Experimental denervation modulates mitochondrial function, where changes in both reactive oxygen species (ROS) and sensitivity to permeability transition are implicated in the resultant muscle atrophy. Notably, although denervation occurs sporadically in ageing muscle, its impact on ageing muscle mitochondria is unknown. Because this information has important therapeutic implications concerning targeting the mitochondrion in ageing muscle, we examined mitochondrial function in skeletal muscle from four groups of humans, comprising two active (mean ± SD age: 23.7 ± 2.7 years and 71.2 ± 4.9 years) and two inactive groups (64.8 ± 3.1 years and 82.5 ± 4.8 years), and compared this with a murine model of sporadic denervation. We tested the hypothesis that, although some alterations of mitochondrial function in aged muscle are attributable to a primary organelle defect, mitochondrial dysfunction would be impacted by persistent denervation in advanced age. Both ageing in humans and sporadic denervation in mice increased mitochondrial sensitivity to permeability transition (humans, P = 0.004; mice, P = 0.01). To determine the contribution of sporadic denervation to mitochondrial function, we pharmacologically inhibited the denervation-induced ROS response. This reduced ROS emission by 60% (P = 0.02) in sporadically denervated mouse muscle, which is similar to that seen in humans older than 75 years (-66%, P = 0.02) but not those younger than 75 years. We conclude that an increased sensitivity to permeability transition is a primary mitochondrial defect in ageing muscle. However, at more advanced age, when muscle atrophy becomes more clinically severe, mitochondrial function changes are markedly impacted by persistent sporadic denervation, making the mitochondrion a less viable therapeutic target.
Normal adult aging is associated with impaired muscle contractile function; however, to what extent cross-bridge kinetics are altered in aging muscle is not clear. We used a slacken restretch maneuver on single muscle fiber segments biopsied from the vastus lateralis of young adults (∼23 yr), older nonathlete (NA) adults (∼80 yr), and age-matched world class masters athletes (MA; ∼80 yr) to assess the rate of force redevelopment (ktr) and cross-bridge kinetics. A post hoc analysis was performed, and only the mechanical properties of "slow type" fibers based on unloaded shortening velocity (Vo) measurements are reported. The MA and NA were ∼54 and 43% weaker, respectively, for specific force compared with young. Similarly, when force was normalized to cross-sectional area determined via the fiber shape angularity data, both old groups did not differ, and the MA and NA were ∼43 and 48% weaker, respectively, compared with young (P < 0.05). Vo for both MA and NA old groups was 62 and 46% slower, respectively, compared with young. Both MA and NA adults had approximately two times slower values for ktr compared with young. The slower Vo in both old groups relative to young, coupled with a similarly reduced ktr, suggests impaired cross-bridge kinetics are responsible for impaired single fiber contractile properties with aging. These results challenge the widely accepted resilience of slow type fibers to cellular aging.
stand the risk of disease (e.g., type 2 diabetes) and/or mortality, at least in part, of an individual and as such provide useful information to health professionals. Therefore, the purpose of the present study was to examine the relationship between long sleep duration and functional capacities in a well-characterized population of sedentary postmenopausal women, a group at increased risk for developing functional capacities. Based on the study of Patel et al., 6 which showed negative health outcomes in long sleepers, we hypothesized that long (> 9 h) sleep duration would be associated with lower functional capacities.
Study Objective:The purpose of the present study was to examine the relationship between long sleep duration and functional capacities. Methods: We conducted a cross-sectional study at the Department of Kinanthropology at the University of Quebec at Montreal. Forty eight non-frail postmenopausal women aged between 49 to 75 years were recruited using advertisements in local papers. Body weight, body mass index, fat mass, skeletal muscle mass, number of steps per day, SF-36 total (healthy questionnaire), resting metabolic rate, total energy intake, sleep duration, knee extensor strength (dynamometer), chair stand test and balance opened eyes test were measured.
Tai chi training improved body composition, muscle strength, functional capacities, and general health perception in postmenopausal women, and this last improvement was more pronounced in type I dynapenic individuals. Therefore, tai chi may be considered as an alternative physical training method in preventing the occurrence of disabilities and frailty in postmenopausal women with type I dynapenia.
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