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).

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.

Organisation of the amygdalo-thalamic pathways in rats.

This study examines the organisation of the pathways from the amygdala to the thalamus. Amygdaloid nuclei (medial, central, basolateral and olfactory groups) of Sprague-Dawley rats were injected with biotinylated dextran using stereotaxic coordinates and their brains were then aldehyde-fixed and processed using standard methods. We have three major findings. First, the amygdala has a distinct set of projections to particular nuclei of the thalamus. The thalamic nuclei with the heaviest amygdaloid terminations include the zona incerta, the mediodorsal and the midline nuclei. Second, nuclei of different amygdaloid groups project to the thalamus in slightly different patterns. For example, some groups of nuclei project to the thalamic reticular nucleus (e.g. medial, olfactory) whilst others do not (e.g. central, basolateral). Thus, there is a certain amount of heterogeneity within the amygdaloid projections to the thalamus. Third, when we compare our results on the amygdalo-thalamic pathways to the many previous descriptions of the thalamo-amygdaloid pathways, we note that they are largely out of register. In other words, some of the thalamic nuclei that project to a given group of amygdaloid nuclei do not necessarily receive a projection back from that same amygdaloid nucleus. Hence, there is no substrate for a strong feed-back relationship between the thalamus and the amygdala, as there has been shown for other centres of the brain (e.g. between the thalamus and neocortex).

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.

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.

Disturbance of thermal homeostasis during post-exercise hyperthermia.

The response of core temperature to exercise was investigated during recovery in order to avoid the antagonistic competition between exercise and thermal reflexes for the same effector systems which control skin blood flow. Five healthy, non-training males [mean (SD) age, 23.8 (2.04) years] were habituated to 29 degrees C at relative 50% humidity for more than 2 h and then exercised by treadmill running at about 75% maximum oxygen uptake for 18 min. They then remained at 29 degrees C for up to 65 min of recovery. Oesophageal (T(es)), rectal (Tre) and skin temperatures (Tsk) were recorded at 5-s intervals throughout. The abrupt fall of temperature gradient from the forearm to finger was used to identify the T(es) for skin vessel dilatation (Tdil) during exercise. Mean (SE) Tes rose from a resting value of 36.67 (0.15) degrees C to 38.22 (0.24) degrees C, mean Tre rose from 37.09 (0.25) degrees C to 38.23 (0.15) degrees C, and Tdil occurred at 37.39 (0.32) degrees C. Within 10 min of recovery mean T(es) fell to 37.31 (0.24) degrees C, where it remained a significant 0.64 degrees C above its pre-exercise (PrEx) level (P < or = 0.018) but insignificantly different from Tdil for the remaining 55 min of recovery. Meanwhile, Tre fell gradually throughout recovery to 37.64 (0.18) degrees C. The Tsk at all non-acral sites except the thigh had recovered to PrEx levels by 20-30 min post-exercise (PoEx).(ABSTRACT TRUNCATED AT 250 WORDS)

Postexercise proteinuria in rowers.

Exercise performance, glomerular filtration rate (GFR), and urinary filtration of proteins during static pool rowing and cycling to exhaustion were studied in trained rowers. The peak VO2 and heart rate were higher during rowing than during cycling. There was a reduction in plasma volume and an increase in lactate concentration after exercise; however, no significant difference was noted between rowing and cycling in either case. Postexercise proteinuria was increased 8 and 11 times, and albuminuria 25 and 20 times after rowing and cycling exercises, respectively. There was no difference between these exercises in terms of protein or albumin excretion. There was no change in postexercise GFR. Albumin clearance was increased 18 and 20 fold after rowing and cycling, respectively. A significant, but low correlation, r = 0.56, was noted between albumin excretion and postexercise blood lactate concentration. Thus, no difference in the effect on kidney response was found between static pool rowing and cycling to exhaustion in these athletes.

The role of the courts, legislatures, and lawyers in treatment decisions.

During the past 10 years, the issues surrounding the right to refuse various forms of treatment have remained complex, and the development of appropriate societal responses has become more elusive. This article considers the role that the judiciary, the legislature, and the legal profession have played in the resolution of these medical, legal, and ethical dilemmas. The courts, legislatures, and lawyers will never be removed completely from involvement in these matters, nor should they be. Yet, a continuation of the medical profession's responsible approach to these issues will insure that their involvement will be kept to a minimum.

Ethics committees in critical care.

Ethics committees have emerged as a way for institutions to evaluate and resolve some of the difficult decisions facing critical care medicine. This article examines their origin, scope, function, and potential problems.