@article{KaufmannGronwaldHeroldetal.2023,
  author    = {Kaufmann, Sebastian and Gronwald, Thomas and Herold, Fabian and Hoos, Olaf},
  title     = {Heart Rate Variability-Derived Thresholds for Exercise Intensity Prescription in Endurance Sports: A Systematic Review of Interrelations and Agreement with Different Ventilatory and Blood Lactate Thresholds},
  series = {Sports Medicine - Open},
  volume    = {9},
  journal   = {Sports Medicine - Open},
  doi       = {10.1186/s40798-023-00607-2},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-357957},
  year      = {2023},
  abstract  = {Background Exercise intensities are prescribed using specific intensity zones (moderate, heavy, and severe) determined by a 'lower' and a 'higher' threshold. Typically, ventilatory (VT) or blood lactate thresholds (LT), and critical power/speed concepts (CP/CS) are used. Various heart rate variability-derived thresholds (HRVTs) using different HRV indices may constitute applicable alternatives, but a systematic review of the proximity of HRVTs to established threshold concepts is lacking. Objective This systematic review aims to provide an overview of studies that determined HRVTs during endurance exercise in healthy adults in comparison with a reference VT and/or LT concept. Methods A systematic literature search for studies determining HRVTs in healthy individuals during endurance exercise and comparing them with VTs or LTs was conducted in Scopus, PubMed and Web of Science (until January 2022). Studies claiming to describe similar physiological boundaries to delineate moderate from heavy (HRVTlow vs. VTlow and/or LTlow), and heavy from severe intensity zone (HRVThigh vs. VThigh and/or LThigh) were grouped and their results synthesized. Results Twenty-seven included studies (461 participants) showed a mean difference in relative HR between HRVTlow and VTlow of - 0.6\%bpm in weighted means and 0.02\%bpm between HRVTlow and LTlow. Bias between HR at HRVTlow and VTlow was 1 bpm (limits of agreement (LoA): - 10.9 to 12.8 bpm) and 2.7 bpm (LoA: - 20.4 to 25.8 bpm) between HRVTlow and LTlow. Mean difference in HR between HRVThigh and VThigh was 0.3\%bpm in weighted means and 2.9\%bpm between HRVThigh and LThigh while bias between HR at HRVThigh and VThigh was - 4 bpm (LoA: - 17.9 to 9.9 bpm) and 2.5 bpm (LoA: - 12.1 to 17.1 bpm) between HRVThigh and LThigh. Conclusion HRVTlow seems to be a promising approach for the determination of a 'lower' threshold comparable to VTlow and potentially for HRVThigh compared to VThigh, although the latter needs further empirical evaluation. LoA for both intensity zone boundaries indicates bias of HRVTs on an individual level. Taken together, HRVTs can be a promising alternative for prescribing exercise intensity in healthy, male athletes undertaking endurance activities but due to the heterogeneity of study design, threshold concepts, standardization, and lack of female participants, further research is necessary to draw more robust and nuanced conclusions.},
  language  = {en}
}
@article{KnopSpilgiesRuflietal.2019,
  author    = {Knop, Janin and Spilgies, Lisanne M. and Rufli, Stefanie and Reinhart, Ramona and Vasilikos, Lazaros and Yabal, Monica and Owsley, Erika and Jost, Philipp J. and Marsh, Rebecca A. and Wajant, Harald and Robinson, Mark D. and Kaufmann, Thomas and W. Wei-Lynn, Wong},
  title     = {TNFR2 induced priming of the inflammasome leads to a RIPK1-dependent cell death in the absence of XIAP},
  series = {Cell Death \& Disease},
  volume    = {10},
  journal   = {Cell Death \& Disease},
  doi       = {10.1038/s41419-019-1938-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-325946},
  year      = {2019},
  abstract  = {The pediatric immune deficiency X-linked proliferative disease-2 (XLP-2) is a unique disease, with patients presenting with either hemophagocytic lymphohistiocytosis (HLH) or intestinal bowel disease (IBD). Interestingly, XLP-2 patients display high levels of IL-18 in the serum even while in stable condition, presumably through spontaneous inflammasome activation. Recent data suggests that LPS stimulation can trigger inflammasome activation through a TNFR2/TNF/TNFR1 mediated loop in xiap-/- macrophages. Yet, the direct role TNFR2-specific activation plays in the absence of XIAP is unknown. We found TNFR2-specific activation leads to cell death in xiap-/- myeloid cells, particularly in the absence of the RING domain. RIPK1 kinase activity downstream of TNFR2 resulted in a TNF/TNFR1 cell death, independent of necroptosis. TNFR2-specific activation leads to a similar inflammatory NF-kB driven transcriptional profile as TNFR1 activation with the exception of upregulation of NLRP3 and caspase-11. Activation and upregulation of the canonical inflammasome upon loss of XIAP was mediated by RIPK1 kinase activity and ROS production. While both the inhibition of RIPK1 kinase activity and ROS production reduced cell death, as well as release of IL-1β, the release of IL-18 was not reduced to basal levels. This study supports targeting TNFR2 specifically to reduce IL-18 release in XLP-2 patients and to reduce priming of the inflammasome components.},
  language  = {en}
}