| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
University of Ottawa, Faculty of Health Sciences, School of Human Kinetics, Human Performance and Environmental Medicine Research Laboratory, Ottawa, Ontario, Canada K1N 6N5
Submitted 30 October 2002 ; accepted in final form 26 February 2003
 |
ABSTRACT |
|---|
 TOP ABSTRACT METHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
|---|
4.0°C/h) until cutaneous vasodilation and sweating occurred. Forearm skin blood flow and arterial blood pressure were measured noninvasively and were used to calculate cutaneous vascular conductance during whole body heating. Sweat rate response was estimated from a 5.0-cm2 ventilated capsule placed on the upper back. Postexercise ThVD and ThSW were both significantly elevated (0.27 ± 0.04°C and 0.25 ± 0.04°C, respectively) compared with the no-exercise trial without LBPP (P < 0.05). However, the postexercise increases in both ThVD and ThSW were reversed with the application of LBPP. Our results support the hypothesis that the postexercise warm thermal responses of cutaneous vasodilation and sweating are attenuated by baroreceptor modulation via lower body venous pooling. blood pressure; skin blood flow; venous pooling; thermoregulation; lower body positive pressure
Dynamic exercise is known to result in a postexercise hypotension in the upright posture (4, 17, 30). Research indicates that venous pooling and a subsequent reduction in stroke volume contributes to the postexercise hypotension in an upright seated position (30). In parallel, it has been shown that acute reductions in central venous pressure delay or decrease the rise in SkBF (21, 19) and sweating during heat stress (3, 21, 19) and possibly result in a sustained postexercise elevation in core temperature (13). Thus it is reasonable to postulate that the postexercise increase in the threshold for cutaneous vasodilation and sweating is a consequence of baroreceptor unloading via lower body venous blood pooling.
In a recent study, our laboratory demonstrated that head-down tilt significantly influences cutaneous vasomotor control during exercise recovery (12). Specifically, the modification of postexercise venous pooling by head-down tilt results in an attenuation of the resting postexercise elevation in the esophageal threshold temperature for cutaneous vasodilation. However, because sweating response was not evaluated, the influence of baroreflex control on postexercise sweating remains unclear. Furthermore, we felt that the limitations in the tilt model warranted further investigation. That is, head-down tilt may have activated postural reflexes (i.e., vestibular, etc.) that could have distorted the primary baroreceptor response (15). Second, because of the fact that mild head-down tilt seems not to modify arterial blood pressure, it is thought that under such conditions only cardiopulmonary baroreceptors are loaded (31). The typical hypotension associated with postexercise venous pooling would tend to unload both cardiopulmonary and sinoaortic baroreceptors (31).
There is limited information regarding the hemodynamic effects of lower body positive pressure (LBPP) in the upright posture. However, it is known that the application of +50 mmHg LBPP in the upright position results in an increase in mean arterial pressure (MAP) and a concomitant increase in cardiac output. The increased cardiac output is primarily determined by a dramatic increase in stroke volume as heart rate (HR) has been shown to decrease (28). Furthermore, the increase in stroke volume during LBPP application is thought to be a result of an increase in central blood volume. As such, the application of LBPP postexercise in the upright position would therefore tend to reverse the postexercise venous pooling observed during postexercise recovery under normal resting conditions. Thus we hypothesized that the application of LBPP (+50 mmHg) postexercise in the upright position would result in a decrease in the esophageal temperature threshold for cutaneous vasodilation and sweating. The upright model was best suited because 1) postexercise hypotension is most commonly reported after a bout of upright dynamic exercise and 2) the postexercise increase in the thresholds for cutaneous vasodilation and sweating were previously measured in an upright position.
|
METHODS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
|---|
Six healthy and physically active men volunteered for this study, which was approved by the Ethics Committee of the University of Ottawa, and written consent was obtained from the participants. Five to 7 days before the experiments, percent body fat was measured by hydrostatic weighing, and peak oxygen consumption (
O2 peak) was measured during a progressive cycle ergometer protocol. The O2 peak data were used to select the submaximal workload for the experimental exercise phase of the study. Subjects were 25 ± 5 yr old and 1.8 ± 0.6 m tall, weighed 82.1 ± 7.5 kg, and had a percentage body fat of 14.9 ± 6.2% (means ± SD). Their mean peak aerobic capacity was 43.7 ± 5.2 ml · kg-1 · min-1.
Instrumentation
Central body temperature [esophageal temperature (Tes)] was monitored continuously by using a pediatric Tes probe (Mon-a-therm, Mallinckrodt Medical, St. Louis, MO) inserted through the nares to a depth one-fourth of the standing height of the subject placing the tip of the thermocouple at the level of the left atrium. Skin temperature was measured at eight sites by use of heat flow sensors (Concept Engineering, Old Saybrook, CT, model FR-025-TH44018-6), and the area-weighted mean skin temperature (
sk) was calculated by assigning the following regional percentages: head 6%, upper arm 9%, forearm 6%, finger 2%, chest 19%, upper back 19%, anterior thigh 21%, and posterior calf 18%.
Oxygen consumption (O2) was calculated by using an automated metabolic analyzer (MedGraphics, St. Paul, MN). MAP was recorded noninvasively from the electrical integration of the pulsatile blood pressure signal obtained from the middle digit of the left hand (Ohmeda, Finapres 2300) referenced at heart level (at the third intercostal space). The Finapres system is based on the volume-clamp method (dynamic unloaded arterial wall principle) introduced by Penaz. These blood pressure data were recorded (with the Finapres servo control on) and stored continuously at 5-s intervals. MAP was also verified throughout the experiment by standard auscultation method of the brachial artery by using a sphygmomanometer and stethoscope. Heart rate was monitored by using a Polar coded transmitter and recorded continuously and stored with a Polar Advantage interface and Polar Precision Performance software (Polar Electro Oy, Kempele, Finland).
SkBF was measured by laser-Doppler velocimetry (Peri-Flux System 5000, main control unit; PF5010 LDPM, function unit; Perimed, Stockholm, Sweden) from the left midanterior forearm. The laser-Doppler flow probes (PR401 Angled Probe, Perimed) were taped to cleaned skin, in an area that did not appear to be superficially vascular and where consistent readings were noted. Cutaneous vascular conductance (CVC) was calculated throughout the experimental protocol by using the ratio of 30-s averages of laser-Doppler flux and MAP.
Sweat rate was estimated from a 5.0-cm2 ventilated capsule placed on the upper back. Anhydrous compressed air was passed through the capsule over the skin surface at a rate of 1 l/min. Water content of the effluent air was measured at known barometric pressure by using the readings from an Omega HX93 humidity and temperature sensor (Omega Engineering, Stamford, CT). Sweat rate was calculated from the product of the difference in water content between effluent and influent air, and the flow rate. This value was normalized for the skin surface area under the capsule (expressed in mg · min-1 · cm-2).
Body core and skin temperatures, sweat rate, and SkBF were recorded (Hewlett-Packard, data-acquisition module, model 3497A), stored (Hewlett-Packard, model PC-312, 9000) and displayed in real time continuously at 10-s intervals.
The LBPP condition was created by inserting the subject up to the hips in a pressure chamber, sealed with a neoprene skirt at the level of the iliac crest. The chamber was custom designed within our laboratory to permit the application of positive pressure to the lower body segments while the subject is in an upright position.
Experimental Protocol
Each subject performed a total of four experimental trials carried out in random order. Experiments were conducted after a 36-h period without physical activity, and subjects were instructed to avoid excessive perambulation or other stresses in the period between awakening and experimentation (i.e., avoid exposure to hot or cold temperatures and minimize physical activity during transit from home to the laboratory). Furthermore, they were asked to fast at least 4 h before experimentation, although water ingestion was maintained during this time.
On arrival to the laboratory, subjects clothed in shorts and athletic shoes were fitted with the appropriate instruments and donned a liquid-conditioned suit (Delta Temax, Pembroke, ON, Canada) covering the torso, arms, and head. The experiments commenced at precisely 0900 after a minimum acclimatization period of 1 h within an environmentally controlled room at an ambient temperature of 25°C. Each of the four experimental trials (carried out in random order) began with a 15-min upright rest period during which baseline measurements were taken (baseline resting). The baseline resting period was carried out within the pressure chamber to ensure maintenance of posture across and within subjects for all measures. Subjects were then either moved to an exercise ergometer (exercise condition) or remained resting in the pressure chamber (no-exercise) for 15 min. For the exercise treatment, the subjects performed 15 min of upright cycling at 65% of their predetermined O2 peak.
Immediately after these respective treatments, subjects were sealed at the level of the iliac crest within the LBPP chamber. The average time to effect this transition was 6.5 ± 1.9 min. Subjects were then exposed to either +50 mmHg LBPP or no LBPP (prewarming period). A schematic representation of the experimental timeline is presented in Fig. 1. During this time, a 20°C water perfusion was started through the liquid-conditioned suit by using a temperature-controlled circulation bath (Endocal, Neslab; and model 20000, Micropump, Vancouver, WA). The temperate water perfusion was performed to control and stabilize skin and core temperature before whole body heating and was continued until forearm cutaneous vasoconstriction was noted (identified as a plateau in SkBF at nadir recorded over 12 consecutive measurements). The average duration of the prewarming phase (defined as the end of the 15-min exercise or no-exercise treatment to the start of the whole body warming) for all experimental trials was 65 min. sk was then increased at a rate of 4.0 ± 0.6°C/h as the water circulating through the suit was progressively increased to 47°C. Once cutaneous vasodilation and sweating were noted (warming phase), whole body warming continued until the rate of increase in both SkBF and sweating achieved a reduced slope and a subsequent sustained elevated value.
|
Data and Statistical Analysis
The Tes threshold for cutaneous vasodilation (ThVD) was defined as the Tes at which there was an increase in CVC measured on the ventral surface of the forearm, observed in three consecutive measurements (19). The Tes threshold for sweating (ThSW) was attained when a rapid increase in sweat rate was observed in at least three consecutive measurements (16). Thermal sensitivity was defined as the slope of the linear portion of the SkBF curve, measured in voltage change per unit change of Tes. The linear portion of the data was selected by visual inspection, and slopes were determined by least squares linear regression analysis.
Hemodynamic and thermoregulatory response thresholds for vasodilation and sweating were identified and compared under each of the conditions as follows: 1) no-exercise/without LBPP; 2) no-exercise/with LBPP; 3) exercise/without LBPP; and 4) exercise/with LBPP. The average response of the different physiological variables was compared for each condition by using ANOVA with repeated measures. In the event of statistical significance (P < 0.05), a Tukey's honestly significant difference test was used to identify significant differences.
|
RESULTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
|---|
sk were similar for all conditions during baseline resting (Table 1).
|
Prewarming Phase
Hemodynamic response. As identified in Table 1, prewarming MAP remained significantly reduced (5 ± 2 mmHg) from baseline resting after exercise (P < 0.05), whereas a significant increase was measured with the application of LBPP. A similar magnitude of increase in MAP was measured for the no-exercise with LBPP condition. MAP remained unchanged throughout the no-exercise without LBPP trial. Application of LBPP reduced the postexercise HR to baseline values before whole body warming, whereas, without LBPP, HR remained significantly elevated (20 beats/min) (P < 0.05). HR remained unchanged from baseline resting during the no-exercise trial without LBPP application. However, HR was significantly reduced when LBPP was applied (-12 beats/min) (P < 0.05).
Thermal response. For both exercise trials, exercise resulted in a similar increase in Tes of 1.0 ± 0.09°C. The application of LBPP postexercise resulted in a decrease in the recovery time required for Tes to return to baseline resting values (P < 0.05) compared with the postexercise Tes response without LBPP. For both no-exercise conditions, Tes remained unchanged from baseline resting until the start of whole body warming, and the application of LBPP had no measurable influence on Tes response (Fig. 2). For all experimental conditions, Tes had returned to baseline resting values and was similar for all conditions before the whole body warming (Fig. 2). sk values before whole body warming were similar for all conditions, although the values were reduced from baseline (Table 1) (P
< 0.05).
|
Warming Phase
The rate of warming for the suit perfusate (19.5°C/h) was similar for all groups, and sk was increased at the same rate of 4.0 ± 0.6°C/h for all subjects in all conditions.
Cutaneous vasodilation. The ThVD was significantly higher (0.27°C) than the no-exercise trial for the without LBPP condition (P < 0.05) (Fig. 3, Table 2). The application of LBPP after exercise resulted in a lowering (0.36°C) of ThVD
compared with the postexercise threshold response measured without LBPP (P < 0.05). In contrast, there was no significant effect of LBPP application in the no-exercise trial on ThVD. sk values at the onset threshold for cutaneous vasodilation were similar for all conditions (Table 3). The sensitivity of the thermal reflex was estimated from the slope of the linear relationship between CVC and Tes. The rate of rise of CVC per unit change in Tes was not significantly different between conditions (Table 3).
|
|
|
Sweating response. As with our findings for cutaneous vasodilation, the ThSW was increased (0.25°C) after exercise compared with the no-exercise condition in the experimental trials performed without LBPP (Fig. 4). The application of LBPP resulted in a decrease (0.28°C) in the postexercise ThSW (P < 0.05), whereas no change was measured in the no-exercise condition. sk at ThSW and the slope of the linear relationship between local upper back sweating and Tes were similar for all conditions (Table 3).
|
|
DISCUSSION |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
|---|
Postexercise Core Temperature Response
Of interest is the observation of an increase in the rate of core temperature decay observed with the application of LBPP postexercise in the upright position. Previously, it has been shown that core temperature remains elevated for a prolonged period after dynamic exercise (33). Although this study was not specifically designed to address postexercise tissue heat exchange, the contrasting response in core temperature, specifically the difference in rates of core temperature decay under LBPP condition, is worthy of note. The changes in hemodynamic response induced by the application of LBPP, such as increase in cardiac output and MAP (an increase in MAP was measured in this study) (28), were sufficient to result in a relative increase in whole body heat loss. On the basis of the data from this study, it is not possible to determine whether this increase in heat loss was due to an increase in the rate of nonevaporative heat loss, evaporative heat loss, or both. However, it has been shown that an increase in the postexercise hypotensive response, induced by exercise of increasing intensity, is paralleled by an increase (0.5°C) in the magnitude of the postexercise elevation in Tes (13). In the present study, the postexercise hypotensive response was reversed with the application of LBPP. Thus, in conjunction with our observation of a baroreceptor-modulation of postexercise vasomotor and sudomotor responses discussed below, it is plausible that the postexercise core temperature response is, to a large extent, influenced by nonthermoregulatory mechanisms like baroreceptors. Further studies are required to examine the kinetics of tissue heat exchange and its relation to blood pressure and/or pooling.
Baroreceptor Modulation of Cutaneous Vasodilation
It has been demonstrated that the cutaneous circulation is on the efferent limb of several nonthermoregulatory reflexes, including the baroreceptor reflex. Baroreceptor unloading has been shown to cause cutaneous vasoconstriction. Studies involving head-up tilt (25) and application of negative pressure to the lower body (29, 31), which displaces blood volume to legs, have proven to provoke cutaneous vasoconstrictor activity in resting humans. Kellogg et al. (11) were able to demonstrate during resting heat stress that baroreceptor unloading caused a withdrawal of active cutaneous vasodilation. Similar baroreflex modulation of cutaneous SkBF has been demonstrated during exercise. Mack et al. (19) showed that baroreceptor unloading induced by the application of -40 mmHg lower body negative pressure during exercise attenuated the threshold for cutaneous vasodilation. This effect was quickly reversed when the lower body negative pressure was removed. Under resting conditions, baroreceptor modulation of cutaneous vasomotor response was noted as a baroreflex modification of the active cutaneous vasodilator system.
Our data support the observation of a similar baroreceptor-mediated response on SkBF. As previously indicated, exercise resulted in a postexercise increase of 0.3°C in ThVD. This exercise-induced increase in the threshold for cutaneous vasodilation was reversed with the application of LBPP. We are confident that our observation of this postexercise increase in the threshold for cutaneous vasodilation was a result of postexercise venous pooling (baroreceptor unloading). Our blood pressure and HR data are consistent with a postexercise hypotensive response. This was manifested as a significant postexercise decrease in MAP and an elevation in HR. These results are consistent with the observations of postexercise hypotension noted in previous studies (17, 30). Second, it has been shown that the resistance vessels in exercised skeletal muscle remain dilated after a bout of dynamic exercise and that the resultant muscle hyperemia persists well into recovery (30). Acute reductions in central venous pressure have been shown to delay or decrease the rise in SkBF during heat stress (22). Thus it is plausible that a baroreceptor-mediated peripheral skin vasoconstriction is elicited in response to the postexercise hypotension. The suppressive reflex on SkBF may reflect a central inhibition of vasodilator outflow due to baroreceptor unloading, because baroreceptor reflexes are known to modulate active vasodilator activity (9), and/or a baroreceptor-mediated decrease in SkBF mediated by an increase in vasoconstrictor tone.
It has been shown that there is a diurnal rhythm in thermoregulatory control and in vasodilator and sudomotor thresholds (1, 2). We believe that this factor had a minimal effect on our results because careful control was taken to commence each experiment at the same time on each experimental day. Each experiment was begun at precisely 0900 to ensure that all experimental evaluations of thermoregulatory thresholds were completed well before 1300. Furthermore, we did observe increases in the onset thresholds for cutaneous vasodilation and sweating in the postexercise period, both of which were attenuated by LBPP. These observations suggest that the main effect was not a result of a circadian shift in threshold response of cutaneous vasodilation and sweating.
Blood volume and plasma osmolality may be changed during certain types of exercise. Studies have shown that hypohydration increases the threshold for sweating and cutaneous vasodilation (5) and that the magnitude of the response is dependent on the level of hypohydration (24). Thus it is possible that the postexercise increase in warm thermal response thresholds may be the result of, or at least accentuated by, relative hypohydration. The hydration status of our subjects was not verified during the experiment because it was unlikely that any significant hypohydration occurred given the type and duration of the exercise. Montain and Coyle (23) demonstrated that 2 h of dynamic exercise (65% maximal O2) in a warm environment (33°C) with no water intake results in a maximum weight loss of 4.2%. Similarly, Mack and Nadel (20) noted that a 70-kg adult could potentially lose on the order of 2.5% of water content per hour of heavy exercise in the heat owing primarily to water loss from sweating. In our study, the short duration of moderate-intensity exercise (only 15 min, 65% O2 peak) performed in a cooler environment (25°C) with unrestricted pretrial water intake is unlikely to have caused more than a 0.5% weight loss. Under this condition, our subjects could be considered euhydrated (8). It is possible to have fluid shift to the interstitial space during intense exercise. In this case it is unlikely that there was a significant change in the interstitial volume during the course of the short-duration, moderate-intensity exercise. It remains to be studied, however, how the application of upright LBPP postexercise affects relative fluid volume balance and how this may potentially impact warm thermal responses.
Factors such as muscle metaboreflex and muscle mechanoreflexes may have contributed to the observations in the present study. It has been shown that LBPP application (up to +60 mmHg) during exercise reduces oxygen saturation in the femoral venous blood and increases lactate release (32). This may in turn activate the muscle metaboreflex and evoke a pressor response. It is felt that the muscle metaboreflex contributed only minimally to our observations for the following reasons: 1) the exercise protocol was performed below anaerobic threshold (65% O2 peak), thus exercise and postexercise lactate production/accumulation would have been minimal; and 2) any metabolites that may have been present postexercise would most likely have cleared by the time the subject was positioned into the LBPP chamber.
It is unlikely that activation of the muscle mechanoreflexes during our LBPP protocol contributed significantly to the observed increases in MAP and the resultant decrease in the postexercise threshold for cutaneous vasodilation. At high levels of LBPP in resting supine position, activation of the muscle mechanoreflex increases sympathetic nerve activity (SNA) and may override the normal baroreflex-mediated withdrawal of SNA (6). In the present study, application of +50 mmHg upright LBPP caused an increase in MAP coupled with bradycardia that would indicate a normal baroreflex response. If the muscle mechanoreflex was primarily responsible for the increase in MAP during upright LBPP, then we would not have noted bradycardia during this time (28). Furthermore, it is unlikely that the muscle mechanoreflex contributed to our observed results because we demonstrated a decrease in the postexercise threshold for vasodilation when LBPP was applied (i.e., as measured in the exercise-with-LBPP trial). Finally, if this reflex was the primary determinant, then because of its impact on SNA this response should have been blunted or opposite to our observed change.
Baroreceptor Modulation of Sweating
Studies have shown that the sweating response during exercise involves not only changes in core and skin temperatures (thermal factors) (7, 26) but also nonthermal factors (central command, mechanoreceptors, metaboreceptors) (26). This is in contrast to passive heating at rest, in which the primary stimuli for sweating are thermal factors (27). Our present finding of a postexercise increase in the ThSW is consistent with our previous studies (14). However, of significant interest was the observation that the postexercise increase in the ThSW was reversed with the application of LBPP. Although the exact mechanism responsible for the postexercise attenuation of the sudomotor response remains to be determined, inferences drawn from previous research would support a baroreceptor-mediated response, comparable to that observed with SkBF regulation.
It is noteworthy that Bini and coworkers (3) previously demonstrated that changes in blood pressure may act to modulate sweat gland activity. Their observation was based on the fact that skin sympathetic nerve recordings from sudomotor fibers showed cardiac rhythmicity. Similarly, Macefield and Wallin (18) found that sudomotor neuronal discharge is modulated by baroreflexes. Although they did not measure skin sympathetic nerve activity, Mack and colleagues (19, 21) showed a greater increase in the ThSW during exercise with baroreceptor unloading. In contrast, Wilson et al. (36) showed that skin sympathetic nerve activity and sweat rate are not modulated by arterial baroreflexes in normothermic or moderately heated individuals. Unlike previous studies, pharmacological manipulation of arterial blood pressure was employed to eliminate the potentially confounding effects associated with using lower body negative pressure to unload baroreceptors (i.e., skin surface cooling). Our present findings would seem to support a possible nonthermal baroreflex modulation of postexercise sweating response. However, in light of the fact that we did not directly measure skin sympathetic nerve activity, there is a potential for confounding effects of non-baroreflex-mediated origin on the postexercise thermal response to sweating yet to be studied.
It is important to note that there remains controversy not only as to whether or not baroreceptor reflexes are involved in the control of sweating (36) but also how it relates to SkBF control (34, 35). As previously indicated, other non-baroreflex-mediated reflexes may act to modulate sudomotor and SkBF response, which were not examined in this study. Thus, although our present observation of a concomitant increase in the postexercise threshold for sweating and cutaneous vasodilation and attenuation thereof with the application of LBPP seem to indicate a similar mechanism of control, further evaluation of the physiological mechanism(s) governing the postexercise control of sweating and cutaneous vasodilation in humans is required.
In summary, this study provides additional insight regarding the competition between thermoregulatory and cardiovascular reflexes and the integrated response. Our results demonstrate that cutaneous vasomotor and sudomotor control are significantly modified during upright exercise recovery. This disturbance in thermal balance (postexercise) and lack thereof during upright postexercise LBPP application illustrates the significant impact of blood pooling on cutaneous vasodilation and sweating after a bout of moderate upright dynamic exercise.
|
ACKNOWLEDGMENTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
|---|
This research was supported by the Natural Science and Engineering Research Council of Canada (grant held by G. P. Kenny).
|
FOOTNOTES |
|---|
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 |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  O. Jay, D. Gagnon, M. B. DuCharme, P. Webb, F. D. Reardon, and G. P. Kenny Human heat balance during postexercise recovery: separating metabolic and nonthermal effects Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1586 - R1592. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Nishiyasu, S. Hayashida, A. Kitano, K. Nagashima, and M. Ichinose Effects of posture on peripheral vascular responses to lower body positive pressure Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H670 - H676. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. Kenny and O. Jay Sex differences in postexercise esophageal and muscle tissue temperature response Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2007; 292(4): R1632 - R1640. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. H. McInnis, W. S. Journeay, O. Jay, E. Leclair, and G. P. Kenny 15{degrees} Head-down tilt attenuates the postexercise reduction in cutaneous vascular conductance and sweating and decreases esophageal temperature recovery time J Appl Physiol, September 1, 2006; 101(3): 840 - 847. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. Kenny, O. Jay, W. M. Zaleski, M. L. Reardon, R. J. Sigal, W. S. Journeay, and F. D. Reardon Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2006; 291(3): R580 - R588. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. Kenny, J. E. Murrin, W. S. Journeay, and F. D. Reardon Differences in the postexercise threshold for cutaneous active vasodilation between men and women Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R172 - R179. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. s. Journeay, F. D. Reardon, N. H. McInnis, and G. P. Kenny Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women J Appl Physiol, November 1, 2005; 99(5): 1816 - 1821. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. W. Wilkins, C. T. Minson, and J. R. Halliwill Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation J Appl Physiol, December 1, 2004; 97(6): 2071 - 2076. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Shibasaki, M. Sakai, M. Oda, and C. G. Crandall Muscle mechanoreceptor modulation of sweat rate during recovery from moderate exercise J Appl Physiol, June 1, 2004; 96(6): 2115 - 2119. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. S. Journeay, F. D. Reardon, C. R. Martin, and G. P. Kenny Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans J Appl Physiol, June 1, 2004; 96(6): 2207 - 2212. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. Kenny, J. Periard, W. S. Journeay, R. J. Sigal, and F. D. Reardon Effect of exercise intensity on the postexercise sweating threshold J Appl Physiol, December 1, 2003; 95(6): 2355 - 2360. [Abstract] [Full Text]
|
|
|
|
|
|
G. P. Kenny, J. Periard, W. S. Journeay, R. J. Sigal, and F. D. Reardon Cutaneous active vasodilation in humans during passive heating postexercise J Appl Physiol, September 1, 2003; 95(3): 1025 - 1031. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
Significant difference from no-exercise (P < 0.05).