Exertional muscle injury: evaluation of concentric versus eccentric actions with serial MR imaging.

Pitman BM, Semmler JG. Reduced short-interval intracortical inhibition after eccentric muscle damage in human elbow flexor muscles. J Appl Physiol 113: 929 -936, 2012. First published July 26, 2012 doi:10.1152/japplphysiol.00361.2012.-The purpose of this study was to use paired-pulse transcranial magnetic stimulation (TMS) to examine the effect of eccentric exercise on short-interval intracortical inhibition (SICI) after damage to elbow flexor muscles. Nine young (22.5 Ϯ 0.6 yr; mean Ϯ SD) male subjects performed maximal eccentric exercise of the elbow flexor muscles until maximal voluntary contraction (MVC) force was reduced by ϳ40%. TMS was performed before, 2 h after, and 2 days after exercise under Rest and Active (5% MVC) conditions with motor-evoked potentials (MEPs) recorded from the biceps brachii (BB) muscle. Peripheral electrical stimulation of the brachial plexus was used to assess maximal Mwaves, and paired-pulse TMS with a 3-ms interstimulus interval was used to assess changes in SICI at each time point. The eccentric exercise resulted in a 34% decline in strength (P Ͻ 0.001), a 41% decline in resting M-wave (P ϭ 0.01), changes in resting elbow joint angle (10°, P Ͻ 0.001), and a shift in the optimal elbow joint angle for force production (18°, P Ͻ 0.05) 2 h after exercise. This was accompanied by impaired muscle strength (27%, P Ͻ 0.001) and increased muscle soreness (P Ͻ 0.001) 2 days after exercise, which is indicative of muscle damage. When the test MEP amplitudes were matched between sessions, we found that SICI was reduced by 27% in resting and 23% in active BB muscle 2 h after exercise. SICI recovered 2 days after exercise when muscle pain and soreness were present, suggesting that delayed onset muscle soreness from eccentric exercise does not influence SICI. The change in SICI observed 2 h after exercise suggests that eccentric muscle damage has widespread effects throughout the motor system that likely includes changes in motor cortex. exercise; motor control; TMS; motor cortex UNACCUSTOMED ECCENTRIC EXERCISE involving the repetitive lengthening of muscle is known to cause significant damage to the ultrastructural and cytoskeletal components of muscle fibers (1) and an impairment in the excitation-contraction coupling process (59). The consequences of this exercise-induced muscle damage are a long-lasting decline in muscle strength, a shift in the optimal muscle length for force generation, muscle swelling, and an increase in passive muscle tension or stiffness (46). Furthermore, muscle pain develops 1 or 2 days after the exercise, which is thought to reflect increased release of noxious chemicals from damaged muscle (39). This delayed onset muscle soreness (DOMS) is not discernible at rest but is elicited under mechanical stimulation such as pressure, stretching, or contraction of the affected muscle (45), which can produce debilitating and long-lasting effects on muscle function (7).Along with these changes in the muscle, several lines of evidence suggest that eccentric muscle damage pro...

Section: Muscle Damage and Neuromotor Performance After Eccentric Exementioning

confidence: 99%

Reduced short-interval intracortical inhibition after eccentric muscle damage in human elbow flexor muscles

Pitman

Semmler

2012

“…A direct relationship among T 2 increase, CK blood level (33, 41), and lactate dehydrogenase activity (41) has been reported in humans during the days following an eccentric exercise, hence indicating that T 2 changes could quantitatively illustrate the damage severity. It has been shown that T 2 increases immediately after a concentric exercise (33, 50) and can remain elevated for a period of 3 mo (43,59). MRI has been used to serially assess skeletal muscle of DMD patients.…”

mentioning

confidence: 99%

Early metabolic changes measured by ¹H MRS in healthy and dystrophic muscle after injury

Pratt

Spangenburg

et al. 2012

Xu S, Pratt SJ, Spangenburg EE, Lovering RM. Early metabolic changes measured by 1 H MRS in healthy and dystrophic muscle after injury. J Appl Physiol 113: 808 -816, 2012. First published June 28, 2012 doi:10.1152/japplphysiol.00530.2012.-Skeletal muscle injury is often assessed by clinical findings (history, pain, tenderness, strength loss), by imaging, or by invasive techniques. The purpose of this work was to determine if in vivo proton magnetic resonance spectroscopy ( 1 H MRS) could reveal metabolic changes in murine skeletal muscle after contraction-induced injury. We compared findings in the tibialis anterior muscle from both healthy wild-type (WT) muscles (C57BL/10 mice) and dystrophic (mdx mice) muscles (an animal model for human Duchenne muscular dystrophy) before and after contraction-induced injury. A mild in vivo eccentric injury protocol was used due to the high susceptibility of mdx muscles to injury. As expected, mdx mice sustained a greater loss of force (81%) after injury compared with WT (42%). In the uninjured muscles, choline (Cho) levels were 47% lower in the mdx muscles compared with WT muscles. In mdx mice, taurine levels decreased 17%, and Cho levels increased 25% in injured muscles compared with uninjured mdx muscles. Intramyocellular lipids and total muscle lipid levels increased significantly after injury but only in WT. The increase in lipid was confirmed using a permeable lipophilic fluorescence dye. In summary, loss of torque after injury was associated with alterations in muscle metabolite levels that may contribute to the overall injury response in mdx mice. These results show that it is possible to obtain meaningful in vivo 1 H MRS regarding skeletal muscle injury.in vivo magnetic resonance spectroscopy; eccentric injury; mdx; muscle damage INTENSE PHYSICAL EXERCISE can cause skeletal muscle damage and inflammation, resulting in pain and a loss of maximal force production. Skeletal muscle injury resulting from high-force lengthening contractions, such as intense physical exercise, is clinically termed a "muscle strain" and is one of the most common ailments seen by physicians. A diagnosis of acute muscle strains is still typically made based on physical exam and patient history. Several direct and indirect indicators of skeletal muscle damage have been observed, including disruption of contractile tissue, cellular accumulation of calcium, delayed onset muscle soreness, a prolonged reduction in muscular strength and range of motion, and an increase in the appearance of muscle proteins in the blood, such as creatine (Cr) kinase (CK), lactate dehydrogenase, and myoglobin (2, 6, 19). Duchenne muscular dystrophy (DMD) is characterized clinically by severe, progressive, and irreversible loss of muscular function. The disease is caused by the lack of dystrophin, a large membrane-associated protein expressed in skeletal muscle and localized to the inner face of the sarcolemma (63). There are significant parallels between the damage incurred after lengthening ("eccentric") contractions ...

“…When quantified on a pixel-by-pixel basis, the areas of muscle demonstrating increased T2 after electrically stimulated exercise [via electromyostimulation (EMS)] (2, 7) have been found to correlate to torque production, allowing T2 magnetic resonance (MR) images to be used as a relative index of muscle activation during exercise (37). Subsequent to eccentric exercise, a delayed increase in the T2 has been observed that peaks 2-6 days after exercise (12,39). This delayed increase correlates to histological assessment of muscle injury in both humans (30) and animals (26) and with changes in other traditional markers of muscle injury such as soreness, serum creatine kinase levels, and isometric force loss (7,12,38).…”

mentioning

confidence: 99%

“…It is well documented that eccentrically exercised muscles demonstrate a delayed increase in T2 that peaks several days after exercise and persists for several weeks (12,39). Debate remains as to the mechanism responsible for this prolonged increase in relaxation time that persists long after other markers of injury have returned to baseline levels.…”

mentioning

confidence: 99%

High specific torque is related to lengthening contraction-induced skeletal muscle injury

Black¹,

Elder²,

Gorgey³

et al. 2008

Black CD, Elder CP, Gorgey A, Dudley GA. High specific torque is related to lengthening contraction-induced skeletal muscle injury. J Appl Physiol 104: 639-647, 2008. First published December 13, 2007 doi:10.1152/japplphysiol.00322.2007.-Animal models implicate multiple mechanical factors in the initiation of exercise-induced muscle injury. Muscle injury has been widely studied in humans, but few data exist regarding the underlying cause of muscle injury. This study sought to examine the role of torque per active muscle volume in muscle injury. Eight subjects performed 80 electrically stimulated [via electromyostimulation (EMS)] eccentric contractions of the right and left quadriceps femoris (QF) through an 80°arc at 120°/s. Specific torque was varied by applying 25-Hz EMS to one thigh and 100-Hz EMS to the contralateral thigh. Transverse relaxation time (T2) magnetic resonance images of the QF were collected before and 3 days after the eccentric exercise bouts. Injury was assessed via changes in isometric force and ratings of soreness over the course of 14 days after exercise and by determining changes in T2 and muscle volume 3 days after exercise. The 100-Hz EMS induced greater force loss (P Ͻ 0. 05), soreness (P Ͻ 0.05), change in muscle volume (P ϭ 0.03), and volume of muscle demonstrating increased T2 (P ϭ 0.005) than the 25-Hz EMS. In addition, injury was found to be similar across the QF in all but the most proximal regions of the QF. Our findings suggest that, in humans, high torque per active volume during lengthening muscle contractions is related to muscle injury. transverse relaxation time magnetic resonance images; electrical stimulation; muscle activation; soreness IT IS WELL ESTABLISHED THAT novel exercise, especially exercise involving lengthening muscle actions, can evoke skeletal muscle injury. Data from animal studies have implicated several mechanical factors as the potential underlying cause or initial event in muscle injury. Contraction force (27, 45), contraction velocity (8, 45), initial muscle length (42), muscle strain (8, 23), and number of eccentric contractions (27,42,46) have been found to contribute to eccentric exercise-induced muscle injury. These studies were performed on a variety of animal species (rabbits, mice, rats) and used multiple in vitro and in situ protocols to induce skeletal muscle injury. It has been suggested that these differences may account for the disparate findings regarding the relative contribution of each factor to muscle injury (11).Few human studies have focused on the underlying mechanisms of exercise-induced muscle injury. As shown in animals, performing contractions at long muscle lengths (29) and increasing the number of eccentric contractions (9) have been shown to cause greater injury. However, the role contraction force plays in muscle injury remains unclear. Eccentric actions recruit fewer motor units to generate a given absolute force (10), and it has been suggested that this is the primary reason eccentric actions cause greater injury than the...