Mechanisms contributing to knee extensor strength loss after prolonged running exercise

The aim of this study was to identify the mechanisms that contribute to the decline in knee extensor (KE) muscles strength after a prolonged running exercise. During the 2 days preceding a 30-km running race [duration 188.7 ± 27.0 (SD) min] and immediately after the race, maximal percutaneous electrical stimulations (single twitch, 0.5-s tetanus at 20 and 80 Hz) were applied to the femoral nerve of 12 trained runners. Superimposed twitches were also delivered during isometric maximal voluntary contraction (MVC) to determine the level of voluntary activation (%VA). The vastus lateralis electromyogram was recorded. KE MVC decreased from pre- to postexercise (from 188.1 ± 25.2 to 142.7 ± 29.7 N · m; P < 0.001) as did %VA (from 98.8 ± 1.8 to 91.3 ± 10.7%; P < 0.05). The changes from pre- to postexercise in these two variables were highly correlated ( R = 0.88; P < 0.001). The modifications in the mechanical response after the 80-Hz stimulation and M-wave peak-to-peak amplitude were also significant ( P < 0.001 and P < 0.05, respectively). It can be concluded that 1) central fatigue, neuromuscular propagation, and muscular factors are involved in the 23.5 ± 14.9% reduction in MVC after a prolonged running bout at racing pace and 2) runners with the greatest KE strength loss experience large activation deficit

Mechanisms contributing to knee extensor strength loss after prolonged running exercise

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Mechanisms contributing to knee extensor strength loss after prolonged running exercise

The aim of this study was to identify the mechanisms that contribute to the decline in knee extensor (KE) muscles strength after a prolonged running exercise. During the 2 days preceding a 30-km running race [duration 188.7 ± 27.0 (SD) min] and immediately after the race, maximal percutaneous electrical stimulations (single twitch, 0.5-s tetanus at 20 and 80 Hz) were applied to the femoral nerve of 12 trained runners. Superimposed twitches were also delivered during isometric maximal voluntary contraction (MVC) to determine the level of voluntary activation (%VA). The vastus lateralis electromyogram was recorded. KE MVC decreased from pre- to postexercise (from 188.1 ± 25.2 to 142.7 ± 29.7 N · m; P < 0.001) as did %VA (from 98.8 ± 1.8 to 91.3 ± 10.7%; P < 0.05). The changes from pre- to postexercise in these two variables were highly correlated ( R = 0.88; P < 0.001). The modifications in the mechanical response after the 80-Hz stimulation and M-wave peak-to-peak amplitude were also significant ( P < 0.001 and P < 0.05, respectively). It can be concluded that 1) central fatigue, neuromuscular propagation, and muscular factors are involved in the 23.5 ± 14.9% reduction in MVC after a prolonged running bout at racing pace and 2) runners with the greatest KE strength loss experience large activation deficit

Asymmetrical after-effects of prism adaptation during goal oriented locomotion

In healthy subjects, sensorimotor after-effects of prism adaptation are known to be symmetric (they appear after using leftward and rightward optical deviations), whereas cognitive after-effects are asymmetric (they appear after using a leftward optical deviation) and rightward oriented. Sensorimotor and cognitive after-effects have been classically studied using different specific tasks. The purpose of the current study was to investigate whether both after-effects may be involved in a same visuo-spatial task. Therefore we compared the amplitude of after-effects following adaptation to a rightward or leftward optical deviation. After-effects were assessed by manual pointing or goal oriented locomotor task. The main result showed a greater amplitude for rightward locomotor after-effects (after adaptation to a leftward deviation) than for leftward locomotor after-effects (after adaptation to a rightward deviation). This means that cognitive after-effects may add to sensorimotor after-effects following adaptation to a leftward optical deviation. This asymmetry challenges the classical distinction between sensorimotor and cognitive after-effects of prism adaptation. Implications for the functional mechanisms and the neuroanatomical substrate of prism adaptation are discussed

Delayed postural control during self-generated perturbations in the frail older adults

Alexandre Kubicki1&ndash;3, Fran&ccedil;ois Bonnetblanc1,2, Geoffroy Petrement3, Yves Ballay1,2, France Mourey2,4&sup1;UFR STAPS, Universit&eacute; de Bourgogne, Dijon, France; &sup2;Motricit&eacute; et Plasticit&eacute;, Institut National de la Sant&eacute; et de la Recherche M&eacute;dicale (INSERM), Dijon, France; &sup3;SARL Fovea Interactive, Campus Industriel &ndash; Espace Entreprises, Chalon sur Sa&ocirc;ne, France; 4UFR M&eacute;decine, Universit&eacute; de Bourgogne, Dijon, FrancePurpose: The aim of this study was to investigate the coordination between posture and movement in pathological aging (frailty) in comparison with normal aging, with the hypothesis that in pathological aging, postural control evolves towards a more reactive mode for which the perturbation induced by the movement is not anticipated and leads to delayed and late postural adjustments.Methods: Elderly subjects performed rapid focal arm-raising movements towards a target, from an upright standing position in two stimuli conditions: simple reaction time and choice reaction time (CRT). Hand and center of pressure (CoP) kinematics were compared between a control group and a frail group of the same age.Results: In frail individuals, the entire movement was impaired and slowed down. In addition, postural adjustments that classically precede and accompany the focal arm movement were delayed and reduced, especially in the CRT condition in which the motor prediction is more limited. Finally, a correlation between the time to CoP maximal velocity and the timed up-and-go score was observed.Conclusion: In these patients, it was concluded that the control of the CoP displacement evolved from a proactive mode in which the perturbation associated with the arm movement is anticipated toward a more reactive mode in which the perturbation is compensated by late and delayed adjustments.Keywords: frailty, anticipatory postural adjustments, backward disequilibriu

Quantifying Paddling Kinematics through Muscle Activation and Whole Body Coordination during Maximal Sprints of Different Durations on a Kayak Ergometer: A Pilot Study

Paddling technique and stroke kinematics are important performance factors in flatwater sprint kayaking and entail significant energetic demands and a high strength from the muscles of the trunk and upper limbs. The various distances completed (from 200 m to 1000 m) require the athletes to optimize their pacing strategy, to maximize power output distribution throughout the race. This study aimed to characterize paddling technique and stroke kinematics during two maximal sprints of different duration. Nine nationally-trained participants (2 females, age: 18 &plusmn; 3 years; BMI: 22.2 &plusmn; 2.0 Kg m&minus;1) performed 40 s and 4 min sprints at maximal intensity on a kayak ergometer. The main findings demonstrated a significantly greater mean stroke power (237 &plusmn; 80 W vs. 170 &plusmn; 48 W; p &lt; 0.013) and rate (131 &plusmn; 8 spm vs. 109 &plusmn; 7 spm; p &lt; 0.001) during the 40 s sprint compared to the 4 min sprint. Athletes used an all-out strategy for the 40 s exercise and a parabolic-shape strategy during the 4 min exercise. Despite the different strategies implemented and the higher muscular activation during the 40 s sprint, no change in paddling technique and body coordination occurred during the sprints. The findings of the present study suggest that the athletes constructed a well-defined profile that was not affected by fatigue, despite a decrease in power output during the all-out strategy. In addition, they regulated their paddling kinematics during the longer exercises, with no change in paddling technique and body coordination

Motor resonance mechanisms are preserved in Alzheimer's disease patients

This study aimed to better characterize the sensorimotor mechanisms underlying motor resonance, namely the relationship between motion perception and movement production in patients suffering from Alzheimer's disease (AD). This work first gives a kinematic description of AD patients' upper limb movements, then it presents a simple paradigm in which a dot with different velocities is moved in front of the participant who is instructed to point to its final position when it stopped. AD patients' actions, as well as healthy elderly participants, were similarly influenced by the dot velocity, suggesting that motor resonance mechanisms are not prevented by pathology. In contrast, only patients had anticipatory motor response: i.e. they started moving before the end of the stimulus motion, unlike what was requested by the experimenter. While the automatic imitation of the stimulus suggests an intact ability to match the internal motor representations with that of the visual model, the uncontrolled motion initiation would indicate AD patients' deficiency to voluntarily inhibit response production. These findings might open new clinical perspectives suggesting innovative techniques in training programs for people with dementia. In particular, the preservation of the motor resonance mechanisms, not dependent on conscious awareness, constitutes an intact basis upon which clinicians could model both physical and cognitive interventions for healthy elderly and AD patients. Furthermore, the evaluation of the inhibitory functions, less sensitive to the level of education than other methods, might be useful for screening test combined with the traditional AD techniques. However, further investigations to understand if this feature is specific to AD or is present also in other neurodegenerative diseases are needed. \ua9 2012 IBRO