Studying organelles in isolation has been proven to be indispensable for deciphering the underlying mechanisms of molecular cell biology. However, observing organelles in intact cells with the use of microscopic techniques reveals a new set of different junctions and contact sites between them that contribute to the control and regulation of various cellular processes, such as calcium and lipid exchange or structural reorganization of the mitochondrial network. In recent years, many studies focused their attention on the structure and function of contacts between mitochondria and other organelles. From these studies, findings emerged showing that these contacts are involved in various processes, such as lipid synthesis and trafficking, modulation of mitochondrial morphology, endoplasmic reticulum (ER) stress, apoptosis, autophagy, inflammation and Ca2+ handling. In this review, we focused on the physical interactions of mitochondria with the endoplasmic reticulum and plasma membrane and summarized present knowledge regarding the role of mitochondria-associated membranes in calcium homeostasis and lipid metabolism.

Literature has shown that children have lower anaerobic capacity and oxidize more lipids during aerobic activity compared with adults. The purpose of the present study was to examine the effects of age on the activity of marker enzymes for anaerobic and aerobic metabolism in human skeletal muscle from relatively sedentary children and adults. The m. obliquus internus abdominis was analyzed for anaerobic [creatine kinase, adenylate kinase, and lactate dehydrogenase (LDH)] and aerobic (carnitine palmitoyltransferase and 2-oxoglutarate dehydrogenase) enzyme activities in 32 male individuals. The subjects were divided into two groups: children (3-11 y; n ϭ 20) and adults (29 -54 y; n ϭ 12). LDH activity was higher in adults (118.2 Ϯ 20.1) compared with children (27.8 Ϯ 10.1) mol · min Ϫ1 · g Ϫ1 wet weight (p Ͻ 0.0002). Creatine kinase activity was 28% (p Ͻ 0.0003) lower in children than in adults, and adenylate kinase activity was 20% (p Ͻ 0.006) lower in children than in adults. In addition, we found higher 2-oxoglutarate dehydrogenase activity in adults compared with children (p Ͻ 0.04), with no effect of age on carnitine palmitoyltransferase activity (NS). When samples were expressed relative to protein content, only LDH activity remained significantly lower in children compared with adults (p Ͻ 0.0001). In conclusion, the lower LDH activity observed in children compared with adults may partially explain decreased anaerobic and lactate generation capacity of the children studied. However, the mechanisms for the relatively deficient anaerobic enzyme activities of children are not clear. The functional characteristics of human skeletal muscle are partially dependent on fiber type; however, modifications to the nature and the capacity of the energy-delivering metabolic pathways can occur independent of fiber type. It is widely known that metabolic enzymes in skeletal muscle have the ability to respond to physiologic stimuli such as exercise (1-4), as well as pathologic processes such as muscular dystrophy, acute respiratory failure, mitochondrial myopathy, denervation, and inactivity (5-9). Although there is some controversy regarding fiber type differences between children and adults (10 -13), there are only minor increases in the proportion of type II fibers with age (10 -12), with no difference in ultrastructure (13). Moreover, there is still disagreement over the effect of age on the enzymatic capacity of skeletal muscle, particularly during the maturation from the pediatric to the adult age group.It has been reported that phosphofructokinase (PFK) was 3-fold lower in the skeletal muscle of children (11-13 y) compared with adults (24 -52 y); however, succinate dehydrogenase activity was not significantly altered by age (11,14). Other studies that have examined anaerobic enzyme activity in children have reported lower glycolytic [PFK, lactate dehydrogenase (LDH)] and higher aerobic (succinate dehydrogenase, fumarase) enzyme activities in children compared with younger adults (14,15). In contrast, one report demon...

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Recently, in terms of amyotrophic lateral sclerosis (ALS), much attention has been paid to the cell structures formed by the mitochondria and the endoplasmic reticulum membranes (MAMs) that are involved in the regulation of Ca2+ signaling, mitochondrial bioenergetics, apoptosis, and oxidative stress. We assumed that remodeling of these structures via swim training may accompany the prolongation of the ALS lifespan. In the present study, we used transgenic mice with the G93A hmSOD1 gene mutation. We examined muscle energy metabolism, oxidative stress parameters, and markers of MAMs (Caveolin-1 protein level and cholesterol content in crude mitochondrial fraction) in groups of mice divided according to disease progression and training status. The progression of ALS was related to the lowering of Caveolin-1 protein levels and the accumulation of cholesterol in a crude mitochondrial fraction. These changes were associated with aerobic and anaerobic energy metabolism dysfunction and higher oxidative stress. Our data indicated that swim training prolonged the lifespan of ALS mice with accompanying changes in MAM components. Swim training also maintained mitochondrial function and lowered oxidative stress. These data suggest that modification of MAMs might play a crucial role in the exercise-induced deceleration of ALS development.

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