Chantigian, Daniel P.

Activation of group III/IV skeletal muscle afferents (ergoreflex) and hypoxia (chemoreflex) are two potent stimuli of the sympathetic nervous system during exercise. Venous distention by graded sub‐systolic occlusion contributes to the ergoreflex during exercise. Although the ergoreflex causes greater increases in blood pressure (BP) compared with the chemoreflex, the interaction of the ergoreflex and hypoxia during lower extremity dynamic exercise is unknown. Objective To determine the effect of hypoxia and graded cuff occlusion on hemodynamic responses during low‐intensity cycling exercise. Methods 19 healthy adults (9 men, 25±5 yr) completed two sessions. Session 1 included a maximal cycle ergometry exercise test. Session 2 included two randomized bouts (hypoxia: 12.5% FiO 2 and normoxia: 21% FiO 2 ) of constant‐load cycling at 30% peak workload for 3 min (control, CTL) followed by randomized inflation of bilateral thigh pressure tourniquets to 20, 40, 60, 80, 100 mmHg for 2 min with 2 min of deflation between occlusions. The bouts were separated by 30 minutes of rest. Blood pressure, heart rate and cardiac output (CO) were measured continuously. Results During hypoxia, the average SPO 2 was 80%. Venous occlusion and hypoxia had differential effects on mean arterial pressure (MAP, occlusion × hypoxia, p=0.02). Significant increases of MAP from CTL occurred at 60 (Δ9 ± 6mmHg), 80 (Δ15 ± 8mmHg), and 100mmHg (Δ17 ± 9mmHg) under normoxia (p<0.05). MAP only increased at 100mmHg (Δ14 ± 9mmHg) under hypoxia (p<0.05). Under hypoxia, MAP was much greater at CTL and 20mmHg as compared to normoxia (p<0.05). SBP exhibited responses similar to MAP under hypoxia (100mmHg increase, p<0.001, occlusion × hypoxia interaction, p=0.02). CO was greater with venous occlusion as mediated by increases in HR (p<0.001). In addition, CO increased under hypoxia (p=0.007) but had no interaction with venous occlusion. Conclusion During low pressure venous occlusion, hypoxia had a greater effect on BP, but as pressure increased (60–100mmHg), there were no significant differences in BP between normoxia and hypoxia. Therefore, sympathetically mediated increases of BP during exercise attributed to hypoxia may negate any responses mediated by the ergoreflex when elicited by venous occlusion at low pressures.

Activation or inhibition of the carotid body chemoreceptors (CBCs) may impact cardiac baroreflex sensitivity (cBRS). The purpose of this study was to test the hypothesis that inhibition of the CBCs will elicit a change in cBRS when compared to normal resting conditions. Young, healthy subjects (n=16, 31±2, 6 women) were given IV saline and a range of IV dopamine (DA) (1‐4 µg/kg/min) for 15 minutes prior to and throughout five hypoxic ventilatory response (HVR) tests. Subjects were initially infused with IV saline. After each HVR, the DA infusion rate was increased by 1 µg/kg/min. A 3‐lead EKG and beat‐by‐beat blood pressure (NexFin) were used to determine cBRS. Data were analyzed from the 5 minutes prior to the HVR associated with the DA dose that elicited the greatest attenuation of the HVR when compared to saline. Heart rate was not significantly different during saline vs. DA (62±3 vs. 65±3, p=0.25). Diastolic blood pressure (77±2 vs. 72±1 mmHg), mean arterial pressure (98±2 vs. 92±2 mmHg), and cBRS “up” sequence (38±7 vs. 21±3 ms/mmHg) were significantly lower during saline vs. DA (p<0.05 for all). cBRS values from the RRI spectrum were not statistically distinguishable between saline and DA (26±4 vs. 21.1±3, p=0.06). In summary, inhibiting the CBCs via DA infusion in young, healthy subjects results in a fall in blood pressure and a reduction in cBRS in response to a rise in blood pressure. These data suggest the CBCs contribute to cBRS and play an important role in modulating parasympathetic control of blood pressure. Funding: NIH R01DK090541

Abstract Background: Occupational stress in resident physicians has profound implications for wellness, professionalism, and patient care. This observational pilot trial measured psychological and physiological stress biomarkers before, during, and after the start of anesthesia residency. Methods: Eighteen physician interns scheduled to begin anesthesia residency were recruited for evaluation at three time points: baseline (collected remotely before residency in June 2013); first-month visit 1 (July); and follow-up visit 2 (residency months 3 to 5, September–November). Validated scales were used to measure stress, anxiety, resilience, and wellness at all three time points. During visits 1 and 2, the authors measured resting heart-rate variability, responses to laboratory mental stress (hemodynamic, catecholamine, cortisol, and interleukin-6), and chronic stress indices (C-reactive protein, 24-h ambulatory heart rate and blood pressure, 24-h urinary cortisol and catecholamines, overnight heart-rate variability). Results: Thirteen interns agreed to participate (72% enrollment). There were seven men and six women, aged 27 to 33 yr. The mean ± SD of all study variables are reported. Conclusion: The novelty of this report is the prospective design in a defined cohort of residents newly exposed to the similar occupational stress of the operating environment. Because of the paucity of literature specific to the measures and stress conditions in this investigation, no data were available to generate a priori definition of primary outcomes and a data analytic plan. These findings will allow power analysis for future design of trials examining occupational stress and stress-reducing interventions. Given the importance of physician burnout in our country, the impact of chronic stress on resident wellness requires further study.