Key pointsr Skin blood flow (SkBF) is an important avenue for heat loss; however, it is rapidly suppressed after exercise despite persistently high core and muscle temperatures.r This has been ascribed to altered active vasodilation; however, recent work has identified a role for adenosine receptors in the decrease in SkBF following passive heating.r In this study, we examined whether adenosine receptors are involved in the postexercise regulation of SkBF by infusion of 4 mM theophylline (a non-selective adenosine receptor antagonist) via microdialysis.r We show that adenosine receptors have a major role in modulating postexercise SkBF, as evidenced by a marked elevation during theophylline infusion compared to a control site.r These results help us to better understand the mechanisms underlying the postexercise reduction in SkBF and subsequently heat loss which is associated with heat-related illness and/or injury.Abstract The time-dependent contributions of active vasodilation (e.g. nitric oxide) and noradrenergic vasoconstriction to the postexercise suppression of cutaneous perfusion despite persistent hyperthermia remain unknown. Moreover, adenosine receptors have been shown to mediate the decrease in cutaneous perfusion following passive heating. We examined the time-dependent modulation of nitric oxide synthase, noradrenergic vasoconstriction and adenosine receptors on postexercise cutaneous perfusion. Eight males performed 15 min of high-intensity (85% V O 2 max ) cycling followed by 60 min of recovery in temperate ambient conditions (25°C). Four microdialysis probes were inserted into the forearm skin and continuously infused with: (1) lactated Ringer solution (Control); (2) 10 mM N G -nitro-L-arginine methyl ester (L-NAME; nitric oxide synthase inhibitor); (3) 10 mM bretylium tosylate (BT; inhibitor of noradrenergic vasoconstriction); or (4) 4 mM theophylline (THEO; adenosine receptor inhibitor). Cutaneous vascular conductance (CVC) was expressed as a percentage of maximum and was calculated as perfusion units (laser Doppler) divided by mean arterial pressure. End-exercise CVC was similar in Control, THEO and BT (P > 0.1), but CVC with L-NAME (39 ± 4%) was lower than Control (59 ± 4%, P < 0.01). At 20 min of recovery, Control CVC (22 ± 3%) returned to baseline levels (19 ± 2%, P = 0.11). Relative to Control, CVC was reduced by L-NAME for the first 10 min of recovery whereas CVC was increased with BT for the first 30 min of recovery (P < 0.03). In contrast, CVC with THEO was elevated throughout the 60 min recovery period (P ࣘ 0.01) compared to Control. We show that adenosine receptors appear to have a major role in postexercise cutaneous perfusion whereas nitric oxide synthase and noradrenergic vasoconstriction are involved only earlier during recovery.

New Findings r What is the central question of this study?Adenosine has been implicated in mediating both vasoconstriction and vasodilatation in a variety of tissues throughout the body. No study has yet examined its influence in cutaneous vasoconstriction elicited by whole-body cooling from normothermia or from hyperthermia. r What is the main finding and its importance?Through the use of the non-selective adenosine receptor antagonist, theophylline, a role for adenosine in the control of the cutaneous circulation when cooling from a state of hyperthermia is suggested.Adenosine has both vasodilatory and vasoconstrictive properties, yet its influence on cutaneous vascular conductance (CVC) during whole-body cooling remains unknown. The present study evaluated the influence of adenosine on reflex cutaneous vasoconstriction. Four microdialysis probes were inserted into the dorsal forearm skin of eight subjects and infused with the following solutions: (i) lactated Ringer solution (CON); (ii) 4 mm theophylline (Theo), a non-selective adenosine receptor antagonist; (iii) 10 mm l-NAME, an inhibitor of nitric oxide synthase; and (iv) combined 4 mm theophylline and 10 mm l-NAME (Theo + l-NAME). Subjects subsequently donned a water-perfusion garment. Following a thermoneutral baseline period, the suit was perfused with water at 10• C for 20 min (Cooling 1). The suit was then perfused with water at 49• C for 45 min (Heating), followed by a second cooling period of 20 min using 10 • C water (Cooling 2). Cutaneous blood flow (laser-Doppler) was measured over each microdialysis probe and used to calculate CVC as a percentage of the maximum determined by sodium nitroprusside infusion and local heating. Cutaneous vascular conductance was significantly elevated at the Theo site relative to CON following Cooling 1 (18 ± 6 versus 8 ± 2%; P = 0.01) and Cooling 2 (27 ± 11 versus 14 ± 5%; P = 0.022). Likewise, CVC at the Theo + l-NAME site remained greater compared with l-NAME after Cooling 1 (13 ± 4 versus 7 ± 3%; P = 0.030) and Cooling 2 (15 ± 3 versus 9 ± 2%; P = 0.009). The present findings demonstrate that non-selective antagonism of adenosine receptors attenuates the decrease in cutaneous vascular conductance during wholebody cooling from hyperthermia.

ä Patellar instability represents a common problem with an evolving understanding and multifactorial pathoetiology.Treatment plans should be based on the identification of contributing anatomical factors and tailored to each individual patient.ä Risks for recurrent instability are dependent on several patient-specific factors including patella alta, increased tibial tubercle-to-trochlear groove (TT-TG) distance, trochlear dysplasia, younger skeletal age, and ligamentous laxity.ä Cartilage or osteochondral lesions and/or fractures are commonly observed in first-time patellar dislocation, and magnetic resonance imaging (MRI) should be strongly considered. Advanced imaging modalities, such as computed tomography (CT) or MRI, should also be obtained preoperatively to identify predisposing factors and guide surgical treatment.ä Medial patellofemoral ligament (MPFL) reconstruction with anatomical femoral tunnel positioning is associated with lower recurrence rates compared with MPFL repair and has become a common and successful reconstructive surgical option in cases of instability.ä Lateral retinacular tightness can be addressed with lateral retinacular release or lengthening, but these procedures should not be performed in isolation.ä Tibial tubercle osteotomy is a powerful reconstructive tool in the setting of underlying skeletal risk factors for instability and can be of particular benefit in the presence of increased TT-TG distance (>20 mm), and/or in the setting of patella alta.ä The indications for trochleoplasty are still developing along with the clinical evidence, but trochleoplasty may be indicated in some cases of severe trochlear dysplasia. Several surgical techniques have indications in specific clinical scenarios and populations, and indications, risks, and benefits to each are progressing with our understanding.ä Combined femoral derotational osteotomy and MPFL reconstruction can be considered for patients with a femoral anteversion angle of >30°to improve patient outcomes and reduce recurrence rates.Patellar dislocations account for 3.3% of all knee injuries, with a reported rate of 42 per 100,000 persons per year 1,2 . These injuries most commonly occur in young girls and women, with >70% of first-time patellar dislocations taking place while participating in sport-related activity 1,3 . The majority of patellar dislocations occur in non-contact injuries when the knee is subject to valgus stress while extended during a planting or pivoting motion 3 . Common risk factors for recurrent lateral patellar instability include patella alta, increased tibial tubercleto-trochlear groove (TT-TG) distance, trochlear dysplasia, younger skeletal age, and ligamentous laxity 4,5 . The overall recurrence rate after a first-time patellar dislocation is approximately 30%, but can increase to >70% when multiple risk factors are present 4 . Predisposing clinical and anatomical variables should Disclosure: The Disclosure of Potential Conflicts of Interest forms are provided with the online version of the article (http://l...

Metaboreceptor activation during passive heating is known to influence cutaneous vascular conductance (CVC) and sweat rate (SR). However, whether metaboreceptors modulate the suppression of heat loss following dynamic exercise remains unclear. On separate days, before and after 15 min of high-intensity treadmill running in the heat (35°C), eight males underwent either 1) no isometric handgrip exercise (IHG) or ischemia (CON), 2) 1 min IHG (60% of maximum, IHG), 3) 1 min IHG followed by 2 min of ischemia (IHG+OCC), 4) 2 min of ischemia (OCC), or 5) 1 min IHG followed by 2 min of ischemia with application of lower body negative pressure (IHG+LBNP). SR (ventilated capsule), cutaneous blood flow (Laser-Doppler), and mean arterial pressure (Finometer) were measured continuously before and after dynamic exercise. Following dynamic exercise, CVC was reduced with IHG exercise (P < 0.05) and remained attenuated with post-IHG ischemia during IHG+OCC relative to CON (39 ± 2 vs. 47 ± 6%, P < 0.05). Furthermore, the reduction in CVC was exacerbated by application of LBNP during post-IHG ischemia (35 ± 3%, P < 0.05) relative to IHG+OCC. SR increased during IHG exercise (P < 0.05) and remained elevated during post-IHG ischemia relative to CON following dynamic exercise (0.94 ± 0.15 vs. 0.53 ± 0.09 mg·min(-1)·cm(-2), P < 0.05). In contrast, application of LBNP during post-IHG ischemia had no effect on SR (0.93 ± 0.09 mg·min(-1)·cm(-2), P > 0.05) relative to post-IHG ischemia during IHG+OCC. We show that CVC is reduced and that SR is increased by metaboreceptor activation following dynamic exercise. In addition, we show that the metaboreflex-induced loading of the baroreceptors can influence the CVC response, but not the sweating response.

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