Increasing exercise duration does not affect the postexercise elevation in esophageal temperature.

It has previously been observed that (a) following 15 min of intense exercise, esophageal temperature (Tes) remains elevated at a plateau value equal to that at which active vasodilation had occurred during exercise (i.e., esophageal temperature threshold for cutaneous vasodilation [ThVD]); and (b) exercise/recovery cycles of identical intensity and duration, when sequential, result in progressively higher Tes at the beginning and end of exercise. In the latter case, parallel increases in both the exercise ThVD and postexercise plateau of Tes were noted. This study was conducted to determine if the elevated postexercise Tes is related to increases in whole-body heat content. On separate occasions, 9 subjects completed 3 bouts of treadmill exercise at 70% VO2 max, 29 degrees C ambient temperature. Each exercise bout lasted either 15, 30, or 45 min and was followed by 60 min of inactive recovery. Esophageal temperatures were similar at the start of each exercise bout, but the rise in Tes during exercise nearly doubled from 1.0 degree C after 15 min of exercise to 1.9 degrees C after 45 min of exercise. There were no intercondition differences among the exercise ThVD (approximately 0.36 degree C above baseline) or postexercise plateau values for Tes (approximately 0.40 degree C above baseline). Thus the relationship between the ThVD during exercise and the postexercise Tes did not appear to be dependent on changes in whole-body heat content as produced by endogenous heating during exercise of different duration.

Changes in exercise and post-exercise core temperature under different clothing conditions.

This study evaluates the effect of different levels of insulation on esophageal (Tes) and rectal (Tre) temperature responses during and following moderate exercise. Seven subjects completed three 18-min bouts of treadmill exercise (75% VO2max, 22 degrees C ambient temperature) followed by 30 min of recovery wearing either: (1) jogging shoes, T-shirt and shorts (athletic clothing); (2) single-knit commercial coveralls worn over the athletic clothing (coveralls); or (3) a Canadian Armed Forces nuclear, bacteriological and chemical warfare protective overgarment with hood, worn over the athletic clothing (NBCW overgarment). Tes was similar at the start of exercise for each condition and baseline Tre was approximately 0.4 degree C higher than Tes. The hourly equivalent rate of increase in Tes during the final 5 min of exercise was 1.8 degrees C, 3.0 degrees C and 4.2 degrees C for athletic clothing, coveralls and NBCW overgarment respectively (P < 0.05). End-exercise Tes was significantly different between conditions [37.7 degrees C (SEM 0.1 degree C), 38.2 degrees C (SEM 0.2 degree C and 38.5 degrees C (SEM 0.2 degree C) for athletic clothing, coveralls and NBCW overgarment respectively)] (P < 0.05). No comparable difference in the rate of temperature increase for Tre was demonstrated, except that end-exercise Tre for the NBCW overgarment condition was significantly greater (0.5 degree C) than that for the athletic clothing condition. There was a drop in Tes during the initial minutes of recovery to sustained plateaus which were significantly (P < 0.05) elevated above pre-exercise resting values by 0.6 degree C, 0.8 degree C and 1.0 degree C, for athletic clothing, coveralls, and NBCW overgarment, respectively. Post-exercise Tre decreased very gradually from end-exercise values during the 30-min recovery. Only the NBCW overgarment condition Tre was significantly elevated (0.3 degree C) above the athletic clothing condition (P < 0.05). In conclusion, Tes is far more sensitive in reflecting the heat stress of different levels of insulation during exercise and post-exercise than Tre. Physiological mechanisms are discussed as possible explanations for the differences in response.

The effect of ambient temperature and exercise intensity on post-exercise thermal homeostasis.

We have previously demonstrated a prolonged (65 min or longer) elevated plateau of esophageal temperature (T(es)) (0.5-0.6 degrees C above pre-exercise values) in humans following heavy dynamic exercise (70% maximal oxygen consumption, VO2max) at a thermoneutral temperature (T(a)) of 29 degrees C. The elevated T(es) value was equal to the threshold T(es) at which active skin vasodilation was initiated during exercise (Th(dil)). A subsequent observation. i.e., that successive exercise/recovery cycles (performed at progressively increasing pre-exercise T(es) levels) produced parallel increases of Th(dil) and the post-exercise T(es), further supports a physiological relationship between these two variables. However, since all of these tests have been conducted at the same T(a) (29 degrees C) and exercise intensity (70% VO2max) it is possible that the relationship is limited to a narrow range of T(a)/exercise intensity conditions. Therefore, five male subjects completed 18 min of treadmill exercise followed by 20 min of recovery in the following T(a)/exercise intensity conditions: (1) cool with light exercise, T(a) = 20 degrees C, 45% VO2max (CL); (2) temperature with heavy exercise, T(a) = 24 degrees C, 75% VO2max (TH); (3) warm with heavy exercise, T(a) = 29 degrees C, 75% VO2max (WH); and (4) hot with light exercise, T(a) = 40 degrees C, 45% VO2max (HL). An abrupt decrease in the forearm-to-finger temperature gradient (T(fa) - T(fi)) was used to identify the Th(dil) during exercise. Mean pre-exercise T(es) values were 36.80, 36.60, 36.72, and 37.20 degrees C for CL, TH, WH, and HL conditions respectively. T(es) increased during exercise, and end post-exercise fell to stable values of 37.13, 37.19, 37.29, and 37.55 degrees C for CL, TH, WH, and HL trials respectively. Each plateau value was significantly higher than pre-exercise values (P < 0.05). Correspondingly, Th(dil) values (i.e., 37.20, 37.23, 37.37, and 37.48 degrees C for CL, TH, WH, and HL) were comparable to the post-exercise T(es) values for each condition. The relationship between Th(dil) and post-exercise T(es) remained intact in all T(a)/exercise intensity conditions, providing further evidence that the relationship between these two variables is physiological and not coincidental.

Intense exercise increases the post-exercise threshold for sweating.

We demonstrated previously that esophageal temperature (T(es)) remains elevated by approximately 0.5 degrees C for at least 65 min after intense exercise. Following exercise, average skin temperature (T(avg)) and skin blood flow returned rapidly to pre-exercise values even though T(es) remained elevated, indicating that the T(es) threshold for vasodilation is elevated during this period. The present study evaluates the hypothesis that the threshold for sweating is also increased following intense exercise. Four males and three females were immersed in water (water temperature, T(w) = 42 degrees C) until onset of sweating (Immersion 1), followed by recovery in air (air temperature, T(a) = 24 degrees C). At a T(a) of 24 degrees C, 15 min of cycle ergometry (70% VO2max) (Exercise) was then followed by 30 min of recovery. Subjects were then immersed again (T(w) = 42 degrees C) until onset of sweating (Immersion 2). Baseline T(es) and T(skavg) were 37.0 (0.1) degrees C and 32.3 (0.3) degrees C, respectively. Because the T(skavg) at the onset of sweating was different during Exercise [30.9 (0.3) degrees C] than during Immersion 1 and Immersion 2 [36.8 (0.2) degrees C and 36.4 (0.2) degrees C, respectively] a corrected core temperature, T((es) (calculated)), was calculated at a single designated skin temperature, T((sk)(designated)), as follows: T((es)(calculated)) = T(es) + [beta/(1-beta)][T(skavg)-T((sk)(designated))]. The T((sk)(designated)) was set at 36.5 degrees C (mean of Immersion 1 and Immersion 2 conditions) and beta represents the fractional contribution of T(skavg) to the sweating response (beta for sweating = 0.1). While T((es)(calculated)) at the onset of sweating was significantly lower during exercise [36.7 (0.2) degrees C] than during Immersion 1 [37.1 (0.1) degrees C], the threshold of sweating during Immersion 2 [37.3 (0.1) degrees C] was greater than during both Exercise and Immersion 1 (P < 0.05). We conclude that intense exercise decreases the sweating threshold during exercise itself, but elicits a subsequent short-term increase in the resting sweating threshold.

Post-exercise thermal homeostasis as a function of changes in pre-exercise core temperature.

We have previously reported that, following continuous exercise, a prolonged elevated plateau of esophageal temperature (Tes) was directly related to the Tes at the time of cutaneous vasodilation (Thdil) during exercise. In order to investigate the hypothesis that the factors which result in an increase of the post-exercise Thdil and define the post-exercise Tes elevation are related to pre-exercise Tes, nine healthy, young [24.0 (1.9) years], non-training males rested at 29 degrees C, 50% humidity for > 1 h (control). They then completed three successive cycles of 15 min treadmill running at 70% maximal oxygen consumption (VO2max) followed by 30 min rest. Esophageal, rectal (Tre) and skin (Tsk) temperatures and forearm cutaneous blood flow were recorded at 5-s intervals throughout. Laser-Doppler flowmetry of forearm skin blood flow was used to identify the Thdil during exercise. Pre-exercise Tes was 36.74 (0.25) degrees C and post-exercise Tes fell to stable and significant (P < 0.05) elevations above pre-exercise values at 37.22 (0.27) degrees C, 37.37 (0.27) degrees C and 37.48 (0.26) degrees C following each successive work bout respectively. Correspondingly, Thdil during each work bout rose in proportion to, and was not different than, the post-exercise Tes in the following recovery [37.20(0.23) degrees C, 37.41 (0.24) degrees C and 37.58 (0.24) degrees C]. Although the increases were less with each successive exercise bout, the differences between each exercise bout, in terms of post-exercise Tes and Thdil values, were significant (P < 0.05). These results reinforce our previous observations of elevations in Thdil and post-exercise Tes after a single exercise bout and lead to the tentative conclusions that (1) pre-exercise Tes has a direct influence on Thdil and post-exercise Tes, and (2) the exercise-induced increase of Thdil persists into recovery, influencing post-exercise thermal recovery.

A comparison of human thermoregulatory response following dynamic exercise and warm-water immersion.

We tested the hypothesis that the prolonged elevated plateau of esophageal temperature (Tes) following moderate exercise is a function of some exercise-related factors and not the increase in heat content and Tes during exercise, by comparing the response to increase Tes during exercise (endogenous heating) and warm-water immersion (exogenous heating). Nine healthy, young [24.0 (1.9) years] subjects performed two separate experiments: (1) 15 min of treadmill exercise at 70% (VO2max) and 15 min rest in a climatic chamber at 29 degrees C, followed by 15 min of immersion in a 42 degrees C water bath and a further 60 min of recovery in the climatic chamber [exercise-water (EW)]; and (2) 15 min of immersion in a 42 degrees C water bath followed by 60 min of recovery in the climatic chamber [water-only (WO)]. Esophageal (Tes) and skin (Tsk) temperatures were recorded at 5-s intervals throughout. The Tes at which the forearm to finger temperature gradient (Tfa-Tfi) abruptly decreases was used to identify the threshold for forearm cutaneous vessel dilation (Thdil) during exercise. Pre-exercise Tes values were 36.64 degrees C and 36.74 degrees C for EW and WO respectively. The EW post-exercise Tes value fell to a stable level of 37.12 degrees C and this value differed by 0.48 degree C (P < 0.05) from baseline, but was similar to Thdil (37.09 degrees C). Despite a 1.2 degrees C increase in Tes during the subsequent warm-water immersion, Tes returned to the post-exercise value (37.11 degrees C). The WO post-immersion Tes fell to a stable plateau of 36.9 degrees C, which was not statistically different from the pre-immersion Tes. The data for both warm-water treatments support the hypothesis that increases in Tes and heat content alone are not the primary mechanisms for the post-exercise elevation in Tes and Thdil. These data also support our previous observation that the exercise-induced elevation in Thdil persists into recovery.

A comparative analysis of physiological responses at submaximal workloads during different laboratory simulations of field cycling.

The purpose of this study was to evaluate the relationships between heart rate (fc), oxygen consumption (VO2), peak force and average force developed at the crank in response to submaximal exercise employing a racing bicycle which was attached to an ergometer (RE), ridden on a treadmill (TC) and ridden on a 400-m track (FC). Eight male trained competitive cyclists rode at three pre-determined work intensities set at a proportion of their maximal oxygen consumption (VO2max): (1) below lactate threshold [work load that produces a VO2 which is 10% less than the lactate threshold VO2 (sub-LT)], (2) lactate threshold VO2 (LT), and (3) above lactate threshold [workload that produces a VO2 which is 10% greater than lactate threshold VO2 (supra-LT)], and equated across exercise modes on the basis of fc. Voltage signals from the crank arm were recorded as FM signals for subsequent representation of peak and average force. Open circuit VO2 measurements were done in the field by Douglas bag gas collection and in the laboratory by automated gas collection and analysis. fc was recorded with a telemeter (Polar Electro Sport Tester, PE3000). Significant differences (P < 0.05) were observed: (1) in VO2 between FC and both laboratory conditions at sub-LT intensity and LT intensities, (2) in peak force between FC and TC at sub-LT intensity, (3) in average force between FC and RE at sub-LT. No significant differences were demonstrated at supra-LT intensity for VO2. Similarly no significant differences were observed in peak and average force for either LT or supra-LT intensities. These data indicate that equating work intensities on the basis of fc measured in laboratory conditions would overestimate the VO2 which would be generated in the field and conversely, that using fc measured in the laboratory to establish field work intensity would underestimate mechanical workload experienced in the field.

The influence of extracellular buffer concentration and propionate on lactate efflux from frog muscle.

Lactate efflux from frog sartorius muscles was measured following a lactate load of about 18 mumol X g-1 induced by a 4-min period of stimulation. Lactate efflux rate was buffer concentration dependent. The initial efflux rate increased from about 150 nmol X g-1 X min-1 in 1 mM MOPS buffer to 400 nmol X g-1 X min-1 in 25 mM MOPS buffer. The addition of 20 mM propionate reduced mean intracellular pH by about 0.2 units and increased lactate efflux rate by 70% at the highest buffer concentration and 400% at the lowest buffer concentration. The observed results are in reasonable agreement with predictions based on a model in which net efflux is limited by diffusion of both buffer and lactate in the extracellular space. Transmembrane lactate efflux appears to consist of two components, one of which is proton linked and carried either by undissociated lactic acid or coupled proton-lactate transport, the other being carried by independent lactate ions.