Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 101: 840-847, 2006. First published June 1, 2006; doi:10.1152/japplphysiol.00382.2006
8750-7587/06 $8.00
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
101/3/840    most recent
00382.2006v1
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 ISI 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 ISI Web of Science (5)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McInnis, N. H.
Right arrow Articles by Kenny, G. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McInnis, N. H.
Right arrow Articles by Kenny, G. P.

15° Head-down tilt attenuates the postexercise reduction in cutaneous vascular conductance and sweating and decreases esophageal temperature recovery time

Natalie H. McInnis,1 W. Shane Journeay,1,2 Ollie Jay,1 Emily Leclair,1 and Glen P. Kenny1

1Laboratory of Human Bioenergetics and Environmental Physiology, School of Human Kinetics, Faculty of Health Sciences, University of Ottawa, Ottawa, Ontario; and 2Toxicology Graduate Program and Department of Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada

Submitted 30 March 2006 ; accepted in final form 23 May 2006


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The following study examined the effect of 15° head-down tilt (HDT) on postexercise heat loss and hemodynamic responses. We tested the hypothesis that recovery from dynamic exercise in the HDT position would attenuate the reduction in the heat loss responses of cutaneous vascular conductance (CVC) and sweating relative to upright seated (URS) recovery in association with an augmented hemodynamic response and an increased rate of core temperature decay. Seven male subjects performed the following three experimental protocols: 1) 60 min in the URS posture followed by 60 min in the 15° HDT position; 2) 15 min of cycle ergometry at 75% of their predetermined VO2 peak followed by 60 min of recovery in the URS posture; or 3) 15 min of cycle ergometry at 75% of their predetermined VO2 peak followed by 60 min of recovery in the 15° HDT position. Mean skin temperature, esophageal temperature (Tes), skin blood flow, sweat rate, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance, and mean arterial pressure (MAP) were recorded at baseline, end exercise, 2, 5, 8, 12, 15, and 20 min, and every 5 min until end of recovery (60 min). Without preceding exercise, HDT decreased HR and increased SV (P ≤ 0.05). During recovery after exercise, a significantly greater MAP, SV, CVC, and sweat rate and a significantly lower HR were found with HDT compared with URS posture (P ≤ 0.05). Subsequently, a significantly lower Tes was observed with HDT after 15 min of recovery onward (P ≤ 0.05). At the end of 60 min of recovery, Tes remained significantly elevated above baseline with URS (P ≤ 0.05); however, Tes returned to baseline with HDT. In conclusion, extended recovery from dynamic exercise in the 15° HDT position attenuates the reduction in CVC and sweating, thereby significantly increasing the rate of Tes decay compared with recovery in the URS posture.

skin blood flow; sweat rate; baroreceptors; exercise recovery

PREVIOUS STUDIES HAVE SHOWN that under thermoneutral conditions, core body temperature remains elevated after an acute bout of dynamic exercise (1, 6, 21, 22, 36, 38). Additionally, sweating (23), skin blood flow (SkBF), and skin temperature (23, 38) return to preexercise values despite the persistent elevation in core temperature.

Research has been conducted to examine the possible factors contributing to altered temperature regulation postexercise. Studies employing recovery modes have attempted to elucidate the relative roles of nonthermal factors such as central command, mechanoreceptors, and baroreceptors in the modulation of heat loss responses during exercise recovery (3, 19, 33, 39). Collectively, the recovery mode studies have determined that attenuating the baroreceptor unloading effect associated with upright inactive recovery, through active or passive recovery, preserves SkBF. Central command did not influence the SkBF response. Sweating, however, can be influenced by central command and mechanoreceptors, albeit the role for baroreceptors remains unresolved.

During upright inactive recovery, there is a growing body of evidence in support of a possible relationship between hemodynamic changes postexercise and heat loss responses. Journeay et al. (18) specifically examined this issue by manipulating postexercise hemodynamics using lower body pressure. They observed a reflex increase in SkBF, sweating, and heat flux with application of +45 mmHg lower body positive pressure (LBPP) in the upright seated (URS) posture. Furthermore, an increase in the rate of core temperature decay was noted after reversal of postexercise hypotension by application of positive pressure to the lower extremities. This effect was not seen under lower body negative pressure or no pressure conditions. It was postulated that LBPP triggered a nonthermal baroreceptor-mediated increase in heat loss responses secondary to a redistribution of blood from the lower extremities to the central circulation.

LBPP produces its effects via increased barometric pressure around the lower extremities. This leads to enhanced microvascular compression in the tissues and produces a pressure gradient that tends to increase central blood volume. With the application of sufficient barometric pressure to the lower extremities, this technique may activate both cardiopulmonary and arterial baroreceptors (7). For example, a study showed that application of +45 mmHg of LBPP postexercise engaged both the cardiopulmonary and arterial baroreceptors (18). Also, it has been suggested that LBPP may activate mechanoreceptors particularly at pressures >20 mmHg (7), whereas others have ruled out mechanoreceptor activation during LBPP (32). One possible limitation of the LBPP technique in thermoregulatory studies is that possible convective airflow to the lower extremities may increase heat loss from the lower extremities. Furthermore, our laboratory has previously observed an enhanced rate of core temperature decay with application of LBPP (18); however, this may not be a convenient cooling strategy in the treatment of hyperthermic individuals due to the time associated with transfer to the pressure box.

In contrast, head-down tilt (HDT) is known to increase central blood volume by promoting venous return through a reduction in the hydrostatic forces present in the upright posture. Specifically, under resting conditions at tilt angles of <30°, this technique is thought to engage the cardiopulmonary baroreceptors without changes in systemic mean arterial pressure (MAP) and therefore reduces the likelihood of engaging the arterial baroreceptors (7–10, 27, 31). Thus HDT is another method by which to manipulate postexercise hemodynamic responses, and it allows for the attenuation of the baroreceptor unloading effect of upright exercise recovery. Additionally, HDT enables us to intervene immediately postexercise and remove the possible effects of mechanoreceptor activation and/or convective airflow on the lower extremities associated with LBPP.

Thus the purpose of this experiment was to examine the effect of HDT, and by extension the role of baroreceptors, on prolonged postexercise heat loss and hemodynamic responses. We tested the hypothesis that recovery from dynamic exercise in the HDT position would augment the heat loss responses of cutaneous vascular conductance and sweating relative to upright recovery in association with an augmented hemodynamic response and increased rate of esophageal temperature (Tes) decay.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects

Seven healthy, physically active men volunteered and gave written consent to participate in this study. The study was approved by the Research Ethics Board at the University of Ottawa. Five to 7 days before the experiments, peak oxygen consumption (VO2 peak) was measured during a progressive cycle ergometer protocol that required the participant to cycle at a cadence of 80 revolutions/min while the ergometer resistance was increased at 0.5 kp every 2 min. The VO2 peak data were used to select the submaximal workload for the experimental exercise phase of the study. Subjects were 20 ± 0.8 (SE) yr old and 182 ± 0.4 cm tall, weighed 78.3 ± 4.2 kg, and had a mean VO2 peak of 56.1 ± 2.6 ml·kg–1·min–1.

Measurements

Heart rate (HR) was monitored using a Polar coded transmitter, recorded continuously and stored with a Polar Advantage interface and Polar Precision Performance software (Polar Electro Oy, Kempele, Finland). MAP was estimated from the integration of a noninvasive recording of blood pressure at the middle digit of the left hand (Finapres 2300, Ohmeda, Madison, WI) fixed at heart level (the third intercostal space). The arm and hand were maintained in position using a cotton arm sling. The position of the hand was verified before all measurements. The Finapres system is based on the Penaz volume clamp method (dynamic unloaded arterial wall principle). MAP was verified periodically throughout the protocol by auscultation. Typically, measurements were verified at 5-min intervals during the first 15 min of recovery and at 10- to 15-min intervals thereafter.

Pulmonary oxygen consumption was estimated using a metabolic cart (model CPX/D, Medgraphics, St. Paul, MN) during VO2 peak assessment preceding the experimental trials. Cardiac output (CO) was estimated using the CPX/D computerized version of the CO2-rebreathing technique of Defares (5). It has been shown that Doppler-derived aortic blood flow (CO) measurements correlate well with the indirect carbon dioxide rebreathing method (11). The Defares method has also been shown to work well in "un-steady-state" testing (14). Stroke volume (SV) was calculated as CO/HR. Total peripheral resistance (TPR) was calculated as MAP/CO.

SkBF was estimated using laser-Doppler velocimetry (PeriFlux System 5000, main control unit; PF5010 LDPM, function unit; Perimed, Stockholm, Sweden) at the left midanterior forearm. The laser-Doppler flow probe (PR 401 angled probe, Perimed) was taped to cleaned skin, in an area that did not appear by visual inspection to be overly vascular and from which consistent readings were noted (28). Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler flow to MAP. At the end of the experiment, local skin temperature was raised to 42°C using a heating element (PF 5020 temperature unit, Perimed) that housed the laser-Doppler flow probe, until peak CVC (CVCpeak) was measured (~30 min) (35). CVCpeak was determined as a sustained elevated plateau in local SkBF. CVC data are presented as a percentage of maximal CVC as determined by local heating (%CVCpeak). All SkBF measures were taken in the period preceding rebreathing to avoid causing fluctuations in SkBF data at each time point. SkBF measures were recorded from the left midanterior forearm such that the arm was level with the heart.

Sweat rate was measured using a 5.0-cm2 ventilated capsule placed over the medial inferior aspect of the trapezius muscle. Anhydrous compressed air was passed through the capsule and over the skin surface (Brooks 5850, mass flow controller, Emerson Electric, Hetfield, PA). The vapor density of the effluent air was calculated from the relative humidity and temperature measured using the Omega HX93 humidity and temperature sensor (Omega Engineering, Stanford, CT). Sweat rate was defined as the product of the difference in water content between effluent and influent air and the flow rate. The flow rate through the capsule was 1.0 l/min. The sweat rate value was adjusted for skin surface area under the capsule (expressed in mg·min–1·cm–2).

Esophageal temperature (Tes) was monitored continuously using a pediatric esophageal temperature 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, whereby the tip of the thermocouple is estimated to be at the level of the left atrium (30). Skin temperature was recorded at 11 sites using 0.3-mm-diameter T-type thermocouples integrated into heat-flow sensors (model FR-025-TH44018-6, Concept Engineering, Old Saybrook, CT). The area-weighted mean skin temperature (Tsk) and heat flux (HFsk) were calculated by assigning the following regional percentages: head 6%, upper arm 9%, forearm 6%, finger 2%, chest 19%, upper back 9.5%, lower back 9.5%, anterior thigh 10%, posterior thigh 10%, anterior calf 9.5%, and posterior calf 9.5% (13). Temperature data were collected and digitized (data acquisition module model 3497A, Hewlett-Packard) at 5-s intervals, displayed graphically in real time and stored on hard disk (model PC-312, 9000, Hewlett-Packard).

The HDT maneuver was performed on a Teeter Hang Ups F5000 inversion table. The upper body only was supported by a meshed cotton and nylon net secured to the upper frame of the tilt table. The 15° HDT position was measured using a Unitek Magnetic Polycast Protractor (model 3310-036, Polytech, Empire Level Manufacturing, Milwaukee, WI).

Experimental Protocol

Each subject performed a total of three experimental trials carried out in random order. Experiments were separated by a minimum of 48 h during which subjects were instructed to avoid physical activity and excessive stressors such as exposure to hot or cold temperatures, particularly during the period between awakening and experimentation and during transit from home to the laboratory. Trials were performed at the same time of day for each subject to avoid circadian variation in Tsk, and Tes. Subjects were asked to fast at least 4 h before experimentation, and water ingestion was permitted ad libitum during this time. On arrival at the laboratory, subjects clothed in shorts and athletic shoes were fitted with the appropriate instruments. All experimental trials were performed at an ambient temperature of 24.0 ± 0.5°C and a relative humidity of 45%.

After instrumentation, subjects remained resting for 10 min during which baseline measures were recorded. Subjects were then required to perform one of three experimental protocols. These were 1) 60 min in the URS posture followed by 60 min in the 15° HDT position; 2) 15 min of cycle ergometry at 75% of their predetermined VO2 peak followed by 60 min of recovery in the URS posture; or 3) 15 min of cycle ergometry at 75% of their predetermined VO2 peak followed by 60 min of recovery in the 15° HDT position. The tilt table was placed adjacent to the cycle ergometer to facilitate the transition from the bike to the tilt table after cessation of exercise. The average time to effect this transition was <30 s.

At the end of each experiment, CVCpeak was determined using a local heating protocol as described previously.

Statistical Analyses

A two-way ANOVA with repeated measures was used to analyze the data using the repeated factors of postexercise recovery time (levels: 2, 5, 8, 12, and 15 min and every 5 min until 60 min) and recovery mode (levels: 15° HDT and URS). The dependent variables employed were the changes from preexercise or baseline rest in Tes, Tsk, HFsk, CO, HR, %CVCpeak, MAP, TPR, SV, and sweat rate. All values represent the means and standard deviation for seven subjects. The exercise and no-exercise sessions were analyzed separately to isolate the effect of recovery mode. For ANOVA main effects, Huynh-Feldt corrected statistics are reported where the assumption of sphericity was not met. Pairwise comparisons were performed using paired sample t-tests. The level of significance was set at an alpha level of 0.05. All analyses were performed using the statistical software package SPSS 12.0 for Windows (SPSS, Chicago, IL).


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Tes Response

Exercise condition.   The change in Tes at the end of exercise relative to preexercise rest was not significantly different between the URS and HDT trials (P = 0.235), with Tes elevated by 1.28°C (SD 0.29) preceding URS and by 1.18°C (SD 0.25) preceding HDT. During recovery, change in Tes from preexercise rest became less with postexercise recovery time [F(1.9,9.4) = 37.0, P < 0.001] and was influenced by recovery mode [F(1,5) = 10.1, P = 0.007]. The interaction between recovery mode and postexercise recovery time for change in Tes [F(2.8,14.1) = 4.7, P = 0.019] is demonstrated by the significantly lower elevation from preexercise rest in Tes during HDT compared with URS (P ≤ 0.05) after 15 min of postexercise recovery and for the remainder of the 60-min recovery period (Fig. 1A). Tes remained significantly (P = 0.006) elevated by 0.22°C (SD 0.12) above preexercise rest after 60 min of URS recovery, but it was 0.15°C (SD 0.08) below preexercise rest after 60 min of HDT recovery.


Figure 1
View larger version (21K):
[in this window]
[in a new window]
  		Fig. 1. Effect of upright seated recovery posture ({square}) and recovery in a 15° head-down tilt recovery position ({triangleup}) after 15 min of cycle ergometry at 75% peak oxygen consumption on esophageal temperature (A), sweat rate (B), forearm cutaneous vascular conductance (CVC; C). *Significant difference between upright seated recovery posture, P ≤ 0.05.

 
No-exercise condition.   Without preceding exercise, change in Tes relative to resting values did not significantly change with time [F(2.1,10.7) = 1.9, P = 0.198] or recovery mode [F(1,5) = 4.7, P = 0.082]; however, a significant interaction was apparent between time and recovery mode [F(1.8, 9.1) = 0.041] as demonstrated by a small (~0.1°C) but significantly (P ≤ 0.05) lower Tes during HDT compared with URS between 15 and 30 min.

Skin Temperature, Dry Heat Loss, Sweating, and %CVCpeak

Exercise condition.   After exercise, the elevations in Tsk from preexercise rest became lower as postexercise recovery time progressed [F(1,6) = 25.8, P = 0.002], with a trend for the influence of recovery mode [F(1,6) = 5.3, P = 0.061]. The interaction between mode and time [F(2.8, 16.8) = 5.8, P = 0.007] is evidenced by a significantly lower Tsk after 12 min of HDT recovery and for the remainder of the 60-min recovery period (P ≤ 0.05). At the end of the postexercise period, Tsk was 0.49°C (SD 0.53) lower after HDT compared with URS. Similarly, the elevations in HFsk from preexercise rest became lower with postexercise recovery time [F(1.6,9.4) = 168.9, P < 0.001]; however, no differences were observed between recovery modes [F(1,6) = 1.2, P = 0.316]. Sweat rate was significantly elevated above preresting values before HDT and URS recovery trials (P ≤ 0.05) and then became reduced throughout postexercise recovery [F(5.3,31.8) = 554.6, P < 0.001]. Furthermore, sweat rate was influenced by recovery mode [F(1,6) = 20.3, P = 0.004], with a significantly greater sweat rate observed during HDT recovery relative to URS between 8 and 45 min postexercise (P ≤ 0.05; Fig. 1B). The elevation in %CVCpeak above preexercise rest after exercise before both HDT and URS recovery trials became lower with postexercise recovery time [F(2.6,13.2) = 17.6, P < 0.001]. Furthermore %CVCpeak was influenced by recovery mode [F(1,5) = 49.4, P = 0.001] with significantly greater values observed throughout the 60-min postexercise recovery period in the HDT position compared with URS (P ≤ 0.05; Fig. 1C).

No-exercise condition.   Without preceding exercise, changes in Tsk, HFsk, %CVCpeak, and sweat rate relative to resting values were not influenced by time or recovery mode (P > 0.05).

Hemodynamic Responses

All hemodynamics data for all conditions are summarized in Table 1.


View this table:
[in this window]
[in a new window]
  		Table 1. Mean relative changes from baseline in cardiac output, stroke volume, heart rate, mean arterial pressure, and total peripheral resistance during the control trials preceded by no exercise

 
Exercise condition.   The elevations in CO after exercise of 15.8 l/min (SD 2.9) before HDT and 16.5 l/min (SD 5.1) before URS were not significantly different (P = 0.818). These elevations from rest in CO became lower during postexercise recovery [F(2.7,13.7) = 151.1, P < 0.001], but they were not influenced by recovery mode [F(1,5) = 0.005, P = 0.948] (Fig. 2A). The elevations in SV after exercise of 46.6 ml (SD 26.0) before HDT and 51.2 ml (SD 34.5) before URS were not significantly different (P = 0.852). However, these elevations from rest in SV became lower with postexercise recovery time [F(3.2,15.8) = 27.3, P < 0.001] and were influenced by recovery mode [F(1,5) = 12.4, P = 0.017] with a significantly greater SV observed during HDT recovery throughout the 60-min postexercise recovery period (P ≤ 0.05; Fig. 2B). After exercise, no significant difference was observed between the elevation in HR of 99.1 beats/min (SD 11.3) before HDT and 97.1 beats/min (SD 12.3) before URS recovery (P = 0.726). HR elevation above rest became lower with postexercise recovery time [F(3.8,23.0) = 297.9, P < 0.001], and it was influenced by recovery mode [F(1,6) = 34.2, P = 0.001] with a significantly lower HR elevation observed during HDT relative to URS throughout the 60-min postexercise recovery period (P ≤ 0.05; Fig. 2C). The changes in MAP from preexercise rest after exercise recovery were not significantly different between HDT and URS (P = 0.376). However, during postexercise recovery, change in MAP was different between recovery modes [F(1,5) = 27.1, P = 0.003], and it was influenced by recovery time [F(2.8, 14.0) = 42.0, P = 0.001] with a significantly higher MAP observed during HDT between 2 and 50 min of postexercise recovery (P ≤ 0.05; Fig. 3A). The changes in TPR from rest after exercise of –10.4 mmHg·l–1·min (SD 1.7) before HDT and –10.5 mmHg·l–1·min (SD 2.5) before URS were not significantly different (P = 0.834). However, change in TPR from preexercise rest became less throughout postexercise recovery [F(5.2,25.8) = 18.0, P < 0.001], but it was not influenced by recovery mode [F(1,5) = 2.2, P = 0.200; Fig. 3B].


Figure 2
View larger version (17K):
[in this window]
[in a new window]
  		Fig. 2. Effect of upright seated recovery posture ({square}) and the 15° head-down tilt recovery position ({triangleup}) after 15-min of cycle ergometry at 75% peak oxygen consumption on cardiac output (CO; A), stroke volume (SV; B), and heart rate (HR; C). *Significant difference between upright seated recovery, P ≤ 0.05.

 

Figure 3
View larger version (21K):
[in this window]
[in a new window]
  		Fig. 3. Effect of upright seated recovery posture ({square}) and recovery in a 15° head-down tilt recovery position ({triangleup}) after 15 min of cycle ergometry at 75% peak oxygen consumption on mean arterial pressure (MAP; A) and total peripheral resistance (TPR; B). *Significant difference between upright seated recovery, P ≤ 0.05.

 
No-exercise condition.   Without preceding exercise, changes in CO, MAP, and TPR relative to resting values were not influenced by time or recovery mode (P > 0.05). The change in HR from resting values was significantly different between recovery modes [F(1,6) = 21.2, P = 0.004]. HR was not influenced by recovery time [F(2.0, 12.1) = 2.7, P = 0.110]; however, a significantly lower HR during HDT compared with URS was observed throughout recovery (P ≤ 0.05). A significant difference between recovery modes was also seen for changes in SV from resting values [F(1,5) = 6.0, P = 0.050], with SV greater during HDT relative to URS between 2 and 50 min of recovery (P ≤ 0.05).

Sweat Rate and %CVCpeak as a Function of Tes

The change of sweat rate (Fig. 4) and CVC (Fig. 5) as a function of Tes after exercise show that after exercise the HDT intervention causes a significantly greater %CVCpeak after 5 min of postexercise recovery (P ≤ 0.05) and a significantly greater sweat rate after 15 min of postexercise recovery. The combination of these increased heat loss responses contribute to a significantly lower Tes after 15 min of recovery in the HDT position (P ≤ 0.05).


Figure 4
View larger version (15K):
[in this window]
[in a new window]
  		Fig. 4. Relationship of esophageal temperature with sweat rate during recovery from 15 min of cycle ergometry at 75% peak oxygen consumption in the upright seated posture (filled symbols) and 15° head-down tilt position (open symbols). *Significant difference between recovery positions at a given time point for sweat rate, P ≤ 0.05. {dagger}Significant difference between recovery positions at a given time point for esophageal temperature, P ≤ 0.05.

 

Figure 5
View larger version (16K):
[in this window]
[in a new window]
  		Fig. 5. Relationship of esophageal temperature with cutaneous vascular conductance during recovery from 15 min of cycle ergometry at 75% peak oxygen consumption in the upright seated posture (filled symbols) and 15° head-down tilt position (open symbols). *Significant difference between recovery positions at a given time point for cutaneous vascular conductance, P ≤ 0.05. {dagger}Significant difference between recovery positions at a given time point for esophageal temperature, P ≤ 0.05.

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
The most important observation from this study is that the manipulation of postexercise hemodynamics using HDT attenuates the fall of MAP, CVC, and sweat rate relative to the URS posture. The augmented MAP and heat loss responses in the HDT condition were also associated with an enhanced rate of Tes decay compared with the URS recovery posture. Thus HDT attenuates the reduction in heat loss responses and MAP in individuals recovering from dynamic exercise. These findings support previous work that employed LBPP to alter postexercise hemodynamics and heat loss (18) and further underscore a baroreceptor-mediated attenuation in heat loss responses during URS exercise recovery.

Our observation of an increased rate of Tes decay in the HDT position is consistent with the elevated heat loss responses of CVC and sweating throughout recovery. In recent studies examining postexercise heat loss responses, it has been shown that there is a significant nonthermal contribution to the control of these responses. Studies employing recovery modes have attempted to elucidate the relative roles of nonthermal factors such as central command, mechanoreceptors, and baroreceptors in the modulation of heat loss responses during exercise recovery (3, 19, 33, 39). In toto these experiments concluded that during upright inactive recovery CVC is influenced predominantly by cardiopulmonary baroreceptors. Two studies exist, however, in men (19) and women (20) where different levels of MAP were observed between recovery modes, and therefore the role of the arterial baroreceptor population in heat loss response modulation cannot be ignored. Additional evidence also exists that attenuating the cardiopulmonary and arterial baroreceptor unloading effect associated with exercise recovery helps preserve the response of CVC (15, 18). Our present study differs from previous work in that we have studied the effect of HDT on prolonged recovery responses, whereas others have employed recovery modes (3, 19, 33, 39) or lower body pressure (18). The present study also supports a cardiopulmonary and arterial baroreceptor-mediated influence on postexercise CVC. This is supported by the fact that the cutaneous circulation is on the efferent arm of the baroreflex (4, 16). In our no-exercise condition, 15° HDT engaged the cardiopulmonary baroreflex as indicated by reflex bradycardia, an increase in SV, and no change in MAP. However, we noted a difference in MAP between HDT and the URS posture postexercise. Thus, whereas 15° HDT may isolate the cardiopulmonary baroreceptors under resting conditions, we observed that during exercise recovery HDT leads to an altered MAP response compared with URS recovery posture. This means that between postexercise recovery positions there are different degrees of arterial baroreceptor loading and thus we cannot rule out a possible role for the arterial baroreceptors in the observed CVC response.

The above-mentioned recovery mode studies demonstrated that sweat rate during postexercise recovery can be modulated by central command, mechanoreceptors, and possibly baroreceptors. Under resting conditions, some researchers did not observe decreases in sweating with baroreceptor unloading (37, 40), whereas others have observed a reduction in the thermosensitivity with baroreceptor unloading at rest (34) and during exercise (17, 29). There remains conflicting information regarding the possible baroreceptor influence on sweating during the postexercise period. Our data support a role for cardiopulmonary and/or arterial baroreceptors in the modulations of sweat rate as inferred by the hemodynamic responses to HDT. Under conditions of LBPP, there may be confounding influences on sweat rate such as air currents in the chamber or mechanoreceptor activation secondary to increased atmospheric pressure around the limbs. In our present study, we employed the HDT technique, thereby removing such possible confounders. We observed that when subjects recovered in the HDT position, sweat rate declined more slowly than during recovery in the URS posture, suggesting that baroreceptors are likely involved in the response. In contrast to previous work whereby applying LBPP stimulated sweat rate after restoring MAP (18), this study commenced the HDT intervention immediately postexercise. A study by Wilson et al. (39) concluded that factors other than thermal or baroreceptor loading status contribute to sweat rate during exercise recovery; however, their observations were limited to 5 min postexercise in the supine posture. We first noted a significant difference after 5 min of recovery. Thus it is possible that a role for baroreceptors in the modulation of postexercise sweat rate might be masked in the initial 5-min period and become more apparent later in recovery. Although speculative, our data support this possibility.

HDT tends to cause a shifting of blood headward by counteracting the hydrostatic pooling of blood seen in the URS posture (31). URS inactive recovery is thought to aid in the accumulation of blood in the venous system of the lower extremities in the absence of the muscle pump (2, 12, 26). This hemodynamic consequence may also contribute to postexercise hypotension (12). Our data indicate that without an exercise treatment, there were no significant effects on hemodynamic variables other than a decrease in HR and a concomitant increase in SV in the HDT recovery position relative to the URS posture. This hemodynamic response of SV is consistent with previous observations of resting subjects in the HDT position (10, 27, 31). However, these studies did not show a decrease in HR. The difference in our observations may be due to the fact that previous studies compared HDT with the supine posture and not the URS posture. Conversely, after exercise, we observed significant differences in SV, HR, and MAP between HDT and URS subjects. This supports the contention that HDT reduced the baroreceptor unloading effect of exercise recovery, thus underscoring the significant effect of HDT when performed after dynamic exercise.

In the URS posture reductions in CVC and sweat rate were observed despite a sustained elevation in Tes. This has been reported previously (15, 18, 23–25, 38) and suggests a possible resetting of the Tes relationship with CVC and sweat rate (see Figs. 4 and 5). When plotting the URS data with the responses observed in the HDT posture, the data points shift upward and to the left. This demonstrates that at a given Tes, the responses of CVC and sweat rate are greater in the HDT posture.

Our observation of an enhanced rate of Tes decay in the HDT condition is significant. Although recovery mode studies have observed augmented heat loss responses, they have not reported significant changes in core temperature even when performed up to 20 min postexercise (19, 20, 33). Conversely, application of +45 mmHg LBPP was effective in increasing the rate of Tes decline in URS subjects postexercise (18). The present study also reported a greater decrement in Tes when HDT was applied postexercise. Moreover, HDT may have some practical significance as it is technically easier to perform than transferring subjects to a lower body pressure chamber. A logical extension to this study for future work includes the examination of the responses of severely hyperthermic individuals (core temperature >39.5°C) to the HDT intervention. This will elucidate the effectiveness of HDT as potentially a more practical alternative for the active cooling methods currently recommended.

We conclude that during recovery from dynamic exercise, heat loss responses are compromised in the URS posture secondary to nonthermal baroreceptors influences. Specifically, application of HDT attenuates the reduction in CVC, sweat rate, and MAP typically observed postexercise. The augmented heat loss responses observed under the HDT position also resulted in an increased rate of Tes decay relative to the URS recovery posture. HDT may therefore promote heat loss in hyperthermic individuals postexercise and provides many technical advantages over LBPP.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This research was supported by a Discovery Grant from the Natural Sciences and Engineering Research Council of Canada (to G. P. Kenny).


   FOOTNOTES
 

Address for reprint requests and other correspondence:: G. P. Kenny, Univ. of Ottawa, School of Human Kinetics, PO Box 450, Station A, 125 Univ., Montpetit Hall, Rm. 367, Ottawa, Ontario, Canada K1N 6N5 (e-mail: gkenny{at}uottawa.ca)

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
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Brown S, Li H, Chitwood L, Anderson E, and Boatwright D. Blood pressure, hemodynamic and thermal responses after cycling exercise. J Appl Physiol 75: 240–245, 1993.[Abstract/Free Full Text]
  2. Carter R III, Watenpaugh DE, Wasmund WL, Wasmund SL, and Smith ML. Muscle pump and central command during recovery from exercise in humans. J Appl Physiol 87: 1463–1469, 1999.[Abstract/Free Full Text]
  3. Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. Effects of mode of exercise recovery on thermoregulatory and cardiovascular responses. J Appl Physiol 93: 1918–1924, 2002.[Abstract/Free Full Text]
  4. Crossley R, Greenfield A, Plassaras G, 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]
  5. Defares JG. Determination of PvCO2 from the exponential CO2 rise during rebreathing. J Appl Physiol 13: 159–164, 1958.[Abstract/Free Full Text]
  6. Franklin PJ, Green DJ, and Cable NT. The influence of thermoregulatory mechanisms on post-exercise hypotension in humans. J Physiol 470: 231–241, 1993.[Abstract/Free Full Text]
  7. Fu Q, Sugiyama Y, Kamiya A, Iwase S, and Mano T. A comparison of the effects of lower body positive pressure and head-down tilt on cardiovascular responses in humans. J Gravit Physiol 6: 111–112, 1999.
  8. Goldsmith SR. Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans. J Appl Physiol 65: 1226–1230, 1988.[Abstract/Free Full Text]
  9. Goldsmith SR. Impaired suppression of plasma norepinephrine during head-down tilt in patients with congestive heart failure. Am Heart J 122: 104–107, 1991.[CrossRef][ISI][Medline]
  10. Goldsmith SR, Francis GS, and Cohn JN. Effect of head-down tilt on basal plasma norepinephrine and renin activity in humans. J Appl Physiol 59: 1068–1071, 1985.[Abstract/Free Full Text]
  11. Hadjis T, Jobin J, Bourbeau J, Desagagnes P, Juneau L, and Sampalis J. Aortic flow velocity indices during upright exercise: reliability and relationship to cardiac output. Can J Cardiol 11: 100–104, 1995.[ISI][Medline]
  12. Halliwill JR. Mechanisms and clinical implications of post-exercise hypotension in humans. Exerc Sport Sci Rev 29: 65–70, 2001.[CrossRef][Medline]
  13. Hardy J and Dubois E. The technique of measuring radiation and convection. J Nutr 15: 461–475, 1938.
  14. Inman MD, Hughson RL, and Jones NL. Comparison of cardiac output during exercise by single-breath and CO2 rebreathing methods. J Appl Physiol 58: 1372–1377, 1985.[Abstract/Free Full Text]
  15. Jackson D and Kenny G. Upright lower body positive pressure application attenuates elevated postexercise resting thresholds for cutaneous vasodilation and sweating in humans. J Appl Physiol 95: 121–128, 2003.[Abstract/Free Full Text]
  16. Johnson JM. Nonthermoregulatory control of human skin blood flow. J Appl Physiol 61: 1613–1622, 1986.[Abstract/Free Full Text]
  17. Johnson JM and Park MK. Effect of upright exercise on threshold for cutaneous vasodilation and sweating. J Appl Physiol 50: 814–818, 1981.[Abstract/Free Full Text]
  18. Journeay WS, Reardon FD, Jean-Gilles S, Martin CR, and Kenny GP. Lower body positive and negative pressure alter thermal and hemodynamic responses after exercise. Aviat Space Environ Med 75: 841–849, 2004.[Medline]
  19. Journeay WS, Reardon FD, Martin CR, and Kenny GP. Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans. J Appl Physiol 96: 2207–2212, 2004.[Abstract/Free Full Text]
  20. Journeay WS, Reardon FD, McInnis N, and Kenny GP. Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women. J Appl Physiol 99: 1816–1821, 2005.[Abstract/Free Full Text]
  21. Kenny GP, Denis PM, Boule N, Proulx CE, Thoden JS, and Reardon FD. Increasing thermal load does not effect the post-exercise elevation in esophageal temperature. Can J Appl Physiol 24: 377–386, 1999.[ISI][Medline]
  22. Kenny GP, Giesbrecht GG, Jette M, Reardon FD, and Thoden JS. The effect of ambient temperature and exercise intensity on the post-exercise thermal homeostasis. Eur J Appl Physiol 76: 109–115, 1997.[CrossRef]
  23. Kenny GP and Neidre PC. The effect of exercise intensity on the post-exercise esophageal temperature response. Eur J Appl Physiol 86: 342–346, 2002.[CrossRef][ISI][Medline]
  24. Kenny GP, Periard J, Journeay WS, Sigal RJ, and Reardon FD. Cutaneous active vasodilation in humans during passive heating postexercise. J Appl Physiol 95: 1025–1031, 2003.[Abstract/Free Full Text]
  25. Kenny GP, Periard J, Journeay WS, Sigal RJ, and Reardon FD. Effect of exercise intensity on the postexercise sweating threshold. J Appl Physiol 95: 2355–2360, 2003.[Abstract/Free Full Text]
  26. Kilgour RD, Gariepy P, and Rehel R. Cardiovascular responses during recovery from exercise and thermal stress. Aviat Space Environ Med 64: 224–229, 1993.[Medline]
  27. London GM, Levenson JA, Safar ME, Simon AC, Guerin AP, and Payen D. Hemodynamic effects of head-down tilt in normal subjects and sustained hypertensive patients. Am J Physiol Heart Circ Physiol 245: H194–H202, 1983.[Abstract/Free Full Text]
  28. Mack GW. Assessment of cutaneous blood flow by using topographical perfusion mapping techniques. J Appl Physiol 85: 353–359, 1998.[Abstract/Free Full Text]
  29. Mack GW, Nishiyasu T, and Shi X. Baroreceptor modulation of cutaneous vasodilator and sudomotor responses to thermal stress. J Physiol 483: 537–547, 1995.[ISI]
  30. Mekjavic IB and Rempel ME. Determination of esophageal probe insertion length based on standing and sitting height. J Appl Physiol 69: 376–379, 1990.[Abstract/Free Full Text]
  31. Nagaya K, Wada F, Nakamitsu S, Sagawa S, and Shiraki K. Responses of the circulatory system and muscle sympathetic nerve activity to head-down tilt in humans. Am J Physiol Regul Integr Comp Physiol 268: R1289–R1294, 1995.[Abstract/Free Full Text]
  32. Nishiyasu T, Nagashima K, Nadel E, and Mack GW. Effect of posture on cardiovascular responses to lower body positive pressure at rest and during dynamic exercise. J Appl Physiol 85: 160–167, 1998.[Abstract/Free Full Text]
  33. Shibasaki M, Sakai M, Oda M, and Crandall CG. Muscle mechanoreceptor modulation of sweat rate during recovery from moderate exercise. J Appl Physiol 96: 2115–2119, 2004.[Abstract/Free Full Text]
  34. Solack SD, Brengelmann GL, and Freund PR. Sweat rate vs. forearm blood flow during lower body negative pressure. J Appl Physiol 58: 1546–1552, 1985.[Abstract/Free Full Text]
  35. Taylor WF, Johnson JM, O'Leary S, and Park M. Effect of high local temperature on reflex cutaneous vasodilation. J Appl Physiol 57: 191–196, 1984.[Abstract/Free Full Text]
  36. Thoden J, Kenny G, Reardon F, Jette M, and Livingstone S. Disturbance of thermal homeostasis during post-exercise hyperthermia. Eur J Appl Physiol 68: 170–176, 1994.[CrossRef]
  37. Vissing S, Scherrer U, and Victor R. 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.[ISI][Medline]
  38. Wilkins BW, Minson CT, and Halliwill JR. Regional hemodynamics during postexercise hypotension II. Cutaneous circulation. J Appl Physiol 97: 2071–2076, 2004.[Abstract/Free Full Text]
  39. Wilson TE, Carter R III, Cutler MJ, Cui J, Smith ML, and Crandall CG. Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance following supine exercise. J Appl Physiol 96: 668–673, 2004.[Abstract/Free Full Text]
  40. Wilson TE, Cui J, and Crandall CG. Absence of arterial baroreflex modulation of skin sympathetic activity and sweat rate during whole-body heating in humans. J Physiol 536: 615–623, 2001.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
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]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
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]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
101/3/840    most recent
00382.2006v1
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 ISI 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 ISI Web of Science (5)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McInnis, N. H.
Right arrow Articles by Kenny, G. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McInnis, N. H.
Right arrow Articles by Kenny, G. P.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.