Voluntary enhanced cocontraction of hamstring muscles during open kinetic chain leg extension exercise: its potential unloading effect on the anterior cruciate ligament.

BACKGROUND: A number of research studies provide evidence that hamstring cocontraction during open kinetic chain knee extension exercises enhances tibiofemoral (TF) stability and reduces the strain on the anterior cruciate ligament. PURPOSE: To determine the possible increase in hamstring muscle coactivation caused by a voluntary cocontraction effort during open kinetic chain leg-extension exercises, and to assess whether an intentional hamstring cocontraction can completely suppress the anterior TF shear force during these exercises. STUDY DESIGN: Descriptive laboratory study. METHODS: Knee kinematics as well as electromyographic activity in the semitendinosus (ST), semimembranosus (SM), biceps femoris (BF), and quadriceps femoris muscles were measured in 20 healthy men during isotonic leg extension exercises with resistance (R) ranging from 10% to 80% of the 1-repetition maximum (1RM). The same exercises were also performed while the participants attempted to enhance hamstring coactivation through a voluntary cocontraction effort. The data served as input parameters for a model to calculate the shear and compressive TF forces in leg extension exercises for any set of coactivation patterns of the different hamstring muscles. RESULTS: For R≤ 40% 1RM, the peak coactivation levels obtained with intentional cocontraction (l) were significantly higher (P < 10(-3)) than those obtained without intentional cocontraction (l 0). For each hamstring muscle, maximum level l was reached at R = 30% 1RM, corresponding to 9.2%, 10.5%, and 24.5% maximum voluntary isometric contraction (MVIC) for the BF, ST, and SM, respectively, whereas the ratio l/l 0 reached its maximum at R = 20% 1RM and was approximately 2, 3, and 4 for the BF, SM, and ST, respectively. The voluntary enhanced coactivation level l obtained for R≤ 30% 1RM completely suppressed the anterior TF shear force developed by the quadriceps during the exercise. CONCLUSION: In leg extension exercises with resistance R≤ 40% 1RM, coactivation of the BF, SM, and ST can be significantly enhanced (up to 2, 3, and 4 times, respectively) by a voluntary hamstring cocontraction effort. The enhanced coactivation levels obtained for R≤ 30% 1RM can completely suppress the anterior TF shear force developed by the quadriceps during the exercise. CLINICAL RELEVANCE: This laboratory study suggests that leg extension exercise with intentional hamstring cocontraction may have the potential to be a safe and effective quadriceps-strengthening intervention in the early stages of rehabilitation programs for anterior cruciate ligament injury or reconstruction recovery. Further studies, including clinical trials, are needed to investigate the relevance of this therapeutic exercise in clinical practice.

Kv1.1 knock-in ataxic mice exhibit spontaneous myokymic activity exacerbated by fatigue, ischemia and low temperature.

Episodic ataxia type 1 (EA1) is an autosomal dominant neurological disorder characterized by myokymia and attacks of ataxic gait often precipitated by stress. Several genetic mutations have been identified in the Shaker-like K(+) channel Kv1.1 (KCNA1) of EA1 individuals, including V408A, which result in remarkable channel dysfunction. By inserting the heterozygous V408A, mutation in one Kv1.1 allele, a mouse model of EA1 has been generated (Kv1.1(V408A/+)). Here, we investigated the neuromuscular transmission of Kv1.1(V408A/+) ataxic mice and their susceptibility to physiologically relevant stressors. By using in vivo preparations of lateral gastrocnemius (LG) nerve-muscle from Kv1.1(+/+) and Kv1.1(V408A/+) mice, we show that the mutant animals exhibit spontaneous myokymic discharges consisting of repeated singlets, duplets or multiplets, despite motor nerve axotomy. Two-photon laser scanning microscopy from the motor nerve, ex vivo, revealed spontaneous Ca(2+) signals that occurred abnormally only in preparations dissected from Kv1.1(V408A/+) mice. Spontaneous bursting activity, as well as that evoked by sciatic nerve stimulation, was exacerbated by muscle fatigue, ischemia and low temperatures. These stressors also increased the amplitude of compound muscle action potential. Such abnormal neuromuscular transmission did not alter fiber type composition, neuromuscular junction and vascularization of LG muscle, analyzed by light and electron microscopy. Taken together these findings provide direct evidence that identifies the motor nerve as an important generator of myokymic activity, that dysfunction of Kv1.1 channels alters Ca(2+) homeostasis in motor axons, and also strongly suggest that muscle fatigue contributes more than PNS fatigue to exacerbate the myokymia/neuromyotonia phenotype. More broadly, this study points out that juxtaparanodal K(+) channels composed of Kv1.1 subunits exert an important role in dampening the excitability of motor nerve axons during fatigue or ischemic insult.

Improvement of stance control and muscle performance induced by focal muscle vibration in young-elderly women: a randomized controlled trial.

UNLABELLED: Filippi GM, Brunetti O, Botti FM, Panichi R, Roscini M, Camerota F, Cesari M, Pettorossi VE. Improvement of stance control and muscle performance induced by focal muscle vibration in young-elderly women: a randomized controlled trial. OBJECTIVE: To determine the effect of a particular protocol of mechanical vibration, applied focally and repeatedly (repeated muscle vibration [rMV]) on the quadriceps muscles, on stance and lower-extremity muscle power of young-elderly women. DESIGN: Double-blind randomized controlled trial; 3-month follow-up after intervention. SETTING: Human Physiology Laboratories, University of Perugia, Italy. PARTICIPANTS: Sedentary women volunteers (N=60), randomized in 3 groups (mean age +/- SD, 65.3+/-4.2y; range, 60-72). INTERVENTION: rMV (100Hz, 300-500microm, in three 10-minute sessions a day for 3 consecutive days) was applied to voluntary contracted quadriceps (vibrated and contracted group) and relaxed quadriceps (vibrated and relaxed group). A third group received placebo stimulation (nonvibrated group). MAIN OUTCOME MEASURES: Area of sway of the center of pressure, vertical jump height, and leg power. RESULTS: Twenty-four hours after the end of the complete series of applications, the area of sway of the center of pressure decreased significantly by approximately 20%, vertical jump increased by approximately 55%, and leg power increased by approximately 35%. These effects were maintained for at least 90 days after treatment. CONCLUSIONS: rMV is a short-lasting and noninvasive protocol that can significantly and persistently improve muscle performance in sedentary young-elderly women.

Inhibition of muscle spindle afferent activity during masseter muscle fatigue in the rat.

The influence of muscle fatigue on the jaw-closing muscle spindle activity has been investigated by analyzing: (1) the field potentials evoked in the trigeminal motor nucleus (Vmot) by trigeminal mesencephalic nucleus (Vmes) stimulation, (2) the orthodromic and antidromic responses evoked in the Vmes by stimulation of the peripheral and central axons of the muscle proprioceptive afferents, and (3) the extracellular unitary discharge of masseter muscle spindles recorded in the Vmes. The masseter muscle was fatigued by prolonged tetanic masseter nerve electrical stimulation. Pre- and postsynaptic components of the potentials evoked in the Vmot showed a significant reduction in amplitude following muscle fatigue. Orthodromic and antidromic potentials recorded in the Vmes also showed a similar amplitude decrease. Furthermore, muscle fatigue caused a decrease of the discharge frequency of masseter muscle spindle afferents in most of the examined units. The inhibition of the potential amplitude and discharge frequency was strictly correlated with the extent of muscle fatigue and was mediated by the group III and IV afferent muscle fibers activated by fatigue. In fact, the inhibitory effect was abolished by capsaicin injection in the masseter muscle that provokes selective degeneration of small afferent muscle fibers containing neurokinins. We concluded that fatigue signals originating from the muscle and traveling through capsaicin-sensitive fibers are able to diminish the proprioceptive input by a central presynaptic influence. In the second part of the study, we examined the central projection of the masseter small afferents sensitive to capsaicin at the electron-microscopic level. Fiber degeneration was induced by injecting capsaicin into the masseter muscle. Degenerating terminals were found on the soma and stem process in Vmes and on the dendritic tree of neurons in Vmot. This suggests that small muscle afferents may influence the muscle spindle activity through direct synapses on somata in Vmes and on dendrites of neurons in Vmot.