I'm posting this separate from the general "got testosterone?" thread as it's of a specific medical nature and potentially very important info. TRT appears highly valuable treatment in SCI to prevent the loss of skeletal muscle post SCI. Obvious limitations of this study is it's an animal model and it's unclear if the effect would continue after the 11 weeks, but an exciting study I thought and worth looking into. Two, I have looked at GH therapy and possible applications to connective tissue/joint degeneration in active populations which readers may find interesting also
Useful summary info from this study:
"...the purpose of this study was to evaluate the effects of TRT on rat skeletal muscles after SCI. It was hypothesized that TRT would at the least attenuate atrophy after SCI based on the effects of androgen replacement in other models of sarcopenia. This study will not address the concerns surrounding testosterone therapy in humans.3 However, it will hopefully serve as an initial step in assessing the efficacy of TRT for reducing several increased health risks after SCI. An increase in affected muscle mass in chronic SCI could increase exercise capacity, and thereby reduce the risk for cardiovascular disease.7 A therapeutically induced increase in muscle mass could also result in increased insulin sensitivity, venous return and metabolic rate with corresponding potential for more favorable body composition and increased bone density, all would have a positive influence on health."
And:
"The most important finding of this study was that TRT ameliorated the decrease in fiber CSA resulting from SCI. TRT also attenuated the slow to fast fiber type shift as well as the decrease in oxidative enzyme activity. To our knowledge, this is the first study to investigate the potential of TRT to prevent atrophy in SCI. TRT in aging sarcopenia and in other diseases with muscle wasting (for example, AIDS) results in favorable effects on bone, muscle size and strength in both low-average and hypogonadal men.19 Increases in muscle CSA were equal, if not greater in TRT only groups than in exercise groups without TRT.20 These data and ours for SCI both demonstrate a positive effect of TRT on muscle size without traditional overload..."
Effects of testosterone replacement therapy on skeletal muscle after spinal cord injury
Abstract
Study design: Randomized control.
Objective: To examine the effects of testosterone replacement therapy (TRT) on skeletal muscle 11 weeks after complete SCI.
Setting: Athens, Georgia USA.
Methods: Soleus (SOL), gastrocnemius (GA), tibialis anterior (TA), vastus lateralis (VL) and triceps brachii (TRI) muscles were taken from twelve young male Charles River rats 11 weeks after complete SCI (T-9 transection, n=8) or sham surgery (n=4). Rats received either TRT (two 5 cm capsules, n=4) or empty capsules (n=8) implanted at surgery. Muscle samples were sectioned and fibers analyzed qualitatively for myosin ATPase and quantitatively for succinate dehydrogenase (SDH), alpha-glycerol-phosphate dehydrogenase (GPDH) and actomyosin ATPase (qATPase) activities using standard techniques.
Results: SCI decreased average fiber size (49plusminus4%) in affected muscles and the percentage of slow fibers in SOL (93plusminus3% to 17plusminus2%). In addition, there was a decrease in SDH and an increase in GPDH and qATPase activities across the four hind-limb muscles of the SCI animals. Fiber size in the TRI was increased (31plusminus2%) by SCI while enzyme activities were not altered. Average fiber size across the four hind limb muscles was decreased by only 30% in TRT SCI animals and their SOL contained 39plusminus2% slow fibers. TRT also attenuated changes in enzyme activities. There was no effect of TRT on the TRI relative to SCI.
Conclusions: TRT was effective in attenuating alterations in myofibrillar proteins during 11 weeks of SCI in affected skelatal muscles.
Full Study HERE
Additional related study of interest:
J Neurobiol. 2004 Sep 5;60(3):348-59.
Exogenous testosterone prevents motoneuron atrophy induced by contralateral motoneuron depletion.
Fargo KN1, Sengelaub DR.
Author information
Abstract
Gonadal steroids exhibit neuroprotective and neurotherapeutic effects. The lumbar spinal cord of male rats contains a highly androgen-sensitive population of motoneurons, the spinal nucleus of the bulbocavernosus (SNB), whose morphology and function are dependent on testosterone in adulthood. Unilateral SNB motoneuron depletion induces dendritic atrophy in contralateral SNB motoneurons, but this atrophy is reversed in previously castrated males treated with testosterone. In the present experiment we test the hypothesis that the morphology of SNB motoneurons is protected from atrophy after contralateral motoneuron depletion by exogenous testosterone alone (i.e., with no delay between castration and testosterone replacement). We unilaterally depleted SNB motoneurons by intramuscular injection of cholera toxin conjugated saporin. Simultaneously, some saporin-injected rats were castrated and immediately given replacement testosterone. Four weeks later, contralateral SNB motoneurons were labeled with cholera toxin conjugated HRP, soma sizes were measured, and dendritic arbors were reconstructed. Contralateral SNB motoneuron depletion induced somal atrophy and dendritic retraction, but testosterone treatment prevented both of these effects. Thus, the presence of high-normal levels of testosterone prevents motoneuron atrophy induced by contralateral motoneuron depletion. These data support a therapeutic role for testosterone in preventing atrophy induced by motoneuron injury.
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