Can whole body vibration exercises promote improvement on quality of life and on chronic pain level of metabolic syndrome patients? A pseudorandomized crossover study.

Quality of life (QoL) is one of the most important health outcome concepts expressed subjectively. Chronic pain (CP) is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Taking into account the poor QoL and the CP already described in metabolic syndrome (MSy) individuals, this study aimed to evaluate the effects of whole body vibration exercises (WBVE) on these parameters in this population. Thirty-three MSy patients were divided in subgroups A [whole body vibration exercise group (WBVeG), n = 17, 15 females/2 males, 61.1 ± 8.4 yr] and B (control group, n = 16, 14 females/2 males, 58.2 ± 9.1 yr). Subgroup A performed 10 sessions (2 times/wk) of WBVE (18 min/session, with a frequency from 5 up to 14 Hz and a peak-to-peak displacement of 2.5, 5.0, and 7.5 mm) on a side-alternating vibrating platform (VP). Subgroup B did the same protocol, but the VP was turned off. The individuals answered the World Health Organization Quality of Life bref (WHOQoL-bref) questionnaire before the first and after the 10th session. The chronic pain level (CPL) was measured by a numeric rating scale (0-10) before and at the end of each session. Significant improvements were found in physical health (P = 0.05) and psychological health (P = 0.04) domains of WHOQoL-bref in WBVeG. A significant acute reduction of the CPL was found in the WBVeG after the protocol, considering the first session and at the last session. WBVE marginally improved physical health and psychological health and decrease the CPL in acute interventions.NEW & NOTEWORTHY Metabolic syndrome patients experience poor quality of life, frequently associated with lack of exercise and bad dietary habits. Additionally, factors such as obesity, neuromusculoskeletal impairment, and peripheral endothelial dysfunction result in a chronic pain level. Whole body vibration exercise might represent a suitable physical therapy, since it is easy to perform, low cost, safe, and capable of promoting an improvement of quality of life and reducing chronic pain level during acute interventions in metabolic syndrome individuals.

Inhibition of mitogen-activated protein/extracellular signal-regulated kinase improves endothelial function and attenuates Ang II-induced contractility of mesenteric resistance arteries from spontaneously hypertensive rats.

OBJECTIVES: Extracellular signal-regulated kinases (ERK1/2) modulate vascular smooth muscle cell (VSMC) growth and contractility, important factors in blood pressure regulation. In the present in vivo study, we investigated whether short-term inhibition of ERK1/2-dependent signaling pathways influences vascular function and blood pressure (BP) in spontaneously hypertensive rats (SHR). METHODS: SHR and Wistar-Kyoto (WKY) rats were injected subcutaneously with either PD98059, selective MEK1/2 inhibitor (20 mg/kg), or vehicle. BP was measured by telemetry. Rats were killed 24 h after injection and small mesenteric arteries mounted as pressurized systems for morphometric analysis and assessment of endothelial function and angiotensin II (Ang II)-induced contractility. ERK1/2 phosphorylation was measured by Western blots, using protein extracts from mesenteric arteries, aorta, heart and kidneys. RESULTS: BP was higher (P < 0.01) in SHR than in WKY rats. PD98059 did not influence BP in either group. Endothelial-dependent relaxation (acetylcholine-induced), which was impaired in SHR, was improved by PD98059 (P < 0.05). Ang II increased contraction, with greater responses in SHR (Emax = 25 +/- 4%) than WKY (Emax = 9 +/- 3%) (P < 0.01). PD98059 reduced Ang II-induced contraction in SHR (Emax = 5.8 +/- 0.4%) and WKY (Emax = 4 +/- 0.4%). Vascular structure was unaltered by PD98059. Vascular and renal ERK1/2 phosphorylation, which was higher in SHR than WKY, was decreased by PD98059 in SHR. CONCLUSION: Short-term treatment with PD98059 improves endothelial function and vascular contractility without influencing BP in SHR. These findings provide evidence that vascular ERK1/2 activity is upregulated and that MEK1/2-sensitive signaling pathways play an important role in the regulation of vascular function in SHR. Acute inhibition of MEK1/2 does not alter blood pressure despite improved endothelial function and reduced arterial reactivity to Ang II.