Muscle Hypertrophy Research Paper
Thomas Warner
Research Paper
Regulation of Muscle Hypertrophy
Our skeletal muscles make up 40-50% of our total mass and are essential for all humans to move, breath, and stand up straight. For the first 20 years of our lives and for those physically active after our muscles are continually growing. Satellite cells are responsible for this growth in our skeletal muscle and are referred to as muscle stem cells. When skeletal muscle cells are traumatized due to physical trauma or disease the regeneration process includes three general processes, destruction, regeneration and remodeling. What regulates these three processes? How are they signaled to initiate the cell cycle and what nutrients and systems do they require to carry out the processes …show more content…
Main Point: Understanding the regulation of muscle hypertrophy requires an understanding of satellite cells (SC), the environment they reside in (niche) and the growth factors that stimulate and inhibit their activation.
Sub Point: Satellite Cells lie in a specific niche that allows them to remain inactive until needed, residing between the sarcolemma and basal membrane of muscle cells (myofibrils). One side of the cell is attached to the basal membrane by two factors. First, the satellite cell has a layer of integrin alpha7beta1 which lies on the side where growth factors and inhibitors from the vasculature, autocrine and motor neuron systems can be received to signal an active or inactive state. Anchoring the satellite cell and its layer of integrin to the basal membrane are laminin, creating a selectively permeable membrane. On the opposite side where the satellite cell resides in a small recess on the myofibril, the satellite cell is attached to …show more content…
There are many systems known and suspected of influencing SC activation and deactivation. Some include the vascular system, the immune system, the neuromuscular system, the autocrine system, and finally the myocyte nucleus. Most of the activation is influenced by the immune system after a muscle cell has been damaged. Once traumatized, Necrophils and Macrophages of the immune system migrate to the site of damage and phagocyte the damaged muscle cell material while releasing growth factors to activate quiescent SCs. At the same time the growth factors stored in the extra cellular matrix, vascular systems, and myocyte nuclei are also released after muscle injury. Examples of the growth factors released by all of these systems are HGF, IGF-1, and IGF-2. These factors bind to satellite cells and initiate SC migration to the damaged cite and start the mitotic cell cycle. Research regarding migration of satellite cells to damaged sites is in its early stages of understanding, what seems to be agreed upon is that factors released from the ECM, immune system, and muscle cells affect the migration of SCs to damaged sites. One factor, TGF-beta, which is released by the immune system is thought to directly attract satellite cells to damaged areas as experiments with a TGF-beta antibody extract reduced SC migration (Griffin, 2009). Activated SCs express MyoD and Myf5 (Broek, Gregte &
Research Paper
Regulation of Muscle Hypertrophy
Our skeletal muscles make up 40-50% of our total mass and are essential for all humans to move, breath, and stand up straight. For the first 20 years of our lives and for those physically active after our muscles are continually growing. Satellite cells are responsible for this growth in our skeletal muscle and are referred to as muscle stem cells. When skeletal muscle cells are traumatized due to physical trauma or disease the regeneration process includes three general processes, destruction, regeneration and remodeling. What regulates these three processes? How are they signaled to initiate the cell cycle and what nutrients and systems do they require to carry out the processes …show more content…
Main Point: Understanding the regulation of muscle hypertrophy requires an understanding of satellite cells (SC), the environment they reside in (niche) and the growth factors that stimulate and inhibit their activation.
Sub Point: Satellite Cells lie in a specific niche that allows them to remain inactive until needed, residing between the sarcolemma and basal membrane of muscle cells (myofibrils). One side of the cell is attached to the basal membrane by two factors. First, the satellite cell has a layer of integrin alpha7beta1 which lies on the side where growth factors and inhibitors from the vasculature, autocrine and motor neuron systems can be received to signal an active or inactive state. Anchoring the satellite cell and its layer of integrin to the basal membrane are laminin, creating a selectively permeable membrane. On the opposite side where the satellite cell resides in a small recess on the myofibril, the satellite cell is attached to …show more content…
There are many systems known and suspected of influencing SC activation and deactivation. Some include the vascular system, the immune system, the neuromuscular system, the autocrine system, and finally the myocyte nucleus. Most of the activation is influenced by the immune system after a muscle cell has been damaged. Once traumatized, Necrophils and Macrophages of the immune system migrate to the site of damage and phagocyte the damaged muscle cell material while releasing growth factors to activate quiescent SCs. At the same time the growth factors stored in the extra cellular matrix, vascular systems, and myocyte nuclei are also released after muscle injury. Examples of the growth factors released by all of these systems are HGF, IGF-1, and IGF-2. These factors bind to satellite cells and initiate SC migration to the damaged cite and start the mitotic cell cycle. Research regarding migration of satellite cells to damaged sites is in its early stages of understanding, what seems to be agreed upon is that factors released from the ECM, immune system, and muscle cells affect the migration of SCs to damaged sites. One factor, TGF-beta, which is released by the immune system is thought to directly attract satellite cells to damaged areas as experiments with a TGF-beta antibody extract reduced SC migration (Griffin, 2009). Activated SCs express MyoD and Myf5 (Broek, Gregte &