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Hemodynamic Response to High- and Low-Load Resistance Exercise in Patients with Coronary Artery Disease: A Randomized, Crossover Clinical Trial.

ABSTRACT: Low-load resistance exercise (LL-RE) is recommended as an adjunct therapy to aerobic exercise during cardiac rehabilitation in patients with coronary artery disease. The safety and hemodynamic response to high-load (HL) RE remain unknown. The aim of this study was to evaluate the hemodynamic response during both HL-RE and LL-RE prior to cardiac rehabilitation. Forty-three patients with coronary artery disease and/or percutaneous coronary intervention performed three sets of leg-press exercise using HL-RE (eight repetitions at the intensity of 80% of one repetition maximum (1-RM)) and LL-RE (16 repetitions at the intensity of 40% 1-RM) in a randomized crossover sequence. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and rating of perceived exertion were measured at baseline, after each set of RE and post-exercise. No clinically relevant changes in HR and BP or in patient-reported symptoms were recorded during HL-RE or LL-RE. Compared with baseline, HR and SBP increased during LL-RE (from 66 bpm to 86 bpm, time effect: p < 0.001; from 129 mmHg to 146 mmHg, time effect: p < 0.001) and HL-RE (from 68 bpm to 86 bpm, time effect: p < 0.001; from 130 mmHg to 146 mmHg, time effect: p < 0.001). Compared with HL-RE, the increase in HR was greater after the final set of LL-RE (32% vs. 28%, p = 0.015), without significant differences in SBP and DBP between LL-RE and HL-RE. Rating of perceived exertion was higher after the 1st set of HL-RE compared with LL-RE (median (interquartile range): 6 (5-7) vs. 6 (5-6), p = 0.010). In patients with coronary artery disease, both HL-RE and LL-RE were safe and well-tolerated. Hemodynamic changes were similar and within the physiological response to RE.

SUBMITTER: Kambic T

PROVIDER: S-EPMC8068143 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Living in neighborhoods characterized by poverty may act as a chronic stressor that results in physiological dysregulation of the sympathetic nervous system. No previous study has assessed neighborhood poverty with hemodynamic, neuroendocrine, and immune reactivity to stress. We used data from 632 patients with coronary artery disease. Patients' residential addresses were geocoded and merged with poverty data from the 2010 American Community Survey at the census-tract level. A z-transformation was calculated to classify census tracts (neighborhoods) as either having 'high' or 'low' poverty. Systolic blood pressure, diastolic blood pressure, heart rate, rate-pressure product, epinephrine, interleukin-6, and high-sensitivity C-reactive protein were measured before and after a public speaking stress task. Multilevel models were used for repeated measures and accounting for individuals nested within census tracts. Adjusted models included demographics, lifestyle and medical risk factors, and medication use. Another set of models included propensity scores weighted by the inverse probability of neighborhood status for sex, age, race, and individual-level income. The mean age was 63 years and 173 were women. After adjusting for potential confounders, participants living in high (vs. low) poverty neighborhoods had similar hemodynamic values at rest and lower values during mental stress for systolic blood pressure (157 mmHg vs. 161 mmHg; p = 0.07), heart rate (75 beats/min vs. 78 beats/min; p = 0.02) and rate-pressure product (11839 mmHg x beat/min vs 12579 mmHg x beat/min; p = 0.01). P-values for neighborhood poverty-by-time interactions were <0.05. Results were similar in the propensity weighted models. There were no significant differences in inflammatory and epinephrine responses to mental stress based on neighborhood poverty status. A blunted hemodynamic response to mental stress was observed among participants living in high poverty neighborhoods. Future studies should explore whether neighborhood poverty and blunted hemodynamic response to stress translate into differences in long-term cardiovascular outcomes.

Project description:BackgroundExercise improves glycemic control but the magnitude, and in some cases, the direction of this effect is variable. Ambient hyperglycemia has been implicated in this exercise response heterogeneity. The current study investigated whether pre-exercise hyperglycemia directly impacts the effect of exercise on glycemic control.MethodsTwelve healthy normal glucose-tolerant males completed four trials in a randomized, crossover design. Each trial consisted of 24-h pre-intervention monitoring, a 7-h intervention, and 24-h post-intervention monitoring. Glycemic control was measured throughout the study by continuous glucose monitoring. The four interventions were no exercise (CON) or 45 min of cycling exercise (70%HRmax) preceded by 3.5 h of either normoglycemia (NG-Ex), steady-state hyperglycemia induced by constant glucose infusion (HG-Ex) or fluctuating glycemia induced by repeated glucose bolus infusions (FG-Ex).ResultsPhysical activity and diet were similar between trials, and energy expenditure during exercise was matched between exercise trials (all P > 0.05). Mean glucose during the 3.5 h ± infusion period was higher in HG-Ex (mean ± SEM; 7.2 ± 0.4 mmol/L) and FG-Ex (7.3 ± 0.3 mmol/L) compared to CON (4.8 ± 0.2 mmol/L) and NG-Ex (5.0 ± 0.2 mmol/L) trials (P < 0.01). Glycemic variability was greatest in FG-Ex (P < 0.01). Following the interventions, the postprandial glucose response (iAUC) was reduced by exercise in NG-Ex compared to CON (321.1 ± 38.6 vs. 445.5 ± 49.7 mmol/L.8h, P < 0.05, d=0.81). This benefit was blunted when exercise was preceded by steady-state (HG-Ex, 425.3 ± 45.7 mmol/L.8h) and fluctuating (FG-Ex, 465.5 ± 39.3 mmol/L.8h) hyperglycemia (both P > 0.05 vs. CON).ConclusionPre-exercise hyperglycemia blunted the glucoregulatory benefits of acute exercise upon postprandial glucose response, suggesting that exposure to hyperglycemia contributes to exercise response heterogeneity.Clinical trial registrationClinicalTrials.gov, identifier NCT03284216.

Project description:Resistance training may be associated with unfavorable cardiovascular responses (such as hemodynamic alterations, anginal symptoms or ventricular arrhythmias). In healthy adults, blood flow-restricted (BFR) resistance training improves muscle strength and hypertrophy improvements at lower loads with minimal systemic cardiovascular adverse responses. The aim of this study was to assess the safety and efficacy of BFR resistance training in patients with coronary artery disease (CAD) compared to usual care. Patients with stable CAD were randomized to either 8 weeks of supervised biweekly BFR resistance training (30-40% 1RM unilateral knee extension) or usual exercise routine. At baseline and after 8 weeks, patients underwent 1-RM knee extension tests, ultrasonographic appraisal of vastus lateralis (VL) muscle diameter and of systemic (brachial artery) flow-mediated dilation, and determination of markers of inflammation (CD40 ligand and tumor necrosis factor alfa), and fasting glucose and insulin levels for homeostatic model assessment (HOMA). A total of 24 patients [12 per group, mean age 60 ± 2 years, 6 (25%) women] were included. No training-related adverse events were recorded. At baseline groups significantly differ in age (mean difference: 8.7 years, p < 0.001), systolic blood pressure (mean difference: 12.17 mmHg, p = 0.024) and in metabolic control [insulin (p = 0.014) and HOMA IR (p = 0.014)]. BFR-resistance training significantly increased muscle strength (1-RM, +8.96 kg, p < 0.001), and decreased systolic blood pressure (-6.77 mmHg; p = 0.030), whereas VL diameter (+0.09 cm, p = 0.096), brachial artery flow-mediated vasodilation (+1.55%; p = 0.079) and insulin sensitivity (HOMA IR change of 1.15, p = 0.079) did not improve significantly. Blood flow restricted resistance training is safe and associated with significant improvements in muscle strength, and may be therefore provided as an additional exercise option to aerobic exercise to improve skeletal muscle functioning in patients with CAD. Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT03087292.

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Hemodynamic Response to High- and Low-Load Resistance Exercise in Patients with Coronary Artery Disease: A Randomized, Crossover Clinical Trial.

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