damage to accumulate rapidly. In the spine, the problem would be exacerbated by exercise-induced strengthening of the back muscles, because most spinal compressive loading comes from back-muscle tension (16). However, the ability of spinal tissues to strengthen in response to increased muscle forces may be restricted by health and age, so that fatigue damage would accumulate most rapidly in sedentary middle-aged people who suddenly became active. Conversely, a carefully regulated build-up of physical activity over many years would lead to a strong spine, as evidenced by the dense vertebrae in elite weightlifters (17) and strong intervertebral discs in the most physically active people (15). The outcome of the "race" between fatigue failure and adaptive remodeling will depend upon the intensity of mechanical loading, the suddenness of its increase, and the age and health of the individual.

Intervertebral discs are vulnerable to fatigue failure

The outcome of the "race" may not be the same in different tissues. Muscles strengthen rapidly --- novice weight-trainers commonly double their poundage for repetitive lifts in 12 months. It is not known how quickly whole bones can strengthen, but professional tennis players have 30% more bone mineral in their racquet arm(18). Lumbar discs are unlikely to keep pace with muscle and bone because metabolite transport within the disc is barely adequate, even for the small population of cells(19) and proteoglycan synthesis is slow (20). Discs adapting more slowly than bones could explain why former elite weightlifters have more bulging discs than former elite runners, but no more end plate defects (4). A small-scale study on cadavers has shown that vertebrae from physically active people appear to strengthen more than the adjacent discs (15). Large and rapid increases in repetitive physical activity may therefore lead to muscle hypertrophy, stronger vertebrae, and fatigue failure in the discs.

Did natural selection get it wrong?

Natural selection may have tolerated the low metabolic rate of lumbar discs because their failure usually occurs after child-bearing age. Natural selection, however works in gene pools, and there may be some advantage in preserving older members of an evolving community. Evolution may not have been able to match the pace of cultural changes in spinal loading patterns such as the overnight change of occupation and of fads in recreational activity. Our evolving spines may never have encountered changes in loading comparable to a lorry driver starting work as a labourer, or a middle-aged mother taking up aerobics.

Do we load our backs excessively?

Sudden increases in repetitive loading would lead to disc failure only if the loading exeeded the fatigue threshold, but this can happen quite easily. Muscle contractions during epileptic fits can crush vertebrae(21), so any event which provokes maximum muscular effort would threaten the tissue-tolerance levels in a single loading cycle, and would certainly exceed the fatigue threshold. Lifting 10 kg weights from the ground without proper care can generate compressive forces on the lumbar spine which exceed the fatigue threshold of the vertebrae (16). The distribution of forces also influences the likelihood of fatigue failure. Culturally-determined habits such as prolonged upright standing concentrate compressive stress on the posterior annuls (22), and may explain why this region often shows the most advanced degenerative changes.

Can we reduce the risks of fatigue failure?

Risks could be reduced by exercising to maintain adequate skeletal strength, by introducing new physical activities slowly, and by modifying tasks which demand high spinal loading. However, it would be counter productive to simply minimise spinal loading, because that might lead to weak backs, vulnerable to injury during slips or falls.

Testing the hypothesis

This could be done by studying back complaints among newcomers to arduous occupations in order to relate increases in spinal loading to clinical signs of disc degeneration. Those studied should have no recent history of back or leg pain, and no recent occupation or pastime as physically demanding as their new occupation. The outcome (painful disc degeneration) should be validated by characteristic findings on magnetic resonance imaging (MRI) (3) or discography (2). MRI scans at the base line would be able to exclude previous disc degeneration, but this may not be important because many common MRI (3) abnormalities are poorly related to pain (3). One longitudinal study of student nurses has shown that back pain is most common after 9-12 months of active training on the wards (23). The cause may possibly have been cumulative fatigue damage to their discs, although no evidence in support of this was reported. The hypothesis could also be tested by primary-care physicians attempting retrospectively to explain MRI or discographic manifestations of disc degeneration in terms of patients' recent occupational and recreational histories. Links between disc degeneration and disc pain are not straightforward --- moderately degenerated discs may be more painful than severely degenerated discs because the reduced height of the latter may cause them to be shielded by the apophyseal joints (1).

The work of the authors is funded by the Arthritis and Rheumatism Council.

Science references

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22 Posture and the compressive strength of the lumbar spine. Adams MA et al. Clin Biomech 1994;9:5-14.

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