References of "Juchmes-Ferir, A"
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See detailEffects of Training on Exercise-Induced Muscle Damage and Interleukin 6 Production
Croisier, Jean-Louis ULg; Camus, G.; Venneman, Ingrid ULg et al

in Muscle & Nerve (1999), 22(2), 208-12

To address the question of whether the increased plasma concentration of interleukin 6 (IL-6) following strenuous muscular work could be related to exercise-induced muscle damage, 5 moderately active male ... [more ▼]

To address the question of whether the increased plasma concentration of interleukin 6 (IL-6) following strenuous muscular work could be related to exercise-induced muscle damage, 5 moderately active male volunteers underwent two isokinetic exercise sessions in the eccentric mode, separated by a period of 3 weeks during which the subjects underwent five training sessions. Before training, exercise was followed by severe muscle pain (delayed-onset muscle soreness; DOMS), and by significant increases in plasma IL-6 level and serum myoglobin concentration (SMb) (P < 0.001). After training, postexercise DOMS and SMb values were significantly lower than those measured before training. There was no significant difference between plasma IL-6 levels measured at the same time points before and after training. We conclude that the hypothetical relationship between exercise-induced muscle damage and increased postexercise levels of circulating IL-6 is not substantiated by the present results. [less ▲]

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See detailEffects of training on myocellular enzyme leakage and delayed onset muscle soreness following maximal isokinetic eccentric exercise
Croisier, Jean-Louis ULg; Camus, Gérard; Duchateau, J. et al

in Mediators of Inflammation (1997), 6

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See detailPiroxicam fails to reduce myocellular enzyme leakage and delayed onset muscle soreness induced by isokinetic eccentric exercise
Croisier, Jean-Louis ULg; Camus, Gérard; Deby-Dupont, G. et al

in Pflügers Archiv : European Journal of Physiology (1996), 431

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See detailMyocellular Enzyme Leakage, Polymorphonuclear Neutrophil Activation and Delayed Onset Muscle Soreness Induced by Isokinetic Eccentric Exercise
Croisier, Jean-Louis ULg; Camus, Gérard; Deby-Dupont, G. et al

in Archives of Physiology & Biochemistry (1996), 104(3), 322-9

To address the question of whether delayed onset muscular soreness (DOMS) following intense eccentric muscle contraction could be due to increased production of the arachidonic acid derived product ... [more ▼]

To address the question of whether delayed onset muscular soreness (DOMS) following intense eccentric muscle contraction could be due to increased production of the arachidonic acid derived product prostaglandin E2 (PGE2). 10 healthy male subjects were submitted to eccentric and concentric isokinetic exercises on a Kin Trex device at 60 degrees/s angular velocity. Exercise consisted of 8 stages of 5 maximal contractions of the knee extensor and flexor muscle groups of both legs separated by 1 min rest phases. There was an interval of at least 30 days between eccentric and concentric testing, and the order of the two exercise sessions was randomly assigned. The subjective presence and intensity of DOMS was evaluated using a visual analogue scale, immediately, following 24 h and 48 h after each test. Five blood samples were drawn from an antecubital vein: at rest before exercise, immediately after, after 30 min recovery, 24 h and 48 h after the tests. The magnitude of the acute inflammatory response to exercise was assessed by measuring plasma levels of polymorphonuclear elastase ([EL]), myeloperoxidase ([MPO]) and PGE2 ([PGE2]). Using two way analysis of variance, it appeared that only eccentric exercise significantly increased [EL] and DOMS, especially of the hamstring muscles. Furthermore, a significant decrease in eccentric peak torque of this muscle group only was observed on day 2 after eccentric work (- 21%; P < 0.002). Serum activity of creatine kinase and serum concentration of myoglobin increased significantly 24 and 48 h after both exercise tests. However, these variables reached significantly higher values following eccentric contractions 48 h after exercise. Mean [PGE2] in the two exercise modes remained unchanged over time and were practically equal at each time point. On the basis of these findings, we conclude that the magnitude of polymorphonuclear (PMN) activation, muscle damage, and DOMS are greater after eccentric than after concentric muscle contractions. However, the hypothesized interplay between muscle damage, increased PGE2 production, DOMS sensations, and reduced isokinetic muscle performance was not substantiated by the present results. [less ▲]

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See detailPiroxicam fails to reduce myocellular enzyme leakage and delayed onset muscle soreness induced by isokinetic eccentric exercise.
Croisier, Jean-Louis ULg; Camus, G.; Monfils, T. et al

in Mediators of Inflammation (1996), 5(3), 230-4

To test the hypothesis that delayed onset muscular soreness (DOMS) following intense eccentric muscle contraction could be due to increased production of prostaglandin E(2) (PGE(2)), ten healthy male ... [more ▼]

To test the hypothesis that delayed onset muscular soreness (DOMS) following intense eccentric muscle contraction could be due to increased production of prostaglandin E(2) (PGE(2)), ten healthy male subjects were studied. Using a double-blind randomized crossover design, each subject performed two isokinetic tests separated by a period of at least 6 weeks: once with placebo, and once with piroxicam (Feldene((R))). They were given one capsule containing either placebo or piroxicam (20 mg) per day for 6 days with initial doses given starting 3 days prior to isokinetic testing. Exercise consisted of eight stages of five maximal contractions of the knee extensor and flexor muscle groups of both legs separated by 1 min rest phases, on a Kin Trex device at 60( degrees )/s angular velocity. The subjective presence and intensity of DOMS were evaluated using a visual analogue scale immediately after, and 24 and 48 h after each test. The mean plasma concentration of PGE(2) measured at rest and after exercise was significantly lower in the group treated with piroxicam (p < 0.05). However, statistical analysis (two-way ANOVA test) revealed that exercise did not cause any significant change of mean plasma PGE(2) over time in either of the two groups. Eccentric work was followed by severe muscle pain in extensor and flexor muscle groups. Maximal soreness was noted 48 h postexercise. Serum creatine kinase activity and the serum concentration of myoglobin increased significantly, and reached peak values 48 h after exercise in both experimental conditions (p < 0.001). By paired t-test, it appeared that there were no significant differences in the serum levels of these two markers of muscle damage between the two groups at any time point. We conclude that: (1) oral administration of piroxicam fails to reduce muscle damage and DOMS caused by strenuous eccentric exercise; and (2) the hypothetical role of increased PGE(2) production in eccentric exercise-induced muscle damage, DOMS, and reduced isokinetic performance is not substantiated by the present results. [less ▲]

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See detailAnaphylatoxin C5a Production During Short-Term Submaximal Dynamic Exercise in Man
Camus, G.; Duchateau, J.; Deby, Ginette ULg et al

in International Journal of Sports Medicine (1994), 15(1), 32-5

We studied the effects of short-term submaximal exercise on the plasma levels of myeloperoxidase ([MPO]) and C5a anaphylatoxin ([C5a]), taken as specific markers of polymorphonuclear neutrophil (PMN) and ... [more ▼]

We studied the effects of short-term submaximal exercise on the plasma levels of myeloperoxidase ([MPO]) and C5a anaphylatoxin ([C5a]), taken as specific markers of polymorphonuclear neutrophil (PMN) and complement activation, respectively. Eleven young, healthy male volunteers were subjected to a constant-load concentric exercise on a cycle ergometer (20 min at 80% maximal oxygen uptake). Mean resting MPO and C5a concentrations were 437 +/- 113 and 0.47 +/- 0.21 ng/ml, respectively. During exercise, [MPO] and [C5a] increased significantly (p < 0.001) towards respective peak values of 649 +/- 131 and 1.3 +/- 0.6 ng/ml. A rapid decrease of both [MPO] and [C5a] was observed during recovery. The similar time course of [MPO] and [C5a] changes and the highly significant relationship between these two variables (r = 0.651; p < 0.001) argues for the possible involvement of the complement anaphylatoxin C5a in the process of PMN degranulation. During exercise, the number of circulating PMN increased (+80%; p < 0.001) and remained practically unchanged up to 20 minutes of recovery. As [MPO] and PMN count were not significantly related (r = 0.2; p < 0.1), we concluded that the activation of PMN was independent of their mobilization. [less ▲]

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