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.

Influence of initial foot dorsal flexion on vertical jump and running performance.

Several studies (on an inclined platform or with special shoes) have reported improved jump performance when the ankle was in a dorsiflexion (DF) position. The present study aims to test whether shoes inducing moderate DF modify vertical jump performance and energy cost. Twenty-one young, healthy female subjects (30 +/- 6 yr, 58 +/- 6 kg, O2max 45 +/- 3 mLxkg-1xmin-1, mean +/- SD) participated in the study. Jump performance was tested with subjects either wearing 4 degrees DF or standard (S) shoes. The jump tests (performed on a force platform) consisted of squat jump (SJ), countermovement jump (CMJ), and continuous jumps (CJ) during 15 seconds. Measured parameters were jump height, speed at take off, and maximal and average power. Oxygen uptake was measured on a treadmill while subjects ran at 95% of the anaerobic threshold during a 7-minute steady-state period. As compared with S shoes, DF shoes significantly improved the height of SJ (31 +/- 4 cm vs. 34 +/- 4 cm, p = 0.0001), CMJ (32 +/- 4 cm vs. 34 +/- 4 cm, p = 0.0004), and CJ (17.5 +/- 4.2 cm vs. 22.0 +/- 6.0 cm, p = 0.0001). Speed at take off was also significantly higher. Mean power significantly increased in SJ and CJ but not in CMJ. Oxygen uptake was not different between conditions (p = 0.40). Dorsiflexion shoes induce a significant increase in jump performance. These results are in accordance with the concept that a DF of the ankle may induce an increase of the length and strength of the triceps surae (higher torque). However, wearing DF shoes did not require more energy during running. Dorsiflexion shoes could be used to increase jump performance in several sports such as volleyball in which jump height is essential.

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.

Mirtazapine decreases the pain feeling in healthy participants.

OBJECTIVES: The treatment of neuropathic pain is mainly based on antiepileptics, tricyclic antidepressants, and opiates. These drugs have important side effects disturbing the patient's quality of life. Mirtazapine (MTZ) is a new and well-tolerated tricyclic antidepressants with both monoaminergic and opioid properties that might favorably influence pain. The aim of this study was to assess whether MTZ can reduce the pain induced by a standardized stimulus presented to healthy human participants. The nociceptive flexion reflex (NFR) to an electric stimulus was chosen to determine the pain threshold. METHODS: The effect of MTZ compared to placebo was assessed on 10 healthy participants in a double-blinded cross-over design. The NFR was measured the day after a single oral dose of drug (30 mg) or placebo. RESULTS: A significant increase in upper limb (+29%, P=0.006) NFR threshold was observed. DISCUSSION: MTZ increases the pain tolerance in healthy participants. The potential benefit of this effect on pain should be investigated more thoroughly in chronic neuropathic pain patients. The NFR might serve as an additional tool for the monitoring of these patients.

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 (p70(s6k) and GSK-3beta) 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, p70(s6k), and GSK-3beta. 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.

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+/-11.3kg; height, 1.74+/-0.08m) 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.

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 < 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 < 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 < 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.

Lipid peroxidation in skeletal muscle of obese as compared to endurance-trained humans: a case of good vs. bad lipids?

Intra-myocellular triglycerides (IMTG) accumulate in the muscle of obese and endurance-trained (ET) humans and are considered a pathogenic factor in the development of insulin resistance, in the former. We postulate that this paradox may be associated with the peroxidation status of the IMTG. IMTG content was the same in the obese and ET subjects. The lipid peroxidation/IMTG ratio was 4.2-fold higher in the obese subjects. Hence, obesity results in an increased level of IMTG peroxidation while ET has a protective effect on IMTG peroxidation. This suggests a link between the lipid peroxidation/IMTG ratio and insulin resistance.

Biopsychosocial complexity is correlated with psychiatric comorbidity but not with perceived pain in complex regional pain syndrome type 1 (algodystrophy) of the knee.

AIM: The aim of this study was to compare the characteristics of patients suffering from complex regional pain syndrome type 1 ([CRPS], also known as reflex sympathetic dystrophy or algodystrophy) of the knee with those of a matched group of patients experiencing post-traumatic knee pain. The comparisons looked at biopsychosocial complexity (simple versus complex), psychiatric comorbidity and pain intensity. METHODS: Cross-sectional, single-centre, case-control study using the INTERMED scale, psychiatric diagnostic tools (ICD-10) and visual analogue pain scale. Contingency table and Chi2 tests. One-way analysis of variance for continuous dependent variables. Difference between groups: Tukey's variance test, after the event. For nominal dependent variables, multivariate logistic analysis. RESULTS: Biopsychosocial complexity did not differ between the two groups (p = 0.7). The "complex" patients displayed significantly more psychiatric comorbidity (odds ratio 2.94, 95% confidence interval 1.1-7.8, p < 0.01), independently of whether or not CRPS was present. The pain perceived varied with biopsychosocial complexity only in the control group. The "complex" control patients reported more pain than the "simple" control patients (p < 0.05). The perceived intensity of pain was not different between the "simple" and "complex" patients with CRPS. CONCLUSIONS: Biopsychosocial complexity was comparable between the two groups, and was strongly associated with the presence of psychiatric comorbidity. However, unlike with other pain syndromes, with CRPS the intensity of the perceived pain did not vary with biopsychosocial complexity. Early identification of "complex" patients could make it possible to quickly institute targeted management for both groups of patients.

Rehabilitation outcomes for orthopaedic trauma individuals as measured by the INTERMED.

PURPOSE: Bio-psychosocial characteristics of patients after orthopaedic traumas may be a strong predictor of poor outcome. The objective of this prospective study was to assess whether the INTERMED, a measure of bio-psychosocial complexity, identifies complex inpatients during rehabilitation including vocational aspects with a poor outcome 1 year after discharge. METHOD: At entry, the INTERMED scores of 118 inpatients were used to assign patients to the high or low complexity group. A questionnaire evaluated 1 year after discharge whether patients: (1) returned to work, (2) still have therapies, (3) take psychoactive drugs, (4) take medication against pain and (5) were satisfied with vocational therapy. Univariate logistic regressions identified which variables predict INTERMED case complexity during hospitalisation as well as predictors (i.e. INTERMED case complexity, French as preferred language, duration of the disability, accident at work, work qualification, severity of the injury, psychiatric co-morbidities, pain) of the five measured outcomes 1 year after discharge. RESULTS: During hospitalisation, the high complexity group was associated with a high prevalence of psychiatric co-morbidities, a higher level of pain and a weaker perception of treatment effects. One year after discharge, the INTERMED was the sole variable to predict all outcomes. CONCLUSION: The INTERMED identifies complex patients during vocational rehabilitation after orthopaedic trauma and is a good predictor of poor outcome 1 year after discharge.

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-3beta 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-beta (GSK-3beta), mammalian target of rapamycin (mTOR), eukaryotic initiation factor 4E binding protein 1 (4E-BP1), and p70(s6kinase) 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-3beta (54%; P < 0.05), 4E-BP1 (48%; P < 0.05), and p70(s6kinase) (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-3beta, and 4E-BP1, would reduce the ability to increase protein synthesis rates.

Sciatica in the female patient: anatomical considerations, aetiology and review of the literature.

The principal author was confronted few years ago with the case of a 38-year-old woman with a 5-month history of ill-defined L5 sciatic pain that was referred to an orthopaedic department for investigation and eventual surgical treatment for what was suspected to be herniated disc-related sciatica. Removal of her enlarged uterus found unexpectedly close to the sacroiliac joint upon lumbar MRI abolished her symptoms. Review of the literature showed that the lumbosacral trunk is vulnerable to pressure from any abdominal mass originating from the uterus and the ovaries. Physiological processes in the female patient and gynaecological diseases may be the source of sciatica, often not readily searched for, leading to fruitless investigations and surgical treatments. The aim of the paper is to highlight gynaecological and obstetrical causes of sciatica and sciatica-like symptoms. To prevent unproductive expenses and morbidity, a thorough gynaecological examination should be done even though neurological examination may be suggestive of a herniated intervertebral disc, and the cyclic pattern of pain related to menses should be routinely asked for.

Akt signalling through GSK-3beta, mTOR and Foxo1 is involved in human skeletal muscle hypertrophy and atrophy.

Skeletal muscle size is tightly regulated by the synergy between anabolic and catabolic signalling pathways which, in humans, have not been well characterized. Akt has been suggested to play a pivotal role in the regulation of skeletal muscle hypertrophy and atrophy in rodents and cells. Here we measured the amount of phospho-Akt and several of its downstream anabolic targets (glycogen synthase kinase-3beta (GSK-3beta), mTOR, p70(s6k) and 4E-BP1) and catabolic targets (Foxo1, Foxo3, atrogin-1 and MuRF1). All measurements were performed in human quadriceps muscle biopsies taken after 8 weeks of both hypertrophy-stimulating resistance training and atrophy-stimulating de-training. Following resistance training a muscle hypertrophy ( approximately 10%) and an increase in phospho-Akt, phospho-GSK-3beta and phospho-mTOR protein content were observed. This was paralleled by a decrease in Foxo1 nuclear protein content. Following the de-training period a muscle atrophy (5%), relative to the post-training muscle size, a decrease in phospho-Akt and GSK-3beta and an increase in Foxo1 were observed. Atrogin-1 and MuRF1 increased after the hypertrophy and decreased after the atrophy phases. We demonstrate, for the first time in human skeletal muscle, that the regulation of Akt and its downstream signalling pathways GSK-3beta, mTOR and Foxo1 are associated with both the skeletal muscle hypertrophy and atrophy processes.

Mitofusins 1/2 and ERRalpha expression are increased in human skeletal muscle after physical exercise.

Mitochondrial impairment is hypothesized to contribute to the pathogenesis of insulin resistance. Mitofusin (Mfn) proteins regulate the biogenesis and maintenance of the mitochondrial network, and when inactivated, cause a failure in the mitochondrial architecture and decreases in oxidative capacity and glucose oxidation. Exercise increases muscle mitochondrial content, size, oxidative capacity and aerobic glucose oxidation. To address if Mfn proteins are implicated in these exercise-induced responses, we measured Mfn1 and Mfn2 mRNA levels, pre-, post-, 2 and 24 h post-exercise. Additionally, we measured the expression levels of transcriptional regulators that control mitochondrial biogenesis and functions, including PGC-1alpha, NRF-1, NRF-2 and the recently implicated ERRalpha. We show that Mfn1, Mfn2, NRF-2 and COX IV mRNA were increased 24 h post-exercise, while PGC-1alpha and ERRalpha mRNA increased 2 h post-exercise. Finally, using in vitro cellular assays, we demonstrate that Mfn2 gene expression is driven by a PGC-1alpha programme dependent on ERRalpha. The PGC-1alpha/ERRalpha-mediated induction of Mfn2 suggests a role of these two factors in mitochondrial fusion. Our results provide evidence that PGC-1alpha not only mediates the increased expression of oxidative phosphorylation genes but also mediates alterations in mitochondrial architecture in response to aerobic exercise in humans.

[Tomodensitometry measurements of proximal tibia and acceleration in marathon athletes]. / Mesures tomodensitométriques du tibia proximal et accélérations chez des marathoniens.

We evaluated bone adaptation of the tibia to mechanical stresses in male marathon runners and in sedentary controls in function of the ground impact measured by accelerometry and of the bone mineral density assessed by peripheral quantitative computed tomography (QCT). Sixty-three subjects (51 runners and 12 controls) were enrolled. All had measurements of bone mineral density of the proximal tibia and of acceleration at the same site during a jogging at 9 km/hour. The results show a significant higher cortical BMD in runners with the higher value of late accelerations (at 50 ms after the contact with the ground). The late acceleration might be related to muscle contraction.

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 beta oxidation and oxidative phosphorylation, the more it responds to ETr by a decrease in its UCP3 content.