SFEBES2016 Poster Presentations Neuroendocrinology and pituitary (34 abstracts)
Copeptin as a marker of cardiovascular strain during occupational heat stress
Mike Stacey 1, , David Woods 1, , Lee Macconnachie 4 , Sophie Britland 5 , Simon Delves 5 , Adrian Allsopp 5 , Stephen Brett 2, , Joanne Fallowfield 5 & Christopher Boos 3,
1Royal Centre for Defence Medicine, Birmingham, UK; 2Imperial College, London, UK; 3Leeds Beckett University, Leeds, UK; 4Poole Hospital NHS Trust, Poole, UK; 5Institute of Naval Medicine, Alverstoke, UK; 6Hammersmith Hospital, London, UK.
Background: Regulation of core body temperature (Tc) can cause significant cardiovascular strain, leading to impaired performance, incapacitation and occupational hazard during work in the heat. Where continuous Tc and heart rate (HR) monitoring is not possible (e.g. during firefighting or on military operations), safer working could result from intermittent sampling of an integrated measure of physiological strain.
Aims: To assess the relationship between HR responses to occupational heat stress and copeptin, a 39-amino acid glycopeptide comprising the C-terminal part of the vasopressin precursor (CT-proAVP).
Methods: Peak HR during maximal exercise in the heat (HRpeak) was determined for 25 military volunteers. Following acclimatisation in Cyprus, volunteers participated in 5 h continuous field training (ambient temperature=30 °C). HR was recorded every 10 min by ambulatory ECG. After training (POST), blood was sampled for plasma copeptin and osmolality.
Results: Heart rate during training was 102 [88, 123] b.min−1, or 55 [47, 64] % HRpeak. Compared with baseline rest, training led to significant (P<0.005) increases in copeptin (8.3±3.6 vs 21.0±9.4 pmol/l) and osmolality (293±4 vs 297±4 mOsm/kg). While copeptin associated moderately with POST osmolality (r=0.54), it also correlated with POST HR (r=0.64) and % HRpeak (r=0.73), as well as with maximum % HRpeak achieved during training (r=0.54). Volunteers with copeptin ≥20 (n=13) vs <20 pmol/l (n=12) differed according to % HR peak (54±6 vs 49±4 pmol/l, P<0.05).
Discussion: Moderate-to-severe cardiovascular strain was achieved within ethical limits. Potential stimuli to copeptin/AVP secretion included osmolality, heart rate and other factors (e.g. baroreceptor activation). Copeptin could play a role in the investigation of exertional collapse, or identification of ‘critical’ cardiovascular strain before incapacitation. Its diagnostic/prognostic value should be established in more controlled settings, with higher exertional-heat stress, and in the post-collapse patient population.
Volume 44
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Endocrine Abstracts
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