The Effects of Vertical vs. Horizontal plyometric Training on Sprinting Kinetics in Post Peak Height Female Student Athletes

Plyometric training is a form of jump training that is a useful method to improve sprinting speed due to its propensity to improve neural efficiency, increase joint stiffness and contraction speed. While research has shown that plyometrics can improve jumping and sprinting performance, no studies have compared the effects of different types of plyometric training on sprinting speed in young females. Therefore, the aim of the study was to compare different forms of plyometric training (horizontal and vertical) on sprinting performance in young females. Thirty young females from a private girls college were randomly divided into two groups and trained for seven weeks, twice a week; vertical plyometric (n=11, age 13.50 ± 0.96, peak heigh velocity-PHV: 1.60 ± 1.14), horizontal plyometric training (n=10, 13.40 ± 0.92, PHV:1.60 ± 0.93), and a physical education class as a control (n=15, age, 15.60 ± 0.31, PHV: 2.90 ± 0.55). Participants were tested for sprinting kinetics i.e. force (Fo), maximum power (Pmax), theoretical velocity (Vo), maximal velocity (Vmax), 10, 20 and 30 m split times using a radar gun over 30 m, isometric strength, vertical jump height and horizontal jump distance before and after the intervention. Both the intervention groups significantly improved all performance variables (g= 0.32- 1.30; p<0.05). The vertical group improved all kinetic variables except Fo and Pmax whereas the horizontal group improved all kinetic variables with a greater effect size g= 0.40-1.30. In comparison to the control group, the vertical group significantly improved Vo, Vmax, vertical and broad jump scores whereas the horizontal group significantly improved broad jump and 20 m split time scores (p<0.05). The findings of this study suggest that horizontal plyometric training is more effective in improving sprinting kinetics.

Lack of increased rate of force development after strength training is explained by specific neural, not muscular, motor unit adaptations

While maximal force increases following short-term isometric strength training, the rate of force development (RFD) may remain relatively unaffected. The underlying neural and muscular mechanisms during rapid contractions after strength training are largely unknown. Since strength training increases the neural drive to muscles, it may be hypothesized that there are distinct neural or muscular adaptations determining the change in RFD independently of an increase in maximal force. Therefore, we examined motor unit population data acquired from surface electromyography during the rapid generation of force before and after four weeks of strength training. We observed that strength training did not change the RFD because it did not influence the number of motor units recruited per second or their initial discharge rate during rapid contractions. While strength training did not change motoneuron behaviour in the force increase phase of rapid contractions, it increased the discharge rate of motoneurons (by ~4 spikes/s) when reaching the plateau phase (~150 ms) of the rapid contractions, determining an increase in maximal force production. Computer simulations with a motor unit model that included neural and muscular properties, closely matched the experimental observations and demonstrated that the lack of change in RFD following training is primarily mediated by an unchanged maximal recruitment speed of motoneurons. These results demonstrate that maximal force and contraction speed are determined by different adaptations in motoneuron behaviour following strength training and indicate that increases in the recruitment speed of motoneurons are required to evoke training-induced increases in RFD.

Pain-induced changes in motor unit discharge depend on recruitment threshold and contraction speed

At high forces, the discharge rates of lower and higher threshold motor units (MU) are influenced in a different way by muscle pain. These differential effects may be particularly important for performing contractions at different speeds since the proportion of lower and higher threshold MUs recruited varies with contraction velocity. We investigated whether MU discharge and recruitment strategies are differentially affected by pain depending on their recruitment threshold (RT), across a range of contraction speeds. Participants performed ankle dorsiflexion sinusoidal-isometric contractions at two frequencies (0.25Hz and 1Hz) and two modulation amplitudes [5% and 10% of the maximum voluntary contraction (MVC)] with a mean target torque of 20%MVC. High-density surface electromyography recordings from the tibialis anterior muscle were decomposed and the same MUs were tracked across painful (hypertonic saline injection) and non-painful conditions. Torque variability, mean discharge rate (MDR), DR variability (DRvar), RT and the delay between the cumulative spike train and the resultant torque output (neuromechanical delay, NMD) were assessed. The average RT was greater at faster contraction velocities (p=0.01) but was not affected by pain. At the fastest contraction speed, torque variability and DRvar were reduced (p<0.05) and MDR was maintained. Conversely, MDR decreased and DRvar and NMD increased significantly during pain at slow contraction speeds (p<0.05). These results show that reductions in contraction amplitude and increased recruitment of higher threshold MUs at fast contraction speeds appears to compensate for the inhibitory effect of nociceptive inputs on lower threshold MUs, allowing the exertion of fast submaximal contractions during pain.

Identification of sequence changes in myosin II that adjust muscle contraction velocity

The speed of muscle contraction is related to body size; muscles in larger species contract at slower rates. Since contraction speed is a property of the myosin isoform expressed in a muscle, we investigated how sequence changes in a range of muscle myosin II isoforms enable this slower rate of muscle contraction. We considered 798 sequences from 13 mammalian myosin II isoforms to identify any adaptation to increasing body mass. We identified a correlation between body mass and sequence divergence for the motor domain of the 4 major adult myosin II isoforms (β/Type I, IIa, IIb, and IIx), suggesting that these isoforms have adapted to increasing body mass. In contrast, the non-muscle and developmental isoforms show no correlation of sequence divergence with body mass. Analysis of the motor domain sequence of β-myosin (predominant myosin in Type I/slow and cardiac muscle) from 67 mammals from 2 distinct clades identifies 16 sites, out of 800, associated with body mass (padj < 0.05) but not with the clade (padj > 0.05). Both clades change the same small set of amino acids, in the same order from small to large mammals, suggesting a limited number of ways in which contraction velocity can be successfully manipulated. To test this relationship, the 9 sites that differ between human and rat were mutated in the human β-myosin to match the rat sequence. Biochemical analysis revealed that the rat–human β-myosin chimera functioned like the native rat myosin with a 2-fold increase in both motility and in the rate of ADP release from the actin–myosin crossbridge (the step that limits contraction velocity). Thus, these sequence changes indicate adaptation of β-myosin as species mass increased to enable a reduced contraction velocity and heart rate.

Why humans are stronger but not faster after isometric strength training: specific neural, not muscular, motor unit adaptations

While maximal force increases following short-term isometric strength training, the rate of force development (RFD) may remain relatively unaffected. The underlying neural and muscular mechanisms during rapid contractions after strength training are largely unknown. Since strength training increases the neural drive to muscles, it may be hypothesized that there are distinct neural or muscular adaptations determining the change in RFD independently of an increase in maximal force. Therefore, we examined motor unit population data during the rapid generation of force before and after four weeks of strength training. We observed that strength training did not change the RFD because it did not influence the number of motor units recruited per second or their initial discharge rate during rapid contractions. While strength training did not change motoneuron behaviour in the force increase phase of rapid contractions, it increased the discharge rate of motoneurons (by ∼4 spikes/s) when reaching the plateau phase (∼150 ms) of the rapid contractions, determining an increase in maximal force production. Computer simulations with a motor unit model that included neural and muscular properties, closely matched the experimental observations and demonstrated that the lack of change in RFD following training is primarily mediated by an unchanged maximal recruitment speed of motoneurons. These results demonstrate that maximal force and contraction speed are determined by different adaptations in motoneuron behaviour following strength training and indicate that increases in the recruitment speed of motoneurons are required to evoke training-induced increases in RFD.

EVALUATION OF THE EFFECT OF VERY HEAVY EXERCISE ON MUSCLE ACTIVITY BY TENSIOMYOGRAPHY IN PROFESSIONAL FOOTBALL PLAYERS

Aim: This study was carried out to investigate the changes in muscle contraction parameters after very heavy exercise in professional football players with Tensiomyography, which is a non-invasive method. Method: Professional licensed football players in the A team of the team they play in the Turkish Super League (n = 11), whose age is 27.27 ± 1.55 years, weight is 74.82 ± 1.83kg, and height is 178.1 ± 1.76cm. participated. Tensiomyography measurements are bilateral m. The first measurement was taken from the rectus femoris muscle before heavy exercise (MET = 11) and the second measurement after it. In the measurements made, the muscle; Contraction time (Tc), maintenance time (Ts), relaxation time (Tr), displacement (Dm), lag time (Td) and contraction velocity (Vc) were evaluated. GraphPad Prism 9.0 program was used to analyze the data. Results: In the measurements made, a statistically significant decrease was observed in Dm, Td and Vc values in the right and left extremities compared to the 1st and 2nd measurements (p <0.05). Conclusion: As a result of our study, the change of muscle contraction properties with the acute effect of heavy exercise was performed with tensiography was evaluated. It was observed that heavy exercise created significant differences in muscle displacement, contraction speed and lag time. It is a passive, non-invasive and easy method for evaluating the performance and muscle activities of athletes after heavy exercise. tensiomyography needs to be investigated with further studies.

Use of Ultrasound to Determine Changes in Diaphragm Mechanics During A Spontaneous Breathing Trial

Objective: Assess change in ultrasound measures of diaphragm mechanics over the course of a 30-minute spontaneous breathing trial (SBT). Design: Prospective observational study. Setting: Single intensive care unit (Logan Hospital, Queensland, Australia), patients recruited from August 2016 to April 2018. Participants: Eligible patients were over the age of 18 years, ventilated for >24 hours, and planned to undergo an SBT. In total, 129 patients were screened. Main outcome measures: Ultrasound measures taken at 5 and 30 minutes during SBT: diaphragmatic excursion (DE), diaphragmatic thickening fraction (DTF), and diaphragmatic contraction speed (DCS). Diaphragmatic rapid shallow breathing index (DRSBI) was calculated using DE/respiratory rate. The presence of diaphragmatic dysfunction (DD) was also determined using DTF < 30%, DE < 11 mm, or DRSBI > 1.6. Results: Eighteen patients had ultrasound measures during an SBT. Four were unable to have DTF visualized. There was no significant change in DTF (n = 14, 32.41 ± 32.21 vs 23.19 ± 17.42, P = .33) or DE (n = 18, 1.72 ± 0.63 vs 1.66 ± 0.59, P = .63) over time. Diaphragmatic contraction speed increased over time (n = 18, 2.21 ± 1.25 vs 2.67 ± 1.61, P = .007). Diaphragmatic rapid shallow breathing index worsened over time (n = 18, 1.65 ± 1.02 vs 2.08 ± 1.51, P = .03). There was no significant change in the presence of DD. Diaphragmatic dysfunction by DTF 8/14 versus 10/14, by DE 4/18 versus 3/18, and by DRSBI 7/18 versus 9/18. No patients failed SBT and one patient failed extubation. Conclusions: Diaphragmatic mechanics may change over the course of an SBT. Further research is required to determine the clinical implications of these changes and the optimal timing of diaphragmatic ultrasound to predict weaning outcome. Diaphragmatic ultrasound may be less feasible than the published data suggest.

Dynamic Properties of Heart Fragments from Different Regions and Their Synchronization

The dynamic properties of the heart differ based on the regions that effectively circulate blood throughout the body with each heartbeat. These properties, including the inter-beat interval (IBI) of autonomous beat activity, are retained even in in vitro tissue fragments. However, details of beat dynamics have not been well analyzed, particularly at the sub-mm scale, although such dynamics of size are important for regenerative medicine and computational studies of the heart. We analyzed the beat dynamics in sub-mm tissue fragments from atria and ventricles of hearts obtained from chick embryos over a period of 40 h. The IBI and contraction speed differed by region and atrial fragments retained their values for a longer time. The major finding of this study is synchronization of these fragment pairs physically attached to each other. The probability of achieving this and the time required differ for regional pairs: atrium–atrium, ventricle–ventricle, or atrium–ventricle. Furthermore, the time required to achieve 1:1 synchronization does not depend on the proximity of initial IBI of paired fragments. Various interesting phenomena, such as 1:n synchronization and a reentrant-like beat sequence, are revealed during synchronization. Finally, our observation of fragment dynamics indicates that mechanical motion itself contributes to the synchronization of atria.

Acto-myosin cross-bridge stiffness depends on the nucleotide state of the myosin II

How various myosin isoforms fulfill the diverse physiological requirements of distinct muscle types remains unclear. Myosin II isoforms expressed in skeletal muscles determines the mechanical performance of the specific muscles as fast movers, or slow movers but efficient force holders. Here, we employed a single-molecule optical trapping method and compared the chemo-mechanical properties of slow and fast muscle myosin II isoforms. Stiffness of the myosin motor is key to its force-generating ability during muscle contraction. We found that acto-myosin (AM) cross-bridge stiffness depends on its nucleotide state as the myosin progress through the ATPase cycle. The strong actin bound ‘AM.ADP’ state exhibited > 2 fold lower stiffness than ‘AM rigor’ state. The two myosin isoforms displayed similar ‘rigor’ stiffness. We conclude that the time-averaged stiffness of the slow myosin is lower due to prolonged duration of the AM.ADP state, which determines the force-generating potential and contraction speed of the muscle, elucidating the basis for functional diversity among myosins.