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1.
S Afr J Physiother ; 80(1): 1954, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38322655

RESUMO

Background: Partial vascular occlusion (PVO) can increase muscle strength and hypertrophy without joint overload. However, PVO could increase the possibility of imbalances and injuries during physical activity. Objectives: To identify changes in strength, muscle activation, and postural control during the use of PVO in young women. Method: A total of 14 healthy women aged between 18 and 30 years were evaluated. Dynamometry was used to analyse the strength of the quadriceps muscle, and surface electromyography to evaluate quadriceps muscle activity. A force platform was utilised to assess postural control, static single-legged support, single-legged squat, and climbing and descending stairs. Participants were randomly assigned to the evaluations either with or without PVO. The results were compared and correlated. Results: The performance of static, dynamic, or stair exercises, with or without PVO, did not indicate differences in muscle strength and recruitment (p > 0.05). The use of PVO improved the velocity of anteroposterior (AP) oscillation of static postural control (p = 0.001). We found a moderate negative correlation between muscle strength and postural control during the ascending stairs task with the use of PVO (r = -0.54; r = -0.59), while in the group without PVO, the correlation was moderate to high (r = -0.55; r = -0.76). Conclusion: The use of PVO did not impair muscle strength and recruitment of the quadriceps or postural control in healthy women. Clinical Implications: Partial vascular occlusion can be used during dynamic exercises without impairing the balance and muscle strength of the quadriceps during its execution.

2.
J Cachexia Sarcopenia Muscle ; 14(4): 1621-1630, 2023 08.
Artigo em Inglês | MEDLINE | ID: mdl-37177862

RESUMO

BACKGROUND: Cachexia is a wasting syndrome associated with systemic inflammation and metabolic disruption. Detection of the early signs of the disease may contribute to the effective attenuation of associated symptoms. Despite playing a central role in the control of metabolism and inflammation, the liver has received little attention in cachexia. We previously described relevant disruption of metabolic pathways in the organ in an animal model of cachexia, and herein, we adopt the same model to investigate temporal onset of inflammation in the liver. The aim was thus to study inflammation in rodent liver in the well-characterized cachexia model of Walker 256 carcinosarcoma and, in addition, to describe inflammatory alterations in the liver of one cachectic colon cancer patient, as compared to one control and one weight-stable cancer patient. METHODS: Colon cancer patients (one weight stable [WSC] and one cachectic [CC]) and one patient undergoing surgery for cholelithiasis (control, n = 1) were enrolled in the study, after obtainment of fully informed consent. Eight-week-old male rats were subcutaneously inoculated with a Walker 256 carcinosarcoma cell suspension (2 × 107 cells in 1.0 mL; tumour-bearing [T]; or phosphate-buffered saline-controls [C]). The liver was excised on Days 0 (n = 5), 7 (n = 5) and 14 (n = 5) after tumour cell injection. RESULTS: In rodent cachexia, we found progressively higher numbers of CD68+ myeloid cells in the liver along cancer-cachexia development. Similar findings are described for CC, whose liver showed infiltration of the same cell type, compared with both WSC and control patient organs. In advanced rodent cachexia, hepatic phosphorylated c-Jun N-terminal kinase protein content and the inflammasome pathway protein expression were increased in relation to baseline (P < 0.05). These changes were accompanied by augmented expression of the active interleukin-1ß (IL-1ß) form (P < 0.05 for both circulating and hepatic content). CONCLUSIONS: The results show that cancer cachexia is associated with an increase in the number of myeloid cells in rodent and human liver and with modulation of hepatic inflammasome pathway. The latter contributes to the aggravation of systemic inflammation, through increased release of IL-1ß.


Assuntos
Carcinossarcoma , Neoplasias do Colo , Humanos , Masculino , Ratos , Animais , Caquexia/patologia , Inflamassomos/metabolismo , Fígado/metabolismo , Inflamação/metabolismo , Neoplasias do Colo/complicações , Carcinossarcoma/complicações , Carcinossarcoma/metabolismo
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