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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% V̇o 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- 13 C] glucose ingestion and [6,6- 2 H 2 ] 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., ISIndex MATSUDA ) 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.

Aim: To study if statins, a widely prescribed, inexpensive medication to prevent coronary artery diseases may cause insulin resistance (IR)., Methods: Fasted (HOMA-IR) and post-meal insulin resistance were assessed in 21 pre-diabetic hypercholesterolemic individuals treated with statins (STA trial). Measurements were compared to another trial conducted 96 h after statin withdrawal using placebo pills (PLAC trial). Trials were duplicated 16-18 h after a bout of moderate-intensity exercise (500 kcal of energy expenditure) to reduce IR and better appreciate statin effects (EXER+STA and EXER+PLAC trials)., Results: Statin withdrawal did not affect fasting (HOMA-IR; 2.35 ± 1.05 vs. 2.18 ± 0.87 for STA vs. PLAC trials; p = 0.150) or post-meal insulin resistance (i.e., Matsuda-index, STA 6.23 ± 2.83 vs. PLAC 6.49 ± 3.74; p = 0.536). A bout of aerobic exercise lowered post-meal IR (p = 0.043), but statin withdrawal did not add to the exercise actions (p = 0.564). Statin withdrawal increased post-meal plasma free glycerol concentrations (0.136 ± 0.073 vs. 0.185 ± 0.090 mmol·L -1 for STA vs. PLAC trials; p < 0.001) but not plasma free fatty acids or fat oxidation (p = 0.981, and p = 0.621, respectively). Post-meal fat oxidation was higher in the exercise trials (p = 0.002)., Conclusions: Withdrawal of statin medication does not affect fasting or post-meal insulin resistance in pre-diabetic hypercholesterolemic individuals. Furthermore, statin use does not interfere with the beneficial effects of exercise on lowering IR., (© 2022 The Authors. Scandinavian Journal of Medicine & Science In Sports published by John Wiley & Sons Ltd.)

The purpose of the study was to determine if concurrent training (endurance and resistance in a single session) elicits leg muscular adaptations beyond the ones obtained by endurance training alone in sedentary individuals with metabolic syndrome (MetS). Sixty-six MetS individuals (37% women, age 56 ± 7 years, BMI 32 ± 5 kg m -2 and 3.8 ± 0.8 MetS factors) were randomized to undergo one of the following 16-week isocaloric exercise programs: (i) 4 + 1 bouts of 4 min at 90% of HR MAX of intense aerobic cycling (IAC + IAC group; n = 33), (ii) 4 IAC bouts followed by 3 sets of 12 repetitions of 3 lower-limb free-weight exercises (IAC + RT group; n = 33). We measured the effects of training on maximal cycling power, leg press maximum strength (1RM), countermovement jump height (CMJ), and mean propulsive velocity (MPV) at workloads ranging from 10% to 100% of baseline 1RM leg press. After intervention, MetS components (Z-score) improved similarly in both groups (p = 0.002). Likewise, maximal cycling power during a ramp test improved similarly in both groups (time effect p < 0.001). However, leg press 1RM improved more in IAC + RT than in IAC + IAC (47 ± 5 vs 13 ± 5 kg, respectively, interaction p < 0.001). CMJ only improved with IAC + RT (0.8 ± 0.2 cm, p = 0.001). Leg press MPV at heavy loads (ie, 80%-100% 1RM) improved more with concurrent training (0.12 ± 0.01 vs 0.06 ± 0.02 m s -1 , interaction p = 0.013). In conclusion, in unconditioned MetS individuals, intense aerobic cycling alone improves leg muscle performance. However, substituting 20% of intense aerobic cycling by resistance training further improves 1RM leg press, MPV at high loads, and jumping ability while providing similar improvement in MetS components., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

We sought to determine the effects of substituting parts of aerobic training (AT) by resistance training (RT) on metabolic syndrome (MetS) factors. MetS patients (aged 56 ± 7 years; body mass index 33 ± 5 kg·m -2 and 3.9 ± 0.8 MetS factors) were randomized to undergo 1 of the following isocaloric, 16-week long exercise programs: ( i ) cycling 4 bouts of 4-min at 90% of maximal heart rate (HR max ) followed by 3 sets of 12 repetitions of 3 lower limb free-weight exercises (high-intensity interval training (HIIT)+RT group; n = 33), ( ii ) cycling 5 bouts of 4 min at 90% of HR max (HIIT+HIIT group; n = 33), or ( iii ) no exercise control group ( n = 21). We measured the evolution of all 5 MetS components ( z score), cardiorespiratory fitness (maximal oxygen uptake), leg strength and power (leg press 1-repetition maximum (1RM) and countermovement jump (CMJ)), fasting blood glucose (FG), fasting insulin, and insulin resistance (homeostasis model assessment 2). Both training groups improved maximal oxygen uptake similarly (170 ± 310 and 190 ± 210 mL O 2 ·min -1 ; P  < 0.001) and z score (-0.12 ± 0.29 and -0.12 ± 0.31 for HIIT+RT and HIIT+HIIT, respectively; P  < 0.02). However, only HIIT+RT improved CMJ ( P  = 0.002) and leg press 1RM above the HIIT+HIIT group (21% vs 6%; P  < 0.001). Furthermore, FG only decreased in the HIIT+RT group (5%; P  = 0.026, time × group). Our findings suggest that substitution of part of HIIT by leg RT improves glucose control in MetS individuals. Novelty Most studies addressing the efficacy of endurance versus resistance training are not matched by energy expenditure. We found that substituting 20% of AT with RT reduces hyperglycemia in MetS individuals. Training recommendations to regain glycemic control in MetS individuals should include resistance training.

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]

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]

Purpose: This study aimed to determine the effects of a 5-yr exercise intervention on metabolic syndrome (MetS) and health-related variables and medication use for MetS management. Methods: Participants were randomly assigned to an exercise intervention (n = 25, 54 ± 2 yr, 20% women) or control group (n = 26, 54 ± 2 yr, 38% women). The intervention lasted 4 months per year and consisted of high-intensity interval training on a cycloergometer thrice a week. Outcomes were MetS z-score and medication use score, MetS-related variables (including blood pressure, blood glucose homeostasis, and lipid profile), and cardiorespiratory fitness (CRF, as determined by maximal oxygen uptake). Results: MetS z-score was similarly reduced over time in both groups (P = 0.244 for group--time interaction). A quasi-significant and significant group--time interaction was found for MetS number of factors (P = 0.004) and CRF (P < 0.001), respectively. Thus, MetS factors tended to decrease over time only in the exercise group with no change in the control group, whereas CRF increased from baseline to 5-yr assessment in the exercise group (by 1.1MET, P < 0.001) but decreased in the control group (-0.5MET, P = 0.025).Medicine use score increased twofold frombaseline to 5-yr follow-up in the control group (P < 0.001) but did not significantly change (10%, P = 0.52) in the exercise group (P < 0.001 for group--time interaction). The proportion of medicated patients who had to increase antihypertensive (P < 0.001), glucose-lowering (P = 0.036), or total medication (P < 0.0001) over the 5-yr period was lower in the exercise than that in the control group. Conclusions: Exercise training can attenuate the increase in medication that would be otherwise required to manage MetS over a 5-yr period. [ABSTRACT FROM AUTHOR]