A bout of aerobic exercise in the heat increases carbohydrate use but does not enhance the disposal of an oral glucose load, in healthy active individuals.

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% V̇o2max 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.

Glucose volume of distribution affects insulin sensitivity measured by intravenous glucose tolerance test.

AIM: To determine whether glucose volume of distribution (VdGLUCOSE ) affects the diagnosis of impaired insulin sensitivity (IS) when using an intravenous glucose tolerance test (IVGTT). METHODS: Individuals with distinct levels of IS underwent IVGTT after an overnight fast. The prediabetic group (Prediab; n = 33) differed from the healthy group (Healthy; n = 14) in their larger glycosylated hemoglobin (HbA1c of 5.9 ± 0.3 vs. 5.4 ± 0.1%; 41 ± 4 vs. 36 ± 1 mmol/mol; p < 0.001), percent body fat (37 ± 6 vs. 24 ± 3%; p < 0.001) and cardiovascular fitness level (VO2MAX 22 ± 5 vs. 44 ± 5 mL of O2 ·kg-1 ·min-1 ; p < 0.001). Ten minutes after intravenous infusion of the glucose bolus (i.e., 35 g in a 30% solution), VdGLUCOSE was assessed from the increases in plasma glucose concentration. IS was calculated during the next 50 min using the slope of glucose disappearance and the insulin time-response curve. RESULTS: VdGLUCOSE was higher in Healthy than in Prediab (230 ± 49 vs. 185 ± 21 mL·kg-1 ; p < 0.001). VdGLUCOSE was a strong predictor of IS (ß standardized coefficient 0.362; p = 0.004). VO2MAX was associated with VdGLUCOSE and IS (Pearson r = 0.582 and 0.704, respectively; p < 0.001). However, body fat was inversely associated with VdGLUCOSE and IS (r = -0.548 and -0.555, respectively; p < 0.001). CONCLUSIONS: Since fat mass is inversely related to VdGLUCOSE and in turn, VdGLUCOSE affects the calculations of IS, the IV glucose bolus dose should be calculated based on fat-free mass rather than body weight for a more accurate diagnosis of impaired IS.

Metformin and exercise effects on postprandial insulin sensitivity and glucose kinetics in pre-diabetic and diabetic adults.

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 + EX), and 4) metformin combined with exercise (MET + 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 + EX lower than PLAC and PLAC + EX, respectively; P = 0.023). MET + 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 µmol·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.NEW & NOTEWORTHY Metformin is the most prescribed oral antidiabetic medicine in the world but its mechanism of action and its interactions with exercise are not fully understood. Our stable isotope tracer data suggested that metformin reduces the rates of oral glucose entering the circulation (gut-liver effect). Exercise, in turn, tended to reduce postprandial insulin blood levels potentiating metformin improvements in insulin sensitivity. Thus, exercise potentiates metformin improvements in glycemic control and should be advised to metformin users.

Statins effect on insulin resistance after a meal and exercise in hypercholesterolemic pre-diabetic individuals.

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.

Effects of chronic metformin treatment on training adaptations in men and women with hyperglycemia: A prospective study.

OBJECTIVE: This study aimed to determine whether chronic metformin use interferes with the improvements in insulin resistance (IR) and cardiorespiratory fitness with aerobic training in people with hyperglycemia and metabolic syndrome (MetS). METHODS: A total of 63 middle-aged (53 [7] years) individuals with MetS and obesity (BMI = 32.8 [4.5] kg/m2 ) completed 16 weeks of supervised high-intensity interval training (3 d/wk, 43 min/session). Participants were either taking metformin (EXER+MET; n = 29) or were free of any pharmacological treatment for their MetS factors (EXER; n = 34). Groups were similar in their initial cardiorespiratory fitness (maximal oxygen uptake [VO2MAX ]), age, percentage of women, BMI, and MetS factors (z score). The effects of exercise training on IR (homeostatic model assessment of insulin resistance [HOMA-IR]), MetS z score, VO2MAX , maximal fat oxidation during exercise, and maximal aerobic power output were measured. RESULTS: Fasting insulin and HOMA-IR decreased similarly in both groups with training (EXER+MET: -4.3% and -10.6%; EXER: -5.3% and -14.5%; p value for time = 0.005). However, metformin use reduced VO2MAX improvements by half (i.e., EXER+MET: 12.7%; EXER: 25.3%; p value for time × group = 0.012). Maximal fat oxidation during exercise increased similarly in both groups (EXER+MET: 20.7%; EXER: 25.3%; p value for time = 0.040). VO2MAX gains were not associated with HOMA-IR reductions (EXER+MET: r = -0.098; p = 0.580; EXER: r = -0.255; p = 0.182). CONCLUSIONS: Metformin use was associated with attenuated VO2MAX improvements but did not affect fasting IR reductions with aerobic training in individuals with hyperglycemia and high cardiovascular risk (i.e., MetS).

One Bout of Resistance Training Does Not Enhance Metformin Actions in Prediabetic and Diabetic Individuals.

PURPOSE: This study aimed to determine the separated and combined effects of metformin and resistance exercise on glycemic control, insulin sensitivity, and insulin-like growth factor 1 (IGF-1) in overweight/obese individuals with prediabetes and type 2 diabetes mellitus. METHODS: Fourteen adults with a body mass index of 32.1 ± 4.1 kg·m-2, insulin resistance (HOMA-2 1.6 ± 0.6), and poor glycemic control (glycated hemoglobin, 6.9% ± 0.9%; 51.9 ± 10.7 mmol·mol-1) while taking metformin (1561 ± 470 g·d-1) were recruited. Participants underwent four 72-h long experimental trials in a randomized counterbalanced order, either 1) taking metformin (MET), 2) replacing metformin by placebo pills (PLAC), 3) taking placebo and undergoing a resistance training bout (RT + PLAC), and 4) taking metformin and undergoing the same RT bout (RT + MET). Interstitial fluid glucose concentration was frequently sampled to obtain 72-h glucose area under the curve (GAUC) and the percentage hyperglycemic glucose readings (>180 mg·dL-1; GPEAKS). Insulin sensitivity (i.e., HOMA-2) and IGF-1 were also assessed. RESULTS: HOMA-2 was not affected by treatments. GAUC and GPEAKS were similarly reduced below PLAC during RT + MET and MET (all P < 0.05). In contrast, RT + PLAC did not affect glucose concentration. Metformin decreased serum IGF-1 concentrations (P = 0.006), and RT did not reverse this reduction. CONCLUSIONS: A bout of full-body RT does not interfere or aid on metformin's blood glucose-lowering actions in individuals with prediabetes and type 2 diabetes mellitus.

Endurance Exercise Training reduces Blood Pressure according to the Wilder's Principle.

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; ß=-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.

Concurrent endurance and resistance training enhances muscular adaptations in individuals with metabolic syndrome.

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 HRMAX 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.

Substitution of parts of aerobic training by resistance training lowers fasting hyperglycemia in individuals with metabolic syndrome.

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 (HRmax) 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 HRmax (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 O2·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.

The use of a graded exercise test may be insufficient to quantify true changes in V̇o2max following exercise training in unfit individuals with metabolic syndrome.

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.

Effects of Exercise Training during Christmas on Body Weight and Cardiometabolic Health in Overweight Individuals.

: Individuals with abdominal obesity and metabolic syndrome (MetS) have augmented risk of all-cause mortality. Lifestyle interventions are effective to treat MetS, however, there are periods during the year in which exercise programs are discontinued and improper dietary habits reappear (e.g., Christmas holidays). We aimed to analyze if exercise-training during Christmas holidays would avoid body-weight gains and cardiometabolic deterioration in MetS individuals, using a randomized control trial. Thirty-eight men with MetS undergoing exercise training were randomly allocated to either continue (TRAIN group, n = 16) or discontinue (HOLID group, n = 22) training, during the three weeks of Christmas. Anthropometrics (body weight, fat, and waist circumference), fasting blood metabolites (glucose, insulin, triglycerides, and cholesterol concentrations) and exercise maximal fat oxidation (FOMAX) and oxygen uptake (VO2PEAK) were determined before and after Christmas. Both groups were similar at baseline in all parameters (p > 0.05). HOLID group increased body weight (91.3 ± 13.0 to 92.0 ± 13.4 kg, p = 0.004), mean arterial pressure (94.0 ± 10.6 to 97.1 ± 8.9 mmHg, p = 0.026), blood insulin (10.2 ± 3.8 to 12.5 ± 5.4 µIU·mL-1, p = 0.003) and HOMA (3.2 ± 1.3 to 4.1 ± 2.3, p = 0.003). In contrast, TRAIN prevented those disarrangements and reduced total (170.6 ± 30.6 to 161.3 ± 31.3 mg·dL-1, p = 0.026) and low-density lipoprotein cholesterol (i.e., LDL-C, 104.8 ± 26.1 to 95.6 ± 21.7 mg·dL-1, p = 0.013). TRAIN also prevented the reductions in exercise FOMAX and VO2PEAK that was observed in the HOLID group (p = 0.002). In conclusion, exercise training during Christmas, prevents body weight gains and the associated cardiovascular (increase in blood pressure and LDL-C) and metabolic (reduced insulin sensitivity) health risks are an optimal non-pharmacological therapy for that period of the year.

Effects of statin therapy and exercise on postprandial triglycerides in overweight individuals with hypercholesterolaemia.

AIMS: To determine the effects of statins on postprandial lipaemia (PPL) and to study if exercise could enhance statin actions. METHODS: Ten hypercholesteraemic (blood cholesterol 204 ± 36 mg dL-1 ; low-density lipoprotein-cholesterol 129 ± 32 36 mg dL-1 ) overweight (body mass index 30 ± 4 kg m-2 ), metabolic syndrome individuals chronically medicated with statins (>6 months) underwent 5-hour PPL tests in 4 occasions in a randomized order: (i) substituting their habitual statin medication by placebo for 96 hours (PLAC trial); (ii) taking their habitual statin medicine (STA trial); (iii) placebo combined with a bout of intense aerobic exercise (EXER+PLAC trial); and (iv) combining exercise and statin medicine (EXER+STA trial). RESULTS: Before the fat meal, statin withdrawal (i.e. PLAC and EXER+PLAC) increased blood triglycerides (TG; 24%), low-density lipoprotein-cholesterol (31%) and total cholesterol (19%; all P < .05) evidencing treatment compliance. After the meal, statin withdrawal increased 5-hour postprandial TG (PPTG) compared to its matched trials (94% higher PLAC vs STA and 45% higher EXER+PLAC vs EXER+STA; P < .05). EXER+PLAC trial did not lower PPTG below PLAC (i.e. incremental AUC of 609 ± 152 vs 826 ± 190 mg dL-1 5 h; P = .09). Adding exercise to statin did not result in larger reductions in PPTG (i.e. EXER+STA vs STA incremental area under the curve of 421 ± 87 vs 421 ± 84 mg dL-1 5 h; P = .99). CONCLUSION: In hypercholesteraemic metabolic syndrome individuals, chronic statin therapy blunts the elevations in TG after a fat meal (i.e. incremental area under the curve of PPTG) reducing the cardiovascular risk associated to their atherogenic dyslipidaemia. However, a single bout of intense aerobic exercise before the high fat meal, does not reduce PPTG but also does not interfere with the effects of statin treatment.

Women with metabolic syndrome show similar health benefits from high-intensity interval training than men.

High-intensity interval training (HIIT), is effective to improve cardiorespiratory fitness (CRF) and metabolic syndrome (MetS) components in adults. However, it is unclear if CRF and MetS components respond similarly in men and women after HIIT. For 16 weeks, 63 women (53±7 years) and 56 men (55±8 years) with MetS underwent a three day/week HIIT program. Bodyweight and composition, VO2MAX, surrogate parameters of CRF (Ventilatory threshold (VT), oxygen uptake efficiency slope (OUES) and VE/VCO2 slope), maximal rate of fat oxidation (MFO), and MetS components were assessed before and after training. All reported variables were analyzed by split-plot ANOVA looking for time by sex interactions. Before training men had higher absolute values of VO2MAX (58.6%), and MFO (24.6%), while lower body fat mass (10.5%) than women (all P<0.05). After normalization by fat-free mass (FFM), VO2MAX remained 16.6% higher in men (P<0.05), whereas differences in MFO disappeared (P = 0.292). After intervention VO2MAX (P<0.001), VO2 at VT (P<0.001), OUES (P<0.001), and VE/VCO2 slope (P<0.001) increased without differences by sex (P>0.05). After training MetS Z-score (P<0.001) improved without differences between men and women (P>0.05). From the MetS components, only blood pressure (P<0.001) and waist circumference (P<0.001) improved across time, without differences by sex. In both, women and men, changes in OUES (r = 0.685 and r = 0.445, respectively), and VO2 at VT (r = 0.378, and r = 0.445, respectively), correlated with VO2MAX. While only bodyweight changes correlated with MetS Z-score changes (r = 0.372, and = 0.300, respectively). Despite baseline differences, 16-weeks of HIIT similarly improved MetS, cardiorespiratory and metabolic fitness in women and men with MetS. This suggests that there are no restrictions due to sex on the benefits derived from an intense exercise program in the health of MetS participants. Trial Registration: clinicaltrials.gov NCT03019796.

Post-exercise Hypotension Produced by Supramaximal Interval Exercise is Potentiated by Angiotensin Receptor Blockers.

We studied the effects of supramaximal interval exercise (SIE) with or without antihypertensive medication (AHM) on 21-hr blood pressure (BP) response. Twelve hypertensive patients chronically medicated with AHM, underwent three trials in a randomized order: a) control trial without exercise and substituting their AHM with a placebo (PLAC); b) placebo medicine and a morning bout of SIE (PLAC+SIE), and c) combining AHM and exercise (AHM+SIE). Acute and ambulatory blood pressure responses were measured for 21-hr after treatment. 20 min after treatment, systolic blood pressure (SBP) readings were reduced, similar to readings after PLAC+SIE (-9.7±6.0 mmHg, P<0.001) and AHM+SIE (-10.4±7.9 mmHg, P=0.001). 21 h after treatment, SBP remained reduced after PLAC+SIE (125±12 mmHg, P=0.022) and AHM+SIE (122±12 mmHg, P=0.013) compared to PLAC (132±16 mmHg). The BP reduction in PLAC+SIE faded out at 4 a.m., while in AHM+SIE it continued overnight. At night, BP reduction was larger in AHM+SIE than PLAC+SIE (-5.6±4.0 mmHg, P=0.006). Our data shows that a bout of supramaximal aerobic interval exercise in combination with ARB medication in the morning elicits a sustained blood pressure reduction lasting at least 21-h. Thus, the combination of exercise and angiotensin receptor blocker medication seems superior to exercise alone for acutely decreasing blood pressure.

Effectiveness of Aerobic Exercise Programs for Health Promotion in Metabolic Syndrome.

PURPOSE: Continuous and interval are the two types of aerobic exercise training commonly used for health promotion. We sought to determine which aerobic exercise training program results in larger health improvements in metabolic syndrome (MetS) individuals. METHODS: One hundred twenty-one MetS patients (age, 57 ± 8 yr; weight, 92 ± 15 kg; and MetS factors, 3.8 ± 0.8 components) with low initial cardiorespiratory fitness (CRF) (V˙O2peak, 24.0 ± 5.5 mL·kg·min) were randomized to undergo one of the following 16-wk exercise program: (a) 4 × 4-min high-intensity interval training at 90% of HRMAX (4HIIT group; n = 32), (b) 50-min moderate-intensity continuous training at 70% of HRMAX (MICT group; n = 35), (c) 10 × 1-min HIIT at 100% of HRMAX (1HIIT group; n = 32), or (d) no exercise control group (CONT; n = 22). We measured the evolution of all five MetS components (i.e., MetS Z Score) and CRF (assessed by V˙O2peak) before and after intervention. RESULTS: MetS Z score decreased 41% after 4HIIT (95% confidence interval [CI], 0.25-0.06; P < 0.01) and 52% in MICT (95% CI, 0.24-0.06; P < 0.01), whereas it did not change in 1HIIT (decreased 24%; 95% CI, -0.16 to 0.03; P = 0.21) and CONT (increased 20%; 95% CI, -0.19 to 0.04; P = 0.22). However, the three exercise groups improved similarly their V˙O2peak (4HIIT, 11%; 95% CI, 0.14-0.33; MICT, 12%; 95% CI, 0.18-0.36; and 1HIIT, 14%; 95% CI, 0.21-0.40 L·min; all P < 0.001). CONCLUSIONS: Our findings suggest that in sedentary individuals with MetS and low initial CRF level any aerobic training program of 16 wk with a frequency of three times per week is sufficient stimulus to raise CRF. However, the more intense but shorter 1HIIT training program is not effective on improving MetS Z score, and thus we caution its recommendation for health promotion purposes in this population.

Training intensity relative to ventilatory thresholds determines cardiorespiratory fitness improvements in sedentary adults with obesity.

The aim of the present study was to study if training intensity relative to ventilatory thresholds (VTs) determines the improvements in cardiorespiratory fitness (CRF) in middle-aged sedentary individuals with obesity. Before and after 16-weeks of HIIT (43-min alternating bouts at 70/90% of HRMAX), oxygen consumption ( V˙ O2) and heart rate (HR) at ventilatory threshold 1 ( V˙ O2VT1, HRVT1), ventilatory threshold 2 ( V˙ O2VT2, HRVT2) and at maximal effort ( V˙ O2MAX, HRMAX) were assessed during a graded cycle-ergometer exercise test. Retrospectively, participants were divided into two groups based on whether training intensities were under (UNDER; n = 39) or over (OVER; n = 37) VT1 and VT2. At baseline, age, body composition, V˙ O2VT1, V˙ O2VT2, and HRMAX were similar in both groups. However, V˙ O2MAX was higher in OVER (P = 0.033), whereas HRVT1 and HRVT2 were higher in UNDER (P < 0.05). V˙ O2MAX (9.0%) and HRMAX (2.2%) improved similarly in both groups. V˙ O2VT1 and V˙ O2VT2 improved with training in both groups (P < 0.001) but the improvement was larger in OVER versus UNDER in V˙ O2VT1 (P = 0.013) and tended to be higher in V˙ O2VT2 (P = 0.068). HRVT1 increased only in OVER (P < 0.001), whereas HRVT2 did not change in any group (P = 0.248). A 16-week programme of HIIT improves V˙ O2MAX similarly in individuals training at intensities over or under their VTs. However, individuals training over their VTs showed a larger improvements in V˙ O2VT1 expanding exercise workloads fuelled by oxidative metabolism.

Exercise Periodization over the Year Improves Metabolic Syndrome and Medication Use.

PURPOSE: We aimed to determine if yearly repeated exercise training reduces metabolic syndrome (MetS) and the use of medicines to control MetS components. METHODS: Fifty-five MetS individuals were randomized into a TRAIN group that underwent two yearly programs of 16-wk high-intensity interval training or a nonexercising CONT group. We measured the evolution of all five MetS components, cardiorespiratory fitness (assessed by V˙O2PEAK) and medicine use, at baseline (0 months), mid (12 months), and end-point (24 months). Testing took place 8 months after the last training session to assess the chronic effects of training. RESULTS: Daily physical activity (wristband activity monitors) and calorie intake (3-d nutritional diary) remained similar to baseline at 1 and 2 yr in each group and were not different between groups. Blood triglycerides and glucose concentrations did not significantly vary in any group. However, waist circumference increased only in CONT after 2 yr (107 ± 2 cm to 111 ± 3 cm; P = 0.004). Mean arterial pressure decreased in TRAIN (101 ± 2 mm Hg to 94 ± 2 mm Hg; P = 0.002), whereas it remained unchanged in CONT (98 ± 2 mm Hg to 99 ± 2 mm Hg; P = 1.000) after 2 yr. Starting from similar levels at baseline, after 2 yr V˙O2PEAK was higher (2.32 ± 0.14 L·min vs 1.98 ± 0.11 L·min; P = 0.049) and medicine use lower (1.27 ± 0.22 vs 2.23 ± 0.43; P = 0.043) in TRAIN than CONT. The reduction in MAP in TRAIN commanded a parallel reduction in MetS Z-score from baseline to 2 yr (0.30 ± 0.1 to 0.07 ± 0.1; P = 0.013). CONCLUSIONS: Two yearly 16-wk high-intensity interval training programs are enough exercise to chronically lower MetS while preventing the reductions in cardiorespiratory fitness associated to aging. Of clinical relevance, yearly exercise training halts the increase in medicine use that occurs in non-exercising MetS individuals.

Acute Hypotension after High-Intensity Interval Exercise in Metabolic Syndrome Patients.

The purpose of this study was to compare the magnitude of post-exercise hypotension (PEH) after a bout of cycling exercise using high-intensity interval training (HIIT) in comparison to a bout of traditional moderate-intensity continuous exercise (CE). After supine rest 14 obese (31±1 kg·m-2) middle-age (57±2 y) metabolic syndrome patients (50% hypertensive) underwent a bout of HIIT or a bout of CE in a random order and then returned to supine recovery for another 45 min. Exercise trials were isocaloric and compared to a no-exercise trial (CONT) of supine rest for a total of 160 min. Before and after exercise we assessed blood pressure (BP), heart rate (HR), cardiac output (Q), systemic vascular resistance (SVR), intestinal temperature (TINT), forearm skin blood flow (SKBF) and percent dehydration. HIIT produced a larger post-exercise reduction in systolic blood pressure than CE in the hypertensive group (-20±6 vs. -5±3 mmHg) and in the normotensive group (-8±3 vs. -3±2 mmHg) while HIIT reduced SVR below CE (P<0.05). Percent dehydration was larger after HIIT, and post-exercise TINT and SKBF increased only after HIIT (all P<0.05). Our findings suggest that HIIT is a superior exercise method to CE to acutely reduce blood pressure in MSyn subjects.