Sedentary Work

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Sedentary Work

• Are Chairs Killing us?

2
Not According to R. GunThe Human Cost of Work
2nd Ed

• 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 Canberians have the longest
  longevity of all the states

3
So Whats 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

4
But Wait A Minute

• Dont we all get an achy neck or lower back while
  sitting at our desk ?
• Who doesnt remember the RSI epidemic
• What if everyone sits too much? This would
  obscure differentiation. Isnt there more
  mechanisation than ever before? Are we immersed
  in a medium of sitting?

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Whats the Truth

• When all else fails check
• the
• scientific data base

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Search Profiles

• 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

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Evidence Base

• Weightlessness/microgravity
• Paraplegia/chronic bed ridden
• Geriatrics
• Animal models
• Population studies
• Conceptual Models

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• Lessons
• From
• Outer Space

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Low Gravity AdjustmentsReferences 1,2,3,5

• 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

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• Lessons
• from
• the
• Laboratory

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Poor old RatsRef 3,6,9,10

• 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

12

• Lessons
• from
• the
• Bedside

13
Prolonged Bed RestRef 7,8

• Healthy Women Study (2 month bed rest)
• Reduced microcirculation endothelium-dependant
  function and endothelium damage
• Sixty days bed rest with head tilt down
• Significant reductions in Left and right
  Ventricular volumes ie cardiac atrophy

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Limb Immobilisation (1)Ref 13,14,15,18,19,20,21

• 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.

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Limb Immobilisation (2)

• 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.

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• Lessons
• from
• the
• Population

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Endemic DisordersRef 22

• Cardiovascular Disease, type2 diabetes, metabolic
  syndrome and obesity, Musculoskeletal aches
• 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 RiskRef 23,27,28,29,30,31,35,37

• 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 )

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ObesityRef 24,32,33,34,36,42

• 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

20
Type 2 DiabetesRef 25,26

• 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 lt10h/wk of TV
  andgtor30min/d of brisk walking

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All Praise to Moderation

• Regular energy expenditure by whatever form is
  beneficial and protective from the development of
  type2,obesity and cardiovascular disease.

22
Musculoskeletal AchesRef 38, 39, 40,41,42

• 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

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Disc Pain (1)Ref 43-61

• 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
• XRs 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)

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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

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• Lessons
• from
• Conceptual Modelling

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BonesRef 11,12

• 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

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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

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The Story Thus Far

• 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.

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Pause

• A
• Time
• for
• Reflection
• 
  

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• What is the dose response relationship between
  activity or its inverse variable inactivity and
  the risk of developing physiological disturbance.

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• CauseExposure to Risk Factors

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Risk Factors Considerations

• 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

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A Timely Reminder

• All factors can be either Toxic or Beneficial
  depending on the dose

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Too Much Toxic

• 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

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Too Little Beneficial

• 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

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Concomitant Dilemma

• 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

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Irreversible Pathways

• 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

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Mechanisms of Disease

• inputs mis- match physiological needs

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A Common Error

• A returning Astronaut might be forgiven for
  believing earth was a hostile environment
• (the current environment may not be
  the cause)

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Solutions to Complexity

• 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

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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

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Conclusions

• 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

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Remedies

• Reconstruct Work/Recreation Role (recommended)
• Office Gym
• Pause Gymnastics
• Regular exercise classes
• Weekly sport
• Walk or cycle to work
• Use the stairs
• Dont watch TV

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Final Word

• We are no more designed to sit for prolonged
  periods than we are to live on the moon

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Extra Last Word

• What is the ideal lifestyle/Job ?

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• Questions
• and
• Discussion