Gender differences in parasympathetic reactivation during recovery from Wingate anaerobic test

Background and Purpose: We wanted to investigate gender differences in parasympathetic reactivation from supramaximal exercise. Materials and methods: Parasympathetic reactivation from a Wingate anaerobic test was investigated in 16 male and 15 female volunteers. Heart rate recovery was assessed as the difference between peak exercise heart rate and heart rate recorded following 60 seconds of recovery (HRR60 ). The time constant of the first 30 s post-exercise HR (T30) was determined as a negative reciprocal of the slope of the regression line. Another time constant decay (T) was obtained by fitting the 5 minute post-exercise HRR into a first-order exponential curve. Measures of heart rate variability (HRV) were used to describe the changes in autonomic cardiac regulation following exercise. Results: Post exercise heart rate recovery was faster in male participants, demonstrated through HRR60 (29.5±8.9 vs. 23.4±9.8 seconds respectively) and T30 (292.4±88.7 vs. 409.2±138.3 seconds respectively), but the time constant of the exponential heart rate decay (T) did not differ between the two genders (140.4±55.7 in males and 130.3±49.7seconds in females). The present study demonstrated similar RMSSD, lnHF and HFnu at rest in male and female participants. The time course of RMSSD30 recovery was impaired immediately after exercise. None of the observed vagal HRV indices have restored after five minutes of recovery following the 30-s Wingate test, but the post-exercise lnHF2-5min was significantly smaller in females (3.3±0.9 ms 2 in males vs. 2.5±1.0 ms 2 in females). Conclusion: The immediate HRR and parasympathetic reactivation was affected by gender and was attenuated in female participants

Ventilation inhibits sympathetic action potential recruitment even during severe chemoreflex stress

© 2017 the American Physiological Society. This study investigated the influence of ventilation on sympathetic action potential (AP) discharge patterns during varying levels of high chemoreflex stress. In seven trained breath-hold divers (age 33 ± 12 yr), we measured muscle sympathetic nerve activity (MSNA) at baseline, during preparatory rebreathing (RBR), and during 1) functional residual capacity apnea (FRCApnea) and 2) continued RBR. Data from RBR were analyzed at matched (i.e., to FRCApnea) hemoglobin saturation (HbSat) levels (RBRMatched) or more severe levels (RBREnd). A third protocol compared alternating periods (30 s) of FRC and RBR (FRC-RBRALT). Subjects continued each protocol until 85% volitional tolerance. AP patterns in MSNA (i.e., providing the true neural content of each sympathetic burst) were studied using wavelet-based methodology. First, for similar levels of chemoreflex stress (both HbSat: 71 ± 6%; P = NS), RBRMatched was associated with reduced AP frequency and APs per burst compared with FRCApnea (both P _ 0.001). When APs were binned according to peak-to-peak amplitude (i.e., into clusters), total AP clusters increased during FRCApnea (+10 ± 2; P \u3c 0.001) but not during RBRMatched (+1 ± 2; P = NS). Second, despite more severe chemoreflex stress during RBREnd (Hb-Sat: 56 ± 13 vs. 71 ± 6%; P = 0.001), RBREnd was associated with a restrained increase in the APs per burst (FRCApnea: +18 ± 7; RBREnd: +11 ± 5) and total AP clusters (FRCApnea: +10 ± 2; RBREnd: +6 ± 4) (both P \u3c 0.01). During FRC-RBRALT, all periods of FRC elicited sympathetic AP recruitment (all P \u3c 0.001), whereas all periods of RBR were associated with complete withdrawal of AP recruitment (all P = NS). Presently, we demonstrate that ventilation per se restrains and/or inhibits sympathetic axonal recruitment during high, and even extreme, chemoreflex stress. NEW & NOTEWORTHY The current study demonstrates that the sympathetic neural recruitment patterns observed during chemoreflex activation induced by rebreathing or apnea are restrained and/or inhibited by the act of ventilation per se, despite similar, or even greater, levels of severe chemoreflex stress. Therefore, ventilation modulates not only the timing of sympathetic bursts but also the within-burst axonal recruitment normally observed during progressive chemoreflex stress

Impaired dynamic cerebral autoregulation in trained breath-hold divers

Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breathhold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11 ± 9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-tostand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (δCVRi/δT)/δBP]. The BHD demonstrated slower RoR than controls (P ≤ 0.001, d = 1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls (P = 0.004, d = 1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls (P = 0.01, d = 0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia

Severe hypoxaemic hypercapnia compounds cerebral oxidative-nitrosative stress during extreme apnoea: implications for cerebral bioenergetic function

We examined to what extent apnoea-induced extremes of oxygen demand/carbon dioxide production impact redox-regulation of cerebral bioenergetic function. Ten ultra-elite apnoeists (6 men, 4 women) performed two maximal dry apnoeas preceded by, [1] normoxic normoventilation resulting in severe end-apnoea hypoxaemic hypercapnia and [2] hyperoxic hyperventilation designed to ablate hypoxaemia resulting in hyperoxaemic hypercapnia. Transcerebral exchange of ascorbate radicals (A·-, electron paramagnetic resonance spectroscopy) and nitric oxide metabolites (NO, tri-iodide chemiluminescence) were calculated as the product of global cerebral blood flow (gCBF, duplex ultrasound) and radial arterial (a) to internal jugular venous (v) concentration gradients. Apnoea duration increased from 306 ± 62 s during hypoxaemic hypercapnia to 959 ± 201 s in hyperoxaemic hypercapnia (P = <0.001). Apnoea generally increased gCBF (all P = <0.001) but was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose (P = 0.015 to 0.044). This was associated with a general net cerebral output (v>a) of A·- that was greater in hypoxaemic hypercapnia (P = 0.046 vs. hyperoxaemic hypercapnia) and coincided with a selective suppression in plasma nitrite (〖"NO" 〗_"2" ^"-" ) uptake (a>v) and gCBF (P = 0.034 to <0.001 vs. hyperoxaemic hypercapnia), implying reduced consumption and delivery of NO consistent with elevated cerebral oxidative-nitrosative stress (OXNOS). In contrast, we failed to observe equidirectional gradients consistent with S-nitrosohaemoglobin consumption and plasma S-nitrosothiol delivery during apnoea (all P = >0.05). Collectively, these findings highlight a key catalytic role for hypoxaemic hypercapnia in cerebral OXNOS

HEART RATE RECOVERY AFTER SUBMAXIMAL EXERCISE IN FOUR DIFFERENT RECOVERY PROTOCOLS IN MALE ATHLETES AND NON-ATHLETES

The effects of different recovery protocols on heart rate recovery (HRR) trend through fitted heart rate (HR) decay curves were assessed. Twenty one trained male athletes and 19 sedentary male students performed a submaximal cycle exercise test on four occasions followed by 5 min: 1) inactive recovery in the upright seated position, 2) active (cycling) recovery in the upright seated position, 3) supine position, and 4) supine position with elevated legs. The HRR was assessed as the difference between the peak exercise HR and the HR recorded following 60 seconds of recovery (HRR60). Additionally the time constant decay was obtained by fitting the 5 minute post-exercise HRR into a first-order exponential curve. Within- subject differences of HRR60 for all recovery protocols in both groups were significant (p < 0. 001) except for the two supine positions (p > 0.05). Values of HRR60 were larger in the group of athletes for all conditions (p < 0.001). The time constant of HR decay showed within-subject differences for all recovery conditions in both groups (p < 0.01) except for the two supine positions (p > 0.05). Between group difference was found for active recovery in the seated position and the supine position with elevated legs (p < 0.05). We conclude that the supine position with or without elevated legs accelerated HRR compared with the two seated positions. Active recovery in the seated upright position was associated with slower HRR compared with inactive recovery in the same position. The HRR in athletes was accelerated in the supine position with elevated legs and with active recovery in the seated position compared with non-athlete

Highs and lows of hyperoxia : physiological, performance, and clinical aspects

Molecular oxygen (O2) is a vital element in human survival and plays a major role in a diverse range of biological and physiological processes. Although normobaric hyperoxia can increase arterial oxygen content CaO2, it also causes vasoconstriction and hence reduces O2 delivery in various vascular beds including the heart, skeletal muscle, and brain. Thus, a seemingly paradoxical situation exists in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Nevertheless, with various degrees of effectiveness, and not without consequences, supplemental oxygen is used clinically in an attempt to correct tissue hypoxia (e.g. brain ischemia, traumatic brain injury, carbon monoxide poisoning, etc.), chronic hypoxemia (e.g. severe COPD, etc.), and to help with wound healing, necrosis, or reperfusion injuries (e.g. compromised grafts). Hyperoxia has also been used liberally by athletes in a belief that it offers performance enhancing benefits; such benefits also extend to hypoxemic patients both at rest and during rehabilitation. This review aims to provide a comprehensive overview of the effects of hyperoxia in humans from the ‘bench-to-bedside’. The first section will focus on the basic physiological principles of partial pressure of arterial O2, CaO2, barometric pressure and how these changes lead to variation in regional O2 delivery. The next section provides an overview of the evidence for and against the use of hyperoxia as an aid to enhance physical performance. The final section addresses pathophysiological concepts, clinical studies, and implications for therapy. The potential of O2 toxicity and future research directions are also considered

HEART RATE VARIABILITY BEFORE AND AFTER CYCLE EXERCISE IN RELATION TO DIFFERENT BODY POSITIONS

The purpose of this study was to assess the effect of three different body positions on HRV measures following short-term submaximal exercise. Thirty young healthy males performed submaximal cycling for five minutes on three different occasions. Measures of HRV were obtained from 5-min R to R wave intervals before the exercise (baseline) and during the last five minutes of a 15 min recovery (post-exercise) in three different body positions (seated, supine, supine with elevated legs). Measures of the mean RR normal-to-normal intervals (RRNN), the standard deviation of normal-to-normal intervals (SDNN), the root mean square of successive differences (RMSSD) and the low-frequency (LF) and the high-frequency (HF) spectral power were analyzed. Post-exercise RRNN, RMSSD were significantly higher in the two supine positions (p < 0. 01) compared with seated body position. Post-exercise ln LF was significantly lower in the supine position with elevated legs than in the seated body position (p < 0.05). No significant difference was found among the three different body positions for post-exercise ln HF (p > 0.05). Post-exercise time domain measures of HRV (RRNN, SDNN, RMSSD) were significantly lower compared with baseline values (p < 0.01) regardless body position. Post-exercise ln LF and ln HF in all three positions remained significantly reduced during recovery compared to baseline values (p < 0.01). The present study suggests that 15 minutes following short-term submaximal exercise most of the time and frequency domain HRV measures have not returned to pre-exercise values. Modifications in autonomic cardiac regulation induced by body posture present at rest remained after exercise, but the post-exercise differences among the three positions did not resemble the ones established at res