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A supervised intense aerobic exercise program improves the health of individuals with metabolic syndrome (MetS). However, it is unclear whether the timing of training within the 24 h day would influence those health benefits. The present study aimed to determine the influence of morning vs. afternoon exercise on body composition, cardiometabolic health and components of MetS. One hundred thirty‐nine individuals with MetS were block randomized into morning (AMEX; n = 42) or afternoon (PMEX; n = 59) exercise training groups, or a non‐training control group (Control; n = 38). Exercise training was comprised of 48 supervised high‐intensity interval sessions distributed over 16 weeks. Body composition, cardiorespiratory fitness (assessed by V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$), maximal fat oxidation (FOmax), blood pressure and blood metabolites were assessed before and after the intervention. Compared with the non‐training Control, both exercise groups improved similarly body composition (–0.7% fat loss; P = 0.002), waist circumference (–2.1 cm; P < 0.001), diastolic blood pressure (–3.8 mmHg; P = 0.004) and V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$ (3.5 mL kg−1 min−1; P < 0.001) with no differences between training groups. AMEX, in comparison with PMEX, reduced systolic blood pressure (–4% vs. –1%; P = 0.019), plasma fasting insulin concentration (–12% vs. –5%; P = 0.001) and insulin resistance (–14% vs. –4%; P = 0.006). Furthermore, MetS Z score was further reduced in the AMEX compared to PMEX (–52% vs. –19%; P = 0.021) after training. In summary, high‐intensity aerobic exercise training in the morning in comparison to training in the afternoon is somewhat more efficient at reducing cardiometabolic risk factors (i.e. systolic blood pressure and insulin sensitivity). Key points: The effect of exercise time of day on health promotion is an area that has gained interest in recent years; however, large‐scale, randomized‐control studies are scarce.People with metabolic syndrome (MetS) are at risk of developing cardiometabolic diseases and reductions in this risk with exercise training can be precisely gauged using a compound score sensitive to subtle evolution in each MetS component (i.e. Z score).Supervised aerobic exercise for 16 weeks (morning and afternoon), without dietary restriction, improved cardiorespiratory and metabolic fitness, body composition and mean arterial pressure compared to a non‐exercise control group.However, training in the morning, without changes in exercise dose or intensity, reduced systolic blood pressure and insulin resistance further compared to when training in the afternoon.Thus, high‐intensity aerobic exercise training in the morning is somewhat more efficient in improving the health of individuals with metabolic syndrome. [ABSTRACT FROM AUTHOR]

Objective: To determine whether statin medication in individuals with obesity, dyslipidemia, and metabolic syndrome affects their capacity to mobilize and oxidize fat during exercise. Methods: Twelve individuals with metabolic syndrome pedaled during 75 min at 54 ± 13% ...O2max (5.7 ± 0.5 metabolic equivalents) while taking statins (STATs) or after 96-hr statin withdrawal (PLAC) in a randomized double-blind fashion. Results: At rest, PLAC increased low-density lipoprotein cholesterol (i.e., STAT 2.55 ± 0.96 vs. PLAC 3.16 ± 0.76 mmol/L; p = .004) and total cholesterol blood levels (i.e., STAT 4.39 ± 1.16 vs. PLAC 4.98 ± 0.97 mmol/L; p = .008). At rest, fat oxidation (0.99 ± 0.34 vs. 0.76 ± 0.37 μmol⋅kg-1⋅min-1 for STAT vs. PLAC; p = .068) and the rates of plasma appearance of glucose and glycerol (i.e., Ra glucose-glycerol) were not affected by PLAC. After 70 min of exercise, fat oxidation was similar between trials (2.94 ± 1.56 vs. 3.06 ± 1.94 μmol⋅kg-1⋅min-1, STA vs. PLAC; p = .875). PLAC did not alter the rates of disappearance of glucose in plasma during exercise (i.e., 23.9 ± 6.9 vs. 24.5 ± 8.2 μmol⋅kg-1⋅min-1 for STAT vs. PLAC; p = .611) or the rate of plasma appearance of glycerol (i.e., 8.5 ± 1.9 vs. 7.9 ± 1.8 μmol⋅kg-1⋅min-1 for STAT vs. PLAC; p = .262). Conclusions: In patients with obesity, dyslipidemia, and metabolic syndrome, statins do not compromise their ability to mobilize and oxidize fat at rest or during prolonged, moderately intense exercise (i.e., equivalent to brisk walking). In these patients, the combination of statins and exercise could help to better manage their dyslipidemia. [ABSTRACT FROM AUTHOR]

We investigated if a bout of exercise in a hot environment (HEAT) would reduce the postprandial hyperglycemia induced by glucose ingestion. The hypothesis was that HEAT stimulating carbohydrate oxidation and glycogen use would increase the disposal of an ingested glucose load [i.e., oral glucose tolerance test (OGTT); 75 g of glucose]. Separated by at least 1 wk, nine young healthy individuals underwent three trials after an overnight fast in a randomized order. Two trials included 50 min of pedaling at 58 ± 5% V̇ o 2max either in a thermoneutral (21 ± 1°C; NEUTRAL) or in a hot environment (33 ± 1°C; HEAT) eliciting similar energy expenditure (503 ± 101 kcal). These two trials were compared with a no-exercise trial (NO EXER). Twenty minutes after exercise (or rest), subjects underwent an OGTT, while carbohydrate oxidation (CHOxid, using indirect calorimetry) plasma blood glucose, insulin concentrations (i.e., [glucose], [insulin]), and double tracer glucose kinetics ([U-13C] glucose ingestion and [6,6-2H2] glucose infusion) were monitored for 120 min. At rest, [glucose], [insulin], and rates of appearance/disappearance of glucose in plasma (glucose Ra/Rd) were similar among trials. During exercise, heart rate, tympanic temperature, [glucose], glycogen oxidation, and total CHOxid were higher during HEAT than NEUTRAL (i.e., 149 ± 35 vs. 124 ± 31 µmol·kg−1·min−1, P = 0.010). However, during the following OGTT, glucose Rd was similar in HEAT and NEUTRAL trials (i.e., 25.1 ± 3.6 vs. 25.2 ± 5.3 µmol·kg−1·min−1, P = 0.981). Insulin sensitivity (i.e., ISIndexMATSUDA) only improved in NEUTRAL compared with NO EXER (10.1 ± 4.6 vs. 8.8 ± 3.7 au; P = 0.044). In summary, stimulating carbohydrate use with exercise in a hot environment does not improve postprandial plasma glucose disposal or insulin sensitivity in a subsequent OGTT. NEW & NOTEWORTHY: Exercise in the heat increases estimated muscle glycogen use. Reduced muscle glycogen after exercise in the heat could increase insulin-mediated glucose uptake during a subsequent oral glucose tolerance test (OGTT). However, plasma glucose kinetics are not improved during the OGTT in response to a bout of exercise in the heat, and insulin sensitivity worsens. Heat stress activates glucose counterregulatory hormones whose actions may linger during the OGTT, preventing increased glucose uptake. [ABSTRACT FROM AUTHOR]

Background The risk for atherogenic plaque formation is high after ingestion of meals in individuals with high blood lipid levels (ie, dyslipidemia). Statins and exercise reduce the rise of blood triglyceride concentrations after a meal, but the effect of their combination is unclear. Methods In a randomized crossover design, 11 individuals with dyslipidemia and metabolic syndrome treated with statins underwent a mixed-meal (970 ± 111 kcal, 24% fat, and 34% carbohydrate) tolerance test. Plasma lipid concentrations, fat oxidation, glucose, and glycerol kinetics were monitored immediately prior and during the meal test. Trials were conducted with participants under their habitual statin treatment and 96 hours after blinded statin withdrawal. Trials were duplicated after a prolonged bout of low-intensity exercise (75 minutes at 53 ± 4% maximal oxygen consumption) to study the interactions between exercise and statins. Results Statins reduced postprandial plasma triglycerides from 3.03 ± 0.85 to 2.52 ± 0.86 mmol·L−1 (17%; P =.015) and plasma glycerol concentrations (ie, surrogate of whole-body lipolysis) without reducing plasma free fatty acid concentration or fat oxidation. Prior exercise increased postprandial plasma glycerol levels (P =.029) and fat oxidation rates (P =.024). Exercise decreased postprandial plasma insulin levels (241 ± 116 vs 301 ± 172 ρmol·L−1; P =.026) but not enough to increase insulin sensitivity (P =.614). Neither statins nor exercise affected plasma glucose appearance rates from exogenous or endogenous sources. Conclusions In dyslipidemic individuals, statins reduce blood triglyceride concentrations after a meal, but without limiting fat oxidation. Statins do not interfere with exercise lowering the postprandial insulin that likely promotes fat oxidation. Last, statins do not restrict the rates of plasma incorporation or oxidation of the ingested glucose. [ABSTRACT FROM AUTHOR]

The potential interaction between metformin and exercise on glucose-lowering effects remains controversial. We studied the separated and combined effects of metformin and/or exercise on fasting and postprandial insulin sensitivity in individuals with pre-diabetes and type 2 diabetes (T2D). Eight T2D adults (60 ± 4 yr) with overweight/obesity (32 ± 4 kg·m-2) under chronic metformin treatment (9 ± 6 yr; 1281 ± 524 mg·day-1) underwent four trials; 1) taking their habitual metformin treatment (MET), 2) substituting during 96 h their metformin medication by placebo (PLAC), 3) placebo combined with 50 min bout of high-intensity interval exercise (PLAC þ EX), and 4) metformin combined with exercise (MET þ EX). Plasma glucose kinetics using stable isotopes (6,6-2H2 and [U-13C] glucose), and glucose oxidation by indirect calorimetry, were assessed at rest, during exercise, and in a subsequent oral glucose tolerance test (OGTT). Postprandial glucose and insulin concentrations were analyzed as mean and incremental area under the curve (iAUC), and insulin sensitivity was calculated (i.e., MATSUDAindex and OGISindex). During OGTT, metformin reduced glucose iAUC (i.e., MET and MET þ EX lower than PLAC and PLAC þ EX, respectively; P = 0.023). MET þ EX increased MATSUDAindex above PLAC (4.8 ± 1.4 vs. 3.3 ± 1.0, respectively; P = 0.018) and OGISindex above PLAC (358 ± 52 vs. 306 ± 46 mL·min-1·m-2, respectively; P = 0.006). Metformin decreased the plasma appearance of the ingested glucose (Ra OGTT; MET vs. PLAC, -3.5; 95% CI -0.1 to -6.8 lmol·kg-1·min-1; P = 0.043). Metformin combined with exercise potentiates insulin sensitivity during an OGTT in individuals with pre-diabetes and type 2 diabetes. Metformin's blood glucose-lowering effect seems mediated by decreased oral glucose entering the circulation (gut-liver effect) an effect partially blunted after exercise. [ABSTRACT FROM AUTHOR]

Context: Statins blunt cardiorespiratory fitness improvements after exercise training and may affect fat oxidation adaptations to training. Objective: To determine if long-term statin use in dyslipidemic individuals restricts the improvements in fat oxidation typically observed after an intense exercise-training program. Methods: A total of 106 metabolic syndrome individuals either chronically medicated with statins (ie, statin group; n=46) or statin naive (ie, control group; n= 60) completed a 16-week supervised high-intensity interval training program. Maximal rates of oxygen consumption (VO2MAX), fat oxidation (FOMAX), and the shape of the workload-fat oxidation curve were assessed before and 48 hours after training in an overnight fasted state. Results: Starting from a similar value at baseline, both groups increased VO2MAX after training, but the increase was larger in the control than in the statin group (19.4% vs 12.6%; P= .013). Before training, FOMAX in the statin group was lower (0.19± 0.08 vs 0.23±0.07 g·min−1 ; P=.023) and took place at a lower workload (33±21 vs 37± 19 W; P=.015) than in the control group. After training, FOMAX improved similarly in both groups (0.06±0.08; 95% CI, 0.03-0.08 g·min−1 and 0.05±0.09; 95% CI, 0.03-0.07 g·min−1, for statin and control groups, respectively; (P < .001). Still, after training, FOMAX occurred at a 28% lower workload in the statin group (38±26 vs 53±32 W; P= .048). The VO-2 workload slope decreased after training in both groups (both P<.001) along with reductions in the respiratory exchange ratio-workload slope. Fat oxidation increased at all workloads after training regardless of the use of statins. Conclusion: Long-term statin treatment is associated with blunted exercise fat oxidation before exercise training. However, statin use does not attenuate the improvements in exercise fat oxidation (FOMAX) derived from intense aerobic exercise training. This finding should encourage statin users to exercise-train to benefit from increased fat oxidation once their fitness level improves. [ABSTRACT FROM AUTHOR]

The effect of antihypertensive medicine (AHM) is larger the higher the pre-treatment blood pressure level. It is unknown whether this Wilder's principle, also applies for the exercise-training blood pressure (BP) lowering effect. One hundred seventy-eight (n=178) middle-aged individuals (55±8 y) with metabolic syndrome (MetS), underwent high intensity interval training (3 days·week–1) for 16 weeks. Participants were divided into medicated (Med; n=103) or not medicated (No Med; n=75) with AHM. Office BP was evaluated before and after the exercise-training. Correlations and stepwise regression analysis were used to determine which variable better predicted the reductions in systolic BP (SBP) with training. After training, participants with hypertension lowered SBP by a similar magnitude regardless of if they were in the Med (–15 mmHg, 95% CI–12,–19; P <0.001) or No Med group (–13 mmHg, 95% CI–9,–16; P <0.001). However, SBP did not decrease among normotensive groups (P =0.847 for Med and P =0.937 for No Med). Pre-treatment SBP levels was the best predictor of exercise-training lowering effect (r=–0.650; β=–0.642; P <0.001). For each 10 mmHg higher pre-training SBP there were a 5 mmHg deeper SBP reduction (Wilder principle). Furthermore, AHM does not interfere with exercise-training BP-lowering effect. [ABSTRACT FROM AUTHOR]

Aims: To determine if the combination of exercise and statin could normalize postprandial triglyceridaemia (PPTG) in hypercholesteraemic individuals. Methods: Eight hypercholesteraemic (blood cholesterol 182 ± 38 mg dL−1; low‐density lipoprotein–cholesterol [LDL‐c] 102 ± 32 mg dL−1) overweight (body mass index 30 ± 4 kg m−2) individuals with metabolic syndrome (MetS) were compared to a group of 8 metabolically healthy (MetH) controls (blood cholesterol 149 ± 23 mg dL−1; LDL‐c 77 ± 23 mg dL−1, and body mass index 23 ± 2 kg m−2). Each group underwent 2 PPTG tests, either 14 hours after a bout of intense exercise or without previous exercise. Additionally, MetS individuals were tested 96 hours after withdrawal of their habitual statin medication to study medication effects. Results: A bout of exercise before the test meal did not reduce PPTG in MetS (P =.347), but reduced PPTG by 46% in MetH (413 ± 267 to 224 ± 142 mg dL−1 for 5 h incremental area under the curve; P =.02). In both trials (i.e., either after a bout of intense exercise or without previous exercise), statin withdrawal in MetS greatly increased PPTG (average 65%; P <.01), mean LDL‐c (average 25%; P <.01), total cholesterol (average 16%; P <.01) and apolipoprotein (Apo) B48 (24%; P <.01), without interference from exercise. However, Apo B100 was not affected by statin withdrawal. Conclusion: Hypercholesteraemic MetS individuals (compared to MetH controls) fail to show an effect of exercise on reducing PPTG. However, chronic statin medication blunts the elevations in triglyceride after a fat meal (i.e., incremental area under the curve of PPTG) reducing their cardiovascular risk associated with their atherogenic dyslipidaemia. Statin decreases PPTG by reducing the secretion or accelerating the catabolism of intestinal Apo B48. [ABSTRACT FROM AUTHOR]

We studied the accuracy of graded exercise testing (GXT) to assess improvements in maximal oxygen uptake (V̇o2max) with exercise training in unfit individuals with metabolic syndrome (MetS). Forty-four adults with MetS (58 ± 7 yr, 36% women, BMI 31.8 ± 4.8 kg/m−2) underwent 4 mo of supervised high-intensity interval exercise training. V̇o2max was assessed using GXT, followed by a constant-load verification test (VerT) at 110% of the maximal work rate achieved during GXT. V̇o2 data from GXT and VerT were compared using repeated-measures ANOVA. The mean improvement in V̇o2max following exercise training was similar when using GXT only or VerT. However, before training, 18 subjects achieved a higher V̇o2max during the verification test that was (+159 mLO2/min) higher than the GXT (P < 0.001). After training, the underestimation of V̇o2max by GXT was reduced but still present (+64 mLO2/min). As a result, improvements in V̇o2max following exercise training as assessed using GXT only almost doubled the “real” increase in V̇o2max as measured by VerT in these 18 individuals. In the remaining 26 subjects, GXT scored below VerT only after training (+54 mLO2/min, P = 0.046). As a consequence, GXT underestimated the actual V̇o2max increases (−49 mLO2/min, P = 0.013) in these individuals. Assessment of changes in V̇o2max following exercise training using only GXT over- or underestimates V̇o2max gains in unfit individuals with MetS. Thus, a verification test may be required to 1) identify the highest V̇o2max during a maximal exercise test on a cycle ergometer and 2) accurately quantify the true changes in cardiorespiratory fitness following exercise training in unfit individuals with MetS. NEW & NOTEWORTHY It is unclear whether the traditional GXT is suitable to assess V̇o2max changes in unfit individuals with metabolic syndrome. Mean changes in V̇o2max following exercise training were similar using GXT or VerT. However, we showed that the GXT overestimated V̇o2max improvements in 41% and underestimated V̇o2max improvements in 59% of subjects. Our data suggest the need for a verification test to appropriately determine training-induced improvements in V̇o2max in unfit individuals with metabolic syndrome. [ABSTRACT FROM AUTHOR]