Article from 'The Lancet'. A peer reviewed medical journal
Kindly sent in by Trevor Baylis
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.
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.
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
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
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
1 Stress distribution inside intervertebral discs: the effects
of age and degeneration. -Adams MA et al. Bone Jt Surg 1996; 78:
2 Reported pain during lumbar discography as a function of annular
ruptures and disc degeneration. Moneta GB et al. Spine 1994; 19:
3 The diagnostic accuracy of MRI, work perception, and psychosocial
factors in identifying symptomatic disc herniations. Boos et al.
Spine 1995: 20: 2613-25.
4 The long term effects of physical loading and exercise lifestyles
on back-related symptoms, disability, and spinal pathology among
men. Videman T et al. Spine 1995; 20: 699-709.
5 An epidemiological study of lifting and twisting on the job and
risk for acute prolapsed lumbar intervertebral disc. Kelsey JL et
al. J Orthop Res 1984;2:61-66.
6 Gradual disc prolapse. Adams MA et al. Spine 1985; 10:524-31.
7 Prolapsed intervertebral disc. A hyper flexion injury. Adams
et al Spine 1982;7:184-91.
8 Internal disruption of an intervertebral disc can be caused by
previous damage to an adjacent vertebral body. Adams MA et al. Presented
to the International Society for the Study of the Lumbar Spine.
Helsinki, Finland, June 1995.
9 Annulus tears and intervertebral disc degeneration: an experimental
study using an animal model. Osti OL et al. Spine 1990; 15: 762
10 Effects of hydro static pressure on matrix synthesis in different
region of the intervertebral disc. Ishihara H et al. J Appl Physiol
1996; 80: 839-46.
11 Determinants of lumbar disc degeneration. A study relating lifetime
exposures and MRI findings in identical twins. Battie MC et al.
Spine 1995; 20: 2601-12.
12 Tensile properties of the annulus fibrosus. Part 2 ultimate
tensile strength and fatigue in life. Green TP et al. Euro Spine
13 Mechanically adaptive bone remodeling. Lanyon LE et al. J Biomech
14 Structural properties of the anterior longitudinal ligament.
Correlation with lumbar bone mineral content. Neumann P et al. Spine
15 Physical activity and the strength of the lumbar spine. Porter
RW et al. Spine 1989;14:201-03.
16 Bending and compressive stresses acting on the lumbar spine
during lifting activities. Dolan P et al. J Biomech 1994;27:1237-48.
17 The loads on the lumbar spine during extreme weight lifting.
Granhed H et al. Spine 1987;12:146-49.
18 Humeral hypertrophy in response to exercise. Jones HH. J Bone
19 Factors involved in the nutrition of the human lumbar intervertebral
disc: cellularity and diffusion of glucose in vitro. Maroudas A
et al. J anat 1975;120:113-30.
20 Proteoglycan synthesis in the human intervertebral disc. Variation
with age, region and pathology. Bayliss MT. Spine 1988;13:972-81.
21 Compression fractures of the vertebra during major epileptic
seizures. Vascancelos D. Epilepsia 1973;14:323-28.
22 Posture and the compressive strength of the lumbar spine. Adams
MA et al. Clin Biomech 1994;9:5-14.
23 A longitudinal study of low back pain in student nurses. Klaber
Moffett JA et al. Int Nurs Stud 1993;30:197-212.