Objectives This systematic review aimed to identify published observational methods assessing biomechanical exposures in occupational settings and evaluate them with reference to the needs of different users. Methods We searched scientific databases and the internet for material from 1965 to September 2008. Methods were included if they were primarily based on the systematic observation of work, the observation target was the human body, and the method was clearly described in the literature. A systematic evaluation procedure was developed to assess concurrent and predictive validity, repeatability, and aspects related to utility. At least two evaluators independently carried out this evaluation. Results We identified 30 eligible observational methods. Of these, 19 had been compared with some other method(s), varying from expert evaluation to data obtained from video recordings or through the use of technical instruments. Generally, the observations showed moderate to good agreement with the corresponding assessments made from video recordings; agreement was the best for large-scale body postures and work actions. Postures of wrist and hand as well as trunk rotation seemed to be more difficult to observe correctly. Intra- and inter-observer repeatability were reported for 7 and 17 methods, respectively, and were judged mostly to be good or moderate. Conclusions With training, observers can reach consistent results on clearly visible body postures and work activities. Many observational tools exist, but none evaluated in this study appeared to be generally superior. When selecting a method, users should define their needs and assess how results will influence decision-making.

Background Occupational and leisure-time physical activity are considered to provide similar health benefits. The authors tested this hypothesis. Methods A representative sample of Danish employees (n=7144, 52% females) reported levels of occupational and leisure-time physical activity in 2005. Long-term sickness absence (LTSA) spells of ≥3 consecutive weeks were retrieved from a social-transfer payment register from 2005 to 2007. Results 341 men and 620 females experienced a spell of LTSA during the period. Cox analyses adjusted for age, gender, smoking, alcohol, body mass index, chronic disease, social support from immediate superior, emotional demands, social class and occupational or leisure-time physical activity showed a decreased risk for LTSA among workers with moderate (HR 0.85, CI 0.72 to 1.01) and high (HR 0.77, CI 0.62 to 0.95) leisure-time physical activity in reference to those with low leisure-time physical activity. In contrast, an increased risk for LTSA was shown among workers with moderate (HR 1.59, CI 1.35 to 1.88) and high (HR 1.84, CI 1.55 to 2.18) occupational physical activity referencing those with low occupational physical activity. Conclusion The hypothesis was rejected. In a dose–response manner, occupational physical activity increased the risk for LTSA, while leisure-time physical activity decreased the risk for LTSA. The findings indicate opposing effects of occupational and leisure-time physical activity on global health.

Since it became clear that K⁺shifts with exercise are extensive and can cause more than a doubling of the extracellular [K⁺] ([K⁺]_s) as reviewed here, it has been suggested that these shifts may cause fatigue through the effect on muscle excitability and action potentials (AP). The cause of the K⁺shifts is a transient or long-lasting mismatch between outward repolarizing K⁺currents and K⁺influx carried by the Na⁺-K⁺pump. Several factors modify the effect of raised [K⁺]_sduring exercise on membrane potential ( E_m) and force production. 1) Membrane conductance to K⁺is variable and controlled by various K⁺channels. Low relative K⁺conductance will reduce the contribution of [K⁺]_sto the E_m. In addition, high Cl⁻conductance may stabilize the E_mduring brief periods of large K⁺shifts. 2) The Na⁺-K⁺pump contributes with a hyperpolarizing current. 3) Cell swelling accompanies muscle contractions especially in fast-twitch muscle, although little in the heart. This will contribute considerably to the lowering of intracellular [K⁺] ([K⁺]_c) and will attenuate the exercise-induced rise of intracellular [Na⁺] ([Na⁺]_c). 4) The rise of [Na⁺]_cis sufficient to activate the Na⁺-K⁺pump to completely compensate increased K⁺release in the heart, yet not in skeletal muscle. In skeletal muscle there is strong evidence for control of pump activity not only through hormones, but through a hitherto unidentified mechanism. 5) Ionic shifts within the skeletal muscle t tubules and in the heart in extracellular clefts may markedly affect excitation-contraction coupling. 6) Age and state of training together with nutritional state modify muscle K⁺content and the abundance of Na⁺-K⁺pumps. We conclude that despite modifying factors coming into play during muscle activity, the K⁺shifts with high-intensity exercise may contribute substantially to fatigue in skeletal muscle, whereas in the heart, except during ischemia, the K⁺balance is controlled much more effectively.

Six subjects performed one-legged dynamic knee-extension. Blood samples were drawn from the femoral artery and vein, and muscle biopsies were obtained from the quadriceps muscle. Leg blood flow was measured by the thermodilution technique, and 3H-inulin was infused for determination of extra- and intracellular muscle water shifts. During the submaximal work load (S) muscle lactate increased, whereas muscle pH remained almost constant; after maximal exercise (M) the values markedly increased for lactate and decreased for pH. Except for a release of lactate from the exercising muscles, K was continuously released throughout S, and this release increased during M. Immediately when the muscles relaxed, the K release was converted to a K re-uptake. The calculated K loss, based on v- a and flow values, agreed with the decrease in muscle K content from 458 mmol/kg dw at rest to 414 mmol/kg dw at exhaustion (P less than 0.05), as analyzed on the muscle biopsies. Muscle water content increased during S mainly because of an increased extracellular H2O, whereas during M the largest increase occurred in intracellular H2O (H2Oi). Because of the simultaneous K loss and H2Oi increase in the exercising muscle the intracellular [K] was calculated to decrease from 165 mM at rest to 129 mM at exhaustion. This decrease and an increase in extracellular [K] from 4.5 mM at rest to greater than 6.0 mM at exhaustion affects the muscle membrane excitability. Muscle fatigue may thus not only be caused by changes within the cell, affecting energy metabolism or actin-myosin reaction, but may be located at the membrane protecting the cell against overload.