Current guidelines recommend weight-bearing activities, preferably strength training for improving skeletal health in patients with osteoporosis. What type of strength training that is most beneficial for these patients is not established. Maximal strength training (MST) is known to improve 1-repetition maximum (1RM) and rate of force development (RFD), which are considered as important covariables for skeletal health. Squat exercise MST might serve as an effective intervention for patients with low bone mass. We hypothesized that 12 weeks of squat exercise MST would improve 1RM and RFD in postmenopausal women with osteoporosis or osteopenia and that these changes would coincide with improved bone mineral density (BMD) and bone mineral content (BMC), and serum markers of bone metabolism. The participants were randomized to a training group (TG, n = 10) or control group (CG, n = 11). The TG underwent 12 weeks of supervised squat exercise MST, 3 times a week, with emphasis on rapid initiation of the concentric part of the movement. The CG was encouraged to follow current exercise guidelines. Measurements included 1RM, RFD, BMD, BMC, and serum bone metabolism markers; type 1 collagen amino-terminal propeptide (P1NP) and type 1 collagen C breakdown products (CTX). At posttest, 8 participants remained in each group for statistical analyses. The TG improved the 1RM and RFD by 154 and 52%, respectively. Lumbar spine and femoral neck BMC increased by 2.9 and 4.9%. The ratio of serum P1NP/CTX tended to increase (p = 0.09), indicating stimulation of bone formation. In conclusion, squat exercise MST improved 1RM, RFD, and skeletal properties in postmenopausal women with osteopenia or osteoporosis. The MST can be implemented as a simple and effective training method for patients with reduced bone mass.
Peripheral arterial disease (PAD) patients have reduced muscle strength and impaired walking ability. The aim of this study was to examine the effects of maximal strength training (MST) on walking economy and walking performance in PAD patients. Ten patients with mild to moderate-severe claudication, classified as Fontaine stage II PAD and with functional limitations from intermittent claudication were recruited and went through an 8-week control period followed by an 8-week, three times a week, MST period. The patients performed four sets of five repetitions dynamic leg press with emphasis on maximal mobilization of force in the concentric action and with a progressive adjusted intensity corresponding to 85-90% of one repetition maximum (1 RM). After the MST period, leg press 1 RM significantly increased by 35.0 ± 10.8 kg (31.3%). Dynamic rate of force development, measured on a force plate installed on the leg press, increased by 1424 ± 1217 N/s (102.7%). The strength improvements led to a significant increase in walking economy of 9.7% when walking horizontally, and to a significant increase in walking performance of 13.6% measured on an incremental treadmill test to exhaustion. No changes were apparent after the control period. No changes in body mass or peak oxygen uptake were observed. MST increases strength in Fontaine stage II PAD patients and leads to improved walking economy. These results suggest that application of MST could accompany aerobic endurance training as a part of the treatment of PAD patients with mild to moderate-severe claudication.
This study examined whether a training intervention likely to elicit adaptations in the leg could result in reduced leg pain and increased whole body physical capacity. Twenty-seven peripheral arterial disease (PAD) patients were randomized to either an individual leg plantar flexion training group (TG) training 4 x 4 min intervals at 80% of maximal work rate three times per week for 8 weeks or a control group. The TG significantly increased plantar flexion peak oxygen uptake and power output by 23.5 and 43.9%, respectively. Treadmill peak oxygen uptake (VO(2peak)) significantly increased 12.3% in the TG and was associated with a significant increased time to exhaustion of 20.0% when treadmill walking. Eleven of 14 patients no longer reported leg pain limitations at VO(2peak). No differences in cardiac output measured at VO(2peak), or walking economy were observed. Plantar flexion training was effective in increasing VO(2peak) and walking performance, and may be a useful strategy in treatment of PAD.
Background: There is increasing evidence that reduced ocular blood flow plays a role in the pathogenesis of glaucoma. In patients with normal-tension glaucoma, ocular blood flow abnormalities may be associated with dysfunction of the endothelin 1 (ET-1) regulation system. Objective: To test the hypothesis that unoprostone, a topical docosanoid, may affect ET-1-induced vasoconstriction in the human choroid. Methods: In a placebo-controlled, randomized, doublemasked, 2-way crossover design, ET-1 (2.5 ng/kg per minute for 150 minutes) was administered intravenously to 24 healthy individuals. Thirty minutes after the start of ET-1 infusion, 1 drop of unoprostone or placebo was instilled into the right eye. After another 30 minutes, 2 drops of unoprostone or placebo was topically administered. This procedure was continued and the dose was increased further until 4 drops of unoprostone or placebo was reached. Subfoveal and pulsatile choroidal blood flow were assessed using laser Doppler flowmetry and laser interferometric measurement of fundus pulsation amplitude, respectively. Results: Administration of exogenous ET-1 decreased choroidal blood flow (mean±SEM, 17%±2%; PϽ.001) and fundus pulsation amplitude (mean±SEM, 19%±2%; PϽ.001). This effect was significantly blunted when topical unoprostone was coadministered (mean ± SEM decrease in choroidal blood flow, 7%±2%; P =.04 vs placebo; mean±SEM decrease in fundus pulsation amplitude, 12%±2%; PϽ.001 vs placebo). Conclusion: There is a functional antagonism between ET-1 and topical unoprostone in the choroidal vasculature. Clinical Relevance: Our findings of a functional antagonism between ET-1 and topical unoprostone in the choroidal vasculature may be important in vascular eye diseases associated with increased ET-1.
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