Search

R1908 --> 753.1 --> To date, more than 46 million people in the United States have contracted the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), which causes COVID‐19. Over 700 thousand total cases have been linked to American colleges and universities. Post‐acute sequelae of SARS‐CoV‐2 infection may affect varied systems. It was reported that sympathetic nerve activity following SARS‐CoV‐2 infection was elevated in young individuals. Cardiovascular autonomic function post‐acute SARS‐CoV‐2 infection in other populations such as athletes, however, has not been thoroughly investigated. Collegiate athletes are a unique population given that they might have a high level of physical fitness before the infection. The present study examined 16 collegiate athletes (12 men and 4 women, age: 20±1 yrs, height: 181±10 cm, weight: 81±18 kg) who were evaluated ~2 weeks after testing positive for SARS‐CoV‐2 by polymerase chain reaction assay. These subjects were asymptomatic or with mild/moderate symptoms during infection. None of the subjects had been hospitalized for COVID‐19 and all subjects were asymptomatic at the time of the study. Beat‐by‐beat blood pressure (BP) with Finometer, and heart rate (HR) from ECG were recorded during 10 minutes of supine rest, Valsalva maneuver, slow breathing (6 breaths/min), handgrip exercise, and 10 minutes of standing. BP, HR, heart rate variability (HRV), and cardiac baroreflex sensitivity (CBRS), and venous blood aldosterone and renin levels were analyzed. The vagal tone index from HRV in 3 of 16 athletes was lower than normative values. The responses in BP to Valsalva maneuver during phases IIa (i.e., "early") and IIb (i.e., "late") were mildly abnormal in 4 athletes and moderately abnormal in one athlete. The Valsalva ratio was below the normal range in 6 athletes. In response to slow breathing, the respiratory sinus arrhythmia amplitude was below the normal range in 3 athletes. In response to handgrip exercise, one athlete had an atypical response where BP decreased while HR was increased from baseline. Three of the subjects were unable to tolerate an orthostatic challenge for 10 minutes. Four out of 16 athletes had abnormally elevated renin activity and 1 out 16 elevated aldosterone levels. It is important to note that while several athletes had abnormal responses to the various autonomic tests, these abnormalities did not correlate with symptoms seen during the infection. Our data suggest that SARS‐CoV‐2 infection may reduce parasympathetic and increase sympathetic tone and may contribute to the autonomic disfunction associated in a subset of collegiate athletes even after recovering from COVID‐19. This study provides further evidence for potential long‐term cardiovascular autonomic effects of Covid‐19 infection even in healthy young trained athletes. Further studies with a larger patient population as well as suitable healthy control subjects are warranted. [ABSTRACT FROM AUTHOR]

Renal sympathetic nerve activation is essential for the development of stress-induced hypertension. High dietary salt (HDS) also contributes to the development of some forms of hypertension. However, it is unclear whether HDS modulates sympathetically mediated renal vascular resistance (RVR) responses during physiological stress in humans. We hypothesized that renal vasoconstrictor responses during stress would be enhanced with HDS. Beat-by-beat measurements of renal blood flow velocity (RBV), blood pressure (BP) and heart rate were obtained in nine normotensive subjects during graded static handgrip (HG) and lower body negative pressure (LBNP) protocols before and after 7 days of HDS. RVR index was calculated by dividing mean BP by RBV. Baseline hemodynamics and plasma norepinephrine were unchanged whereas epinephrine was increased (P < .01) with HDS. In contrast to our hypothesis, increases in RVR during 15 s HG at 70% maximum voluntary contraction were less (P < .04) in the subjects who showed a "large" reduction (>70%) in PRA after HDS. Importantly, the magnitude of this attenuation correlated directly to the drop in PRA after HDS (r = .84; P < .02). RVR responses were also less within the same subjects during LBNP at -10 mmHg after HDS (P < .02) although the responses were similar at -30 and -50 mmHg. In conclusion, HDS attenuates the RVR responses during high intensity handgrip especially in subjects with a large reduction in PRA. We speculate that diminished renin-angiotensin system after HDS led to enhanced arterial baroreflex restraint of the muscle mechanoreflex induced renal vasoconstriction during exercise. [ABSTRACT FROM AUTHOR]

Augmentation index (AI) is used as a measure of arterial stiffness. It represents the augmentation in central aortic pressure due to the effect of returning reflected pulse wave. The aim of the study was to assess the relationship between acute changes in renal vascular resistance (RVR) and arterial stiffness (assessed by AI) during static exercise. Nine subjects (mean age 31.7±9.1 years, 5 males) performed two protocols: First, handgrip (HG) for 15 sec at 30% and 70% of maximum voluntary contraction (MVC). Second, HG to fatigue (HGF) at 40% of MVC followed by post handgrip circulatory arrest (CA) for 2 min. RVR was calculated as the quotient of blood pressure (beat-by-beat) to renal artery velocity (Duplex). AI% was computed by the SphygmoCor software from the aortic pressure waveform, derived from the radial artery waveform recorded by a micromanometer. The AI% was logarithmically transformed and corrected for heart rate. The increase in Log AI% accompanied by increase in RVR index was more pronounced in the HGF and CA protocol. Conclusion: During static exercise, renal vascular resistance and arterial stiffness (measured by augmentation index) increase in a parallel way reflecting sympathetic activation. [ABSTRACT FROM AUTHOR]

It was speculated that muscle metabolites can sensitize muscle mechanoreceptors, and accentuate muscle sympathetic nerve activity (MSNA) responses to mechanoreceptors stimulation in exercise. However, this hypothesis has not been verified directly in healthy subjects. To test whether the MSNA response to passive stretch could be accentuated with increasing metabolites in the muscles, MSNA, ECG and blood pressure (BP) were recorded in 14 young healthy subjects. Subjects performed static isometric handgrip at 30% maximum voluntary contraction (MVC) until fatigue followed by 4 min post exercise ischemia (PEMI). After 2 min of PEMI, the hand was passively stretched (dorsiflexion). In 10 of the subjects, the stretch protocol was also performed without preceding handgrip or ischemia, ischemia alone, and following non-fatigue handgrip at 30% MVC followed by ischemia. During the PEMI after fatigue handgrip, stretch induced significant increase in MSNA (26.4±2.6 to 30.7±2.8 bursts/min, P=0.002) and mean BP (106±2 to 108±2 mmHg, P=0.01). Stretch performed under the other 3 conditions had no significant effect on MSNA. The present data suggest that muscle metabolites accentuate MSNA response to mechanoreceptors stimulation, probably via sensitizing the mechanoreceptors. [ABSTRACT FROM AUTHOR]

During exercise muscle mechanoreflex mediated sympathoexcitation evokes renal vasoconstriction (RV). Animal studies suggest that prostaglandins (PG) generated within the contracting muscle sensitizes muscle mechanoreflexes. Thus, we hypothesized that local PG blockade would attenuate RV during muscle stretch. Accordingly, 9 healthy subjects performed static handgrip before and after locally PG blockade (6 mg ketorolac-tromethamine infused into the exercising forearm) via Bier block. Renal blood flow velocity (RBV; Duplex Ultrasound), mean arterial pressure (MAP; Finapres) and heart rate (ECG) were obtained during post-handgrip circulatory arrest (PHG-CA) followed by PHG-CA with passive forearm muscle stretch (PMS). Increases in renal vascular resistance (RVR, calculated as RBV/MAP) from baseline were greater during PHG-CA + PMS than during PHG-CA alone (Δ43±11% vs. Δ34±10%; P<.02). Similar results were found after a saline Bier block control (Δ59±15% vs. Δ39±11%; P<.02). However, after a ketorolac Bier block the RVR was not increased by PMS (Δ43<10% vs. Δ47±13%; P=NS). HR and MAP responses were similar during PHG-CA and PHG-CA + PMS (P=NS). PMS engages muscle mechanoreflexes and our data show that PMS with PHG-CA evokes RV. Since PG blockade attenuated the RV response, this suggests that PG sensitizes muscle mechanoreflexes in humans. [ABSTRACT FROM AUTHOR]

Animal reports suggest that reflex activation of cardiac sympathetic nerves can evoke coronary vasoconstriction. Conversely, physiologic stress may induce coronary vasodilation to meet an increased metabolic demand. The ability of the sympathetic nervous system to modulate coronary vasomotor tone in response to stress in humans is unclear. Coronary blood flow velocity (CBV), an index of coronary blood flow, can be measured in humans by noninvasive Duplex ultrasound. Accordingly we studied 11 healthy volunteers and measured beat-by-beat changes in CBV, diastolic blood pressure (DBP) and heart rate during: a) static handgrip (HG) for 20 s at 10% and 70% maximal voluntary contraction (MVC); b) lower body negative pressure (LBNP) at -10 and -30 mmHg for 3 min each; c) cold pressor test (CPT) for 90 s; and d) hypoxia (FiO2 0.1), hyperoxia (FiO2 1.0) and hypercapnia (FiCO2 0.05) for 5 min each. Coronary vascular resistance (CVR) index was calculated as DBP/CBV. CVR increased by 28% during HG at 70% MVC (P<0.01), both levels of LBNP (31%, P<0.04; and 44%, P<0.01, respectively) and hyperoxia by 20% (P<0.01). Conversely, hypoxia led to an 18% decrease in CVR (P<0.01). No significant changes were noted in CVR during the other protocols. Thus, in general, physiologic stress known to be associated with sympathetic activation is associated with coronary vasoconstriction. However, contrasting responses were noted during systemic hypoxia and hyperoxia where mechanisms independent of autonomic influences appear to dominate the vascular end organ effects. [ABSTRACT FROM AUTHOR]