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Peer-reviewedCC BY 4.0Pain Research & Management

The Role of Cardiovascular Function in Endogenous Pain Modulation

  • Joëlle Katharina Metzger1,2
  • Shane James Timothy Balthazaar1,2,3,4
  • Sophie Sturzenegger1
  • Tom Edward Nightingale3,4
  • Michèle Hubli1,2
4 affiliations
  1. 1Spinal Cord Injury Center Balgrist University Hospital University of Zurich Zurich Switzerland balgrist.ch
  2. 2Neuroscience Center Zurich (ZNZ) University of Zurich and ETH Zurich Zurich Switzerland ethz.ch
  3. 3School of Sport, Exercise and Rehabilitation Sciences University of Birmingham Birmingham UK birmingham.ac.uk
  4. 4International Collaboration on Repair Discoveries University of British Columbia Vancouver British Columbia Canada ubc.ca
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Abstract

Structural and functional overlap between the nociceptive and cardiovascular systems establish a bidirectional coupling that supports dynamic regulation across both systems. Disruption of this coupling could contribute to impaired endogenous pain modulation in chronic pain conditions. Thus, this study aimed to investigate the relationship between endogenous pain modulation and cardiovascular function in healthy participants. Thirty participants underwent assessment of pain modulatory capacity using offset analgesia (OA; 47–48°C‐47°C) and conditioned pain modulation (CPM), with pressure pain thresholds as test stimuli and a cold pressor test (CPT) as conditioning stimulus. Resting heart rate variability (HRV) and baroreflex sensitivity (BRS) were derived from 5‐min baseline recordings of continuous electrocardiography and beat‐to‐beat blood pressure. Blood pressure reactivity during the CPT was calculated as the relative difference between peak blood pressure during the CPT and baseline. Associations between pain modulation (OA, CPM) and cardiovascular function (HRV, BRS, blood pressure reactivity) were examined. In this healthy cohort (N = 30), participants exhibited pronounced pain inhibitory capacity, with OA at −85.7% ± 21.8% and CPM at −19.0% ± 14.7%. Higher resting BRS was related to higher OA (rho = −0.48, p = 0.030) and CPM capacity (rho = −0.52, p = 0.021). Moreover, higher CPM capacity was associated with larger blood pressure responses in both parallel (rho = −0.48, p = 0.021) and sequential designs (rho = −0.49, p = 0.033). Increased OA capacity was linked to higher HRV (rho = −0.50, p = 0.030) at rest. Using a multimodal approach, these findings support a functional coupling between endogenous pain modulation and cardiovascular regulation in healthy individuals, emphasizing the role of cardiovascular adaptability in shaping pain inhibitory processes. Understanding this pain‐cardiovascular coupling may help explain interindividual variability in endogenous pain modulation in healthy individuals and might offer insight into its disruption in chronic pain conditions.

Trial Registration: ClinicalTrials.gov identifier: NCT06443281

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Cite

BibTeXRIS
BibTeX
@article{metzger2026role,
  title = {{The Role of Cardiovascular Function in Endogenous Pain Modulation}},
  author = {Joëlle Katharina Metzger and Shane James Timothy Balthazaar and Sophie Sturzenegger and Tom Edward Nightingale and Michèle Hubli},
  journal = {Pain Research \& Management},
  year = {2026},
  month = nov,
  doi = {10.1155/prm/8018460},
  url = {https://doi.org/10.1155/prm/8018460},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - The Role of Cardiovascular Function in Endogenous Pain Modulation
AU  - Joëlle Katharina Metzger
AU  - Shane James Timothy Balthazaar
AU  - Sophie Sturzenegger
AU  - Tom Edward Nightingale
AU  - Michèle Hubli
PY  - 2026
DA  - 2026/11/05
JO  - Pain Research & Management
DO  - 10.1155/prm/8018460
UR  - https://doi.org/10.1155/prm/8018460
AB  - Structural and functional overlap between the nociceptive and cardiovascular systems establish a bidirectional coupling that supports dynamic regulation across both systems. Disruption of this coupling could contribute to impaired endogenous pain modulation in chronic pain conditions. Thus, this study aimed to investigate the relationship between endogenous pain modulation and cardiovascular function in healthy participants. Thirty participants underwent assessment of pain modulatory capacity using offset analgesia (OA; 47–48°C‐47°C) and conditioned pain modulation (CPM), with pressure pain thresholds as test stimuli and a cold pressor test (CPT) as conditioning stimulus. Resting heart rate variability (HRV) and baroreflex sensitivity (BRS) were derived from 5‐min baseline recordings of continuous electrocardiography and beat‐to‐beat blood pressure. Blood pressure reactivity during the CPT was calculated as the relative difference between peak blood pressure during the CPT and baseline. Associations between pain modulation (OA, CPM) and cardiovascular function (HRV, BRS, blood pressure reactivity) were examined. In this healthy cohort (N = 30), participants exhibited pronounced pain inhibitory capacity, with OA at −85.7% ± 21.8% and CPM at −19.0% ± 14.7%. Higher resting BRS was related to higher OA (rho = −0.48, p = 0.030) and CPM capacity (rho = −0.52, p = 0.021). Moreover, higher CPM capacity was associated with larger blood pressure responses in both parallel (rho = −0.48, p = 0.021) and sequential designs (rho = −0.49, p = 0.033). Increased OA capacity was linked to higher HRV (rho = −0.50, p = 0.030) at rest. Using a multimodal approach, these findings support a functional coupling between endogenous pain modulation and cardiovascular regulation in healthy individuals, emphasizing the role of cardiovascular adaptability in shaping pain inhibitory processes. Understanding this pain‐cardiovascular coupling may help explain interindividual variability in endogenous pain modulation in healthy individuals and might offer insight into its disruption in chronic pain conditions.  Trial Registration: ClinicalTrials.gov identifier: NCT06443281
SN  - 1203-6765
SN  - 1918-1523
ER  -