Respiratory, cardiovascular and musculoskeletal mechanisms involved in the pathophysiology of pulmonary hypertension: An updated systematic review of preclinical and clinical studies.

BACKGROUND: Progressive exercise intolerance is a hallmark of pulmonary hypertension (pH), severely impacting patients' independence and quality of life (QoL). Accumulating evidence over the last decade shows that combined abnormalities in peripheral reflexes and target organs contribute to disease progression and exercise intolerance. OBJECTIVE: The aim of this study was to review the literature of the last decade on the contribution of the cardiovascular, respiratory, and musculoskeletal systems to pathophysiology and exercise intolerance in pH. METHODS: A systematic literature search was conducted using specific terms in PubMed, SciELO, and the Cochrane Library databases for original pre-clinical or clinical studies published between 2013 and 2023. Studies followed randomized controlled/non-randomized controlled and pre-post designs. RESULTS: The systematic review identified 25 articles reporting functional or structural changes in the respiratory, cardiovascular, and musculoskeletal systems in pH. Moreover, altered biomarkers in these systems, lower cardiac baroreflex, and heightened peripheral chemoreflex activity seemed to contribute to functional changes associated with poor prognosis and exercise intolerance in pH. Potential therapeutic strategies acutely explored involved manipulating the baroreflex and peripheral chemoreflex, improving cardiovascular autonomic control via cardiac vagal control, and targeting specific pathways such as GPER1, GDF-15, miR-126, and the JMJD1C gene. CONCLUSION: Information published in the last 10 years advances the notion that pH pathophysiology involves functional and structural changes in the respiratory, cardiovascular, and musculoskeletal systems and their integration with peripheral reflexes. These findings suggest potential therapeutic targets, yet unexplored in clinical trials, that could assist in improving exercise tolerance and QoL in patients with pH.

Impact of an active lifestyle on cardiovascular autonomic modulation and oxidative stress in males with overweight and parental history of hypertension.

Family history of hypertension is associated with early autonomic dysfunction and increased oxidative stress. These alterations have been found to be reinforced by the overweight factor. Conversely, an active lifestyle is effective in improving the mechanisms regulating blood pressure control. Hence, we ought to investigate the effects of an active lifestyle on the hemodynamic, autonomic and oxidative stress parameters in individuals carrying both family history of hypertension and overweight risk factors. Fifty-six normotensive males were divided into four groups: eutrophic offspring of normotensive parents (EN, n = 12), eutrophic and inactive with hypertensive parents (EH, n = 14), overweight and inactive with hypertensive parents (OH, n = 13), and overweight and physically active with hypertensive parents (OAH, n = 17). Cardiovascular autonomic modulation was assessed by heart rate (HRV) and blood pressure (BPV) variability indexes. Oxidative stress included pro/antioxidant markers and nitrite concentration. Inactive offspring of hypertensive parents (EH and OH) showed higher LFSBP (vs EN), an indicator of sympathetic outflow to the vasculature and reduced anti-oxidant activity (vs EN), while higher pro-oxidant markers were found exclusively in OH (vs EN and EH). Conversely, the OAH group showed bradycardia, higher vagally-mediated HFabs index (vs OH and EN), lower sympathovagal balance (vs OH) and preserved LFSBP. Yet, the OAH showed preserved pro/antioxidant markers and nitrite levels. Our findings indicates that overweight offspring of hypertensive parents with an active lifestyle have improved hemodynamic, cardiac autonomic modulation and oxidative stress parameters compared to their inactive peers.

Cardiac baroreflex dysfunction in patients with pulmonary arterial hypertension at rest and during orthostatic stress: role of the peripheral chemoreflex.

The baroreflex integrity in early-stage pulmonary arterial hypertension (PAH) remains uninvestigated. A potential baroreflex impairment could be functionally relevant and possibly mediated by enhanced peripheral chemoreflex activity. Thus, we investigated 1) the cardiac baroreflex in nonhypoxemic PAH; 2) the association between baroreflex indexes and peak aerobic capacity [i.e., peak oxygen consumption (V̇o2peak)]; and 3) the peripheral chemoreflex contribution to the cardiac baroreflex. Nineteen patients and 13 age- and sex-matched healthy adults (HA) randomly inhaled either 100% O2 (peripheral chemoreceptor inhibition) or 21% O2 (control session) while at rest and during a repeated sit-to-stand maneuver. Beat-by-beat analysis of R-R intervals and systolic blood pressure provided indexes of cardiac baroreflex sensitivity (cBRS) and effectiveness (cBEI). The PAH group had lower cBEI for all sequences (cBEIALL) at rest [means ± SD: PAH = 0.5 ± 0.2 vs. HA = 0.7 ± 0.1 arbitrary units (a.u.), P = 0.02] and lower cBRSALL (PAH = 6.8 ± 7.0 vs. HA = 9.7 ± 5.0 ms·mmHg-1, P < 0.01) and cBEIALL (PAH = 0.4 ± 0.2 vs. HA= 0.6 ± 0.1 a.u., P < 0.01) during the sit-to-stand maneuver versus the HA group. The cBEI during the sit-to-stand maneuver was independently correlated to V̇o2peak (partial r = 0.45, P < 0.01). Hyperoxia increased cBRS and cBEI similarly in both groups at rest and during the sit-to-stand maneuver. Therefore, cardiac baroreflex dysfunction was observed under spontaneous and, most notably, provoked blood pressure fluctuations in nonhypoxemic PAH, was not influenced by the peripheral chemoreflex, and was associated with lower V̇o2peak, suggesting that it could be functionally relevant.NEW & NOTEWORTHY Does the peripheral chemoreflex play a role in cardiac baroreflex dysfunction in patients with pulmonary arterial hypertension (PAH)? Here we provide new evidence of cardiac baroreflex dysfunction under spontaneous and, most notably, provoked blood pressure fluctuations in patients with nonhypoxemic PAH. Importantly, impaired cardiac baroreflex effectiveness during provoked blood pressure fluctuations was independently associated with poorer functional capacity. Finally, our results indicated that the peripheral chemoreflex did not mediate cardiac baroreflex dysfunction among those patients.

The cardiovascular consequences of fatiguing expiratory muscle work in otherwise resting healthy humans.

In 11 healthy adults (25 ± 4 yr; 2 female, 9 male subjects), we investigated the effect of expiratory resistive loaded breathing [65% maximal expiratory mouth pressure (MEP), 15 breaths·min-1, duty cycle 0.5; ERLPm] on mean arterial pressure (MAP), leg vascular resistance (LVR), and leg blood flow ([Formula: see text]). On a separate day, a subset of five male subjects performed ERL targeting 65% of maximal expiratory gastric pressure (ERLPga). ERL-induced expiratory muscle fatigue was confirmed by a 17 ± 5% reduction in MEP (P < 0.05) and a 16 ± 12% reduction in the gastric twitch pressure response to magnetic nerve stimulation (P = 0.09) from before to after ERLPm and ERLPga, respectively. From rest to task failure in ERLPm and ERLPga, MAP increased (ERLPm = 31 ± 10 mmHg, ERLPga = 18 ± 9 mmHg, both P < 0.05), but group mean LVR and [Formula: see text] were unchanged (ERLPm: LVR = 0.78 ± 0.21 vs. 0.97 ± 0.36 mmHg·mL-1·min, [Formula: see text] = 133 ± 34 vs. 152 ± 74 mL·min-1; ERLPga: LVR = 0.70 ± 0.21 vs. 0.84 ± 0.33 mmHg·mL-1·min, [Formula: see text] = 160 ± 48 vs. 179 ± 110 mL·min-1) (all P ≥ 0.05). Interestingly, [Formula: see text] during ERLPga oscillated within each breath, increasing (∼66%) and decreasing (∼50%) relative to resting values during resisted expirations and unresisted inspirations, respectively. In conclusion, fatiguing expiratory muscle work did not affect group mean LVR or [Formula: see text] in otherwise resting humans. We speculate that any sympathetically mediated peripheral vasoconstriction was counteracted by transient mechanical effects of high intra-abdominal pressures during ERL.NEW & NOTEWORTHY Fatiguing expiratory muscle work in otherwise resting humans elicits an increase in sympathetic motor outflow; whether limb blood flow ([Formula: see text]) and leg vascular resistance (LVR) are affected remains unknown. We found that fatiguing expiratory resistive loaded breathing (ERL) did not affect group mean [Formula: see text] or LVR. However, within-breath oscillations in [Formula: see text] may reflect a sympathetically mediated vasoconstriction that was counteracted by transient increases in [Formula: see text] due to the mechanical effects of high intra-abdominal pressure during ERL.

Uncovering the mechanisms of exertional dyspnoea in combined pulmonary fibrosis and emphysema.

The prevailing view is that exertional dyspnoea in patients with combined idiopathic pulmonary fibrosis (IPF) and emphysema (CPFE) can be largely explained by severe hypoxaemia. However, there is little evidence to support these assumptions.We prospectively contrasted the sensory and physiological responses to exercise in 42 CPFE and 16 IPF patients matched by the severity of exertional hypoxaemia. Emphysema and pulmonary fibrosis were quantified using computed tomography. Inspiratory constraints were assessed in a constant work rate test: capillary blood gases were obtained in a subset of patients.CPFE patients had lower exercise capacity despite less extensive fibrosis compared to IPF (p=0.004 and 0.02, respectively). Exertional dyspnoea was the key limiting symptom in 24 CPFE patients who showed significantly lower transfer factor, arterial carbon dioxide tension and ventilatory efficiency (higher minute ventilation (V'E)/carbon dioxide output (V'CO2 ) ratio) compared to those with less dyspnoea. However, there were no between-group differences in the likelihood of pulmonary hypertension by echocardiography (p=0.44). High dead space/tidal volume ratio, low capillary carbon dioxide tension emphysema severity (including admixed emphysema) and traction bronchiectasis were related to a high V'E/V'CO2 ratio in the more dyspnoeic group. V'E/V'CO2 nadir >50 (OR 9.43, 95% CI 5.28-13.6; p=0.0001) and total emphysema extent >15% (2.25, 1.28-3.54; p=0.01) predicted a high dyspnoea burden associated with severely reduced exercise capacity in CPFEContrary to current understanding, hypoxaemia per se is not the main determinant of exertional dyspnoea in CPFE. Poor ventilatory efficiency due to increased "wasted" ventilation in emphysematous areas and hyperventilation holds a key mechanistic role that deserves therapeutic attention.

Carotid chemoreflex activity restrains post-exercise cardiac autonomic control in healthy humans and in patients with pulmonary arterial hypertension.

KEY POINTS: Dysfunction of post-exercise cardiac autonomic control is associated with increased mortality risk in healthy adults and in patients with cardiorespiratory diseases. The afferent mechanisms that regulate the post-exercise cardiac autonomic control remain unclear. We found that afferent signals from carotid chemoreceptors restrain the post-exercise cardiac autonomic control in healthy adults and patients with pulmonary arterial hypertension (PAH). Patients with PAH had higher carotid chemoreflex sensitivity, and the magnitude of carotid chemoreceptor restraint of autonomic control was greater in patients with PAH as compared to healthy adults. The results demonstrate that the carotid chemoreceptors contribute to the regulation of post-exercise cardiac autonomic control, and suggest that the carotid chemoreceptors may be a potential target to treat post-exercise cardiac autonomic dysfunction in patients with PAH. ABSTRACT: Dysfunction of post-exercise cardiac autonomic control predicts mortality, but its underlying mechanisms remain unclear. We tested whether carotid chemoreflex activity restrains post-exercise cardiac autonomic control in healthy adults (HA), and whether such restraint is greater in patients with pulmonary arterial hypertension (PAH) who may have both altered carotid chemoreflex and altered post-exercise cardiac autonomic control. Twenty non-hypoxaemic patients with PAH and 13 age- and sex-matched HA pedalled until 90% of peak work rate observed in a symptom-limited ramp-incremental exercise test. Recovery consisted of unloaded pedalling for 5 min followed by seated rest for 6 min. During recovery, subjects randomly inhaled either 100% O2 (hyperoxia) to inhibit the carotid chemoreceptor activity, or 21% O2 (normoxia) as control. Post-exercise cardiac autonomic control was examined via heart rate (HR) recovery (HRR; HR change after 30, 60, 120 and 300 s of recovery, using linear and non-linear regressions of HR decay) and HR variability (HRV; time and spectral domain analyses). As expected, the PAH group had higher carotid chemosensitivity and worse post-exercise HRR and HRV than HA. Hyperoxia increased HRR at 30, 60 and 120 s and absolute spectral power HRV in both groups. Additionally, hyperoxia resulted in an accelerated linear HR decay and increased time domain HRV during active recovery only in the PAH group. In conclusion, the carotid chemoreceptors restrained recovery of cardiac autonomic control from exercise in HA and in patients with PAH, with the restraint greater for some autonomic indexes in patients with PAH.

Ischemic preconditioning boosts post-exercise but not resting cardiac vagal control in endurance runners.

PURPOSE: High cardiac vagal control in endurance athletes has been generally associated with adequate recovery from training and readiness to cope high-intensity training. A method that improves cardiac vagal control in endurance athletes could therefore be advantageous. Accordingly, we sought to test whether ischemic preconditioning (IPC) could enhance cardiac vagal control in endurance runners. METHODS: Fifteen subjects underwent IPC, sham ultrasound (SHAM) or control (CT), in random order. Subjects were informed both IPC and SHAM would be beneficial vs. CT (i.e., similar placebo induction), and IPC would be harmless despite ischemia sensations (i.e., nocebo avoidance). Resting cardiac vagal control was assessed via respiratory sinus arrhythmia (RSA) and heart rate variability (HRV) indexes. Post-exercise cardiac vagal control was assessed via heart rate recovery [HR time constant decay (T30) and absolute HR decay (HRR30s)] during 30-s breaks of a discontinuous incremental test. Capillary blood samples were collected for lactate threshold identification. RESULTS: RSA and HRV were similar among interventions at pre- and post-intervention assessments. Lactate threshold occurred at 85 ± 4% of maximal effort. T30 was similar among interventions, but IPC increased HRR30s at 70% and 75% of maximal effort vs. SHAM and CT (70%: IPC = 31 ± 2 vs. SHAM = 26 ± 3 vs. CT = 26 ± 2 bpm, mean ± SEM, P < 0.01; 75%: IPC = 29 ± 2 vs. SHAM = 25 ± 2 vs. CT = 24 ± 2 bpm, P < 0.01). CONCLUSION: IPC did not change resting cardiac vagal control, but boosted fast post-exercise cardiac vagal reactivation at exercise intensities below lactate threshold in endurance runners.

Hyperadditive ventilatory response arising from interaction between the carotid chemoreflex and the muscle mechanoreflex in healthy humans.

Physical exercise potentiates the carotid chemoreflex control of ventilation (VE). Hyperadditive neural interactions may partially mediate the potentiation. However, some neural interactions remain incompletely explored. As the potentiation occurs even during low-intensity exercise, we tested the hypothesis that the carotid chemoreflex and the muscle mechanoreflex could interact in a hyperadditive fashion. Fourteen young healthy subjects inhaled randomly, in separate visits, 12% O2 to stimulate the carotid chemoreflex and 21% O2 as control. A rebreathing circuit maintained isocapnia. During gases administration, subjects either remained at rest (i.e., normoxic and hypoxic rest) or the muscle mechanoreflex was stimulated via passive knee movement (i.e., normoxic and hypoxic movement). Surface muscle electrical activity did not increase during the passive movement, confirming the absence of active contractions. Hypoxic rest and normoxic movement similarly increased VE [change (mean ± SE) = 1.24 ± 0.72 vs. 0.73 ± 0.43 l/min, respectively; P = 0.46], but hypoxic rest only increased tidal volume (Vt), and normoxic movement only increased breathing frequency (BF). Hypoxic movement induced greater VE and mean inspiratory flow (Vt/Ti) increase than the sum of hypoxic rest and normoxic movement isolated responses (VE change: hypoxic movement = 3.72 ± 0.81 l/min vs. sum = 1.96 ± 0.83 l/min, P = 0.01; Vt/Ti change: hypoxic movement = 0.13 ± 0.03 l/s vs. sum = 0.06 ± 0.03 l/s, P = 0.02). Moreover, hypoxic movement increased both Vt and BF. Collectively, the results indicate that the carotid chemoreflex and the muscle mechanoreflex interacted, mediating a hyperadditive ventilatory response in healthy humans. NEW & NOTEWORTHY The main finding of this study was that concomitant carotid chemoreflex and muscle mechanoreflex stimulation provoked greater ventilation increase than the sum of ventilation increase induced by stimulation of each reflex in isolation, which, consequently, supports that the carotid chemoreflex and the muscle mechanoreflex interacted, mediating a hyperadditive ventilatory response in healthy humans.

Immediate and 24-h blood pressure-lowering effects of arm crank exercise in patients with traumatic lower-limb amputation: a randomized cross-over study.

AIM: This study aimed to investigate the clinic and 24-h postexercise hypotension (PEH) after a moderate-intensity arm crank exercise session in individuals with traumatic lower-limb amputation. PARTICIPANTS AND METHODS: Nine men (46±17 years) with unilateral traumatic lower-limb amputation participated in two experimental sessions conducted randomly: an aerobic exercise (EXE: arm crank ergometer, 30 min) or a control session (CON: participants remained seated on the cycle ergometer, 30 min). Clinic and 24-h systolic, diastolic, and mean blood pressure (BP) response were measured after both sessions. The clinical measurements of blood flow and forearm vascular resistance (FVR) were also performed. RESULTS: Compared with the preintervention period, the BP levels did not change in the CON session. However, EXE resulted in a significant hypotensive effect in systolic (-10±0.9 mmHg, P≤0.05), diastolic (-11±1.5 mmHg, P≤0.05), and mean BP (-11±1.2 mmHg, P≤0.05) during the entire postexercise period. The PEH was accompanied by a decreased FVR over the entire postintervention period (P≤0.05). Significant reductions were found for 24-h average systolic, diastolic, and mean BP levels (P=0.03, 0.01, and 0.02, respectively) following EXE compared with the CON session. CONCLUSION: These results showed, for the first time, that individuals with traumatic lower-limb amputation presented immediate and 24-h PEH after a single bout of arm crank exercise testing. The PEH at the clinic condition was justified, at least in part, by the reduction in peripheral FVR.

Methods of assessment of the post-exercise cardiac autonomic recovery: A methodological review.

The analysis of post-exercise cardiac autonomic recovery is a practical clinical tool for the assessment of cardiovascular health. A reduced heart rate recovery - an indicator of autonomic dysfunction - has been found in a broad range of cardiovascular diseases and has been associated with increased risks of both cardiac and all-cause mortality. For this reason, over the last several years, non-invasive methods for the assessment of cardiac autonomic recovery after exercise - either based on heart rate recovery or heart rate variability indices - have been proposed. However, for the proper implementation of such methods in daily clinical practice, the discussion of their clinical validity, physiologic meaning, mathematical formulation and reproducibility should be better addressed. Therefore, the aim of this methodological review is to present some of the most employed methods of post-exercise cardiac autonomic recovery in the literature and comprehensively discuss their strengths and weaknesses.

Increased peripheral vascular resistance in male patients with traumatic lower limb amputation: one piece of the cardiovascular risk puzzle.

AIM: The increased morbidity and mortality in traumatic lower limb amputees can be explained by the development of risk factors, among which high blood pressure plays an important role. However, the possible mechanisms underlying increased blood pressure levels observed in this population remain unclear. Thus, we aimed to test the hypothesis that peripheral vascular resistance is increased at rest in patients with traumatic lower limb amputation. PATIENTS AND METHODS: In a cross-sectional study, eight patients with traumatic unilateral lower limb amputation (amputee group) and eight healthy individuals without amputation (control group) were included. Resting blood pressure, heart rate, and forearm blood flow were recorded simultaneously and thus, forearm vascular resistance was calculated. RESULTS: The amputee group showed higher systolic (126±2 vs. 118±5 mmHg, P<0.01), diastolic (78±2 vs. 63±3 mmHg, P<0.01), mean blood pressure (94±2 vs. 81±3 mmHg, P<0.01), and heart rate (74±5 vs. 65±8 bpm, P=0.02) compared with the control group. Despite the similar forearm blood flow response between groups, patients with traumatic lower limb amputation presented increased peripheral vascular resistance at rest compared with the control group (31.3±3.8 vs. 25.7±6.5 U, P=0.05). CONCLUSION: Patients with traumatic amputation present increased peripheral vascular resistance. Our findings clarify one possible mechanism underlying the higher blood pressure levels observed in this population.

Water intake accelerates parasympathetic reactivation after high-intensity exercise.

UNLABELLED: It has been shown that water intake (WI) improves postexercise parasympathetic recovery after moderate-intensity exercise session. However, the potential cardiovascular benefit promoted by WI has not been investigated after high-intensity exercise. PURPOSE: To assess the effects of WI on post high-intensity parasympathetic recovery. METHODS: Twelve recreationally active young men participated in the study (22 ± 1.4 years, 24.1 ± 1.6 kg.m(-2)). The experimental protocol consisted of two visits to the laboratory. Each visit consisted in the completion of a 30-min high-intensity [~80% of maximal heart rate (HR)] cycle ergometer aerobic session performing randomly the WI or control (CON, no water consumption) intervention at the end of the exercise. HR and RR intervals (RRi) were continuously recorded by a heart rate monitor before, during and after the exercise. Differences in HR recovery [e.g., absolute heart rate decrement after 1 min of recovery (HRR60s) and time-constant of the first order exponential fitting curve of the HRR (HRRτ)] and in postexercise vagal-related heart rate variability (HRV) indexes (rMSSD30s, rMSSD, pNN50, SD1 and HF) were calculated and compared for WI and CON. RESULTS: A similar HR recovery and an increased postexercise HRV [SD1 = 9.4 ± 5.9 vs. 6.0 ± 3.9 millisecond, HF(ln) = 3.6 ± 1.4 vs. 2.4 ± 1.3 millisecond(2), for WI and CON, respectively; p < .05] was observed in WI compared with CON. CONCLUSION: The results suggest that WI accelerates the postexercise parasympathetic reactivation after high-intensity exercise. Such outcome reveals an important cardioprotective effect of WI.

Effect of water intake on postexercise cardiovascular recovery / Efeito da ingestao hidrica sobre a recuperacao cardiovascular pos-exercicio

Physical exercise elicits an increase in heart rate (HR), blood pressure (BP) and, consequently, in the rate-pressure product (RPP). Recovery of HR immediately after exercise indicates cardiovascular health. Blood pressure also decreases after exercise, occasionally reaching values lower than pre-exercise levels (postexercise hypotension). Studies have shown a positive effect of water intake on HR recovery after exercise. However, little is known about the effect of water intake on postexercise BP and RPP responses. The objective of this study was to evaluate the effects of water intake on postexercise cardiac work assessed by HR, BP and RPP. Fourteen healthy volunteers (22 ± 1.4 years) participated in the study. The experimental session consisted of HR, systolic (SBP) and diastolic BP (DBP) recording at rest, followed by submaximal exercise on a cycle ergometer. Next, the subjects consumed water and the cardiovascular variables were recorded during recovery. In addition, a control session without postexercise water intake was performed. The RPP was calculated from the product of HR and SBP. Water intake prevented a postexercise hypotensive effect on DBP, but accelerated postexercise HR and RPP reduction during recovery when compared to the control session. It was concluded that water intake is an effective strategy to reduce postexercise cardiac work.

O exercício físico promove a elevação da frequência cardíaca (FC), pressão arterial (PA) e, por consequência, do duplo produto (DP). Imediatamente após o término do exercício, há a recuperação da FC; resposta que indica boa saúde cardiovascular. A PA também apresenta queda pós-exercício, atingindo, eventualmente, valores abaixo do repouso (hipotensão pós-exercício; HPE). Estudos têm demonstrado efeito positivo da ingestão hídrica (IH) sobre a recuperação da FC pós-exercício. Pouco se sabe a respeito do efeito dessa estratégia sobre o comportamento da PA e do DP nesse período. O objetivo do estudo foi investigar o efeito da IH sobre o trabalho cardiovascular pós-exercício, por meio da avaliação da FC, PA e DP. Quatorze voluntários saudáveis (22 ± 1,4 anos) participaram desse estudo. A sessão experimental constou do registro da FC e PA sistólica (PAS) e diastólica (PAD) de repouso, seguido de exercício físico submáximo em cicloergômetro. Posteriormente, realizou-se a IH e registro das variáveis cardiovasculares na recuperação. Adicionalmente, realizou-se uma sessão controle, excluindo-se a IH pós-exercício. O DP foi calculado a partir do produto da FC pela PAS. A IH impediu a ocorrência de HPE na PAD, porém acelerou a redução da FC e do DP, no período da recuperação pós-exercício, quando comparada à sessão controle. Pode-se concluir que a IH é uma estratégia eficiente na redução do trabalho cardiovascular pós-exercício.

Post-exercise heart rate variability recovery: a time-frequency analysis.

OBJECTIVE: Most studies investigating the effects of non-pharmacological interventions, such as physical training (PT), on cardiac autonomic control, assessed the HRV only in resting conditions. Recently, a new time-frequency mathematical approach based on the short-time Fourier transform (STFT) method has been validated for the assessment of HRV in non-stationary conditions such as the immediate post-exercise period. The aim of this study was to evaluate the effects of the PT on post-exercise cardiac autonomic control using the time-frequency STFT analysis of the HRV. METHODS: Twenty-one healthy male volunteers participated in this study. The subjects were initially evaluated for their physical exercise/sport practice and allocated to groups of low physical training ((Low)PT, n = 13) or high physical training (H(igh)PT, n = 8). The post-exercise HRV was assessed by the STFT method, which provides the analysis of dynamic changes in the power of the low- and high-frequency spectral components (LF and HF, respectively) of the HRV during the whole recovery period. RESULTS: Greater LF (from the min 5 to 10) and HF (from the min 6 to 10) in the post-exercise period in the H(igh)PT compared to the (Low)PT group (P < 0.05) was observed. CONCLUSION: These results indicate that exercise training exerts beneficial effects on post-exercise cardiac autonomic control.