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Biomedical subjects

G P Kenny

Publications and source records attributed to G P Kenny.

At least 19 recordsLinked to original sources
PubMed2005

Safe cooling limits from exercise-induced hyperthermia.

We evaluated the cooling rate of hyperthermic subjects, as measured by three estimates of deep core temperatures (esophageal, rectal and aural canal temperatures), during immersion in a range of water temperatures. The objective of the study was to compare the three indices of core temperature and define safe cooling limits when using rectal temperature to avoid the development of hypothermia. On 4 separate days, seven subjects (four males, three females) exercised for 45.4+/-4.1 min at 65% V(O2)max at an ambient temperature of 39 degrees C, RH: 36.5%, until rectal temperature (T (re)) increased to 40.0 degrees C (39.5 degrees C for two subjects). Following exercise, the subjects were immersed in a circulated water bath controlled at 2, 8, 14 and 20 degrees C until T (re) returned to 37.5 degrees C. When T (re) reached normothermia during the cooling period (37.5+/-0.05 degrees C), both esophageal (T (es)) (35.6+/-1.3 degrees C) and aural canal (T (ac)) (35.9+/-0.9 degrees C) temperatures were approaching or reaching hypothermia, particularly during immersion in 2 degrees C water (T (es)=34.5+/-1.2 degrees C). On the basis of the heat loss data, the heat gained during the exercise was fully eliminated after 5.4+/-1.5, 7.9+/-2.9, 10.4+/-3.8 and 13.1+/-2.8 min of immersion in 2, 8, 14 and 20 degrees C water, respectively, with the coldest water showing a significantly faster cooling rate. During the immersion in 2 degrees C water, a decrease of only 1.5 degrees C in T (re) resulted in the elimination of 100% of the heat gained during exercise without causing hypothermia. This study would therefore support cooling the core temperature of hyperthermic subjects to a rectal temperature between 37.8 degrees C (during immersion in water >10 degrees C) and 38.6 degrees C (during immersion in water <10 degrees C) to eliminate the heat gained during exercise without causing hypothermia.

Adult↗
PubMed2003

Meta-analysis of the effect of structured exercise training on cardiorespiratory fitness in Type 2 diabetes mellitus.

AIMS/HYPOTHESIS: Low cardiorespiratory fitness is a powerful and independent predictor of mortality in people with diabetes. Several studies have examined the effects of exercise on cardiorespiratory fitness in Type 2 diabetic individuals. However, these studies had relatively small sample sizes and highly variable results. Therefore the aim of this study was to systematically review and quantify the effects of exercise on cardiorespiratory fitness in Type 2 diabetic individuals. METHODS: MEDLINE, EMBASE, and four other databases were searched up to March 2002 for randomized, controlled trials evaluating effects of structured aerobic exercise interventions of 8 weeks or more on cardiorespiratory fitness in adults with Type 2 diabetes. Cardiorespiratory fitness was defined as maximal oxygen uptake (VO(2max)) during a maximal exercise test. RESULTS: Seven studies, presenting data for nine randomized trials comparing exercise and control groups (overall n=266), met the inclusion criteria. Mean exercise characteristics were as follows: 3.4 sessions per week, 49 min per session for 20 weeks. Exercise intensity ranged from 50% to 75% of VO(2max). There was an 11.8% increase in VO(2max) in the exercise group and a 1.0% decrease in the control group (post intervention standardized mean difference =0.53, p<0.003). Studies with higher exercise intensities tended to produce larger improvements in VO(2max). Exercise intensity predicted post-intervention weighted mean difference in HbA(1c) (r=-0.91, p=0.002) to a larger extent than did exercise volume (r=-0.46, p=0.26). CONCLUSIONS/INTERPRETATION: Regular exercise has a statistically and clinically significant effect on VO(2max) in Type 2 diabetic individuals. Higher intensity exercise could have additional benefits on cardiorespiratory fitness and HbA(1c).

Databases, Factual↗
PubMed2003

Muscle temperature transients before, during, and after exercise measured using an intramuscular multisensor probe.

Seven subjects (1 woman) performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their maximal oxygen consumption during bilateral knee extensions (Vo(2 sp)). A multisensor thermal probe was inserted into the left vastus medialis (middiaphysis) under ultrasound guidance. The deepest sensor (tip) was located approximately 10 mm from the femur and deep femoral artery (T(mu 10)), with additional sensors located 15 (T(mu 25)) and 30 mm (T(mu 40)) from the tip. Esophageal temperature (T(es)) was measured as an index of core temperature. Subjects rested in an upright seated position for 60 min in an ambient condition of 22 degrees C. They then performed 15 min of isolated bilateral knee extensions (60% of Vo(2 sp)) on a Kin-Com, followed by 60 min of recovery. Resting T(es) was 36.80 degrees C, whereas T(mu 10), T(mu 25), and T(mu 40) were 36.14, 35.86, and 35.01 degrees C, respectively. Exercise resulted in a T(es) increase of 0.55 degrees C above preexercise resting, whereas muscle temperature of the exercising leg increased by 2.00, 2.37, and 3.20 degrees C for T(mu 10), T(mu 25), and T(mu 40), respectively. Postexercise T(es) showed a rapid decrease followed by a prolonged sustained elevation approximately 0.3 degrees C above resting. Muscle temperature decreased gradually over the course of recovery, with values remaining significantly elevated by 0.92, 1.05, and 1.77 degrees C for T(mu 10), T(mu 25), and T(mu 40), respectively, at end of recovery (P < 0.05). These results suggest that the transfer of residual heat from previously active musculature may contribute to the sustained elevation in postexercise T(es).

Adult↗
PubMed2002

Effect of water temperature on cooling efficiency during hyperthermia in humans.

We evaluated the cooling rate of hyperthermic subjects, as measured by rectal temperature (T(re)), during immersion in a range of water temperatures. On 4 separate days, seven subjects (4 men, 3 women) exercised at 65% maximal oxygen consumption at an ambient temperature of 39 degrees C until T(re) increased to 40 degrees C (45.4 +/- 4.1 min). After exercise, the subjects were immersed in a circulated water bath controlled at 2, 8, 14, or 20 degrees C until T(re) returned to 37.5 degrees C. No difference in cooling rate was observed between the immersions at 8, 14, and 20 degrees C despite the differences in the skin surface-to-water temperature gradient, possibly because of the presence of shivering at 8 and 14 degrees C. Compared with the other conditions, however, the rate of cooling (0.35 +/- 0.14 degrees C/min) was significantly greater during the 2 degrees C water immersion, in which shivering was seldom observed. This rate was almost twice as much as the other conditions (P < 0.05). Our results suggest that 2 degrees C water is the most effective immersion treatment for exercise-induced hyperthermia.

Adult↗
PubMed2001

Effects of exercise on glycemic control and body mass in type 2 diabetes mellitus: a meta-analysis of controlled clinical trials.

CONTEXT: Exercise is widely perceived to be beneficial for glycemic control and weight loss in patients with type 2 diabetes. However, clinical trials on the effects of exercise in patients with type 2 diabetes have had small sample sizes and conflicting results. OBJECTIVE: To systematically review and quantify the effect of exercise on glycosylated hemoglobin (HbA(1c)) and body mass in patients with type 2 diabetes. DATA SOURCES: Database searches of MEDLINE, EMBASE, Sport Discuss, Health Star, Dissertation Abstracts, and the Cochrane Controlled Trials Register for the period up to and including December 2000. Additional data sources included bibliographies of textbooks and articles identified by the database searches. STUDY SELECTION: We selected studies that evaluated the effects of exercise interventions (duration >/=8 weeks) in adults with type 2 diabetes. Fourteen (11 randomized and 3 nonrandomized) controlled trials were included. Studies that included drug cointerventions were excluded. DATA EXTRACTION: Two reviewers independently extracted baseline and postintervention means and SDs for the intervention and control groups. The characteristics of the exercise interventions and the methodological quality of the trials were also extracted. DATA SYNTHESIS: Twelve aerobic training studies (mean [SD], 3.4 [0.9] times/week for 18 [15] weeks) and 2 resistance training studies (mean [SD], 10 [0.7] exercises, 2.5 [0.7] sets, 13 [0.7] repetitions, 2.5 [0.4] times/week for 15 [10] weeks) were included in the analyses. The weighted mean postintervention HbA(1c) was lower in the exercise groups compared with the control groups (7.65% vs 8.31%; weighted mean difference, -0.66%; P<.001). The difference in postintervention body mass between exercise groups and control groups was not significant (83.02 kg vs 82.48 kg; weighted mean difference, 0.54; P =.76). CONCLUSION: Exercise training reduces HbA(1c) by an amount that should decrease the risk of diabetic complications, but no significantly greater change in body mass was found when exercise groups were compared with control groups.

Adult↗
PubMed2000

Acute head-down tilt decreases the postexercise resting threshold for forearm cutaneous vasodilation.

The purpose of this study was to evaluate the role of baroreceptor control on the postexercise threshold for forearm cutaneous vasodilation. On four separate days, six subjects (1 woman) were randomly exposed to 65 degrees head-up tilt and to 15 degrees head-down tilt during a No-Exercise and Exercise treatment protocol. Under each condition, a whole body water-perfused suit was used to regulate mean skin temperature (T(sk)) in the following sequence: 1) cooling until the threshold for vasoconstriction was evident; 2) heating ( approximately 7.0 degrees C/h) until vasodilation occurred; and 3) cooling until esophageal temperature (T(es)) and (T(sk)) returned to baseline values. The Exercise treatment consisted of 15 min of cycling exercise at 70% maximal O(2) uptake, followed by 15 min of recovery in the head-up tilt position. The No-Exercise treatment consisted of 30 min resting in the head-up tilt position. After the treatment protocols, subjects were returned to their pretreatment condition, then cooled and warmed again consecutively. The calculated T(es) threshold for cutaneous vasodilation increased 0.24 degrees C postexercise during head-up tilt (P < 0.05), whereas no difference was measured during head-down tilt. In contrast, sequential measurements without exercise demonstrate a time-dependent decrease for head-up tilt (0.17 degrees C) and no difference for head-down tilt. Pretreatment thresholds were significantly lower during head-down tilt compared with head-up tilt. We have shown that manipulating postexercise venous pooling by means of head-down tilt, in an effort to reverse its impact on baroreceptor unloading, resulted in a relative lowering of the resting postexercise elevation in the T(es) for forearm cutaneous vasodilation.

Adult↗
PubMed2000

Moderate exercise increases the post exercise resting warm thermoregulatory response thresholds.

BACKGROUND: The purpose of this study was to evaluate the effect of exercise on the subsequent post-exercise core temperature thresholds for vasodilation and sweating. METHODS: On two separate days, with 6 subjects (3 males and 3 females), a whole-body water-perfused suit decreased mean skin temperature until the threshold for vasoconstriction was demonstrated. Mean skin temperature was then slowly increased (approximately 5.0 degrees C x h(-1)) until thresholds for vasodilation and sweating were clearly established. Subjects were cooled by decreasing water temperature until both esophageal and mean skin temperatures returned to near baseline values. Subjects then either performed 15 min of cycle ergometry (60% V(O2max)) followed by 30 min of recovery (Exercise), or remained seated with no exercise for 45 min (Control). Subjects were then cooled again until the onset of cutaneous vasoconstriction followed by a second warming period. The core temperature thresholds for vasodilation and sweating increased significantly by 0.49 degrees C and 0.19 degrees C post-exercise, respectively (p < 0.05). In order to compare thresholds between conditions in which both esophageal and mean skin temperatures were changing, we mathematically compensated for changes in skin temperatures using the established linear cutaneous contribution of skin to the control of vasodilation and sweating (10%). RESULTS: The calculated core temperature threshold (at a designated skin temperature of 36.0 degrees C) for vasodilation increased significantly from 36.56 +/- 0.12 degrees C to 37.11 +/- 0.21 degrees C post-exercise (p < 0.01). Likewise, the sweating threshold increased from 36.79 +/- 0.18 degrees C to 37.05 +/- 0.23 degrees C postexercise (p < 0.01). In contrast, sequential measurements, without exercise, demonstrate a time-dependent decrease (0.18 degrees C) in the sweating threshold, with no difference in the vasodilation threshold. CONCLUSION: These data indicate that exercise has a prolonged effect by increasing the post-exercise thresholds for both warm thermoregulatory responses.

Body Temperature Regulation↗
PubMed1999

The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion.

The purpose of this study was to evaluate the effect of exercise on the subsequent post-exercise thresholds for vasoconstriction and shivering measured during water immersion. On 2 separate days, seven subjects (six males and one female) were immersed in water (37.5 degrees C) that was subsequently cooled at a constant rate of approximately 6.5 degrees C x h(-1) until the thresholds for vasoconstriction and shivering were clearly established. Water temperature was then increased to 37.5 degrees C. Subjects remained immersed for approximately 20 min, after which they exited the water, were towel-dried and sat in room air (22 degrees C) until both esophageal temperature and mean skin temperature (Tsk) returned to near-baseline values. Subjects then either performed 15 min of cycle ergometry (at 65% maximal oxygen consumption) followed by 30 min of recovery (Exercise), or remained seated with no exercise for 45 min (Control). Subjects were then cooled again. The core temperature thresholds for both vasoconstriction and shivering increased significantly by 0.2 degrees C Post-Exercise (P < 0.05). Because the Tsk at the onset of vasoconstriction and shivering was different during Pre- and Post-Exercise Cooling, we compensated mathematically for changes in skin temperatures using the established linear cutaneous contribution of skin to the control of vasoconstriction and shivering (20%). The calculated core temperature threshold (at a designated skin temperature of 32.0 degrees C) for vasoconstriction increased significantly from 37.1 (0.3) degrees C to 37.5 ( 0.3) degrees C post-exercise (P < 0.05). Likewise, the shivering threshold increased from 36.2 (0.3) degrees C to 36.5 (0.3) degrees C post-exercise (P < 0.05). In contrast to the post-exercise increase in cold thermal response thresholds, sequential measurements demonstrated a time-dependent similarity in the Pre- and Post-Control thresholds for vasoconstriction and shivering. These data indicate that exercise has a prolonged effect on the post-exercise thresholds for both cold thermoregulatory responses.

Adult↗
PubMed1999

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.

Adult↗
PubMed1999

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.

Adult↗
PubMed1998

Moderate exercise increases postexercise thresholds for vasoconstriction and shivering.

The purpose of this study was to evaluate the effect of exercise on the subsequent postexercise thresholds for vasoconstriction and shivering. On two separate days, with six subjects (3 women), a whole body water-perfused suit slowly decreased mean skin temperature (approximately 7.0 degreesC/h) until thresholds for vasoconstriction and shivering were clearly established. Subjects were then rewarmed by increasing water temperature until both esophageal and mean skin temperatures returned to near-baseline values. Subjects either performed 15 min of cycle ergometry (65% maximal O2 consumption) followed by 30 min of recovery (Exercise) or remained seated with no exercise for 45 min (Control). Subjects were then cooled again. We mathematically compensated for changes in skin temperatures by using the established linear cutaneous contribution of skin to the control of vasoconstriction and shivering (20%). The calculated core temperature threshold (at a designated skin temperature of 30.0 degreesC) for vasoconstriction increased significantly from 36.64 +/- 0.20 to 36.89 +/- 0.22 degreesC postexercise (P < 0.01). Similarly, the shivering threshold increased from 35.73 +/- 0.13 to 36.13 +/- 0.12 degreesC postexercise (P < 0.01). In contrast, sequential measurements, without exercise, demonstrate a time-dependent decrease in both the vasoconstriction (0.10 degreesC) and shivering (0.12 degreesC) thresholds. These data indicate that exercise has a prolonged effect by increasing the postexercise thresholds for both cold thermoregulatory responses.

Adult↗
PubMed1997

Clonidine decreases vasoconstriction and shivering thresholds, without affecting the sweating threshold.

PURPOSE: This study was conducted to test the hypothesis that clonidine produces a dose-dependent increase in the sweating threshold and dose-dependent decreases in vasoconstriction and shivering thresholds. METHODS: Six healthy subjects (two female) were studied on four days after taking clonidine in oral doses of either 0 (control), 3, 6 or 9 micrograms.kg-1. The order followed a balanced design in a double-blind fashion. Oesophageal temperature and mean skin temperature (from 12 sites) were measured. Subjects were seated in 37 degrees C water which was gradually warmed until sweating occurred (sweat rate increased above 50 g.m-2.h-1). The water was then cooled gradually until thresholds for vasoconstriction (onset of sustained decrease in fingertip blood flow) and shivering (sustained elevation in metabolism) were determined. Thresholds were then referred to as the core temperature, adjusted to a designated mean skin temperature of 33 degrees C. RESULTS: High dose clonidine similarly decreased the adjusted core temperature thresholds for vasoconstriction by 1.16 +/- 0.30 degrees C and for shivering by 1.63 +/- 0.23 degrees C (P < 0.01). The dose response effects were linear for both cold responses with vasoconstriction and shivering thresholds decreasing by 0.13 +/- 0.05 and 0.19 +/- 0.09 degree C.microgram-1 respectively (P < 0.0001). The sweating threshold was unaffected by clonidine, however the interthreshold range between sweating and vasoconstriction thresholds increased from control (0.19 +/- 0.48 degree C) to high dose clonidine (1.31 +/- 0.54 degrees C). CONCLUSION: The decreases in core temperature thresholds for cold responses and increased interthreshold range are consistent with the effects of several anaesthetic agents and opioids and is indicative of central thermoregulatory inhibition.

Adrenergic alpha-Agonists↗
PubMed1997

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.

Adult↗
PubMed1997

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.

Adult↗
PubMed1997

Inhibition of shivering increases core temperature afterdrop and attenuates rewarming in hypothermic humans.

During severe hypothermia, shivering is absent. To simulate severe hypothermia, shivering in eight mildly hypothermic subjects was inhibited with meperidine (1.5 mg/kg). Subjects were cooled twice (meperidine and control trials) in 8 degrees C water to a core temperature of 35.9 +/- 0.5 (SD) degrees C, dried, and then placed in sleeping bags. Meperidine caused a 3.2-fold increase in core temperature afterdrop (1.1 +/- 0.6 vs. 0.4 +/- 0.2 degree C), a 4.3-fold increase in afterdrop duration (89.4 +/- 31.4 vs. 20.9 +/- 5.7 min), and a 37% decrease in rewarming rate (1.2 +/- 0.5 vs. 1.9 +/- 0.9 degrees C/h). Meperidine inhibited overt shivering. Oxygen consumption, minute ventilation, and heart rate decreased after meperidine injection but subsequently returned toward preinjection values after 45 min postimmersion. This was likely due to the increased thermoregulatory drive with the greater afterdrop and the short half-life of meperidine. These results demonstrate the effectiveness of shivering heat production in attenuating the postcooling afterdrop of core temperature and potentiating core rewarming. The meperidine protocol may be valuable for comparing the efficacy of various hypothermia rewarming methods in the absence of shivering.

Adult↗
PubMed1997

Efficacy of forced-air and inhalation rewarming by using a human model for severe hypothermia.

We recently developed a nonshivering human model for severe hypothermia by using meperidine to inhibit shivering in mildly hypothermic subjects. This thermal model was used to evaluate warming techniques. On three occasions, eight subjects were immersed for approximately 25 min in 9 degrees C water. Meperidine (1.5 mg/kg) was injected before the subjects exited the water. Subjects were then removed, insulated, and rewarmed in an ambient temperature of -20 degrees C with either 1) spontaneous rewarming (control), 2) inhalation rewarming with saturated air at approximately 43 degrees C, or 3) forced-air warming. Additional meperidine (to a maximum cumulative dose of 2.5 mg/kg) was given to maintain shivering inhibition. The core temperature afterdrop was 30-40% less during forced-air warming (0.9 degree C) than during control (1.4 degrees C) and inhalation rewarming (1.2 degrees C) (P < 0.05). Rewarming rate was 6- to 10-fold greater during forced-air warming (2.40 degrees C/h) than during control (0.41 degree C/h) and inhalation rewarming (0.23 degree C/h) (P < 0.05). In nonshivering hypothermic subjects, forced-air warming provided a rewarming advantage, but inhalation rewarming did not.

Adult↗
PubMed1996

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.

Adult↗