Journal of Applied Physiology Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 96: 1019-1025, 2004. First published October 31, 2003; doi:10.1152/japplphysiol.00928.2003
8750-7587/04 $5.00
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
96/3/1019    most recent
00928.2003v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Scremin, G.
Right arrow Articles by Kenney, W. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scremin, G.
Right arrow Articles by Kenney, W. L.

Aging and the skin blood flow response to the unloading of baroreceptors during heat and cold stress

Glaucio Scremin and W. Larry Kenney

Noll Physiological Research Center and Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania 16802-6900

Submitted 29 August 2003 ; accepted in final form 27 October 2003


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Control of skin blood flow (SkBF) is on the efferent arm of both thermoregulatory and nonthermoregulatory reflexes. To what extent aging may affect the SkBF response when these two reflex systems interact is unknown. To determine the response of aged skin to the unloading of baroreceptors in thermoneutral, cold stress, and heat stress conditions, sequential bouts of nonhypotensive lower body negative pressure (LBNP) were applied at -10, -20, and -30 mmHg in 14 young (18–25 yr) and 14 older (63–78 yr) men. SkBF was measured by laser-Doppler velocimetry (averaged over 2 forearm sites), and data are expressed as percentage of maximal cutaneous vascular conductance (%CVCmax). Total forearm blood flow was measured by venous occlusion plethysmography, and forearm vascular conductance (FVC) was calculated as the ratio of forearm blood flow to mean arterial pressure. In young men, all three intensities of LBNP in thermoneutrality decreased FVC significantly (P < 0.05), but FVC at -10 mmHg did not change in the older men. There were no significant LBNP effects on %CVCmax. Application of LBNP during cold stress did not significantly change %CVCmax or FVC in either age group. During heat stress, -10 to -30 mmHg of LBNP decreased FVC significantly (P < 0.05) in both age groups, but these decreases were attenuated in the older men (P < 0.05). %CVCmax decreased at -30 mmHg in the younger men only. These results suggest that older men have an attenuated skin vasoconstrictor response to the unloading of baroreceptors in heat stress conditions. Furthermore, the forearm vasoconstriction elicited by LBNP in older men reflects that of underlying tissue (i.e., muscle) rather than that of skin, whereas -30 mmHg LBNP also decreases SkBF in young hyperthermic men.

lower body negative pressure; cutaneous blood flow; hyperthermia; vasoconstriction

THE SKIN CIRCULATION IS CONTROLLED by thermoregulatory and nonthermoregulatory reflexes (8, 9, 14, 17, 21). Thermoregulatory reflexes, which include skin blood flow (SkBF) responses to heat and cold stresses, exert their effects on the skin circulation of hairy skin through two branches of the sympathetic nervous system: a noradrenergic vasoconstrictor branch and an active vasodilator branch. Nonthermoregulatory reflexes, which include SkBF responses to changes in arterial and central venous pressure (CVP) and exercise stresses, also operate through the two aforementioned branches of the sympathetic nervous system; however, these reflexes act through different efferent mechanisms under different thermal conditions (17). For instance, during hyperthermia, skin blood vessels vasoconstrict in response to a nonthermoregulatory stimulus (e.g., unloading of baroreceptors) via a withdrawal of active vasodilation (17). During hypo- and normothermia, skin blood vessels constrict via an increase in noradrenergic vasoconstriction.

Lower body negative pressure (LBNP) elicits a relative central hypovolemia and causes sustained vasoconstrictor responses in several vascular beds (3, 14, 27) via baroreflexes. In heat stress conditions, the skin vascular bed receives blood flow as high as 7–8 l/min (15) and, therefore, may become an important site for the control in response to changes in arterial and CVP when baroreceptors are unloaded. Furthermore, it has been hypothesized (9) that the baroreflexes predominate over thermoregulatory reflexes in the control of SkBF when baroreceptor unloading is superimposed on heat stress. However, those data are hard to reconcile with data (1, 20) showing an increased susceptibility to syncope in heat stress when a blood pressure (BP) challenge is applied.

Aging is associated with functional and structural changes in the ability of the cardiovascular system to adapt to physiological stress (6, 7, 10–12, 23, 28). SkBF responses to thermoregulatory stresses decrease with aging (18, 26). Furthermore, baroreflex control of the peripheral circulation in response to changes in arterial and/or central blood volume also decreases with aging (6, 7, 10, 23, 28). Because heat stress is associated with an increased incidence of syncope during a BP challenge (e.g., head-up tilt, LBNP) and aging is associated with an increased susceptibility to orthostatic hypotension and heat syncope (5, 30, 33), a better understanding of how aging affects the baroreflex control of the skin circulation is warranted (1, 20).

In a previous study (22), our laboratory showed that, during head-up tilt in heat-stress conditions, forearm vascular resistance increased significantly less in the older men than in the young men. However, specifically how aging affects the baroreflex control of the skin circulation when baroreceptor unloading is superimposed on heat and cold stresses remains unknown. We hypothesized that aged skin would vasoconstrict less than younger skin in response to baroreceptor unloading at low intensities of LBNP (-10 to -30 mmHg) during thermal neutral, cold-stress, and heat-stress conditions. To test this hypothesis, we used laser-Doppler flowmetry (LDF) and venous occlusion plethysmography techniques to assess the SkBF and total forearm blood flow (FBF) responses, respectively, in young and older men to sequential nonhypotensive bouts of LBNP while the skin was cooled or heated using water-perfused suits. Cold stress was induced by whole body skin cooling, and heat stress involved increasing both skin and core temperatures.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects. All procedures used in this investigation were approved in advance by the Biomedical Committee of the Institutional Review Board for the Protection of Human Subjects of the Office of Regulatory Compliance of The Pennsylvania State University. After approved informed consent procedures, 14 young (18–25 yr) and 14 older (63–78 yr) men agreed to participate in the study. All subjects were healthy, as determined by a physical examination. The physical was performed before subjects engaged in any experimental procedure and included blood analysis (CHEM-24), a physical examination by a physician, measurement of skin folds as an estimate of adiposity (2), a resting 12-lead ECG, and a maximal graded exercise test on a treadmill to determine maximal oxygen consumption (19). Exclusion criteria included body mass index >=30 or <=20 kg/m2, smoking, medications that could alter any cardiovascular or thermoregulatory variables, hypertension (resting systolic pressure >140 mmHg and/or diastolic pressure >90 mmHg), signs of cardiovascular and/or metabolic disease, or any abnormalities observed in the resting or exercise electrocardiogram. See Table 1 for subjects' physical characteristics.


View this table:
[in this window]
[in a new window]
  		Table 1. Subjects' physical characteristics

 

Measurements. Sublingual temperature (Tsl) was measured under the tongue as surrogate of core temperature by placement of a copper-constantan thermocouple. Each subject was asked to keep his mouth closed at all times to avoid any possible confounding effects of air movement over the thermocouple. A modified mouthpiece was used to secure the tip of the sublingual thermocouple in place. Mean skin temperature (sk) was calculated as the unweighted average of six copper-constantan thermocouples placed on the upper right arm, chest, back, abdomen, right thigh, and right calf. As both sk and Tsl have their effects on vasomotor and sudomotor responses to thermal stress, mean body temperature (b) was calculated during thermoneutral and cold stress as 0.66·Tsl + 0.33·sk (4) and during heat stress as 0.9·Tsl + 0.1·sk (13). During the peripheral vascoconstriction that accompanies cold stress, the contribution of the "shell" relative to the core increases and thus the greater weighting of sk during whole body cooling (4). Heart rate (HR) and mean arterial pressure (MAP) were monitored using a finger cuff placed on the right middle or index finger of each subject (Finapres blood pressure monitor, model 2300, Ohmeda, Madison, WI). Brachial auscultation was used to validate the plethysmographic MAP readings. LDF single-fiber probes (DRT4 laser-Doppler perfusion and temperature monitor, Moor Instruments) were used to measure SkBF (flux) at two sites in the right forearm. Cutaneous vascular conductance (CVC) was calculated as the ratio of flux to MAP. Total FBF was measured by venous occlusion plethysmography (model EC4 plethysmograph, Hokanson, Belleview, WA), and forearm vascular conductance (FVC) was calculated as the ratio of FBF to MAP. Urine osmolarity was measured by freezing-point depression (DigiMatic osmometer model 3D2, Advanced Instruments, Needham Heights, MA) to assess hydration status before testing. Values between 500 and 800 mosmol/kgH2O for urine osmolality were considered normal.

Experimental procedures. On the day before the scheduled experiment date, each subject was asked to consume eight glasses of a nonalcoholic beverage of choice to ensure proper hydration. Subjects were also instructed to refrain from consuming any alcohol or caffeine at least 12 h before their arrival to the laboratory. All experiments were conducted between 0800 and 1400. On arrival, a urine sample was collected to document hydration status, and nude weight was recorded. Subjects were instrumented with six skin thermocouples and ECG leads and dressed in a water-perfused suit (Diving Unlimited, San Diego, CA), which covered all body parts except the head, right and left forearms, hands, and feet. To prevent heat loss through sweat evaporation, subjects wore rubberized pants and a jacket over the water-perfused suit and had their feet covered by plastic bags. Subjects were then placed and sealed below their iliac crests into an acrylic LBNP box. Last, the subject right and left forearms were prepared for LDF and venous occlusion plethysmography, respectively.

A 15-min baseline period followed, during which water at 35°C was perfused through the suit. At the end of the 15-min baseline period, three consecutive bouts of LBNP at -10, -20, and -30 mmHg were applied with each bout lasting 3 min. These intensities of LBNP (-10, -20, and -30 mmHg) were chosen to primarily unload cardiopulmonary and possibly sinoaortic baroreceptors (8). For the next 20–30 min, sk was slowly lowered from 35 to 30°C. When the desired sk of 30°C stabilized, LBNP was again applied as described above. Hyperthermia was then induced by clamping sk between 38 and 40°C and allowing Tsl to rise by 0.3°C. When Tsl increased 0.3°C above baseline, sequential LBNP was again applied. This procedure was repeated when Tsl increased by 0.6°C and again at 0.9°C above baseline. Each subject was then returned to normothermia by perfusing water at 20°C into the water-perfused suit. Finally, local heaters surrounding the LDF probes were used to slowly increase local skin temperature (Tsk) from 34 to 42°C in ~10 min. Tsk was kept at 42°C for ~30 min to ensure maximal vasodilation of skin blood vessels in that area (32). Values for CVC at each of the local heated sites were expressed as percentages of maximum CVC (%CVCmax). After the end of the experimental protocol, subjects were removed from the LBNP box, and a final nude weight was recorded.

Data analysis. All data, except FBF and BP measured by brachial auscultation, were monitored continuously by a personal computer and averaged over 1-min periods by a data-acquisition system (LabView). Brachial auscultation was done in regular intervals of 10 min throughout the entire length of the experimental protocol. FBF was measured 2 min before a bout of LBNP and after the first minute at each of the three consecutive bouts of LBNP. FBF was measured four times per minute for 1 min and recorded as the average of those four measurements. %CVCmax data were given as the average of the two forearm sites.

Statistical analysis. An independent t-test was used to determine any statistically significant differences between age groups in the physical characteristics of the subjects, weight loss, and urine osmolality. A two-way (age x experimental stage) repeated-measures ANOVA was done on all dependent variables (HR, MAP, %CVCmax, FVC, sk, b, Tsl) to compare any age differences between the averaged data from 5 min before application of LBNP with the last minute of data for each of the 3-min bouts of LBNP in all three thermal conditions. All data are presented as means ± SE.


   RESULTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
In normothermia (sk = 34.6 ± 0.09 and 34.8 ± 0.29°C and Tsl = 36.8 ± 0.05 and 36.9 ± 0.10°C in young and older men, respectively), application of LBNP at -10 to -30 mmHg decreased FVC significantly (P < 0.05) from pre-LBNP values in the young men (Table 2 and Figs. 1 and 2). Application of LBNP did not significantly change %CVCmax. HR increased significantly (P < 0.05) from pre-LBNP values only at -30 mmHg of LBNP in the young men. In the older men, FVC and %CVCmax responses to application of LBNP were similar to those of the young men, with the exception of application of LBNP at -10 mmHg, which did not significantly change FVC (Table 2). Application of LBNP in normothermia did not increase HR significantly in the older men and did not change MAP significantly in either age group (Table 2, Fig. 1).


View this table:
[in this window]
[in a new window]
  		Table 2. Hemodynamic and thermoregulatory variables throughout different stages of experimental protocol

 


View larger version (31K):
[in this window]
[in a new window]
  		Fig. 1. Representative data from 1 young (A) and 1 older subject (B) from the entire experimental protocol. %CVCmax, percentage of maximal cutaneous vascular conductance; FVC, forearm vascular conductance; HR, heart rate; MAP, mean arterial pressure; sk, mean skin temperature; b, mean body temperature; Tsl, sublingual temperature; LBNP, lower body negative pressure; bpm, beats/min.

 


View larger version (19K):
[in this window]
[in a new window]
  		Fig. 2. Mean (±SE) changes ({Delta}) in %CVCmax ({Delta}%CVCmax; A) and FVC ({Delta}FVC; B) in older and young subjects during application of LBNP at -10, -20, and -30 mmHg in normo-, hypo-, and hyperthermia at {Delta}Tsl = 0.9°C. Data from {Delta}Tsl = 0.3 and 0.6°C are not shown. (For absolute data, see Table 2.)

 

Cold stress led to a significant drop (P < 0.05) in sk from 34.6 ± 0.09 to 30.0 ± 0.10°C and from 34.8 ± 0.29 to 30.0 ± 0.12°C in the young and older men, respectively. The drop in sk led to a significant reduction (P < 0.05) in FVC and %CVCmax and a significant increase (P < 0.05) in MAP in both age groups (Table 2). Exposure to LBNP during cold stress failed to elicit any further significant changes in HR, MAP, FVC, or %CVCmax in either age group.

Passive heat stress led to the desired increases (P < 0.05) in Tsl (0.3 ± 0.07, 0.6 ± 0.08, and 0.9 ± 0.07 and 0.3 ± 0.06, 0.6 ± 0.07, and 0.9 ± 0.11°C in young and older men, respectively). The rise in Tsl, in turn, led to significant increases (P < 0.05) in FVC, HR, and %CVCmax in both age groups. However, FVC was significantly lower (P < 0.05) in the older than in the younger men at each change in Tsl ({Delta}Tsl) (Table 2), as was HR (P < 0.05). Passive heat stress did not change MAP significantly in either age group (Table 2).

In the young men, application of LBNP at -30 mmHg significantly decreased (P < 0.05) %CVCmax and significantly increased HR at each {Delta}Tsl interval. Also in the young men, FVC decreased significantly (P < 0.05) at LBNP intensities of -10 to -30 mmHg when {Delta}Tsl = 0.3, 0.6, and 0.9°C. At {Delta}Tsl = 0.6°C, HR also increased significantly (P < 0.05) during LBNP at -20 mmHg. Application of LBNP failed to elicit any significant changes in MAP in the young men.

Exposure to LBNP during hyperthermia did not significantly change %CVCmax in the older men. At {Delta}Tsl = 0.3 and 0.9°C, application of LBNP from -10 to -30 mmHg led to a significant drop (P < 0.05) in FVC in the older men; however, this response was significantly smaller (P < 0.05) than that of the young men (Table 2, Fig. 1). At {Delta}Tsl = 0.6°C, application of LBNP elicited a significant drop (P < 0.05) in FVC only at -30 mmHg in older men (Table 2). Exposure to LBNP during hyperthermia did not significantly change HR or MAP in the older men (Table 2, Fig. 1).

Application of LBNP paradoxically and consistently increased %CVCmax at {Delta}Tsl = 0.3 and 0.6°C in 3 of the 14 older men. At 0.9°C {Delta}Tsl, this response was even more frequent, taking place in six older men (Fig. 1). In contrast, LBNP increased %CVCmax only in two young subjects at {Delta}Tsl = 0.9°C. When the results from the subjects who showed an increase in %CVCmax during LBNP are removed from the analysis, we still see an age-related attenuation in skin vasoconstrictor response to the unloading of baroreceptors during heat stress. For instance, during -30 mmHg of LBNP at {Delta}Tsl = 0.9°C, SkBF dropped by 16.5 ± 3.4% CVCmax (P < 0.05) in the young men vs. only 4.1 ± 0.2% CVCmax (P > 0.05) in the older men.


   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
In this study, we provide evidence that supports our hypothesis that aged skin vasoconstricts less than younger skin in response to unloading of baroreceptors when SkBF is elevated during heat stress. Support for this finding stems from the data showing that, at elevated core temperature and Tsk, the application of -30-mmHg LBNP elicited significant reductions in %CVCmax only in the young men. The significant drop in FVC observed during application of LBNP during heat stress in the older group suggests vasoconstriction of underlying tissue (i.e., muscle) rather than that of skin. This finding is further supported by the fact that, in the older men, the decrease in FVC observed during LBNP in hyperthermia was similar in magnitude to that observed in normothermia (Table 2). Because blood flow to the underlying musculature does not increase during whole body passive heating (15), greater reductions in FBF with application of LBNP in hyperthermia than in normothermia would be due to reductions in SkBF. Therefore, the greater reduction in FVC in the young men than in the older during LBNP in hyperthermia supports the idea that, in the young men, both skin and underlying tissue vasconstricted as opposed to only underlying tissue in the older men.

However, we failed to show an attenuated skin and muscle vasoconstrictor response to baroreceptor unloading in thermoneutral and cold stress conditions. Our results are in conflict with other reports in the literature suggesting an age-related difference in the FVC response to the unloading of baroreceptors in normothermia (6, 7). Cléroux et al. (6,7) have shown that, in thermoneutrality, a similar drop in CVP between young and old subjects led to a smaller reduction in FBF in the older than in the younger subjects. The discrepancy between our results and those of Cléroux et al. may be explained by the fact that, in our study, the baseline FBF and FVC were similar between the two age groups (Table 2), whereas, in the study reported by Cléroux et al., baseline FBF was significantly lower in the older than in the young subjects. The consequence of a lower baseline FBF is that any FBF changes triggered by the application of LBNP (expressed as absolute FBF changes) would result in a smaller FBF change. Other investigations have also observed no age-related differences in FBF or FVC responses to the unloading of baroreceptors in normothermia (28, 31).

Mechanistically, the reduced ability of baroreceptors to reflexly modulate SkBF during hyperthermia in older men may be due to any one or a combination of the following mechanisms. First, it is possible that the afferent branch of the baroreceptor reflex is impaired in aging (6, 34). Cléroux et al. (6, 7) have shown that cardiac compliance is reduced with aging, suggesting that the increase in cardiac stiffness may impair the ability of the cardiac volume receptors to sense central blood volume changes caused by LBNP. Second, it is possible that central nervous system integration of the baroreceptor reflex arc is affected (6, 34). Shi et al. (28) have reported that, during LBNP at -15 mmHg, no facilitatory interaction between cardiopulmonary and carotid baroreflexes was observed in the older subjects. They attributed this finding to the fact that aging affects the central nervous system integration of the afferent nerve traffic from the carotid and cardiopulmonary baroreceptors. Central nervous system cell degeneration, decreased cell affinity to neurotransmitters and/or receptor density, and altered release of neurotransmitters related to the aging process could all account for the impairment in the central integration of the low-pressure baroreceptor reflex (6). Last, because data analysis was performed on the differences between pre-LBNP values with the last minute of LBNP during each thermal condition, a lower baseline value would result in less change in the variable of interest in response to the unloading of baroreceptors. Because the pre-LBNP values for %CVCmax and FVC at each {Delta}Tsl are lower in the older men than in the young men, it is possible that this could explain the lower SkBF response to LBNP in the older men. However, two lines of evidence argue against this possibility. First, LBNP decreased %CVCmax significantly at each {Delta}Tsl only in the young men (Table 2, Fig. 2). Second, LBNP changed FVC significantly less at each {Delta}Tsl in the older men, not only when expressed as absolute FVC but also when expressed as either change in FVC or percent change in FVC. For example, at {Delta}Tsl = 0.9°C, FVC significantly decreased from 23.3 ± 4.01 to 13.5 ± 3.40 ml·100 ml-1·min-1·100 mmHg-1, a 42% drop in FVC (P < 0.05), and from 10 ± 1.68 to 8.1 ± 1.48 ml·100 ml-1·min-1·100 mmHg-1, a 19% drop in FVC (P < 0.05), during LBNP at -30 mmHg in the young and older men, respectively.

Although it is well established that SkBF decreases with application of LBNP during heat stress (8, 17), other explanations have also been proposed to explain the reflex-mediated skin vasoconstriction response during LBNP. Neurophysiological studies have demonstrated skin sympathetic nerve activity to be unaffected by maneuvers affecting baroreflexes (35). For instance, Vissing et al. (35) reported that application of LBNP from -5 to -15 mmHg yielded no significant changes in skin sympathetic nerve activity when sk increased from 34.1 to 35°C. Application of LBNP at -15 mmHg did reduce SkBF, but this reduction was also observed during application of sham LBNP with a similar reduction in sk. Vissing et al. attributed this apparent conflict to the fact that the reflex-mediated skin vasoconstriction during application of LBNP is due to a thermal rather than a baroreceptor reflex. The thermal reflex is triggered from the drop in sk that occurs during LBNP. In the present study, application of LBNP during heat stress led to reductions in sk by as much as 2.0°C (Table 2). Although we cannot completely rule out the idea that thermal reflexes may have played a part in the reduction of SkBF to the application of LBNP, we believe that this was not the case in this study for three reasons. First, LBNP at -10 and -20 mmHg led to a reduction in sk without any significant changes in SkBF. Second, application of LBNP at -30 mmHg at {Delta}Tsl = 0.9°C in the older group led to a reduction in sk of 2.0°C, on average, which was not associated with a reduction in SkBF (Table 2). Third, reflex thermoregulatory control of SkBF during hyperthermia is predominantly governed by core rather than sk (21, 24). Tsl increased and b stayed constant. Therefore, small reductions in sk that may occur during application of LBNP are not sufficient to account for the reflex-mediated skin vasoconstriction in response to LBNP.

A surprising finding of this study was that, in 3 of the 14 older men, application of LBNP actually increased %CVCmax consistently at each {Delta}Tsl (at {Delta}Tsl = 0.9°C, %CVCmax rose in six older men and in two young subjects). Similar anomalous findings have been previously reported in young subjects. Peters et al. (25) reported that nonhypotensive LBNP failed to reduce SkBF in hyperthermia in young men and women. He attributed this response to the marked heterogeneity in the SkBF response to LBNP demonstrated in investigations using laser-Doppler scanning techniques. In addition, Johnson et al. (16) have reported that one limitation of LDF techniques is that the area under observation is too small to produce uniform responses and that venous occlusion plethysmography may better represent the blood flow responses to LBNP. In the present study, we tried to overcome this limitation by averaging results from two adjacent LDF skin forearm sites as well as by using venous occlusion plethysmography on the contralateral arm. In a previous study conducted in our laboratory (26), we used laser-Doppler imaging to examine reflex vasodilation in response to passive heating in young and older subjects. In this investigation, the older men responded to passive heating with a smaller vasodilated area of skin than that of the young men when esophageal temperature increased from baseline by 0.2–0.6°C. Therefore, it is possible that the LDF skin forearm sites unresponsive to LBNP were the sites that corresponded to nonvasodilated areas of skin. However, this is mere speculation, because no studies on the spatial distribution and heterogeneity of reflex-mediated skin noradrenergic skin vasoconstriction during LBNP in older people have been conducted using laser-Doppler scanning techniques.

Impairment of baroreceptor reflexes with aging has been reported in the control of HR and peripheral circulation (6, 7, 29, 30). Our results lend further credence to this hypothesis by providing evidence that aging is also associated with a decreased ability of low-pressure baroreceptors to reflexly modulate SkBF.

In summary, aged skin vasoconstricts less than younger skin in response to baroreceptor unloading during heat stress. The inability of baroreceptors to reflexly modulate SkBF when unloaded may play a role in the decreased ability of the elderly to properly regulate central blood volume and maintain BP during a BP challenge, especially in heat stress environments.

Limitations. An assumption of this study was that application of LBNP decreased CVP equally in both age groups. However, Minson et al. (22) have reported that "CVP fell 1.7 mmHg more in the young men than in the older men during the assumption of the upright posture, suggesting less stimulus to the cardiopulmonary baroreceptors in the older men."

If a similar differential response occurred in the present study, it is possible that the drop in CVP during heat stress caused by LBNP in the older group was not sufficient to cause a significant decrease in CVC. Although the stresses were not exactly the same (i.e., upright tilt vs. LBNP), we cannot rule out the idea that an unequal drop in CVP between the two age groups could have occurred, because no direct measurement of CVP was used in the present study.

Air leakage associated with LBNP decreased sk during LBNP. Although we cannot totally disregard the possibility that skin cooling-associated LBNP may have contributed to some degree in the reduction in CVP in some subjects, as reported by Johnson et al. (14), this was not the major drive for skin vasoconstriction during LBNP in the majority of the subjects studied. In addition, the drop in sk was not significantly different between young and older men. Furthermore, because Tsl slightly increased during LBNP as sk slightly decreased b remained unchanged. Therefore, the weighted averages of the two thermoregulatory variables (sk, Tsl) responsible for the reflex thermoregulatory control of SkBF in hyperthermia added no further thermal input signals that may have confounded the reflex-mediated skin vasoconstriction response during LBNP.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
The authors thank the volunteers who participated in the present study and acknowledge the technical assistance of Jane M. Pierzga, Caitlin Thompson, Rose Moffitt, Lindsay Baker, and Thayne Munce, and the medical assistance of the General Clinical Research Center.

GRANTS

This study was funded by the National Institute on Aging Grant RO1 AG-07004.


   FOOTNOTES
 

Address for reprint requests and other correspondence: G. Scremin, 119 Noll Physiological Research Center, The Pennsylvania State Univ., Univ. Park, PA 16802-6900 (E-mail: gxs229{at}psu.edu).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Allan JR and Crossley RJ. Effect of controlled elevation of body temperature on human tolerance to +Gz acceleration. J Appl Physiol 33: 418-420, 1972.[Free Full Text]
  2. Allen TH, Peng MT, Chen KP, Huang TF, Chang C, and Fang HS. Prediction of blood volume and adiposity in man from body weight and cube of height. Metabolism 5: 328-345, 1956.[Web of Science][Medline]
  3. Beiser GD, Zelis R, Epstein SE, Mason DT, and Braunwald E. The role of skin and muscle resistance vessels in reflexes mediated by the baroreceptor system. J Clin Invest 49: 225-231, 1970.[Medline]
  4. Burton AC. Human calorimetry. II. The average temperature of the tissues of the body. J Nutr 9: 261-268, 1935.[Abstract/Free Full Text]
  5. Caruso C and Posey V. Heat waves threaten the old. Geriatr Nurs 6: 209-212, 1985.[Medline]
  6. Cléroux J, Giannattasio C, Bolla G, Cuspidi C, Grassi G, Mazzola C, Sampieri L, Seravalle G, Valsecchi M, and Mancia G. Decreased cardiopulmonary reflexes with aging in normotensive humans. Am J Physiol Heart Circ Physiol 257: H961-H968, 1989.[Abstract/Free Full Text]
  7. Cléroux J, Giannattasio C, Grassi G, Seravalle G, Sampieri L, Cuspidi C, Bolla G, Valsecchi M, Mazzola C, and Mancia G. Effects of ageing on the cardiopulmonary receptor reflex in normotensive humans. J Hypertens Suppl 6: S141-S144, 1988.[Medline]
  8. Crandall CG, Johnson JM, Kosiba WA, and Kellogg DL Jr. Baroreceptor control of the cutaneous active vasodilator system. J Appl Physiol 81: 2192-2198, 1996.[Abstract/Free Full Text]
  9. Crossley RJ, Greenfield AD, Plassaras GC, and Stephens D. The interrelation of thermoregulatory and baroreceptor reflexes in the control of the blood vessels in the human forearm. J Physiol 183: 628-636, 1966.[Abstract/Free Full Text]
  10. Giannattasio C, Ferrari AU, and Mancia G. Alterations in neural cardiovascular control mechanisms with ageing. J Hypertens Suppl 12: S13-S17, 1994.[CrossRef][Medline]
  11. Hajduczok G, Chapleau MW, and Abboud FM. Increase in sympathetic activity with age. II. Role of impairment of cardiopulmonary baroreflexes. Am J Physiol Heart Circ Physiol 260: H1121-H1127, 1991.[Abstract/Free Full Text]
  12. Hajduczok G, Chapleau MW, and Abboud FM. Rapid adaptation of central pathways explains the suppressed baroreflex with aging. Neurobiol Aging 12: 601-604, 1991.[CrossRef][Web of Science][Medline]
  13. Hammel HT. Regulation of internal body temperature. Annu Rev Physiol 30: 641-710, 1968.[CrossRef][Web of Science][Medline]
  14. Johnson JM, Niederberger M, Rowell LB, Eisman MM, and Brengelmann GL. Competition between cutaneous vasodilator and vasoconstrictor reflexes in man. J Appl Physiol 35: 798-803, 1973.[Free Full Text]
  15. Johnson JM and Proppe DW. Cardiovascular adjustments to heat stress. In: Handbook of Physiology. Environmental Physiology. Bethesda, MD: Am. Physiol. Soc., 1996, sect. 4, vol. I, chapt. 11, p. 215-243.
  16. Johnson JM, Taylor WF, Shepherd AP, and Park MK. Laser-Doppler measurement of skin blood flow: comparison with plethysmography. J Appl Physiol 56: 798-803, 1984.[Abstract/Free Full Text]
  17. Kellogg DL Jr, Johnson JM, and Kosiba WA. Baroreflex control of the cutaneous active vasodilator system in humans. Circ Res 66: 1420-1426, 1990.[Abstract/Free Full Text]
  18. Kenney WL, Morgan AL, Farquhar WB, Brooks EM, Pierzga JM, and Derr JA. Decreased active vasodilator sensitivity in aged skin. Am J Physiol Heart Circ Physiol 272: H1609-H1614, 1997.[Abstract/Free Full Text]
  19. Kohl HW, Gibbons LW, Gordon NF, and Blair SN. An empirical evaluation of the ACSM guidelines for exercise testing. Med Sci Sports Exerc 22: 533-539, 1990.
  20. Lind AR, Leithead CS, and McNicol GW. Cardiovascular changes during syncope induced by tilting men in the heat. J Appl Physiol 25: 268-276, 1968.[Free Full Text]
  21. Mack G, Nishiyasu T, and Shi X. Baroreceptor modulation of cutaneous vasodilator and sudomotor responses to thermal stress in humans. J Physiol 483: 537-547, 1995.[Abstract/Free Full Text]
  22. Minson CT, Wladkowski SL, Pawelczyk JA, and Kenney WL. Age, splanchnic vasoconstriction, and heat stress during tilting. Am J Physiol Regul Integr Comp Physiol 276: R203-R212, 1999.[Abstract/Free Full Text]
  23. Monahan KD, Dinenno FA, Seals DR, Clevenger CM, Desouza CA, and Tanaka H. Age-associated changes in cardiovagal baroreflex sensitivity are related to central arterial compliance. Am J Physiol Heart Circ Physiol 281: H284-H289, 2001.[Abstract/Free Full Text]
  24. Pergola PE, Kellogg DL Jr, Johnson JM, and Kosiba WA. Reflex control of active cutaneous vasodilation by skin temperature in humans. Am J Physiol Heart Circ Physiol 266: H1979-H1984, 1994.[Abstract/Free Full Text]
  25. Peters JK, Nishiyasu T, and Mack GW. Reflex control of the cutaneous circulation during passive body core heating in humans. J Appl Physiol 88: 1756-1764, 2000.[Abstract/Free Full Text]
  26. Pierzga JM, Frymoyer A, and Kenney WL. Delayed distribution of active vasodilation and altered vascular conductance in aged skin. J Appl Physiol 94: 1045-1053, 2003.[Abstract/Free Full Text]
  27. Rowell LB, Detry JM, Blackmon JR, and Wyss C. Importance of the splanchnic vascular bed in human blood pressure regulation. J Appl Physiol 32: 213-220, 1972.[Free Full Text]
  28. Shi X, Gallagher KM, Welch-O'Connor RM, and Foresman BH. Arterial and cardiopulmonary baroreflexes in 60- to 69- vs. 18- to 36-yr-old humans. J Appl Physiol 80: 1903-1910, 1996.[Abstract/Free Full Text]
  29. Smith JJ, Hughes CV, Ptacin MJ, Barney JA, Tristani FE, and Ebert TJ. The effect of age on hemodynamic response to graded postural stress in normal men. J Gerontol 42: 406-411, 1987.
  30. Smith JJ and Porth CJ. Posture and the circulation: the age effect. Exp Gerontol 26: 141-162, 1991.[CrossRef][Web of Science][Medline]
  31. Taylor JA, Hand GA, Johnson DG, and Seals DR. Sympathoadrenalcirculatory regulation of arterial pressure during orthostatic stress in young and older men. Am J Physiol Regul Integr Comp Physiol 263: R1147-R1155, 1992.[Abstract/Free Full Text]
  32. Taylor WF, Johnson JM, O'Leary D, and Park MK. Effect of high local temperature on reflex cutaneous vasodilation. J Appl Physiol 57: 191-196, 1984.[Abstract/Free Full Text]
  33. Tsutsui Y, Sagawa S, Yamauchi K, Endo Y, Yamazaki F, and Shiraki K. Cardiovascular responses to lower body negative pressure in the elderly: role of reduced leg compliance. Gerontology 48: 133-139, 2002.[CrossRef][Web of Science][Medline]
  34. Van Merode T, Hick PJ, Hoeks AP, Rahn KH, and Reneman RS. Carotid artery wall properties in normotensive and borderline hypertensive subjects of various ages. Ultrasound Med Biol 14: 563-569, 1988.[CrossRef][Web of Science][Medline]
  35. Vissing SF, Scherrer U, and Victor RG. Increase of sympathetic discharge to skeletal muscle but not to skin during mild lower body negative pressure in humans. J Physiol 481: 233-241, 1994.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Eur Heart JHome page
D. J. Green, A. J. Maiorana, J. H. J. Siong, V. Burke, M. Erickson, C. T. Minson, W. Bilsborough, and G. O'Driscoll
Impaired skin blood flow response to environmental heating in chronic heart failure
Eur. Heart J., February 1, 2006; 27(3): 338 - 343.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
T. Ito, T. Itoh, T. Hayano, K. Yamauchi, and A. Takamata
Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2005; 289(2): R432 - R440.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
96/3/1019    most recent
00928.2003v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Scremin, G.
Right arrow Articles by Kenney, W. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scremin, G.
Right arrow Articles by Kenney, W. L.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.