Muscle Compensation: A Case Study

At the molecular level of explanation these processes are dependent on the interplay between glutamate receptors, Ca2+ channels, the increase of intracellular Ca2+ levels, Ca2+-dependent proteins like Akt, ERK, mTOR and neurotrophins such as brain derived neurotrophic factor (BDNF) (24, 25).

Next, to determine if contraction via the EMC pathway requires extracellular or intracellular calcium, the second type of stimulus was used and the tissue was stimulated using calcium free K+-depolarising solution. The bathing solution in this experiment was calcium free solution to make sure all extracellular calcium was eliminated, as without calcium, the EMC pathway is expected to produce no response.

Both electrical and chemical forces combine to determine the resting membrane potential of the cell. Although the resting membrane potential of most cells is normally negative, the selective permeability of the membrane allows certain ions in and out, causing the neuronal membrane voltage to become depolarized (more positive), or hyperpolarized (more negative). Key ions involved in muscle membrane potential are sodium, potassium, and chloride, which move via passive or active diffusion through ion channels and transporter pumps (Baierlein et al. 2011). The Nernst equation predicts the membrane voltage based on the assumption that the membrane is only permeable to one type of ion. In this investigation, we are seeking to understand the basis for how different ions interact to produce the membrane potential of DEM, DEL1, and DEL2 crayfish muscle

Calcium needs to be released first and needs to be obtained in the body in order for the body to carry out its function. Calcium or calcium ion (Ca2+) is stored in the sacroplasmic reticulum (SR) to start contraction for the muscles.11 In the case of the cardiac muscle, it would start contraction through the Sodium-Calcium exchange (NCX) and with limited help of the SR. Sodium ions (Na+) would enter from the dyadic cleft, the space where the cell membrane and SR are in close proximity.11 This would cause Ca2+ to flow out of the cell. In order for Ca2+ to reenter it has to go through Ca2+ channels and so Ca2+ would be released.11 Excitation-contraction coupling relies on the dyadic cleft of Ca2+ to be released. Understanding how NCX works could help provide treatment for HF because the cardiac muscle could be manipulated to contract. It may be possible to remove the NCX because it can cause too much Ca2+ to be stored in the SR and cause arrhythmias and cell death.11 This would lead to a pathway to fixing any heart failure

The ryanodine receptors (RyRs) are intracellular Ca2+ channels that are a cellular mediator for calcium-induced calcium release (CICR) (1). The inositol 1,4,5-triphosphate receptors (IP3R) are intracellular Ca2+ channels that act as a cellular mediator for CICR through their activation of a second messenger that causes the release of Ca2+ (1). In the process of CICR Ca2+ is released from intracellular storage (3). In the development of epilepsy, a dysregulation of intracellular calcium ([Ca2+] i) by inositol 1,4,5-triphosphate receptors (IP3R) and ryanodine receptors (RyR)

Your wrist hurts, now your bicep hurts, then your shoulder hurts, and you are now wondering why your whole arm hurts. Muscle compensation happens when people hurt one muscle and they try to make up for their weakened strength. The Fleet Feet Sports Webpage, a webpage dedicated to runners and their health, says, “The body uses compensation patterns to perform motions when strength and mobility are not sufficient” (“Compensation Patterns”). Compensation can lead to a multitude of serious problems. During a job shadowing experience, I saw a patient experience multiple injuries due to a muscle compensation pattern. Muscle compensation can lead to a magnitude of injuries, as demonstrated by a patient I observed.

Muscles contract through an action potential moving along a motor neuron toward the skeletal muscle and they connect to a neuromuscular junction  acetylcholine vesicles being released  binding on the sarcolemma  causes Na+ influx in the muscle fiber generating an action potential within the muscle fiber  action potential moves through the T-tubules Calcium channels open calcium is released into the cytoplasm  actin-myosin binding sites and cross-bridges are activated by calcium ions between the actin/ myosin heads  ATP is hydrolyzed to flex myosin head  this flexion makes the actin filaments move close to the middle of the sarcomere  The length of the sarcomere becomes shorter  contraction. I would like to define a few terms discussed within this

Moreover, channelopathies produce changes in neurotransmitter release through alterations in calcium channels (4). Any event that disrupts

When the action potential is no longer generated, Ca2+ are actively transported back into the sarcoplasmic reticulum.

Gamma motor neurons are a type of lower motor neuron that take part in the process of muscle contraction. Their cell bodies are located in the anterior horn of the spinal cord. Gamma motor neurons innervate intrafusal fibers, which contract only slightly. The function of intrafusal fiber contraction is not to provide force to the muscle; rather, gamma activation of the intrafusal fiber is necessary to keep the muscle spindle taut, and therefore sensitive to stretch, over a wide range of muscle lengths. If a resting muscle is stretched, the muscle spindle becomes stretched in parallel, sending signals through the primary and secondary afferents. A subsequent contraction of the muscle, however, removes the pull on the spindle, and it becomes

While the dynamics of CaMKII in LTP had thus far been elucidated, it still begged the question as to why postsynaptic depolarization alone could not induce LTP across the dendritic shaft. Since it was known that postsynaptic depolarization caused a large, sustained increase in Ca2+ in spines, 8 the authors

(regulate Ca2+ pump) that encodes SR to see the rate at which calcium is being uptake/released

ClC-1 is thought to be the main chloride channel responsible for muscle cell repolarisation, although not all ‘whole muscle’ experiments support this – the majority of muscle cell repolarisation is attributable to action of voltage-gated K+ channels, but ClC-1 channel activity is nonetheless significant. The physiological role of ClC-1 is demonstrated by the pathophysiology of myotonia congenital – which occurs from mutations in the CLCN1 gene. ClC-1 channel inhibitors, such as A-9-C and CPP, can induce myotonia – a condition in which a single action potential (AP) at the neuromuscular junction causes repetitive AP firing, and thus delayed muscle relaxation. Immunohistochemical evidence suggests ClC-1 is concentrated in the sarcolemmal membrane rather than the t-tubular membrane, which was not expected – as repeated muscle stimulation accumulates K+ in the t-tubular membrane, hence it would be expected to find the majority of chloride conductance localised here (Figure 2). This differs greatly from previous physiological localisation of ClC-1, which suggested up to 80% of chloride conductance may be associated with the t-tubular membrane [6]. Interestingly, no clear physiological significance of ClC-1 channels has been detected in other tissues [5].

Relaxation only occurs when the simulation of the motor nerve actually stops. Calcium is pumped back in to the Sarcoplasmic Reticulum and prevents the link between the actin and myosin filaments. The phase of relaxation only

Specific signal molecules open and close ion channel receptors that permit the passing of ions in and out of the cell. These ions include Na+, K+, Ca2+, or Cl-, necessary for sending chemical signals.