The effect of exercise intensity on the post-exercise esophageal temperature response

Kenny, Glen P.; Niedre, Peter C.

doi:10.1007/s00421-001-0538-4

Cited by 43 publications

(45 citation statements)

References 17 publications

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“…This finding suggests that temperature is not simply intensity dependent, which contrasts previous research (Kenny and Niedre 2002). However, the exercise intensity of 93% _ VO 2 max used in that study was much higher than that used in our current study or other research by the same group.…”

Section: Discussioncontrasting

confidence: 79%

“…These responses in skin blood flow and temperature have been reported previously by Wilkins et al (2004) who found that skin blood flow does not play and obligatory role in PEH. Furthermore, the data in this study provides support for a cardiopulmonary baroreceptor-mediated influence on postexercise skin blood flow in order to increase TPR, and suggests that post-exercise temperature regulation may be preceded by the need to regulate post-exercise blood pressure as proposed by Kenny and Niedre (2002). In summary the unique finding from this study is that the magnitude of acute PEH is clinically similar when the ''dose'' (intensity · duration) of exercise is the same for normotensive individuals.…”

Section: Discussionmentioning

confidence: 58%

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Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

et al. 2007

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The purpose of this study was to investigate the effects of exercise intensity on the magnitude of acute post-exercise hypotension while controlling for total work done over the exercise bout. Seven normotensive physically active males aged 28 +/- 6 years (mean +/- SD) completed four experimental trials, a no exercise control, 30 min of semi-recumbent cycling at 70% VO2peak (INT), cycling for 30 min at 40% VO2peak (SMOD) and cycling at 40% VO2peak for a time which corresponded to the same total work done as in the intense trial (LMOD). Blood pressure (BP), heart rate, stroke volume, cardiac output, total peripheral resistance, core body temperature and forearm skin and limb blood flow were measured prior to and for 20 min following the exercise bout. Post-exercise summary statistics were compared between trials with a one-factor general linear model. The change in systolic BP, averaged over the 20-min post-exercise period was significantly lower only following the INT (-5 +/- 3 mm Hg) and LMOD exercise (-1 +/- 7 mm Hg) compared to values in control (P < 0.04). The changes in systolic BP and MAP following INT and LMOD were not significantly different from each other (P > 0.05). Similar results were obtained when the minimum values of these variables recorded during the post-exercise period were compared. Mean changes in cardiac output (1.9 +/- 0.3 l min(-1)) and total peripheral resistance (-3 +/- 1 mm Hg l(-1 )min(-1)) after INT exercise were also different from those in CON (P < 0.0005). The acute post-exercise reduction in BP was clinically similar following high intensity short duration exercise and moderate intensity longer duration exercise that was matched for total work done.

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Section: Discussioncontrasting

confidence: 79%

Section: Discussionmentioning

confidence: 58%

Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

et al. 2007

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“…A number of studies have shown that the duration of the postexercise hypotension in normotensive individuals may vary between 1 and 2 h after exercise (17) and that the magnitude of the response is influenced by the intensity of exercise (12). The blood pressure and HR data are consistent with a postexercise hypotensive response.…”

Section: Discussionsupporting

confidence: 66%

Effect of exercise intensity on the postexercise sweating threshold

Kenny

Périard

Journeay³

et al. 2003

Journal of Applied Physiology

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The hypothesis that the magnitude of the postexercise onset threshold for sweating is increased by the intensity of exercise was tested in eight subjects. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects remained seated resting for 15 min (no exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption (V O2 peak) followed by a 20-min seated recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The suit was first perfused with 20°C water to control and stabilize skin and core temperature before whole body heating. Subsequently, the skin was heated (ϳ4.0°C/h) until sweating occurred. Exercise resulted in an increase in the onset threshold for sweating of 0.11 Ϯ 0.02, 0.23 Ϯ 0.01, and 0.33 Ϯ 0.02°C above that measured for the no-exercise resting values (P Ͻ 0.05) for the 55, 70, and 85% of V O2 peak exercise conditions, respectively. We did note that there was a greater postexercise hypotension as a function of exercise intensity as measured at the end of the 20-min exercise recovery. Thus it is plausible that the increase in postexercise threshold may be related to postexercise hypotension. It is concluded that the sweating response during upright recovery is significantly modified by exercise intensity and may likely be influenced by the nonthermal baroreceptor reflex adjustments postexercise. sudomotor activity; baroreceptor reflexes; heat loss; thermoregulation RECENT STUDIES INDICATE THAT exercise induces a residual effect on thermal control, resulting in an increase in the postexercise esophageal temperature at which sweating occurs (11,13). Although the mechanism(s) for thermoregulatory control of sweating before and during exercise has been evaluated, there remains a lack of information on its nature and role during postexercise temperature regulation. Various studies have shown that the sweating response during exercise not only involves changes in thermal factors, such as core and skin temperatures (4, 23, 24), but also nonthermal factors, including central command, baroreceptors, mechanoreceptors, and metaboreceptors (15,24,30). This is in contrast to passive heating at rest, in which the primary stimuli for sweating is thought to be a factor of thermal origin (25).More recently, it has been shown that the postexercise sweating response is to some degree influenced by nonthermal baroreflex control (10). Specifically, the modification of postexercise venous pooling by lower body positive pressure results in a lowering of the resting postexercise elevation in the onset threshold for sweating. However, the mechanism of control is still unknown. Dynamic exercise is known to result in postexercise hypotension in the upright position (3,6,7,14,18,26,27). During postexercise hypotension, mean arterial pressure (MAP) is reduced subsequent to both neural and vascular activity (6-8). This postexercise hypotension is ...

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“…Specifically, exercise induces a residual effect on thermal control, resulting in an increase of ~0.3-0.4 °C in the postexercise esophageal temperature at which cutaneous vasodilation and sweating (Kenny et al, 2000a) occurs. Furthermore, an increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was shown to result in a relative increase in the onset thresholds for cutaneous vasodilation (Kenny et al, 2003a) and ecrrine sweating (Kenny et al, 2003b), an overall decrease in the rate of heat loss, and a concomitant increase in the postexercise core temperature recovery time (Kenny and Neidre, 2002). These observations suggest a possible physiological link between the observed postexercise cardiovascular changes and the altered thermal response thresholds for cutaneous vasodilation and sweating.…”

Section: Introductionmentioning

confidence: 94%

The Postexercise Increase in the Threshold for Cutaneous Vasodilation and Sweating is Not Observed With Extended Recovery

Kenny

Journeay²

2005

Can. J. Appl. Physiol.

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The following study was conducted to evaluate the hypothesis that an increase in the postexercise onset threshold for cutaneous vasodilation (Th(VD)) and sweating (Th(SW)) would not be observed upon the restoration of baseline mean arterial pressure (MAP). Subjects remained either seated resting for 15 min or performed 15 min of treadmill running at 70% VO2peak followed by either 20- (short) or 60-min (extended) recovery. At the end of each recovery protocol (20 and 60 min) a water perfusion suit was then used to increase mean skin temperature until Th(VD) and Th(SW) was noted. Exercise resulted in an increase in Th(VD) and Th(SW) of 0.24 +/- 0.03 and 0.24 +/- 0.02 degrees C, respectively, above no-exercise for the short recovery (p < 0.05). No increase was measured for the extended recovery. Postexercise MAP was significantly reduced prior to whole-body warming for the short recovery whereas no reduction was measured for the extended recovery. The increase in Th(VD) and Th(SW), measured during the early stages of recovery, is reversed with the reestablishment of baseline MAP.

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The effect of exercise intensity on the post-exercise esophageal temperature response

Cited by 43 publications

References 17 publications

Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

Effect of exercise intensity on the postexercise sweating threshold

The Postexercise Increase in the Threshold for Cutaneous Vasodilation and Sweating is Not Observed With Extended Recovery

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