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We investigated the locomotor muscle metaboreflex control of ventilation, circulation, and dyspnea in patients with chronic obstructive pulmonary disease (COPD). Ten patients [forced expiratory volume in 1 second (FEV1; means ± SD) = 43 ± 17% predicted] and nine age- and sex-matched controls underwent 1) cycling exercise followed by postexercise circulatory occlusion (PECO) to activate the metaboreflex or free circulatory flow to inactivate it, 2) cold pressor test to interpret whether any altered reflex response was specific to the metaboreflex arc, and 3) muscle biopsy to explore the metaboreflex arc afferent side. We measured airflow, dyspnea, heart rate, arterial pressure, muscle blood flow, and vascular conductance during reflexes activation. In addition, we measured fiber types, glutathione redox balance, and metaboreceptor-related mRNAs in the vastus lateralis. Metaboreflex activation increased ventilation versus free flow in patients (â¼15%, P < 0.020) but not in controls (P > 0.450). In contrast, metaboreflex activation did not change dyspnea in patients (P = 1.000) but increased it in controls (â¼100%, P < 0.001). Other metaboreflex-induced responses were similar between groups. Cold receptor activation increased ventilation similarly in both groups (P = 0.46). Patients had greater type II skeletal myocyte percentage (14%, P = 0.010), lower glutathione ratio (-34%, P = 0.015), and lower nerve growth factor (NGF) mRNA expression (-60%, P = 0.031) than controls. Therefore, COPD altered the locomotor muscle metaboreflex control of ventilation. It increased type II myocyte percentage and elicited redox imbalance, potentially producing more muscle metaboreceptor stimuli. Moreover, it decreased NGF expression, suggesting a downregulation of metabolically sensitive muscle afferents.NEW & NOTEWORTHY This study's integrative physiology approach provides evidence for a specific alteration in locomotor muscle metaboreflex control of ventilation in patients with COPD. Furthermore, molecular analyses of a skeletal muscle biopsy suggest that the amount of muscle metaboreceptor stimuli derived from type II skeletal myocytes and redox imbalance overcame a downregulation of metabolically sensitive muscle afferents.
Assuntos
Fator de Crescimento Neural , Doença Pulmonar Obstrutiva Crônica , Humanos , Fator de Crescimento Neural/metabolismo , Reflexo/fisiologia , Músculo Esquelético/fisiologia , Dispneia , Glutationa/metabolismo , Pressão Sanguínea/fisiologiaRESUMO
Abnormalities in the muscle metaboreflex concur to exercise intolerance and greater cardiovascular risk. Exercise training benefits neurocardiovascular function at rest and during exercise, but its role in favoring muscle metaboreflex in health and disease remains controversial. While some authors demonstrated that exercise training enhanced the sensitization of muscle metabolically afferents and improved neurocardiovascular responses to muscle metaboreflex activation, others reported unaltered responses. This narrative review aimed to: (a) highlight the current evidence on the effects of exercise training upon cardiovascular and autonomic responses to muscle metaboreflex activation; (b) analyze the role of training components and indicate potential mechanisms of metaboreflex adaptations; and (c) address key methodological features for future research. Though limited, accumulated evidence suggests that muscle metaboreflex adaptations depend on the individual clinical status, exercise modality, and training duration. In healthy populations, most trials negated the hypothesis of metaboreflex improvement due to chronic exercise, irrespective of the training duration. Favorable changes in patients with impaired metaboreflex, particularly chronic heart failure, mostly resulted from long-term interventions (> 16 weeks) including aerobic exercise of moderate to high intensity, performed in isolation or within multimodal training. Potential mechanisms of metaboreflex improvements include enhanced sensitivity of channels and receptors, greater antioxidant capacity, lower metabolite accumulation, increased functional sympatholysis, and muscle perfusion. Future research should investigate: (1) the dose-response relationship of training components within different exercise modalities to elicit improvements in individuals showing intact or impaired muscle metaboreflex; and (2) potential and specific underlying mechanisms of metaboreflex improvements in individuals with different medical conditions.
Assuntos
Adaptação Fisiológica/fisiologia , Sistema Nervoso Autônomo/fisiologia , Fenômenos Fisiológicos Cardiovasculares , Exercício Físico/fisiologia , Músculo Esquelético/fisiologia , Reflexo/fisiologia , HumanosRESUMO
A parasympathetic reactivation is an underlying mechanism mediating the rapid fall in heart rate (HR) at the onset of post-exercise ischemia (PEI) in humans. Herein, we tested the hypothesis that, compared to men, women present a slower HR recovery at the cessation of isometric handgrip exercise (i.e., onset of PEI) due to an attenuated cardiac vagal reactivation. Forty-seven (23 women) young and healthy volunteers were recruited. Subjects performed 90s of isometric handgrip exercise at 40% of maximal voluntary contraction followed by 3-min of PEI. The onset of PEI was analyzed over the first 30s in 10s windows. Cardiac vagal reactivation was indexed using the HR fall and by HR variability metrics (e.g., RMSSD and SDNN) immediately after the cessation of the exercise. HR was significantly increased from rest during exercise in men and women and increases were similar between sexes. However, following the cessation of exercise, the HR recovery was significantly slower in women compared to men regardless of the time point (women vs. men: ∆-14 ± 8 vs. ∆-18 ± 6 beats.min-1 at 10s; ∆-20 ± 9 vs. ∆-25 ± 8 beats.min-1 at 20s; ∆-22 ± 10 vs. ∆-27 ± 9 beats.min-1 at 30s; P = .027). RMSSD and SDNN increased at the cessation of exercise in greater magnitude in men compared to women. These findings demonstrate that women had a slower HR recovery at the cessation of isometric handgrip exercise and onset of PEI compared to men, suggesting a sex-related difference in cardiac vagal reactivation in healthy young humans.
Assuntos
Sistema Nervoso Autônomo/fisiologia , Exercício Físico/fisiologia , Mãos/fisiologia , Frequência Cardíaca/fisiologia , Músculo Esquelético/fisiologia , Reflexo/fisiologia , Caracteres Sexuais , Adulto , Feminino , Humanos , Masculino , Músculo Esquelético/metabolismo , Adulto JovemRESUMO
The incidence of Parkinson's disease is increasing worldwide. The motor dysfunctions are the hallmark of the disease, but patients also experience non-motor impairments, and over 40% of the patients experience coexistent abnormalities, such as orthostatic hypotension. Exercise training has been suggested as a coping resource to alleviate Parkinson's disease symptoms and delay disease progression. However, the body of knowledge is showing that the cardiovascular response to exercise in patients with Parkinson's disease is altered. Adequate cardiovascular and hemodynamic adjustments to exercise are necessary to meet the metabolic demands of working skeletal muscle properly. Therefore, since Parkinson's disease affects parasympathetic and sympathetic branches of the autonomic nervous system and the latter are crucial in ensuring these adjustments are adequately made, the understanding of these responses during exercise in this population is necessary. Several neural control mechanisms are responsible for the autonomic changes in the cardiovascular and hemodynamic systems seen during exercise. In this sense, the purpose of the present work is to review the current knowledge regarding the cardiovascular responses to dynamic and isometric/resistance exercise as well as the mechanisms by which the body maintains appropriate perfusion pressure to all organs during exercise in patients with Parkinson's disease. Results from patients with Parkinson's disease and animal models of Parkinson's disease provide the reader with a well-rounded knowledge base. Through this, we will highlight what is known and not known about how the neural control of circulation is responding during exercise and the adaptations that occur when individuals exercise regularly.
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Blood flow restriction training (BFRT) is an increasingly widespread method of exercise that involves imposed restriction of blood flow to the exercising muscle. Blood flow restriction is achieved by inflating a pneumatic pressure cuff (or a tourniquet) positioned proximal to the exercising muscle before, and during, the bout of exercise (i.e., ischemic exercise). Low-intensity BFRT with resistance training promotes comparable increases in muscle mass and strength observed during high-intensity exercise without blood flow restriction. BFRT has expanded into the clinical research setting as a potential therapeutic approach to treat functionally impaired individuals, such as the elderly, and patients with orthopedic and cardiovascular disease/conditions. However, questions regarding the safety of BFRT must be fully examined and addressed before the implementation of this exercise methodology in the clinical setting. In this respect, there is a general concern that BFRT may generate abnormal reflex-mediated cardiovascular responses. Indeed, the muscle metaboreflex is an ischemia-induced, sympathoexcitatory pressor reflex originating in skeletal muscle, and the present review synthesizes evidence that BFRT may elicit abnormal cardiovascular responses resulting from increased metaboreflex activation. Importantly, abnormal cardiovascular responses are more clearly evidenced in populations with increased cardiovascular risk (e.g., elderly and individuals with cardiovascular disease). The evidence provided in the present review draws into question the cardiovascular safety of BFRT, which clearly needs to be further investigated in future studies. This information will be paramount for the consideration of BFRT exercise implementation in clinical populations.
Assuntos
Sistema Nervoso Autônomo/fisiologia , Células Quimiorreceptoras/metabolismo , Isquemia , Contração Muscular , Músculo Esquelético/anormalidades , Músculo Esquelético/inervação , Condicionamento Físico Humano/métodos , Reflexo , Oclusão Terapêutica , Adaptação Fisiológica , Animais , Metabolismo Energético , Feminino , Hemodinâmica , Humanos , Masculino , Músculo Esquelético/metabolismo , Condicionamento Físico Humano/efeitos adversos , Fluxo Sanguíneo Regional , Medição de Risco , Oclusão Terapêutica/efeitos adversosRESUMO
In animals, the blockade of acid-sensing ion channels (ASICs), cation pore-forming membrane proteins located in the free nerve endings of group IV afferent fibers, attenuates increases in arterial pressure (AP) and sympathetic nerve activity (SNA) during muscle contraction. Therefore, ASICs play a role in mediating the metabolic component (skeletal muscle metaboreflex) of the exercise pressor reflex in animal models. Here we tested the hypothesis that ASICs also play a role in evoking the skeletal muscle metaboreflex in humans, quantifying beat-by-beat mean AP (MAP; finger photoplethysmography) and muscle SNA (MSNA; microneurography) in 11 men at rest and during static handgrip exercise (SHG; 35% of the maximal voluntary contraction) and postexercise muscle ischemia (PEMI) before (B) and after (A) local venous infusion of either saline or amiloride (AM), an ASIC antagonist, via the Bier block technique. MAP (BAM +30 ± 6 vs. AAM +25 ± 7 mmHg, P = 0.001) and MSNA (BAM +14 ± 9 vs. AAM +10 ± 6 bursts/min, P = 0.004) responses to SHG were attenuated under ASIC blockade. Amiloride also attenuated the PEMI-induced increases in MAP (BAM +25 ± 6 vs. AAM +16 ± 6 mmHg, P = 0.0001) and MSNA (BAM +16 ± 9 vs. AAM +8 ± 8 bursts/min, P = 0.0001). MAP and MSNA responses to SHG and PEMI were similar before and after saline infusion. We conclude that ASICs play a role in evoking pressor and sympathetic responses to SHG and the isolated activation of the skeletal muscle metaboreflex in humans. NEW & NOTEWORTHY We showed that regional blockade of the acid-sensing ion channels (ASICs), induced by venous infusion of the antagonist amiloride via the Bier block anesthetic technique, attenuated increases in arterial pressure and muscle sympathetic nerve activity during both static handgrip exercise and postexercise muscle ischemia. These findings indicate that ASICs contribute to both pressor and sympathetic responses to the activation of the skeletal muscle metaboreflex in humans.
Assuntos
Canais Iônicos Sensíveis a Ácido/fisiologia , Pressão Sanguínea/fisiologia , Força da Mão/fisiologia , Contração Muscular/fisiologia , Músculo Esquelético/fisiologia , Reflexo/fisiologia , Adulto , Humanos , Masculino , Sistema Nervoso Simpático/fisiologia , Adulto JovemRESUMO
KEY POINTS: The activation of the group III/IV skeletal muscle afferents is one of the principal mediators of cardiovascular responses to exercise; however, the neuronal circuitry mechanisms that are involved during the activation of group III/IV muscle afferents in humans remain unknown. Recently, we showed that GABAergic mechanisms are involved in the cardiac vagal withdrawal during the activation of mechanically sensitive (predominantly mediated by group III fibres) skeletal muscle afferents in humans. In the present study, we found that increases in muscle sympathetic nerve activity and mean blood pressure during isometric handgrip exercise and postexercise ischaemia were significantly greater after the oral administration of diazepam, a benzodiazepine that increases GABAA activity, but not after placebo administration in young healthy subjects. These findings indicate for the first time that GABAA receptors modulate sympathetic vasomotor outflow and the pressor responses to activation of metabolically sensitive (predominantly mediated by group IV fibres) skeletal muscle afferents in humans. ABSTRACT: Animal studies have indicated that GABAA receptors are involved in the neuronal circuitry of the group III/IV skeletal muscle afferent activation-induced neurocardiovascular responses to exercise. In the present study, we aimed to determine whether GABAA receptors modulate the neurocardiovascular responses to activation of metabolically sensitive (predominantly mediated by group IV fibres) skeletal muscle afferents in humans. In a randomized, double-blinded, placebo-controlled and cross-over design, 17 healthy subjects (eight women) performed 2 min of ischaemic isometric handgrip exercise at 30% of the maximal voluntary contraction followed by 2 min of postexercise ischaemia (PEI). Muscle sympathetic nerve activity (MSNA), blood pressure (BP) and heart rate (HR) were continuously measured and trials were conducted before and 60 min after the oral administration of either placebo or diazepam (10 mg), a benzodiazepine that enhances GABAA activity. At rest, MSNA was reduced, whereas HR and BP did not change after diazepam administration. During ischaemic isometric handgrip, greater MSNA (pre: ∆13 ± 9 bursts min-1 vs. post: ∆29 ± 15 bursts min-1 , P < 0.001), HR (pre: ∆23 ± 11 beats min-1 vs. post: ∆31 ± 17 beats min-1 , P < 0.01) and mean BP (pre: ∆33 ± 12 mmHg vs. post: ∆37 ± 12 mmHg, P < 0.01) responses were observed after diazepam. During PEI, MSNA and mean BP remained elevated from baseline before diazepam (∆10 ± 8 bursts min-1 and ∆25 ± 14 mmHg, respectively) and these elevations were increased after diazepam (∆17 ± 12 bursts min-1 and ∆28 ± 13 mmHg, respectively) (P ≤ 0.05). Importantly, placebo pill had no effect on neural, cardiac and pressor responses. These findings demonstrate for the first time that GABAA receptors modulate MSNA and the pressor responses to skeletal muscle metaboreflex activation in humans.
Assuntos
Pressão Sanguínea/fisiologia , Contração Muscular/fisiologia , Músculo Esquelético/fisiologia , Receptores de GABA-A/metabolismo , Reflexo/fisiologia , Sistema Nervoso Simpático/fisiologia , Adulto , Diazepam/farmacologia , Feminino , Moduladores GABAérgicos/farmacologia , Humanos , Masculino , Sistema Nervoso Simpático/efeitos dos fármacos , Adulto JovemRESUMO
PURPOSE: To investigate the effect of isolated muscle metaboreflex activation on spontaneous cardiac baroreflex sensitivity (cBRS), and to characterize the potential sex-related differences in this interaction in young healthy subjects. METHODS: 40 volunteers (20 men and 20 women, age: 22 ± 0.4 year) were recruited. After 5-min rest period, the subjects performed 90 s of isometric handgrip exercise at 40% of maximal voluntary contraction followed by 3 min of post-exercise ischemia (PEI). Beat-to-beat heart rate and arterial blood pressure were continuously measured by finger photopletysmography. Spontaneous cBRS was assessed using the sequence technique and heart rate variability was measured in time (RMSSD-standard deviation of the RR intervals) and frequency domains (LF-low and HF-high frequency power). RESULTS: Resting cBRS was similar between men and women. During PEI, cBRS was increased in men (Δ3.0 ± 1.1 ms mmHg- 1, P = 0.03) but was unchanged in women (Δ-0.04 ± 1.0 ms mmHg- 1, P = 0.97). In addition, RMSSD and HF power of heart rate variability increased in women (Δ7.4 ± 2.6 ms, P = 0.02; Δ373.4 ± 197.3 ms2; P = 0.04, respectively) and further increased in men (Δ26.4 ± 7.1 ms, P < 0.01; Δ1874.9 ± 756.2 ms2; P = 0.02, respectively). Arterial blood pressure increased from rest during handgrip exercise and remained elevated during PEI in both groups, however, these responses were attenuated in women. CONCLUSIONS: These findings allow us to suggest a sex-related difference in spontaneous cBRS elicited by isolated muscle metaboreflex activation in healthy humans.
Assuntos
Barorreflexo , Pressão Sanguínea , Frequência Cardíaca , Isquemia Miocárdica/fisiopatologia , Condicionamento Físico Humano/fisiologia , Adulto , Feminino , Força da Mão , Humanos , Contração Isométrica , Masculino , Isquemia Miocárdica/etiologia , Condicionamento Físico Humano/efeitos adversos , Fatores SexuaisRESUMO
Patients with Parkinson's disease (PD) exhibit attenuated cardiovascular responses to exercise. The underlying mechanisms that are potentially contributing to these impairments are not fully understood. Therefore, we sought to test the hypothesis that patients with PD exhibit blunted cardiovascular responses to isolated muscle metaboreflex activation following exercise. For this, mean blood pressure, cardiac output, and total peripheral resistance were measured using finger photoplethysmography and the Modelflow method in 11 patients with PD [66 ± 2 yr; Hoehn and Yahr score: 2 ± 1 a.u.; time since diagnosis: 7 ± 1 yr; means ± SD) and 9 age-matched controls (66 ± 3 yr). Measurements were obtained at rest, during isometric handgrip exercise performed at 40% maximal voluntary contraction, and during postexercise ischemia. Also, a cold pressor test was assessed to confirm that blunted cardiovascular responses were specific to exercise and not representative of generalized sympathetic responsiveness. Changes in mean blood pressure were attenuated in patients with PD during handgrip (PD: ∆25 ± 2 mmHg vs. controls: ∆31 ± 3 mmHg; P < 0.05), and these group differences remained during postexercise ischemia (∆17 ± 1 mmHg vs. ∆26 ± 1 mmHg, respectively; P < 0.01). Additionally, changes in total peripheral resistance were attenuated during exercise and postexercise ischemia, indicating blunted reflex vasoconstriction in patients with PD. Responses to cold pressor test did not differ between groups, suggesting no group differences in generalized sympathetic responsiveness. Our results support the concept that attenuated cardiovascular responses to exercise observed in patients with PD are, at least in part, explained by an altered skeletal muscle metaboreflex. NEW & NOTEWORTHY Patients with Parkinson's disease (PD) presented blunted cardiovascular responses to exercise. We showed that cardiovascular response evoked by the metabolic component of the exercise pressor reflex is blunted in patients with PD. Furthermore, patients with PD presented similar pressor response during the cold pressor test compared with age-matched controls. Altogether, our results support the hypothesis that attenuated cardiovascular responses to exercise observed in patients with PD are mediate by an altered skeletal muscle metaboreflex.
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Pressão Sanguínea , Exercício Físico , Músculo Esquelético/fisiologia , Doença de Parkinson/fisiopatologia , Reflexo , Idoso , Débito Cardíaco , Força da Mão , Humanos , Masculino , Pessoa de Meia-Idade , Músculo Esquelético/fisiopatologia , VasoconstriçãoRESUMO
The exercise pressor reflex (EPR) is comprised of group III and IV skeletal muscle afferents and is one of the principal mediators of the cardiovascular response to exercise. In animals, capsaicin-based analgesic balm (CAP) attenuates the pressor response to muscle contraction, indicating the transient receptor potential vanilloid 1 (TRPv1) receptor (localized on the group IV afferent neuron) as an important mediator of the EPR. However, whether these findings can be extrapolated to humans remains unknown. Here, we tested the hypothesis that CAP would attenuate blood pressure (BP) and muscle sympathetic nerve activity (MSNA) responses to isolated muscle metaboreflex activation in healthy men. MSNA (microneurography) and beat-to-beat heart hate (HR, by electrocardiography), and BP (finger photoplethysmography) were continuously measured in eight healthy males (23 ± 5 yr) at rest, during isometric handgrip exercise, and during postexercise ischemia (PEI). Trials were performed before and 30 and 60 min after the topical application of CAP (0.1%, CAPZASIN-HP) over the volar forearm of the subject's exercising arm. Isometric exercise evoked increases in mean BP (∆32 ± 4 mmHg) and MSNA (∆26 ± 5 bursts/min; ∆19 ± 5 bursts/100 heart beats). The increases in BP during handgrip were not affected by CAP, but the increase in MSNA was lower after 60 min of CAP application. During PEI, the increases in BP and MSNA were all significantly less than those before CAP (all P < 0.05). In conclusion, CAP attenuated BP and sympathetic responses evoked by PEI in humans. These data provide evidence that transient receptor potential vanilloid 1 receptors potentially contribute to the EPR in humans, via its metabolic component. NEW & NOTEWORTHY We found that topical application of capsaicin-based analgesic balm attenuates arterial blood pressure and muscle sympathetic nerve activity during isolated muscle metaboreflex activation following isometric handgrip exercise in healthy humans. These findings suggest that the transient receptor potential vanilloid 1 may contribute to the exercise pressor reflex in humans via its metabolic component.
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Analgésicos/farmacologia , Capsaicina/farmacologia , Músculo Esquelético/efeitos dos fármacos , Reflexo/efeitos dos fármacos , Adulto , Pressão Sanguínea/efeitos dos fármacos , Sistema Cardiovascular/efeitos dos fármacos , Exercício Físico/fisiologia , Antebraço/fisiologia , Força da Mão/fisiologia , Voluntários Saudáveis , Frequência Cardíaca/efeitos dos fármacos , Humanos , Isquemia/tratamento farmacológico , Masculino , Contração Muscular/efeitos dos fármacos , Sistema Nervoso Simpático/efeitos dos fármacos , Adulto JovemAssuntos
Pressão Arterial , Barorreflexo , Artérias , Exercício Físico , Frequência Cardíaca , HumanosRESUMO
Isolated muscle metaboreflex activation with posthandgrip exercise ischemia (PEI) increases sympathetic nerve activity and partially maintains the exercise-induced increase in blood pressure, but a smaller heart rate (HR) response occurs. The cardiopulmonary baroreceptors, mechanically sensitive receptors that respond to changes in central blood volume and pressure, are strongly associated with changes in body position and upon activation elicit reflex sympathoinhibition. Here, we tested the hypothesis that postural changes modulate the sympathetically mediated cardiac response to PEI in humans. Beat-to-beat HR (electrocardiography) and blood pressure (finger photoplethysmography) were continuously measured, and cardiac function was assessed by echocardiography in 13 healthy men (21 ± 3 yr). After a 15-min rest period, 90-s static handgrip at 40% maximum voluntary contraction was performed followed by 3 min of PEI. Four trials were randomly conducted during either seated or supine position with and without ß1-adrenergic blockade (25 mg atenolol). During PEI under control conditions, HR remained elevated from baseline in the seated [change (Δ): 4 ± 1 beats/min] but not in the supine (change: -1 ± 1 beats/min) position. Similarly, stroke volume and cardiac output were increased from baseline in the seated (∆13.0 ± 2.4 ml and ∆1.1 ± 0.2 l/min, respectively) but not in the supine (∆2.5 ± 2.9 ml and ∆0.13 ± 0.20 l/min, respectively) position. During ß1-adrenergic blockade, HR, stroke volume, and cardiac output remained unchanged in both conditions. We conclude that sympathetically mediated cardiac responses to PEI are influenced by changes in body position. These findings indicated that muscle metaboreflex and cardiopulmonary baroreflex have an interactive influence on the neural control of cardiovascular function in humans. NEW & NOTEWORTHY In the present study, we demonstrated that muscle metaboreflex activation increases heart rate, stroke volume, and cardiac output in the seated position but not in the supine position and not after ß1-adrenergic blockade. These findings indicate that sympathetically mediated cardiac responses to isolated muscle metaboreflex activation after exercise are modulated by central blood volume mobilization.
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Barorreflexo , Células Quimiorreceptoras/metabolismo , Metabolismo Energético , Exercício Físico , Coração/inervação , Hemodinâmica , Contração Muscular , Músculo Esquelético/inervação , Postura , Sistema Nervoso Simpático/fisiopatologia , Antagonistas de Receptores Adrenérgicos beta 1/administração & dosagem , Pressão Arterial , Atenolol/administração & dosagem , Barorreflexo/efeitos dos fármacos , Débito Cardíaco , Força da Mão , Frequência Cardíaca , Hemodinâmica/efeitos dos fármacos , Humanos , Masculino , Músculo Esquelético/metabolismo , Pressorreceptores/metabolismo , Pressorreceptores/fisiopatologia , Distribuição Aleatória , Postura Sentada , Decúbito Dorsal , Sistema Nervoso Simpático/efeitos dos fármacos , Fatores de Tempo , Adulto JovemRESUMO
KEY POINTS: Recent evidence indicates that metaboreflex regulates heart rate recovery after exercise (HRR). An increased metaboreflex activity during the post-exercise period might help to explain the reduced HRR observed in hypertensive subjects. Using lower limb circulatory occlusion, the present study showed that metaboreflex activation during the post-exercise period delayed HRR in never-treated hypertensive men compared to normotensives. These findings may be relevant for understanding the physiological mechanisms associated with autonomic dysfunction in hypertensive men. ABSTRACT: Muscle metaboreflex influences heart rate (HR) regulation after aerobic exercise. Therefore, increased metaboreflex sensitivity may help to explain the delayed HR recovery (HRR) reported in hypertension. The present study assessed and compared the effect of metaboreflex activation after exercise on HRR, cardiac baroreflex sensitivity (cBRS) and heart rate variability (HRV) in normotensive (NT) and hypertensive (HT) men. Twenty-three never-treated HT and 25 NT men randomly underwent two-cycle ergometer exercise sessions (30 min, 70% VÌO2 peak ) followed by 5 min of inactive recovery performed with (occlusion) or without (control) leg circulatory occlusion (bilateral thigh cuffs inflated to a suprasystolic pressure). HRR was assessed via HR reduction after 30, 60 and 300 s of recovery (HRR30s, HRR60s and HRR300s), as well as by the analysis of short- and long-term time constants of HRR. cBRS was assessed by sequence technique and HRV by the root mean square residual and the root mean square of successive differences between adjacent RR intervals on subsequent 30 s segments. Data were analysed using two- and three-way ANOVA. HRR60s and cBRS were significant and similarly reduced in both groups in the occlusion compared to the control session (combined values: 20 ± 10 vs. 26 ± 9 beats min-1 and 2.1 ± 1.2 vs. 3.2 ± 2.4 ms mmHg-1 , respectively, P < 0.05). HRR300s and HRV were also reduced in the occlusion session, although these reductions were significantly greater in HT compared to NT (-16 ± 11 vs. -8 ± 15 beats min-1 for HRR300s, P < 0.05). The results support the role of metaboreflex in HRR and suggest that increased metaboreflex sensitivity may partially explain the delayed HRR observed in HT men.