Evaluation of muscle oxygenation by near infrared spectroscopy in patients with facioscapulohumeral muscular dystrophy.

UNLABELLED: The purpose of the study was to determine muscle metabolism adaptation to exercise in facioscapulohumeral muscular dystrophy patients (FSHD) and to study the correlation with clinical functional status (6-min walk test). 8 FSHD patients and 15 age-matched healthy controls (Controls) performed two isokinetic constant-load knee extension exercises: (1) at 20% of their maximal extensors' peak torque (i.e., the same relative workload) and (2) at (20N⋅m) (the same absolute workload) for up to 4 min. All exercises consisted of rhythmic, voluntary, isokinetic, concentric contractions of the quadriceps femoris at 90°/s, whereas the flexion was performed passively at the same speed. Muscle oxygenation in the vastus lateralis was evaluated using near-infrared spectroscopy (NIRS). The FSHD patients displayed a lower maximal peak torque than controls (-41%, p < 0.05). During the two-exercise modalities, deoxygenated haemoglobin (HHb) and total haemoglobin volume (tHb) were lower in the FSHD patients (p < 0.05). The initial muscle deoxygenation time delay was shorter in the control group (FSHD: 15.1 ± 4.1 s vs. CONTROLS: 10.4 ± 2.1 s, p < 0.05). Mean response time and maximal peak torque were both correlated with functional impairment (walking endurance). The results suggest that FSHD patients present an impairment in their capacity to deliver or to use oxygen.

Carbon monoxide pollution impairs myocardial perfusion reserve: implication of coronary endothelial dysfunction.

Chronic exposure to simulated urban CO pollution is reported to be associated with cardiac dysfunction. Despite the potential implication of myocardial perfusion alteration in the pathophysiology of CO pollution, the underlying mechanisms remain today still unknown. Therefore, the aim of this work was to evaluate the effects of prolonged exposure to simulated urban CO pollution on the regulation of myocardial perfusion. Cardiac hemodynamics and myocardial perfusion were assessed under basal conditions and during the infusion of a ß-Adrenergic agonist. The effects of CO exposure on capillary density, coronary endothelium-dependent vasodilatation, eNOS expression and eNOS uncoupling were also evaluated. Our main results were that prolonged CO exposure was associated with a blunted myocardial perfusion response to a physiological stress responsible for an altered contractile reserve. The impairment of myocardial perfusion reserve was not accounted for a reduced capillary density but rather by an alteration in coronary endothelium-dependent vasorelaxation (-45% of maximal relaxation to ACh). In addition, though chronic CO exposure did not change eNOS expression, it significantly increased eNOS uncoupling. Therefore, the present work underlines the fact that chronic CO exposure, at levels found in urban air pollution, is associated with reduced myocardial perfusion reserve. This phenomenon is explained at the coronary-vessel level by deleterious effects of CO exposure on the endothelium NO-dependent vasorelaxation via eNOS uncoupling.

Moderate exercise prevents impaired Ca2+ handling in heart of CO-exposed rat: implication for sensitivity to ischemia-reperfusion.

Sustained urban carbon monoxide (CO) exposure exacerbates heart vulnerability to ischemia-reperfusion via deleterious effects on the antioxidant status and Ca(2+) homeostasis of cardiomyocytes. The aim of this work was to evaluate whether moderate exercise training prevents these effects. Wistar rats were randomly assigned to a control group and to CO groups, living during 4 wk in simulated urban CO pollution (30-100 parts/million, 12 h/day) with (CO-Ex) or sedentary without exercise (CO-Sed). The exercise procedure began 4 wk before CO exposure and was maintained twice a week in standard filtered air during CO exposure. On one set of rats, myocardial ischemia (30 min) and reperfusion (120 min) were performed on isolated perfused rat hearts. On another set of rats, myocardial antioxidant status and Ca(2+) handling were evaluated following environmental exposure. As a result, exercise training prevented CO-induced myocardial phenotypical changes. Indeed, exercise induced myocardial antioxidant status recovery in CO-exposed rats, which is accompanied by a normalization of sarco(endo)plasmic reticulum Ca(2+)-ATPase 2a expression and then of Ca(2+) handling. Importantly, in CO-exposed rats, the normalization of cardiomyocyte phenotype with moderate exercise was associated with a restored sensitivity of the myocardium to ischemia-reperfusion. Indeed, CO-Ex rats presented a lower infarct size and a significant decrease of reperfusion arrhythmias compared with their sedentary counterparts. To conclude, moderate exercise, by preventing CO-induced Ca(2+) handling and myocardial antioxidant status alterations, reduces heart vulnerability to ischemia-reperfusion.

Simulated urban carbon monoxide air pollution exacerbates rat heart ischemia-reperfusion injury.

Myocardial damages due to ischemia-reperfusion (I/R) are recognized to be the result of a complex interplay between genetic and environmental factors. Epidemiological studies suggested that, among environmental factors, carbon monoxide (CO) urban pollution can be linked to cardiac diseases and mortality. The aim of this work was to evaluate the impact of exposure to CO pollution on cardiac sensitivity to I/R. Regional myocardial I/R was performed on isolated perfused hearts from rats exposed for 4 wk to air enriched with CO (30-100 ppm). Functional variables, reperfusion ventricular arrhythmias (VA) and cellular damages (infarct size, lactate dehydrogenase release) were assessed. Sarcomere length shortening and Ca(2+) handling were evaluated in intact isolated cardiomyocytes during a cellular anoxia-reoxygenation protocol. The major results show that prolonged CO exposure worsens myocardial I/R injuries, resulting in increased severity of postischemic VA, impaired recovery of myocardial function, and increased infarct size (60 +/- 5 vs. 33 +/- 2% of ischemic zone). The aggravating effects of CO exposure on I/R could be explained by a reduced myocardial enzymatic antioxidant status (superoxide dismutase -45%; glutathione peroxidase -49%) associated with impaired intracellular Ca(2+) handling. In conclusion, our results are consistent with the idea that chronic CO pollution dramatically increases the severity of myocardial I/R injuries.

Active epidemiological surveillance of musculoskeletal disorders in a shoe factory.

AIMS: (1) To evaluate an active method of surveillance of musculoskeletal disorders (MSDs). (2) To compare different criteria for deciding whether or not a work situation could be considered at high risk of MSDs in a large, modern shoe factory. METHODS: A total of 253 blue collar workers were interviewed and examined by the same physician in 1996; 191 of them were re-examined in 1997. Risk factors of MSDs were assessed for each worker by standardised job site work analysis. Prevalence and incidence rates of carpal tunnel syndrome, rotator cuff syndrome, and tension neck syndrome were calculated for each of the nine main types of work situation. Different criteria used to assess situations with high risk of MSDs were compared. RESULTS: On the basis of prevalence data, three types of work situation were detected to be at high risk of MSDs: cutting, sewing, and assembly preparation. The three types of work situations identified on the basis of incidence data (sewing preparation, mechanised assembling, and finishing) were different from those identified by prevalence data. At least one recognised risk factor for MSDs was identified for all groups of work situations. The ergonomic risk could be considered as serious for the four types of work situation having the highest ergonomic scores (sewing, assembly preparation, pasting, and cutting). CONCLUSION: The results of the health surveillance method depend largely on the definition of the criteria used to define the risk of MSDs. The criteria based on incidence data are more valid than those based on prevalence data. Health and risk factor surveillance must be combined to predict the risk of MSDs in the company. However, exposure assessment plays a greater role in determining the priorities for ergonomic intervention.