Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+ release by various mechanisms, and the effects of reactive oxygen species. Many different activities lead to fatigue, and an important challenge is to identify the various mechanisms that contribute under different circumstances. Most of the mechanistic studies of fatigue are on isolated animal tissues, and another major challenge is to use the knowledge generated in these studies to identify the mechanisms of fatigue in intact animals and particularly in human diseases.

/pdf/skeletal-muscle-fatigue-cellular-mechanisms-d0dzk4w31g.pdf

Skeletal Muscle Fatigue: Cellular Mechanisms

Background: Multiple laboratory tests are used in the diagnosis and management of patients with diabetes mellitus The quality of the scientific evidence supporting the use of these assays varies substantially

Approach: An expert committee drafted evidence-based recommendations for the use of laboratory analysis in patients with diabetes An external panel of experts reviewed a draft of the guidelines, which were modified in response to the reviewers’ suggestions A revised draft was posted on the Internet and was presented at the AACC Annual Meeting in July, 2000 The recommendations were modified again in response to oral and written comments The guidelines were reviewed by the Professional Practice Committee of the American Diabetes Association

Content: Measurement of plasma glucose remains the sole diagnostic criterion for diabetes Monitoring of glycemic control is performed by the patients, who measure their own plasma or blood glucose with meters, and by laboratory analysis of glycated hemoglobin The potential roles of noninvasive glucose monitoring, genetic testing, autoantibodies, microalbumin, proinsulin, C-peptide, and other analytes are addressed

Summary: The guidelines provide specific recommendations based on published data or derived from expert consensus Several analytes are of minimal clinical value at the present time, and measurement of them is not recommended

/pdf/guidelines-and-recommendations-for-laboratory-analysis-in-547km3houz.pdf

Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus

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Textbook Of Work Physiology Physiological Bases Of Exercise

http://academic.oup.com/auk/article-pdf/102/3/661/30080634/auk0661.pdf

Scaling: why is animal size so important?

Capabilities in health monitoring enabled by capture and quantitative chemical analysis of sweat could complement, or potentially obviate the need for, approaches based on sporadic assessment of blood samples. Established sweat monitoring technologies use simple fabric swatches and are limited to basic analysis in controlled laboratory or hospital settings. We present a collection of materials and device designs for soft, flexible, and stretchable microfluidic systems, including embodiments that integrate wireless communication electronics, which can intimately and robustly bond to the surface of the skin without chemical and mechanical irritation. This integration defines access points for a small set of sweat glands such that perspiration spontaneously initiates routing of sweat through a microfluidic network and set of reservoirs. Embedded chemical analyses respond in colorimetric fashion to markers such as chloride and hydronium ions, glucose, and lactate. Wireless interfaces to digital image capture hardware serve as a means for quantitation. Human studies demonstrated the functionality of this microfluidic device during fitness cycling in a controlled environment and during long-distance bicycle racing in arid, outdoor conditions. The results include quantitative values for sweat rate, total sweat loss, pH, and concentration of chloride and lactate.

A soft, wearable microfluidic device for the capture, storage, and colorimetric sensing of sweat

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.

/pdf/regional-variations-in-transepidermal-water-loss-eccrine-4gnldib7li.pdf

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

Thermal energy is transferred within and between bodies via several avenues, but for most unprotected human cold exposures, particularly during immersion, convective heat loss dominates. Lower tissue temperatures stimulate thermoreceptors, and the resultant afferent flow elicits autonomic homoeostatic responses (thermogenesis and vasoconstriction) that regulate body temperature within a narrow range. The most powerful effector responses occur when both superficial and deep thermoreceptors are cooled simultaneously, but thermoeffector activation can also occur as a result of peripheral cooling alone. The responses to cold, and the hazards associated with cold exposure, are moderated by factors which influence heat production and heat loss, including the severity and duration of cold stimuli, accompanying exercise, the magnitude of the metabolic response, and individual characteristics such as body composition, age, and gender. Cold stress can quickly overwhelm human thermoregulation with consequences ranging from impaired performance to death. This review provides a comprehensive overview of the human physiological responses to acute cold exposure.

Human physiological responses to cold exposure.

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

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.

Human heat adaptation

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 degrees C), and mild (-4 degrees C) and moderate (-11 degrees 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 degrees 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 degrees 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.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2004.081562

Nigel A.S. Taylor

Papers

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

Human physiological responses to cold exposure.

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

Human heat adaptation

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