To study if statins, a widely prescribed, inexpensive medication to prevent coronary artery diseases may cause insulin resistance (IR).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).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).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.
We studied if dehydrating exercise would reduce muscle water ( H 2 O muscle ) and affect muscle electrolyte concentrations. Vastus lateralis muscle biopsies were collected prior, immediately after, and 1 and 4 h after prolonged dehydrating exercise (150 min at 33 ± 1 °C, 25% ± 2% humidity) on nine endurance‐trained cyclists ( VO 2max = 54.4 ± 1.05 mL/kg/min). Plasma volume ( PV ) changes and fluid shifts between compartments ( Cl − method) were measured. Exercise dehydrated subjects 4.7% ± 0.3% of body mass by losing 2.75 ± 0.15 L of water and reducing PV 18.4% ± 1% below pre‐exercise values ( P < 0.05). Right after exercise H 2 O muscle remained at pre‐exercise values (i.e., 398 ± 6 mL/100 g dw muscle −1 ) but declined 13% ± 2% (342 ± 12 mL/100 g dw muscle −1 ; P < 0.05) after 1 h of supine rest. At that time, PV recovered toward pre‐exercise levels. The Cl − method corroborated the shift of fluid between extracellular and intracellular compartments. After 4 h of recovery, PV returned to pre‐exercise values; however, H 2 O muscle remained reduced at the same level. Muscle Na + and K + increased ( P < 0.05) in response to the H 2 O muscle reductions. Our findings suggest that active skeletal muscle does not show a net loss of H 2 O during prolonged dehydrating exercise. However, during the first hour of recovery H 2 O muscle decreases seemly to restore PV and thus cardiovascular stability.
Purpose The purpose of this study was to determine, i) the reliability of blood lactate and ventilatory-based thresholds, ii) the lactate threshold that corresponds with each ventilatory threshold (VT1 and VT2) and with maximal lactate steady state test (MLSS) as a proxy of cycling performance. Methods Fourteen aerobically-trained male cyclists ( 62.1±4.6 ml·kg-1·min-1) performed two graded exercise tests (50 W warm-up followed by 25 W·min-1) to exhaustion. Blood lactate, and data were collected at every stage. Workloads at VT1 (rise in ;) and VT2 (rise in ) were compared with workloads at lactate thresholds. Several continuous tests were needed to detect the MLSS workload. Agreement and differences among tests were assessed with ANOVA, ICC and Bland-Altman. Reliability of each test was evaluated using ICC, CV and Bland-Altman plots. Results Workloads at lactate threshold (LT) and LT+2.0 mMol·L-1 matched the ones for VT1 and VT2, respectively (p = 0.147 and 0.539; r = 0.72 and 0.80; Bias = -13.6 and 2.8, respectively). Furthermore, workload at LT+0.5 mMol·L-1 coincided with MLSS workload (p = 0.449; r = 0.78; Bias = -4.5). Lactate threshold tests had high reliability (CV = 3.4–3.7%; r = 0.85–0.89; Bias = -2.1–3.0) except for DMAX method (CV = 10.3%; r = 0.57; Bias = 15.4). Ventilatory thresholds show high reliability (CV = 1.6%–3.5%; r = 0.90–0.96; Bias = -1.8–2.9) except for RER = 1 and V-Slope (CV = 5.0–6.4%; r = 0.79; Bias = -5.6–12.4). Conclusions Lactate threshold tests can be a valid and reliable alternative to ventilatory thresholds to identify the workloads at the transition from aerobic to anaerobic metabolism.
Abstract 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/m 2 ) 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 [VO 2MAX ]), 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, VO 2MAX , 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 VO 2MAX 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). VO 2MAX 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 VO 2MAX improvements but did not affect fasting IR reductions with aerobic training in individuals with hyperglycemia and high cardiovascular risk (i.e., MetS).
Cross sectional data reveal that individuals with high cardiorespiratory fitness (i.e., CRF assessed by VO2max) have lower prevalence of metabolic syndrome (i.e., MetS; Hassinen et al., 2010). However, there is a scarcity of exercise-training intervention trials with serial measures of CRF to confirm that exercise training reduces MetS through increases in CRF. We recently found that two consecutive years of 4-month aerobic interval training are required to chronically improve MetS (Morales-Palomo et al., 2017). PURPOSE: To determine the chronic effects of two consecutive 4 months-a-year training program on the relationship between increased CRF and reduced MetS continuous z score-(Z-MetS). METHODS: Using a repeated-measures, randomized control design, MetS subjects were allocated to either a training group (TRAIN; n=20) or a control group (CONT; n=22) that remained sedentary. TRAIN extended for 4 months every year (November-mid-March) consisting in 3 sessions per week of aerobic interval training (Mora-Rodriguez et al., 2014). At baseline and after 7 months of the last training program, VO2max, Z-MetS, 10 yrs atherosclerotic cardiovascular disease risk index (ASCVD) and medicine use were assessed. RESULTS: From a similar level at baseline, VO max increased by 1.31±0.96 mL·kg·min-1 after 2 yrs in TRAIN (9%; P=0.05) being 12% higher than CONT (P=0.05). Z-MetS decrease after 2 yrs in TRAIN (0.48±0.12 to 0.24±0.10; P=0.033) but remained unaltered in the CONT. ASCVD did not change in TRAIN but worsen in the CONT group after 2 yrs (7.8±1.3% to 10.4±1.9%; p=0.004). The correlation between the changes in VO2max and Z-MetS was significant for the TRAIN group (r=-0.571; P=0.013; r2=33%). After 2 yrs, a higher percentage of subjects in the CONT group in comparison to the TRAIN used cholesterol lowering medicine (45 vs 15%) and two medicines (45 vs 20%) in comparison to the TRAIN group. CONCLUSION: Two consecutive years of a 4-month intense aerobic exercise program raises CRF in association with a reduction in Z-MetS. The amount of variance in the reduction in Z-MetS that could be explained by the increase in VO2max is 32% which suggest that exercise could be an important clinical non-pharmacological treatment to reduce the progression of MetS and the concomitant cardiovascular risk.
Dyslipidemia and insulin resistance (IR) are intertwined. In overweight individuals, excessive plasma free fatty acids turnover in conjunction with reduced fat oxidation, results in IR. In turn, IR increases hepatic production of large VLDL while reducing postprandial activation of lipoprotein lipase. Thus, it would be expected that correcting dyslipidemia with statin should also ease IR. However, warnings against the use of statin in diabetic individuals is habitual in clinical practice. PURPOSE: To determine if statins are causing glycemic disbalance in metabolic syndrome individuals. METHODS: Eight hypercholesteremic, pre-diabetic, and statin users individuals, ingested a meal test (86 ± 7 g carbohydrates) after an overnight fast to assess insulin resistance (IR). Trials were conducted with subjects under their habitual statin medication (STA trials) and after 96-h statin withdrawal (PLAC trials). To better detect statin effect on insulin resistance, those trials were duplicated after a bout of intense exercise the previous evening (EXER+STA and EXER+PLAC) since exercise reduces IR. RESULTS: Compared to resting trials, aerobic exercise 14-h prior to glucose ingestion improved whole-body Matsuda index (MISI) (9.7 ± 6.6 vs 6.3 ± 3.6; exercise effect, P = 0.035). However, 96-h statin withdrawal had no effects on IR (HOMA2-IR, P = 0.361 or MISI P = 0.840). Statin decreased lipolysis (i.e., blood glycerol concentrations; P = 0.009) but not resting fat oxidation (P = 0.684) while exercise tended to increase fat oxidation (P = 0.052). We could not find significant associations between lipolysis or fat oxidation and IR. CONCLUSION: 96-h statin withdrawal in pre-diabetic hypercholesteremic MetS individuals did not improve their IR which suggests that the reverse may be true and chronic statin medication does not blunt insulin actions. Interestingly, statins do not impede the exercise-induced lowering of IR.
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.
We studied if salt and water ingestion alleviates the physiological strain caused by dehydrating exercise in the heat. Ten trained male cyclists ( : 60 ± 7 m L /kg/min) completed three randomized trials in a hot‐dry environment (33 ° C , 30% rh, 2.5 m/s airflow). Ninety minutes before the exercise, participants ingested 10 m L of water/kg body mass either alone ( CON trial) or with salt to result in concentrations of 82 or 164 m M Na + ( ModNa + or HighNa + trial, respectively). Then, participants cycled at 63% of for 120 min immediately followed by a time‐trial. After 120 min of exercise, the reduction in plasma volume was lessened with ModNa + and HighNa + trials (−11.9 ± 2.1 and −9.8 ± 4.2%) in comparison with CON (−16.4 ± 3.2%; P < 0.05). However, heat accumulation or dissipation (forearm skin blood flow and sweat rate) were not improved by salt ingestion. In contrast, both salt trials maintained cardiac output (∼1.3 ± 1.4 L/min; P < 0.05) and stroke volume (∼10 ± 11 mL/beat; P < 0.05) above CON after 120 min of exercise. Furthermore, the salt trials equally improved time‐trial performance by 7.4% above CON (∼289 ± 42 vs 269 ± 50 W , respectively; P < 0.05). Our data suggest that pre‐exercise ingestion of salt plus water maintains higher plasma volume during dehydrating exercise in the heat without thermoregulatory effects. However, it maintains cardiovascular function and improves cycling performance.
To determine the effect of circadian rhythm on neuromuscular responses and kinematics related to physical tennis performance, after a standardised warm-up, 13 highly competitive male tennis players were tested twice for serve velocity/accuracy (SVA), countermovement vertical jump (CMJ), isometric handgrip strength (IS), agility T-test (AGIL) and a 10-m sprint (10-m RUN). In a randomised, counter-balance order, tennis players underwent the test battery twice, either in the morning (i.e., AM; 9:00 h) and in the afternoon (i.e., PM; 16:30 h). Paired t-tests were used to analyse differences due to time-of-day in performance variables. Comparison of morning versus afternoon testing revealed that SVA (168.5 ± 6.5 vs. 175.2 ± 6.1 km · h−1; P = 0.003; effect size [ES] = 1.07), CMJ (32.2 ± 0.9 vs. 33.7 ± 1.1 cm; P = 0.018; ES = 1.46), AGIL (10.14 ± 0.1 vs. 9.91 ± 0.2 s; P = 0.007; ES = 1.23) and 10-m RUN time (1.74 ± 0.1 vs. 1.69 ± 0.1 s; P = 0.021; ES = 0.67) were significantly blunted during the morning testing. However, IS was not affected by time-of-day (P = 0.891). Thus, tennis performance may be reduced when competing in the morning in comparison to early evening. Therefore, coaches and tennis players should focus on schedule the SVA, power, speed and agility training sessions in the afternoon.
Objective There is a growing tendency for physicians to prescribe exercise in accordance with the ‘exercise is medicine’ global health initiative. However, the exercise-pharmacologic interactions for controlling blood pressure are not well described. Our purpose was to study whether angiotensin II receptor type 1 blocker (ARB) antihypertensive medicine enhances the blood pressure-lowering effects of intense exercise. Participants and methods Fifteen hypertensive individuals with metabolic syndrome chronically medicated with ARB underwent two exercise trials in a blind randomized order. One trial was conducted after taking their habitual dose of ARB (ARB MED trial) and another after 48 h of placebo medicine (i.e. dextrose; PLAC trial). Results After placebo medication, brachial systolic blood pressure increased by 5.5 mmHg [P=0.009; effect size (ES)=0.476] and diastolic by 2.5 mmHg (P=0.030; ES=0.373). Exercise reduced systolic and diastolic blood pressures to the same extent in ARB MED and PLAC trials (7 and 8 mmHg, respectively, for systolic and 5 and 4 mmHg, respectively, for diastolic, all P<0.05). Pulsatile measures of arterial stiffness did not reveal an interaction effect between exercise and medication. However, postocclusion reactive hyperemia increased after exercise only in the ARB MED trial (361±169 to 449±240% from baseline; P=0.033; ES=0.429). Conclusion ARBs and a bout of intense exercise each have an independent effect on lowering blood pressure in hypertensive individuals, and these effects are additive.
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