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Heart Rate Variability during Heat Exposure is not Affected by Short‐term Passive Heat Acclimation in Young Healthy Participants
Author(s) -
Gendron Philippe,
Gravel Hugo,
Barry Hadiatou,
Gag Daniel
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.09183
Subject(s) - acclimatization , heart rate , heart rate variability , hyperthermia , bradycardia , cardiology , medicine , zoology , stroke volume , chemistry , blood pressure , biology , botany
Heat acclimation attenuates the increase in heart rate during heat exposure. This heat acclimation‐induced bradycardia has been associated with increased stroke volume due to blood volume expansion. However, exercise‐induced heat acclimation also modulates cardiac parasympathetic activity, as measured through heart rate variability (HRV). Therefore, it is possible that modulation of cardiac autonomic activity could contribute to the effect of heat acclimation on heart rate during heat exposure. The purpose of this study was to determine if HRV during heat exposure is modified by short‐term passive heat acclimation. METHODS Fifteen healthy adults (27 ± 5 years, 5 females/10 males) underwent heat exposure in a water‐perfused suit to increase esophageal temperature (Tes) by 1.2°C, before and after a 7‐day controlled hyperthermia protocol. During heat exposure, R‐R interval was measured continuously with a 5‐lead electrocardiogram and used to calculate heart rate (HR), mean normal‐to‐normal intervals (NN), standard deviation of NN intervals (SDNN), root mean square of successive NN interval differences (RMSSD), low‐frequency (LF) and high‐frequency spectral power (HF) and the LF‐to‐HF power ratio (LF/HF). The acclimation protocol consisted of hot water immersion to elevate and subsequently maintain rectal temperature ≥38.6°C for 60 minutes once a day for 7 consecutive days. Variables were compared between the pre and post acclimation visit at baseline and at increases in Tes of 0.6°C and 1.2°C. RESULTS Heat acclimation lowered resting Tes (36.81 ± 0.29 to 36.53 ± 0.32°C, P <0.001) and, consequently absolute Tes during heat exposure. When analyzed as a function of the change in Tes from baseline, no difference was observed for HR ( P =0.072) at baseline (59 ± 10 vs. 57 ± 9 bpm), +0.6°C (88 ± 12 vs. 86 ± 11 bpm), and +1.2°C (103 ± 13 to 99 ± 12 bpm). Similarly, NN (baseline: 1049 ± 172 vs. 1081 ± 162 ms, +0.6°C: 691 ± 104 vs. 705 ± 100 ms, +1.2°C: 595 ± 74 vs. 600 ± 96 ms, P =0.295), SDNN (baseline: 84 ± 38 vs. 90 ± 37 ms, +0.6°C: 43 ± 15 vs. 45 ± 15 ms, +1.2°C: 28 ± 9 vs. 31 ± 8 ms, P =0.294) and RMSSD (baseline: 83 ± 49 vs. 93 ± 57 ms, +0.6°C: 19 ± 9 vs. 19 ± 14 ms, +1.2°C: 9 ± 4 vs. 9 ± 3 ms, P =0.336) did not differ after heat acclimation. No effect of heat acclimation was also observed for LF ( P =0.339), HF ( P =0.509) and LF/HF ratio ( P =0.449). CONCLUSIONS These results suggest that short‐term, passive and isothermic heat acclimation does not modulate cardiac autonomic activity during passive heat exposure in healthy young adults. Support or Funding Information Natural Sciences and Engineering Research Council of Canada, Canada Foundation for Innovation and Montreal Heart Institute Foundation.

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