Reduction In Muscle Stiffness Research Articles

THE EFFECT OF STATIC STRETCHING OF THE BICEPS BRACHII ON TORQUE, ELECTROMYOGRAPHY, AND MECHANOMYOGRAPHY.

Recent research has indicated that acute static stretching of a muscle prior to maximal muscular performance may negatively impact strength production, however, the mechanisms responsible for this phenomenon remain unclear. PURPOSE The purpose of this study was to determine the effect of an acute static stretching bout of the biceps brachii on torque, electromyography (EMG), and mechanomyography (MMG) during concentric isokinetic muscle actions. METHODS Eighteen (men, n = 10; women, n = 8) adult subjects (M±SD age = 22.7±2.8 yrs; weight = 78.0±17.0 kg; height = 177.9±11.0 cm) performed maximal isokinetic (30 and 270°s−1) forearm flexion strength testing on two occasions while EMG and MMG were recorded. Subjects were randomly assigned to stretching (STR) or non-stretching (NSTR) protocols before strength testing. RESULTS Two-way ANOVAs with repeated measures revealed no significant (p < 0.05) two-way interaction but a significant main effect for torque (NSTR = M±SEM = 36.9±3.3 Nm; STR = 35.2±3.3 Nm). In addition, a significant two-way interaction for MMG revealed greater amplitude values for STR versus NSTR for 30°s−1 (STR = 93.5±14.4 mV; NSTR = 63.1±10.6 mV) and 270°s−1 (STR = 207.6±35.6 mV; NSTR = 136.4±31.7 mV). For EMG amplitude, there was no significant two-way interaction or main effect for protocol. CONLUSION These results indicated that a greater ability to produce torque without prior stretching is related to the musculotendinous stiffness of the muscle rather than the number of motor units activated. This suggests that performing activities that reduce muscle stiffness (such as stretching or warming up) may be detrimental to performance.

Overnight use of continuous low-level heatwrap therapy for relief of low back pain

Nadler SF, Steiner DJ, Petty SR, Erasala GN, Hengehold DA, Weingand KW. Overnight use of continuous low-level heatwrap therapy for relief of low back pain. Arch Phys Med Rehabil 2003;84:335-42. Objective: To evaluate of the efficacy and safety of 8 hours of continuous, low-level heatwrap therapy administered during sleep. Design: Prospective, randomized, parallel, single-blind (investigator), placebo-controlled, multicenter clinical trial. Setting: Two community-based research facilities. Participants: Seventy-six patients, aged 18 to 55 years, with acute, nonspecific low back pain. Interventions: Subjects were stratified by baseline pain intensity and gender and randomized to one of the following treatments: evaluation of efficacy (heatwrap, n=33; oral placebo, n=34) or blinding (unheated wrap, n=5; oral ibuprofen, n=4). All treatments were administered for 3 consecutive nights with 2 days of follow-up. Main Outcome Measures: Primary: morning pain relief (hour 0) on days 2 through 4 (0[ndash ]5-point verbal response scale). Secondary: mean daytime pain relief score (days 2[ndash ]4, hours 0[ndash ]8), mean extended pain relief score (day 4, hour 0; day 5, hour 0), muscle stiffness, lateral trunk flexibility, and disability (Roland-Morris Disability Questionnaire). Results: Heatwrap therapy was significantly better than placebo at hour 0 on days 2 through 4 for mean pain relief ( P=.00005); at hours 0 through 8 on days 2 through 4 for pain relief ( P[lt ].001); at hour 0 on day 4 and at hour 0 on day 5 for mean pain relief ( P[lt ].001); on day 4 in reduction of morning muscle stiffness ( P[lt ].001); for increased lateral trunk flexibility on day 4 ( P[lt ].002); and for decreased low back disability on day 4 ( P=.005). Adverse events were mild and infrequent. Conclusions: Overnight use of heatwrap therapy provided effective pain relief throughout the next day, reduced muscle stiffness and disability, and improved trunk flexibility. Positive effects were sustained more than 48 hours after treatments were completed. [copy ] 2003 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Relation between changes in long-latency stretch reflexes and muscle stiffness in Parkinson's disease – comparison before and after unilateral pallidotomy

Objective: To study the effects of posteroventral pallidotomy on both the size of long-latency stretch reflex (LLR) and the muscle stiffness in the wrist flexor muscles. Patients and methods: Eleven consecutive patients (right-handed, 6 men and 5 women) underwent left-side microelectrode-guided pallidotomy. The LLR of the contralesional forearm was studied at baseline and 2–3 months after surgery while patients continued to take their optimal medical regimens (‘on’ period). Patients were instructed not to respond to the perturbation (passive mode) or to oppose the mechanical extensor perturbation (active mode). Results: The stretch reflex evoked by extension perturbations of the wrist consisted of a short-latency reflex (M1) and an LLR (M2). Pallidotomy had no effects on the size of M1 components in both passive and active mode and on that of M2 component in the passive mode, however, it significantly reduced M2 component in the active mode ( P<0.05). The inherent muscle stiffness over 60 ms period of mechanical stretch was not influenced by pallidotomy in any experimental condition (preoperative vs. postoperative or passive mode vs. active mode). The hand displacement following M2 component increased significantly after pallidotomy in both passive ( P<0.005) and active mode ( P<0.05). The inverted value of the displacement following M2 component correlated with the size of M2 component ( r=0.60, P<0.001). Conclusions: Pallidotomy decreased the transcortical reflex gain, probably at cortical level, and consequently reduced muscle stiffness.

Botulinum toxin A in cerebral palsy: Functional outcomes

Botulinum toxin A in cerebral palsy: Functional outcomes

Can exercise-induced muscle damage be avoided?

All athletes have experienced the discomfort and debilitating effects of exercise-induced muscle damage. Symptoms are most common at the beginning of the season when intense training is reintroduced after a period of relative inactivity. A plethora of scientific data describes exercise conditions that lead to muscle damage. It is well accepted that damage occurs with unfamiliar exercise, primarily involving eccentric contractions. For example, downhill running places a large eccentric stress on the quadriceps muscle group and commonly results in muscle damage.1 However, muscles that have been preconditioned with eccentric contractions are protected against damage from subsequent bouts of eccentric exercise. This muscle damage is known as the “repeated-bout effect” and has been shown with various forms of exercise in both humans and animal models.2 Despite the many studies describing muscle damage and its various clinical symptoms, few have identified intrinsic causative factors or suitable interventions for limiting the symptoms. Clinically, it is important to first identify people at risk of developing more severe symptoms and then to design interventions that might limit those symptoms. Three recent experimental studies provide clinically relevant information for athletes and physicians.3,4,5 Controlled experimental studies have shown wide variation in symptoms between subjects after a bout of unfamiliar eccentric exercise. These data indicate that some people are more susceptible to damage than others, but it is not clear why. Recently musculoskeletal flexibility has been shown to be an important factor affecting the severity of symptoms after eccentric exercise.3 Flexibility was quantified according to a measure of passive muscle stiffness, and subjects' muscles were categorized as “stiff,” “normal,” or “compliant.” After a bout of eccentric exercise, subjects with stiff muscles had significantly greater loss of strength, pain, muscle tenderness, and elevation of plasma creatine kinase activity than those with compliant muscles. Greater apparent muscle damage was attributed to the inability of the tendon and aponeurosis of stiffer muscles to absorb the lengthening imposed by the eccentric contractions. Warm-up and stretching are known to greatly reduce muscle stiffness.6 Because stiffness seems to predispose muscles to damage, it follows that appropriately warming up before exercise may reduce the severity of exercise-induced muscle damage. It has also been shown that warm-up reduces subsequent symptoms of muscle damage.4 Eccentric contractions of the elbow flexors preceded by a warm-up resulted in significantly less loss of strength and elevation of plasma creatine kinase activity than eccentric contractions without a prior warm-up. The protective effect was attributed to decreased passive muscle stiffness, although actual stiffness measurements were not made. Besides the possible role of warm-ups in limiting the symptoms of muscle damage, preconditioning the muscle with eccentric contractions clearly provides a protective effect (repeated-bout effect). Recent data suggest that it may not be necessary to damage the muscle with the initial bout to provide a protective effect.5 Brown and associates showed that as few as 10 maximal eccentric contractions of the knee extensors were sufficient to reduce symptoms appreciably after a subsequent bout of 50 maximal contractions performed three weeks later. There was a clear repeated-bout effect despite that 10 contractions did not result in appreciable muscle damage. These data indicate that preconditioning muscles with a few maximal eccentric contractions can considerably reduce symptoms after a subsequent, more intense, bout of eccentric exercise. The key elements for the repeated-bout effect are that the preconditioning contractions are eccentric, that high-intensity contractions are performed, and that the preconditioning contractions affect the same muscle groups that will be working eccentrically in the repeated bout. All dynamic sports activities involve a large component of high-intensity eccentric contractions, whether the activity is in a game or a practice. Athletes typically experience considerable symptoms of muscle damage when returning to these activities after a prolonged layoff because of injury or between seasons. The severity of these symptoms may be reduced by maintaining good flexibility, especially of the principal muscle groups involved in the given sport; preconditioning the principal muscle groups with a few high-intensity eccentric contractions one to two weeks before returning to full activities; and performing specific warm-up exercises for the principal muscle groups immediately before the first few training sessions or games. Increasing the athletes' awareness of the cause of symptoms will increase compliance with any intervention directed at limiting muscle damage. This is especially important in sports that do not place a large emphasis on warm-up or flexibility.

Effects of cold water immersion on the symptoms of exercise-induced muscle damage

Cryotherapy is an effective treatment for acute sports injury to soft tissue, although the effect of cryotherapy on exercise-induced muscle damage is unclear. The aim of this study was to assess the effects of cold water immersion on the symptoms of exercise-induced muscle damage following strenuous eccentric exercise. After performing a bout of damage-inducing eccentric exercise (eight sets of five maximal reciprocal contractions at 0.58 rad .s-1) of the elbow flexors on an isokinetic dynamometer, 15 females aged 22.0 2.0 years (mean s) were allocated to a control group (no treatment, n=7) or a cryotherapy group (n=8). Subjects in the cryotherapy group immersed their exercised arm in cold water (15 C) for 15 min immediately after eccentric exercise and then every 12 h for 15 min for a total of seven sessions. Muscle tenderness, plasma creatine kinase activity, relaxed elbow angle, isometric strength and swelling (upper arm circumference) were measured immediately before and for 3 days after eccentric exercise. Analysis of variance revealed significant ( P < 0.05) main effects for time for all variables, with increases in muscle tenderness, creatine kinase activity and upper arm circumference, and decreases in isometric strength and relaxed elbow angle. There were significant interactions ( P < 0.05) of group time for relaxed elbow angle and creatine kinase activity. Relaxed elbow angle was greater and creatine kinase activity lower for the cryotherapy group than the controls on days 2 and 3 following the eccentric exercise. We conclude that although cold water immersion may reduce muscle stiffness and the amount of post-exercise damage after strenuous eccentric activity, there appears to be no effect on the perception of tenderness and strength loss, which is characteristic after this form of activity.

Reduced stretch reflex sensitivity and muscle stiffness after long-lasting stretch-shortening cycle exercise in humans.

It has been suggested that during repeated long-term stretch-shortening cycle (SSC) exercise the decreased neuromuscular function may result partly from alterations in stiffness regulation. Therefore, interaction between the short latency stretch-reflex component (M1) and muscle stiffness and their influences on muscle performance were investigated before and after long lasting SSC exercise. The test protocol included various jumps on a sledge ergometer. The interpretation of the sensitivity of the reflex was based on the measurements of the patellar reflexes and the M1 reflex components. The peak muscle stiffness was measured indirectly and calculated as a coefficient of the changes in the Achilles tendon force and the muscle length. The fatigue protocol induced a marked impairment of the neuromuscular function in maximal SSC jumps. This was demonstrated by a 14.1%-17.7% (n.s. - P < 0.001) reduction in the mean eccentric forces and a 17.3%-31.8% (n.s. - P < 0.05) reduction in the corresponding M1 area under the electromyograms. Both of these methods of assessing the short latency reflex response showed a clear deterioration in the sensitivity of the reflex after fatigue (P < 0.05-0.001). This was also the case for the eccentric peak stiffness of the soleus muscle which declined immediately after fatigue by 5.4% to 7.1% (n.s. - P < 0.05) depending on the jump condition. The results observed would suggest that the modulation of neural input to the muscle was at least partly of reflex origin from the contracting muscle, and furthermore, that the reduced muscle stiffness which accompanied the decreased reflex sensitivity could have been partly responsible for the weakened muscle performance due to impaired utilization of elastic energy.