Resistance training and cardiometabolic risk in women with metabolically healthy and unhealthy obesity.

Despite some reported benefits, there is a low quality of evidence for resistance training (RT) improving metabolic health of individuals with overweight or obesity. We evaluated the impact of RT on body composition, cardiorespiratory fitness (CRF) and physical performance, lipid-lipoprotein profile, inflammation, and glucose-insulin homeostasis in 51 postmenopausal women versus 29 controls matched for age, obesity, and physical activity. Exercised women were further subdivided for comparison of RT effects into those presenting metabolically healthy obesity (MHO) and those with metabolically unhealthy obesity (MUHO) classified according to Karelis and Rabasa-Lhoret or an approach based on adipose tissue secretory dysfunction using the plasma adiponectin(A)/leptin (L) ratio. Participants followed a 4-month weekly RT program targeting major muscle groups (3 × 10 repetitions at 80% one repetition maximum (1-RM)). Percent fat marginally decreased and lean body mass increased (0.01 < p < 0.05) while CRF and muscular strength improved in all women, after RT (effect size (ES): 0.11-1.21 (trivial to large effects), p ˂ 0.01). Fasting plasma triacylglycerol and high-density lipoprotein-cholesterol levels slightly increased and decreased, respectively, in participants with MHO using the A/L ratio approach (ES: -0.47 to 1.07 (small to large effects), p ˂ 0.05). Circulating interleukin-6 soluble receptor decreased in both groups and soluble tumor necrosis factor receptor-1/soluble tumor necrosis factor receptor-2 in women with MUHO only, irrespective of definition (ES: -0.42 to -0.84 (small to large effects), p ˂ 0.05). Glucose-insulin homeostasis was unchanged regardless of group or definition. RT improved physical performance and body composition but had a lesser impact on cardiometabolic risk in women with obesity, irrespective of their metabolic phenotype.

Plasma adiponectin/leptin ratio associates with subcutaneous abdominal and omental adipose tissue characteristics in women.

BACKGROUND: A better understanding of adipose tissue (AT) dysfunction, which includes morphological and functional changes such as adipocyte hypertrophy as well as impaired adipogenesis, lipid storage/mobilization, endocrine and inflammatory responses, is needed in the context of obesity. One dimension of AT dysfunction, secretory adiposopathy, often assessed as a low plasma adiponectin (A)/leptin (L) ratio, is commonly observed in obesity. The aim of this study was to examine markers of AT development and metabolism in 67 women of varying age and adiposity (age: 40-62 years; body mass index, BMI: 17-41 kg/m2) according to levels of adiponectinemia, leptinemia or the plasma A/L ratio. METHODS: Body composition, regional AT distribution and circulating adipokines were determined. Lipolysis was measured from glycerol release in subcutaneous abdominal (SCABD) and omental (OME) adipocytes under basal, isoproterenol-, forskolin (FSK)- and dibutyryl-cyclic AMP (DcAMP)-stimulated conditions. Adipogenesis (C/EBP-α/ß/δ, PPAR-γ2 and SREBP-1c) and lipid metabolism (ß2-ARs, HSL, FABP4, LPL and GLUT4) gene expression (RT-qPCR) was assessed in both fat depots. Participants in the upper versus lower tertile of adiponectin, leptin or the A/L ratio were compared. RESULTS: Basal lipolysis was similar between groups. Women with a low plasma A/L ratio were characterized by higher adiposity and larger SCABD and OME adipocytes (p<0.01) compared to those with a high ratio. In OME adipocytes, women in the low adiponectinemia tertile showed higher isoproterenol-stimulated lipolysis (0.01

No benefit of vitamin D supplementation on muscle function and health-related quality of life in primary cardiovascular prevention patients with statin-associated muscle symptoms: A randomized controlled trial.

BACKGROUND: Statins are the leading lipid-lowering drugs, reducing blood cholesterol by controlling its synthesis. Side effects are linked to the use of statins, in particular statin-associated muscle symptoms (SAMS). Some data suggest that vitamin D supplementation could reduce SAMS. OBJECTIVE: The purpose of this study was to evaluate the potential benefits of vitamin D supplementation in a randomized controlled trial. METHODS: Men (n = 23) and women (n = 15) (50.5 ± 7.7 years [mean ± SD]) in primary cardiovascular prevention, self-reporting or not SAMS, were recruited. Following 2 months of statin withdrawal, patients were randomized to supplementation (vitamin D or placebo). After 1 month of supplementation, statins were reintroduced. Before and 2 months after drug reintroduction, muscle damage (creatine kinase and myoglobin) was measured. Force (F), endurance (E) and power (P) of the leg extensors (ext) and flexors (fle) and handgrip strength (FHG) were also measured with isokinetic and handheld dynamometers, respectively. The Short Form 36 Health Survey (SF-36) questionnaire and a visual analog scale (VAS) were administrated to assess participants' self-reported health-related quality of life and SAMS intensity, respectively. Repeated-measures analysis was used to investigate the effects of time, supplementation, and their interaction, according to the presence of SAMS. RESULTS: Despite no change for objective measures, subjective measures worsened after reintroduction of statins, independent of supplementation (VAS, SF-36 mental component score, all p < 0.05). However, no interaction between time and supplementation according to the presence of SAMS was observed for any variables. CONCLUSIONS: Vitamin D supplementation does not appear to mitigate SAMS.

Impact of statin withdrawal on perceived and objective muscle function.

BACKGROUND AND AIMS: Statin-associated muscle symptoms (SAMS) are frequently reported. Nevertheless, few data on objective measures of muscle function are available. Recent data suggesting an important nocebo effect with statin use could confound such effects. The objective was to assess if subjective and objective measures of muscle function improve after drug withdrawal in SAMS reporters. METHODS: Patients (59 men, 33 women, 50.3±9.6 yrs.) in primary cardiovascular prevention composed three cohorts: statin users with (SAMS, n = 61) or without symptoms (No SAMS, n = 15), and controls (n = 16) (registered at clinicaltrials.gov, NCT01493648). Force (F), endurance (E) and power (P) of the leg extensors (ext) and flexors (fle) and handgrip strength (Fhg) were measured using isokinetic and handheld dynamometers, respectively. A 10-point visual analogue scale (VAS) was used to self-assess SAMS intensity. Measures were taken before and after two months of withdrawal. RESULTS: Following withdrawal, repeated-measures analyses show improvements for the entire cohort in Eext, Efle, Ffle, Pext and Pfle (range +7.2 to +13.3%, all p≤0.02). Post-hoc analyses show these changes to occur notably in SAMS (+8.8 to +16.6%), concurrent with a decrease in subjective perception of effects in SAMS (VAS, from 5.09 to 1.85). Fhg was also improved in SAMS (+4.0 to +6.2%) when compared to No SAMS (-1.7 to -4.2%) (all p = 0.02). CONCLUSIONS: Whether suffering from "true" SAMS or nocebo, those who reported SAMS had modest but relevant improvements in muscle function concurrent with a decrease in subjective symptoms intensity after drug withdrawal. Greater attention by clinicians to muscle function in frail statin users appears warranted. TRIAL REGISTRATION: This study is registered in clinicaltrials.gov (NCT01493648).

Intra-abdominal adipose depot variation in adipogenesis, lipogenesis, angiogenesis, and fibrosis gene expression and relationships with insulin resistance and inflammation in premenopausal women with severe obesity

Although severe obesity is associated with insulin resistance (IR) and inflammation, secretory function of intra-abdominal adipose tissues and their relationships with IR and inflammation markers remain poorly understood. Aims were to measure gene expression of adipogenic (C/EBPα/β, PPARγ-1/2, SREBP-1c, LXRα), lipogenic (SCD1, DGAT-1/2), angiogenic (VEGFα, leptin), and fibrotic (LOX, COL6A3) factors in the round ligament (RL), omental (OM), and mesenteric (ME) fat depots and to evaluate their relationships with IR and inflammation markers in 48 women with severe obesity undergoing bariatric surgery. Gene expression was assessed by RT-qPCR, and plasma glucose and insulin (HOMA-IR calculated), PAI-1, IL-6, TNFα, adiponectin, and leptin levels were determined. C/EBPβ and PPARγ-1/2 mRNA levels were more expressed in the OM (0.001

Contribution of markers of adiposopathy and adipose cell size in predicting insulin resistance in women of varying age and adiposity.

Adipose tissue (AT) dysfunctions, such as adipocyte hypertrophy, macrophage infiltration and secretory adiposopathy (low plasma adiponectin/leptin, A/L, ratio), associate with metabolic disorders. However, no study has compared the relative contribution of these markers to cardiometabolic risk in women of varying age and adiposity. Body composition, regional AT distribution, lipid-lipoprotein profile, glucose homeostasis and plasma A and L levels were determined in 67 women (age: 40-62 years; BMI: 17-41 kg/m2). Expression of macrophage infiltration marker CD68 and adipocyte size were measured from subcutaneous abdominal (SCABD) and omental (OME) fat. AT dysfunction markers correlated with most lipid-lipoprotein levels. The A/L ratio was negatively associated with fasting insulinemia and HOMA-IR, while SCABD or OME adipocyte size and SCABD CD68 expression were positively related to these variables. Combination of tertiles of largest adipocyte size and lowest A/L ratio showed the highest HOMA-IR. Multiple regression analyses including these markers and TAG levels revealed that the A/L ratio was the only predictor of fasting insulinemia and HOMA-IR. The contribution of the A/L ratio was superseded by adipose cell size in the model where the latter replaced TAGs. Finally, leptinemia was a better predictor of IR than adipocyte size and the A/L ratio in our participants sample.

Intra-abdominal adipose depot variation in adipogenesis, lipogenesis, angiogenesis, and fibrosis gene expression and relationships with insulin resistance and inflammation in premenopausal women with severe obesity.

Although severe obesity is associated with insulin resistance (IR) and inflammation, secretory function of intra-abdominal adipose tissues and their relationships with IR and inflammation markers remain poorly understood. Aims were to measure gene expression of adipogenic (C/EBPα/ß, PPARγ-1/2, SREBP-1c, LXRα), lipogenic (SCD1, DGAT-1/2), angiogenic (VEGFα, leptin), and fibrotic (LOX, COL6A3) factors in the round ligament (RL), omental (OM), and mesenteric (ME) fat depots and to evaluate their relationships with IR and inflammation markers in 48 women with severe obesity undergoing bariatric surgery. Gene expression was assessed by RT-qPCR, and plasma glucose and insulin (HOMA-IR calculated), PAI-1, IL-6, TNFα, adiponectin, and leptin levels were determined. C/EBPß and PPARγ-1/2 mRNA levels were more expressed in the OM (0.001

Ischemic Preconditioning Enhances Aerobic Adaptations to Sprint-Interval Training in Athletes Without Altering Systemic Hypoxic Signaling and Immune Function.

Optimizing traditional training methods to elicit greater adaptations is paramount for athletes. Ischemic preconditioning (IPC) can improve maximal exercise capacity and up-regulate signaling pathways involved in physiological training adaptations. However, data on the chronic use of IPC are scarce and its impact on high-intensity training is still unknown. We investigated the benefits of adding IPC to sprint-interval training (SIT) on performance and physiological adaptations of endurance athletes. In a randomized controlled trial, athletes included eight SIT sessions in their training routine for 4 weeks, preceded by IPC (3 × 5 min ischemia/5 min reperfusion cycles at 220 mmHg, n = 11) or a placebo (20 mmHg, n = 9). Athletes were tested pre-, mid-, and post-training on a 30 s Wingate test, 5-km time trial (TT), and maximal incremental step test. Arterial O2 saturation, heart rate, rate of perceived exertion, and quadriceps muscle oxygenation changes in total hemoglobin (Δ[THb]), deoxyhemoglobin (Δ[HHb]), and tissue saturation index (ΔTSI) were measured during exercise. Blood samples were taken pre- and post-training to determine blood markers of hypoxic response, lipid-lipoprotein profile, and immune function. Differences within and between groups were analyzed using Cohen's effect size (ES). Compared to PLA, IPC improved time to complete the TT (Mid vs. Post: -1.6%, Cohen's ES ± 90% confidence limits -0.24, -0.40;-0.07) and increased power output (Mid vs. Post: 4.0%, ES 0.20, 0.06;0.35), Δ[THb] (Mid vs. Post: 73.6%, ES 0.70, -0.15;1.54, Pre vs. Post: 68.5%, ES 0.69, -0.05;1.43), Δ[HHb] (Pre vs. Post: 12.7%, ES 0.24, -0.11;0.59) and heart rate (Pre vs. Post: 1.4%, ES 0.21, -0.13;0.55, Mid vs. Post: 1.6%, ES 0.25, -0.09;0.60). IPC also attenuated the fatigue index in the Wingate test (Mid vs. Post: -8.4%, ES -0.37, -0.79;0.05). VO2peak and maximal aerobic power remained unchanged in both groups. Changes in blood markers of the hypoxic response, vasodilation, and angiogenesis remained within the normal clinical range in both groups. We concluded that IPC combined with SIT induces greater adaptations in cycling endurance performance that may be related to muscle perfusion and metabolic changes. The absence of elevated markers of immune function suggests that chronic IPC is devoid of deleterious effects in athletes, and is thus a safe and potent ergogenic tool.

Similar Recovery of Maximal Cycling Performance after Ischemic Preconditioning, Neuromuscular Electrical Stimulation or Active Recovery in Endurance Athletes.

This study investigated the efficacy of ischemic preconditioning (IPC) on the recovery of maximal aerobic performance and physiological responses compared with commonly used techniques. Nine endurance athletes performed two 5-km cycling time trials (TT) interspersed by 45 minutes of recovery that included either IPC, active recovery (AR) or neuromuscular electrical stimulation (NMES) in a randomized crossover design. Performance, blood markers, arterial O2 saturation (SpO2), heart rate (HR), near-infrared spectroscopy-derived muscle oxygenation parameters and perceptual measures were recorded throughout TTs and recovery. Differences were analyzed using repeated-measures ANOVAs and Cohen's effect size (ES). The decrement in chronometric performance from TT1 to TT2 was similar between recovery modalities (IPC: -6.1 sec, AR: -7.9 sec, NMES: -5.4 sec, p = 0.84, ES 0.05). The modalities induced similar increases in blood volume before the start of TT2 (IPC: 13.3%, AR: 14.6%, NMES: 15.0%, p = 0.79, ES 0.06) and similar changes in lactate concentration and pH. There were negligible differences between conditions in bicarbonate concentration, base excess of blood and total concentration of carbon dioxide, and no difference in SpO2, HR and muscle O2 extraction during exercise (all p > 0.05). We interpreted these findings to suggest that IPC is as effective as AR and NMES to enhance muscle blood volume, metabolic by-products clearance and maximal endurance performance. IPC could therefore complement the athlete's toolbox to promote recovery.

Comparing an adiposopathy approach with four popular classifications schemes to categorize the metabolic profile of postmenopausal women.

Numerous classifications are used to discern metabolically healthy obese (MHO) from metabolically abnormal obese (MAO) individuals. The goal of this study was to compare a single phenotype approach, adiposopathy (i.e., the plasma adiponectin/leptin ratio), with four commonly used classifications (International Diabetes Federation (IDF), Karelis, Lynch, Wildman), all based on obesity with other risk factors), for their ability to discern phenotypic differences between MAO and MHO postmenopausal women. Anthropometry, body composition, blood pressure, cardiorespiratory fitness (CRF), lipid-lipoprotein, hepatic, inflammatory, and adipokine profiles, as well as glucose-insulin homeostasis, were assessed in 79 obese sedentary postmenopausal women (60 ± 5 years; body mass index, BMI, 34.0 ± 3.7 kg/m2). Abdominal subcutaneous adipose tissue (SCAT) expression of selected genes involved in fatty acid metabolism and inflammation was used as markers of tissue state (n = 48). Beyond their intrinsic criteria, adiposopathy was almost as effective as the Karelis definition in discerning differences in MHO for adiposity (reduced body weight, BMI, waist circumference, and fat mass), lipid-lipoprotein (lower triacylglycerol and higher HDL-cholesterol levels, reduced atherogenic ratios) and adipokine (higher adiponectin and lower leptin levels) profiles, and glucose-insulin homeostasis (lower insulin resistance) as well as for some SCAT gene expression related to lipolysis and lipogenesis, but was the only one able to distinguish these subjects for greater CRF. The other classifications revealed fewer differences between MAO and MHO women. These data suggest that considering a marker of AT dysfunction such as adiposopathy either alone or in addition to other criteria could be potentially interesting in discerning the MHO phenotype.

The relationship between adiposopathy and glucose-insulin homeostasis is not affected by moderate-intensity aerobic training in healthy women with obesity

The contribution of adiposopathy to glucose-insulin homeostasis remains unclear. This longitudinal study examined the potential relationship between the adiponectin/leptin ratio (A/L, a marker of adiposopathy) and insulin resistance (IR: homeostasis model assessment (HOMA)), insulin sensitivity (IS: Matsuda), and insulin response to an oral glucose tolerance test before and after a 16-week walking program, in 29 physically inactive pre- and postmenopausal women with obesity (BMI, 29-35 kg/m2; age, 47-54 years). Anthropometry, body composition, VO2max, and fasting lipid-lipoprotein and inflammatory profiles were assessed. A/L was unchanged after training (p = 0.15), despite decreased leptin levels (p < 0.05). While the Matsuda index tended to increase (p = 0.07), HOMA decreased (p < 0.05) and fasting insulin was reduced (p < 0.01) but insulin area under the curve (AUC) remained unchanged (p = 0.18) after training. Body fatness and VO2max were improved (p < 0.05) while triacylglycerols increased and HDL-CHOL levels decreased after training (p < 0.05). At baseline, A/L was positively associated with VO2max, HDL-CHOL levels, and Matsuda (0.37 < ρ < 0.56; p < 0.05) but negatively with body fatness, HOMA, insulin AUC, IL-6, and hs-CRP levels (− 0.41 < ρ < − 0.66; p < 0.05). After training, associations with fitness, HOMA, and inflammation were lost. Multiple regression analysis revealed A/L as an independent predictor of IR and IS, before training (partial R2 = 0.10 and 0.22), although A/L did not predict the insulin AUC pre- or post-intervention. A significant correlation was found between training-induced changes to A/L and IS (r = 0.38; p < 0.05) but not with IR or insulin AUC. Although changes in the A/L ratio could not explain improvements to glucose-insulin homeostasis indices following training, a relationship with insulin sensitivity was revealed in healthy women with obesity

High ApoD protein level in the round ligament fat depot of severely obese women is associated with an improved inflammatory profile.

PURPOSE: Apolipoprotein D (ApoD) is a lipocalin participating in lipid transport. It binds to a variety of ligands, with a higher affinity for arachidonic acid, and is thought to have a diverse array of functions. We investigated a potential role for ApoD in insulin sensitivity, inflammation, and thrombosis-processes related to lipid metabolism-in severely obese women. METHODS: We measured ApoD expression in a cohort of 44 severely obese women including dysmetabolic and non-dysmetabolic patients. Physical and metabolic characteristics of these women were determined from anthropometric measurements and blood samples. ApoD was quantified at the mRNA and protein levels in samples from three intra-abdominal adipose tissues (AT): omental, mesenteric and round ligament (RL). RESULTS: ApoD protein levels were highly variable between AT of the same individual. High ApoD protein levels, particularly in the RL depot, were linked to lower plasma insulin levels (-40%, p = 0.015) and insulin resistance (-47%, p = 0.022), and increased insulin sensitivity (+10%, p = 0.008). Lower circulating pro-inflammatory PAI-1 (-39%, p = 0.001), and TNF-α (-19%, p = 0.030) levels were also correlated to high ApoD protein in the RL AT. CONCLUSIONS: ApoD variability between AT was consistent with different accumulation efficiencies and/or metabolic functions according to the anatomic location of fat depots. Most statistically significant correlations implicated ApoD protein levels, in agreement with protein accumulation in target tissues. These correlations associated higher ApoD levels in fat depots with improved metabolic health in severely obese women.

The relationship between adiposopathy and glucose-insulin homeostasis is not affected by moderate-intensity aerobic training in healthy women with obesity.

The contribution of adiposopathy to glucose-insulin homeostasis remains unclear. This longitudinal study examined the potential relationship between the adiponectin/leptin ratio (A/L, a marker of adiposopathy) and insulin resistance (IR: homeostasis model assessment (HOMA)), insulin sensitivity (IS: Matsuda), and insulin response to an oral glucose tolerance test before and after a 16-week walking program, in 29 physically inactive pre- and postmenopausal women with obesity (BMI, 29-35 kg/m2; age, 47-54 years). Anthropometry, body composition, VO2max, and fasting lipid-lipoprotein and inflammatory profiles were assessed. A/L was unchanged after training (p = 0.15), despite decreased leptin levels (p < 0.05). While the Matsuda index tended to increase (p = 0.07), HOMA decreased (p < 0.05) and fasting insulin was reduced (p < 0.01) but insulin area under the curve (AUC) remained unchanged (p = 0.18) after training. Body fatness and VO2max were improved (p < 0.05) while triacylglycerols increased and HDL-CHOL levels decreased after training (p < 0.05). At baseline, A/L was positively associated with VO2max, HDL-CHOL levels, and Matsuda (0.37 < ρ < 0.56; p < 0.05) but negatively with body fatness, HOMA, insulin AUC, IL-6, and hs-CRP levels (- 0.41 < ρ < - 0.66; p < 0.05). After training, associations with fitness, HOMA, and inflammation were lost. Multiple regression analysis revealed A/L as an independent predictor of IR and IS, before training (partial R2 = 0.10 and 0.22), although A/L did not predict the insulin AUC pre- or post-intervention. A significant correlation was found between training-induced changes to A/L and IS (r = 0.38; p < 0.05) but not with IR or insulin AUC. Although changes in the A/L ratio could not explain improvements to glucose-insulin homeostasis indices following training, a relationship with insulin sensitivity was revealed in healthy women with obesity.

High-intensity interval training improves acute plasma volume responses to exercise that is age dependent.

Plasma volume (PV) is affected by several factors including age, physical training and, acutely, by exercise intensity. The purpose of this study was to investigate the effects of 6 weeks of high-intensity interval training (HIT) on PV and blood pressure (BP) changes among sedentary individuals. Thirty subjects aged between 18 and 71 years [body mass index=30.1(1.2) kg/m2 ] completed a 6-weeks HIT program. Anthropometric and fitness variables were obtained at pre- and post- HIT. PV variations during warm-up and after supramaximal cycling test (SCT) were calculated using two methods based on Hematocrit (Ht) and Hemoglobin (Hb) measures. After both the warm-up and SCT, PV decreased significantly among participants at pre- and at post-HIT (P < 0.01). However, PV decreases were significantly greater at pre-HIT compared with post-HIT during warm-up and after SCT (P < 0.01, respectively). In addition, at pre-HIT, a positive relationship was found between age and both PV variations at warm-up and after SCT (r2  = 0.55 and r2  = 0.46; P < 0.01 respectively). However, no relationship was found during the post-HIT period. After SCT and after both visits, only body weight predicted 22% of PV variations. In the current study, a significant relationship was found between systolic and diastolic BP improvements and PV variations in post-HIT (r2  = 0.54 and r2 =0.56, P < 0.05, respectively). Our results suggest that HIT may improve PV values and reduce the effects of age on the decrease in PV. These interventions led to improvements in systolic and diastolic BP values among participants.

Ischemic Preconditioning Improves Time Trial Performance at Moderate Altitude.

PURPOSE: Endurance athletes often compete and train at altitude where exercise capacity is reduced. Investigating acclimation strategies is therefore critical. Ischemic preconditioning (IPC) can improve endurance performance at sea level through improved O2 delivery and utilization, which could also prove beneficial at altitude. However, data are scarce, and there is no study at altitudes commonly visited by endurance athletes. METHODS: In a randomized, crossover study, we investigated performance and physiological responses in 13 male endurance cyclists during four 5-km cycling time trials (TT), preceded by either IPC (3 × 5 min ischemia/5-min reperfusion cycles at 220 mm Hg) or SHAM (20 mm Hg) administered to both thighs, at simulated low (FIO2 0.180, ~1200 m) and moderate (FIO2 0.154, ~2400 m) altitudes. Time to completion, power output, cardiac output (Q˙), arterial O2 saturation (SpO2), quadriceps tissue saturation index (TSI) and RPE were recorded throughout the TT. Differences between IPC and SHAM were analyzed at every altitude using Cohen effect size (ES) and compared with the smallest worthwhile change. RESULTS: At low altitude, IPC possibly improved time to complete the TT (-5.2 s, -1.1%; Cohen ES ± 90% confidence limits -0.22, -0.44; 0.01), power output (2.7%; ES 0.21, 0.08; 0.51), and Q˙ (5.0%; ES 0.27, 0.00; 0.54), but did not alter SpO2, muscle TSI, and RPE. At moderate altitude, IPC likely enhanced completion time (-7.3 s; -1.5%; ES -0.38, -0.55; -0.20), and power output in the second half of the TT (4.6%; ES 0.28, -0.15; 0.72), increased SpO2 (1.0%; ES 0.38, -0.05; 0.81), and decreased TSI (-6.5%; ES -0.27, -0.73; 0.20) and RPE (-5.4%, ES -0.27, -0.48; -0.06). CONCLUSIONS: Ischemic preconditioning may provide an immediate and effective strategy to defend SpO2 and enhance high-intensity endurance performance at moderate altitude.

The effects of diurnal Ramadan fasting on energy expenditure and substrate oxidation in healthy men.

The study aimed to examine the effects of diurnal Ramadan fasting (RF) on substrate oxidation, energy production, blood lipids and glucose as well as body composition. Nine healthy Muslim men (fasting (FAST) group) and eight healthy non-practicing men (control (CNT) group) were assessed pre- and post-RF. FAST were additionally assessed at days 10, 20 and 30 of RF in the morning and evening. Body composition was determined by hydrodensitometry, substrate oxidation and energy production by indirect calorimetry, blood metabolic profile by biochemical analyses and energy balance by activity tracker recordings and food log analyses. A significant group×time interaction revealed that chronic RF reduced body mass and adiposity in FAST, without changing lean mass, whereas CNT subjects remained unchanged. In parallel to these findings, a significant main diurnal effect (morning v. evening) of RF on substrate oxidation (a shift towards lipid oxidation) and blood metabolic profile (a decrease in glucose and an increase in total cholesterol and TAG levels, respectively) was observed, which did not vary over the course of the Ramadan. In conclusion, although RF induces diurnal metabolic adjustments (morning v. evening), no carryover effect was observed throughout RF despite the extended daily fasting period (18·0 (sd 0·3) h) and changes in body composition.

Anatomical distribution of primary amine oxidase activity in four adipose depots and plasma of severely obese women with or without a dysmetabolic profile

Semicarbazide-sensitive amine oxidase (SSAO), identical to primary amine oxidase or vascular adhesion protein-1, is a membrane enzyme that generates hydrogen peroxide. SSAO is highly expressed at the adipocyte surface, and its plasma levels increase with type 2 diabetes. Since visceral adipose tissue (AT) is more tightly associated with obesity complications than subcutaneous (SC) abdominal fat, we compared SSAO activity in plasma and 4 distinct AT locations in 48 severely obese women (body mass index (BMI), averaging 54 ± 11 kg/m2), with or without a dysmetabolic profile. Higher glucose and triacylglycerol levels vs lower high-density lipoprotein (HDL)-cholesterol characterized dysmetabolic women (DYS; n = 25) from non-dysmetabolic (NDYS; n = 23), age- and weight-matched subjects. SC, mesenteric (ME), omental (OM), and round ligament (RL) fat locations were collected during bariatric surgery. SSAO capacity to oxidize up to 1 mM benzylamine was determined in AT and plasma with radiometric and fluorimetric methods. Plasma SSAO was higher in the DYS group. SSAO activity was higher in fat than in plasma, when expressed as radiolabeled benzaldehyde per milligram of protein. In ATs from DYS women, protein content was 10 % higher, and basal hydrogen peroxide release lower than in NDYS subjects, except for RL location. The SSAO affinity towards benzylamine did not exhibit regional variation and was not altered by a dysmetabolic profile (K m averaging 184 ± 7 μM; n = 183). Although radiometric and fluorimetric methods gave different estimates of oxidase activity, both indicated that AT SSAO activity did not vary according to anatomical location and/or metabolic status in severely obese women

High-intensity interval training improves performance in young and older individuals by increasing mechanical efficiency.

This study evaluated the effects of 6 weeks of high-intensity interval training (HIIT) on mechanical efficiency (ME) in young and older groups. Seventeen healthy young adults [26.2(2.4) year], and thirteen healthy older adults [54.5(2.3) year] completed a 6-week HIIT intervention (three sessions per week) on an electromagnetically braked cycle ergometer. Each HIIT session contained six repetitions of supramaximal exercise intervals (6 seconds each) with 2 min of passive recovery between each repetition. ME (%) were computed in net terms across stages corresponding to ventilator thresholds 1 (VT1) and 2 (VT2) and at 100% of maximal oxygen consumption (VO2max) of an incremental maximal cycling test. After 6 weeks, the ME values did not differ between the two groups and were significantly higher than the ones at baseline (P < 0.01). In this study, the multiple linear regression analysis demonstrated the increases in maximal power (Pmax) contributed significantly to ME increases over 6 weeks at VT1, VT2 and at 100% of VO2max This model accounted respectively for 28, 38, and 42%, of the increases. In older adults, ME determined during incremental maximal cycling test increases at VT1, VT2 and at 100% over 6-week HIIT intervention, and the increment appeared to be related to increases in Pmax. HIIT can be recommended as a strategy aimed at improving muscle efficiency among older adults.

Perilipin 5 fine-tunes lipid oxidation to metabolic demand and protects against lipotoxicity in skeletal muscle.

Lipid droplets (LD) play a central role in lipid homeostasis by controlling transient fatty acid (FA) storage and release from triacylglycerols stores, while preventing high levels of cellular toxic lipids. This crucial function in oxidative tissues is altered in obesity and type 2 diabetes. Perilipin 5 (PLIN5) is a LD protein whose mechanistic and causal link with lipotoxicity and insulin resistance has raised controversies. We investigated here the physiological role of PLIN5 in skeletal muscle upon various metabolic challenges. We show that PLIN5 protein is elevated in endurance-trained (ET) subjects and correlates with muscle oxidative capacity and whole-body insulin sensitivity. When overexpressed in human skeletal muscle cells to recapitulate the ET phenotype, PLIN5 diminishes lipolysis and FA oxidation under basal condition, but paradoxically enhances FA oxidation during forskolin- and contraction- mediated lipolysis. Moreover, PLIN5 partly protects muscle cells against lipid-induced lipotoxicity. In addition, we demonstrate that down-regulation of PLIN5 in skeletal muscle inhibits insulin-mediated glucose uptake under normal chow feeding condition, while paradoxically improving insulin sensitivity upon high-fat feeding. These data highlight a key role of PLIN5 in LD function, first by finely adjusting LD FA supply to mitochondrial oxidation, and second acting as a protective factor against lipotoxicity in skeletal muscle.