An evaluation of heart rate variability in female youth soccer players following soccer heading: A pilot study

Most head impacts in soccer occur from purposeful heading; however, the link between heading and neurological impairment is unknown. Previous work suggests concussion may result in an uncoupling between the autonomic nervous system and cardiovascular system. Accordingly, heart rate variability (HRV) may be a sensitive measure to provide meaningful information regarding repetitive heading in soccer. The purpose of this pilot study assesses the feasibility of measuring HRV to evaluate autonomic function following soccer heading. Sixteen youth female participants underwent heart rate monitoring during a heading and footing condition. Participants completed a five minute resting supine trial at the start and end of each testing session. Standard 450 g soccer balls were projected at 6 m/s towards participants. Participants performed five headers, for the header condition, and five footers for the footer condition. The HRV for resting supine trials, pre-and post-header and footer conditions were assessed for both time and frequency domains. HRV effect sizes were small when comparing conditions, except absolute low frequency (d = 0.61) and standard deviation of the normal-normal (NN) intervals (d = 0.63). Participant retention and adherence were high, without adverse events. Findings suggest HRV is a feasible measure for evaluating the effects of heading on autonomic function

Corrigendum to "Electrodiagnostic assessment of the autonomic nervous system: A consensus statement endorsed by the American Autonomic Society, American Academy of Neurology, and the International Federation of Clinical Neurophysiology" [Clin. Neurophysiol. 132(2) (2021) 666-682].

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The effects of neurotrophins on neurite growth in cultured adult sensory neurons

The compartmented culture method was used to study the regulation of adult sensory neurite growth by neurotrophins. We examined the effects of the neurotrophins nerve growth factor (NGF), neurotrophin-3 (NT3), and brain derived neurotrophic factor (BDNF) on neurite elongation from adult rat dorsal root ganglion (DRG) neurons. Initial proximal neurite growth (within center compartments) did not require neurotrophins. Subsequent elongation into distal compartments resulted from NGF but not NT3 or BDNF treatment. After neurites had extended into distal compartments, treatment with anti-NGF resulted in the cessation of growth with no significant neurite retraction. After axotomy of growing neurites in distal compartments, NGF was necessary to support regrowth. In the same paradigm, both NT3 and BDNF did not result regrowth. The results demonstrated that unlike in vivo nerve regeneration, in vitro regrowth does require NGF. -- Given the above results, the next focus of study was to determine the individual contributions ofthe NGF receptors to the growth response. The requirement of both TrkA and the p75 neurotrophin receptor in neurite growth was examined using several experimental interventions. As expected, inhibition of TrkA activation using K252a totally blocked distal neurite extension into NGF containing compartments. Results showed using BDNF to interfere with NGF binding to p75, found that the addition of BDNF to NGF containing distal compartments reduced distal neurite extension. In contrast MC192 which alters the interaction of NGF with p75, completely inhibited NGF dependent neurite growth. Both compounds were found to partially attenuate NGF induced TrkA phosphorylation. However only MC192 appeared to activate p75 based on immunocytochemical evidence showing nuclear localization of NFk-B. -- These results demonstrate that both TrkA and p75 play a role in neurite growth response to NGF. Furthermore our evidence suggests that any alteration in optimal TrkA-p75 interactions, or direct activation of p75 at the expense of TrkA, results in an inhibition of NGF-dependent neurite growth. -- NGF/TrkA signaling has a number of common pathways in which to elicit various physiological responses. Many of the same pathways are used by other growth factors that also are capable of producing neurite growth in adult sensory neurons. To investigate the influence of other growth factors in addition to NGF, the effects of IGF-1 EGF and FGF on neurite growth from adult rat dorsal root ganglion (DRG) neurons were examined. As expected, NGF elicited robust neuritic growth in both the dissociated and compartmented cultures. The growth response to IGF-1 was similar. There was minimal neurite growth in response to EGF or FGF. In addition, IGF-1 (but neither FGF nor EGF), when applied to cell bodies in compartmented cultures, potentiated the distal neurite growth into NGF- containing side compartments. -- In order to determine the contribution of signaling intermediates downstream of receptor activation, we used pharmacological inhibitors and western blotting. The PI 3- kinase inhibitor, LY294002 attenuated neurite growth evoked by NGF, IGF and EGF in dissociated cultures, while the MEK inhibitor PD98059 only diminished growth in IGF treated cultures. Immunoprecipitation and western blotting results demonstrated differential activation of MAPK, PI 3-kinase, PLCyl and SNT by the different factors. Activation of PI 3-kinase and SNT by both NGF and IGF-1 correlated with their effects on neurite growth. These results support the hypothesis that the PI 3-kinase pathway, and the SNT protein play an important role in neurogenesis. -- In conclusion neurite growth of adult DRG neurons is mediated by NGF in vitro and required TrkA activation. In comparison these results indicate that inhibition of NGF binding to p75 partially inhibits growth while activation of the receptor abolishes the response. Further assessment of NGF-TrkA signaling pathways, using other growth factors for comparison (i.e. IGF-1 and EGF) indicate that PI 3-kinase and SNT signaling intermediates are important contributors to the growth process. These experiments are a part of a larger focus on NGF and its role in neurite growth in neurons (adult DRG neurons) that do not require this factor for survival. Furthermore these studies will hopefully contribute to elucidating the processes involved in neurite growth

An updated normative data-set from the Autonomic Reflex Screen representative of Southwestern Ontario

In evaluating autonomic dysfunction, the autonomic reflex screen (ARS) is an established set of standardized tests to evaluate the presence and severity of autonomic dysfunction. Our laboratory previously reported normative data on 121 healthy individuals; however, the sample size in older individuals was reduced compared with other age groups. Therefore, the objective of the current study was to provide updated normative values representative of young, middle-aged, and older individuals from Southwestern Ontario. Two hundred and fifty-two healthy individuals completed quantitative sudomotor axon reflex testing, heart rate responses to deep breathing (HRDB), and Valsalva maneuver using standard protocols of the ARS. All 4 sweat sites demonstrated a significant effect of sex (p < 0.001). In addition, the proximal leg, distal leg, and foot were all significantly affected by age (p < 0.001). Cardiovagal parameters, measured via HRDB and Valsalva ratio revealed a significant regression with age (p < 0.001). These results show similar trends with previously reported normative data sets. All normative data as a function of age and sex, where appropriate, are expressed as percentiles (2.5th, 5th, 95th, 97.5th). The current study provides updated normative data describing autonomic functioning in healthy individuals obtained from the sudomotor and cardiovagal components of the ARS. METHODS: 252 healthy individuals completed quantitative sudomotor axon reflex testing, heart rate responses to deep breathing (HRDB), and Valsalva maneuver using standard protocols of the ARS. RESULTS: All four sweat sites demonstrated a significant effect of sex (pThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author