Short-term sleep deprivation and human thermoregulatory function during thermal challenges

New Findings: What is the topic of this review? It is generally accepted that sleep deprivation constitutes a predisposing factor to the development of thermal injury. This review summarizes the available human-based evidence on the impact of sleep loss on autonomic and behavioural thermoeffectors during acute exposure to low and high ambient temperatures. What advances does it highlight? Limited to moderate evidence suggests that sleep deprivation per se impairs thermoregulatory defence mechanisms during exposure to thermal extremes. Future research is required to establish whether inadequate sleep enhances the risk for cold- and heat-related illnesses. Abstract: Relatively short periods of inadequate sleep provoke physiological and psychological perturbations, typically leading to functional impairments and degradation in performance. It is commonly accepted that sleep deprivation also disturbs thermal homeostasis, plausibly enhancing susceptibility to cold- and heat-related illnesses. Herein, we summarize the current state of human-based evidence on the impact of short-term (i.e., ≤4 nights) sleep deprivation on autonomic and behavioural thermoeffectors during acute exposure to low and high ambient temperatures. The purpose of this brief narrative review is to highlight knowledge gaps in the area and stimulate future research to investigate whether sleep deprivation constitutes a predisposing factor for the development of thermal injuries. © 2021 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Societ

The role of muscle pump in the development of cardiovascular drift

This study examined the role of muscle pump in the development of cardiovascular drift (CVdrift) during cycling. Twelve healthy males (23.4±0.5 years, mean ±SE) exercised for 90 min with 40 and 80 pedal revolutions per minute (rpm) at the same oxygen consumption, in two separate days. CVdrift was developed in both conditions as indicated by the drop in stroke volume (SV) and the rise in heart rate (HR) from the 20th min onwards (ΔSV = -16.2±2.0 and -17.1±1.0 ml beat-1; ΔHR = 18.3±2.0 and 17.5±3.0 beats min-1 for 40 and 80 rpm, respectively, P < 0.05) but without difference between conditions. Mean cardiac output (CO2 rebreathing) was 14.7±0.3 l min-1 and 15.0±0.3 l min-1, and mean arterial pressure was 100.0±1.0 mmHg and 96.7±0.8 mmHg for 40 and 80 rpm, respectively, without significant changes over time, and without difference between conditions. Electromyographic activity (iEMG) was lower throughout exercise with 80 rpm (35.6±1.2% and 11.0±1.0% for 40 and 80 rpm, respectively). Similarly, total hemoglobin, determined with near-infrared spectroscopy (NIRS) was 58.0±0.8 (AU) for 40 rpm and 53.0±1.4 (arbitrary units) for 80 rpm, from 30th min onwards (P < 0.05), an indication of lower leg blood volume during the faster pedal rate condition. Thermal status (rectal and mean skin temperature), blood and plasma volume changes, blood lactate concentration, muscle oxygenation (NIRS signal) and the rate of perceived exertion were similar in the two trials. It seems that muscle pump is not an important factor for the development of CVdrift during cycling, at least under the present experimental conditions. © Springer-Verlag 2008

Forearm-finger skin temperature gradient as an index of cutaneous perfusion during steady-state exercise

The purpose of this study was to examine whether the forearm-finger skin temperature gradient (Tforearm-finger), an index of vasomotor tone during resting conditions, can also be used during steady-state exercise. Twelve healthy men performed three cycling trials at an intensity of ~60% of their maximal oxygen uptake for 75 min separated by at least 48 h. During exercise, forearm skin blood flow (BFF) was measured with a laser-Doppler flowmeter, and finger skin blood flow (PPG) was recorded from the left index fingertip using a pulse plethysmogram. Tforearm-finger of the left arm was calculated from the values derived by two thermistors placed on the radial side of the forearm and on the tip of the middle finger. During exercise, PPG and BFF increased (P<0·001), and Tforearm-finger decreased (P<0·001) from their resting values, indicating a peripheral vasodilatation. There was a significant correlation between Tforearm-finger and both PPG (r = -0·68; P<0·001) and BFF (r = -0·50; P<0·001). It is concluded that Tforearm-finger is a valid qualitative index of cutaneous vasomotor tone during steady-state exercise. © 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd

Heterogeneous sensitivity of cerebral and muscle tissues to acute normobaric hyperoxia at rest

The purpose was to investigate the effects of acute normobaric hyperoxia at rest on cerebral, respiratory and leg muscle oxygenation. Ten healthy men were studied twice in a single-blinded counterbalanced crossover study protocol. On one occasion they breathed air and on the other 100% normobaric O2 for a 2-hour time period. Oxygenated (δ[O2Hb]), deoxygenated (δ[HHb]) and total (δ[tHb]) hemoglobin in the cerebral frontal cortex, and in the intercostal and vastus lateralis muscles were simultaneously monitored with near-infrared spectroscopy. The hyperoxic stimulus promptly increased δ[O2Hb] (~2μM) and decreased δ[HHb] (~3.6μM) in the frontal cortex. These cerebral responses were directly and fully countered by resumption of normoxic air breathing. In contrast, δ[HHb] significantly decreased due to the acute hyperoxic stimulus in both intercostal and vastus lateralis muscles. The temporal changes in muscle oxygenation were slower compared to those in the cerebral area; and they only partially recovered during the 15-min normoxic-recovery period. Acute supplementation of normobaric O2 at rest influences cerebral, leg and respiratory muscle oxygenation of healthy individuals, but not in the same manner. Namely, the frontal cortex seems to be more sensitive to hyperoxia than are the skeletal muscle regions. © 2012 Elsevier Inc