Decrease In Muscle Force Research Articles

Gait and Neuromuscular Asymmetries after Acute Anterior Cruciate Ligament Rupture

The decreased internal knee extensor moment is a significant gait asymmetry among patients with anterior cruciate ligament (ACL) deficiency, yet the muscular strategy driving this altered moment for the injured limb is unclear. This study aimed to determine whether patients with ACL deficiency and characteristic knee instability would demonstrate normal extensor and increased flexor muscle force to generate a decreased internal extensor moment (i.e., use a hamstring facilitation strategy). Gait analysis was performed on 31 athletes with acute ACL rupture who exhibited characteristic knee instability after injury. Peak internal knee extensor moment was calculated using inverse dynamics, and muscle forces were estimated using an electromyography-driven modeling approach. Comparisons were made between the injured and contralateral limbs. As expected, patients demonstrated decreased peak knee flexion (P = 0.028) and internal knee extensor moment (P = 0.0004) for their injured limb but exhibited neither an isolated decrease in extensor force (quadriceps avoidance) nor an isolated increase in flexor force (hamstring facilitation) at peak knee moment. Instead, they exhibited decreased muscle force from both flexor (P = 0.0001) and extensor (P = 0.0103) groups. This strategy of decreased muscle force may be explained in part by muscle weakness that frequently accompanies ACL injury or by apprehension, low confidence, and fear of further injury. This is the first study to estimate muscle forces in the ACL-deficient knee using an electromyography-driven approach. These results affirm the existence of neuromuscular asymmetries in the individuals with ACL deficiency and characteristic knee instability.

Leaky ryanodine receptors in β-sarcoglycan deficient mice: a potential common defect in muscular dystrophy

BackgroundDisruption of the sarcolemma-associated dystrophin-glycoprotein complex underlies multiple forms of muscular dystrophy, including Duchenne muscular dystrophy and sarcoglycanopathies. A hallmark of these disorders is muscle weakness. In a murine model of Duchenne muscular dystrophy, mdx mice, cysteine-nitrosylation of the calcium release channel/ryanodine receptor type 1 (RyR1) on the skeletal muscle sarcoplasmic reticulum causes depletion of the stabilizing subunit calstabin1 (FKBP12) from the RyR1 macromolecular complex. This results in a sarcoplasmic reticular calcium leak via defective RyR1 channels. This pathological intracellular calcium leak contributes to reduced calcium release and decreased muscle force production. It is unknown whether RyR1 dysfunction occurs also in other muscular dystrophies.MethodsTo test this we used a murine model of Limb-Girdle muscular dystrophy, deficient in β-sarcoglycan (Sgcb−/−).ResultsSkeletal muscle RyR1 from Sgcb−/− deficient mice were oxidized, nitrosylated, and depleted of the stabilizing subunit calstabin1, which was associated with increased open probability of the RyR1 channels. Sgcb−/− deficient mice exhibited decreased muscle specific force and calcium transients, and displayed reduced exercise capacity. Treating Sgcb−/− mice with the RyR stabilizing compound S107 improved muscle specific force, calcium transients, and exercise capacity. We have previously reported similar findings in mdx mice, a murine model of Duchenne muscular dystrophy.ConclusionsOur data suggest that leaky RyR1 channels may underlie multiple forms of muscular dystrophy linked to mutations in genes encoding components of the dystrophin-glycoprotein complex. A common underlying abnormality in calcium handling indicates that pharmacological targeting of dysfunctional RyR1 could be a novel therapeutic approach to improve muscle function in Limb-Girdle and Duchenne muscular dystrophies.

Skeletal muscle force is preserved in NOX4 deficient mice

NADPH oxidase levels are elevated in various cardiovascular diseases. The NOX4 isoform of NADPH oxidase generates reactive oxygen species that promotes calcium release in skeletal muscle. NOX4 knockdown depresses maximal tetanic force in mouse EDL muscle. We tested the hypotheses that NOX4 deficient mice would have decreased muscle force, rightward shift in the force‐frequency relationship, and accelerated fatigue in vitro. We studied intact soleus muscle from genetic control (C57BL/6J) and NOX 4 knockout mice (n = 7/group; 2 males/group) at 95%O2 and 37°C. Our initial experiments suggest no difference in maximal soleus tetanic force (Po) between groups (in N/cm2; Control 32 ± 6, NOX 4−/− 36 ± 4). Neither the stimulus frequency that elicited 50% Po (Control 53 ± 3 Hz; NOX4−/− 53 ± 8 Hz) nor muscle fatigue (not shown) was affected by NOX4 deficiency. Our study suggests that skeletal muscle force is preserved in mice lacking NOX4 isoform of NADPH oxidase.

Urocortins Improve Dystrophic Skeletal Muscle Structure and Function through Both PKA- and Epac-Dependent Pathways

In Duchenne muscular dystrophy, the absence of dystrophin causes progressive muscle wasting and premature death. Excessive calcium influx is thought to initiate the pathogenic cascade, resulting in muscle cell death. Urocortins (Ucns) have protected muscle in several experimental paradigms. Herein, we demonstrate that daily s.c. injections of either Ucn 1 or Ucn 2 to 3-week-old dystrophic mdx(5Cv) mice for 2 weeks increased skeletal muscle mass and normalized plasma creatine kinase activity. Histological examination showed that Ucns remarkably reduced necrosis in the diaphragm and slow- and fast-twitch muscles. Ucns improved muscle resistance to mechanical stress provoked by repetitive tetanizations. Ucn 2 treatment resulted in faster kinetics of contraction and relaxation and a rightward shift of the force-frequency curve, suggesting improved calcium homeostasis. Ucn 2 decreased calcium influx into freshly isolated dystrophic muscles. Pharmacological manipulation demonstrated that the mechanism involved the corticotropin-releasing factor type 2 receptor, cAMP elevation, and activation of both protein kinase A and the cAMP-binding protein Epac. Moreover, both STIM1, the calcium sensor that initiates the assembly of store-operated channels, and the calcium-independent phospholipase A(2) that activates these channels were reduced in dystrophic muscle by Ucn 2. Altogether, our results demonstrate the high potency of Ucns for improving dystrophic muscle structure and function, suggesting that these peptides may be considered for treatment of Duchenne muscular dystrophy.

Fluvastatin-induced alterations of skeletal muscle function in hypercholesterolaemic rats

Although statins, the most widely used drugs in the treatment of hyperlipidaemia, are generally accepted as efficient and safe drugs their side-effects on skeletal muscle have been reported with increasing frequency. The lack of an animal model in which these side effects would consistently be observed is one of the important drawbacks in studying statin associated myopathy. To overcome this and enable the studying of the effects of fluvastatin on skeletal muscles an animal model with high blood cholesterol levels was developed. In these animals cholesterol levels rose more than seven fold (from 1.5 ± 0.1 to 10.7 ± 2.0 mmol/l; n = 15 and 16) with a dramatic increase in low density lipoprotein/high density lipoprotein ratio (from 0.29 ± 0.02 to 1.56 ± 0.17). While the latter was reversed by statin treatment, an elevation in blood creatine kinase (CK) level indicated the presence of muscle wasting. Fibers from m. extensor digitorum longus (EDL) showed significant reduction in cross sectional area in the statin treated groups. Statin treatment also decreased the proliferation and fusion of skeletal myotubes in culture. In line with this, resting intracellular calcium concentration ([Ca(2+)](i)) was reduced in statin treated satellite cells and myotubes. On the other hand, in adult skeletal muscle fibers statin treatment increased resting [Ca(2+)](i) (116 ± 4 nM vs. 151 ± 5 nM; n = 33 and 34) and decreased both twitch and tetanic force both in EDL and m. soleus. In addition, in m. soleus the duration of twitch and tetanic force was shortened. These results clearly indicate that statin administration in these animals results in a myopathy characterized by decreased muscle force and elevated plasma CK level.

Catechins attenuate eccentric exercise-induced inflammation and loss of force production in muscle in senescence-accelerated mice

Catechins have a great variety of biological actions. We evaluated the potential benefits of catechin ingestion on muscle contractile properties, oxidative stress, and inflammation following downhill running, which is a typical eccentric exercise, in senescence-accelerated prone mice (SAMP). Downhill running (13 m/min for 60 min; 16° decline) induced a greater decrease in the contractile force of soleus muscle and in Ca(2+)-ATPase activity in SAMP1 compared with the senescence-resistant mice (SAMR1). Moreover, compared with SAMR1, SAMP1 showed greater downhill running-induced increases in plasma CPK and LDH activity, malondialdehyde, and carbonylated protein as markers of oxidative stress; and in protein and mRNA expression levels of the inflammatory mediators such as tumor necrosis factor-α and monocyte chemoattractant protein-1 in muscle. SAMP1 exhibited aging-associated vulnerability to oxidative stress and inflammation in muscle induced by downhill running. Long-term (8 wk) catechin ingestion significantly attenuated the downhill running-induced decrease in muscle force and the increased inflammatory mediators in both plasma and gastrocnemius muscle. Furthermore, catechins significantly inhibited the increase in oxidative stress markers immediately after downhill running, accompanied by an increase in glutathione reductase activity. These findings suggest that long-term catechin ingestion attenuates the aging-associated loss of force production, oxidative stress, and inflammation in muscle after exercise.

Tea catechins prevent contractile dysfunction in unloaded murine soleus muscle: A pilot study

Objective Extended periods of muscle disuse, physical inactivity, immobilization, and bedrest result in a loss of muscle mass and a decrease in muscle force, which are accompanied by an increase in oxidative stress. We investigated the effects of the intake of green tea catechins on unloading-induced muscle dysfunction in tail-suspended mice. Methods Ten-week-old male BALB/c mice were fed a purified control diet or a diet containing 0.5% tea catechins for 14 d. Thereafter, the mice were subjected to continuous tail suspension for 10 d. On the final day, muscle mass, contractile force production, antioxidant potential, and carbonylated protein levels were evaluated. Results Hind limb unloading caused a loss of soleus muscle weight and muscle force. Intake of tea catechins significantly inhibited the unloading-induced decrease in force in isolated soleus muscle by 19% compared with the control group, although tea catechins did not affect muscle weight. In addition, intake of tea catechins suppressed the decrease in antioxidant potential and the increase in carbonyl myofibrillar protein. Conclusion Ingestion of tea catechins minimized contractile dysfunction in skeletal muscle and muscle atrophy in unloaded muscle. This effect might be partly due to the lower oxidative modification of myofibrillar protein through the antioxidant activity of tea catechins.

Early exercise and attenuation of myopathy in the patient with sepsis in ICU

Background: Many survivors of severe illness and intensive care admission have decreased quality of life of which decreased physical recovery plays a major part. Those with sepsis syndromes in particular have been shown to have increased mortality and poor quality of life compared to other survivors in intensive care.Objectives: This review aimed to discuss mechanics of myopathy in sepsis and examine the evidence that these are able to be prevented by early activity in intensive care.Major findings: There are a number of exercise trials conducted in general intensive care patients. These have positive findings indicating that early intervention with exercise is able to prevent critical illness weakness syndromes, and loss of muscle mass, decrease duration of mechanical ventilation, length of hospital and intensive care unit (ICU) stay and improve overall quality of life. Specific changes and mechanisms responsible for decreases in muscle force and muscle mass in sepsis syndromes and possible interventions are discussed. As many of these findings are extrapolated from animal studies, there is a need for further research into mechanisms of myopathy in intensive care patients.Conclusions: Controlled clinical trials need to be conducted specifically on patients with sepsis syndromes. Longer term outcomes such as health related quality of life, mortality, duration of ventilation and length of ICU stay are important to investigate. It is also important to identify specific effects of exercise on the mechanisms of myopathy in sepsis. Once this has been proven, research needs to be undertaken so specific levels of exercise can be safely recommended.

Low level laser therapy before eccentric exercise reduces muscle damage markers in humans

The purpose of the present study was to determine the effect of low level laser therapy (LLLT) treatment before knee extensor eccentric exercise on indirect markers of muscle damage. Thirty-six healthy men were randomized in LLLT group (n = 18) and placebo group (n = 18). After LLLT or placebo treatment, subjects performed 75 maximal knee extensors eccentric contractions (five sets of 15 repetitions; velocity = 60° seg(-1); range of motion = 60°). Muscle soreness (visual analogue scale--VAS), lactate dehydrogenase (LDH) and creatine kinase (CK) levels were measured prior to exercise, and 24 and 48 h after exercise. Muscle function (maximal voluntary contraction--MVC) was measured before exercise, immediately after, and 24 and 48 h post-exercise. Groups had no difference on kineanthropometric characteristics and on eccentric exercise performance. They also presented similar baseline values of VAS (0.00 mm for LLLT and placebo groups), LDH (LLLT = 186 IU/l; placebo = 183 IU/l), CK (LLLT = 145 IU/l; placebo = 155 IU/l) and MVC (LLLT = 293 Nm; placebo = 284 Nm). VAS data did not show group by time interaction (P = 0.066). In the other outcomes, LLLT group presented (1) smaller increase on LDH values 48 h post-exercise (LLLT = 366 IU/l; placebo = 484 IU/l; P = 0.017); (2) smaller increase on CK values 24 h (LLLT = 272 IU/l; placebo = 498 IU/l; P = 0.020) and 48 h (LLLT = 436 IU/l; placebo = 1328 IU/l; P < 0.001) post-exercise; (3) smaller decrease on MVC immediately after exercise (LLLT = 189 Nm; placebo = 154 Nm; P = 0.011), and 24 h (LLLT = 249 Nm; placebo = 205 Nm; P = 0.004) and 48 h (LLLT = 267 Nm; placebo = 216 Nm; P = 0.001) post-exercise compared with the placebo group. In conclusion, LLLT treatment before eccentric exercise was effective in terms of attenuating the increase of muscle proteins in the blood serum and the decrease in muscle force.

Effect Of Local Vibration Treatment On Muscle Damage Parameters Following Eccentric Muscle Contractions.

It is well known that eccentric muscle contractions induce muscle damage resulting in prolonged decrease in muscle force and increases in muscle soreness and serum creatine kinase activity. Numerous studies have examined several interventions to reduce muscle damage and induce faster recovery but the results from studies are controversial. PURPOSE: To investigate the effect of local vibration treatment on muscle force production(%MVC), muscle soreness(SOR), and blood parameters including creatine kinase(CK) and aspartate transaminase(AST) following high force eccentric muscle contractions. METHODS: Twenty four healthy male subjects were randomly assigned to either control(CON, n=8), single vibration treatment(SVG, n=8), or 3-day vibration treatment(3VG, n=8) group. Each subject performed 2 sets of 25 maximal eccentric muscle contractions of elbow flexors using modified arm curl machine. SVG performed 10-min vibration immediately after exercise using whole body vibration equipment where both hands were placed on the vibrating surface of the equipment on each subject's knees and the frequency of vibration was 20Hz. 3VG performed 10-min vibration at 24, 48, and 72 hours after exercise. %MVC, SOR and blood parameters were measured pre, immediately after, 24, 48, 72, and 96 hours after exercise. To determine the effect of group by time interaction, one-way ANOVA repeated measure was used. RESULTS: There was a significant group by time interaction in %MVC(p< 0.001) where 3VG had a faster recovery at 48, 72, and 96 hours after exercise compared to CON and SVG. Additionally, there was a significant group by time interaction in SOR(p<0.05) where 3VG had a lower SOR and a faster recovery at 48, 72, and 96 hours after exercise compared to CON and SVG. However, there were no significant group by time effects in CK (p=1.00) and AST(p=0.89). CONCLUSIONS: The local vibration treatment following eccentric muscle contractions may be a beneficial intervention to elicit a faster recovery in muscle force generation and muscle soreness when the multiple treatments are conducted.

Influence of electrical stimulation frequency on skeletal muscle force and fatigue

Objective The aim of this study is to determine the impact of electrical stimulation frequency on muscle force and fatigue and propose application modalities in regards to sports or clinical rehabilitation training. Methods The maximal voluntary contraction (MVC) force of the quadriceps femoris muscle was recorded before, during and after electrical stimulation in 26 healthy adults during 20-minute sessions corresponding to 60 of 5-second contractions separated by 15-second rest periods. Three different frequencies were used: 100, 50 and 20 Hz. Results With a frequency of 100 Hz, we obtained 71% of the MVC force at the beginning of the session (MVCb). The decrease in muscle force at the end of the session is significantly greater for the highest frequencies respectively 27, 33 and 38% of MVCb for 100, 50 and 20 Hz. Conclusion The impact of electrical stimulation to improve muscle force seems to be dependent on frequency, intensity pulse trains and number of contractions per session. Higher intensity and higher frequency induce stronger muscular contractions, but also a stronger decline in force and thus quick-setting muscle fatigue. Classical 20-minute training sessions with many contractions (60 or more) do not seem appropriate for sports training or clinical rehabilitation programs.

Prolonged Muscle Damage Depends on Force Variability

Skeletal muscle damage frequently occurs after eccentric exercise, however, the relationship between intraindividual variability of eccentric exercise and skeletal muscle damage is not clear yet. The aim of the study was to test the hypothesis that prolonged decrease in skeletal muscle force depends on intraindividual variability of eccentric exercise. Eleven healthy men were asked to perform knee eccentric extension of 10 series with 12 repetitions (EE) with maximal intensity at 160 degrees/s. The maximal voluntary knee extension isometric torque (MVC) of the quadriceps muscle and isokinetic concentric torque (IT) at 30 degrees/s of knee angles were established before and 2 min, 60 min, 24 h and 14 days after EE. At 24 h and 48 h after EE muscle soreness and creatine kinase activity before and at 48 h after EE were calculated. The intraindividual variability of EE and autocorrelation coefficient of EE were calculated. We observed a significant decrease in MVC and IT after EE. The maximal isokinetic torque shifted to longer muscle length after EE. It was concluded that longer lasting (within 14 days) indirect symptoms of exercise induced muscle damage (decrease in muscle force) are closely related to variability of EE.

The effect of triangular fibrocartilage complex injury on extensor carpi ulnaris function and friction

Background It has been previously shown that injury to the triangular fibrocartilage complex increases the moment arm of the extensor carpi ulnaris. This will reduce the force producing capacity of the muscle in some situations, but will also increase its mechanical advantage. It is also possible that the change in the tendon path may increase tendon friction, predisposing the patient to future repetitive motion injury. It is the purpose of this study to determine the effects of triangular fibrocartilage complex injury on extensor carpi ulnaris moment producing capacity and tendon friction. Methods A simple simulation was used to examine muscle moment producing capacity throughout the range of motion, at varying speeds and in both injured and healthy states. Six fresh frozen human cadaveric wrists were used to determine the effect of injury on tendon friction. A custom made device was used to move the wrists through a range of motion, while a constant force was applied to the proximal tendon and force was recorded at the distal tendon. Friction was measured before and after the creation of injury. Findings The decreases in muscle force following injury were small, even in the worse case. The moment producing capacity of the muscle was increased following injury. Tendon friction during flexion–extension was decreased following injury. The friction during radial-ulnar deviation was unchanged. Interpretation When making surgical decisions about triangular fibrocartilage complex repair, it is not necessary to consider extensor carpi ulnaris moment producing capacity or tendon friction.

Is interstitial K+ accumulation a key factor in the fatigue process under physiological conditions?

Muscle fatigue, i.e. the decrease in muscle force in response to prolonged or repeated contractions, can originate from any impairment along the neuromuscular system, from a reduction in central neural drive to impaired contractile protein interaction. At the muscle level, a decrease in the force-generating capacity can result from (i) an impaired force per cross-bridge, (ii) a reduced myofibrillar Ca2+ sensitivity and (iii) a decreased Ca2+ release from the sarcoplasmic reticulum (SR). During prolonged activity, the interstitial K+ increases and concentrations of 10–12 mm have been observed. Therefore, resultant sarcolemmal excitability, leading to a reduction in the amplitude of the action potential, can result in impaired SR Ca2+ release. This last factor was the point of interest in a recent article in The Journal of Physiology by Clausen & Nielsen (2007), that investigated the effect of excitability failure on force production during fatigue of rat soleus muscle exposed to different bath K+ concentrations ([K+]o). Clausen & Nielsen showed that the rate of force decline was greater when muscle was pre-exposed for 10–40 min to a high [K+]o (10 mm) and then electrically stimulated compared with low [K+]o (4 mm). They also showed that this increased fatigability could be counteracted by applying different agents known to directly or indirectly stimulate the Na+–K+ pumps. Thus, the data obtained by Clausen & Nielsen (2007) strongly indicate that these high [K+]o values induce a reduction in sarcolemmal excitability, leading to a decrease in soleus endurance which can be prevented by the stimulation of the Na+–K+ pump. Nevertheless, it is possible that these results are confined to the experimental conditions used to induce fatigue. In their study, Clausen & Nielsen (2007) stimulated soleus muscle continuously at 60 Hz for 1 min; muscle endurance was then assessed by calculating the rate of force decline over the first 20 s of stimulation. In this letter, the possibility that a rise in [K+]o may not be a critical factor of muscle fatigue under physiological conditions is discussed.

Markers of inflammation and disuse in vastus lateralis of chronic obstructive pulmonary disease patients

Disuse and/or local inflammation in the muscle cannot be excluded as potential influences for the decreased muscle force in patients hospitalised due to an acute chronic obstructive pulmonary disease (COPD) exacerbation. This study aims to compare expression levels of markers of disuse (insulin-like growth factor-1 (IGF-I), MyoD and myogenin) and inflammation [interleukin-6 (IL-6), IL-8 and tumour necrosis factor-alpha (TNF-alpha)] in the muscle of hospitalised and stable COPD patients and healthy elderly. Muscle biopsies (m. vastus lateralis) were taken in 14 hospitalised COPD patients (aged 68 +/- 8), 11 clinically stable COPD patients (aged 68 +/- 9) and seven healthy subjects (aged 70 +/- 7) to analyse local mRNA expression levels of IL-6, IL-8, TNF-alpha, IGF-I and protein expression levels of IGF-I, MyoD and myogenin. Relationships of these expression levels with lung and skeletal muscle function were investigated. IGF-I mRNA and MyoD protein levels were significantly lower in hospitalised patients compared to healthy subjects. MyoD protein levels were positively related to quadriceps force. Muscle IL-6 and IL-8 expression in hospitalised patients was similar compared to stable patients and healthy subjects and was not related to expression levels of muscle markers of disuse or quadriceps force. Muscle TNF-alpha and myogenin were not detected. Decreased expression levels of muscle IGF-I and MyoD in hospitalised patients suggest a potential influence of disuse in the increased muscle weakness during an acute COPD exacerbation. This study did not find any evidence supporting local inflammation via IL-6, IL-8 and/or TNF-alpha in the vastus lateralis muscle of COPD patients.

Effects of chronic sepsis on rat motor units: Experimental study of critical illness polyneuromyopathy

Critical illness polyneuromyopathy (CIP) leads to major muscle weakness correlated with peripheral nerve and/or muscle alterations. Because sepsis seems to be the main factor, we used an experimental model of chronic sepsis in rats to study the localization of the first alterations on isolated motor units of soleus muscle. Seven days of chronic sepsis leads to a decrease in muscle force and an increase in muscle fatigability. Muscle twitch contraction time is also slower and all the motor units exhibit a slow profile in septic rats. Motor axon conduction velocity remains normal. We observed a significant increase in the latency between nerve and muscle action potentials but no modifications in the electromechanical delay. The first action of sepsis on motor units seems to be a delayed trigger of muscle action potential along with a muscle weakness but without nerve conduction impairment.

Decreased motor unit firing rate and force control in older men

Introduction Ageing is related to muscle atrophy that leads to decreases in muscle force. The largest changes are found in fast muscle fibres and fast force production, reducing the capability to recover from sudden balance disturbances. Also ageing-related decrease in force control has been found, as indicated by an increase in force fluctuations and motor unit (MU) firing variability (Galganski et al. 1993). Possibly due to differences in measurement protocols and muscles, the results concerning the effects of ageing on motor unit firing rate are, however, somewhat contradictory (for review, see Roos et al. 1997). The purpose of the present study was to investigate the age-related changes in the firing properties of the Soleus muscle, which has an important role in locomotion and balance.

Effect of stretching on agonist–antagonist muscle activity and muscle force output during single and multiple joint isometric contractions

Eight moderately active male subjects where tested for peak force in an isometric knee extension test and peak force and rate of force development in an isometric squat test. Both tests where performed at a 100 degrees knee angle and average integrated electromyography (IEMG) was measured from the vastus medialis (VM), vastus lateralis (VL) and biceps femoris (BF) muscles. Subjects performed the two conditions, stretching (S) or control (C) in a randomized order. Subjects where tested for baseline strength measures in both the isometric knee extension and isometric squat and then either stretched or sat quietly for 10 min. Following S or C subjects where then tested at six time points. Following S peak force in the isometric knee extension was significantly (P < or = 0.05) less than C at 1, 2, 8 and 16 min post. No significant difference in peak force was found between S and C in the isometric squat. However, following S the rate of force development in the isometric squat was significantly less than C at immediately post. No significant differences where observed in IEMG of the VM or VL between S and C in either the isometric knee extension or isometric squat. However, IEMG significantly decreased in the BF at 1 min post after S in comparison with C in both the isometric knee extension and isometric squat. Stretching appears to decrease muscle force output in a single joint isometric contraction and rate of force development in a multiple joint isometric contraction. Possible changes in agonist-antagonist muscle activity patterns need to be further examined.

The Effects Of Stretching On Lower Body Strength And Functional Power Performance

Many athletes stretch prior to competition or practice with the expectation that increased flexibility will translate into better on-field performance. This is based on studies indicating that a pre-stretched skeletal muscle that is immediately stimulated to contract will exhibit greater contractile performance. However, results from other studies indicate that stretching a muscle prior to contraction produces a decrease in muscle force generating ability. PURPOSE The purpose of this study was to determine whether prior static stretching has any adverse influence on the performance of lower body strength and functional power performance. METHODS 14 male soccer players ages 18–22 were divided into stretch (S) and control (C) groups and tested on subsequent days. Day 1 assessed the effect of stretching on vertical jump. Following a warm-up, both groups were allowed three jump attempts followed by a five minute rest period. Following the five minute rest period, the S group performed three sets of thirty seconds passive stretch using the sit and reach, standing quad stretch and a standing calf stretch while the C group rested. The vertical jump of both groups was then re-evaluated as previously stated. Day 2 assessed the effect of stretching on strength performance via a 3-Repitition Maximum (3-RM) barbell squat test. Following a warm-up, both groups were tested for their 3-RM barbell squat followed by a 5 minute rest period. Following the five minute rest period, the S group performed three sets of thirty second passive individual stretch as previously described, while the C group rested. Both groups were then re-evaluated for their 3-RM barbell squat. RESULTS Following the stretching exercises the vertical jump of the S group experienced a significant (p=0.000) decrease, from 25.9 ± 2.2 in (mean ± SD) to 24.6 ± 2.5 in. While the vertical jump of the C group remained the same (24.2 ± 3.5 in and 23.9 ± 3.7 in) (p=0.059). However, following the stretching exercises; although there were deceases in 3-RM for both groups, there were no significant reductions in the 3-RM barbell squat subsequent to the stretch (S group p=0.125 and C group p=0.094). CONCLUSIONS These data indicate that stretching prior to competition may hamper on-field performance, particularly in those sports requiring jumping. Therefore, stretching should be limited and performed for relative short durations in order to prevent injuries or other warm up techniques should be used. Although, the 3-RM squat was reduced for both groups the difference between the groups was not significant indicating that maximal strength was not effected.

The Effects Of Stretching On Lower Body Strength And Functional Power Performance

Many athletes stretch prior to competition or practice with the expectation that increased flexibility will translate into better on-field performance. This is based on studies indicating that a pre-stretched skeletal muscle that is immediately stimulated to contract will exhibit greater contractile performance. However, results from other studies indicate that stretching a muscle prior to contraction produces a decrease in muscle force generating ability. PURPOSE The purpose of this study was to determine whether prior static stretching has any adverse influence on the performance of lower body strength and functional power performance. METHODS 14 male soccer players ages 18–22 were divided into stretch (S) and control (C) groups and tested on subsequent days. Day 1 assessed the effect of stretching on vertical jump. Following a warm-up, both groups were allowed three jump attempts followed by a five minute rest period. Following the five minute rest period, the S group performed three sets of thirty seconds passive stretch using the sit and reach, standing quad stretch and a standing calf stretch while the C group rested. The vertical jump of both groups was then re-evaluated as previously stated. Day 2 assessed the effect of stretching on strength performance via a 3-Repitition Maximum (3-RM) barbell squat test. Following a warm-up, both groups were tested for their 3-RM barbell squat followed by a 5 minute rest period. Following the five minute rest period, the S group performed three sets of thirty second passive individual stretch as previously described, while the C group rested. Both groups were then re-evaluated for their 3-RM barbell squat. RESULTS Following the stretching exercises the vertical jump of the S group experienced a significant (p=0.000) decrease, from 25.9 ± 2.2 in (mean ± SD) to 24.6 ± 2.5 in. While the vertical jump of the C group remained the same (24.2 ± 3.5 in and 23.9 ± 3.7 in) (p=0.059). However, following the stretching exercises; although there were deceases in 3-RM for both groups, there were no significant reductions in the 3-RM barbell squat subsequent to the stretch (S group p=0.125 and C group p=0.094). CONCLUSIONS These data indicate that stretching prior to competition may hamper on-field performance, particularly in those sports requiring jumping. Therefore, stretching should be limited and performed for relative short durations in order to prevent injuries or other warm up techniques should be used. Although, the 3-RM squat was reduced for both groups the difference between the groups was not significant indicating that maximal strength was not effected.