VALIDATION OF A 3-DIMENSIONAL VIDEO MOTION CAPTURE SYSTEM FOR DETERMINING BARBELL POWER AND VELOCITY DURING THE BENCH PRESS

Andrew C. Fry, Luke Bradford, Trent Herda, Joseph Weir FACSM, Michael Lane, Matthew Andre, Andrea Hudy, J. Deckert and J. Siedlik.Neuromechanics Laboratory and Kansas Athletics Inc., University of Kansas, Lawrence, KS Analyses of barbell kinetics and kinematics have typically required the use of force plates, tether-based position transducers, or digitized video analysis. PURPOSE: To determine the validity of a 3-dimensional video markerless motion capture system for determining barbell kinetics and kinematics. METHODS: Two 3-D video cameras sampling at 30 Hz and mounted on the top of a power rack were interfaced with a self-contained computer and software system, and operated with a touch screen (EliteForm, Lincoln, NE). For laboratory comparison purposes, a ceiling–mounted linear position transducer (Unimeasure, Corvallis, OR) was attached via a tether to the barbell. Data from the position transducer was sampled at 1000 Hz using a BioPac data acquisition system (Goleta, CA). Velocity (m.s-1) and power (W) were derived using LabView software (National Instruments, Austin, TX). One weight-trained male subject (age = 25 yrs, hgt = 1.75 m, BW = 82.6 kg, 1 RM = 161.0 kg) performed the barbell bench press exercise for 10 sets x 1 repetition at 30, 40, 50, 60, 70 and 80% 1 RM loads using maximal acceleration during the concentric phase. Dependent variables included peak (PV) and X̅ velocity (MV) and peak (PP) and X̅ power (MP). Linear regressions between lab-derived and 3-D video-derived data provided correlation coefficients, and regression slopes (b). Bland-Altman plots were used to determine X̅ differences, from which effect sizes (Cohen’s D) and % error for the 3-D camera system was determined. RESULTS: Lab-derived mean values for all loads ranged as follows; MV = 0.36 – 1.00 m.s-1, PV = 0.47 – 1.60 m.s-1, MP = 460.9 – 621.6 W, and PP = 619.9 – 1055.6 W. CONCLUSION: The 3-D video markerless motion capture system provided accurate and valid barbell velocity and power data for the bench press exercise. Supported in part by Nebraska Global LL

Instrument-assisted Soft Tissue Mobilization: Effects on the Properties of Human Plantar Flexors

The effect of instrument-assisted soft tissue mobilization (ISTM) on passive properties and inflammation in human skeletal muscle has not been evaluated. Passive properties of muscle, inflammatory myokines and subjective reporting of functional ability were used to identify the effects of ISTM on the plantar flexors. 11 healthy men were measured for passive musculotendinous stiffness (MTS), passive range of motion (PROM), passive resistive torque (PASTQ) and maximum voluntary contraction peak torque (MVCPT) for plantar flexor muscles of the lower leg. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured from muscle biopsies from the gastrocnemius, and subjective measurements of functional ability were taken using the perception of functional ability questionnaire (PFAQ). MTS, PROM, PRT and MVCPT were measured in the treatment leg (TL) and control leg (CL) before, immediately after, 24 h, 48 h and 72 h following IASTM. Biopsies for IL-6 and TNF-α and PFAQ responses were collected before as well as 24 h, 48 h and 72 h after IASTM. There were no significant differences in MTS, PROM, PASTQ, MVCPT, IL-6 and TNF-α between the TL or CL. A significant decrease in the perception of function and a significant increase in pain for the TL were found following IASTM

Mechanism of KMT5B haploinsufficiency in neurodevelopment in humans and mice.

Pathogenic variants in KMT5B, a lysine methyltransferase, are associated with global developmental delay, macrocephaly, autism, and congenital anomalies (OMIM# 617788). Given the relatively recent discovery of this disorder, it has not been fully characterized. Deep phenotyping of the largest (n = 43) patient cohort to date identified that hypotonia and congenital heart defects are prominent features that were previously not associated with this syndrome. Both missense variants and putative loss-of-function variants resulted in slow growth in patient-derived cell lines. KMT5B homozygous knockout mice were smaller in size than their wild-type littermates but did not have significantly smaller brains, suggesting relative macrocephaly, also noted as a prominent clinical feature. RNA sequencing of patient lymphoblasts and Kmt5b haploinsufficient mouse brains identified differentially expressed pathways associated with nervous system development and function including axon guidance signaling. Overall, we identified additional pathogenic variants and clinical features in KMT5B-related neurodevelopmental disorder and provide insights into the molecular mechanisms of the disorder using multiple model systems

Mechanism of KMT5B haploinsufficiency in neurodevelopment in humans and mice.

Pathogenic variants in KMT5B, a lysine methyltransferase, are associated with global developmental delay, macrocephaly, autism, and congenital anomalies (OMIM# 617788). Given the relatively recent discovery of this disorder, it has not been fully characterized. Deep phenotyping of the largest (n = 43) patient cohort to date identified that hypotonia and congenital heart defects are prominent features that were previously not associated with this syndrome. Both missense variants and putative loss-of-function variants resulted in slow growth in patient-derived cell lines. KMT5B homozygous knockout mice were smaller in size than their wild-type littermates but did not have significantly smaller brains, suggesting relative macrocephaly, also noted as a prominent clinical feature. RNA sequencing of patient lymphoblasts and Kmt5b haploinsufficient mouse brains identified differentially expressed pathways associated with nervous system development and function including axon guidance signaling. Overall, we identified additional pathogenic variants and clinical features in KMT5B-related neurodevelopmental disorder and provide insights into the molecular mechanisms of the disorder using multiple model systems

Regulation of tissue morphodynamics: an important role for actomyosin contractility

Forces arising from contractile actomyosin filaments help shape tissue form during morphogenesis. Developmental events that result from actomyosin contractility include tissue elongation, bending, budding, and collective migration. Here, we highlight recent insights into these morphogenetic processes from the perspective of actomyosin contractility as a key regulator. Emphasis is placed on a range of results obtained through live imaging, culture, and computational methods. Combining these approaches in the future has the potential to generate a robust, quantitative understanding of tissue morphodynamics

Microfabricated tissues for investigating traction forces involved in cell migration and tissue morphogenesis

Cell-generated forces drive an array of biological processes ranging from wound healing to tumor metastasis. Whereas experimental techniques such as traction force microscopy are capable of quantifying traction forces in multidimensional systems, the physical mechanisms by which these forces induce changes in tissue form remain to be elucidated. Understanding these mechanisms will ultimately require techniques that are capable of quantifying traction forces with high precision and accuracy in vivo or in systems that recapitulate in vivo conditions, such as microfabricated tissues and engineered substrata. To that end, here we review the fundamentals of traction forces, their quantification, and the use of microfabricated tissues designed to study these forces during cell migration and tissue morphogenesis. We emphasize the differences between traction forces in two- and three-dimensional systems, and highlight recently developed techniques for quantifying traction forces

COMPUTERIZED NEUROCOGNITIVE ASSESSMENTS AND DETECTION OF THE MALINGERING ATHLETE

Jacob Siedlik1, Spyros Siscos1, Philip Gallagher1, Jennifer Seeley2, Adam Rolf3, Karen Evans3, Phillip Vardiman1. 1Applied Physiology Laboratory, University of Kansas, Lawrence, KS; 2Department of Psychology and Research in Education, University of Kansas, Lawrence KS; 3Lawrence Memorial Hospital, Lawrence, KS. In the United States it is estimated that 1.6 to 3.6 million concussions occur each year. Computerized neurocognitive assessment tools (NCAT) are commonly used by athletic trainers and physicians to measure cognitive abilities in healthy, non-concussed athletes. The systems are designed to measure post-concussion cognitive ability in order to thoroughly evaluate and monitor the athlete’s recovery to ensure proper return to play decisions. However, researchers are concerned that athletes would be capable of intentionally underperforming on baseline tests to expedite their return to the field following a concussion. PURPOSE: There were two specific aims of this study: 1. To investigate the test-taker’s ability to alter their NCAT baseline test scores, malingering baseline (MB) relative to a non-malingering baseline (NMB), 2. To assess the NCAT’s ability to detect MB compared to a physician trained in evaluation of results from this version of NCAT. METHODS: 20 male, collegiate rugby players completed this study (23±4yrs). Participants completed 2 NCAT assessments within a 7-day interval. Participants were initially deceived to believe this was a pre-test/post-test assessment. The NMB was measured following the NCAT’s normal sequence of instructions where they were asked to perform to the best of their abilities. Immediately prior to the second assessment (MB), each participant was debriefed about the prior deception and instructed to “underperform on the test” without specific direction on techniques to do so. NMB and MB clinical reports were generated by the NCAT system, blinded and sent to the physicians for secondary analysis. RESULTS: MB test scores were significantly lower (p \u3c .05) than NMB scores for 12 of the 13 variables assessed as part of this study. The NCAT system detected 70% (n=14) of the MB tests, whereas the physician detected the same 14 MB tests and 2 additional (80%) from NCAT reports. CONCLUSIONS: There is a possibility that athletes would be able to malinger and alter their baseline scores using an NCAT system. This possibility is reduced with oversight by a properly trained physician familiar with the particular NCAT software. In-person clinical assessment coupled with NCAT provides the most reliable method to avoid malingering by athletes. Supported by the University of Kansas Undergraduate Research Award