This study investigated the influence of age on the functional status of mitochondria isolated from skeletal muscle of C57BL/6 mice aged 3 and 18 months. We hypothesized that skeletal muscle mitochondria isolated from aged animals will exhibit a decreased respiratory function. Mitochondrial respiratory functional measures (ie, State 3 and 4 respiration, respiratory control ratio and number of nanomoles of ADP phosphorylated by nanomoles of O(2) consumed per mitochondrion) and biochemical markers of oxidative damage (aconitase activity, protein carbonyl derivatives, sulfhydryl groups, and malondialdehyde) were measured in isolated mitochondrial suspensions. Along with traditional tests of mitochondrial function, an in vitro repetitive ADP-stimulation test was used to evaluate the mitochondrial capacity to reestablish the homeostatic balance between successive ADP stimulations. The number of mitochondria per mitochondrial suspension, calculated by transmission electron microscopy, was used to normalize functional and biochemical data. Our results confirm the existence of an age-associated decline in mitochondrial function of mixed skeletal muscle, which is significantly correlated with higher levels of mitochondrial oxidative damage.

Aging can be characterized as a time dependent decline of maximal functionality that affects tissues and organs of the whole body. Such is induced by the progressive loss of redundant components and leads to an increased susceptibility to disease and risk of death. Regarding the aging of skeletal muscle, it has been pointed out that mitochondria is a key factor behind the loss of redundancy and functionality, since this organelle has a major role in cellular homeostasis particularly at the level of the bioenergetic status. Decreased activities of the mitochondrial electron transport chain complexes and an increased release of reactive oxygen species from mitochondria are well documented with age; it is suggested that the mitochondrial loss of function results from the increased oxidative damage to proteins, lipids, and DNA of this organelle. However, it is important to be aware that the mitochondrial loss of function could also be a consequence, rather than a cause, of the cellular deterioration with age, which compromises mitochondrial biogenesis, mitochondrial protein turnover and autophagocytosis of damaged mitochondria. In this review several topics will be addressed regarding the age-related loss of skeletal muscle redundancy associated with mitochondrial dysfunction, emphasizing hypotheses for underlying mechanisms. In addition, we discuss some of the cellular mechanisms that can be pointed out as being responsible for the age-related mitochondrial dysfunction.

The purpose of the current study was to assess and to compare the hydrodynamics of the first and second gliding positions of the breaststroke underwater stroke used after starts and turns, considering drag force (D), drag coefficient (CD) and cross-sectional area (S). Twelve national-level swimmers were tested (6 males and 6 females, respectively 18.2 ± 4.0 and 17.3 ± 3.0 years old). Hydrodynamic parameters were assessed through inverse dynamics from the velocity to time curve characteristic of the underwater armstroke of the breaststroke technique. The results allow us to conclude that, for the same gliding velocities (1.37 ± 0.124 m/s), D and the swimmers’ S and CD values obtained for the first gliding position are significantly lower than the corresponding values obtained for the second gliding position of the breaststroke underwater stroke (31.67 ± 6.44 N vs. 46.25 ± 7.22 N; 740.42 ± 101.89 cm2 vs. 784.25 ± 99.62 cm2 and 0.458 ± 0.076 vs. 0.664 ± 0.234, respectively). These differences observed for the total sample were not evident for each one of the gender’s subgroups.

This study investigated the impact of lifelong sedentariness on skeletal muscle mass and mitochondrial function. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young-Y; old sedentary-OS; old active-OA). Young animals were sacrificed after 1 week of quarantine, and OS and OA groups were individually placed into standard cages and in cages with running wheels, respectively, until sacrifice (25 months). Body weights and hind-limb skeletal muscle wet weights were obtained from all groups. Mitochondrial respiratory functional measures (i.e., state 3 and 4 respiration, respiratory control ratio, and ratio of nanomoles of ADP phosphorylated by nanomoles of O2 consumed [ADP/O]) and biochemical markers of oxidative damage (aconitase activity, protein carbonyl derivatives, sulfhydryl groups) were measured in isolated mitochondrial suspensions. Our results reveal that lifelong sedentary behavior has a negative impact on the age-related loss of skeletal muscle mass and on the isolated mitochondrial function of mixed skeletal muscle of mice, which is associated with an increased oxidative damage to mitochondrial biomolecules.

Several in vitro studies about age-associated skeletal muscle mitochondrial dysfunction are somewhat conflicting, and this might be related to different normalization procedures. The objective of this study was to normalize the functional and biochemical data per number of mitochondria present in a mitochondrial suspension. Functional and biochemical parameters were obtained in mitochondrial suspensions from murine skeletal muscle of different ages. Mitochondrial respiratory function was polarographically measured using a Clark-type oxygen electrode. Biochemical analyses included determination of citrate synthase (CS) activity and total protein content in the mitochondrial suspension. Electron microscopy analysis of the suspensions allowed calculation of the number of mitochondria per milligram of protein. Our results conclude that advanced age is associated with mitochondrial dysfunction; moreover, from the correlation between morphological and biochemical data, it is evident that CS activity in the mitochondrial suspensions is a more accurate marker of mitochondrial mass than is total protein content.