Hemodynamic responses to neuromuscular electrical stimulation and to metaboreflex activation.

BACKGROUND: Metabolites produced during muscle exercise can sensitize types III and IV fibers, which account for increasing blood pressure (BP) and vascular resistance in non-exercising limbs, as well as for redistributing the blood flow to active muscles; reflex response is called metaboreflex. Neuromuscular electrical stimulation (NMES) induces greater local muscle metabolic demand than voluntary isometric contractions. Metabolic accumulation is essential to activate muscle metaboreflex; thus, the hypothesis of the current study is that one NMES session can induce metaboreflex with different hemodynamic responses in upper and lower limbs. Objective - to investigate whether one acute NMES session could activate metaboreflex by inducing different hemodynamic responses between arms and legs. METHODS: Twenty (20) healthy subjects (mean age = 47.7±9.4 years, 13 women, mean body mass index = 26 ± 3 kg/m2) participated in this randomized crossover study. All participants were subjected to two NMES interventions, one in the upper limbs (UPL) and the other in the lower limbs (LL). Mean blood pressure (MBP), blood flow (BF) and vascular resistance (VR) were used to selectively evaluate metaboreflex responses at baseline, during NMES interventions, and recovery periods with, and without, postexercise circulatory occlusion (PECO+ and PECO-, respectively) through the area under the curve (AUC) in VR. RESULTS: MBP increased by 13% during UPL interventions and only remained high during PECO+. Changes in MBP were not observed in LL, although BF in the contralateral leg has decreased by 14% during PECO+ protocol. Muscle metaboreflex activation (AUC differences in VR between PECO+ and PECO-) was not different between UPL and LL (P=0.655). CONCLUSIONS: Acute NMES session has induced similar metaboreflex activation in both arms and legs, although hemodynamic responses differed between interventions.

Inspiratory muscle strength and six-minute walking distance in heart failure: Prognostic utility in a 10 years follow up cohort study.

BACKGROUND: Maximal inspiratory pressure (PImax) and 6-minutes walk distance test (6MWD) may be more available and feasible alternatives for prognostic assessment than cardiopulmonary testing. We hypothesized that the PImax and 6MWD combination could improve their individual accuracy as risk predictors. We aimed to evaluate PImax ability as a mortality predictor in HF and whether the combination to 6MWD could improve risk stratification. METHODS: Prospective cohort from HF Clinics of three University Hospitals. PImax, 6MWD and pVO2 were obtained at baseline. The end point was all cause mortality. RESULTS: Consecutive 256 individuals (50% woman, 57.4±10.4years) with low ejection fraction (LVEF) (31.8±8.6%) were followed up to 10years. During a median follow-up of 34.7 (IQR 37) months, 110 participants died. Mean±SD values were: pVO2 14.9±5.1mL/kg/min, PImax 5.5±1.3kPa and 6MWD 372±118m. In multivariate Cox regression, pVO2, PImax, 6MWD and LVEF were independent mortality predictors. The pVO2 showed gold standard accuracy, followed by PImax (AUC = 0.84) and 6MWD (AUC = 0.74). Kaplan-Meier mean survival time (MST±SE) for lower (≤5.0kPa) and higher (>6.0kPa) PImax tertiles, were 37.9±2.8months and 105.0±5.2months respectively, and addition of 6MWD did not restratified risk. For intermediate PImax tertile, MST was 81.5±5.5months, but adding 6MWD, MST was lower (53.3±7.6months) if distance was ≤350m and higher (103.1±5.7months) for longer distances. CONCLUSION: PImax is an independent mortality predictor in HF, more accurate than 6MWD and LVEF. Addition of 6MWD empowers risk stratification only for intermediate PImax tertile. Although less accurate than pVO2, this simpler approach could be a feasible alternative as a prognostic assessment.

Cardiorespiratory fitness of a Brazilian regional sample distributed in different tables.

BACKGROUND: Most classification tables of cardiorespiratory fitness (CRF) used in clinical practice are international and have not been validated for the Brazilian population. That can result in important discrepancies when that classification is extrapolated to our population. OBJECTIVE: To assess the use of major CRF tables available in a Brazilian population sample of the Central High Plan of the state of Rio Grande do Sul (RS). METHODS: This study assessed the retrospective data of 2,930 individuals, living in 36 cities of the Central High Plan of the state of RS, and considered the following: presence of risk factors for cardiovascular disease and estimated maximum oxygen consumption (VO2peak) values obtained through exercise test with Bruce protocol. To classify CRF, the individuals were distributed according to sex, inserted in their respective age groups in the Cooper, American Heart Association (AHA) and Universidade Federal de São Paulo (Unifesp) tables, and classified according to their VO2peak. RESULTS: Women had lower VO2peak values as compared with those of men (23.5 ± 8.5 vs. 31.7 ± 10.8 mL.kg-1.min-1, p < 0.001). Considering both sexes, VO2peak showed an inverse and moderate correlation with age (R = -0.48, p < 0.001). An important discrepancy in the CRF classification levels was observed between the tables, ranging from 49% (Cooper x AHA) to 75% (Unifesp x AHA). CONCLUSION: Our findings indicate important discrepancy in the CRF classification levels of the tables assessed. Future studies could assess whether international tables could be used for the Brazilian population and populations of different regions of Brazil.

The contribution of inspiratory muscles function to exercise limitation in heart failure: pathophysiological mechanisms / Contribuição da musculatura inspiratória na limitação ao exercício na insuficiência cardíaca: mecanismos fisiopatológicos

BACKGROUND: Heart failure induces histological, metabolic and functional adaptations in the inspiratory muscles. This inspiratory muscle weakness, which occurs in 30% to 50% of the heart failure patients, is associated with reduction in the functional capacity, reduction in the quality of life and with a poor prognosis in these individuals. OBJECTIVES: The objective of this review was to discuss the pathophysiological mechanisms that may explain the role of the inspiratory muscles in the exercise limitation with focus in the reflexes that control the ventilation and the circulation during the exercise. METHOD: We performed searches in the PUBMED database using the terms "inspiratory muscles", "inspiratory muscle training", "metaboreflex" and chemoreflex" and including studies published since 1980. RESULTS: Inspiratory muscle weakness is associated with exercise intolerance and with an exaggerated inspiratory chemoreflex and metaboreflex in heart failure. The inspiratory metaboreflex may be attenuated by the inspiratory muscle training or by the aerobic exercise training improving the exercise performance. CONCLUSIONS: Patients with heart failure may present changes in the inspiratory muscle function associated with inspiratory chemoreflex and metaboreflex hyperactivity, which exacerbate the exercise intolerance.

CONTEXTUALIZAÇÃO: A insuficiência cardíaca (IC) acarreta alterações histológicas, metabólicas e funcionais dos músculos inspiratórios. A fraqueza dos músculos inspiratórios, que ocorre em 30% a 50% dos pacientes com IC, associa-se com a redução da capacidade funcional, prejuízos para a qualidade de vida e piora no prognóstico desses indivíduos. OBJETIVOS: Discutir os mecanismos fisiopatológicos que potencialmente explicam o papel da musculatura inspiratória na limitação ao exercício, abordando-se os reflexos que controlam a ventilação e a circulação durante o exercício. MÉTODO: Foram realizadas pesquisas na base de dados PUBMED, utilizando os termos inspiratory muscles, inspiratory muscle training, metaborreflex e chemoreflex e incluindo estudos publicados desde 1980. RESULTADOS: A fraqueza muscular inspiratória está relacionada com intolerância ao exercício e com exacerbação do quimiorreflexo e do metaborreflexo inspiratório na IC. O metaborreflexo inspiratório pode ser atenuado pelo treinamento muscular inspiratório ou pelo treinamento aeróbico, melhorando o desempenho ao exercício. CONCLUSÕES: Os pacientes com IC podem apresentar alterações da função muscular inspiratória associadas com hiperatividade quimiorreflexa e metaborreflexa inspiratória, as quais podem agravar a intolerância ao exercício.

The contribution of inspiratory muscles function to exercise limitation in heart failure: pathophysiological mechanisms.

BACKGROUND: Heart failure induces histological, metabolic and functional adaptations in the inspiratory muscles. This inspiratory muscle weakness, which occurs in 30% to 50% of the heart failure patients, is associated with reduction in the functional capacity, reduction in the quality of life and with a poor prognosis in these individuals. OBJECTIVES: The objective of this review was to discuss the pathophysiological mechanisms that may explain the role of the inspiratory muscles in the exercise limitation with focus in the reflexes that control the ventilation and the circulation during the exercise. METHOD: We performed searches in the PUBMED database using the terms "inspiratory muscles", "inspiratory muscle training", "metaboreflex" and chemoreflex" and including studies published since 1980. RESULTS: Inspiratory muscle weakness is associated with exercise intolerance and with an exaggerated inspiratory chemoreflex and metaboreflex in heart failure. The inspiratory metaboreflex may be attenuated by the inspiratory muscle training or by the aerobic exercise training improving the exercise performance. CONCLUSIONS: Patients with heart failure may present changes in the inspiratory muscle function associated with inspiratory chemoreflex and metaboreflex hyperactivity, which exacerbate the exercise intolerance.

Age-related effects of vagotonic atropine on cardiovagal baroreflex gain.

Impaired neural transduction of barosensory vessel stretch into vagal outflow is a primary determinant of reduced cardiovagal baroreflex gain with human aging. We set out to determine whether age-related reductions in this neural component of the baroreflex might be offset by enhancing the central integration/efferent responsiveness of the neural arc. Low vagotonic doses of atropine were employed to enhance central neural outflow and peripheral sinus node effects. Baroreflex gain and its neural and mechanical components were pharmacologically assessed before and after intravenous vagotonic atropine in 16 older and 14 young healthy subjects. Vagotonic atropine increased cardiovagal baroreflex gain (∼30%) and its neural component (∼20%) in older but not young individuals. Moreover, the atropine-induced increases in integrated gain and in its neural component were inversely related to baseline levels. Thus, age-related neural deficits in the baroreflex arc appear to play a determining role in reduced cardiovagal baroreflex gain with age and the compromised neural baroreflex function can be acutely improved by a single pharmacologic intervention.

Attenuated inspiratory muscle metaboreflex in endurance-trained individuals.

The inspiratory metaboreflex is activated during loaded breathing to task failure and induces sympathetic activation and peripheral vasoconstriction that may limit exercise performance. Inspiratory muscle training appears to attenuate the inspiratory metaboreflex in healthy subjects. Since whole body aerobic exercise training improves breathing endurance and inspiratory muscle strength, we hypothesized that endurance-trained individuals would demonstrate a blunted inspiratory muscle metaboreflex in comparison to sedentary individuals. We studied 9 runners (23±0.7 years; maximal oxygen uptake [VO2 max] = 53 ± 4 ml kg(-1) min(-1)) and 9 sedentary healthy volunteers (24±0.7 years; VO2 max = 37 ±2 ml kg(-1) min(-1)). The inspiratory muscle metaboreflex was induced by breathing against an inspiratory load of 60% of maximal inspiratory pressure (MIP), with prolonged duty cycle. Arterial pressure, popliteal blood flow, and heart rate were measured throughout the protocol. Loaded breathing to task failure increased mean arterial pressure in both sedentary and endurance-trained individuals (96±3 to 100±4 mmHg and 101±3 to 110±5 mmHg). Popliteal blood flow decreased in sedentary but not in trained individuals (0.179±0.01 to 0.141±0.01 cm/s, and 0.211±0.02 to 0.214±0.02 cm/s). Similarly, popliteal vascular resistance increased in sedentary but not in trained individuals (559±35 to 757±56 mmHg s/cm, and 528±69 to 558±64 mmHg s/cm). These data demonstrate that endurance-trained individuals have an attenuated inspiratory muscle metaboreflex.

Augmented peripheral chemoreflex in patients with heart failure and inspiratory muscle weakness.

We hypothesized that heart failure patients with inspiratory muscle weakness (IMW) present greater peripheral chemoreflex responsiveness and augmented exercise ventilatory oscillation compared to patients with preserved inspiratory muscle strength. We studied 19 heart failure patients: 9 with IMW (maximal inspiratory pressure [PImax]<70% of predicted) and 10 with preserved inspiratory muscle strength. Inspiratory muscle strength was measured via pressure transducer. Peripheral chemoreflex was evaluated by the single-breath CO(2) test. Exercise ventilatory oscillation was determined as the ratio between amplitude and mean of each oscillation during incremental exercise. Patients with IMW had greater peripheral chemoreflex response (0.11+/-0.03 l min(-1) Torr(-1)) than those with preserved inspiratory muscle strength (0.07+/-0.03 l min(-1) Torr(-1), p=0.02). Moreover, there was a significant and inverse correlation between PImax and peripheral chemoreflex response (r=-0.57, p=0.01). Likewise, there was a significant and inverse correlation between PImax and ventilatory oscillations (r=-0.46, p=0.04). Our findings indicate that IMW is linked to increased peripheral chemoreflex and augmented exercise ventilatory oscillation in patients with chronic heart failure.