Exercise-based cardiac rehabilitation after myocardial revascularization: a systematic review and meta-analysis.

BACKGROUND: The present study aimed to analyze the effects of exercise-based cardiac rehabilitation (CR) on physical performance after myocardial revascularization. In addition, we compared the type and duration of exercise-based CR protocols to determine which ones produced the best performance improvements. METHODS: This systematic review and meta-analysis was conducted and reported in accordance with PRISMA statement. A systematic search of PubMed, Web of Science, SPORTDiscus and ProQuest, was performed in July 2020. Studies that met the following criteria were included: (i) participants submitted to myocardial revascularization (i.e., coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI)), (ii) participants submitted to exercise-based CR, and (iii) participants submitted to protocols for assessing physical performance before and after the exercise-based CR. RESULTS: Thirteen and eleven studies evaluating the effects of exercise-based CR after myocardial revascularization were included in the systematic review and meta-analysis, respectively. Exercise-based CR increased physical performance after myocardial revascularization (mean effect size (ES) 0.75; 95% confidence interval (CI) 0.62, 0.88), particularly when aerobic (ES 0.85; 95% CI 0.68, 1.01) and combined training (ES 1.04; 95% CI 0.70, 1.38) lasting 8-12 weeks (ES 1.20; 95% CI 0.87, 1.53) was prescribed. CONCLUSIONS: The present systematic review and meta-analysis indicates that exercise-based CR increases physical performance after myocardial revascularization. The prescription of physical training for these patients should emphasize aerobic and combined training lasting at least 8-12 weeks, which is more effective in improving physical performance. IMPACT: Our findings demonstrate the effectiveness of physical training in improving physical performance after myocardial revascularization.

Inhibition of nNOS in the paraventricular nucleus of hypothalamus decreases exercise-induced hyperthermia.

The paraventricular nucleus of the hypothalamus (PVN) is an important site for autonomic control, which integrates thermoregulation centers and sympathetic outflow to thermoeffector organs. PVN neurons express the neuronal isoform of nitric oxide synthase (nNOS) whose expression is locally upregulated by physical exercise. Thus, the aim of the present study was to evaluate the role of nNOS in the PVN in the exercise-induced hyperthermia. Seven days after surgery, male Wistar rats received bilateral intra-PVN microinjections of the selective nNOS inhibitor Nw-Propyl-L-Arginine (NPLA) or vehicle (saline) and were submitted to an acute progressive exercise session on a treadmill until fatigue. Abdominal and tail skin temperature (Tabd and Ttail, respectively) were measured, and the threshold (Hthr; °C) and sensitivity (Hsen) for heat dissipation calculated. Performance variables were also collected. During the progressive exercise protocol, all animals displayed an increase in the Tabd. However, compared to vehicle group, the microinjection of NPLA in the PVN attenuated the exercise-induced hyperthermia. There was no difference in Ttail or Hthr between NPLA and control rats. In contrast, Hsen was increased in the NPLA group compared to vehicle. In addition, heat storage was lower in NPLA-treated animals. Despite the temperature differences, inhibition of nNOS in the PVN did not affect running performance on the treadmill. These results suggest that nitrergic signaling within the PVN, under nNOS activation, drives the increase of body temperature, being necessary for the proper thermal regulatory mechanisms during progressive exercise-induced hyperthermia.

Impaired thermoregulation in spontaneously hypertensive rats during physical exercise is related to reduced hypothalamic neuronal activation.

This study aimed to evaluate the physical exercise-induced neuronal activation in brain nuclei controlling thermoregulatory responses in hypertensive and normotensive rats. Sixteen-week-old male normotensive Wistar rats (NWRs) and spontaneously hypertensive rats (SHRs) were implanted with an abdominal temperature sensor. After recovery, the animals were subjected to a constant-speed treadmill running (at 60% of the maximum aerobic speed) for 30 min at 25 °C. Core (Tcore) and tail-skin (Tskin) temperatures were measured every minute during exercise. Ninety minutes after the exercise, the rats were euthanized, and their brains were collected to determine the c-Fos protein expression in the following areas that modulate thermoregulatory responses: medial preoptic area (mPOA), paraventricular hypothalamic nucleus (PVN), and supraoptic nucleus (SON). During treadmill running, the SHR group exhibited a greater increase in Tcore and an augmented threshold for cutaneous heat loss relative to the NWR group. In addition, the SHRs showed reduced neuronal activation in the mPOA (< 49.7%) and PVN (< 44.2%), but not in the SON. The lower exercise-induced activation in the mPOA and PVN in hypertensive rats was strongly related to the delayed onset of cutaneous heat loss. We conclude that the enhanced exercise-induced hyperthermia in hypertensive rats can be partially explained by a delayed cutaneous heat loss, which is, in turn, associated with reduced activation of brain areas modulating thermoregulatory responses.