Biological sex-related differences in the postprandial triglyceride response to intermittent hypoxaemia in young adults: a randomized crossover trial.

Obstructive sleep apnoea is characterized by chronic intermittent hypoxaemia and is independently associated with an increased risk of metabolic comorbidities (e.g. type II diabetes and ischaemic heart disease). These comorbidities could be attributable to hypoxaemia-induced alterations in blood lipid profiles. However, it remains unclear whether intermittent hypoxaemia alters triglyceridaemia differently between biological sexes. Therefore, we used a randomized crossover design to examine whether 6 h of moderate intermittent hypoxaemia (15 hypoxaemic cycles/h, 85% oxyhaemoglobin saturation) alters plasma triglyceride levels differently between men and women after a high-fat meal. Relative to men, women displayed lower levels of total triglycerides, in addition to denser triglyceride-rich lipoprotein triglycerides (TRL-TG; mainly very low-density lipoprotein triglycerides and chylomicron remnant triglycerides) and buoyant TRL-TG (mainly chylomicron triglycerides) during normoxia (ambient air) and intermittent hypoxaemia (sex × time: all P ≤ 0.008). Intermittent hypoxaemia led to higher triglyceride levels (condition: all P ≤ 0.016); however, this effect was observed only in men (sex × condition: all P ≤ 0.002). Compared with normoxia, glucose levels were higher in men and lower in women during intermittent hypoxaemia (sex × condition: P < 0.001). The different postprandial responses between biological sexes occurred despite similar reductions in mean oxyhaemoglobin saturation and similar elevations in insulin levels, non-esterified fatty acid levels and mean heart rate (sex × condition: all P ≥ 0.185). These results support growing evidence showing that intermittent hypoxaemia impacts men and women differently, and they might help to explain biological sex-related discrepancies in the rate of certain comorbidities associated with intermittent hypoxaemia. KEY POINTS: Intermittent hypoxaemia is a key characteristic of obstructive sleep apnoea and alters lipid metabolism in multiple tissues, resulting in increased circulating triglyceride levels, an important risk factor for cardiometabolic diseases. Circulating triglyceride levels are regulated differently between biological sexes, with women typically displaying much lower fasting and postprandial triglyceride levels than men, partly explaining why women of all ages experience lower mortality rates from cardiometabolic diseases. In this study, healthy young men and women consumed a high-fat meal and were then exposed to 6 h of intermittent hypoxaemia or ambient air. We show that postprandial triglyceride levels are significantly lower in women compared with men and that intermittent hypoxaemia leads to higher postprandial triglyceride levels in men only. These results might help us to understand better why women living with obstructive sleep apnoea experience lower rates of cardiometabolic diseases (e.g. type II diabetes and ischaemic heart disease) than men living with obstructive sleep apnoea.

No impact of a high-fat meal coupled with intermittent hypoxemia on acute kidney injury biomarkers in adults with and without obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxemia, which is associated with progressive loss of kidney function, where postprandial fluctuations in renal physiology may further compromise oxygen supply and kidney function. Therefore, we measured biomarkers of acute kidney injury (AKI) following a high-fat meal with and without intermittent hypoxemia. Eighteen healthy young men (mean age [SD]: 22.7 years [3.1]) and seven middle-aged to older individuals with OSA (54.4 years [6.4]) consumed a high-fat meal during normoxia or intermittent hypoxemia (~15 hypoxic cycles per hour, ~85% oxyhemoglobin saturation) for 6 h. We observed no changes in estimated glomerular filtration rate and plasma concentrations of creatinine, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) at any measured time points. In both groups, plasma concentrations of interleukin-18 (IL-18) increased after 6 h during normoxia only (p = 0.033, ηp 2 = 0.122), and plasma concentrations of liver-type fatty acid-binding protein (L-FABP) transiently decreased after 3 h in both conditions (p = 0.008, ηp 2 = 0.152). These findings indicate that AKI biomarkers are not acutely elevated during the postprandial state with or without intermittent hypoxemia, suggesting that other mechanisms may play more important roles in the progression of kidney disease in OSA.

Human Preadipocytes Differentiated under Hypoxia following PCB126 Exposure during Proliferation: Effects on Differentiation, Glucose Uptake and Adipokine Profile.

Persistent organic pollutants (POPs) accumulation and hypoxia are two factors proposed to adversely alter adipose tissue (AT) functions in the context of excess adiposity. Studies have shown that preadipocytes exposure to dioxin and dioxin-like POPs have the greatest deleterious impact on rodent and immortalized human preadipocyte differentiation, but evidence on human preadipocytes is lacking. Additionally, hypoxia is known to strongly interfere with the dioxin-response pathway. Therefore, we tested the effects of pre-differentiation polychlorinated biphenyl (PCB)126 exposure at 10 µM for 3 days and subsequent differentiation under hypoxia on human subcutaneous adipocytes (hSA) differentiation, glucose uptake and expression of selected metabolism- and inflammation-related genes. Pre-differentiation PCB126 exposure lowered the adenosine triphosphate (ATP) content, glucose uptake and leptin expression of mature adipocytes but had limited effects on differentiation under normoxia (21% O2). Under hypoxia (3% O2), preadipocytes ability to differentiate was significantly reduced as reflected by significant decreased lipid accumulation and downregulation of key adipocyte genes such as peroxisome proliferator-activated receptor gamma (PPARγ) and adiponectin. Hypoxia increased glucose uptake and glucose transporter 1 (GLUT1) expression but abolished the adipocytes insulin response and GLUT4 expression. The expression of pro-inflammatory adipokine interleukin-6 (IL-6) was slightly increased by both PCB126 and hypoxia, while IL-8 expression was significantly increased only following the PCB126-hypoxia sequence. These observations suggest that PCB126 does not affect human preadipocyte differentiation, but does affect the subsequent adipocytes population, as reflected by lower ATP levels and absolute glucose uptake. On the other hand, PCB126 and hypoxia exert additive effects on AT inflammation, an important player in the development of chronic diseases such as type 2 diabetes and cardiovascular diseases.

The Effect of Acute Intermittent and Continuous Hypoxia on Plasma Circulating ßOHB Levels Under Different Feeding Statuses in Humans.

Introduction: Acute hypoxia is known to increase circulating nonesterified fatty acid (NEFA) levels. Adipose tissue lipolysis is a major source of NEFA into circulation and insulin suppresses this process when the tissue is insulin sensitive. NEFA can be esterified to triglycerides and/or completely/partially oxidized, the latter leading to ketogenesis in the liver. To our knowledge, the effect of hypoxia on ketogenesis, more specifically ß-hydroxybutyrate (ßOHB) levels, remains unknown in humans. Therefore, the objective of this study was to determine the effect of acute intermittent and continuous hypoxia on circulating ßOHB levels under different feeding status. Methods: Plasma samples from three different randomized crossover studies were assessed for ßOHB concentrations. In the first study, 14 healthy men (23 ± 3.5 years) were exposed to 6 h of normoxia or intermittent hypoxia (IH-Fed) (15 hypoxic events/hour) following an isocaloric meal. In the second study, 10 healthy men (26 ± 5.6 years) were exposed to 6 h of continuous normobaric hypoxia (CH-Fasted) (FiO2 = 0.12) or normoxia in the fasting state. In the third study (CH-Fed), 9 healthy men (24 ± 4.5 years) were exposed to 6 h of normoxia or CH in a constant prandial state. ßOHB, NEFA and insulin levels were measured during all sessions. Results: In the IH-Fed study, ßOHB and NEFA levels tended to be greater over 6 h of IH (condition × time interaction, ßOHB p = 0.108 and NEFA p = 0.062) compared to normoxia. In the CH-Fasted study, ßOHB and NEFA levels increased over time in both experimental conditions, this effect being greater under CH (condition × time interaction, ßOHB p = 0.070; NEFA p = 0.046). In the CH-Fed study, ßOHB levels slightly increased up to 180 min before falling back to initial concentrations by the end of the protocol in both normoxia and CH (main effect of time, p = 0.062), while NEFA were significantly higher under CH (p = 0.006). Conclusion: Acute normobaric hypoxia exposure tends to increase plasma ßOHB concentrations over time in healthy men. The stimulating effect of hypoxia on plasma ßOHB levels is however attenuated during postprandial and prandial states.

CYP1A1, VEGFA and Adipokine Responses of Human Adipocytes Co-exposed to PCB126 and Hypoxia.

It is increasingly recognized that hypoxia may develop in adipose tissue as its mass expands. Adipose tissue is also the main reservoir of lipophilic pollutants, including polychlorinated biphenyls (PCBs). Both hypoxia and PCBs have been shown to alter adipose tissue functions. The signaling pathways induced by hypoxia and pollutants may crosstalk, as they share a common transcription factor: aryl hydrocarbon receptor nuclear translocator (ARNT). Whether hypoxia and PCBs crosstalk and affect adipokine secretion in human adipocytes remains to be explored. Using primary human adipocytes acutely co-exposed to different levels of hypoxia (24 h) and PCB126 (48 h), we observed that hypoxia significantly inhibits the PCB126 induction of cytochrome P450 (CYP1A1) transcription in a dose-response manner, and that Acriflavine (ACF)-an HIF1α inhibitor-partially restores the PCB126 induction of CYP1A1 under hypoxia. On the other hand, exposure to PCB126 did not affect the transcription of the vascular endothelial growth factor-A (VEGFA) under hypoxia. Exposure to hypoxia increased leptin and interleukin-6 (IL-6), and decreased adiponectin levels dose-dependently, while PCB126 increased IL-6 and IL-8 secretion in a dose-dependent manner. Co-exposure to PCB126 and hypoxia did not alter the adipokine secretion pattern observed under hypoxia and PCB126 exposure alone. In conclusion, our results indicate that (1) hypoxia inhibits PCB126-induced CYP1A1 expression at least partly through ARNT-dependent means, suggesting that hypoxia could affect PCB metabolism and toxicity in adipose tissue, and (2) hypoxia and PCB126 affect leptin, adiponectin, IL-6 and IL-8 secretion differently, with no apparent crosstalk between the two factors.

Acute Ingestion of Ketone Monoesters and Precursors Do Not Enhance Endurance Exercise Performance: A Systematic Review and Meta-Analysis.

There has been much consideration over whether exogenous ketone bodies have the capacity to enhance exercise performance through mechanisms such as altered substrate metabolism, accelerated recovery, or neurocognitive improvements. This systematic review aimed to determine the effects of both ketone precursors and monoesters on endurance exercise performance. A systematic search was conducted in PubMed, SPORTDiscus, and CINAHL for randomized controlled trials investigating endurance performance outcomes in response to ingestion of a ketone supplement compared to a nutritive or nonnutritive control in humans. A meta-analysis was performed to determine the standardized mean difference between interventions using a random-effects model. Hedge's g and 95% confidence intervals (CI) were reported. The search yielded 569 articles, of which eight were included in this review (80 participants; 77 men and three women). When comparing endurance performance among all studies, no significant differences were found between ketone and control trials (Hedges g = 0.136; 95% CI [-0.195, 0.467]; p = .419). Subanalyses based on type of endurance tests showed no significant differences in time to exhaustion (Hedge's g = -0.002; 95% CI [-0.312, 0.308]; p = .989) or time trial (Hedge's g = 0.057; 95% CI [-0.282, 0.395]; p = .744) values. Based on these findings, exogenous ketone precursors and monoesters do not exert significant improvements on endurance exercise performance. While all studies reported an increase in blood ketone concentrations after ingestion, ketone monoesters appear to be more effective at raising concentrations than precursors.

Physiological Responses to Hypoxia on Triglyceride Levels.

Hypoxia is a condition during which the body or specific tissues are deprived of oxygen. This phenomenon can occur in response to exposure to hypoxic environmental conditions such as high-altitude, or because of pathophysiological conditions such as obstructive sleep apnea. Circumstances such as these can restrict supply or increase consumption of oxygen, leading to oxyhemoglobin desaturation and tissue hypoxia. In certain cases, hypoxia may lead to severe health consequences such as an increased risk of developing cardiovascular diseases and type 2 diabetes. A potential explanation for the link between hypoxia and an increased risk of developing cardiovascular diseases lies in the disturbing effect of hypoxia on circulating blood lipids, specifically its capacity to increase plasma triglyceride concentrations. Increased circulating triglyceride levels result from the production of triglyceride-rich lipoproteins, such as very-low-density lipoproteins and chylomicrons, exceeding their clearance rate. Considerable research in murine models reports that hypoxia may have detrimental effects on several aspects of triglyceride metabolism. However, in humans, the mechanisms underlying the disturbing effect of hypoxia on triglyceride levels remain unclear. In this mini-review, we outline the available evidence on the physiological responses to hypoxia and their impact on circulating triglyceride levels. We also discuss mechanisms by which hypoxia affects various organs involved in the metabolism of triglyceride-rich lipoproteins. This information will benefit scientists and clinicians interested in the mechanistic of the regulatory cascade responsible for the response to hypoxia and how this response could lead to a deteriorated lipid profile and an increased risk of developing hypoxia-related health consequences.

The effect of acute intermittent hypoxia on postprandial triglyceride levels in humans: a randomized crossover trial.

BACKGROUND: Obstructive sleep apnea (OSA), a sleep disorder frequently observed in individuals living with obesity, consists of repeated involuntary breathing obstructions during sleep, leading to intermittent hypoxia (IH). In humans, acute continuous hypoxia slightly increases plasma triglycerides (TG). However, no study yet compared the postprandial TG response of individuals with or without OSA under intermittent hypoxia. METHODS: Using a randomized crossover design, seven individuals diagnosed with moderate OSA and eight healthy individuals without OSA were given a meal after which they were exposed for 6 h to normoxia or intermittent hypoxia (e.g., 15 hypoxic events per hour). Blood lipid levels were measured hourly during each session. RESULTS: Peak postprandial TG concentrations tended to be 22% higher under IH irrespective of group (IH × time interaction, p = 0.068). This trend toward higher total plasma TG was attributable to increased levels of denser TG-rich lipoproteins such as very low-density lipoproteins (VLDL) and chylomicrons (CM) remnants. Irrespective of group, the postprandial TG concentrations in denser TG-rich lipoproteins was 20% higher under IH (IH × time interaction, p = 0.036), although IH had virtually no impact on denser TG-rich lipoprotein concentrations in the OSA group. CONCLUSION: Acute intermittent hypoxia tends to negatively affect postprandial TG levels in healthy individuals, which is attributable to an increase in denser TG-carrying lipoprotein levels such as VLDL and CM remnants. This altered postprandial TG response to acute intermittent hypoxia was not observed in individuals with OSA.

Effects of different oxygen tensions on differentiated human preadipocytes lipid storage and mobilisation.

Adipose tissue expansion has been suggested to impair oxygen (O2) diffusion in the adipose tissue and cause hypoxia. This study aimed at characterising the effects of hypoxia on adipocyte lipid storage and mobilisation functions. Human preadipocytes were exposed to different O2 tensions (3, 10 and 21%) either acutely for 24 h after differentiation (acute exposure) or during differentiation (14d, chronic hypoxia). Lipoprotein lipase (LPL) activity was decreased dose-dependently by both acute and chronic hypoxia (p < .05). Acute exposure to 3, and 10% O2 stimulated the expression of lipid storage gene, while chronic exposure to 3% O2 inhibited the expression of genes involved in lipid storage and mobilisation (p < .05). Acute hypoxia dose-dependently stimulated basal lipolysis. Conversely, chronic hypoxia did not affect basal lipolysis but significantly decreased isoproterenol-stimulated lipolysis (p < .05). In conclusion, the effects of hypoxia on human adipocyte lipid storage and mobilisation functions are complex but could favour ectopic fat deposition.

Normobaric hypoxia does not alter the critical environmental limits for thermal balance during exercise-heat stress.

NEW FINDINGS: What is the central question of this study? Hypoxia reportedly does not impair thermoregulation during exercise in compensable heat stress conditions: does it have an impact on maximal heat dissipation and therefore the critical environmental limit for the physiological compensability of core temperature? What is the main finding and its importance? Although skin blood flow was higher in hypoxia, no differences in sweat rates or the critical environmental limit for the physiological compensability of core temperature - an indicator of maximal heat loss - were found compared to exercise in normoxia, indicating no influence of normobaric hypoxia on thermoregulatory capacity in warm conditions. ABSTRACT: Altered control of skin blood flow (SkBF) in hypoxia does not impair thermoregulation during exercise in compensable conditions, but its impact on maximal heat dissipation is unknown. This study therefore sought to determine whether maximum heat loss is altered by hypoxia during exercise in warm conditions. On separate days, eight males exercised for 90 min at a fixed heat production of ∼500 W in normoxia (NORM) or normobaric hypoxia (HYP, FIO2  = 0.13) in a 34°C environment. Ambient vapour pressure was maintained at 2.13 kPa for 45 min, after which it was raised 0.11 kPa every 7.5 min. The critical ambient vapour pressure at which oesophageal temperature inflected upward (Pcrit ) indicated that maximum heat dissipation had been reached. Neither local sweat rates on the upper arm, back and forehead (average NORM: 1.46 (0.15) vs. HYP: 1.41 (0.16) mg cm-2  min-1 ; P = 0.59) nor whole-body sweat losses (NORM: 1029 (137) g vs. HYP: 1025 (150) g; P = 0.95) were different between trials. Laser-Doppler flux values (LDF; arbitrary units), an index of SkBF, were not different between NORM and HYP on the forearm (P = 0.23) or back (P = 0.73); however, when normalized as a percentage of maximum, LDF values tended to be higher in HYP compared to NORM at the forearm (condition effect, P = 0.05) but not back (P = 0.19). Despite potentially greater SkBF in hypoxia, there was no difference in Pcrit between conditions (NORM: 3.67 (0.35) kPa; HYP: 3.46 (0.39) kPa; P = 0.22). These findings suggest that hypoxia does not independently alter thermoregulatory capacity during exercise in warm conditions.

A retrospective analysis to determine if exercise training-induced thermoregulatory adaptations are mediated by increased fitness or heat acclimation.

NEW FINDINGS: What is the central question of this study? Are fitness-related improvements in thermoregulatory responses during uncompensable heat stress mediated by aerobic capacity V̇O2max or is it the partial heat acclimation associated with training? What is the main finding and its importance? During uncompensable heat stress, individuals with high and low V̇O2max displayed similar sweating and core temperature responses whereas exercise training in previously untrained individuals resulted in a greater sweat rate and a smaller rise in core temperature. These observations suggest that it is training, not V̇O2max per se, that mediates thermoregulatory improvements during uncompensable heat stress. ABSTRACT: It remains unclear whether aerobic fitness, as defined by the maximum rate of oxygen consumption V̇O2max , independently improves heat dissipation in uncompensable environments, or whether the thermoregulatory adaptations associated with heat acclimation are due to repeated bouts of exercise-induced heat stress during regular aerobic training. The present analysis sought to determine if V̇O2max independently influences thermoregulatory sweating, maximum skin wettedness (ωmax ) and the change in rectal temperature (ΔTre ) during 60 min of exercise in an uncompensable environment (37.0 ± 0.8°C, 4.0 ± 0.2 kPa, 64 ± 3% relative humidity) at a fixed rate of heat production per unit mass (6 W kg-1 ). Retrospective analyses were performed on 22 participants (3 groups), aerobically unfit (UF; n = 7; V̇O2max : 41.7 ± 9.4 ml kg-1  min-1 ), aerobically fit (F; n = 7; V̇O2max : 55.6 ± 4.3 ml kg-1  min-1 ; P < 0.01) and aerobically unfit (n = 8) individuals, before (pre; V̇O2max : 45.8 ± 11.6 ml kg-1  min-1 ) and after (post; V̇O2max : 52.0 ± 11.1 ml kg-1  min-1 ; P < 0.001) an 8-week training intervention. ωmax was similar between UF (0.74 ± 0.09) and F (0.78 ± 0.08, P = 0.22). However, ωmax was greater post- (0.84 ± 0.08) compared to pre- (0.72 ± 0.06, P = 0.02) training. During exercise, mean local sweat rate (forearm and upper-back) was greater post- (1.24 ± 0.20 mg cm-2  min-1 ) compared to pre- (1.04 ± 0.25 mg cm-2  min-1 , P < 0.01) training, but similar between UF (0.94 ± 0.31 mg cm-2  min-1 , P = 0.90) and F (1.02 ± 0.30 mg cm-2  min-1 ). The ΔTre at 60 min of exercise was greater pre- (1.13 ± 0.16°C, P < 0.01) compared to post- (0.96 ± 0.14°C) training, but similar between UF (0.85 ± 0.29°C, P = 0.22) and F (0.95 ± 0.22°C). Taken together, aerobic training, not V̇O2max per se, confers an increased ωmax , greater sweat rate, and smaller rise in core temperature during uncompensable heat stress in fit individuals.

Beyond the mechanical lens: Systemic inflammatory responses to repetitive lifting under varying loads and frequencies.

OBJECTIVE: Currently, low back disorder (LBD) research focuses primarily on mechanical variables to assess whether task demands exceed tissue capacity; however, it is important to assess how other nonmechanical variables affect tissue capacity in a time-dependent manner. The current investigation sought to explore physiological responses to an acute lifting task, as lifting has been implicated as a risk factor in the development of LBDs. METHODS: Twelve participants completed two sessions of 2 h of repetitive symmetrical lifting from floor to knuckle height under two conditions, matched for total external work (Low Force High Repetition (LFHR) and High Force Low Repetition (HFLR)). Full-body kinematics and ground reaction forces were measured throughout. Interleukin 6 (IL-6) and interleukin 8 (IL-8), markers of systemic inflammation, were assessed from blood sampling at Baseline, 0, 4 and 24 h post-lifting on both days. Dual x-ray absorptiometry (DEXA) scans were also performed on participants to quantify body composition. RESULTS: Significant load (HFLR and LFHR) * time (Baseline, 0, 4, 24 h) interaction effects were found for both IL-6 and IL-8, where the LFHR condition resulted in greater responses at 0 and 4 h post-lifting. CONCLUSIONS: This was the first study of its kind to concurrently measure peak and cumulative spinal moments and their relationship to systemic inflammation in both sexes, while strictly controlling for confounding variables (e.g. physical activity, caloric intake, body composition, etc.). Greater levels of IL-6 and IL-8 were seen in the LFHR condition, likely due to the greater cumulative spinal moments in this condition.

[The controversial effects of low-calorie sweeteners]. / Les édulcorants de la controverse.

Substantial reviews of the most recent evidence report a strong relationship between the consumption of sugar-sweetened beverages and adverse health effects, such as the prevalence of obesity and metabolic diseases. Various public policies were recently undertaken by many countries in the hope of reducing sugar-sweetened beverage consumption amongst their population. This has led the food industries to promote low-calorie sweeteners (sugar substitutes) as a healthy alternative that would limit caloric intake without compromising the sweet taste of food and beverages. However, is the use of low-calorie sweeteners as a means of limiting or reducing energy intake without consequences for our health? This review aims to discuss the effects of low-calorie sweeteners consumption on health and to elucidate whether their use should be recommended by health professionals to their patients as part of weight management.

TITLE: Les édulcorants de la controverse. ABSTRACT: La littérature révèle un lien important entre la consommation de boissons sucrées et des effets néfastes sur la santé humaine, comme la prévalence de l'obésité et des maladies métaboliques. Différentes stratégies ont été adoptées par de nombreux pays afin d'inciter la population à réduire leur consommation de boissons sucrées. Les industries alimentaires ont, quant à elles, promu les substituts de sucre (ou édulcorants), les présentant comme une saine alternative qui permettrait de réduire l'apport calorique sans avoir à compromettre l'agréable goût sucré des aliments et des boissons. Toutefois, l'utilisation des substituts de sucre comme moyen de limiter ou de réduire l'apport énergétique est-elle sans conséquence pour la santé ? Cette revue vise à discuter des différents effets associés à la consommation d'édulcorants sur la santé et à élucider si leur utilisation devrait être recommandée par les professionnels de la santé à leurs patients dans le cadre de la gestion de leur poids.

Steady-state sweating during exercise is determined by the evaporative requirement for heat balance independently of absolute core and skin temperatures.

KEY POINTS: When exercise was prescribed to elicit a fixed evaporative heat balance requirement (Ereq ), no differences in steady-state sweat rates were observed with different absolute oesophageal and/or skin temperatures, secondary to differences in time of the day (i.e. morning (AM) vs. afternoon (PM)) and ambient temperature (i.e. 23°C vs. 33°C). Exercise at a fixed metabolic heat production (Hprod ), but a different Ereq (due to differences in air temperature), yielded higher steady-state sweat rates with a higher Ereq , irrespective of absolute oesophageal temperature. Circadian rhythm did not alter the change in core temperature prior to the onset for sudomotor activation, nor the thermosensitivity, resulting in similar cumulative whole-body sweat rates irrespective of time of day at a fixed Ereq . Collectively, these data indicate that during exercise in a compensable environment, steady-state sudomotor responses are influenced by Ereq rather than absolute core and skin temperatures, or Hprod . ABSTRACT: The present study sought to determine whether absolute core temperature (modified via diurnal variation) and absolute skin temperature (modified by different air temperatures (Ta )) alters the steady-state sweating response to exercise at a fixed evaporative heat balance requirement (Ereq ). Ten males exercised for 60 min on six occasions. Three Ta /heat production (Hprod ) combinations (23°C/525 W, 33°C/400 W, 33˚C/525 W) were completed in the morning (08.00 h, AM) and afternoon (16.00 h, PM), to yield: (1) the same Ereq (200 or 275 W·m-2 ) with different absolute core temperatures (AM vs. PM); (2) the same Ereq (200 W·m-2 ) with different skin temperatures (Ta : 23˚C vs. 33˚C); (3) the same heat production (525 W) with different Ereq (200 vs. 275 W·m-2 ). Oesophageal temperature (Toes ), local sweat rate (LSR) on the arm and upper-back, and whole-body sweat rate (WBSR) were measured. Steady-state Toes was always higher in PM versus AM at an Ereq of 200 W·m-2 (23°C, P = 0.001; 33°C, P = 0.004) and 275 W·m-2 , (33°C, P = 0.001). However steady-state mean LSR (200 W·m-2 /23°C: P = 0.25; 200 W·m-2 /33°C: P = 0.86; 275 W·m-2 /33°C: P = 0.53) and WBSR (200 W·m-2 /23°C: P = 0.79; 200 W·m-2 /33°C: P = 0.48; 275W·m-2 /33°C: P = 0.32) were similar. When Ereq was matched (200 W·m-2 ) with different Ta (23°C vs. 33°C), steady-state LSR (P > 0.17) and WBSR (P > 0.93) were similar despite different skin temperatures. For the same Hprod (525 W) but different Ereq (200 vs. 275 W·m-2 ), mean LSR (P < 0.001), and WBSR (P < 0.001) were higher with a greater Ereq . Collectively, steady-state sweating during exercise is altered by Ereq but not Toes , skin temperature, or Hprod .

Thermoregulatory adaptations with progressive heat acclimation are predominantly evident in uncompensable, but not compensable, conditions.

This study assessed whether, notwithstanding lower resting absolute core temperatures, alterations in time-dependent changes in thermoregulatory responses following partial and complete heat acclimation (HA) are only evident during uncompensable heat stress. Eight untrained individuals underwent 8 wk of aerobic training (i.e., partial HA) followed by 6 days of HA in 38°C/65% relative humidity (RH) (i.e., complete HA). On separate days, esophageal temperature (Tes), arm (LSRarm), and back (LSRback) sweat rate, and whole body sweat rate (WBSR) were measured during a 45-min compensable (37°C/30% RH) and 60-min uncompensable (37°C/60% RH) heat stress trial pre-training (PRE-TRN), post-training (POST-TRN), and post-heat acclimation (POST-HA). For compensable heat stress trials, resting Tes was lower POST-TRN (36.74 ± 0.27°C, P = 0.05) and POST-HA (36.60 ± 0.27°C, P = 0.001) compared with PRE-TRN (36.99 ± 0.19°C); however, ΔTes was similar in all trials (PRE-TRN:0.40 ± 0.23°C; POST-TRN:0.42 ± 0.20°C; POST-HA:0.43 ± 0.12°C, P = 0.97). While LSRback was unaltered by HA (P = 0.94), end-exercise LSRarm was higher POST-TRN (0.70 ± 0.14 mg·cm-2·min-1, P < 0.001) and POST-HA (0.75 ± 0.16 mg·cm-2·min-1, P < 0.001) compared with PRE-TRN (0.61 ± 0.15 mg·cm-2·min-1). Despite matched evaporative heat balance requirements, steady-state WBSR (31st-45th min) was greater POST-TRN (12.7 ± 1.0 g/min, P = 0.02) and POST-HA (12.9 ± 0.8 g/min, P = 0.004), compared with PRE-TRN (11.7 ± 0.9 g/min). For uncompensable heat stress trials, resting Tes was lower POST-TRN (36.77 ± 0.22°C, P = 0.05) and POST-HA (36.62 ± 0.15°C, P = 0.03) compared with PRE-TRN (36.86 ± 0.24°C). But ΔTes was smaller POST-TRN (0.77 ± 0.19°C, P = 0.05) and POST-HA (0.75 ± 0.15°C, P = 0.04) compared with PRE-TRN (1.10 ± 0.32°C). LSRback and LSRarm increased with HA (P < 0.007), supporting the greater WBSR with HA (POST-TRN:14.4 ± 2.4 g/min, P < 0.001; POST-HA:16.8 ± 2.8 g/min, P < 0.001) compared with PRE-TRN (12.7 ± 3.2 g/min). In conclusion, the thermal benefits of HA are primarily evident when conditions challenge the physiological capacity to dissipate heat.NEW & NOTEWORTHY We demonstrate that neither partial nor complete heat acclimation alters the change in core temperature during compensable heat stress compared with an unacclimated state, despite a marginally greater whole body sweat rate. However, the greater local and whole body sweat rate with partial and complete heat acclimation reduced the rise in core temperature during 60 min of uncompensable heat stress compared with an unacclimated state, suggesting the improvements in heat dissipation associated with heat acclimation are best observed when the upper physiological limits for evaporative heat loss are challenged.

The Effect of Acute Continuous Hypoxia on Triglyceride Levels in Constantly Fed Healthy Men.

INTRODUCTION: Elevated plasma triglyceride (TG) concentrations are an important contributor to deleterious metabolic alterations. Evidence in animals suggest that acute exposure to an environment with reduced oxygen inhibits plasma TG clearance and causes important rise in plasma TG, especially in the postprandial state. The objective of this study was to characterize the effects of an acute exposure to normobaric hypoxia on prandial TG levels in 2 distinct lipoprotein subtypes in healthy humans: chylomicrons which are secreted by the intestine and carry dietary lipids, and denser TG carriers (mainly VLDL), which are secreted by the liver and carry endogenous lipids. Plasma lipolytic activity was also assessed. It was hypothesized that hypoxia would reduce prandial plasma lipolytic activity and raise prandial TG levels in both lipoprotein subtypes. METHODS: Using a randomized crossover design, 9 healthy young men were studied for 6 h in a constantly fed state while being exposed to either normobaric hypoxia (FiO2 = 0.12) and normoxic conditions on two different days. Prandial glucose, TG, non-esterified fatty acid (NEFA), and post-heparin plasma lipolytic activity were measured during each session. RESULTS: Six hours of exposure to hypoxia marginally increase prandial glycemia (+5%, p = 0.06) while increasing insulinemia by 40% (p = 0.04). Hypoxia induced a 30% rise in prandial NEFA levels and tended to slightly increased total prandial TG levels by 15% (p = 0.11). No difference was observed in TG concentrations and metabolism of chylomicrons between conditions. However, TG in the VLDL containing fraction decreased significantly overtime under normoxia but not under hypoxia (time × condition interaction, p = 0.02). No difference was observed in post-heparin plasmatic lipolytic activity between conditions. CONCLUSION: Acute hypoxia in healthy men tends to increase prandial VLDL-TG levels. These results lend support to the increased blood lipid levels reported in animals exposed acutely to lower partial pressures of oxygen.

Are Fruit Juices Healthier Than Sugar-Sweetened Beverages? A Review.

Free sugars overconsumption is associated with an increased prevalence of risk factors for metabolic diseases such as the alteration of the blood lipid levels. Natural fruit juices have a free sugar composition quite similar to that of sugar-sweetened beverages. Thus, could fruit juice consumption lead to the same adverse effects on health as sweetened beverages? We attempted to answer this question by reviewing the available evidence on the health effects of both sugar-sweetened beverages and natural fruit juices. We determined that, despite the similarity of fruits juices to sugar-sweetened beverages in terms of free sugars content, it remains unclear whether they lead to the same metabolic consequences if consumed in equal dose. Important discrepancies between studies, such as type of fruit juice, dose, duration, study design, and measured outcomes, make it impossible to provide evidence-based public recommendations as to whether the consumption of fruit juices alters the blood lipid profile. More randomized controlled trials comparing the metabolic effects of fruit juice and sugar-sweetened beverage consumption are needed to shape accurate public health guidelines on the variety and quantity of free sugars in our diet that would help to prevent the development of obesity and related health problems.

No effect of acute normobaric hypoxia on plasma triglyceride levels in fasting healthy men.

Circulating fatty acids are a major systemic energy source in the fasting state as well as a determinant of hepatic triglycerides (TG)-rich very-low-density lipoprotein production. Upon acute hypoxia, sympathetic arousal induces adipose tissue lipolysis, resulting in an increase in circulating nonesterified fatty acids (NEFA). Animal studies suggest that TG clearance may also be strongly reduced under hypoxia, though this effect has been shown to be dependent on temperature. Whether the hypoxia-induced rise in blood fatty acid concentrations affects fasting TG levels in humans under thermoneutral conditions remains unknown. TG, NEFA, and glycerol levels were measured in fasted healthy young men (n = 10) exposed for 6 h to either normoxia (ambient air) or acute hypoxia (fraction of inspired oxygen = 0.12) in a randomized, crossover design. Participants were casually clothed and rested in front of a fan in an environmental chamber maintained at 28 °C during each trial. Under hypoxia, a significantly greater increase in NEFA occurred (condition × time interaction, p = 0.049) and glycerol levels tended to be higher (condition × time, p = 0.104), suggesting an increase in adipose tissue lipolysis. However, plasma TG levels did not change over time and did not differ between the normoxia and hypoxia conditions. In conclusion, acute exposure to normobaric hypoxia under thermoneutral condition in healthy men during fasting state increased lipolysis without affecting circulating TG.