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    Detraining:

    Detraining may result in decreased mitochondrial biogenesis. In a study of nine healthy males that participated in an endurance training program for six weeks, and then a detraining period of three weeks, Wibom et al. (1992) found mitochondrial ATP production rate and mitochondrial enzyme activity decreased.28 The changes in ATP production rate and enzymes result in a decrease in the volume of mitochondria.  

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    In this image, one can observe the dramatic loss in mitochondrial content of the muscle fibers when detrained. Also, note how low the content of the untrained is compared to that of the trained.12

     

    The image below shows the difference between mitochondrial content of fiber types in the trained and untrained.13

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    There are obviously many health benefits of endurance exercise. The increase in work capacity is one benefit that is directly related to the mitochondria. When the number of mitochondria are increased, the muscles can remove more oxygen from the blood therefore increasing work capacity.28

     

    Aging:

    During the aging process, there are many aspects of metabolism that deteriorate.28 The literature is not conclusive concerning what exactly happens to the mitochondria during aging. However, at least two changes have been noted. The first concerns reactive oxygen species (ROS) that initiate a cell suicide mechanism. Mutations in mtDNA have been found to collect in aging muscle. Alterations in mtDNA structure have been found to increase the formation of ROS in the muscle, creating a ROS imbalance. The imbalance causes the apoptotic pathway to be triggered more, therefore increasing the number of cell deaths. The second mitochondrial change due to aging concerns the PGC-1ɑ. A decrease in PGC-1ɑ reduces biogenesis.5

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    This cartoon helps to put all of the mitochondrial changes that occur due to increased ROS and decreased PGC-1ɑ in perspective.14

     

    Chronic Muscle Disuse:

    The phrase chronic muscle disuse refers to disuse such as immobilization of limbs, bed rest, or space flight.When the muscles are not being used, biogenesis is stunted. Both the intermyofibrillar mitochondria and subsarcolemmal mitochondria are affected by muscle disuse, but they are affected differently. The subsarcolemmal experience a fast decrease in number of mitochondria which affects ATP production. However, the intermyofibrillar mitochondria experience a much slower decrease. Therefore, there are more of intermyofibrillar mitochondria present during muscle disuse than the subsarcolemmal mitochondria. The intermyofibrillar mitochondria are more vulnerable to proapoptotic proteins. Atrophy then occurs because the odds for cell death via apoptosis are increased.15

    More information about the effects of apoptosis on mitochondria can be found here:

    http://ajpcell.physiology.org/content/289/4/C994

     

    In conclusion, decreased performance is noticeable during aging, detraining, and chronic muscle disuse. This phenomenon is partially expalined by the fact that all three of these conditions result in decreased mitochondrial biogenesis. Although biogenesis is affected differently by all 3 conditions, the end result is hindered energy production. If the volume of mitochondria is reduced, ATP production suffers. 

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