title: Sweat loss during heat stress contributes to subsequent reductions in lower-body negative pressure tolerance.
abstract: The contribution of sweating to heat stress-induced reductions in haemorrhagic tolerance is not known. This study tested the hypothesis that fluid loss due to sweating contributes to reductions in simulated haemorrhagic tolerance in conditions of heat stress. Eight subjects (35 ± 8 years old; 77 ± 5 kg) underwent a normothermic time control and two heat stress trials (randomized). The two heat stress trials were as follows: (i) with slow intravenous infusion of lactated Ringer solution sufficient to offset sweat loss (IV trial); or (ii) without intravenous infusion (dehydration; DEH trial). Haemorrhage was simulated via progressive lower-body negative pressure (LBNP) to presyncope after core body (intestinal) temperature was raised by ~1.5 °C using a water-perfused suit or a normothermic time control period. The LBNP tolerance was quantified via a cumulative stress index. Middle cerebral artery blood velocity (transcranial Doppler) and mean blood pressure (Finometer®) were measured continuously. Relative changes in plasma volume were calculated from haematocrit and haemoglobin. Increases in core body temperature and sweat loss (~1.6% body mass deficit) were similar (P > 0.05) between heat stress trials. Slow intravenous infusion (1.2 ± 0.3 litres) prevented heat-induced reductions in plasma volume (IV trial, -0.6 ± 6.1%; and DEH trial, -6.6 ± 5.1%; P = 0.01). Intravenous infusion improved LBNP tolerance (632 ± 64 mmHg min) by ~20% when compared with the DEH trial (407 ± 117 mmHg min; P = 0.01), yet tolerance remained 44% lower in the IV trial relative to the time control normothermic trial (1138 ± 183 mmHg min; P < 0.01). These data indicate that although sweat-induced dehydration impairs simulated haemorrhagic tolerance, this impairment is secondary to the negative impact of heat stress itself.
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, TX 75231, USA.
authors.forename: Rebekah A I
authors.initials: RA
authors.lastname: Lucas
authors.forename: Matthew S
authors.initials: MS
authors.lastname: Ganio
authors.forename: James
authors.initials: J
authors.lastname: Pearson
authors.forename: Craig G
authors.initials: CG
authors.lastname: Crandall
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002560:Cerebrovascular Circulation; D003681:Dehydration / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D005260:Female; D005440:Fluid Therapy; D018882:Heat Stress Disorders / Q000097:blood / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D018869:Heat-Shock Response; D006400:Hematocrit; D006454:Hemoglobins / Q000378:metabolism; D006470:Hemorrhage / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D006706:Homeostasis; D006801:Humans; D006979:Hyperthermia, Induced; D007262:Infusions, Intravenous; D007552:Isotonic Solutions / Q000008:administration & dosage; D008150:Lower Body Negative Pressure; D008297:Male; D020768:Middle Cerebral Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D010953:Plasma Volume; D000077325:Ringer's Lactate; D013546:Sweating; D013575:Syncope / Q000097:blood / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D013781:Texas; D013997:Time Factors; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D015415:Biomarkers; D006454:Hemoglobins; D007552:Isotonic Solutions; D000077325:Ringer's Lactate