Unaccustomed exercise consisting of eccentric (i.e., lengthening) muscle contractions often results in muscle damage characterized by ultrastructural alterations in muscle tissue, clinical signs, and symptoms (e.g., reduced muscle strength and range of motion, increased muscle soreness and swelling, efflux of myocellular proteins). The time course of recovery following exercise-induced muscle damage depends on the extent of initial muscle damage, which in turn is influenced by the intensity and duration of exercise, joint angle/muscle length, and muscle groups used during exercise. The effects of these factors on muscle strength, soreness, and swelling are well characterized. By contrast, much less is known about how they affect intramuscular inflammation and molecular aspects of muscle adaptation/remodeling. Although inflammation has historically been viewed as detrimental for recovery from exercise, it is now generally accepted that inflammatory responses, if tightly regulated, are integral to muscle repair and regeneration. Animal studies have revealed that various cell types, including neutrophils, macrophages, mast cells, eosinophils, CD8 and T-regulatory lymphocytes, fibro-adipogenic progenitors, and pericytes help to facilitate muscle tissue regeneration. However, more research is required to determine whether these cells respond to exercise-induced muscle damage. A large body of research has investigated the efficacy of physicotherapeutic, pharmacological, and nutritional interventions for reducing the signs and symptoms of exercise-induced muscle damage, with mixed results. More research is needed to examine if/how these treatments influence inflammation and muscle remodeling during recovery from exercise.

Sh relationships among the measures. Peak soreness is experienced 2–3 d postexercise while peak swelling occurs 5 d postexercise. Maximal strength and the ability to fully flex the arm show the greatest decrements immediately after exercise with a linear restoration of these functions over the next 10 d. Blood creatine kinase (CK) levels increase precipitously at 2 d after exercise which is also the time when spontaneous muscle shortening is most pronounced. Whether the similarity in the time courses of some of these responses implies that they are caused by similar factors remains to be determined. Performance of one bout of eccentric exercise produces an adaptation such that the muscle is more resistant to damage from a subsequent bout of exercise. The length of the adaptation differs among the measures such that when the exercise regimens are separated by 6 wk, all measures show a reduction in response on the second, compared with the first, bout. After 10 wk, only CK and muscle shortening show a reduction in response. After 6 months only the CK response is reduced. A combination of cellular factors and neurological factors may be involved in the adaptation process. ©1992The American College of Sports Medicine...

This study examined muscle swelling and changes in inflammatory markers in the blood following eccentric exercise-induced muscle damage. Subjects(N = 14) who had not been involved in a resistance training program performed 24 maximal eccentric actions of the elbow flexors. Muscle swelling was assessed by measures of the upper arm circumference (CIR), ultrasonography(USG), and magnetic resonance imaging (MRI). Plasma concentrations of interleukin-1α, interleukin-1β, interleukin-2, interleukin-6, tumor necrosis factor-α, and plasma levels of C-reactive protein, cortisol, and zinc were analyzed. Established indicators of muscle damage (maximal isometric force, range of motion, muscle soreness, and plasma creatine kinase, aspartate aminotransferase, and lactate dehydrogenase activities) were also measured. All measures, including CIR and USG, except for MRI, were assessed immediately before and after and for 5 d post-exercise. MRI was taken at pre- and 1, 3, 6, 10, 23, 31, and 58 d post-exercise. All muscle damage indicators changed significantly after exercise. A large increase in CIR (>20 mm) was found 4-5 d after exercise, and this coincided with USG, showing an increase in muscle thickness. The echointensity of USG increased with the enlargement of the elbow flexors. MRI displayed enlargement of the biceps brachii and brachialis cross-sectional area that started at 1 d, and lasted until 23 d, post-exercise. The most profound increase in the enlargement and signal intensity of the MRI was found 3 or 6 d after exercise. However, none of the plasma levels of inflammatory makers showed significant changes. It is concluded that exercise-induced muscle damage caused muscle swelling, which is indicative of muscle edema, but the inflammatory responses after exercise appear to be different from those accompanying infection or tissue injury.

To examine the effect of progressive resistance training on muscle function, functional performance, balance, body composition, and muscle thickness in men receiving androgen deprivation for prostate cancer. Ten men aged 59-82 yr on androgen deprivation for localized prostate cancer undertook progressive resistance training for 20 wk at 6- to 12-repetition maximum (RM) for 12 upper- and lower-body exercises in a university exercise rehabilitation clinic. Outcome measures included muscle strength and muscle endurance for the upper and lower body, functional performance (repeated chair rise, usual and fast 6-m walk, 6-m backwards walk, stair climb, and 400-m walk time), and balance by sensory organization test. Body composition was measured by dual-energy x-ray absorptiometry and muscle thickness at four anatomical sites by B-mode ultrasound. Blood samples were assessed for prostate specific antigen (PSA), testosterone, growth hormone (GH), cortisol, and hemoglobin. Muscle strength (chest press, 40.5%; seated row, 41.9%; leg press, 96.3%; P < 0.001) and muscle endurance (chest press, 114.9%; leg press, 167.1%; P < 0.001) increased significantly after training. Significant improvement (P < 0.05) occurred in the 6-m usual walk (14.1%), 6-m backwards walk (22.3%), chair rise (26.8%), stair climbing (10.4%), 400-m walk (7.4%), and balance (7.8%). Muscle thickness increased (P < 0.05) by 15.7% at the quadriceps site. Whole-body lean mass was preserved with no change in fat mass. There were no significant changes in PSA, testosterone, GH, cortisol, or hemoglobin. Progressive resistance exercise has beneficial effects on muscle strength, functional performance and balance in older men receiving androgen deprivation for prostate cancer and should be considered to preserve body composition and reduce treatment side effects.

One bout of eccentric exercise produces an adaptation that reduces muscle damage in subsequent bouts. Because it is not known how long this adaptation lasts, the present study investigated the maximal length of the attenuated changes in muscle damage indicators after high-force eccentric exercise. Male students (N = 35) were placed into three groups and performed two bouts of eccentric exercise of the nondominant elbow flexors separated by either 6 (N = 14), 9 (N = 11), or 12 (N = 10) months. Maximal isometric force (MIF), range of motion (ROM), upper arm circumference (CIR), muscle soreness (SOR), and plasma creatine kinase activity (CK) were measured before and for 5 d after exercise. Magnetic resonance (MR) images of the transverse and longitudinal scans of the upper arm were taken 4 d after exercise. Changes in the criterion measures were compared between the first and second bouts and between groups by a two-way repeated measures ANOVA. A faster recovery in MIF was evident after a second bout performed at 6 or 9 months, and reduced SOR as well as smaller increases in CIR, CK, and T2 relaxation time of MR images also occurred after the second exercise bout at 6 months compared with initial responses. No significant differences between the bouts were found for ROM, and the 12-month group did not show any repeated bout effect. These results show that the repeated bout effect for most of the criterion measures lasts at least 6 months but is lost between 9 and 12 months.