Peripheral Revascularization Reverses the Decline in Active Muscle Oxygen Saturation in Peripheral Artery Disease

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Effect of cadence on locomotor–respiratory coupling during upper-body exercise

Introduction: Asynchronous arm-cranking performed at high cadences elicits greater cardiorespiratory responses compared to low cadences. This has been attributed to increased postural demand and locomotor–respiratory coupling (LRC), and yet, this has not been empirically tested. This study aimed to assess the effects of cadence on cardiorespiratory responses and LRC during upper-body exercise. Methods: Eight recreationally-active men performed arm-cranking exercise at moderate and severe intensities that were separated by 10 min of rest. At each intensity, participants exercised for 4 min at each of three cadences (50, 70, and 90 rev min−1) in a random order, with 4 min rest-periods applied in-between cadences. Exercise measures included LRC via whole- and half-integer ratios, cardiorespiratory function, perceptions of effort (RPE and dyspnoea), and diaphragm EMG using an oesophageal catheter. Results: The prevalence of LRC during moderate exercise was highest at 70 vs. 50 rev min−1 (27 ± 10 vs. 13 ± 9%, p = 0.000) and during severe exercise at 90 vs. 50 rev min−1 (24 ± 7 vs. 18 ± 5%, p = 0.034), with a shorter inspiratory time and higher mean inspiratory flow (p < 0.05) at higher cadences. During moderate exercise, (Formula presented.) and fC were higher at 90 rev min−1 (p < 0.05) relative to 70 and 50 rev min−1 ((Formula presented.) 1.19 ± 0.25 vs. 1.05 ± 0.21 vs. 0.97 ± 0.24 L min−1; fC 116 ± 11 vs. 101 ± 13 vs. 101 ± 12 b min−1), with concomitantly elevated dyspnoea. There were no discernible cadence-mediated effects on diaphragm EMG. Conclusion: Participants engage in LRC to a greater extent at moderate-high cadences which, in turn, increase respiratory airflow. Cadence rate should be carefully considered when designing aerobic training programmes involving the upper-limbs

ACUTE ELECTRONIC CIGARETTE USE DOES NOT ALTER INDICATORS OF THORACIC GAS COMPRESSION

Austin Gooch, Marc A. Augenreich, Jonathon L. Stickford. Appalachian State University, Boone, NC. Background: Electronic cigarette (EC) use has been shown to increase airway resistance, which may lead to alterations in thoracic gas compression volume during maximal expiratory maneuvers. Furthermore, changes to gas compression volume could potentially confound the measurement of forced expiratory volume in one second (FEV1). Purpose: To investigate the acute effects of EC use on three separate indicators of thoracic gas compression volume. Methods: Ten (N=10) male adults participated in all testing procedures over the course of two laboratory visits. Participants inhaled from an EC with (EC+) or without (EC-) the nicotine cartridge in a randomized order. After each use of the EC (EC+ or EC-) participants completed pulmonary function testing. The area under the curve (AUC) between the maximal expiratory flow-lung volume loop and the maximal expiratory flow-mouth volume loop was quantified in each condition. The differences (Δ) in forced expiratory flow at 25% (FEF25%), 50% (FEF50%), and 75% (FEF75%) of forced vital capacity (FVC) between the lung volume and mouth volume loops were measured. Additionally, the Δ in volume between the maximal expiratory flow-lung volume loop and the maximal expiratory flow-mouth volume loop at peak expiratory flow (PEF), FEF25%, FEF50%, and FEF75%were also evaluated for both conditions. All values are expressed as mean ± SD. Results: The AUC between the lung volume and mouth volume loops was not different between conditions (EC+: 3.68 ± 1.42 L2·s; EC-: 3.47 ± 1.44 L2·s; P \u3e 0.05). There were no significant differences in ΔFEF25%, FEF50%, and FEF75% between the two conditions (all P \u3e 0.05). However, the ΔFEF decreased alongside lung volume, independent of condition (P \u3c 0.05). Additionally, there was a reduction in the volume difference at FEF50% and FEF75% compared with PEF and FEF25% (P \u3c 0.05) but no differences were detected between conditions (P \u3e 0.05). Conclusion: We observed no change in the volume of thoracic gas compression during the maximal expiratory maneuver following acute EC use. We interpret this to mean the thoracic gas compression volume does not change spirometry measurements (in particular, FEV1) in relation to pulmonary function testing immediately after acute EC use. Funding provided by the Appalachian State University Office of Student Research and the University Research Council

NO CHANGES IN SYMPATHETIC NEURAL ACTIVITY OR TRANSDUCTION OVER SIX MONTHS RECOVERY FROM SARS-COV-2

Shawn Roberts, Abigail Stickford, Jonathon Stickford, Rachel Szeghy, Stephen Ratchford, Nina Stute, Marc Augenreich, Valesha Province. Appalachian State University, Boone, NC. BACKGROUND: Otherwise healthy young adults recently infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have acutely elevated muscle sympathetic nerve activity (MSNA) compared with non-infected individuals. METHODS: Participants (n=9, 7M/2F, age 21.2±1.4 y) were tested three times following a positive SARS-CoV-2 polymerase chain reaction test (V1:47±15, V2:107±25, V3:170±19 days post-positive). Resting MSNA burst frequency, incidence, and total activity, heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressure were measured at each visit. Data were collected for 5 min of supine rest. MSNA and HR were continuously measured and averaged over 5 min. Blood pressure was measured at the brachial artery at the first and fourth minute, then averaged. Sympathetic transduction to blood pressure was calculated as the absolute (mmHg) and relative (%) changes in mean arterial pressure (MAP) following a sympathetic burst and in response to sympathetic quiescence. RESULTS: Resting MSNA burst frequency (V1: 17±7, V2: 16±7, V3: 14±3 bursts∙min-1), incidence (V1: 31±12, V2: 28±13, V3: 25±4 bursts∙100 heart beats-1), and total activity (V1: 255±105, V2: 230±97, V3: 224±84 a.u.∙min-1) did not change across visits (p\u3e0.05). SBP (V1: 135±11, V2: 127±8, V3: 121±11 mmHg, p=0.037) and DBP (V1: 77±7, V2: 71±7, V3: 67±6 mmHg, p=0.001) both decreased throughout recovery, while HR (V1: 57±9, V2: 60±6, V3: 57±8 bpm, p=0.163) did not change. The absolute (p=0.252) and relative (p=0.435) ΔMAP following an MSNA burst showed no significant changes over time Similarly, there were no changes in the absolute (p=0.169) or relative (p=0.127) ΔMAP following a non-bursting cardiac cycle. CONCLUSION: Despite cross-sectional data indicating elevated sympathetic activity following mild cases of COVID-19, longitudinal data suggests no change in sympathetic neural parameters over six months recovery. The diverging findings may indicate a) no effect of SARS-CoV-2 infection on sympathetic activity or, alternatively, b) prolonged recovery of autonomic function. However, the current results indicate clear reductions in DBP and SBP throughout six months of recovery from SARS-CoV-2. Given the lack of change in neural measures, changes in pressure are likely a result of other mechanisms

Tracking peripheral vascular function for six months in young adults following SARS‐CoV‐2 infection

Abstract SARS‐CoV‐2 infection is known to instigate a range of physiologic perturbations, including vascular dysfunction. However, little work has concluded how long these effects may last, especially among young adults with mild symptoms. To determine potential recovery from acute vascular dysfunction in young adults (8 M/8F, 21 ± 1 yr, 23.5 ± 3.1 kg⋅m−2), we longitudinally tracked brachial artery flow‐mediated dilation (FMD) and reactive hyperemia (RH) in the arm and hyperemic response to passive limb movement (PLM) in the leg, with Doppler ultrasound, as well as circulating biomarkers of inflammation (interleukin‐6, C‐reactive protein), oxidative stress (thiobarbituric acid reactive substances, protein carbonyl), antioxidant capacity (superoxide dismutase), and nitric oxide bioavailability (nitrite) monthly for a 6‐month period post‐SARS‐CoV‐2 infection. FMD, as a marker of macrovascular function, improved from month 1 (3.06 ± 1.39%) to month 6 (6.60 ± 2.07%; p  0.05). Circulating markers of inflammation, oxidative stress, antioxidant capacity, and nitric oxide bioavailability did not change during the 6 months (p > 0.05). Together, these results suggest some improvements in macrovascular, but not microvascular function, over 6 months following SARS‐CoV‐2 infection. The data also suggest persistent ramifications for cardiovascular health among those recovering from mild illness and among young, otherwise healthy adults with SARS‐CoV‐2

Monthly transthoracic echocardiography in young adults for 6 months following SARS‐CoV‐2 infection

Abstract Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) can elicit acute and long‐term effects on the myocardium among survivors, yet effects among otherwise healthy young adults remains unclear. Young adults with mild symptoms of SARS‐CoV‐2 (8M/8F, age: 21 ± 1 years, BMI: 23.5 ± 3.1 kg·m−2) underwent monthly transthoracic echocardiography (TTE) and testing of circulating cardiac troponin‐I for months 1–6 (M1–M6) following a positive polymerase chain reaction test to better understand the acute effects and post‐acute sequelae of SARS‐CoV‐2 on cardiac structure and function. Left heart structure and ejection fraction were unaltered from M1–M6 (p > 0.05). While most parameters of septal and lateral wall velocities, mitral and tricuspid valve, and pulmonary vein (PV) were unaltered from M1–M6 (p > 0.05), lateral wall s′ wave velocity increased (M1: 0.113 ± 0.019 m·s−1, M6: 0.135 ± 0.022 m·s−1, p = 0.013); PV S wave velocity increased (M1: 0.596 ± 0.099 m·s−1, M6: 0.824 ± 0.118 m·s−1, p < 0.001); the difference between PV A wave and mitral valve (MV) A wave durations decreased (M1: 39.139 ± 43.715 ms, M6: 18.037 ± 7.227 ms, p = 0.002); the ratio of PV A duration to MV A duration increased (M1: 0.844 ± 0.205, M6: 1.013 ± 0.132, p = 0.013); and cardiac troponin‐I levels decreased (M1: 0.38 ± 0.20 ng·ml−1, M3: 0.28 ± 0.34 ng·ml−1, M6: 0.29 ± 0.16 ng·ml−1; p = 0.002) over time. While young adults with mild symptoms of SARS‐CoV‐2 lacked changes to cardiac structure, the subclinical improvements to cardiac function and reduced inflammatory marker of cardiac troponin‐I over 6 months following SARS‐CoV‐2 infection provide physiologic guidance to post‐acute sequelae and recovery from SARS‐CoV‐2 and its variants using conventional TTE