The effect of direct and indirect hand heating on finger blood flow and dexterity during cold exposure

1. The aim of this study was to investigate if finger temperature or finger blood flow is the critical factor for maintenance of finger dexterity during cold exposure.

2. Subjects were exposed twice to −25°C air for 3 h by using a Torso Heating Test (THT) where the torso was maintained to 42°C with a heating vest while the hands were bare, and a Hand Heating Test (HHT) where the hands were heated with heated gloves.

3. Despite similar finger temperatures, finger blood flow was eight times lower and finger dexterity was decreased in HHT as compared to THT.

4. It is concluded that finger blood flow is the critical factor to maintain finger dexterity in the cold.

Nitric oxide and neurally mediated regulation of skin blood flow during local heating.

The mechanisms underlying the skin blood flow (SkBF) response to local heating are complex and poorly understood. Our goal was to examine the role of axon reflexes and nitric oxide (NO) in the SkBF response to a local heating protocol. We performed 40 experiments following a standardized heating protocol with different interventions, including blockade of the axon reflex (EMLA cream), antebrachial nerve blockade (0.5% bupivacaine injection), and NO synthase (NOS) inhibition (> or =10 mM N(G)-nitro-L-arginine methyl ester; microdialysis). Appropriate controls were performed to verify the efficacy of the various blocks. Values are expressed as a percentage of maximal SkBF (SkBF(max); 50 mM sodium nitroprusside). At the initiation of local heating, SkBF rose to an initial peak, followed by a brief nadir, and a secondary, progressive rise to a plateau. Axon reflex block decreased the initial peak from 75+3 to 32 +/- 2% SkBF(max) (P < 0.01 vs. control) but did not affect the plateau. NOS inhibition before and throughout local heating reduced the initial peak from 75 +/- 3 to 56 +/- 3% SkBF(max) (P < 0.01) and the plateau from 87 +/- 4 to 40 +/- 5%. NOS inhibition during axon reflex block did not further reduce the initial SkBF peak compared with axon reflex block alone. Antebrachial nerve block did not affect the local heating SkBF response. The primary finding of these studies is that there are at least two independent mechanisms contributing to the rise in SkBF during nonpainful local heating: a fast-responding vasodilator system mediated by the axon reflexes and a more slowly responding vasodilator system that relies on local production of NO.     

Influence of localized auxiliary heating on hand comfort during cold exposure

There is a needfor a hand-heating system that will keep the hands warm during coldexposure without hampering finger dexterity. The purpose of this studywas to examine the effects of torso heating on the vasodilativeresponses and comfort levels of cooled extremities during a 3-hexposure to 15°C air. Subjects were insulated, but theirupper extremities were left exposed to the cold ambient air. The effectof heating the torso [torso-heating test (THT)] on handcomfort was compared with a control condition in which no torso heatingwas applied, but Arctic mitts were worn [control test(CT)]. The results indicate that mean finger temperature, meanfinger blood flow, mean toe temperature, mean body skin temperature, body thermal comfort, mean finger thermal comfort, and rate of bodyheat storage were all significantly (P < 0.05) higher on average (n = 6)during THT. Mean body heat flow was significantly (P < 0.05) lower during THT. Therewere no significant differences (P  0.05) in rectal temperature between CT and THT. Mean unheated body skintemperature and mean unheated body heat flow (both of which did notinclude the torso area in the calculation of mean body skin temperatureand mean body heat flow) were also calculated. There were nosignificant differences (P  0.05) inmean unheated body skin temperature and mean unheated body heat flowbetween CT and THT. It is concluded that the application of heat to the torso can maintain finger and toe comfort for an extended period oftime during cold exposure.

     

Investigating high-amplitude oscillations in rat tail skin blood flow during core heating and cooling

In a separate paper, we describe high-amplitude oscillations in human skin blood flow (Q˙_sk). Using an open-loop model in rats, we independently modulated and clamped hypothalamic and skin temperatures. Central heating reliably induced these high-amplitude oscillations in tail Q˙_sk, which occurred at 0.41±0.03 Hz spanning 758.1±25.7 ms, and were comprised of high-amplitude peaks (496.8±87.6 AU) arising from a stable baseline (114.1±27.6 AU). Central cooling significantly reduced Q˙_sk, but not the amplitude, the frequency, width or baseline of the oscillations. These observations indicate that such high-amplitude oscillations are not primarily mediated via central thermal state. Instead, we believe these oscillations to be turned on by an elevated skin temperature.     

Aging and the skin blood flow response to the unloading of baroreceptors during heat and cold stress.

Control of skin blood flow (SkBF) is on the efferent arm of both thermoregulatory and nonthermoregulatory reflexes. To what extent aging may affect the SkBF response when these two reflex systems interact is unknown. To determine the response of aged skin to the unloading of baroreceptors in thermoneutral, cold stress, and heat stress conditions, sequential bouts of nonhypotensive lower body negative pressure (LBNP) were applied at -10, -20, and -30 mmHg in 14 young (18-25 yr) and 14 older (63-78 yr) men. SkBF was measured by laser-Doppler velocimetry (averaged over 2 forearm sites), and data are expressed as percentage of maximal cutaneous vascular conductance (%CVC(max)). Total forearm blood flow was measured by venous occlusion plethysmography, and forearm vascular conductance (FVC) was calculated as the ratio of forearm blood flow to mean arterial pressure. In young men, all three intensities of LBNP in thermoneutrality decreased FVC significantly (P < 0.05), but FVC at -10 mmHg did not change in the older men. There were no significant LBNP effects on %CVC(max). Application of LBNP during cold stress did not significantly change %CVC(max) or FVC in either age group. During heat stress, -10 to -30 mmHg of LBNP decreased FVC significantly (P < 0.05) in both age groups, but these decreases were attenuated in the older men (P < 0.05). %CVC(max) decreased at -30 mmHg in the younger men only. These results suggest that older men have an attenuated skin vasoconstrictor response to the unloading of baroreceptors in heat stress conditions. Furthermore, the forearm vasoconstriction elicited by LBNP in older men reflects that of underlying tissue (i.e., muscle) rather than that of skin, whereas -30 mmHg LBNP also decreases SkBF in young hyperthermic men.     

Hypohydration effect on finger skin temperature and blood flow during cold-water finger immersion.

This study was conducted to determine whether hypohydration (Hy) alters blood flow, skin temperature, or cold-induced vasodilation (CIVD) during peripheral cooling. Fourteen subjects sat in a thermoneutral environment (27 degrees C) during 15-min warm-water (42 degrees C) and 30-min cold-water (4 degrees C) finger immersion (FI) while euhydrated (Eu) and, again, during Hy. Hy (-4% body weight) was induced before FI by exercise-heat exposure (38 degrees C, 30% relative humidity) with no fluid replacement, whereas during Eu, fluid intake maintained body weight. Finger pad blood flow [as measured by laser-Doppler flux (LDF)] and nail bed (T(nb)), pad (T(pad)), and core (T(c)) temperatures were measured. LDF decreased similarly during Eu and Hy (32 +/- 10 and 33 +/- 13% of peak during warm-water immersion). Mean T(nb) and T(pad) were similar between Eu (7.1 +/- 1.0 and 11.5 +/- 1.6 degrees C) and Hy (7.4 +/- 1.3 and 12.6 +/- 2.1 degrees C). CIVD parameters (e.g., nadir, onset time, apex) were similar between trials, except T(pad) nadir was higher during Hy (10.4 +/- 3.8 degrees C) than during Eu (7.9 +/- 1.6 degrees C), which was attributed to higher T(c) in six subjects during Hy (37.5 +/- 0.2 degrees C), compared with during Eu (37.1 +/- 0.1 degrees C). The results of this study provide no evidence that Hy alters finger blood flow, skin temperature, or CIVD during peripheral cooling.     

Assessment of the changes in regulatory systems of human's skin blood flow during local heating

The mechanisms of thermal regulation of skin blood flow during local heating to 35, 40 and 45 'C have been studied by the method of laser Doppler flowmetry in healthy volunteers. To estimate the state of microvascular bed the continuous wavelet-transform spectral analysis has been used. The amplitudes of fluxmotions in the range of blood flow active modulation significantly increase during local heating to 35 degrees C. The amplitudes of blood flow oscillations in the ranges of cardiorhythm and respiratory rhythm increase during local heating to 40 degrees C. The high amplitude oscillations in the range of myogenic activity are maintained. The amplitude of oscillations in the range of endothelial activity distinctly decreases and the oscillations in the range of neurogenic activity are inhibited. Local heating to 45 degrees C results in a significant decreasing of the oscillation amplitudes in the range of myogenic activity, and the amplitudes of cardio- and respiratory spectral components amount to their peak values among the temperatures of local heating under study.     

Effect of alterations in ambient temperature on blood flow in the skin.

The effect of changing ambient temperature on skin temperature was recorded in human subjects; also, its effect on blood flow was measured using venous occlusion and optical plethysmography. When cold stimulus was removed in stages using a heating cabinet, it was found that a biphasic flow response occurred in the fingers with each step change in temperature. There was a rapid transient rise followed by a decline to an equilibrium flow level. The transient rise occurred even when the temperature rose from 37 to 40 degrees C, although at this level the equilibrium remained unchanged. It is suggested that the transient rise was due to stimulation of Hensel's dynamic warmth receptors, whereas the rise in equilibrium temperature was due to removal of cold stimulus, which at low ambient temperatures maintains reflex vasoconstriction through activation of static cold receptors. Upper arm skin responded to removal of cold stimulus by a fall in temperature. Immersion of a different limb in cold water produced vasoconstriction in fingers but vasodilatation in the upper arm skin. It is suggested that this may be due to neurogenic vasodilatation, though the present work gives no indication as to pathways.     

The effect of local heating on blood flow in the finger and the forearm skin

Blood flow of the finger and the forearm were measured in five male subjects by venous occlusion plethysmography using mercury-in-Silastic strain gauges in either a cool-dry (COOL: 25 degrees C, 40% relative humidity), a hot-dry (WARM: 35 degrees C, 40% relative humidity), or a hot-wet (HOT: 35 degrees C, 80% relative humidity) environment. One hand or forearm was immersed in a water bath, the temperature (Tw) of which was raised every 10 min by steps of 2 degrees C until it reached 41 degrees or 43 degrees C. While the other hand or forearm was kept immersed in a water bath (Tw, 35 degrees C), blood flow in the heated side (BFw) was compared with the corresponding blood flow in the control side (BFc). Under WARM or HOT conditions, finger BFw was significantly lower than finger BFc at a Tw of 39-41 degrees C in the majority of subjects. When Tw was raised to 43 degrees C, however, finger BFw became higher than BFc in nearly half of the subjects. In the COOL state, finger BFw did not decrease but increased steadily when Tw increased from 37 degrees to 43 degrees C. In the forearm, BFw increased steadily with increasing Tw even in WARM-HOT environments. No such heat-induced vasoconstriction was observed in the forearm. From these results we conclude that in hyperthermic subjects, the rise in local temperature to above core temperature produces vasoconstriction in the fingers, an area where no thermal sweating takes place.     

Infrared cameras overestimate skin temperature during rewarming from cold exposure

ObjectiveThe primary aim of this study was to assess the accuracy of an infrared camera and that of a skin thermistor, both commercially available. The study aimed to assess the agreement over a wide range of skin temperatures following cold exposure.MethodsFifty-two males placed their right hand in a thin plastic bag and immersed it in 8 °C water for 30 min whilst seated in an air temperature of 30 °C. Following hand immersion, participants removed the bag and rested their hand at heart level for 10 min. Index finger skin temperature (T_sk) was measured with a thermistor, affixed to the finger pad, and an infrared camera measured 1 cm distally to the thermistor. Agreement between the infrared camera and thermistor was assessed by mean difference (infrared camera minus thermistor) and 95% limits of agreement analysis, accounting for the repeated measures over time. The clinically significant threshold for T_sk differences was set at ±0.5 °C and limits of agreement ±1 °C.ResultsAs an average across all time points, the infrared camera recorded T_sk 1.80 (SD 1.16) °C warmer than the thermistor, with 95% limits of agreement ranging from −0.46 °C to 4.07 °C.ConclusionCollectively, the results show the infrared camera overestimated T_sk at every time point following local cooling. Further, measurement of finger T_sk from the infrared camera consistently fell outside the acceptable level of agreement (i.e. mean difference exceeding ±0.5 °C). Considering these results, infrared cameras may overestimate peripheral T_sk following cold exposure and clinicians and practitioners should, therefore, adjust their risk/withdrawal criteria accordingly.     

Effects of atropine and L-NAME on cutaneous blood flow during body heating in humans.

We sought to investigate further the roles of sweating, ACh spillover, and nitric oxide (NO) in the neurally mediated cutaneous vasodilation during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured with a laser-Doppler flowmeter. After a rise in core temperature (1. 0 +/- 0.1 degrees C) and the establishment of cutaneous vasodilation, atropine and subsequently the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) were given to the forearm via a brachial artery catheter. After atropine infusion, cutaneous vascular conductance (CVC) remained constant in five of six subjects, whereas L-NAME administration blunted the rise in CVC in three of six subjects. A subsequent set of studies using intradermal microdialysis probes to selectively deliver drugs into forearm skin confirmed that atropine did not affect CVC. However, perfusion of L-NAME resulted in a significant decrease in CVC (37 +/- 4%, P < 0.05). The results indicate that neither sweating nor NO release via muscarinic receptor activation is essential to sustain cutaneous dilation during heating in humans.