An initial response to whole-body or local exposure of the extremities to cold is a strong vasoconstriction, leading to a rapid decrease in hand and foot temperature. This impairs tactile sensitivity, manual dexterity, and muscle contractile characteristics while increasing pain and sympathetic drive, decreasing gross motor function, occupational performance, and survival. A paradoxical and cyclical vasodilatation often occurs in the fingers, toes, and face, and this has been termed the hunting response or cold-induced vasodilatation (CIVD). Despite being described almost a century ago, the mechanisms of CIVD are still disputed; research in this area has remained largely descriptive in nature. Recent research into CIVD has brought increased standardization of methodology along with new knowledge about the impact of mediating factors such as hypoxia and physical fitness. Increasing mechanistic analysis of CIVD has also emerged along with improved modeling and prediction of CIVD responses. The present review will survey work conducted during this century on CIVD, its potential mechanisms and modeling, and also the broader context of manual function in cold conditions.

Hyperthermia is thought to increase limb blood flow through the activation of thermosensitive mechanisms within the limb vasculature, but the precise vascular locus in which hyperthermia modulates perfusion remains elusive. We tested the hypothesis that local temperature‐sensitive mechanisms alter limb hemodynamics by regulating microvascular blood flow. Temperature and oxygenation profiles and leg hemodynamics of the common (CFA), superficial (SFA) and profunda (PFA) femoral arteries, and popliteal artery (POA) of the experimental and control legs were measured in healthy participants during: (1) 3 h of whole leg heating (WLH) followed by 3 h of recovery (n = 9); (2) 1 h of upper leg heating (ULH) followed by 30 min of cooling and 1 h ULH bout (n = 8); and (3) 1 h of lower leg heating (LLH) (n = 8). WLH increased experimental leg temperature by 4.2 ± 1.2ºC and blood flow in CFA, SFA, PFA, and POA by ≥3‐fold, while the core temperature essentially remained stable. Upper and lower leg blood flow increased exponentially in response to leg temperature and then declined during recovery. ULH and LLH similarly increased the corresponding segmental leg temperature, blood flow, and tissue oxygenation without affecting these responses in the non‐heated leg segment, or perfusion pressure and conduit artery diameter across all vessels. Findings demonstrate that whole leg hyperthermia induces profound and sustained elevations in upper and lower limb blood flow and that segmental hyperthermia matches the regional thermal hyperemia without causing thermal or hemodynamic alterations in the non‐heated limb segment. These observations support the notion that heat‐activated thermosensitive mechanisms in microcirculation regulate limb tissue perfusion during hyperthermia.

Raynaud's phenomenon (RP) is a condition characterized by episodic, excessive vasoconstriction in the fingers and toes, triggered by cold or stress. This leads to a distinctive sequence of color changes in the digits. Pallor indicates reduced blood flow due to oxygen deprivation, while erythema appears as reperfusion. RP can be primary, with no identifiable underlying cause, or secondary, associated with other conditions. These conditions include autoimmune diseases, most commonly systemic sclerosis, vascular diseases; and neurological conditions. While the exact cause of RP remains unclear, genetic and hormonal (estrogen) factors are likely contributors. The pathogenesis of RP involves a complex interaction between the vascular wall, nerves, hormones, and humoral factors, disrupting the balance between vasoconstriction and vasodilation. In primary RP, the vascular abnormalities are primarily functional. However, in secondary RP, both functional and structural components occur in blood vessels. This explains why digital tissue damage frequently occurs in secondary RP but not primary RP. Diagnosis of RP is primarily clinical. Recent advancements in imaging techniques have aided in diagnosis and monitoring, but nail fold capillaroscopy remains the gold standard for distinguishing between primary and secondary RP. If there are signs of acute ischemic injury, vascular imaging, particularly preoperatively, is crucial to rule out other vaso-occlusive conditions. Management of RP focuses on alleviating symptoms and preventing tissue damage. Vasodilator medications are the first-line treatment when general measures like warmth and stress management are not sufficient. Dihydropyridine calcium channel blockers (CCBs), such as nifedipine, are commonly used for vasodilation. Phosphodiesterase-5 inhibitors and prostaglandin analogs are alternative options for patients who do not respond to CCBs or have ischemic tissue damage. Bosentan, an endothelin-1 receptor antagonist, has shown effectiveness in treating and preventing digital ulcers, especially in patients with multiple ulcers. For severe cases, botulinum toxin injections or sympathectomy surgery can be used to control RP symptoms. However, botulinum toxin injections require repeated administration, and sympathectomy's long-term effectiveness is uncertain. Fat grafting is a promising surgical therapy for promoting healing and preventing tissue injury.

Nearly a century ago, cold-induced vasodilation (CIVD) was first described as repeated episodes of warm blood flow to the fingers during cold-water immersion. Since then, hundreds of studies have examined this phenomenon, yet no comprehensive synthesis exists. To address this gap, we conducted a meta-analysis of studies in which the hand, or parts thereof, were immersed for 30 minutes in water below 20°C. A total of 80 studies met the inclusion criteria. Across studies, the weighted onset time of CIVD averaged 7.9 minutes [7.4-8.3], and the mean finger temperature averaged 10.0°C [9.5-10.6]. Onset time was weakly related to finger temperature during immersion (<i>r</i> = -0.21 to -0.27), supporting the theory that the onset of CIVD is triggered by low local tissue temperatures, while the magnitude is dependent on sympathetic activity. Onset time was longer for hand versus finger-only immersion, for individuals with a larger surface area, and for males compared to females. Onset time was shorter with higher ambient temperatures, in cold-indigenous populations, and with increasing age. To enrich the meta-analysis, we conducted a narrative literature review of the individual factors and previously proposed mechanisms of CIVD. Current evidence suggests that CIVD is mediated by 1) impaired transfer of noradrenaline from sympathetic nerves to the smooth muscle of the arterio-venous anastomoses or 2) nitric oxide release from these nerves, however, further research is needed to confirm these mechanisms. Future investigations should prioritize including more females and older adults, as these populations remain underrepresented in the literature.