Cold environmental temperatures increase sympathetic nerve activity and blood pressure, and increase the risk of acute cardiovascular events in aged individuals. The acute risk of cardiovascular events increases with aortic pulse wave velocity as well as elevated central and peripheral pulse pressures. The aim of this study was to examine the independent influence of aortic pulse wave velocity upon central and peripheral pressor responses to sympathetic activation via the cold pressor test (CPT). Twenty‐two healthy subjects (age: 18–73 years) completed a CPT with the left hand immersed in 2–4°C water for 3 min. During the CPT, central (from: 36 ± 7 to: 51 ± 12 mmHg) and peripheral pulse pressure increased (from: 54 ± 7 to: 66 ± 11; both P < 0.05). In all subjects the increase in central pulse pressure during the CPT was independently associated with baseline aortic pulse wave velocity (r 2 = 0.221, P = 0.027) but not age (P > 0.05). In a subset of subjects with higher arterial stiffness, the increase in peripheral pulse pressure during the CPT was independently associated with baseline aortic pulse wave velocity (r 2 = 0.415, P = 0.032) but not age (P > 0.05). These data indicate that central and peripheral pulse pressure responses during sympathetic activation are positively and independently associated with aortic pulse wave velocity through a wide age range. Decreasing aortic pulse wave velocity in aged individuals with elevated arterial stiffness may help reduce the incidence of acute cardiovascular events upon exposure to cold environmental temperatures.
Individuals who are exposed to an increased risk of experiencing a hemorrhagic insult, such as soldiers and firefighters, are often required to complete intermittent high intensity exercise in the presence of environmental heat stress. In normothermic conditions, increases in heart rate and reductions in vascular resistance can be greater following high intensity interval exercise relative to continuous steady state exercise. These hemodynamic alterations following high intensity interval exercise may reduce the capacity to withstand a hemorrhagic insult. We investigated whether high intensity interval exercise reduces tolerance to a simulated hemorrhagic challenge (lower body negative pressure; LBNP) relative to steady state exercise in heat stressed individuals. Eight healthy participants (Age: 27 ± 5 years; Ht: 179 ± 9 cm; Wt: 78.9 ± 18.7 kg) completed two trials (Steady state and Interval). Participants performed cycling exercise either by alternating between 10 and 88% (Interval) or continuously at 38% (Steady state) of the predetermined maximal aerobic power output whilst wearing a warm water perfused suit until core temperatures increased by 1.40 ± 0.21°C. Participants then underwent progressive LBNP (−20mmHg, −30mmHg, etc.) to pre syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Following exercise and prior to LBNP, mean skin temperatures were similarly elevated from baseline in both trials (from: 32.35 ± 0.42 to 37.95 ± 0.59°C, P < 0.05). Mean arterial pressure was not different between trials prior to LBNP (Interval: 79 ± 6 vs. Steady state: 77 ± 7 mmHg; P = 0.57) and were similarly reduced in both trials at pre syncope (to 63 ± 6 and 62 ± 6 mmHg respectively, both P < 0.05). CSI was lower in the interval trial relative to the steady state trial (280 ± 204 vs. 518 ± 285 mmHg*min, respectively; P = 0.024). In heat stressed individuals, tolerance to a simulated hemorrhagic challenge was reduced following high intensity interval exercise relative to steady state exercise. These findings have implications for individuals who exercise at intermittent high intensities in hot environments and are at increased risk of experiencing a hemorrhagic injury (e.g. soldiers, firefighters and miners). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
We investigated whether small reductions in skin temperature 60 s after the onset of a simulated hemorrhagic challenge would improve tolerance to lower body negative pressure (LBNP) after exercise heat stress. Eleven healthy subjects completed two trials (High and Reduced). Subjects cycled at ~55% maximal oxygen uptake wearing a warm water-perfused suit until core temperatures increased by ~1.2°C before lying supine and undergoing LBNP to presyncope. LBNP tolerance was quantified as cumulative stress index (CSI; product of each LBNP level multiplied by time; mmHg·min). Skin temperature was similarly elevated from baseline before LBNP and remained elevated 60 s after the onset of LBNP in both High (37.72 ± 0.52°C) and Reduced (37.95 ± 0.54°C) trials (both P < 0.0001). At 60%CSI skin temperature remained elevated in the High trial (37.51 ± 0.56°C) but was reduced to 34.97 ± 0.72°C by the water-perfused suit in the Reduced trial ( P < 0.0001 between trials). Cutaneous vascular conductance was not different between trials [High: 1.57 ± 0.43 vs. Reduced: 1.39 ± 0.38 arbitrary units (AU)/mmHg; P = 0.367] before LBNP but decreased to 0.67 ± 0.19 AU/mmHg at 60%CSI in the Reduced trial while remaining unchanged in the High trial ( P = 0.002 between trials). CSI was higher in the Reduced (695 ± 386 mmHg·min) relative to the High (441 ± 290 mmHg·min; P = 0.023) trial. Mean arterial pressure was not different between trials at presyncope (High: 62 ± 10 vs. Reduced: 62 ± 9 mmHg; P = 0.958). Small reductions in skin temperature after the onset of a simulated hemorrhagic challenge improve LBNP tolerance after exercise heat stress. This may have important implications regarding treatment of an exercise heat-stressed individual (e.g., soldier) who has experienced a hemorrhagic injury.
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