Download Sedentary Work - Dr David McGrath

Sedentary Work
Are Chairs Killing us?
Not According to R. Gun
“The Human Cost of Work” 2nd Ed
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Industrial Injury rates
Occupational cancer rate
Overall Cancer rate
Musculoskeletal Injuries
Physical Exposure to Risk Factors
Occupational Respiratory Disease
Occupational Skin Disease
Infections and Parasitic Diseases
Psychological Disorders
Heart Disease
Outcomes from chemical exposures
In all of these Situations, sedentary occupations are protective compared to other occupations
There is an increased rate of compensation claims in the public sector for stress disorders but
NOT an actual increase in psychological disorder (ie employment culture with increased reporting)
In addition Canberian’s have the longest longevity of all the states
So What’s the Fuss
 Is
there anything to worry about at all?
 Does the public sector just attract just a
bunch of wingers ?
 When things go wrong the first explanation
becomes “Its my chair doc”, followed by
OHS review and a new chair
 Failure to recover, is followed by a compo
claim
But Wait A Minute
 Don’t
we all get an achy neck or lower
back while sitting at our desk ?
 Who doesn’t remember the RSI epidemic
 What if everyone sits too much? This
would obscure differentiation. Isn’t there
more mechanisation than ever before? Are
we immersed in a medium of sitting?
What’s the Truth
When all else fails check
the
scientific data base
Search Profiles
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Inactivity Physiology
Disuse Paradigm
Prolonged Weightlessness
Muscle Activation and Disuse
Physical activity and cancer
Physical activity and disease
Physical activity and health
Sedentary
Chairs and pain
Office Ergonomics
Bed Rest
Disc Disease
Awkward Postures
Postures
Evidence Base
 Weightlessness/microgravity
 Paraplegia/chronic
bed ridden
 Geriatrics
 Animal
models
 Population studies
 Conceptual Models
Lessons
From
Outer Space
Low Gravity Adjustments
References 1,2,3,5
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During Spaceflight
A drop in Blood Pressure and Respiratory Frequency
Stable Heart Rate and Heart Rate Variability
On Return to Earth
Large changes in all variables before returning to earth values
Author Conclusions
Functional adaptation in space physiological impairment on return to earth
Impairments include orthostatic intolerance, bone demineralisation, muscular atrophy,
neurovestibular symptoms, increased urinary supersaturation of renal chemicals,
decreased urinary output
Longer duration flights result in more severe and more prolonged disability
The concept of safe duration of exposure in hostile microgravity environment
Changes correlate with relatively immobile terrestrial patients eg spinal cord, geriatric
or prolonged best rest patients
Lessons
from
the
Laboratory
Poor old Rats
Ref 3,6,9,10
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Tails up heads down
Disrupted cerebrovascular autoregulation, negative calcium balance with bone loss
Lower Limb Suspension (4 weeks)
Changes to muscle bulk and excitability which is muscle group and type dependant
Immobilisation
Marked increase in the number of neutrophils, monocytes, eosinophils. No change in
Lymphocytes. Ie Natural immunity cells increase
Lessons
from
the
Bedside
Prolonged Bed Rest
Ref 7,8
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Healthy Women Study (2 month bed rest)
Reduced microcirculation endothelium-dependant function and endothelium damage
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Sixty days bed rest with head tilt down
Significant reductions in Left and right Ventricular volumes ie cardiac atrophy
Limb Immobilisation (1)
Ref 13,14,15,18,19,20,21
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Neuromuscular Components of Loss
Neurological component to strength loss/gain generally greater than muscle
component. (48% neurological, 39% muscle) (56% and 36% Ref20)
Changes in neurological components distributed widely. Loss of firing rate in motor
neuron. Changes to muscle receptors with functional loss proprioception.
Unloading produces severe muscle atrophy and slow to fast muscle type transitions
Loss of phosphokinase levels and muscle excitability. Altered ion channels.
Reduced postural control through loss of slow twitch postural muscle type
Muscle shortening through loss of loss of sarcomeres in series (ends of muscle
necrosis) Altered length-tension functional relationship. Single joint muscles the most
because of type1 dominance. EMG activity changes.
Increase in connective tissue relative to contractile mass. Functional increase in
muscle stiffness. Decreased joint range.
Decreased synthesis, increased catabolism.
Changes in the musculotendinous junction. Decreased contact area.
Limb Immobilisation (2)
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Inflammatory mediators
Acute and chronic disorders can be associated with free radical mediated
inflammatory alterations to muscle strength and mass. Ie concomitant risk for bed
ridden in addition to disuse. Acute intense exercise induces inflammation.
Age Related Differences
Muscle volume loss greater in older but similar loss in strength
Long Term Disuse
Speed and power more affected than strength. A future risk factor for falls.
Lessons
from
the
Population
Endemic Disorders
Ref 22
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Cardiovascular Disease, type2 diabetes, metabolic syndrome
and obesity, Musculoskeletal aches
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Daily Sitting or low nonexercise activity levels (NEAT) may have a direct connection
The effects (negative ) of prolonged sitting may be distinct from the effects (positive )
of structured exercise
NEAT is greater component of energy expenditure than exercise
Brief but frequent muscular contraction throughout the day may be necessary to
oppose unhealthy molecular signals causing metabolic disease
LPL activity more influenced by daily low intensity activity than adding vigorous
exercise. Inactivity produced chemical changes qualitatively different than exercise.
Concept of Volume of intermittent nonexercise physical activity in everyday life.
(inactivity physiology paradigm) and (non exercise activity )
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Cardiovascular Risk
Ref 23,27,28,29,30,31,35,37
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Physical inactivity profound effects on lipoprotein metabolism. Modest exercise
prevented these changes creating sustained VLDL-TG lowering. Intense exercise did
not but increased HDL.
Physical inactivity reduces LPL activity in muscles and TG clearance
Brisk walking and vigorous exercise have substantial and similar reduction in the
incidence of coronary events among women (regardless of BMI, race etc )
Prolonged sitting predicts cardiovascular risk
Moderate intensity exercise such as walking is associated with a substantial risk
reduction for total and ischemic stroke in a dose-response manner in women
Average weekly exercise intensity in men was associated with reduced CHD
(coronary heart disease) independent of MET hours in physical activity
At least 1 hour/week of walking in women lowered CHD risk. Time spent walking but
not pace predicted lower risk.
High intensity exercise produces the greatest change in lipid profile
May be safer to exercise in afternoons (HR and V(o2) max reactivity )
Obesity
Ref 24,32,33,34,36,42
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NEAT non exercise activity thermogenesis is highly individual and controlled by the
environment (employment). Up to 2000kcal/day range
NEAT is critical to fat deposition
Obese individuals exhibit an innate tendency to be seated 2.5 hours more than
sedentary lean counterparts
The equivalent of 11 miles walking/week at low or moderate intensity prevented
accumulation of visceral fat
A modest increase over above level resulted in significant decreases in visceral fat
Walking 19km/week at 40-55% peak V(o2) sufficient to increase aerobic fitness.
Higher levels increased fitness further.
Metabolic cardiovascular syndrome is strongly associated with reduced habitual
energy expenditure
Sitting 7.4 hours /day strongly associated with obesity
Working women only ½ as likely to be obese
Type 2 Diabetes
Ref 25,26
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A similar and significant risk reduction for type2 diabetes with equivalent energy
expenditure by either walking or vigorous activity
Independent of energy levels, sedentary behaviour especially TV watching was
associated with significant elevation of risk of type2 and obesity
Risk of type2 prevented by <10h/wk of TV and>or=30min/d of brisk walking
All Praise to Moderation
 Regular
energy expenditure by whatever
form is beneficial and protective from the
development of type2,obesity and
cardiovascular disease.
Musculoskeletal Aches
Ref 38, 39, 40,41,42
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Ergonomic Intervention Programs report very modest reduction in moderate to severe
pain levels (20% to 16% prevalence)
Computer workstations have high prevalence of aches (shoulder pains 45%,back
pains 43%, wrist pains 30%, neck pain 30% typical levels )
Only a 10% take up rate of advice regarding computer workstations. (poor
compliance)
Prognostic factors for aches were, time at the keyboard, and speed of work
Disc Pain (1)
Ref 43-61
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Degeneration with degraded collagen can occur as early as 2nd decade
Static Compressive loads can initiate a number of harmful responses in
dose/response manner (rat experiments )
Endplate calcification (mechanical stress) limits solute diffusion into the disc
Disc degeneration can be induced by axial loading (rabbit)
Endplate degeneration correlates with disc degeneration (52,55)
Chondrocyte apoptosis induced by static mechanical load
Endplate cartilage damage increases with age and reduces diffusion
Aging and degeneration two separate processes (49)
Axial Distraction can induce disc regeneration (rabbit) (54)
Density of openings in osseous end plate correlate with disc degeneration
XR’s more accurate than MRI in determining stage of disc degeneration(56)
Damage to endplate correlates with disc degeneration (pigs) (57)
End Plate is the main route of solute entry into the disc (60)
Disc Pain (2)
 Any
mechanism that damages the
Vertebral End Plate with loss of Perfusion
can lead to nuclear, followed by annular
damage (degeneration)
 It is not clear about the contribution,
overall and in particular of cyclic and static
loading versus acute trauma
Lessons
from
Conceptual Modelling
Bones
Ref 11,12
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Osteocyte Signals
Reduced loading leads to reduced osteoblast activity and increased osteoclast
activity.
Most force environments sufficient to maintain osteoblast activity
Remodelling Threshold
Restoration of normal architecture by remodelling is a high threshold event.
Increasing bone mass by physical exercise is difficult in adults. Remodelling is part of
youth. Exercise may stop further bone loss however.
Disc Models
Focus on finite modelling with an emphasis on diffusion gradients and osmosis
affected by various force environments
Skeleton Summary
 Musculoskeletal
inactivity has the potential
to develop muscular contractures,
weakness, tissue type changes, disruption
to disc architecture, loss of neural
connectedness, biomechanical inefficiency
The Story Thus Far
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Prolonged sitting has the potential to disturb
chemistry and cellular signalling, shorten and
stiffen muscles, weaken bones, change
neurological connectedness, upset energy
regulation and be an input for the development
of type2 diabetes, metabolic syndrome, obesity,
musculoskeletal aches, osteoporosis and
cardiovascular disease. There is also an
increased risk of injury and falls.
Pause
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A
Time
for
Reflection
 What
is the dose response relationship
between activity or its inverse variable
inactivity and the risk of developing
physiological disturbance.
 Cause=Exposure
to Risk Factors
Risk Factors Considerations
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Exposure Dosage
Good or Bad
Extrinsic and Intrinsic
Sequential or Concomitant
Intermittent or Continuous
Counterbalancing Positive Factors
Inadequate Recovery & Re-exposure
Age at time of exposure
Circadian and other periodicities
Intensity and Volume
Rate of Change
A Timely Reminder
 “All
factors can be either Toxic or
Beneficial depending on the dose”
Too Much “Toxic”
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Generally blue collar occupations have more exposure to physical and chemical
hazards
There are exceptions such as hairdressing and sections of cosmetic industry with
unusual toxic exposure.
Sedentary usually implies less exposure to “Toxic” and is protective
Too Little “Beneficial”
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Insufficient outdoors reduces exposure to fresh air or vitamin D producing UV
Insufficient sitting (Prolonged standing) can produce foot pathology
Insufficient Vitamins lead to malnutrition
Insufficient Energy expenditure may lead to physiological disturbance and disease
Insufficient Movement may lead to faulty movement patterns and altered perfusion
dynamics
Concomitant Dilemma
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“Toxic” and “Beneficial” inputs can occur together
Prolonged sitting means less exposure to beneficial movement inputs (B) while
reducing exposure to hazardous inputs. (T)
Is the reduction in “T” greater than the loss of “B” ?
“Climbing a mountain is both rewarding
and dangerous”
“Not Climbing a mountain is both safe and
unrewarding”
Irreversible Pathways
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Exercise is not an antidote for non activity (LPL example)
Gravity is not an antidote for prolonged weightlessness
Surgery is not an antidote for joint destruction
Stretch is not an antidote for shortening
“climbing a cliff face may not return one to
the top after rolling down a slope”
Mechanisms of Disease
“inputs mis- match physiological needs”
A Common Error
 A returning Astronaut
might be forgiven for
believing earth was a hostile environment
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(the current environment may not be the cause)
Solutions to Complexity
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R.Gun suggests that we stop trying to codify risk and institute an information based
system based on “situations”. He advocates this for toxicology and manual handling.
This is similar to “near miss reporting” system utilised by the airline industry.
For exposures which are more pervasive like a creeping temperature rise or
sedentary life perhaps a new approach is needed. How about a thermometer? Detect
early and change the pertinent exposures to correct the temperature.
Detect signs and symptoms of Sedentary life or
excessive sitting early and reduce exposure. Apply
antidotes if available. ie Early secondary intervention
Early Detectors
 Symptoms
of fatigue, stiffness, aches
 Signs of low aerobic capacity, loss of
flexibility, muscle tenderness, central
obesity, rising BP, fasting glucose, innate
inflammatory markers, resting HR
Conclusions
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Sedentary occupations are generally protective from other toxic inputs
There appears to be a non risk exposure dosage for sitting
Excess sitting may be negative and comparable to impairment produced by outer
space exposure. This is due to loss of usual antigravity inputs and disruption to
energy regulation.
Chronic excess sitting may insidiously create metabolic and structural harm which is
difficult to reverse
Some of the negative effects of excess can be obviated by moderate exercise
Regular standing and walking are antidotes for some harm development
A higher NEAT produced by above is protective
Remedies
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Reconstruct Work/Recreation Role (recommended)
Office Gym
Pause Gymnastics
Regular exercise classes
Weekly sport
Walk or cycle to work
Use the stairs
Don’t watch TV
Final Word
We are no more designed to sit for
prolonged periods than we are to live on
the moon
Extra Last Word
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What is the ideal lifestyle/Job ?
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Questions
and
Discussion