ABSTRACT 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˙O 2peak , 24.0 ± 5.5 mL·kg −1 ·min −1 ) were randomized to undergo one of the following 16-wk exercise program: (a) 4 × 4-min high-intensity interval training at 90% of HR MAX (4HIIT group; n = 32), (b) 50-min moderate-intensity continuous training at 70% of HR MAX (MICT group; n = 35), (c) 10 × 1-min HIIT at 100% of HR MAX (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˙O 2peak ) 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˙O 2peak (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 −1 ; 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.
Abstract 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.
BACKGROUND: Statin is the most prescribed medicine worldwide to lower cardiovascular risk. Its blood triglyceride lowering effect, may limit fat mobilization/oxidation during exercise. METHODS: Nine individuals with metabolic syndrome, chronically treated with statins to correct their dyslipidemia exercised at three increasing intensities (40, 70, and 85% VO2 MAX) while taking statins or placebo using a randomized double-blind crossover design. Indirect calorimetry and stable isotope tracer techniques were combined to assess plasma substrate kinetic and oxidation. RESULTS: As expected, statin use lowered resting plasma triglyceride concentration (i.e., PLAC 1.4 ± 0.7 vs STAT 1.1 ± 0.5 mmol·L-1, p = 0.003), and also plasma triglyceride concentration during exercise (i.e., PLAC 1.7 ± 0.8 vs STAT 1.2 ± 0.5 mmol·L-1; p < 0.001). Ra glycerol (i.e., index of whole-body lipolysis) increased along with exercise intensity but the increase was attenuated by statins (p < 0.014) at the 85% VO2 MAX exercise intensity (i.e., PLAC 7.4 ± 1.9 vs STAT 5.8 ± 2.2 mM·kg·min-1; p = 0.046). This 21% lower lipolysis during STAT did not limit fat oxidation that was similarly low in PLAC and STAT (i.e., PLAC 0.7 ± 2.1 vs STAT 0.8 ± 2.2 mM·kg·min-1; p = 0.459). STAT increased resting plasma glucose concentration (i.e., PLAC 6.6 ± 1.6 vs STAT 6.8 ± 1.6 mmol·L-1, p = 0.036) but did not affect exercise glucose or insulin plasma. Rates of glucose appearance (i.e., Ra glucose, index of liver glucose output) were similar during PLAC and STAT at rest and during exercise. Glucose disappearance rates increased during the first two exercise intensities (i.e., 40 and 70% VO2 MAX), but decreased in both groups at 85% VO2 explaining the ensuing hyperglycaemia at this intensity. SUMMARY: Statin reduces exercise lipolysis during high intensity exercise, without affecting the already low rates of fat oxidation at that intensity. However, statin use does not affect plasma glucose kinetics or carbohydrate oxidation during exercise in a wide range of intensities in individuals chronically medicated with this drug.
Aims: To determine if the combination of exercise and statin could normalize postprandial triglyceridemia (PPTG) in hypercholesteraemic individuals. Mehods: Eight hypercholesteraemic (blood cholesterol 182±38 mg·dL-1; LDL-c 102±32 mg·dL-1) overweight (BMI 30±4 kg·m-2) individuals with metabolic syndrome (i.e., Met Synd) were compared to a group of eight metabolically healthy controls (i.e., MetH, blood cholesterol 149±23 mg·dL-1; LDL-c 77±23 mg·dL-1, and BMI 23±2 kg·m-2). Each group underwent two PPTG tests, either 14-h after a bout of intense exercise (EXER) or without previous exercise (REST). Additionally, Met Synd individuals were tested 96 h after withdrawal of their habitual statin medication (PLAC trials) to study medication effects. Results: A bout of exercise before the test meal did not reduce PPTG in Met Synd (P=0.347), but reduced PPTG by 46% in MetH (224±142 to 413±267 mg·dL-1·for 5 h iAUC; P=0.02). In both trials (i.e., REST and EXER) statin withdrawal in Met Synd greatly increased PPTG (average 65%; P<0.01), mean LDL-c (average 25%; P<0.01), total cholesterol (average 16%; P<0.01) and Apo B48 (24%; P<0.01), without interference from exercise. However, Apo B100 was not affected by statin withdrawal. Conclusions: Hypercholesteraemic Met Synd individuals (compared to metabolically healthy controls) are resistant to the effects of exercise on reducing PPTG. However, chronic statin medication blunts the elevations in TG after a fat meal (i.e., iAUC of PPTG) reducing their cardiovascular risk associated to their atherogenic dyslipidemia. Statin decreases PPTG by reducing the secretion or accelerating the catabolism of intestinal Apo B48.
Objective: In hypertensive individuals with metabolic syndrome (MetS), antihypertensive medications (AHM) are prescribed in conjunction with lifestyle advice (i.e., exercise) to reduce blood pressure (BP). However, if the combination of both treatments results in better BP control remains unknown. The objective of this study was to analyze the separated and combined effects of AHM and exercise training on ambulatory blood pressure (ABP). Design and method: Thirty-six hypertensive individuals with MetS under long-term prescription with AHM targeting the renin-angiotensin-aldosterone system (RAAS) were recruited. Before and after a 4-month aerobic interval training their AHM prescription was withdrawn during 3 days (i.e., PLAC trials) and 24-h ABP compared to when individuals held their habitual dose of medication (i.e., AHM trial) using a double-blind, randomized design. Plasma renin activity (PRA) and aldosterone concentration were measured to confirm withdrawal effects on RAAS. Urine albumin and creatinine ratio (UACR) was measured to assess kidney function. Results: Before the intervention AHM reduced 24-h mean arterial pressure (MAP) by -5 ± 5 mmHg (P < 0.001, Figure 1). After 4-months of aerobic training AHM reduced MAP an additional -3 ± 5 mmHg (92 ± 9 to 89 ± 8 mmHg; P = 0.014). However, BP lowering effect was not observed when AHM was withdrawn after training (97 ± 8 vs 96 ± 8 mmHg; P = 507). AHM increased PRA before and after training (P < 0.005) whilst had no effect on plasma aldosterone concentration (P = 1.000). Aerobic training did not significantly reduced RAAS hormones or the UACR. Conclusions: Aerobic training and AHM in conjunction reduce BP to a higher extent than each treatment in isolation. These findings support the combination of habitual AHM with exercise training with the goal to reduce BP in hypertensive MetS individuals.
We aimed to determine if yearly repeated exercise training reduces metabolic syndrome (MetS) and the use of medicines to control MetS components.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.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).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.
Abstract Aim To determine whether glucose volume of distribution (Vd GLUCOSE ) 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 (VO 2MAX 22 ± 5 vs. 44 ± 5 mL of O 2 ·kg −1 ·min −1 ; p < 0.001). Ten minutes after intravenous infusion of the glucose bolus (i.e., 35 g in a 30% solution), Vd GLUCOSE 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 Vd GLUCOSE was higher in Healthy than in Prediab (230 ± 49 vs. 185 ± 21 mL·kg −1 ; p < 0.001). Vd GLUCOSE was a strong predictor of IS (β standardized coefficient 0.362; p = 0.004). VO 2MAX was associated with Vd GLUCOSE and IS (Pearson r = 0.582 and 0.704, respectively; p < 0.001). However, body fat was inversely associated with Vd GLUCOSE and IS ( r = −0.548 and −0.555, respectively; p < 0.001). Conclusions Since fat mass is inversely related to Vd GLUCOSE and in turn, Vd GLUCOSE 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.
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