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The purpose of the present study was to compare total knee arthroplasty (TKA) rehabilitation with and without whole-body vibration (WBV) to 1) understand if WBV is a useful treatment during TKA rehabilitation to increase quadriceps strength and function, and 2) to investigate the effect of WBV on quadriceps voluntary muscle activation. Subject and Methods. Individuals post TKA (WBV n=8, control n=8) received physical therapy with and without WBV for four weeks. Quadriceps strength and muscle activation, function, perceived pain, and knee range of motion were measured. Results. No adverse side effects were reported in either group. There was a significant increase in strength and function for both groups (P<0.01). There was no difference pre to posttest between groups for strength, muscle activation, or pain (Hotelling’s T2=0.42, P=.80) or for function (F=0.54, P=0.66). Discussion and Conclusion. In individuals with TKA, WBV showed equal strength and function improvement to physical therapy directed progressive resistive exercise. Influence of WBV on muscle activation remains unclear, as initial muscle activation was near established normal quadriceps levels and remained so post treatment.

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Context: Knee pain is a common symptom in knee pathology and is associated with alterations in quadriceps activation and movement patterns. Reducing pain through intervention may help reestablish neuromuscular function. The independent effects of knee pain are difficult to examine and unclear. Objective: To investigate the effects of transcutaneous electrical nerve stimulation (TENS) on quadriceps activation and vertical ground reaction force (VGRF) during walking. Design: Crossover. Setting: Laboratory. Subjects: 15 in the TENS group (10M and 5F, 23.5 ± 2.8 yrs, 70.5 ± 12.5 kg, 178.1 ± 7.4 cm), and 15 in the sham group (10M and 5F, 22.5 ± 2.0 yrs, 72.1 ± 13.7 kg, 177.5 ± 9.3 cm). Interventions: Subjects underwent three experimental conditions (pain, sham, and control). Measurements were recorded across four time points (preinfusion, infusion, treatment, and posttreatment). Hypertonic or isotonic saline, respectively, was infused into the infrapatellar fat pad for 48 minutes (total 7.7 mL). The TENS group received a 20-minute treatment. A sham treatment was administered to the sham group. Main Outcome Measures: Perceived knee pain on a 10-cm visual analog scale, knee extension maximum voluntary isometric contraction (MVIC) normalized to body mass, knee extension central activation ratio (CAR), and VGRF. Results: Knee pain peaked at 4 cm during infusion and remained consistent across time in the sham group (F2,28 = 49.90, P < 0.0001), while knee pain gradually decreased to 1.5 cm following TENS treatment (F2,28 = 23.11, P < 0.0001). A group x condition x time interaction was detected for both the MVIC (F6,168 = 2.92, P < 0.01) and CAR (F6,168 = 3.03, P < 0.008) measurements. Post hoc analysis revealed that the infusion of hypertonic saline reduced knee extension MVIC by 29% in the TENS group, and by 26% in the sham group (P < 0.05). However, while the MVIC remained depressed by 26% following sham treatment, the MVIC was found to improve by 12% following TENS treatment (P < 0.05). Similarly, a 10% decrease in CAR was detected in both sham and TENS groups prior to treatment. This 10% deficit held, with a 9% deficit following sham treatment, while the deficit of CAR was improved by 4% following TENS treatment (P < 0.05). For the TENS group, infusion of hypertonic saline changed VGRF at initial loading, midstance, and push-off phase. VGRF was only different at initial loading and push-off phase following TENS treatment. For the sham group however, sham treatment did not restore VGRF, showing alterations in initial loading, midstance, and push-off phase (α = 0.05). Conclusions: Infusion of hypertonic saline increased perceived knee pain, reduced knee extension MVIC, reduced CAR, and altered VGRF over some of stance phase. TENS lessened the deficits in MVIC, CAR, and VGRF, suggesting decreased muscle inhibition and improved movement function.

En relation avec sa position anatomique, la détection portale de nutriments se situe au coeur de l’impact de la composition nutritionnelle d’un repas sur la prise alimentaire et le métabolisme énergétique. Ainsi, la détection portale de glucose, produit par exemple en réponse aux protéines alimentaires, induit un signal nerveux à l’origine d’une induction de la satiété et d’une amélioration de l’homéostasie glucidique. Grâce à des travaux physiologiques et anatomiques chez le rat, nous proposons un modèle pour cette détection dans lequel deux modes interviennent, soit un transport et un catabolisme intracellulaire, soit une détection purement extracellulaire du glucose. La glycémie portale est détectée par l’un ou l’autre de ces mécanismes en fonction de sa différence avec la glycémie artérielle, reflet du statut nutritionnel et métabolique des individus. Un signal nerveux est ensuite initié dans les neurones périportaux, dont les axones aboutissent à proximité de la lumière veineuse. Les études immunohistochimiques réalisées ont permis de montrer que ce signal induit une activation cérébrale étendue en relation avec les effets multiples du glucose portal, dans le tronc cérébral, les systèmes sensoriels et cortico-limbiques, et l’hypothalamus. Dans ce dernier, la nature cellulaire de l’activation conforte notamment l’hypothèse de l’implication du signal glucose portal dans l’effet de satiété induit par les régimes riches en protéines. / Nutrient sensing in the portal vein occurs in a strategic location to relay the effects of the diet on food intake and energy metabolism. The portal sensing of glucose produced for instance in response to dietary proteins initiates a nervous signal that ultimately induces satiety and a better control of glucose metabolism. Our physiological and anatomical approaches enable us to propose a sensing model in which two different mechanisms can occur, involving either the intracellular transport and catabolism of glucose or a direct extracellular detection. Portal glycaemia is detected by one pathway or the other depending on its difference with arterial blood glucose, which reflects the nutritional and metabolic state of the subject. A nervous signal is then initiated in periportal neurons, whose axons terminate close to the venous lumen. Our immunohistochemical studies have shown that this signal induces a widespread activation in the brain that relates to the multiple effects of portal glucose appearance, in the brainstem, the sensory and cortico-limbic systems and the hypothalamus. In this latter area, the cellular nature of the activation supports the hypothesized central role of portal glucose appearance in the satiety effect of high-protein diets.

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No description available.