The Effect of Recalled Previous Work Environment on Return to Work After a Rehabilitation Program Including Vocational Aspects for Trauma Patients

Introduction The aim of the present study was to assess the association between remembered previous work place environment and return to work (RTW) after hospitalisation in a rehabilitation hospital. Methods A cohort of 291 orthopedic trauma patients discharged from hospital between 15 December 2004 and 31 December 2005 was included in a study addressing quality of life and work-related questions. Remembered previous work environment was measured by Karasek's 31-item Job Content Questionnaire (JCQ), given to the patients during hospitalisation. Post-hospitalisation work status was assessed 3months, 1, and 2years after discharge, using a questionnaire sent to the ex-patients. Logistic regression models were used to test the role of four JCQ variables on RTW at each time point while controlling for relevant confounders. Results Subjects perceiving a higher physical demand were less likely to return to work 1year after hospital discharge. Social support at work was positively associated with RTW at all time points. A high job strain appeared to be positively associated with RTW 1year after rehabilitation, with limitations due to large confidence intervals. Conclusions Perceptions of previous work environment may influence the probability of RTW. In a rehabilitation setting, efforts should be made to assess those perceptions and, if needed, interventions to modify them should be applie

The effect of recalled previous work environment on return to work after a rehabilitation program including vocational aspects for trauma patients.

INTRODUCTION: The aim of the present study was to assess the association between remembered previous work place environment and return to work (RTW) after hospitalisation in a rehabilitation hospital. METHODS: A cohort of 291 orthopedic trauma patients discharged from hospital between 15 December 2004 and 31 December 2005 was included in a study addressing quality of life and work-related questions. Remembered previous work environment was measured by Karasek's 31-item Job Content Questionnaire (JCQ), given to the patients during hospitalisation. Post-hospitalisation work status was assessed 3 months, 1, and 2 years after discharge, using a questionnaire sent to the ex-patients. Logistic regression models were used to test the role of four JCQ variables on RTW at each time point while controlling for relevant confounders. RESULTS: Subjects perceiving a higher physical demand were less likely to return to work 1 year after hospital discharge. Social support at work was positively associated with RTW at all time points. A high job strain appeared to be positively associated with RTW 1 year after rehabilitation, with limitations due to large confidence intervals. CONCLUSIONS: Perceptions of previous work environment may influence the probability of RTW. In a rehabilitation setting, efforts should be made to assess those perceptions and, if needed, interventions to modify them should be applied

Predictors of nonresponse in a questionnaire-based outcome study of vocational rehabilitation patients.

OBJECTIVE: To identify predictors of nonresponse to a self-report study of patients with orthopedic trauma hospitalized for vocational rehabilitation between November 15, 2003, and December 31, 2005. The role of biopsychosocial complexity, assessed using the INTERMED, was of particular interest. DESIGN: Cohort study. Questionnaires with quality of life, sociodemographic, and job-related questions were given to patients at hospitalization and 1 year after discharge. Sociodemographic data, biopsychosocial complexity, and presence of comorbidity were available at hospitalization (baseline) for all eligible patients. Logistic regression models were used to test a number of baseline variables as potential predictors of nonresponse to the questionnaires at each of the 2 time points. SETTING: Rehabilitation clinic. PARTICIPANTS: Patients (N=990) hospitalized for vocational rehabilitation over a period of 2 years. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: Nonresponse to the questionnaires was the binary dependent variable. RESULTS: Patients with high biopsychosocial complexity, foreign native language, or low educational level were less likely to respond at both time points. Younger patients were less likely to respond at 1 year. Those living in a stable partnership were less likely than singles to respond at hospitalization. Sex, psychiatric, and somatic comorbidity and alcoholism were never associated with nonresponse. CONCLUSIONS: We stress the importance of assessing biopsychosocial complexity to predict nonresponse. Furthermore, the factors we found to be predictive of nonresponse are also known to influence treatment outcome and vocational rehabilitation. Therefore, it is important to increase the response rate of the groups of concern in order to reduce selection bias in epidemiologic investigations

Criterion validity of 3D trunk accelerations to assess external work and power in able-bodied gait

Evaluative quantification of gait disorder minimizing time-consuming and cost-intensive laboratory installations remains a challenging task in movement analysis. We examined the criterion validity of global gait mechanics assessed by trunk accelerometry. Eight female and four male volunteer subjects (mean age, 27.5 years; S.D., 5.1 years; weight, 68.7 ± 11.3 kg; height, 1.74 ± 0.08 m) without gait dysfunction participated in the study. They walked barefoot over two adjacent force-platforms at self-selected speeds. In addition to ground reaction forces, vertical, anterior–posterior and medio-lateral accelerations of the trunk were simultaneously measured by means of a light tri-axial accelerometer. Mean acceleration cycles of the trunk and the body centre of mass were calculated. Acceleration vectors were integrated twice to obtain velocity and displacement vectors of the trunk and the centre of mass, respectively. Temporal boundaries of right and left functional stance phases were defined by the two intermediate moments between maximum anterior–posterior velocity and minimal vertical displacement. Cross-correlations of the kinematics of the trunk and the centre of mass were determined. External work and corresponding symmetry indicators were computed for both methods. Centre of mass anterior–posterior displacement lagged behind the trunk by 3.5% of the gait cycle. External power correlated highly (r > 0.82) between the trunk model and the centre of mass. Work correlated moderately high (r = 0.77) between the two methods. Work and power asymmetry indexes correlated moderately high (r > 0.64). Our findings suggest that accelerometry has the potential to assess functional kinematics and energy-related outcomes in large cohorts

Proximal tibia volumetric bone mineral density is correlated to the magnitude of local acceleration in male long-distance runners

The beneficial effect of physical exercise on bone mineral density (BMD) is at least partly explained by the forces exerted directly on the bones. Male runners present generally higher BMD than sedentary individuals. We postulated that the proximal tibia BMD is related to the running distance, as well as to the magnitude of the shocks (while running) in male runners. A prospective study (three yearly measurements) included 81 healthy male subjects: 16 sedentary lean subjects, and 3 groups of runners (5–30 km/wk, n = 19; 30–50 km/wk, n = 29; 50–100 km/wk, n = 17). Several measurements were performed at the proximal tibia level: volumetric BMD (vBMD) and cortical index (CI), i.e., an index of cortical bone thickness and peak accelerations (an index of shocks during heel strike) while running (measured by a three-dimensional accelerometer). A general linear model assessed the prediction of vBMD or CI by 1) simple effects (running distance, peak accelerations, time); and 2) interactions (for instance, if vBMD prediction by peak acceleration depends on running distance). CI and vBMD 1) increase with running distance to reach a plateau over 30 km/wk; and 2) are positively associated with peak accelerations over 30 km/wk. Running may be associated with high peak accelerations to have beneficial effects on BMD. More important strains are needed to be associated with the same increase in BMD during running sessions of short duration than those of long duration. CI and vBMD are associated with the magnitude of the shocks during heel strike in runners

Atrogin-1, MuRF1, and FoXo, as well as phosphorylated GSK-3β and 4E-BP1 are reduced in skeletal muscle of chronic spinal cord-injured patients

Chronic complete spinal cord injury (SCI) is associated with severe skeletal muscle atrophy as well several atrophy and physical-inactivity-related comorbidity factors such as diabetes, obesity, lipid disorders, and cardiovascular diseases. Intracellular mechanisms associated with chronic complete SCI-related muscle atrophy are not well understood, and thus their characterization may assist with developing strategies to reduce the risk of comorbidity factors. Therefore, the aim of this study was to determine whether there was an increase in catabolic signaling targets, such as atrogin-1, muscle ring finger-1 (MuRF1), forkhead transcription factor (FoXO), and myostatin, and decreases in anabolic signaling targets, such as insulin-like growth factor (IGF), v-akt murine thymoma viral oncogene (Akt), glycogen synthase kinase-β (GSK-3β), mammalian target of rapamycin (mTOR), eukaryotic initiation factor 4E binding protein 1 (4E-BP1), and p70s6kinase in chronic complete SCI patients. In SCI patients, when compared with controls, there was a significant reduction in mRNA levels of atrogin-1 (59%; P < 0.05), MuRF1 (55%; P < 0.05), and myostatin (46%; P < 0.01), and in protein levels of FoXO1 (72%; P < 0.05), FoXO3a (60%; P < 0.05), and atrogin-1 (36%; P < 0.05). Decreases in the protein levels of IGF-1 (48%; P < 0.001) and phosphorylated GSK-3β (54%; P < 0.05), 4E-BP1 (48%; P < 0.05), and p70s6kinase (60%; P = 0.1) were also observed, the latter three in an Akt-and mTOR-independent manner. Reductions in atrogin-1, MuRF1, FoXO, and myostatin suggest the existence of an internal mechanism aimed at reducing further loss of muscle proteins during chronic SCI. The downregulation of signaling proteins that regulate anabolism, such as IGF, GSK-3β, and 4E-BP1, would reduce the ability to increase protein synthesis rates. © 2009 Wiley Periodicals, Inc

Human skeletal muscle atrophy in amyotrophic lateral sclerosis reveals a reduction in Akt and an increase in atrogin-1

The molecular mechanisms influencing muscle atrophy in humans are poorly understood. Atrogin-1 and MuRF1, two ubiquitin E3-ligases, mediate rodent and cell muscle atrophy and are suggested to be regulated by an Akt/Forkhead (FKHR) signaling pathway. Here we investigated the expression of atrogin-1, MuRF1, and the activity of Akt and its catabolic (FKHR and FKHRL1) and anabolic (p70s6k and GSK-3&beta;) targets in human skeletal muscle atrophy. The muscle atrophy model used was amyotrophic lateral sclerosis (ALS). All measurements were performed in biopsies from 22 ALS patients and 16 healthy controls as well as in G93A ALS mice. ALS patients had a significant increase in atrogin-1 mRNA and protein content, which was associated with a decrease in Akt activity. There was no difference in the mRNA and protein content of FKHR, FKHRL1, p70s6k, and GSK-3&beta;. Similar observations were made in the G93A ALS mice. Human skeletal muscle atrophy, as seen in the ALS model, is associated with an increase in atrogin-1 and a decrease in Akt. The transcriptional regulation of human atrogin-1 may be controlled by an Akt-mediated transcription factor other than FKHR or via another signaling pathway. <br /

Endurance training in humans leads to fiber type-specific increases in levels of peroxisome proliferator-activated receptor-[gamma] coactivator-1 and peroxisome proliferator-activated receptor-[alpha] in skeletal muscle

The peroxisome proliferator-activated receptor (PPAR)-&gamma; coactivator-1 (PGC-1) can induce mitochondria biogenesis and has been implicated in the development of oxidative type I muscle fibers. The PPAR isoforms &alpha;, &beta;/&delta;, and &gamma; control the transcription of genes involved in fatty acid and glucose metabolism. As endurance training increases skeletal muscle mitochondria and type I fiber content and fatty acid oxidative capacity, our aim was to determine whether these increases could be mediated by possible effects on PGC-1 or PPAR-&alpha;, -&beta;/&delta;, and -&gamma;. Seven healthy men performed 6 weeks of endurance training and the expression levels of PGC-1 and PPAR-&alpha;, -&beta;/&delta;, and -&gamma; mRNA as well as the fiber type distribution of the PGC-1 and PPAR-&alpha; proteins were measured in biopsies from their vastus lateralis muscle. PGC-1 and PPAR-&alpha; mRNA expression increased by 2.7- and 2.2-fold (P &lt; 0.01), respectively, after endurance training. PGC-1 expression was 2.2- and 6-fold greater in the type IIa than in the type I and IIx fibers, respectively. It increased by 2.8-fold in the type IIa fibers and by 1.5-fold in both the type I and IIx fibers after endurance training (P &lt; 0.015). PPAR-&alpha; was 1.9-fold greater in type I than in the II fibers and increased by 3.0-fold and 1.5-fold in these respective fibers after endurance training (P &lt; 0.001). The increases in PGC-1 and PPAR-&alpha; levels reported in this study may play an important role in the changes in muscle mitochondria content, oxidative phenotype, and sensitivity to insulin known to be induced by endurance training.<br /

UCP3 Protein Regulation in Human Skeletal Muscle Fibre Types I, IIa and IIx is Dependent on Exercise Intensity

It has been proposed that mitochondrial uncoupling protein 3 (UCP3) behaves as an uncoupler of oxidative phosphorylation. In a cross-sectional study, UCP3 protein levels were found to be lower in all fibre types of endurance-trained cyclists as compared to healthy controls. This decrease was greatest in the type I oxidative fibres, and it was hypothesised that this may be due to the preferential recruitment of these fibres during endurance training. To test this hypothesis, we compared the effects of 6 weeks of endurance (ETr) and sprint (STr) running training on UCP3 mRNA expression and fibre-type protein content using real-time PCR and immunofluorescence techniques, respectively. UCP3 mRNA and protein levels were downregulated similarly in ETr and STr (UCP3 mRNA: by 65 and 50 %, respectively; protein: by 30 and 27 %, respectively). ETr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 54, 29 and 16 %, respectively. STr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 24, 31 and 26 %, respectively. The fibre-type reductions in UCP3 due to ETr, but not STr, were significantly different from each other, with the effect being greater in type I than in type IIa, and in type IIa than in type IIx fibres. As a result, compared to STr, ETr reduced UCP3 expression significantly more in fibre type I and significantly less in fibre types IIx. This suggests that the more a fibre is recruited, the more it adapts to training by a decrease in its UCP3 expression. In addition, the more a fibre type depends on fatty acid β oxidation and oxidative phosphorylation, the more it responds to ETr by a decrease in its UCP3 content