Although the ability to sense skin wetness and humidity is critical for behavioral and autonomic adaptations, humans are not provided with specific skin receptors for sensing wetness. It has been proposed that we "learn" to perceive the wetness experienced when the skin is in contact with a wet surface or when sweat is produced through a multisensory integration of thermal and tactile inputs generated by the interaction between skin and moisture. However, the individual roles of thermal and tactile cues and how these are integrated peripherally and centrally by our nervous system is still poorly understood. Here we tested the hypothesis that the central integration of coldness and mechanosensation, as subserved by peripheral A-nerve afferents, might be the primary neural process underpinning human wetness sensitivity. During a quantitative sensory test, we found that individuals perceived warm-wet and neutral-wet stimuli as significantly less wet than cold-wet stimuli, although these were characterized by the same moisture content. Also, when cutaneous cold and tactile sensitivity was diminished by a selective reduction in the activity of A-nerve afferents, wetness perception was significantly reduced. Based on a concept of perceptual learning and Bayesian perceptual inference, we developed the first neurophysiological model of cutaneous wetness sensitivity centered on the multisensory integration of cold-sensitive and mechanosensitive skin afferents. Our results provide evidence for the existence of a specific information processing model that underpins the neural representation of a typical wet stimulus. These findings contribute to explaining how humans sense warm, neutral, and cold skin wetness.

Undoubtedly, adjusting our thermoregulatory behavior represents the most effective mechanism to maintain thermal homeostasis and ensure survival in the diverse thermal environments that we face on this planet. Remarkably, our thermal behavior is entirely dependent on the ability to detect variations in our internal (i.e. body) and external environment, via sensing changes in skin temperature and wetness. In the past 30 years, we have seen a significant expansion of our understanding of the molecular, neuroanatomical and neurophysiological mechanisms that allow humans to sense temperature and humidity. The discovery of temperature-activated ion channels which gate the generation of action potentials in thermosensitive neurons, along with the characterization of the spino-thalamo-cortical thermosensory pathway, and the development of neural models for the perception of skin wetness, are only some of the recent advances which have provided incredible insights on how biophysical changes in skin temperature and wetness are transduced into those neural signals which constitute the physiological substrate of skin thermal and wetness sensations. Understanding how afferent thermal inputs are integrated and how these contribute to behavioral and autonomic thermoregulatory responses under normal brain function is critical to determine how these mechanisms are disrupted in those neurological conditions which see the concurrent presence of afferent thermosensory abnormalities and efferent thermoregulatory dysfunctions. Furthermore, advancing the knowledge on skin thermal and wetness sensations is crucial to support the development of neuro-prosthetics. In light of the above, this review will focus on the peripheral and central neurophysiological mechanisms underpinning skin thermal and wetness sensations in humans.

Cold sensations are suggested as the primary inducer of the perception of skin wetness.However, limited data are available on the effects of skin cooling. Hence, we investigated the role of peripheral cold afferents in the perception of wetness. Six cold-dry stimuli (producing skin cooling rates in a range of 0.02 to 0.41°C/s) were applied on the forearm of 9 female participants.Skin temperature and conductance, thermal and wetness perception were recorded. Five out of 9 participants perceived wetness as a result of cold-dry stimuli with cooling rates in a range of 0.14 to 0.41°C/s, while 4 did not perceive skin wetness at all. Although skin cooling and cold sensations play a role in evoking the perception of wetness, these are not always of a primary importance and other sensory modalities (i.e. touch and vision), as well as the inter-individual variability in thermal sensitivity, might be equally determinant in characterising this perception.

AbstractThe central integration of thermal (i.e. cold) and mechanical (i.e. pressure) sensory afferents is suggested as to underpin the perception of skin wetness. However, the role of temperature and mechanical inputs, and their interaction, is still unclear. Also, it is unknown whether this intra-sensory interaction changes according to the activity performed or the environmental conditions. Hence, we investigated the role of peripheral cold afferents, and their interaction with tactile afferents, in the perception of local skin wetness during rest and exercise in thermo-neutral and warm environments. Six cold-dry stimuli, characterised by decreasing temperatures [i.e. -4, -8 and -15°C below the local skin temperature (Tsk)] and by different mechanical pressures [i.e. low pressure (LP): 7 kPa; high pressure (HP): 10 kPa], were applied on the back of 8 female participants (age 21 ± 1 years), while they were resting or cycling in 22 or 33°C ambient temperature. Mean and local Tsk, thermal and wetness perceptions were recorded during the tests. Cold-dry stimuli produced drops in Tsk with cooling rates in a range of 0.06 to 0.4°C/s. Colder stimuli resulted in increasing 4 coldness and in stimuli being significantly more often perceived as wet, particularly when producing skin cooling rates of 0.18°C/s and 0.35°C/s. However, when stimuli were applied with HP, local wetness perceptions were significantly attenuated.Wetter perceptions were recorded during exercise in the warm environment. We conclude that thermal inputs from peripheral cutaneous afferents are critical in characterizing the perception of local skin wetness. However, the role of these inputs might be modulated by an intra-sensory interaction with the tactile afferents. These findings indicate that human sensory integration is remarkably multimodal.Keywords: Keywords: Keywords: Keywords: skin wetness; thermo-receptors; mechano-receptors; sensory integration; perception 5The perception of skin wetness is a complex somatosensory experience which seems to result from the intra-sensory integration of temperature and mechanical inputs (Ackerley et al. 2012;Bergmann Tiest et al. 2012;Bentley, 1900). Although humidity-receptors have been previously described in some insects (Yokohari and Tateda, 1976), these receptors have not been identified in human skin (Clark and Edholm, 1985). It is currently suggested that as human beings, we "learn" to perceive the wetness experienced when our skin is in contact with a wet surface, when a liquid is touched, or when sweat is produced (Bergmann Tiest et al. 2012) through a complex multisensory integration (Driver and Spence, 2000;Gescheider and Wright, 2012). The physical processes which occur when the skin is in contact with moisture (i.e. heat transfer and mechanical interactions between the skin and the environment) generate thermal and mechanical inputs which could be integrated and combined at different anatomical levels through specific multisensory pathways (Cappe et al. 2009). Hence, it ...

The ability to perceive thermal changes in the surrounding environment is critical for survival. However, sensing temperature is not the only factor among the cutaneous sensations to contribute to thermoregulatory responses in humans. Sensing skin wetness (i.e. hygrosensation) is also critical both for behavioral and autonomic adaptations. Although much has been done to define the biophysical role of skin wetness in contributing to thermal homeostasis, little is known on the neurophysiological mechanisms underpinning the ability to sense skin wetness. Humans are not provided with skin humidity receptors (i.e., hygroreceptors) and psychophysical studies have identified potential sensory cues (i.e. thermal and mechanosensory) which could contribute to sensing wetness. Recently, a neurophysiological model of human wetness sensitivity has been developed. In helping clarifying the peripheral and central neural mechanisms involved in sensing skin wetness, this model has provided evidence for the existence of a specific human hygrosensation strategy, which is underpinned by perceptual learning via sensory experience. Remarkably, this strategy seems to be shared by other hygroreceptor-lacking animals. However, questions remain on whether these sensory mechanisms are underpinned by specific neuromolecular pathways in humans. Although the first study on human wetness perception dates back to more than 100 years, it is surprising that the neurophysiological bases of such an important sensory feature have only recently started to be unveiled. Hence, to provide an overview of the current knowledge on human hygrosensation, along with potential directions for future research, this review will examine the psychophysical and neurophysiological bases of human skin wetness perception.

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.

Sensing skin wetness is linked to inputs arising from cutaneous cold-sensitive afferents. As thermosensitivity to cold varies significantly across the torso, we investigated whether similar regional differences in wetness perception exist. We also investigated the regional differences in thermal pleasantness and whether these sensory patterns are influenced by ambient temperature. Sixteen males (20 ± 2 yr) underwent a quantitative sensory test under thermo-neutral [air temperature (Tair) = 22°C; relative humidity (RH) = 50%] and warm conditions (Tair = 33°C; RH = 50%). Twelve regions of the torso were stimulated with a dry thermal probe (25 cm(2)) with a temperature of 15°C below local skin temperature (Tsk). Variations in Tsk, thermal, wetness, and pleasantness sensations were recorded. As a result of the same cold-dry stimulus, the skin-cooling response varied significantly by location (P = 0.003). The lateral chest showed the greatest cooling (-5 ± 0.4°C), whereas the lower back showed the smallest (-1.9 ± 0.4°C). Thermal sensations varied significantly by location and independently from regional variations in skin cooling with colder sensations reported on the lateral abdomen and lower back. Similarly, the frequency of perceived skin wetness was significantly greater on the lateral and lower back as opposed to the medial chest. Overall wetness perception was slightly higher under warm conditions. Significantly more unpleasant sensations were recorded when the lateral abdomen and lateral and lower back were stimulated. We conclude that humans present regional differences in skin wetness perception across the torso, with a pattern similar to the regional differences in thermosensitivity to cold. These findings indicate the presence of a heterogeneous distribution of cold-sensitive thermo-afferent information.

Multiple sclerosis (MS) is an autoimmune neurodegenerative disease characterized by demyelination of the central nervous system (CNS). The exact cause of MS is still unknown; yet its incidence and prevalence rates are growing worldwide, making MS a significant public health challenge. The heterogeneous distribution of demyelination within and between MS patients translates in a complex and varied array of autonomic, motor, sensory and cognitive symptoms. Yet a unique aspect of MS is the highly prevalent (60-80%) temperature sensitivity of its sufferers, where neurological symptoms are temporarily exacerbated by environmental-or exercise-induced increases (or decreases) in body temperature. MS temperature sensitivity is primarily driven by temperature-dependent slowing or blocking of neural conduction within the CNS due to changes in internal (core) temperature; yet changes in skin temperature could also contribute to symptom exacerbation (e.g. during sunlight and warm ambient exposure). The impact of temperature sensitivity, and particularly of increases in core temperature, on autonomic (e.g. thermoregulatory/cardiovascular function) and motor symptoms (e.g. fatigue) is well described. However, less attention has been given to how increases (and decreases) in core and skin temperature affect sensory and cognitive symptoms. Furthermore, it remains uncertain whether changes in skin temperature alone could also trigger worsening of symptoms. Here we review the impact of temperature sensitivity on MS sensory and cognitive function and discuss additional factors (e.g. changes in skin temperature) that potentially contribute to temperature-induced worsening of symptoms in the absence of alteration in core temperature.