Although IL-6 is a key modulator of immune function, it also plays a role in regulating substrate metabolism. To determine whether IL-6 affects lipid metabolism, 18 healthy men were infused for 3 h with saline (Con; n = 6) or a high dose (High-rhIL6; n = 6) or a low dose (Low-rhIL6; n = 6) of recombinant human IL-6 (rhIL-6). The IL-6 concentration during Con, Low-rhIL6, and High-rhIL6 was at a steady state after 30 min of infusion at approximately 4, 140, and 320 pg/ml, respectively. Either dose of rhIL-6 was associated with a similar increase in fatty acid (FA) concentration and endogenous FA rate of appearance (R_a) from 90 min after the start of the infusion. The FA concentration and FA R_a continued to increase until the cessation of rhIL-6 infusion, reaching levels approximately 50% greater than Con values. The elevated levels reached at the end of rhIL-6 infusion persisted at least 3 h postinfusion. Triacylglycerol concentrations were unchanged during rhIL-6 infusion, whereas whole body fat oxidation increased after the second hour of rhIL-6 infusion. Of note, during Low-rhIL6, the induced elevation in FA concentration and FA R_a occurred in the absence of any change in adrenaline, insulin, or glucagon, and no adverse side effects were observed. In conclusion, the data identify IL-6 as a potent modulator of fat metabolism in humans, increasing fat oxidation and FA reesterification without causing hypertriacylglyceridemia.

Respiratory rate is a fundamental vital sign that is sensitive to different pathological conditions (e.g., adverse cardiac events, pneumonia, and clinical deterioration) and stressors, including emotional stress, cognitive load, heat, cold, physical effort, and exercise-induced fatigue. The sensitivity of respiratory rate to these conditions is superior compared to that of most of the other vital signs, and the abundance of suitable technological solutions measuring respiratory rate has important implications for healthcare, occupational settings, and sport. However, respiratory rate is still too often not routinely monitored in these fields of use. This review presents a multidisciplinary approach to respiratory monitoring, with the aim to improve the development and efficacy of respiratory monitoring services. We have identified thirteen monitoring goals where the use of the respiratory rate is invaluable, and for each of them we have described suitable sensors and techniques to monitor respiratory rate in specific measurement scenarios. We have also provided a physiological rationale corroborating the importance of respiratory rate monitoring and an original multidisciplinary framework for the development of respiratory monitoring services. This review is expected to advance the field of respiratory monitoring and favor synergies between different disciplines to accomplish this goal.

There is an ever-growing demand for measuring respiratory variables during a variety of applications, including monitoring in clinical and occupational settings, and during sporting activities and exercise. Special attention is devoted to the monitoring of respiratory rate because it is a vital sign, which responds to a variety of stressors. There are different methods for measuring respiratory rate, which can be classed as contact-based or contactless. The present paper provides an overview of the currently available contact-based methods for measuring respiratory rate. For these methods, the sensing element (or part of the instrument containing it) is attached to the subject’s body. Methods based upon the recording of respiratory airflow, sounds, air temperature, air humidity, air components, chest wall movements, and modulation of the cardiac activity are presented. Working principles, metrological characteristics, and applications in the respiratory monitoring field are presented to explore potential development and applicability for each method.

The mechanisms that mediate the tightly controlled production and clearance of glucose during muscular work are unclear, and it has been suggested that an unidentified “work factor” exists that influences the contraction-induced increase in endogenous glucose production (EGP). The cytokine interleukin (IL)-6 is released from skeletal muscle during contraction. Here we show that IL-6 contributes to the contraction-induced increase in EGP. Six men performed 2 h of bicycle exercise on three separate occasions, at a relatively high intensity (HI) or at a low intensity with (LO + IL-6) or without (LO) an infusion of recombinant human IL-6 that matched the circulating concentration of IL-6 seen in HI exercise. The stable isotope 6,6 ²H₂ glucose was infused to calculate EGP (rate of glucose appearance [R_a]), whole-body glucose disposal (rate of glucose disappearance [R_d]), and metabolic clearance rate (MCR) of glucose. Glucose R_a, R_d, and MCR were higher (P < 0.05) at HI than at LO. Throughout exercise at LO + IL-6, glucose R_a and R_d were higher (P < 0.05) than LO, even though the exercise intensity was identical. In addition, MCR was higher (P < 0.05) at LO + IL-6 than at LO at 90 min. Insulin, glucagon, epinephrine, norepinephrine, cortisol, and growth hormone were identical when comparing LO + IL-6 with LO. These data suggest that IL-6 influences glucose homeostasis during exercise. Our results provide potential new insights into factors that mediate glucose production and disposal and implicates IL-6 in the so-called “work factor.”

To determine whether IL-6 increases lipolysis and fat oxidation in patients with type 2 diabetes and/or whether it exerts this effect independently of changes to the hormonal milieu, patients with type 2 diabetes (D) and healthy control subjects (CON) underwent recombinant human (rh)IL-6 infusion for 3 h. Rates of appearance (R_a) and disappearance (R_d) of [U-¹³C]palmitate and [6,6-²H₂]glucose were determined. rhIL-6 infusion increased ( P < 0.05) palmitate R_a and R_d in a similar fashion in both groups. Neither plasma glucose concentration nor glucose R_a/R_d was affected by rhIL-6 infusion in either group, whereas rhIL-6 infusion resulted in a reduction ( P < 0.05) in circulating insulin in D. Plasma growth hormone (GH) was increased ( P < 0.05) by IL-6 in CON, and cortisol increased ( P < 0.05) in response to IL-6 in both groups. To determine whether IL-6 was exerting its effect directly or through activation of these hormones, we performed cell culture experiments. Fully differentiated 3T3-L1 adipocytes were treated with PBS (control) IL-6, or IL-6 plus dexamethasone and GH. IL-6 treatment alone increased ( P < 0.05) lipolysis, but this effect was reduced by the addition of dexamethasone and GH such that IL-6 plus dexamethasone and GH had blunted ( P < 0.05) lipolysis compared with IL-6 alone. To assess whether IL-6 increases fat oxidation, L6 myotubes were treated with PBS (Control), IL-6, or AICAR, a compound known to increase lipid oxidation. Both IL-6 and AICAR markedly increased ( P < 0.05) oxidation of [¹⁴C]palmitate compared with Control. Acute IL-6 treatment increased fatty acid turnover in D patients as well as healthy CON subjects. Moreover, IL-6 appears to be activating lipolysis independently of elevations in GH and/or cortisol and appears to be a potent catalyst for fat oxidation in muscle cells.