ABSTRACT
BACKGROUND: At present, it is unclear whether older, obese persons with or without sarcopenia respond differently to training. Furthermore, there are no differentiated recommendations for resistance training for this special target group. OBJECTIVES: The objectives are to investigate the changes in the physical parameters of older, obese men caused by training and to reappraise the modalities of resistance training for older persons. DESIGN: Pre-test-post-test design. PARTICIPANTS: The participants were 33 physically inactive and obese older men (≥ 65 years, BMI ≥30 kg/m2), with-out severe diseases. Subjects were divided into two groups: NSAR (no or presarcopenia, n= 15) or SAR (sarcopenia, n= 18). INTERVENTION: The intervention consisted of progressive resistance training, twice a week for 16 weeks with finally 80-85% of maximum strength and three sets with 8-12 repetitions. The training contained six exercises for the major muscle groups. MEASUREMENTS: Sarcopenia was assessed using the Short Physical Performance Battery (SPPB), hand-grip strength, skeletal muscle mass index (SMI), and gait speed over a 6-meter walkway. Furthermore, the maximum dynamic strength (1 RM) was assessed. RESULTS: At baseline, the NSAR group had significantly better values in SMI, SPPB score, hand-grip strength, and 1 RM. After training, the results in both groups displayed an increase in 1 RM at the lower limbs (NSAR 18%, SAR 38%) and the upper limbs (NSAR 12%, SAR 14%). Also, the SPPB score (NSAR 11%, SAR 15%) and the 6-m-gait speed (NSAR 5%, SAR 10%) increased. The SAR group was able to increase their right hand-grip strength by 12%, whereas the NSAR group maintained their initial high strength values. SMI did not change in both groups. CONCLUSIONS: Both groups show improvements after resistance training with slightly more benefits for men with sarcopenia. Results of this study can be used to define specific training regimens for N(SAR) subjects.
ABSTRACT
Phenytoin (pht) is an anticonvulsant drug commonly used for the prevention of seizures. A common side effect of PHT therapy is gingival hyperplasia, occasionally so severe that it requires surgical intervention. Cyclosporine A (CSA) is a drug widely used for the control of rejection phenomena following solid organ and bone marrow transplantation. A frequent side effect of CSA administration is gingival overgrowth. As yet, the molecular mechanisms of drug-induced gingival hyperplasia are unknown although it has been postulated that certain drugs increase fibroblastic activity through alterations in levels of various growth factors and cytokines. The purpose of this study was to: 1) evaluate monocyte/macrophage platelet-derived growth factor (PDGF) and interleukin (IL)-1 beta production in vitro after exposure to CSA; 2) determine the levels of PDGF-B and IL-1 beta gene expression in minimally inflamed gingival tissues of control patients and PHT-treated patients exhibiting gingival overgrowth as well as patients with severe gingival inflammation; and 3) combine characterization of macrophage phenotype with clinical presentation and expression of PDGF-B and IL-1 beta in gingival tissues from the control and PHT-treated patients. For the in vitro studies, commercial ELISA kits were used to measure PDGF-A/PDGF-B and IL-1 beta levels in conditioned media from rat and human monocyte/macrophage cell cultures. CSA caused a significant elevation of PDGF but did not cause any changes in IL-1 beta levels. For the in vivo studies, quantitative competitive reverse transcription polymerase chain reaction (QC-RTPCR) techniques were utilized to measure PDGF-B and IL-1 beta mRNA levels in experimental groups. PHT-treated patients exhibiting gingival overgrowth demonstrated a significant increase in PDGF-B mRNA compared with minimally inflamed controls. Patients with severe gingival inflammation also demonstrated a significant increase in PDGF-B mRNA however, PHT-induced PDGF-B upregulation is approximately 6 times larger than PDGF-B upregulation produced by inflammation alone. PHT-treated patients exhibiting gingival overgrowth demonstrated no significant increase in IL-1 beta mRNA; however, IL-1 beta mRNA levels in the severely inflamed gingival samples demonstrated a significant increase. Additionally, for the clinical samples, macrophage phenotype was characterized immunohistochemically in adjacent sections using specific monoclonal antibodies for inflammatory and reparative/proliferative phenotypes. There were no significant differences in the numbers of either macrophage phenotype in minimally inflamed gingival tissues; however, in the severely inflamed tissue, there was a significant increase in the inflammatory macrophage phenotype and in the hyperplastic gingival tissue, there was a significant increase in the reparative/proliferative macrophage phenotype. The results of this investigation indicate that the clinical presentation of inflamed and hyperplastic gingival tissues is associated with specific macrophages phenotypes which express the pro-inflammatory cytokine IL-1 beta in inflamed tissues or the essential polypeptide growth factor PDGF-B in PHT-induced hyperplastic tissues.
