Nine untrained men (22-29 yr) performed 45 min of downhill running (16% incline, 70% of maximum heart rate). Needle biopsies of the vastus lateralis were performed before, 45 min after, and 5 days after exercise. Immunohistochemical staining of muscle cross sections revealed a 135% increase in muscle interleukin-1 beta (IL-1 beta) immediately after and a 250% increase (P < 0.03) 5 days after exercise. Using a rating scale (0-3) for the presence of neutrophils, light microscopic examination showed a significant accumulation of neutrophils in muscle biopsies taken 45 min after and 5 days after exercise [before: 0.5 +/- 0.2, 45 min after: 1.5 +/- 0.3 (P < 0.01), and 5 days after: 1.2 +/- 0.2 (P < 0.04)]. In addition, electron microscopic analysis showed an increase in the percentage of damaged Z-bands relative to total Z-bands [before: 4.8 +/- 3.5%, 45 min after: 32.5 +/- 8.6% (P < 0.05), and 5 days after: 14.1 +/- 3.2%]. Neutrophil accumulation was positively correlated to intracellular Z-band damage (rho = 0.66, P < 0.001). Immunohistochemical staining for IL-1 beta was related to neutrophil accumulation in muscle (rho = 0.38, P < 0.06) and to plasma creatine kinase levels (rho = 0.416, P < 0.04). These data indicate that after eccentric exercise ultrastructural damage to skeletal muscle is associated with neutrophil infiltration and muscle IL-1 beta accumulation.
To assess muscle remodeling and functional adaptation to exercise and diet interventions, 26 men and women aged 72–98 yr underwent a vastus lateralis biopsy before and after placebo control condition, and progressive resistance training, multinutrient supplementation, or both. Type II atrophy, Z band, and myofibril damage were present at baseline. Combined weight lifting and nutritional supplementation increased strength by 257 ± 62% ( P = 0.0001) and type II fiber area by 10.1 ± 9.0% ( P = 0.033), with a similar trend for type I fiber area (+12.8 ± 22.2%). Exercise was associated with a 2.5-fold increase in neonatal myosin staining ( P = 0.0009) and an increase of 491 ± 137% ( P < 0.0001) in IGF-I staining. Ultrastructural damage increased by 141 ± 59% after exercise training ( P = 0.034). Strength increases were largest in those with the greatest increases in myosin, IGF-I, damage, and caloric intake during the trial. Age-related sarcopenia appears largely confined to type II muscle fibers. Frail elders respond robustly to resistance training with musculoskeletal remodeling, and significant increases in muscle area are possible with resistance training in combination with adequate energy intakes.
Many countries have carried out over the past decade a series of reforms and measures to encourage longer working lives and to respond to the looming challenges of rapid population ageing. But have these steps gone far enough and have the necessary measures been taken? Much of the focus of this policy action has been on old-age pension reform but, as stressed in the report Live Longer, Work Longer (OECD 2006), a more comprehensive set of reform may be necessary to encourage work at an older age. This includes policy action in three broad areas to: (1) reward work, (2) change employer practices, and (3) improve the employability of workers. The aim of this paper is to provide an overview of recent policy initiatives to give older people better work incentives and choices implemented in France, The Netherlands, Norway and Switzerland since 2006 as well as to identify areas where more could be done, covering both supply-side and demand-side aspects.
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