Linda Maxwell

Delayed Onset Muscle Soreness Treatment Strategies and Performance Factors

AbstractDelayed onset muscle soreness (DOMS) is a familiar experience for the elite or novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year. Eccentric activities induce micro-injury at a greater frequency and severity than other types of muscle actions. The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion, shock attenuation and peak torque. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury if a premature return to sport is attempted.A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms. Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. Athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1–2 days following intense DOMS-inducing exercise. Alternatively, exercises targeting less affected body parts should be encouraged in order to allow the most affected muscle groups to recover. Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of, or during, the sporting season in order to reduce the level of physical impairment and/or training disruption. There are still many unanswered questions relating to DOMS, and many potential areas for future research.

Exercise-enhanced satellite cell proliferation and new myonuclear accretion in rat skeletal muscle

The effects of increased functional loading on early cellular regenerative events after exercise-induced injury in adult skeletal muscle were examined with the use of in vivo labeling of replicating myofiber nuclei and immunocyto- and histochemical techniques. Satellite cell proliferation in the soleus (Sol) of nonexercised rats (0.4 +/- 0.2% of fibers) was unchanged after an initial bout of declined treadmill exercise but was elevated after two (1.0 +/- 0.2%, P < or = 0.01), but not four or seven, daily bouts of the same task. Myonuclei produced over the 7-day period comprised 0.9-1.9% of myonuclei in isolated fibers of Sol, tibialis anterior, and vastus intermedius of nonexercised rats. The accretion of new myonuclei was enhanced (P < or = 0.05) in Sol and vastus intermedius by the initial exercise followed by normal activity (to 3.1-3.4% of myonuclei) and more so by continued daily exercise (4.2-5.3%). Observed coincident with a lower incidence of histological fiber injury and unchanged fiber diameter and myonuclei per millimeter, the greater new myonuclear accretion induced by continued muscle loading may contribute to an enhanced fiber repair and regeneration after exercise-induced injury.

Anti-oxidant therapy improves microvascular ultrastructure and perfusion in postischemic myocardium

To determine the contribution of oxygen-derived free radicals to the changes in microvascular structure and function which follow reperfusion of ischemic myocardium, isolated perfused rat hearts were subjected to 15 or 45 min of global ischemia followed by 5 min of oxygenated reperfusion. Hearts were then fixed by perfusion with glutaraldehyde and perfused with nuclear track photographic emulsion to identify competent capillaries in scanning and transmission electron micrographs. Reperfusion after 15 min caused a significant reduction in the density of competent capillaries in the subendocardial third of the left ventricle, but this reduction was lessened but not eliminated by the addition of 0.61 mmole/liter desferrioxamine, but not by 60,000 U/liter superoxide dismutase plus 60,000 U/liter catalase, to the perfusate. After 45 min of ischemia both interventions prevented the myocyte swelling, endothelial cell changes, bleb formation, and reduction in microvascular lumina characteristic of unprotected reperfusion, but only desferrioxamine significantly improved microvascular competence. This suggests that the hydroxyl radical rather than superoxide and/or hydrogen peroxide has a pathogenic role, although desferrioxamine may have other effects as nonspecific chelator. Postischemic reductions in capillary function also occur in reversibly injured myocardium in the absence of structural abnormality. Preventing postischemic microvascular incompetence has the potential to minimize ischemic cell injury and to enhance repair following myocardial infarction, but it also may increase the risk of hemorrhage from venules.

Differences Between Heart Valve Allografts and Xenografts in the Incidence and Initiation of Dystrophic Calcification

&NA; Following surgical removal because of primary tissue failure, 30 antibiotic‐sterilized human aortic valve allografts and 27 glutaraldehyde‐treated porcine aortic valve xenografts were examined for macroscopic and microscopic evidence of dystrophic calcification. These grafts had been mounted on stents and used for from 34 to 166 months to replace diseased mitral valves. After explantation the grafts were carefully examined then prepared for light microscopy, for transmission electron microscopy and for energy dispersive X‐ray microanalysis. Gross calcification occurred significantly (p = 0.002) more frequently in xenografts (89%), and was more extensive than in allografts (53%). Calcification usually appeared as nodular excrescences on the cusps, although occasionally it formed plates within them. This reduced tissue pliability and was usually associated with either valvular stenosis or regurgitation. The calcified deposits contained calcium and phosphate in ratios approaching those of hydroxyapatite. In xenograft valves the smallest discrete deposits of calcification were spherical and usually associated with membranous debris of porcine donor fibroblasts, but allografts did not contain donor cell remnants and early calcification was linearly arranged along collagen fibres.

ENDOTHELIN-3-INDUCED MICROVASCULAR INCOMPETENCE AND MITOCHONDRIAL DAMAGE IN RAT MYOCARDIUM

1. To determine the possible role of an endothelin in the development of postischaemic microvascular incompetence, isolated buffer‐perfused rat hearts were perfused with endothelin‐3 (ET‐3) in phosphate buffer.

The Spatial and Temporal Distribution of Insulin-Like Growth Factor-1 Following Experimental Myocardial Infarction in the Rat

Insulin-like growth factor-1 (IGF-1) is believed to be involved in the repair and adaptation that follow ischemic injury to the myocardium. The aim of this study was to elucidate the role of IGF-1 by defining the changes that occur in its distribution following regional myocardial infarction. The left anterior descending coronary artery was ligated in adult male Wistar rats, and hearts were examined microscopically from 6 hours to 20 days later. IGF-1 was identified histochemically using the avitin-biotin-peroxidase method with a polyclonal antibody to IGF-1 and was quantified by optical density measurements of standard fields in sections of hearts prepared in a single batch. Immunoreactivity was located in the cytoplasm of viable myocytes, vascular smooth-muscle cells, mast cells, leukocytes, endothelial cells, and fibroblasts. The zone of viable myocardium immediately adjacent to infarcts reacted significantly more intensely for IGF-1 than all other regions at all stages, with a maximum optical density (617% higher than sham-operated control myocardium, p < .001) 24 hours after coronary artery ligation. Immunoreactivity in myocardium tissue distant from the infarcts also increased during the first day (382% at 24 hours), but this increase was not statistically significant thereafter. These temporal and spatial changes in the distribution and amount of IGF-1 indicate that this finding is predominantly associated with a localized response to injury by the viable myocytes adjacent to infarcts.

The pathology and pathogenesis of asthma

Until recently, most of the knowledge of the pathology and pathogenesis of asthma was derived largely from necropsy studies of patients dying from asthma. In status asthmaticus, mucous plugs, changes to the bronchial epithelium, basement membrane thickening, smooth muscle hypertrophy and inflammatory cell infiltration of the bronchial wall are all observed. The development of animal models of asthma and the use of the fibre-optic bronchoscope have contributed to what is known of the pathological features present between attacks or in mild asthma and to the pathogenesis of this enigmatic disease. Structural and functional abnormalities of the airway epithelium may result in increased bronchial hyper-responsiveness and, with the demonstration of the pro-inflammatory properties of the eosinophil, the hypothesis that these cells merely modulate the actions of other cells now requires revision.