scholarly journals Initial stay times for uncompensable occupational heat stress in young and older men: a preliminary assessment

Author(s):  
Sean R. Notley ◽  
Ashley Akerman ◽  
Glen P. Kenny

During uncompensable occupational heat stress, heat-mitigation controls are required to prevent core temperature exceeding recommended limits (≥38°C). However, the initial stay time before employing controls remained unknown. We estimated these times for moderate-intensity work at 26, 28, 30, and 32°C wet-bulb globe temperatures (WBGT) in 50 young (18-30 years) and older (50-70 years), non-heat acclimatized men. Initial stay time was 111 min at 26°C WBGT and declined exponentially to 44 min at 32°C WBGT. Novelty point • We provide estimates of the moderate-intensity work duration before heat-mitigation is required in wet-bulb globe temperatures between 26-32°C for young and older, non-heat acclimatized men.

2019 ◽  
Vol 317 (1) ◽  
pp. R113-R120 ◽  
Author(s):  
Gregory W. McGarr ◽  
Naoto Fujii ◽  
Caroline M. Muia ◽  
Takeshi Nishiyasu ◽  
Glen P. Kenny

Our objective in this study was to examine the separate and combined effects of potassium (K+) channels and nitric oxide synthase (NOS) on cutaneous vasodilation and sweating in older men during rest and exercise in the heat. In 13 habitually active men (61 ± 4 yr), cutaneous vascular conductance and local sweat rate were assessed at six dorsal forearm skin sites continuously perfused with either 1) lactated Ringer (control), 2) 10 mM NG-nitro-l-arginine methyl ester (l-NAME, NOS inhibitor), 3) 50 mM tetraethylammonium (TEA; Ca2+-activated K+ channel blocker), 4) 5 mM glybenclamide (GLY; ATP-sensitive K+ channel blocker), 5) 50 mM TEA + 10 mM l-NAME, and 6) 5 mM GLY + 10 mM l-NAME via microdialysis. Participants rested in non-heat stress (25°C) and heat stress (35°C) conditions for ∼60 min each, followed by 50 min of moderate-intensity cycling (∼55% V̇o2peak) and 30 min of recovery in the heat. During rest and exercise in the heat, l-NAME, TEA + l-NAME, and GLY + l-NAME attenuated CVC relative to control (all P ≤ 0.05), although l-NAME was not different from TEA + l-NAME or GLY + l-NAME (all P > 0.05). TEA attenuated CVC during rest, whereas GLY attenuated CVC during exercise (both P ≤ 0.05). Additionally, whereas neither l-NAME nor TEA altered sweating throughout the protocol (all P > 0.05), combined TEA + l-NAME attenuated sweating during exercise in the heat ( P ≤ 0.05). We conclude that in habitually active older men blockade of KCa and KATP channels attenuates cutaneous vasodilation during rest and exercise in the heat, respectively, and these effects are NOS dependent. Furthermore, combined NOS inhibition and KCa channel blockade attenuates sweating during exercise in the heat.


2019 ◽  
Vol 126 (4) ◽  
pp. 1129-1137 ◽  
Author(s):  
Robert D. Meade ◽  
Naoto Fujii ◽  
Gregory W. McGarr ◽  
Lacy M. Alexander ◽  
Pierre Boulay ◽  
...  

Age-related impairments in cutaneous vascular conductance (CVC) and sweat rate (SR) during exercise may result from increased arginase activity, which can attenuate endogenous nitric oxide (NO) production. We therefore evaluated whether arginase inhibition modulates these heat-loss responses in young ( n = 9, 23 ± 3 yr) and older ( n = 9, 66 ± 6 yr) men during two 30-min bouts of moderate-intensity cycling (Ex1 and Ex2) in the heat (35°C). CVC and SR were measured at forearm skin sites perfused with 1) lactated Ringer’s (control), 2) NG-nitro-L-arginine methyl ester (L-NAME; NO synthase-inhibited), or 3) Nω-hydroxy-nor-arginine and S-(2-boronoethyl)-l-cysteine (Nor-NOHA + BEC; arginase-inhibited). In both groups, CVC was reduced at L-NAME relative to control and Nor-NOHA + BEC (both P < 0.01). Likewise, SR was attenuated with L-NAME compared with control and Nor-NOHA + BEC during each exercise bout in the young men (all P ≤ 0.05); however, no influence of treatment on SR in the older men was observed ( P = 0.14). Based on these findings, we then evaluated responses in 7 older men (64 ± 7 yr) during passively induced elevations in esophageal temperature (∆Tes) equal to those in Ex1 (0.6°C) and Ex2 (0.8°C). L-NAME reduced CVC by 18 ± 20% CVCmax at a ∆Tes of 0.8°C ( P = 0.03) compared with control, whereas Nor-NOHA + BEC augmented CVC by 20 ± 18% CVCmax, on average, throughout heating (both P ≤ 0.03). SR was not influenced by either treatment ( P = 0.80) Thus, arginase inhibition does not modulate CVC or SR during exercise in the heat but, consistent with previous findings, does augment CVC in older men during passive heating. NEW & NOTEWORTHY In the current study, we demonstrate that local arginase inhibition does not influence forearm cutaneous vasodilatory and sweating responses in young or older men during exercise-heat stress. Consistent with previous findings, however, we observed augmented cutaneous blood flow with arginase inhibition during whole-body passive heat stress. Thus, arginase differentially affects cutaneous vasodilation depending on the mode of heat stress but does not influence sweating during exercise or passive heating.


2019 ◽  
Vol 597 (5) ◽  
pp. 1383-1399 ◽  
Author(s):  
Yannick Molgat‐Seon ◽  
Andrew H. Ramsook ◽  
Carli M. Peters ◽  
Michele R. Schaeffer ◽  
Paolo B. Dominelli ◽  
...  

2013 ◽  
Vol 84 (11) ◽  
pp. 1153-1158 ◽  
Author(s):  
Jayme D. Limbaugh ◽  
Gregory S. Wimer ◽  
Lynn H. Long ◽  
William H. Baird

2005 ◽  
Vol 288 (5) ◽  
pp. E922-E929 ◽  
Author(s):  
M. Sheffield-Moore ◽  
D. Paddon-Jones ◽  
A. P. Sanford ◽  
J. I. Rosenblatt ◽  
A. G. Matlock ◽  
...  

We sought to determine whether exercise-induced muscle protein turnover alters the subsequent production of hepatically derived acute-phase plasma proteins, and whether age affects how these proteins are regulated. We measured arteriovenous (a-v) balance and the synthesis of mixed muscle protein, albumin (A) and fibrinogen (F) before exercise (REST) and from the beginning of exercise to 10, 60, and 180 min following a single bout of moderate-intensity leg extension exercise (POST-EX) in postabsorptive untrained older ( n = 6) and younger ( n = 6) men using l-[ ring-2H5]phenylalanine (Phe). Subjects performed 6 sets of 8 repetitions of leg extension at 80% of their 1-RM (one-repetition maximum). All data are presented as the difference from REST (Δ from REST at 10, 60, and 180 min POST-EX). Mixed muscle fractional synthesis rate (FSR-M) increased significantly from the beginning of exercise until 10 min POST-EX in the older men (ΔFSR-M: 0.044%/h), whereas FSR-M in the younger men was not elevated until 180 min POST-EX (ΔFSR-M: 0.030%/h). FSR-A and FSR-F increased at all POST-EX periods in the older men (ΔFSR-A = 10 min: 1.90%/day; 60 min: 2.72%/day; 180 min: 2.78%/day; ΔFSR-F = 10 min: 1.00%/day; 60 min: 3.01%/day; 180 min: 3.73%/day). No change occurred in FSR-A in the younger men, but FSR-F was elevated from the beginning of exercise until 10 and 180 min POST-EX (10 min: 3.07%/day and 180 min: 3.96%/day). Net balance of Phe was positive in the older men in the immediate POST-EX period. Our data indicate that mixed muscle and hepatic derived protein synthesis is differentially regulated in younger and older men in response to a single bout of moderate-intensity leg extension exercise. Moreover, our data suggest that with age may come a greater need to salvage or make available amino acids from exercise-induced muscle protein breakdown to mount an acute-phase response.


2000 ◽  
Vol 25 (6) ◽  
pp. 536-545 ◽  
Author(s):  
William A. Latzka ◽  
Michael N. Sawka

Hyperhydration or increasing body water content above normal (euhydration) level was thought to have some benefit during exercise heat-stress; however, attempts to overdrink have been minimized by a rapid diuretic response. The perception that hyperhydration might be beneficial for exercise performance and for thermoregulation arose from the adverse consequences of hypohydration. Many studies had examined the effects of hyperhydration on thermoregulation in the heat; however, most of them suffer from design problems that confound their results. The design problems included control conditions not representing euhydration but hypohydration, control conditions not adequately described, cold fluid ingestion that reduced core temperature, and/or changing heat acclimation status. Several investigators reported lower core temperatures during exercise after hyperhydration, while other studies do not. Some investigators reported higher sweating rates with hyperhydration, while other studies do not. Recent research that controlled for these confounding variables reported that hyperhydration (water or glycerol) did not alter core temperature, skin temperature, whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or heart rate responces compared to euhydration trail. If euhydration is maintained during exercise-heat stress then hyperhydration appears to have no meaningful advantage. Key words: Hydration, fluid replacement, exercise heat-stress, total body water exercise


1997 ◽  
Vol 272 (2) ◽  
pp. H776-H784 ◽  
Author(s):  
H. M. Stauss ◽  
D. A. Morgan ◽  
K. E. Anderson ◽  
M. P. Massett ◽  
K. C. Kregel

To investigate the effects of hyperthermia and aging on baroreceptor-heart rate reflex sensitivity (BRS), cardiovascular parameters were recorded during a progressive rise in core temperature in conscious mature and senescent Fischer 344 rats. BRS was calculated from spontaneous changes in blood pressure and interbeat interval. Low- (LF, 0.01-0.20 Hz) and mid- (MF, 0.2-0.5 Hz) frequency blood pressure power were also determined. In both age groups, hyperthermia caused an increase in blood pressure, renal resistance, and LF but no changes in renal nerve activity, whereas a tachycardia was only observed in the older rats. Increases in BRS (0.80 +/- 0.14 vs. 1.72 +/- 0.34 ms/mmHg, P < 0.05) and MF (3.10 +/- 0.55 vs. 7.81 +/- 1.89 mmHg2, P < 0.05) and a positive correlation between BRS and MF (r = 0.50, P < 0.01) were observed with heating in mature but not senescent rats. These results indicate that LF, which increased with elevated core temperature, may be modulated by thermal stimuli. The augmented BRS in the mature group may contribute to the hemodynamic adjustments that occur with hyperthermia, whereas the lack of an increase in BRS during heat stress in the senescent group suggests that baroreceptor reflex modulation is impaired with aging. The positive correlation between BRS and MF in mature rats, together with the lack of an increase in renal sympathetic nerve activity, indicates that MF may reflect the modulating influence of the efferent sympathetic portion of the baroreceptor reflex loop on arterial blood pressure rather than merely the activity of the peripheral sympathetic nervous system.


2013 ◽  
Vol 304 (8) ◽  
pp. R651-R656 ◽  
Author(s):  
Brett J. Wong

We tested the hypothesis that inhibition of cutaneous sensory nerves would attenuate reflex cutaneous vasodilation in response to an increase in core temperature. Nine subjects were equipped with four microdialysis fibers on the forearm. Two sites were treated with topical anesthetic EMLA cream for 120 min. Sensory nerve inhibition was verified by lack of sensation to a pinprick. Microdialysis fibers were randomly assigned as 1) lactated Ringer (control); 2) 10 mM nitro-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase; 3) EMLA + lactated Ringer; and 4) EMLA + l-NAME. Laser-Doppler flowmetry was used as an index of skin blood flow, and blood pressure was measured via brachial auscultation. Subjects wore a water-perfused suit, and oral temperature was monitored as an index of core temperature. The suit was perfused with 50°C water to initiate whole body heat stress to raise oral temperature 0.8°C above baseline. Cutaneous vascular conductance (CVC) was calculated and normalized to maximal vasodilation (%CVCmax). There was no difference in CVC between control and EMLA sites (67 ± 5 vs. 69 ± 6% CVCmax), but the onset of vasodilation was delayed at EMLA compared with control sites. The l-NAME site was significantly attenuated compared with control and EMLA sites (45 ± 5% CVCmax; P < 0.01). Combined EMLA + l-NAME site (25 ± 6% CVCmax) was attenuated compared with control and EMLA ( P < 0.001) and l-NAME only ( P < 0.01). These data suggest cutaneous sensory nerves contribute to reflex cutaneous vasodilation during the early, but not latter, stages of heat stress, and full expression of reflex cutaneous vasodilation requires functional sensory nerves and NOS.


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