Sedentary Work

1. Sedentary Work Are Chairs Killing us?

2. Not According to R. Gun“The 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 Canberian’s have the longest longevity of all the states

3. 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

4. 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?

5. What’s the Truth When all else fails check the scientific data base

6. 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

7. Evidence Base • Weightlessness/microgravity • Paraplegia/chronic bed ridden • Geriatrics • Animal models • Population studies • Conceptual Models

8. Lessons From Outer Space

9. 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

10. Lessons from the Laboratory

11. 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

14. 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.

15. 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.

16. Lessons from the Population

17. 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 )

18. 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 )

19. 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 <10h/wk of TV and>or=30min/d of brisk walking

21. 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

23. 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 • 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)

24. 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

25. Lessons from Conceptual Modelling

26. 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

27. 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

28. 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.

29. Pause • A • Time • for • Reflection

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

31. Cause=Exposure to Risk Factors

32. 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

33. A Timely Reminder • “All factors can be either Toxic or Beneficial depending on the dose”

34. 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

35. 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

36. 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”

37. 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”

38. Mechanisms of Disease “inputs mis- match physiological needs”

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

40. 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

41. 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

42. 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

43. Remedies • 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

44. Final Word We are no more designed to sit for prolonged periods than we are to live on the moon

45. Extra Last Word • What is the ideal lifestyle/Job ?

46. Questions • and • Discussion