Muscle injury

Obviously, if you wish to treat a skin condition or infection, a preparation that can be applied topically would be the preferred option. Similarly, inhalation would be the first choice if trying to treat a pulmonary or bronchial condition, such as asthma. Dermal application would also be the first choice for localized tissue treatments (e.g. muscle injury), provided that the drug can be absorbed through the skin. However, in most other situations it is necessary for drugs to enter the bloodstream in order for them to be transported to their site of action. This is most commonly achieved by ingestion, or by intravenous (i.v.), intramuscular (i.m.) or subcutaneous (s.c.) injection when the oral route is not suitable. 

Muscle fatigue during this intensity range may be due to other factors besides lack of CHO substrate. The potential mechanisms include dehydration, electrolyte imbalances, and the onset of muscle injury and soreness. As these potential fatigue factors are common to the range of intensities in this section and exercise below 60% VO2 max, they will be discussed in the following section. 

Warren, J.A., Jenkins, R.R, Packer, L., Witt, E.H. and Armstrong, P.B. (1992). Elevated muscle vitamin E does not attenuate eccentric exercise-induced muscle injury. J. Appl. Physiol. 72, 2168-2175. 

Musculoskeletal Effects. Muscular rigidity was observed in humans after acute cyanide poisoning (Grandas et al. 1989) and rhabdomyolysis, a clinical syndrome characterized by skeletal muscle injury, was observed in a man who ingested 0.57 mg CNVkg in a suicide attempt (Saincher et al. 1994). 

Skeletal myoblasts are adult, tissue-specific stem cells [73] located between the basal lamina and the sarcolemma on the periphery of the mature skeletal-muscle fiber [74]. Also known as muscle satellite cells, these small, mononuclear cells are activated by biochemical signals to divide and differentiate into fusion-competent cells after muscle injury. 

Cyclobenzaprine Poorly understood inhibition of muscle stretch reflex in spinal cord Reduction in hyperactive muscle reflexes antimuscarinic effects Acute spasm due to muscle injury inflammation Hepatic metabolism duration, 4-6 h Toxicities Strong antimuscarinic effects... 

Diazepam Facilitates GABAergic transmission in central nervous system (see Chapter 22) Increases interneuron inhibition of primary motor afferents in spinal cord central sedation Chronic spasm due to cerebral palsy, stroke, spinal cord injury acute spasm due to muscle injury Hepatic metabolism duration, 12-24 h Toxicities See Chapter 22... 

At the same time that the motor neurons send signals to the muscles, branches travel into other parts of the brain including the olivary nuclei, which send neurons into the cerebellum. The cerebellum acts as a kind of computer needed for fine tuning of the impulses to the muscles. Injury to the cerebellum leads to difficulty in finely coordinated motions. Input to the Purkinje cells arises from the climbing fibers, which originate in the inferior olive of the brain stem. Each climbing fiber activates a single Purkinje cell, but the dendrites of each Purkinje cell also form as many as 200,000 different synapses with parallel fibers that run across the cortex of the cerebellum (Fig. 30-15). 

A3 receptors in affording skeletal muscle protection was investigated. The A3 receptor-selective agonist Cl-IBMECA exerted a potent reduction of skeletal muscle injury when it was administered before the onset of ischemia. The reduced skeletal muscle injury was reversed by the presence of the A3 receptor-selective antagonist MRS 1191 but not by that of DPCPX (Fig. 13.2). These data demonstrated for the first time a protective function of the A3 receptor in skeletal muscle. 

Taken together, using a mouse model of hindlimb skeletal muscle injury, all three adenosine receptor subtypes could each individually induce protection from ischemia-reperfusion injury in skeletal muscle. Due to the lack of a highly selective A2B receptor agonist and antagonist, its role in mediating an anti-ischemic effect in skeletal muscle remains to be determined. 

Fig. 13.4 (continued) (c) CCPA was effective in preventing the ischemia/reperfusion-induced injury in these mice, (d) A structurally distinct A3 receptor agonist MRS3558 was also able to reduce skeletal muscle injury in WT mice (representative of eight mice)... 

Feng et al. 2006 Tapiero and Tew 2003 Miles et al. 2000). Marked induction of MT mRNA is evident in skeletal muscle of animals and humans under conditions that promote decreased protein synthesis and increased protein degradation, such as, muscle injury and disuse (Jagoe et al. 2002 Lecker et al. 2004 Kondo et al. 1994 Penkowa et al. 2005). 

Tidball JG (1995) Inflammatory cell response to acute muscle injury. Med Sci Sports Exerc 27 1022-32... 

Warren GL, Summan M, Gao X, Chapman R, Hulderman T, Simeonova PP (2007) Mechanisms of skeletal muscle injury and repair revealed by gene expression studies in mouse models. J Physiol 582 825-41... 

Furuno, K., and Goldberg, A.L., 1986, The activation of protein degradation in muscle by Ca2+ or muscle injury does not involve a lysosomal mechanism, Biochem J, 237, pp 859-864. 

Pedowitz RA, Gershuni DH, Schmidt AH, Friden J, Rydevik BL, Hargens AR. Muscle injury induced beneath and distal to a pneumatic tourniquet a quantitative animal study of effects of tourniquet pressure and duration. J Hand Surg Am 1991 16 610-21. 

As of early 2002, controlled clinical studies had not discovered any direct link between creatine use and muscle pain or strains when supplements are taken according to generally accepted guidelines. In fact, preliminary results from an Arkansas State University study of college baseball players found that those who used creatine did not have any more cramping or muscle injuries than nonsupplementing players. 

Bromelain has found application in a wide variety of inflammatory conditions. These include thrombophlebitis, skeletal muscle injuries, hematomas, oral inflammations, diabetic ulcers, and athletic injuries [2,5,88,93]. 

Van Nieuwenhoven, F.A., A.H. Kleine, K.W.H. Wodzig, W.T. Hermens, H.A. Kragten, J.G. Maessen, C.K. Punt, M.P. Van Dieijen, G.J. Van der Vusse, and J.F.C. Glatz (1995). Discrimination between myocardial and skeletal muscle injury by assessment of the plasma ratio of myoglobin over fatty acid binding protein. Circulation 92 2848-2854. 

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