Pulled muscle pain

*Please note that the following content is solely a brief introduction to myofascial pain syndrome / pulled muscle / muscle pain for the purpose of promoting the clarification of chiropractic care.

Myofascial pain syndrome or known as a muscle trigger point is a sore and tender spot in a muscle which may become progressively worse with time, cause referred pain and muscle weakness, and may have significant detrimental impact on the athlete or active individual. It is important to note, that myofascial pain syndrome is the most common cause of muscle pain and is a major contributor to joint pain and headaches. At Vincere Health Chiropractic we use the most modern and advanced therapeutic equipment, modalities and techniques in the treatment of myofascial pain syndrome, including joint manipulation/ mobilization; Extracoporeal Shock Wave therapy; dry needling; myofascial release; kinesio and dynamic taping; and stretching and strengthening of the affected muscle(s) (rehabilitation).

A myofascial trigger point (MFTP) or known as myofascial pain syndrome can be defined as an area of hyperirritable or palpable tender, taut nodules/ bands of muscle fibers with possible accompanied referred pain, muscle spasm, motor weakness and autonomic effects. MFTPs are very common and are the major cause of muscle pain and a major contributor to headaches and joint pain.

The pathophysiology behind MFTPs is not entirely clear. Several causes/ contributors have been linked to the development of MFTPs, of which the primary causes include; postural strain; overweight; trauma; overload of muscles; weak muscles; joint dysfunction; nutritional deficiency, particularly zinc, magnesium and vitamin B12; drug-induced myalgia, particularly cholesterol-lowering drugs (statins), anti-malarial drugs (such as chloroquine and hydroxychloroquine), corticosteroids (glucocorticoids such as for inflammation), and HIV therapy; and of importance to note stress (stress-induced myalgia). Myofascial pain syndrome is postulated to stem from an abnormal increase in the production and release of the neurotransmitter acetylcholine (ACh) which induce sustained depolarization of the post-junctional membrane of the muscle fibers with subsequent continuous release and uptake of calcium ions; sustained shortening of the sarcomeres; muscle ischemia; and the release of sensitizing substances/ cytokines such as substance P, bradykinin, calcitonin gene-related peptide (CGRP), tumor necrosis factor, and interleukin expressions. A vicious cycle develops, the nociceptors are sensitized and the muscle ischemia is aggravated; the nociceptors threshold of Aδ-fibre and C-fibre afferents in the muscle fibers are lowered with an increase in their nociceptive responsiveness in the periphery to stimulation of their receptive fields, causing non-noxious stimuli such as light touch or normal joint movement to depolarize and activate their nociceptors and cause their firing.

During the normal physiological contraction of a muscle the capillary blood flow is temporarily obstructed. The blood flow in the muscle immediately recovers after the contraction. The dynamic muscle contraction-relaxation rhythm serves as a muscular pump to enhance intramuscular blood flow. In the setting of a sustained muscle contraction or when the muscle is overloaded by excessive muscle activity; the muscle metabolism is highly dependent on oxygen and glucose of which are in short supply, due to the induced reduced intramuscular blood circulation by the contraction. Studies have affirmed that only 10 % of maximum voluntary muscle contraction may produce intramuscular pressure which is high enough to impair the intramuscular blood circulation significantly.

Oxygen and glucose are required for the synthesis of adenosine monophosphate (ATP) to provide energy to the muscle to contract. In the setting of sustained contraction or when the muscle is overloaded by excessive muscle activity; a local energy crisis develops due to the lack of energy. The human body can counteract the local energy crisis, by switching from the aerobic to the anaerobic glycolysis energy system, to guarantee an adequate supply of ATP. In an aerobic state when there is enough oxygen and glucose supply in the muscle due to adequate intramuscular blood flow; oxygen reacts with pyruvic acid to produce high amounts of ATP, 16 molecules of ATP per pyruvic acid molecule; carbon dioxide and water. In an anaerobic state when there is not enough oxygen and glucose supply in the muscle due to the insufficient intramuscular blood supply induced by the overload muscle; the glycolysis system (sugar splitting) initially brakes down 1 glucose molecule into 2 pyruvic acid molecules which release enough energy to form 2 ATP molecules. As the muscle becomes more anaerobic; the majority of the formed pyruvic acids are converted into lactic acid which decreases the intramuscular acidity (pH). In the normal physiological functioning of a muscle; the majority of formed lactic acids diffuse out of the muscle cells into the bloodstream. Studies have affirmed that post-exercise lactic acid is washed out of a muscle within 30 minutes after exercise. To the contrary, in the setting of sustained contraction or when the muscle is overloaded by excessive muscle activity; the intramuscular blood flow is restricted and impairs the ability of the human body to wash out lactic acid from muscles.

Studies have shown that low intramuscular pH (below 5) can excite and sensitize nociceptors which are distributed in the intramuscular connective tissue and investing fascial envelops, by causing an increase in the hydrogen (H+) ion concentration in the muscle tissue, of which the muscle nociceptive ion channels are susceptive to. Furthermore, the low intramuscular pH may cause the downregulation of acetylcholinesterase (AChE), decrease the amount of these enzymes, and thereby increase the efficacy of ACh and subsequently maintain sarcomere contraction. AChE is an enzyme which hydrolyses ACh and thereby terminates synaptic transmission at cholinergic synapses, in order to prevent the excessive binding of ACh to their nicotinic acetylcholine receptors (AChR) at their neuromuscular junctions. In addition, low intramuscular pH have been found to trigger the release of several nociceptive substances/ cytokines particularly CGRP, which further enhance the release of ACh, decrease the effectiveness of AChE in the synaptic cleft, as well as cause the upregulation of AChRs in the sarcomere (muscle cell membrane). In the normal physiological functioning of a muscle; each ACh ligand binding to its nicotinic cholinergic receptor will generate a small postsynaptic potential change of a fixed size at each depolarized motor end plate, known as the miniature end-plate potential (mepp). The binding of several ACh neurotransmitters to their nicotinic cholinergic receptors will produce mepp summation and result in the generation of a larger depolarization of each motor end plate, to generate an end-plate potential (EPP). When the EPP is large enough and reaches the threshold, the generation of an action potential will result and cause contraction of each recruited muscle fiber. The mepp activity is dependent on the state of the AChR and the local concentration of ACh, of which is the result of ACh-release, ACh-reuptake, and ACh-breakdown by ACHe; of which all are adversely affected by the induced lower intramuscular pH.

The biomechanical relaxation of a muscle occurs when the myosin-actin cross-bridges detach within the sarcomere (contraction unit of a muscle cell/ muscle fiber), of which ATP is required for. When ATP attach to the myosin molecule; the link between the myosin and actin myofilaments weakens which allow the myosin head to detach from actin, or in more simpler terms; the cross-bridge between the myosin and actin “breaks”. At the same time of the myosin-actin cross-bridge detachment; calcium (Ca2+) ions detach from troponin molecules of actin, which blocks the tropomyosin-myosin binding site on actin. In the normal physiological functioning of a muscle; large amounts of the detached Ca2+ ions from the actin will re-enter the sarcoplasmic reticulum found within the muscle cell by the presence of a Ca2+ pumps driven by calcium ATPase, which in turn place a high demand on ATP during muscle relaxation. In the setting of a sustained muscle contraction or when the muscle is overloaded by excessive muscle activity; the sarcomeres may stay in a state of contraction until enough ATP is available in the muscle cell to resolve the intracellular accumulation of Ca2+ ions; induced by the reduced intramuscular blood supply by the contraction.


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