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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:ImportanceThe clinical significance of hemodynamic reactivity to mental stress in the population with coronary artery disease (CAD) is unclear.ObjectiveTo investigate the association between hemodynamic reactivity to mental stress and the risk of adverse cardiovascular events in patients with stable CAD.Design, setting, and participantsThis cohort study included individuals with stable CAD from 2 prospective studies from a university-based hospital network: the Mental Stress Ischemia Prognosis Study (MIPS) and the Myocardial Infarction and Mental Stress Study 2 (MIMS2). Participants were enrolled between June 2011 and March 2016 and followed up for a median of 6.0 (IQR, 5.6-6.0) years in MIPS and 4.6 (IQR, 3.8-5.3) years in MIMS2. Data were analyzed from December 1, 2022, to February 15, 2023.ExposuresThe rate-pressure product (RPP) was calculated as the mean systolic blood pressure times the mean heart rate at rest. Rate-pressure product reactivity was calculated as the maximum RPP during a standardized mental stress test minus the RPP at rest.Main outcomes and measuresThe primary outcome was a composite of cardiovascular death or nonfatal myocardial infarction. The secondary end point additionally included hospitalizations for heart failure.ResultsFrom the total of 938 individuals from the pooled cohort (mean [SD] age, 60.2 [10.1] years; 611 [65.1%] men), 631 participated in MIPS and 307 in MIMS2. A total of 373 individuals (39.8%) were Black, 519 (55.3%) were White, and 46 (4.9%) were of unknown race or ethnicity. The RPP increased by a mean (SD) of 77.1% (23.1%) during mental stress (mean [SD] absolute change, 5651 [2878]). For every SD decrease in RPP reactivity with mental stress, the adjusted hazard ratios for the primary and secondary end points were 1.30 (95% CI, 1.04-1.72) and 1.30 (95% CI, 1.06-1.56), respectively, in MIPS and 1.41 (95% CI, 1.06-1.97) and 1.21 (95% CI, 1.02-1.60), respectively, in MIMS2. In the pooled sample, when RPP reactivity to mental stress was added to a model including traditional clinical risk characteristics, model discrimination for adverse events improved (increase in C statistic of 5% for the primary end point; P = .009).Conclusions and relevanceIn this cohort study of individuals with stable CAD, a blunted cardiovascular reactivity to mental stress was associated with adverse outcomes. Future studies are needed to assess the clinical utility of mental stress reactivity testing in this population.

Project description:IntroductionThe post-exercise recovery is a period of vulnerability of the cardiovascular system in which autonomic nervous system plays a key role in cardiovascular deceleration. It is already known that individuals with coronary artery disease (CAD) are at greater risk due to delayed vagal reactivation in this period. Water ingestion has been studied as a strategy to improve autonomic recovery and mitigate the risks during recovery. However, the results are preliminary and need further confirmation. Therefore, our aim was to investigate the influence of individualized water drinking on the non-linear dynamics of heart rate during and after aerobic exercise in CAD subjects.Methods30 males with CAD were submitted to a control protocol composed of initial rest, warming up, treadmill exercise, and passive recovery (60 min). After 48 hours they performed the hydration protocol, composed of the same activities, however, with individualized water drinking proportional to the body mass lost in the control protocol. The non-linear dynamics of heart rate were assessed by indices of heart rate variability extracted from the recurrence plot, detrended fluctuation analysis, and symbolic analysis.Results and discussionDuring exercise, the responses were physiological and similar in both protocols, indicating high sympathetic activity and reduced complexity. During recovery, the responses were also physiological, indicating the rise of parasympathetic activity and the return to a more complex state. However, during hydration protocol, the return to a more complex physiologic state occurred sooner and non-linear HRV indices returned to resting values between the 5th and 20th minutes of recovery. In contrast, during the control protocol, only a few indices returned to resting values within 60 minutes. Despite that, differences between protocols were not found. We conclude that the water drinking strategy accelerated the recovery of non-linear dynamics of heart rate in CAD subjects but did not influence responses during exercise. This is the first study to characterize the non-linear responses during and after exercise in CAD subjects.

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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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