above title appeared on the shelves of some university and hospital libraries. The numbers were not large, and the locations were predominantly in North America. Actually, the first sentence is not quite accurate, because what appears above was preceded by the letters CRC, the acronym of Chemical Rubber Company, based in Boca Raton, Florida, USA. The company was then a major force in chemistry, proud publisher of a series of handbooks that were holy writ to scientists in virtually all disciplines at the time and with which no working laboratory could be without. The journal in question was one of a whole series launched from the same source around the same time, differing in name only in the subject matter purported to be covered. This initiative was accompanied by a series of authoritative but expensive monographs in the biomedical field that were beyond the means of private individuals but highly sought after by these impecunious souls through their institutions that, in those halcyon days, were much better placed than they are today to respond to the extravagant whims of their constituents. This financial recklessness was compounded by the absence of sponsorship by scientific societies and by the fact that these journals refused to sully their pristine pages with anything that smelled of money, such as advertisements or announcements. CRC paid the eventual price, but in more ways than one. Apart from the publishers themselves, the founding fathers and joint editors were John W King, MD, PhD, of the Cleveland Clinic, and Willard R Faulkner, PhD, from Vanderbilt Medical Center. One has to admire their energy and vision. The very first issue (Vol 1, Pt 1 ) had no fewer than 192 pages and 15 “articles”. Seven of these were full reviews (the longest contained 46 pages and the shortest only five), and the remaining items were fillers of various sorts, including abstracts of future papers, a catalogue of clinical references, and a Classification of Standard Reagents for Enteroviruses. Gradually, these utilitarian distractions were phased out, and the content became restricted to full reviews, as the journal title demanded. The year of its birth coincided with a period of particularly explosive growth in the laboratory sciences, fuelled by earlier advances in the basic sciences, and there was a real need for something more insightful than a merely descriptive account of advances and new developments in the various fields. What was required was an expert and critical author who, by separating the wheat from the chaff, the sheep from the goats, and the ducks from the geese, could stand egalitarianism on its head, drawing attention to those papers and their respective authors whose work was most worthy of attention and emulation. This wishful thought has been fulfilled sufficiently often over the ensuing years to raise the journal to the pinnacle of its class in comparative awareness surveys. King and Faulkner, from the very beginning, introduced some important innovations that have stood the test of time. First of all, each author and his chosen topic were carefully selected and the subject of a personal invitation. Each paper was scrutinized by an expert referee in an open review process. The name of the referee appeared below that of the authors, and he was paid a token honorarium, but in many instances he received more than he had bargained for: credit as a coauthor of the paper. This practice is rampant throughout the early and middle periods of the journal in the electronic editions posted on the Informa website, but, fortunately, the PubMed abstracts have avoided this error. Neither do the dates of the various volumes always correspond between these sources and the printed version. Compilers of bibliographies should take heed. The table of contents included a synopsis (not a summary ) of the paper and a brief biography of the authors. The former has now evolved into the Statement of Significance, and authors must be judged by their present work without biographical knowledge of their past accomplishments. The second issue (Vol 1, Pt 2) leaned heavily in the direction of hematology, and, of the nine papers comprising Vol 1, Pt 3, no fewer than seven concerned various aspects of hemoglobin. The other disciplines within the laboratory sciences were more evenly distributed, and the authors, albeit exclusively from North America, were among the most renowned in their fields. In Vol 1, Pt 4, which brought the page count for the year to 684, the American monopoly was broken with three of the five papers coming wholly or in part from UK institutions. The following year, Vol 2 Critical Reviews in Clinical Laboratory Science, 2010; 47(1): 1–4

Critical reviews in clinical laboratory sciences.

The human body constantly exchanges heat with the environment. Temperature regulation is a homeostatic feedback control system that ensures deep body temperature is maintained within narrow limits despite wide variations in environmental conditions and activity-related elevations in metabolic heat production. Extensive research has been performed to study the physiological regulation of deep body temperature. This review focuses on healthy and disordered human temperature regulation during heat stress. Central to this discussion is the notion that various morphological features, intrinsic factors, diseases, and injuries independently and interactively influence deep body temperature during exercise and/or exposure to hot ambient temperatures. The first sections review fundamental aspects of the human heat stress response, including the biophysical principles governing heat balance and the autonomic control of heat loss thermoeffectors. Next, we discuss the effects of different intrinsic factors (morphology, heat adaptation, biological sex, and age), diseases (neurological, cardiovascular, metabolic, genetic), and injuries (spinal cord injury, deep burns, heat stroke), with emphasis on the mechanisms by which these factors enhance or disturb the regulation of deep body temperature during heat stress. We conclude with key unanswered questions in this field of research.

Human temperature regulation under heat stress in health, disease, and injury.

Under normothermic, resting conditions, humans dissipate heat from the body at a rate approximately equal to heat production. Small discrepancies between heat production and heat elimination would, over time, lead to significant changes in heat storage and body temperature. When heat production or environmental temperature is high the challenge of maintaining heat balance is much greater. This matching of heat elimination with heat production is a function of the skin circulation facilitating heat transport to the body surface and sweating, enabling evaporative heat loss. These processes are manifestations of the autonomic control of cutaneous vasomotor and sudomotor functions and form the basis of this review. We focus on these systems in the responses to hyperthermia. In particular, the cutaneous vascular responses to heat stress and the current understanding of the neurovascular mechanisms involved. The available research regarding cutaneous active vasodilation and vasoconstriction is highlighted, with emphasis on active vasodilation as a major responder to heat stress. Involvement of the vasoconstrictor and active vasodilator controls of the skin circulation in the context of heat stress and nonthermoregulatory reflexes (blood pressure, exercise) are also considered. Autonomic involvement in the cutaneous vascular responses to direct heating and cooling of the skin are also discussed. We examine the autonomic control of sweating, including cholinergic and noncholinergic mechanisms, the local control of sweating, thermoregulatory and nonthermoregulatory reflex control and the possible relationship between sudomotor and cutaneous vasodilator function. Finally, we comment on the clinical relevance of these control schemes in conditions of autonomic dysfunction.

Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans.

Key points
Previous studies implicate nitric oxide (NO) in the control of sweating during exercise in the heat; however, it is unclear whether cyclooxygenase (COX) is also involved.
We demonstrated that exercise-induced sweating at a moderate heat production (400 W, ∼40% VO2 max ) was similarly reduced when COX and NO synthase were inhibited separately and in combination.
Alternatively, inhibiting COX and/or NO synthase did not influence exercise-induced sweating at a high heat production (700 W, ∼70% VO2 max ).
We show that both COX and NO are involved in sweating during exercise at moderate heat production and that the effects may not be independent. However, roles for COX and NO are less evident when heat production is elevated.
The results lead to better understanding of the mechanisms of sweating and indicate that COX inhibitors (e.g. aspirin) may impair core body temperature regulation and thereby increase the risk of heat-related illness.


Abstract
Our recent work implicated nitric oxide (NO) in the control of sweating during intermittent exercise; however, it is unclear if cyclooxygenase (COX) is also involved. On separate days, ten healthy young (24 ± 4 years) males cycled in the heat (35°C). Two 30 min exercise bouts were performed at either a moderate (400 W, moderate heat load) or high (700 W, high heat load) rate of metabolic heat production and were followed by 20 and 40 min of recovery, respectively. Forearm sweating (ventilated capsule) was evaluated at four skin sites that were continuously perfused via intradermal microdialysis with: (1) lactated Ringer solution (Control), (2) 10 mm ketorolac (a non-selective COX inhibitor), (3) 10 mm NG-nitro-l-arginine methyl ester (l-NAME; a non-selective NO synthase inhibitor) or (4) a combination of 10 mm ketorolac + 10 mm l-NAME. During the last 5 min of the first exercise at moderate heat load, forearm sweating (mg min−1 cm−2) was equivalently reduced with ketorolac (0.54 ± 0.08), l-NAME (0.55 ± 0.07) and ketorolac+l-NAME (0.56 ± 0.08) compared to Control (0.67 ± 0.06) (all P   0.05). We show that (1) although both COX and NO modulate forearm sweating during intermittent exercise bouts in the heat at a moderate heat load, the effects are not additive, and (2) the contribution of both enzymes to forearm sweating is less evident during intermittent exercise when the heat load is high and during recovery.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2014.280651

Evidence for cyclooxygenase‐dependent sweating in young males during intermittent exercise in the heat

Nitric oxide (NO) is a signalling molecule that contributes to the control of many physiological pathways, including the heat-loss response of skin vasodilatation. Recently, NO has been implicated in the control of sweating during exercise in young adults. We tested the hypothesis that ageing reduces NO-dependent sweating during exercise in the heat. Ten young (23 ± 3 years old) and 10 older men (64 ± 5 years old), matched for body surface area, performed three successive 15 min bouts of exercise (Ex1, Ex2 and Ex3) at the same rate of metabolic heat production (300 W m(-2)) in the heat (35°C, 20% relative humidity). Exercise periods were interspersed with 15 min recovery periods. Local sweat rate (ventilated capsule) was measured on two forearm skin sites, which were continuously perfused via intradermal microdialysis with 0.9% saline as control (CON) or 10 mm N(G)-nitro-l-arginine methyl ester (L-NAME), a non-selective NO synthase inhibitor. Local sweat rate at the end of Ex1 was lower in the CON conditions in the older versus young men (0.69 ± 0.19 versus 0.90 ± 0.17 mg min(-1) cm(-2), P = 0.018). In the young men, local sweat rate was reduced in the L-NAME-treated conditions compared with the CON conditions at the end of Ex1 (0.67 ± 0.14 versus 0.90 ± 0.17 mg min(-1) cm(-2), P = 0.004), Ex2 (0.78 ± 0.20 versus 1.03 ± 0.20 mg min(-1) cm(-2), P = 0.013) and Ex3 (0.78 ± 0.20 versus 1.03 ± 0.21 mg min(-1) cm(-2), P = 0.014). In the older men, there was no main effect of treatment conditions on local sweat rate (P = 0.537) such that local sweat rates in the L-NAME-treated and CON conditions were similar (Ex1, 0.65 ± 0.20 versus 0.69 ± 0.19 mg min(-1) cm(-2); Ex2, 0.80 ± 0.27 versus 0.91 ± 0.29 mg min(-1) cm(-2); and Ex3, 0.84 ± 0.31 versus 0.94 ± 0.38 mg min(-1) cm(-2)). We conclude that ageing attenuates the influence of NO in the control of local forearm sweating observed in young adults during short 15 min bouts of exercise in the heat. This mechanism may, in part, explain the age-related impairments in sweating.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/expphysiol.2013.077644

Diminished nitric oxide-dependent sweating in older males during intermittent exercise in the heat

The purpose of the current study was to determine the effect of a locally administered nonselective β-adrenergic antagonist on sweat gland function during exercise. Systemically administered propra...

Localized β-adrenergic receptor blockade does not affect sweating during exercise

The purpose of the current study was to investigate the role of in vivo β-adrenergic stimulation on sweat production during exercise. To do this, atropine was used to block the cholinergic component of sweating, thus isolating any potential β-adrenergic response during exercise. The subjects for this study were 11 healthy volunteers. Atropine (1% solution) and aminophylline (1% solution) were administered to a 5 cm2 area of the flexor surface of one forearm via iontophoresis. The opposing arm underwent iontophoresis with a saline solution. Each subject then exercised at 75% of their age-predicted maximum heart rate. During exercise, mean ± SD sweat rate in the control forearm was 0.63 ± 0.50 mg/cm2/min. There was no measurable sweat production in the arm pre-treated with atropine and aminophylline. Following exercise, iontophoresis of pilocarpine verified complete cholinergic blockade in the treated forearm. The results of the current study suggest that in vivo β-adrenergic stimulation alone is not sufficient to elicit sweating in exercising humans. Such data supports previous studies that have suggested that the role of β-adrenergic stimulation in vivo is to potentiate cholinergic sweating.

The role of in vivo β-adrenergic stimulation on sweat production during exercise

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Localized β-adrenergic receptor blockade does not affect sweating during exercise

The role of in vivo β-adrenergic stimulation on sweat production during exercise