A Comparison of Fatigue Failure Responses of Old

Versus Middle-Aged Lumbar Motion Segments in

Simulated Flexed Lifting

Sean Gallagher, PhD, CPE,*

From the *NIOSH Pittsburgh Research Laboratory, Pittsburgh, PA;

William S. Marras, PhD, CPE,† Alan S. Litsky, MD, ScD,†

John Landoll, PhD,† and Velimir Matkovic, MD, PhD†

†Ohio State University, Columbus, OH;

Deborah Burr, PhD,‡

and ‡University of Florida,

Gainesville, FL.

Study Design. Survival analysis techniques were used

to compare the fatigue failure responses of elderly motion segments to a middle-aged sample.

Objectives. To compare fatigue life of a middle-aged

sample of lumbosacral motion segments to a previously

tested elderly cohort. An additional objective was to evaluate the influence of bone mineral content on cycles to

failure.

Summary of Background Data. A previous investigation evaluated fatigue failure responses of 36 elderly lumbosacral motion segments (average age, 81 ± 8 years)

subjected to spinal loads estimated when lifting a 9-kg

load in 3 torso flexion angles (0°, 22.5°, and 45°). Results

demonstrated rapid fatigue failure with increased torso

flexion; however, a key limitation of this study was the old

age of the specimens.

Methods. Each lumbosacral spine was dissected into 3

motion segments (L1–L2, L3–L4, and L5–S1). Motion segments within each spine were randomly assigned to a

spinal loading condition corresponding to lifting 9 kg in 3

torso flexion angles (0°, 22.5°, or 45°). Motion segments

were statically loaded and allowed to creep for 15 minutes, then cyclically loaded at 0.33 Hz. Fatigue life was

taken as the number of cycles to failure (10 mm displacement after creep loading).

Results. Compared with the older sample of spines,

the middle-aged sample exhibited increased fatigue life

(cycles to failure) in all the torso flexion conditions. Increased fatigue life of the middle-aged specimens was

associated with the increased bone mineral content

(BMC) in younger motion segments (mean ± SD, 30.7 ±

11.1 g per motion segment vs. 27.8 ± 9.4 g). Increasing

bone mineral content had a protective influence with each

additional gram increasing survival times by approximately 12%.

Conclusion. Younger motion segments survive considerably longer when exposed to similar spine loading

conditions that simulate repetitive lifting in neutral and

flexed torso postures, primarily associated with the increased bone mineral content possessed by younger motion segments. Cycles to failure of young specimens at

22.5° flexion were similar to that of older specimens at

0° flexion, and survivorship of young specimens at 45°

flexion was similar to the older cohort at 22.5°.

Key words: biomechanics, low back disorders, fatigue

failure, age, motion segments, vertebral endplate fractures, torso flexion, lifting, bone mass.

Low back disorders (LBDs) are a major cause of both

short- and long-term occupational disability in the

United States,1 and it is clear that workers in certain

occupations are more susceptible to LBD.2–5 Specifically,

epidemiologic studies have shown that jobs involving

heavy physical demands such as construction,2,3 mining,2,4 and farming,5 engender increased risk of back

pain. These occupations are thought to experience high

LBD rates as a result of their extreme postural and manual lifting demands. Studies have shown that jobs involving significant lifting6 –9 and jobs that involve frequent

bending10–12 are associated with increased LBD risk.

Workers in the mining industry, in particular, often

have to lift heavy materials in restricted workspaces that

compel torso flexion. An understanding of the impact of

repeated loading of the spine in flexion on fatigue failure

of spinal tissues is thus a critical issue for our research

agency, which is concerned with reducing the pain and

disability associated with LBD in the mining industry.

It is well accepted that loads experienced by the spine

during manual lifting tasks are sufficient to cause fractures in the endplates of lumbar vertebrae, particularly

on repeated loading.13–15 Endplate fractures may not be

painful in and of themselves16

; however, evidence suggests that the process of internal disc disruption and disc

degeneration may be initiated via endplate fractures.16,17

It has been shown that endplate damage will alter the

distribution of stress in the disc, resulting in buckling of

the lamellas of the internal anulus.17 Once this process

has been initiated, repeated spine loading will cause additional disruption of the anular fibers, resulting in formation of significant fissures or tears.18–20 If these tears

occur near or extend close to the outer portions of the

anulus, a wound healing process is initiated, which involves infiltration of mast cells, macrophages, and release of cytokines and growth factors.21 The presence of

these infiltrates has been strongly linked to discogenic

low back pain.21,22 Indeed, for patients experiencing

chronic low back pain, the prevalence of internal disc

disruption is at least 39%,19 which represents the most
common cause of chronic low back pain that has been

demonstrated objectively.16

The ability to resist endplate fractures appears highly

related to the amount of mineralized tissue of which the

vertebra is comprised.23–26 Studies have found that the

relationship between the ultimate compressive strength

of a vertebral body and bone mineral content (BMC) is

essentially linear.23,24,27,28 There is a decrease in vertebral strength with age, particularly beyond the age of 40

years, which is linked with a reduction in bone mineral in

the vertebrae.28,29 Specifically, there appears to be a significant loss of horizontally oriented trabeculae, particularly in the central portion of the vertebral body.30,31

The departure of horizontal trabeculae deprives the vertically oriented trabecular “posts” of important reinforcement, and the load-bearing capability of the center

of the vertebral body becomes degraded as a result.32

The body appears unable to reconstruct the horizontal

trabeculae; instead, bone is deposited in a manner to

thicken or reinforce the vertically oriented members.16

The decreased strength of the cancellous core of the vertebral body as aging takes place is associated with a shift

in the load-bearing responsibilities from cancellous to

cortical bone.32 However, complex regional loadsharing responsibilities also appear to exist. Specifically,

Eswaran et al33 report that the cortical shell provides

45% of the support in the narrowest region of the vertebral body, but only 15% near the endplates.

The age-related changes detailed above undoubtedly

impact the vulnerability of the endplates to fatigue failure. Specifically, the weakened trabecular network underlying the endplates permits increased deformation of

the cartilaginous endplates and may increase the propensity to fracture.32 The finding of increased fracturing in

the endplates with increasing age appears to bear testimony to this development.34 The purpose of the present

investigation is to compare and contrast the fatigue failure responses of older motion segments to loads simulating a lift of 9 kg in 3 torso flexion postures(0°, 22.5°, and

45°),15 to those of a younger cohort, and further, to

evaluate the influence of BMC on fatigue life.

Materials and Methods

The biomaterials testing methods used for the younger cohort

in this comparative analysis follow exactly those described in

the article involving tests on the older spines,15 where additional detail may be obtained. The current manuscript summarizes these procedures and additionally provides data on collection and analysis of BMC and bone mineral density (BMD),

which were not detailed in the previous paper.

Three replications of a randomized block partially confounded factorial design were performed using a total of 18

lumbar spines (54 motion segments), none of which died of

causes relating to spine pathology. The first 2 replications (12

spines or 36 motion segments) consisted of an older cohort of

specimens (mean ± SD age, 80.7 ± 7.8 years).15 This older

sample was comprised of 8 male and 4 female spines. The third

replication (6 spines or 18 motion segments) was performed

using a younger group of specimens (mean ± SD age, 49.2 ±

17.3 years) and was comprised of 3 male and 3 female spines.

Each spine was frozen in plastic bags until needed and subsequently defrosted before dissection into 3 motion segments

(L1–L2, L3–L4, and L5–S1). Excess musculature, adipose tissue, and fascia were removed from the motion segments and

ligaments spanning multiple levels were sectioned. Ligaments

confined to a single motion segment were preserved.

Bone mineral density (BMD) and BMC for vertebral bodies

L1–L4 of each spine were measured by means of dual radiograph absorptiometry using a Lunar DPX machine (Lunar,

Madison, WI). Specimens were positioned on a bed of rice (to

simulate body tissue) with the anterior aspect of the spine facing up. The BMD of the specimen was expressed in grams

divided by the projected area of the bone. BMC was derived

from the BMD and area measurements. BMD, projected area

of the vertebral bone, and BMC for L1–L2 and L3–L4 segments

individually were provided in standard reports. Table 1 provides information regarding the age of each specimen along

with data on BMC and BMD for L1–L2 and L3–L4 motion

segments from each spine.

Table 1. Age, Bone Mineral Content, and Bone Mineral Density for L1–L2 and L3–L4 Motion Segments From Old and

Middle-Aged Lumbar Spines

Older Spines Middle-Aged Spines

L1–L2 L3–L4 L1–L2 L3–L4

Spine ID Age (yr) BMC (g) BMD (g/cm2

) BMC (g) BMD (g/cm2) Spine ID Age (yr) BMC (g) BMD (g/cm2) BMC (g) BMD (g/cm2)

M11

M8

M1

F9

M7

F6

F17

M10

F13

M16

M12

M14

85

74

77

85

65

82

93

80

91

79

84

73

28.6

33.7

28.9

18.3

11.5

23.2

11.9

34.6

17.2

26.2

31.2

25.0

1.030

1.121

0.897

0.686

0.635

0.995

0.652

0.890

0.751

0.946

0.870

0.894

38.6

40.0

33.3

28.2

14.0

29.9

15.9

45.6

24.4

32.8

41.7

31.3

1.263

1.095

0.958

0.917

0.647

1.071

0.745

1.068

0.902

1.044

1.030

0.958

F20

M23

M21

F22

M18

F19

55

60

61

42

60

17

13.9

39.6

25.0

33.5

29.4

20.5

0.615

1.152

0.793

1.368

0.991

0.932

18.8

53.7

29.5

40.0

39.0

25.8

0.679

1.264

0.793

1.317

1.140

0.999

Mean

SD

80.7

7.8

24.2

7.9

0.864

0.154

31.3

9.7

0.975

0.163

49.2

17.3

27.0

9.2

0.975

0.265

34.5

12.4

1.032

0.257
Anterior-posterior and left lateral radiographs of each motion segment were taken at 50 kV, 5 mA, and a film focus

distance of 38 in. These initial radiographs served to detect the

presence of existing defects in individual motion segments and

were used to determine the relative angles of all 4 endplates of

the motion segment. A dynamic EMG-assisted biomechanical

model35 was used to develop appropriate loads and load rates

associated with lifting a 9-kg load starting at 3 trunk flexion

angles: 0° (neutral), 22.5° (partial flexion), and 45° (full flexion). These spinal load estimates were obtained from an existing large database of lifting tasks. Resultant loads were 1300

N, 2400 N, and 3150 N for these torso flexion angles, respectively. Since the spine is composed of viscoelastic tissues, it was

considered vital that the rate of loading also be correctly modeled in each posture. Average model estimates of load rate for

the 3 postures were 700 N/s, 2100 N/s, and 4800 N/s, with

increasing load rates in more flexed postures. Motion segments

were flexed according to endplate angles obtained in a radiographic study of subjects performing torso flexion in vivo.

36

Motion segments were potted in trays containing polymethylmethacrylate, the flexion angle of each motion segment being

confirmed by endplate measurements obtained via multiple radiographs during the fixation process. This flexion angle was

maintained constantly throughout the cyclic loading regimen

for a given specimen. All tests were conducted in a humidified

environmental chamber at a temperature of 37 C. Motion segments were statically loaded for 15 minutes (at 500, 750, or

1050 N depending on torso flexion angle) and then cyclically

loaded at 0.33 Hz until failure or the maximum number of

cycles (10,020) was completed using a hydraulic materials testing machine (MTS Systems Corp., Eden Prairie, MN). Failure

was defined as a displacement of 10 mm after termination of

the period of creep deformation. The primary dependent measure was the number of cycles to failure.

Comparisons of the fatigue failure responses of specimens

were achieved via survival analysis techniques, specifically via

Kaplan-Meier Product Limit Estimation and Cox Regression

Analysis. Kaplan-Meier Product Limit Estimation, and mean

survival times were obtained separately on the younger specimens (18 motion segments) and older specimens (36 motion

segments). Plots of survivorship functions for each group were

obtained. Variables included in the Cox regression models included simulated torso flexion angle, lumbar level, BMC,

BMD, and weight of the motion segment. Both young and old

specimens were included in Cox models to better evaluate the

influence of a range of bone mineral values. Since this regression analysis incorporated bone mineral data, L5–S1 segments

(from which BMC data were not obtained) were omitted from

this analyses. Alpha levels for all tests of significance were set at

0.05.

Results

Kaplan-Meier Product-Limit estimation demonstrated

longer survival times and an increased number of censored observations (i.e., the number of motion segments

surviving the entire 10,020 cycles of the test) for the

younger cohort of specimens compared with the older

group. Figures 1A and B illustrate the survivorship functions s(t) at each angle of torso flexion for older and

younger spines, respectively.

Figure 1. A, Survivorship functions for old spines by torso flexion

angle (n = 36). B, Survivorship functions for young spines by torso

flexion angle (n = 18). For each motion segment tested at 0° flexion,

maximum load was 1300 N (load rate, 700 N/s), at 22.5° flexion maximum

load was 2400 N (load rate, 2100 N/s), and at 45° flexion maximum

load was 3150 N (load rate, 4800 N/s).

As can be seen from these

figures, increased loads and load rates associated with

greater torso flexion were associated with decreased survival of specimens in both groups. However, the survivorship functions for younger spines show a dramatically improved fatigue life forthe simulated lifting task at

all torso flexion levels. Table 2 details the difference between these groups in terms of censored observations

and mean survival time. In all cases, survival was significantly enhanced in the younger sample.

Table 2. Comparison of Censored Observations and Mean Survival Times for Old and Middle-Aged Spine Motion

Segments Using Spinal Loads Predicted When Lifting a 9-kg Load in Three Torso Flexion Postures

0° 22.5° 45°

% of Censored

Observations

Mean Cycles

to Failure

% of Censored

Observations

Mean Cycles

to Failure

% of Censored

Observations

Mean Cycles

to Failure

Older specimens (n = 36)

Middle-aged specimens (n = 18)

67

100

8267

10,020

25

67

3261

7124

0

33

263

3929
Table 3 provides the results of Cox regression models

examining the effects of flexion angle and BMC.

Table 3. Results of Cox Regression Models

Incorporating Effects of Simulated Torso Lifting Loads at

Different Angles of Flexion and Bone Mineral Content of

the Specimens

df Beta SE P Risk Ratio 95% CI for RR

Flexion 2 0.001

22.5° 1 2.756 0.862 0.001 15.741 2.905–85.309

45° 1 3.923 0.921 0.000 50.530 8.310–307.245

BMC 1 -0.127 0.036 0.001 0.881 0.820–0.946

No

other variables input to the model were significant predictors of time to failure. On the average, younger spines

were found to possess approximately 3 additional grams

of bone mineral per motion segment than older spines

(mean ± SD, 30.7 ± 11.1 g vs. 27.8 ± 9.4 g).

As can be seen in the Cox regression analysis presented in Table 3, both flexion angle and BMC were

significant predictors of the time to failure. Compared

with the referent posture (0° flexion), simulated lifting in

22.5° flexion had a 15.7-fold increase in relative risk,

while the 45° condition saw a 50.5-fold increase in relative risk compared with the referent condition. As can be

seen from the negative exponent, increasing BMC exerted a protective influence. According to the model, every gram of BMC resulted in a 12% increase in cycles to

failure for this sample (when controlling for the effects of

flexion).

Table 4 presents a comparison of failure mechanisms

observed in specimens failing via fatigue in the older

versus the younger age samples.

Table 4. Comparison of Fatigue Failure Mechanisms of Older Versus Middle-Aged Motion Segments by Flexion Angle

0° 22.5° 45°

Older Middle-Aged Older Middle-Aged Older Middle-Aged

No. of specimens tested 12 6 12 6 12 6

No. of specimens failing via fatigue 4 0 9 2 12 4

Specimens exhibiting endplate failure

Inferior EP (superior vertebra) 2 0 9 1 10 3

Superior EP (inferior vertebra) 0 0 6 0 6 2

Specimens exhibiting zygapophysial joint damage

Increased laxity 0 0 3 1 4 2

Disruption 2 0 3 0 2 0

Specimens exhibiting vertebral body fracture

Superior VB 2 0 5 1 6 4

Inferior VB 0 0 1 1 2 0

Specimens exhibiting disc failure 0 0 0 1 0 0

Of those specimens failing via fatigue, the proportion of younger specimens experiencing endplate failure appeared somewhat lower in

the more erect postures (0° and 22.5° flexion); however,

a similar proportion of endplate failures were observed

at 45° flexion in both groups. Frank disruption of the

zygapophysial joints was observed in 7 of the 25 older

motion segments failing via fatigue but was never observed in the younger specimens. Increased laxity of the

zygapophysial joints was observed in 3 of the younger

specimens failing via fatigue, however. The sole disc failure observed in fatigue failure specimens was observed in

one of the younger motion segments exposed to the 22.5°

torso loading condition. In general, older specimens

tended to exhibit more extensive damage (i.e., multiple

failure modes) as compared with younger specimens.

Discussion

Failure of spinal tissues may be considered a function of

load magnitude, loading frequency, and load tolerance

(or strength) of the tissue. The current investigation provides data to address all 3 of these potential factors in an

in vitro experiment and provides some insight to the

changes in fatigue tolerance that occur with aging. Results of this study indicated that younger (middle-aged)

spines were found to have considerably increased fatigue

life at all 3 flexion angles compared with an elderly cohort. However, within each age cohort, the increased

spinal load associated with lifting in deeper torso flexion

resulted in a remarkable reduction in cycles to failure.

None of the middle-aged specimens failed at the 0° torso

flexion simulated lift. It may be observed that, for most

materials, repetitive loading at less than 30% of the material’s ultimate strength will not typically result in fatigue failure.37 This is sometimes referred to as the “endurance limit” associated with cyclic loading. One might

infer that the 1300 N load at the 0° flexion condition was

below the endurance limit of all of the younger specimens tested. Furthermore, while none of the older sample survived the maximum of 10,020 cycles at the 45°

torso flexion simulated lift, one third of younger specimens were able to do so. Comparison of the survivorship

functions reveals that survival of young specimens at

22.5° flexion was quite similar to that of older specimens

at 0° flexion, and that the survivorship of young specimens at 45° was similar to that of the older cohort at

22.5° flexion. It would appear that the diminished BMC

in the older specimens was largely responsible for differences in survival between the 2 groups.

Unfortunately, the open-celled sponge-like structural

design of vertebral bone, while being able to deform
more without cracking (compared with long bones), is

not as adept at withstanding high loads.38 When spinal

loads are sufficiently large (as in lifting tasks), microfractures in the trabeculae will occur, invoking the process of

bone remodeling. In trabecular bone, remodeling results

in substantial bone loss (especially compared with cortical bone) due to higher number of remodeling sites per

unit volume, along with the fact that new bone formation lags behind the ability to resorb bone starting early

in midlife. This process will lead to a loss of trabecular

plates and connectivity, resulting in substantial strength

loss.39 More rapid remodeling is associated with decreased bone quality and increased risk of fracture, due

to the decreased density of newly remodeled bone tissue,

more unfilled sites where bone has been resorbed, along

with poorer cross-linking of collagen fibers.38,40 The decreased fatigue life exhibited by older motion segments is

an unfortunate consequence of the depletion of bone

mineral resulting from this slow but steady process.23,30

While the absolute difference in BMC was small between

young and old specimens (less than 3 g per motion segment, on average), the architectural and structural importance of even small changesin BMC was dramatically

apparent in this study.

It is interesting to note that this study found BMC to

be a better predictor of vertebral integrity than BMD, a

finding also observed elsewhere.41 One reason this may

be true is that BMC provides a combined measure of

both the size and density of vertebral bone, whereas

BMD obscures the influence of the specimen size, known

to be positively correlated with vertebral strength.38,40

BMC may thus be a superior measure to use when assessing or predicting vertebral strength. It should not

escape notice that BMC is easily obtained in vivo, and the

findings of this study could have potential clinical relevance in terms of assessing (at least in general terms) a

patient’s risk of damage to spinal tissues, especially if the

patient is engaged in physically demanding lifting tasks.

For example, a job requiring repetitive lifting in flexed

postures in a person with low BMC would clearly be a

recipe for rapid failure of spinal tissues.

It is incumbent on us to consider the relevance of the

current results with respect to potential low back pain

pathways. Indeed, results of this study may have relevance to different pain mechanisms, depending on the

physiologic age of the spine. One possible pathway to

pain is that fatigue failure will lead to endplate fractures

leading to disc degradation, as detailed in the introduction. If one considers a healthy young spine (with no disc

degeneration and with a normal “young” BMC value),

results of this study suggest relatively little risk would be

associated with lifting a 9-kg load repeatedly as long as

an upright posture could be adopted. However, risk of

endplate failure in such young spines would increase substantially when flexed lifting is performed, although a

relatively high number of cycles may be necessary when

lifting a moderate load. Lifting of heavier loads would

obviously accelerate this process, and it should be noted

that, with a sufficiently heavy load, one would not anticipate the upright posture to remain consistently protective. In young spines, trabecular damage (particularly in

the vertebral centrum42) may lead to decreased endplate

support leading to cracks of the endplate, mortared via

scar tissue, and initiating a degenerative cascade in the

disc. It should be noted that the majority of studies examining the association between heavy physical loading

and disc degeneration have found an association,43–55

although it should be noted that this association has not

been universally observed.56–58

The role of inherited traits on disc degeneration has

received increased attention in recent studies44,59 and

merits some discussion with respect to the current research findings. Investigators in these studies examined

monozygotic (MZ) twins discordant for physical loading, and evaluated measures of disc degeneration via

magnetic resonance imaging. Although physical load

was found to have a significant effect on disc degeneration in these investigations, it was asserted that factors

related to inheritance accounted for a more sizeable portion of the variability in disc degeneration. In the context

of the present experiment, one inherited trait that may

help explain this result is that of BMC. It would seem

intuitive that MZ twins, sharing an identical DNA blueprint, would also share a high correspondence in BMC

(i.e., would have comparable vertebral size and bone

density). Indeed, studies over the last 30 years in healthy

twins consistently demonstrate a large genetic contribution to bone mass.60 – 65 Heritability estimates of BMD in

the lumbarspine have been reported at 89%, and lumbar

anthropometric dimension heritability estimates range

from 61% to 83%.65 Thus, it would seem quite plausible

that a high proportion of the variability in disc degeneration attributed to inheritance in these studies may, indeed, be due to differences in vertebral strength between

twin pairs. It would be a reasonable supposition, for

example, that twins with higher BMC would possess

endplates that would be less prone to fracture (due to

enhanced structural support) and less likely to lead to

disc degeneration as a result. Conversely, twins possessing low BMC would be expected to experience more

rapid endplate failure and disc degeneration. As demonstrated in the currentstudy,small differencesin BMC can

have an extraordinary impact on vertebral strength and

fatigue life. Thus, inheritance of bone mineral attributes

may play a large role with respect to the ability to tolerate physical loads on the spine, which may impact the

development of disc degeneration.

The likelihood that a high correlation in BMC exists

within MZ twin pairs raises a related issue regarding the

impact of an identical twins design in evaluating the influence of physical loading on disc degeneration. It

should be readily apparent that tissue failure will be influenced both by the magnitude of an imposed load and

strength of the material on which the load is exposed.

One would anticipate that the effect of this association

would be most prominent when both factors are free to
vary, and particularly when both variables are at their

discordant extremes (i.e., low-load/high material

strength may produce little or no damage, whereas highload/low material strength may produce significant damage). Thus, the effect of changes in magnitudes of physical loading on tissue damage would be expected to be

more apparent when examined in a context of material

strengthsthat comprise a wide range of values. However,

it should be recognized that in a twin design, because of

a high induced correlation in BMC (i.e., material

strength) between twins, the impact of changes in physical load are examined in a somewhat restricted context

(only within materials of similar strength). While such

comparisons are certainly legitimate, they may not be

fully representative of the effect that changes in physical

load would bring to bear if examined over a wide range

of material strengths. This may help to explain why

physical load was found to have a lesser influence on

degenerative changes in the twin studies44,59 (where

physical load effect was restricted to matched levels of

material strength) compared with other epidemiologic

studies(where differencesin physical loading were examined without restrictions in the range of material

strength).43–55

Disc degeneration will alter the mechanical properties

and load distribution within the spinal column, and as

this process evolves with age, additional threats may

emerge that may lead to low back pain when exposed to

repetitive loading. Regional bone loss appears to be related to the degree of disc degeneration, with greater

bone loss seen in the centrum of the vertebra with increased disorganization of the disc. This may be due to a

redistribution of load to the vertebral body periphery

resulting from disc degeneration30 and the development

ofstress concentrationsin the disc.66 The resulting weaknesses in the vertebrae may lead to osteoporotic fractures, which may be a particular risk when the older,

osteoporotic spine is loaded in a flexed posture.67 These

fractures may result in significant pain, deformity, and

disability.68

It is important to note that the number of cycles until

the failure criterion was reached in this biomaterials testing protocol should not be taken as representing a value

that may be sustained before clinically relevant damage

occurring. Indeed, endplate fractures may be initiated

with less compaction than allowed in the present protocol and will usually occur with less that 5 mm.16,17 We

established a higher displacement criterion in our initial

experiment due to the older sample and a desire to maximize experimental variability in fatigue life to better establish the influence of torso flexion. It is not precisely

known how mechanical tests of cadaver specimens relate

to in vivo loading. Some have suggested that the healing

capabilities of bone in vivo may result in less rapid

failure than during in vitro testing.17,69 Others have suggested that osteoclastic resorption in the physiologic

state may actually reduce strength and accelerate in vivo

fatigue failure compared with that observed during in

vitro testing.26,70

While the relationship of in vitro testing to the physiologic state is not entirely clear, results of the present

investigation provide several important findings that

may have clinical relevance with respect to cyclic loading

and failure of spinal tissues. For example, results of this

study suggest that exposure to spinal loads experienced

in flexed lifting of a given weight are likely to result in

much more rapid fatigue failure compared with the reduced loads experienced in upright lifting. These findings

provide strong support for minimizing the amount of

forward bending performed in lifting tasks, especially in

heavy industry such as mining. Future lifting guidelines

should be designed to account for the rapid fatigue failure that may occur in flexion. Results also suggest that

older workers will experience fatigue failure much more

quickly, primarily due to the reduced BMC in their

spines. This suggests that future lifting limits may also

need to consider age-related changes to prevent tissue

damage as bone loss continues to accumulate.

The results presented in thisstudy are not encouraging

for mine workers who are bound to adopt a flexed postures during lifting tasks due to restrictions in vertical

space often present in the underground mining environment (particularly in coal mines with working heights at

or around 1.5 meters). However, these findings may help

explain the high incidence rates for LBD typically observed in mining.2,4 Manual materials handling is a pervasive activity in mining and if workers are forced to

perform such activities in a flexed posture, the results

here suggest more rapid failure of spinal tissues, potentially accelerating the process of disc degeneration. There

are unfortunately limited postural alternatives in restricted spaces and it is more difficult (though not impossible) to provide mechanical-assist devices in restricted

spaces. Lifting in a kneeling posture will help keep the

spine in a more upright orientation and may be a useful

alternative to stoop lifting; however, lifting capacity is

reduced in the kneeling posture and there may certainly

be a trade-off with regard to increased risk of knee disorders. Clearly, results of this study suggest that loads

handled in a stooped posture be minimized to the greatest extent possible. Furthermore, the need for new and

better mechanical aids that can be effectively utilized in

restricted workspaces would seem to be a critical element

in reducing LBD risk in underground mines.

Certain limitations should be considered regarding

the data presented here. These include the possibility that

preexisting medical conditions or loading histories might

have differentially affected the specimens. The chances of

prior damage would certainly be greater in older specimens. In this regard, it is important to realize that, although fatigue failure occurred more rapidly in older

specimens, this does not necessarily imply greater back

pain experience in older osteopenic spines. It is quite

possible (in fact likely) that such spines have already
experienced the degenerative changes that may have led

to pain much earlier in life.

Key Points

● The fatigue failure responses of 18 working age

motion segments (average ± SD age, 49 ± 17

years) exposed to spines loads simulating lifting

tasks at 3 trunk flexion angles were compared with

those of a previously tested elderly cohort (average ± SD age, 81 ± 8 years).

● Compared with the older sample of spines, the

younger sample exhibited a substantial increase in

cycles to fatigue failure in all the torso flexion conditions.

● Bone mineral content was greater in the younger

motion segments, 30.7 g (±11.1 SD) per motion

segment, versus 27.8 g (±9.4 SD) in older spines.

● Cox regression modeling indicated increasing

relative risk of fatigue failure for segments exposed

to simulated spinal loads when lifting at increased

angles of torso flexion (risk ratio for 22.5° flexion = 15.7 compared with 0°; risk ratio for 45° =

50.5 compared with 0°).

● Increased bone mineral content was found to

have a protective influence (i.e., every increase of

1 g BMC led to 12% increase in cycles to failure).

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