Sheila Dervis

Hyperthermia and cardiovascular strain during an extreme heat exposure in young versus older adults

ABSTRACT We examined whether older individuals experience greater levels of hyperthermia and cardiovascular strain during an extreme heat exposure compared to young adults. During a 3-hour extreme heat exposure (44°C, 30% relative humidity), we compared body heat storage, core temperature (rectal, visceral) and cardiovascular (heart rate, cardiac output, mean arterial pressure, limb blood flow) responses of young adults (n = 30, 19–28 years) against those of older adults (n = 30, 55–73 years). Direct calorimetry measured whole-body evaporative and dry heat exchange. Body heat storage was calculated as the temporal summation of heat production (indirect calorimetry) and whole-body heat loss (direct calorimetry) over the exposure period. While both groups gained a similar amount of heat in the first hour, the older adults showed an attenuated increase in evaporative heat loss (p < 0.033) in the first 30-min. Thereafter, the older adults were unable to compensate for a greater rate of heat gain (11 ± 1 ; p < 0.05) with a corresponding increase in evaporative heat loss. Older adults stored more heat (358 ± 173 kJ) relative to their younger (202 ± 92 kJ; p < 0.001) counterparts at the end of the exposure leading to greater elevations in rectal (p = 0.043) and visceral (p = 0.05) temperatures, albeit not clinically significant (rise < 0.5°C). Older adults experienced a reduction in calf blood flow (p < 0.01) with heat stress, yet no differences in cardiac output, blood pressure or heart rate. We conclude, in healthy habitually active individuals, despite no clinically observable cardiovascular or temperature changes, older adults experience greater heat gain and decreased limb perfusion in response to 3-hour heat exposure.

Running economy, not aerobic fitness, independently alters thermoregulatory responses during treadmill running

We sought to determine the independent influence of running economy (RE) and aerobic fitness [maximum oxygen consumption (V̇O 2max)] on thermoregulatory responses during treadmill running by conducting two studies. In study 1, seven high (HI-FIT: 61 ± 5 ml O2 · kg(-1) · min(-1)) and seven low (LO-FIT: 45 ± 4 ml O2 · kg(-1) · min(-1)) V̇O 2max males matched for physical characteristics and RE (HI-FIT: 200 ± 21; LO-FIT: 200 ± 18 ml O2 · kg(-1) · km(-1)) ran for 60 min at 1) 60%V̇O 2max and 2) a fixed metabolic heat production (Hprod) of 640 W. In study 2, seven high (HI-ECO: 189 ± 15.3 ml O2 · kg(-1) · km(-1)) and seven low (LO-ECO: 222 ± 10 ml O2 · kg(-1) · km(-1)) RE males matched for physical characteristics and V̇O 2max (HI-ECO: 60 ± 3; LO-ECO: 61 ± 7 ml O2 · kg(-1) · min(-1)) ran for 60 min at a fixed 1) speed of 10.5 km/h and 2) Hprod of 640 W. Environmental conditions were 25.4 ± 0.8°C, 37 ± 12% RH. In study 1, at Hprod of 640 W, similar changes in esophageal temperature (ΔTes; HI-FIT: 0.63 ± 0.20; LO-FIT: 0.63 ± 0.22°C; P = 0.986) and whole body sweat losses (WBSL; HI-FIT: 498 ± 66; LO-FIT: 497 ± 149 g; P = 0.984) occurred despite different relative intensities (HI-FIT: 55 ± 6; LO-FIT: 39 ± 2% V̇O 2max; P < 0.001). At 60% V̇O 2max, ΔTes (P = 0.029) and WBSL (P = 0.003) were greater in HI-FIT (1.14 ± 0.32°C; 858 ± 130 g) compared with LO-FIT (0.73 ± 0.34°C; 609 ± 123 g), as was Hprod (HI-FIT: 12.6 ± 0.9; LO-FIT: 9.4 ± 1.0 W/kg; P < 0.001) and the evaporative heat balance requirement (Ereq; HI-FIT: 691 ± 74; LO-FIT: 523 ± 65 W; P < 0.001). Similar sweating onset ΔTes and thermosensitivities occurred between V̇O 2max groups. In study 2, at 10.5 km/h, ΔTes (1.16 ± 0.31 vs. 0.78 ± 0.28°C; P = 0.017) and WBSL (835 ± 73 vs. 667 ± 139 g; P = 0.015) were greater in LO-ECO, as was Hprod (13.5 ± 0.6 vs. 11.3 ± 0.8 W/kg; P < 0.001) and Ereq (741 ± 89 vs. 532 ± 130 W; P = 0.007). At Hprod of 640 W, ΔTes (P = 0.910) and WBSL (P = 0.710) were similar between HI-ECO (0.55 ± 0.31°C; 501 ± 88 g) and LO-ECO (0.57 ± 0.16°C; 483 ± 88 g), but running speed was different (HI-ECO: 8.2 ± 0.6; LO-ECO: 7.2 ± 0.4 km/h; P = 0.025). In conclusion, thermoregulatory responses during treadmill running are not altered by V̇O 2max, but by RE because of differences in Hprod and Ereq.

A comparison of thermoregulatory responses to exercise between mass-matched groups with large differences in body fat

We sought to determine 1) the influence of adiposity on thermoregulatory responses independently of the confounding biophysical factors of body mass and metabolic heat production (Hprod); and 2) whether differences in adiposity should be accounted for by prescribing an exercise intensity eliciting a fixed Hprod per kilogram of lean body mass (LBM). Nine low (LO-BF) and nine high (HI-BF) body fat males matched in pairs for total body mass (TBM; LO-BF: 88.7 ± 8.4 kg, HI-BF: 90.1 ± 7.9 kg; P = 0.72), but with distinctly different percentage body fat (%BF; LO-BF: 10.8 ± 3.6%; HI-BF: 32.0 ± 5.6%; P < 0.001), cycled for 60 min at 28.1 ± 0.2 °C, 26 ± 8% relative humidity (RH), at a target Hprod of 1) 550 W (FHP trial) and 2) 7.5 W/kg LBM (LBM trial). Changes in rectal temperature (ΔTre) and local sweat rate (LSR) were measured continuously while whole body sweat loss (WBSL) and net heat loss (Hloss) were estimated over 60 min. In the FHP trial, ΔTre (LO-BF: 0.66 ± 0.21 °C, HI-BF: 0.87 ± 0.18 °C; P = 0.02) was greater in HI-BF, whereas mean LSR (LO-BF 0.52 ± 0.19, HI-BF 0.43 ± 0.15 mg·cm(-2)·min(-1); P = 0.19), WBSL (LO-BF 586 ± 82 ml, HI-BF 559 ± 75 ml; P = 0.47) and Hloss (LO-BF 1,867 ± 208 kJ, HI-BF 1,826 ± 224 kJ; P = 0.69) were all similar. In the LBM trial, ΔTre (LO-BF 0.82 ± 0.18 °C, HI-BF 0.54 ± 0.19 °C; P < 0.001), mean LSR (LO-BF 0.59 ± 0.20, HI-BF 0.38 ± 0.12 mg·cm(-2)·min(-1); P = 0.04), WBSL (LO-BF 580 ± 106 ml, HI-BF 381 ± 68 ml; P < 0.001), and Hloss (LO-BF 1,884 ± 277 kJ, HI-BF 1,341 ± 184 kJ; P < 0.001) were all greater at end-exercise in LO-BF. In conclusion, high %BF individuals demonstrate a greater ΔTre independently of differences in mass and Hprod, possibly due to a lower mean specific heat capacity or impaired sudomotor control. However, thermoregulatory responses of groups with different adiposity levels should not be compared using a fixed Hprod in watts per kilogram lean body mass.

Heart rate variability during high heat stress: a comparison between young and older adults with and without type 2 diabetes

We examined whether older individuals with and without Type 2 diabetes (T2D) experience differences in heart rate variability (HRV) during a 3-h exposure to high heat stress compared with young adults. Young (Young; n = 22; 23 ± 3 yr) and older individuals with (T2D; n = 11; 59 ± 9 yr) and without (Older; n = 25; 63 ± 5 yr) T2D were exposed to heat stress (44°C, 30% relative humidity) for 3 h. Fifty-five HRV measures were assessed for 15 min at baseline and at minutes 82.5-97.5 (Mid) and minutes 165-180 (End) during heat stress. When compared with Young, a similar number of HRV indices were significantly different (P < 0.05) in Older (Baseline: 35; Mid: 29; End: 32) and T2D (Baseline: 31; Mid: 30; End: 27). In contrast, the number of HRV indices significantly different (P < 0.05) between Older and T2D were far fewer (Baseline: 13, Mid: 1, End: 3). Within-group analyses demonstrated a greater change in the Young groups HRV during heat stress compared with Older and T2D; the number of significantly different (P < 0.05) HRV indices between baseline and End were 42, 29, and 20, for Young, Older, and T2D, respectively. Analysis of specific HRV domains suggest that the Young group experienced greater sympathetic activity during heat stress compared with Older and T2D. In conclusion, when compared with young, older individuals with and without T2D demonstrate low HRV at baseline and less change in HRV (including an attenuated sympathetic response) during 3 h high heat stress, potentially contributing to impaired thermoregulatory function.

The effect of plasma osmolality and baroreceptor loading status on postexercise heat loss responses

We examined the separate and combined effects of plasma osmolality and baroreceptor loading status on postexercise heat loss responses. Nine young males completed a 45-min treadmill exercise protocol at 58 ± 2% V̇o2 peak, followed by a 60-min recovery. On separate days, participants received 0.9% NaCl (ISO), 3.0% NaCl (HYP), or no infusion (natural recovery) throughout exercise. In two additional sessions (no infusion), lower-body negative (LBNP) or positive (LBPP) pressure was applied throughout the final 45 min of recovery. Local sweat rate (LSR; ventilated capsule: chest, forearm, upper back, forehead) and skin blood flow (SkBF; laser-Doppler flowmetry: forearm, upper back) were continuously measured. During HYP, upper back LSR was attenuated from end-exercise to 10 min of recovery by ∼0.35 ± 0.10 mg·min(-1)·cm(-2) and during the last 20 min of recovery by ∼0.13 ± 0.03 mg·min(-1)·cm(-2), while chest LSR was lower by 0.18 ± 0.06 mg·min(-1)·cm(-2) at 50 min of recovery compared with natural recovery (all P < 0.05). Forearm and forehead LSRs were not affected by plasma hyperosmolality during HYP (all P > 0.28), which suggests regional differences in the osmotic modulation of postexercise LSR. Furthermore, LBPP application attenuated LSR by ∼0.07-0.28 mg·min(-1)·cm(-2) during the last 30 min of recovery at all sites except the forehead compared with natural recovery (all P < 0.05). Relative to natural recovery, forearm and upper back SkBF were elevated during LBPP, ISO, and HYP by ∼6-10% by the end of recovery (all P < 0.05). We conclude that 1) hyperosmolality attenuates postexercise sweating heterogeneously among skin regions, and 2) baroreceptor loading modulates postexercise SkBF independently of changes in plasma osmolality without regional differences.

Type 1 diabetes modulates cyclooxygenase- and nitric oxide-dependent mechanisms governing sweating but not cutaneous vasodilation during exercise in the heat

Both cyclooxygenase (COX) and nitric oxide synthase (NOS) contribute to sweating, whereas NOS alone contributes to cutaneous vasodilation during exercise in the heat. Here, we evaluated if Type 1 diabetes mellitus (T1DM) modulates these responses. Adults with (n = 11, 25 ± 5 yr) and without (n = 12, 24 ± 4 yr) T1DM performed two bouts of 30-min cycling at a fixed rate of heat production of 400 W in the heat (35°C); each followed by a 20- and 40-min recovery period, respectively. Sweat rate and cutaneous vascular conductance (CVC) were measured at four intradermal microdialysis sites treated with either 1) lactated Ringer (vehicle control site), 2) 10 mM ketorolac (nonselective COX inhibitor), 3) 10 mM NG-nitro-l-arginine methyl ester (nonselective NOS inhibitor), or 4) a combination of both inhibitors. In nondiabetic adults, separate and combined inhibition of COX and NOS reduced exercise sweat rate (P ≤ 0.05), and the magnitude of reductions were similar across sites. In individuals with T1DM, inhibition of COX resulted in an increase in sweat rate of 0.10 ± 0.09 and 0.09 ± 0.08 mg ·: min-1 ·: cm-2 for the first and second exercise bouts, respectively, relative to vehicle control site (P ≤ 0.05), whereas NOS inhibition had no effect on sweating. In both groups, NOS inhibition reduced CVC during exercise (P ≤ 0.05), although the magnitude of reduction did not differ between the nondiabetic and T1DM groups (exercise 1: -28 ± 10 vs. -23 ± 8% max, P = 0.51; exercise 2: -31 ± 12 vs. -24 ± 10% max, P = 0.38). We show that in individuals with T1DM performing moderate intensity exercise in the heat, NOS-dependent sweating but not cutaneous vasodilation is attenuated, whereas COX inhibition increases sweating.