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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, NOSdependent sweating but not cutaneous vasodilation is attenuated, whereas COX inhibition increases sweating. [ABSTRACT FROM AUTHOR]

The purpose of this study was to compare smokers and non-smokers' sudomotor and cutaneous vascular responses to whole-body passive heat stress. 9 regularly smoking (SMK; 29±9 y; 10±6 cigarettes/day) and 13 non-smoking (N-SMK; 27±8 y) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate via ventilated-capsule (LSR), sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via Laser Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared to N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52±0.19 versus 0.35±0.14°C, respectively; p=0.03) and cutaneous vasodilation (0.61±0.21 versus 0.31±0.12°C, respectively; p<0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63±0.21 versus 0.60±0.40 versus Δmg/²/min/°C ΔTb, respectively, p=0.81; CVC: 82.5±46.2 versus 58.9±23.3 Δ%max/°C ΔTb, respectively; p=0.19). However, plateau in LSR during whole-body heating was higher in N-SMK versus SMK (1.00±0.13 versus 0.79±0.26 mg·cm²·min; p=0.03), which was likely a result of higher SGO (8.94±3.99 versus 5.94±3.49 μg·gland-1·min-1, respectively; p=0.08) and not number of SGA (104±7 versus 121±9 glands/cm², respectively; p=0.58). During whole-body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight to local (i.e. forearm) thermoregulatory responses of young smokers during uncompensatory whole-body passive heat stress. [ABSTRACT FROM AUTHOR]

Sleep occurs in close relation to changes in body temperature. Both the monophasic sleep period in humans and the polyphasic sleep periods in rodents tend to be initiated when core body temperature is declining. This decline is mainly due to an increase in skin blood flow and consequently skin warming and heat loss. We have proposed that these intrinsically occurring changes in core and skin temperatures could modulate neuronal activity in sleep-regulating brain areas (Van Someren EJW, Chronobiol Int 17:313-54, 2000). We here provide results compatible with this hypothesis. We obtained 144 sleep-onset latencies while directly manipulating core and skin temperatures within the comfortable range in eight healthy subjects under controlled conditions. The induction of a proximal skin temperature difference of only 0.78 ± 0.03°C (mean ± SE) around a mean of 35.13 ± 0.11°C changed sleep-onset latency by 26%, i.e., by 3.09 minutes [95% confidence interval (CI), 1.91 to 4.28] around a mean of 11.85 mm (CI, 9.74 to 14.41), with faster sleep onsets when the proximal skin was warmed. The reduction in sleep-onset latency occurred despite a small but significant decrease in subjective comfort during proximal skin warming. The induction of changes in core temperature (δ = 0.20 ± 0.02°C) and distal skin temperature (δ = 0.74 ± 0.05°C) were ineffective. Previous studies have demonstrated correlations between skin temperature and sleep-onset latency. Also, sleep disruption by ambient temperatures that activate thermoregulatory defense mechanisms has been shown. The present study is the first to experimentally demonstrate a causal contribution to sleep-onset latency of skin temperature manipulations within the normal nocturnal fluctuation range. Circadian and sleep-appetitive behavior-induced variations in skin temperature might act as an input signal to sleep-regulating systems. [ABSTRACT FROM AUTHOR]

Adenosine (ADO) receptor antagonists (aminophylline, caffeine) blunt the respiratory roll-off response to hypoxia in the newborn. This study was designed to determine the ADO receptor subtype involved in the respiratory depression. Chronically catheterized lambs of 7–16 days of age breathed via face mask a gas mixture with a fraction of inspired 02 of 0.21 (normoxia) or 0.07 (hypoxia), while being infused intravascularly with 9-cyclopentyl- 1 ,3-dipropylxanthine (DPCPX; ADO A1-receptor antagonist, n = 8), ZM-241385 (ADO A2A-receptor antagonist, n = 7), or vehicle. Ventilation was measured at 20°C by a turbine transducer flowmeter. In normoxia [arterial Po2 (Pao2) of ∼83 Torr], infusion of vehicle did not alter cardiorespiratory measurements, whereas hypoxia (Pao2 of ∼31 Torr, 15 min) elicited biphasic effects on mean arterial pressure (transient increase), heart rate (HR; diminishing tachycardia), and minute ventilation. In the latter, hypoxia increased ventilation to a peak value of --2.5 times control within the first 3 mm, which was followed by a significant (P < 0.05) decline to -50% of the maximum increment over the subsequent 7 min. ZM-241385 abolished the hypoxic ventilatory roll-off and blunted the rate of rise in HR without affecting mean arterial pressure or rectal temperature responses. In normoxia, DPCPX increased ventilation and mean arterial pressure but did not change HR. Compared with vehicle, DPCPX did not significantly affect cardiorespiratory responses to hypoxemia (Pao2 of ∼31 Torr, 10 min). It is concluded that 1) ADO A2A receptors are critically involved in the ventilatory roll-off and HR responses to hypoxia, and 2) ADO A1 receptors, which are tonically active in cardiorespiratory control in normoxia, appear to have little impact on hypoxic ventilatory depression. [ABSTRACT FROM AUTHOR]

The criptochrome genes (Cry1 and Cry2) are involved in the molecular mechanism that controls the circadian clock, and mice lacking these genes (Cry1-/-/Cry2-/-) are behaviorally arrhythmic. It has been speculated that the circadian clock modulates the characteristics of thermoregulation, resulting in body temperature (Tb) rhythm. However, there is no direct evidence proving this speculation. We show here that Tb and heat production in Cry1-/-/Cry2-/- mice are arrhythmic under constant darkness. In contrast, both rhythms occur under a light-dark cycle and/or periodical food restriction linked with spontaneous activity and/or eating, although they are not robust as those in wild-type mice. The relationship between heat production and Tb in Cry1-/-/Cry2-/- mice is linear and identical under any conditions, indicating that their Tb rhythm is determined by heat production rhythm associated with activity and eating. However, Tb in wild-type mice is maintained at a relatively higher level in the active phase than the inactive phase regardless of the heat production level. These results indicate that the thermoregulatory responses are modulated according to the circadian phase, and the Cry genes are involved in this mechanism. [ABSTRACT FROM AUTHOR]

Romanovsky, Andrej A. Do fever and anapyrexia exist? Analysis of set point-based definitions. Am J Physiol Regul Integr Comp Physiol 287: R992-R995, 2004. First published June 24, 2004; 10.1152/ ajpregu.00068.2004.—Fever and anapyrexia are the most studied thermoregulatory responses. They are defined as a body temperature (Tb) increase and decrease, respectively, occurring because of a shift in the set point (SP) and characterized by active defense of the new Tb. Although models of Tb control with a single SP (whether obvious or hidden) have been criticized, the SP-based definitions have remained unchallenged. In this article, the SP-based definitions of fever and anapyrexia were subjected to two tests. In test 1, they were compared with experimental data on changes in thresholds for activation of different thermoeffectors. Changes in thresholds were found compatible with an SP increase in some (but not all) cases of fever. In all cases of what is called anapyrexia, its mechanism (dissociation of thresholds of different effectors) was found incompatible with a decrease in a single SP. In test 2, experimental data on the dependence of Tb on ambient temperature (Ta) were analyzed. It was found that the febrile level of Tb is defended in some (but not all) cases. However, strong dependence on Ta was found in all cases of anapyrexia, which agrees with threshold dissociation but not with a decrease of the SP. It is concluded that fever (as defined) has only limited experimental support, whereas anapyrexia (as defined) does not exist. Two solutions are offered. A palliative is to accept that SP-based terms (anapyrexia, cryexia, regulated hypothermia, and such) are inadequate and should be abandoned. A radical solution is to transform all definitions based on comparing Tb with the SP into definitions based on balancing active and passive processes of Tb control. [ABSTRACT FROM AUTHOR]