Nigel A.S. Taylor

Static and dynamic assessment of the Biodex dynamometer

SummaryThe validity and accuracy of the Biodex dynamometer was investigated under static and dynamic conditions. Static torque and angular position output correlated well with externally derived data (r=0.998 andr>0.999, respectively). Three subjects performed maximal voluntary knee extensions and flexions at angular velocities from 60 to 450° · s−1. Using linear accelerometry, high speed filming and Biodex software, data were collected for lever arm angular velocity and linear accelerations, and subject generated torque. Analysis of synchronized angular position and velocity changes revealed the dynamometer controlled angular velocity of the lever arm to within 3.5% of the preset value. Small transient velocity overshoots were apparent on reaching the set velocity. High frequency torque artefacts were observed at all test velocities, but most noticeably at the faster speeds, and were associated with lever arm accelerations accompanying directional changes, application of resistive torques by the dynamometer, and limb instability. Isokinematic torques collected from ten subjects (240, 300 and 400° · s−1) identified possible errors associated with reporting knee extension torques at 30° of flexion. As a result of tissue and padding compliance, leg extension angular velocity exceeded lever arm angular velocity over most of the range of motion, while during flexion this compliance meant that knee and lever arm angles were not always identical, particularly at the start of motion. Nevertheless, the Biodex dynamometer was found to be both a valid and an accurate research tool; however, caution must be expercised when interpreting and ascribing torques and angular velocities to the limb producing motion.

Regional variations in transepidermal water loss, eccrine sweat gland density, sweat secretion rates and electrolyte composition in resting and exercising humans

Literature from the past 168 years has been filtered to provide a unified summary of the regional distribution of cutaneous water and electrolyte losses. The former occurs via transepidermal water vapour diffusion and secretion from the eccrine sweat glands. Daily insensible water losses for a standardised individual (surface area 1.8 m2) will be 0.6–2.3 L, with the hands (80–160 g.h−1) and feet (50–150 g.h−1) losing the most, the head and neck losing intermediate amounts (40–75 g.h−1) and all remaining sites losing 15–60 g.h−1. Whilst sweat gland densities vary widely across the skin surface, this same individual would possess some 2.03 million functional glands, with the highest density on the volar surfaces of the fingers (530 glands.cm−2) and the lowest on the upper lip (16 glands.cm−2). During passive heating that results in a resting whole-body sweat rate of approximately 0.4 L.min−1, the forehead (0.99 mg.cm−2.min−1), dorsal fingers (0.62 mg.cm−2.min−1) and upper back (0.59 mg.cm−2.min−1) would display the highest sweat flows, whilst the medial thighs and anterior legs will secrete the least (both 0.12 mg.cm−2.min−1). Since sweat glands selectively reabsorb electrolytes, the sodium and chloride composition of discharged sweat varies with secretion rate. Across whole-body sweat rates from 0.72 to 3.65 mg.cm−2.min−1, sodium losses of 26.5–49.7 mmol.L−1 could be expected, with the corresponding chloride loss being 26.8–36.7 mmol.L−1. Nevertheless, there can be threefold differences in electrolyte losses across skin regions. When exercising in the heat, local sweat rates increase dramatically, with regional glandular flows becoming more homogeneous. However, intra-regional evaporative potential remains proportional to each local surface area. Thus, there is little evidence that regional sudomotor variations reflect an hierarchical distribution of sweating either at rest or during exercise.

Human heat adaptation

In this overview, human morphological and functional adaptations during naturally and artificially induced heat adaptation are explored. Through discussions of adaptation theory and practice, a theoretical basis is constructed for evaluating heat adaptation. It will be argued that some adaptations are specific to the treatment used, while others are generalized. Regarding ethnic differences in heat tolerance, the case is put that reported differences in heat tolerance are not due to natural selection, but can be explained on the basis of variations in adaptation opportunity. These concepts are expanded to illustrate how traditional heat adaptation and acclimatization represent forms of habituation, and thermal clamping (controlled hyperthermia) is proposed as a superior model for mechanistic research. Indeed, this technique has led to questioning the perceived wisdom of body-fluid changes, such as the expansion and subsequent decay of plasma volume, and sudomotor function, including sweat habituation and redistribution. Throughout, this contribution was aimed at taking another step toward understanding the phenomenon of heat adaptation and stimulating future research. In this regard, research questions are posed concerning the influence that variations in morphological configuration may exert upon adaptation, the determinants of postexercise plasma volume recovery, and the physiological mechanisms that modify the cholinergic sensitivity of sweat glands, and changes in basal metabolic rate and body core temperature following adaptation.

The distribution of cutaneous sudomotor and alliesthesial thermosensitivity in mildly heat‐stressed humans: an open‐loop approach

The distribution of cutaneous thermosensitivity has not been determined in humans for the control of autonomic or behavioural thermoregulation under open‐loop conditions. We therefore examined local cutaneous warm and cool sensitivities for sweating and whole‐body thermal discomfort (as a measure of alliesthesia). Thirteen males rested supine during warming (+4°C), and mild (−4°C) and moderate (−11°C) cooling of ten skin sites (274 cm2), whilst the core and remaining skin temperatures were clamped above the sweat threshold using a water‐perfusion suit and climate chamber. Local thermosensitivities were calculated from changes in sweat rates (pooled from sweat capsules on all limbs) and thermal discomfort, relative to the changes in local skin temperature. Thermosensitivities were examined across local sites and body segments (e.g. torso, limbs). The face displayed stronger cold (−11°C) sensitivity than the forearm, thigh, leg and foot (P= 0.01), and was 2–5 times more thermosensitive than any other segment for both sudomotor and discomfort responses (P= 0.01). The face also showed greater warmth sensitivity than the limbs for sudomotor control and discomfort (P= 0.01). The limb extremities ranked as the least thermosensitive segment for both responses during warming, and for discomfort responses during moderate cooling (−11°C). Approximately 70% of the local variance in sudomotor sensitivity was common to the alliesthesial sensitivity. We believe these open‐loop methods have provided the first clear evidence for a greater facial thermosensitivity for sweating and whole‐body thermal discomfort.

Considerations for the measurement of core, skin and mean body temperatures

Despite previous reviews and commentaries, significant misconceptions remain concerning deep-body (core) and skin temperature measurement in humans. Therefore, the authors have assembled the pertinent Laws of Thermodynamics and other first principles that govern physical and physiological heat exchanges. The resulting review is aimed at providing theoretical and empirical justifications for collecting and interpreting these data. The primary emphasis is upon deep-body temperatures, with discussions of intramuscular, subcutaneous, transcutaneous and skin temperatures included. These are all turnover indices resulting from variations in local metabolism, tissue conduction and blood flow. Consequently, inter-site differences and similarities may have no mechanistic relationship unless those sites have similar metabolic rates, are in close proximity and are perfused by the same blood vessels. Therefore, it is proposed that a gold standard deep-body temperature does not exist. Instead, the validity of each measurement must be evaluated relative to ones research objectives, whilst satisfying equilibration and positioning requirements. When using thermometric computations of heat storage, the establishment of steady-state conditions is essential, but for clinically relevant states, targeted temperature monitoring becomes paramount. However, when investigating temperature regulation, the response characteristics of each temperature measurement must match the forcing function applied during experimentation. Thus, during dynamic phases, deep-body temperatures must be measured from sites that track temperature changes in the central blood volume.

The topography of eccrine sweating in humans during exercise

The purpose of this study was to investigate the distribution of steady-state sweating rates (msw), during stressful exercise and heat exposures. Six men completed 42-min trials: 2-min rest and 40-min cycling at 40% peak power in 36.6° C (relative humidity 46.0%). The msw, was monitored using ventilated capsules at the forehead, and at three additional sites. Repeat trials allowed monitoring from eleven skin surfaces. Auditory canal temperature (Tac) and 11 skin temperatures were measured. After normalising msw to the forehead response within subjects, differences in Tac and onset time thresholds, and transient and steady-state msw were examined. The pooled, lower torso msw onset [mean 45.5 (SEM 42.0) s] preceded that of the head [mean 126.5 (SEM 34.8) s, P<0.05], but was not significantly different from the legs [mean 66.6 (SEM 25.7) s], upper torso [mean 80.2 (SEM 36.8) s] or arms [mean 108.6 (SEM 31.2) s]. Transient msw did not differ among regions (P=0.16). Mean, steady-state forehead msw [3.20 (SEM 0.51) mg · cm−2 · min−1]was not significantly greater than the scapula, forearm, hand, stomach and lower back msw (in descending order), but was greater than the chest [1.6 (SEM 0.2)], upperarm [1.6 (SEM 0.2)], calf [1.5 (SEM 0.3)] and thigh msw [1.0 (SEM 0.2), P<0.05 for all comparisons]. The results did not support the caudal-to-rostral sweat onset evident during supine, resting heat stress. Equivalent Tac sweat thresholds existed between sites, while steady-state msw topography varied among subjects and was not dominated by central regions.

Sustained and generalized extracellular fluid expansion following heat acclimation

We measured intra‐ and extravascular body‐fluid compartments in 12 resting males before (day 1; control), during (day 8) and after (day 22) a 3‐week, exercise–heat acclimation protocol to investigate plasma volume (PV) changes. Our specific focus was upon the selective nature of the acclimation‐induced PV expansion, and the possibility that this expansion could be sustained during prolonged acclimation. Acclimation was induced by cycling in the heat, and involved 16 treatment days (controlled hyperthermia (90 min); core temperature = 38.5°C) and three experimental exposures (40 min rest, 96.9 min (s.d. 9.5 min) cycling), each preceded by a rest day. The environmental conditions were a temperature of 39.8°C (s.d. 0.5°C) and relative humidity of 59.2% (s.d. 0.8%). On days 8 and 22, PV was expanded and maintained relative to control values (day 1: 44.0 ± 1.8; day 8: 48.8 ± 1.7; day 22: 48.8 ± 2.0 ml kg−1; P < 0.05). The extracellular fluid compartment (ECF) was equivalently expanded from control values on days 8 (279.6 ± 14.2versus 318.6 ± 14.3 ml kg−1; n= 8; P < 0.05) and 22 (287.5 ± 10.6 versus 308.4 ± 14.8 ml kg−1; n= 12; P < 0.05). Plasma electrolyte, total protein and albumin concentrations were unaltered following heat acclimation (P > 0.05), although the total plasma content of these constituents was elevated (P < 0.05). The PV and interstitial fluid (ISF) compartments exhibited similar relative expansions on days 8 (15.0 ± 2.2%versus 14.7 ± 4.1%; P > 0.05) and 22 (14.4 ± 3.6%versus 6.4 ± 2.2%; P= 0.10). It is concluded that the acclimation‐induced PV expansion can be maintained following prolonged heat acclimation. In addition, this PV expansion was not selective, but represented a ubiquitous expansion of the extracellular compartment.

Eccrine Sweat Glands

SummaryHeat dissipation, under conditions of thermal stress, is mediated primarily by evaporation of sweat. Physical training has been shown to enhance sweat production by eliciting changes in the sensitivity of eccrine glands, total sweat output and distribution of gland activity. These adaptations afford partial acclimation. Heat acclimation produces similar changes, and also results in reduced sweat thresholds. To account for these different responses it has been hypothesised that physical training induces peripheral adaptations, while acclimation produces both peripheral and central modifications. It is suggested that repeated cutaneous heat detection may be essential to the development of central sudo-motor changes.

Ratings of perceived exertion and affect in hot and cool environments

SummaryThe effects of hot and cool environments on perceptual and physiological responses during steady-state exercise were examined in men (n = 14) performing 30 min of constant exercise (cycle ergometry) at a perceived exertion of “somewhat hard”. Subjects exercised at the same absolute exercise intensity in hot (40°C), neutral (24°C), and cool (8°C) conditions. Data were collected for differential ratings of perceived exertion (RPE), affect, thermal sensation, mean skin (