Regional thermal hyperemia in the human leg: Evidence of the importance of thermosensitive mechanisms in the control of the peripheral circulation

Abstract

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.

Elevate to Alleviate – Evidence Based Vascular Nursing Study

“…Environmental conditions and the clothing that the patients wore during the protocols were evaluated in order to not induce hyperthermia, as it is thought to increase limb blood flow through the activation of thermosensitive mechanisms within the limb vasculature. 10 In particular, environmental temperature of hospital rooms was set at 20°C, and patients wore light cotton pajamas during hospital stay.…”

Physiological Function during Exercise and Environmental Stress in Humans—An Integrative View of Body Systems and Homeostasis

“…Even at these low absolute exercise intensities, however, the elevation in limb blood low is lower than would be expected given the magnitude of hyperaemia observed when heat stress and exercise are studied in isolation. As an example, while severe passive hyperthermia results in elevations in leg blood flow of ~1 L•min −1 [158,[245][246][247][248][249], the superimposition of the same thermal stimulus onto single-leg knee-extensor exercise in the same individuals results in increases of only ~0.5 L•min −1 -an attenuation of 50% of the response seen at rest [158,245,250]. When a larger muscle mass is engaged (e.g., cycling), the hyperthermia-induced augmentation in exercising limb blood flow disappears altogether [35,155,156,240,241] (Figure 5).…”

“…This construct can be used to explain the differential limb hemodynamic responses to dehydration and/or hyperthermia under resting and different exercising conditions (i.e., an increase at rest and small muscle mass exercise vs. a decline during whole-body exercise). In conditions of small muscle mass exercise with dehydration and hyperthermia, it is possible that thermal, fluid and oxygen sensing mechanisms activated by (i) increases in local tissue temperature similar to that observed during local and whole-body passive heating [158,[245][246][247]276,277] (ii) changes in red blood cell deformability and cell volume [278,279] and (iii) elevations in arterial oxygen content concomitant to the dehydration-mediated haemoconcentration [19,168] lead to augmented vasodilator activity in the face of a very low systemic sympathetic activity (e.g., circulating noradrenaline 1.2 to 1.9 nmol•L −1 ). This contrasts with the responses to whole-body prolonged exercise where a similar fall in mean arterial pressure (~8%) is accompanied by a much larger increase in circulating catecholamines (~18 nmol•L −1 ).…”

“…These temporally linked restrictions in skeletal muscle blood flow and Q give rise to the alternative possibility that regulatory events in the peripheral microcirculation play a crucial role in the output of the heart [44,125,[284][285][286]. Several empirical observations support this hypothesis: (i) artificial pacing of heart rate at rest and during exercise up to maximal aerobic capacity leaves Q and exercising limb blood flow unaltered, suggesting that tachycardia independent of peripheral circulatory events is inconsequential to activity of the heart [125,204,209,[287][288][289]; (ii) incremental exercise in a man with an implanted cardiac pacemaker was associated with substantial elevations in end-diastolic volume, stroke volume, ejection fraction, pulmonary wedge pressure and Q, despite constant heart rate at 100 beats•min −1 , whilst systemic blood flow rose in relation to VO 2 up to 2 L•min −1 [3] (p. 181); (iii) increases in conduit artery blood flow during single leg knee-extensor exercise and passive segmental leg heating are accompanied by selective increases in downstream blood flow [246,290]. This is similar to what happens during intense whole-body exercise across the head, with brain blood flow declining when extracranial perfusion increases [35,36]; (iv) blood flow in non-exercising organs and tissues (including in the arm and brain) are relatively unchanged during incremental and constant power exercise, when large increases in Q occur (Figures 1 and 5).…”

“…This is similar to what happens during intense whole-body exercise across the head, with brain blood flow declining when extracranial perfusion increases [35,36]; (iv) blood flow in non-exercising organs and tissues (including in the arm and brain) are relatively unchanged during incremental and constant power exercise, when large increases in Q occur (Figures 1 and 5). This evidence ((iii) and (iv)) suggests that the heart does not determine local blood flow distribution; (v) in ex vivo pressurised preparations of small muscle resistance arteries, pharmacologically-induced alterations in vascular tone evokes substantial changes in blood flow in the absence of a heart [261,291,292]; (vi) infusion of vasodilator or constrictor substances into the femoral artery at rest and during submaximal and maximal aerobic exercise leads to proportional augmentation or blunting in leg blood flow and Q, respectively, but no changes in brain or contralateral limb blood flow [65,116,287,[293][294][295]; (vii) infusion of ATP into the femoral vein (at a rate that causes substantial leg and systemic hyperaemia when infused in the femoral artery), does not change either leg blood flow or Q [65]; (viii) limb blood flow per unit of power is remarkedly similar during different exercise modalities despite very different systemic blood flows [64,125]; (ix) likewise, in the face of large differences in Q, limb blood flow is highly comparable during passive whole-body heat stress and isolated whole-limb and limb segment heating [158,246,247,277]; (x) the reductions in peripheral blood flow associated with exercise-induced dehydration parallel the diminished venous flow to the heart, suggesting that the lowering of Q occurs only when there is an interaction among reduced peripheral blood flow, dehydration-induced hypovolemia and tachycardia [6,44,210]; and (xi) exercising limb blood flow and Q per unit of power are restricted during exercise intensity domains above VO 2max , yet the overall circulatory response is closely tied to contracting muscle aerobic metabolism [259,296]. These observations underscore the need for new integrative models that better explain the regulation of the heart and circulation across the whole range of exercise intensities and environmental stresses that hu...…”