When practicing a motor skill, learners who are expecting to teach it to another person exhibit superior gains in skill execution and declarative knowledge. Since skills acquired with large gains in declarative knowledge are highly susceptible to decrement under psychological pressure, it is possible the advantage of expecting to teach is lost when performing the learned skill under pressure. To test this hypothesis, we had 40 participants practice golf putting with the expectation of teaching (teach group) and 42 participants practice with the expectation of being tested (test group). The next day, all participants performed low-and high-pressure posttests. The teach group outperformed the test group under low pressure but not high pressure, where the teach group's performance declined to that of the test group. Further, the teach group reported using more declarative knowledge during the posttests than the test group, but declarative knowledge use did not mediate the performance decline from low-to high-pressure posttest. Taken together, results suggest expecting to teach benefits skill learning, but this advantage is lost when performing the skill under high pressure. However, whether skill breakdown under high pressure is caused by an increase in declarative knowledge use remains an open question. Public Significance StatementThis study suggests practicing a motor skill with the expectation of teaching it enhances skill learning. However, this improved capability for skill performance is not manifested when the skill is performed under psychological pressure. Thus, it is recommended that people practice skills with the expectation of teaching them and take measures to prevent choking under pressure.
BACKGROUND Augmented beat‐to‐beat blood pressure (BP) variability is prognostic of target organ damage and cardiovascular events. A recent study demonstrated greater BP variability in healthy young Black males compared to White males, but whether these differences appear in females remains unclear. Therefore, we sought to examine race and sex differences in beat‐to‐beat BP variability in healthy young Black and White adults. METHODS 52 adults including 13 Black females (age 21.5 ± 0.8 yrs, BMI 27.0 ± 4.2 kg/m2, resting BP 126 ± 10/78 ± 12 mmHg; Mean ± SD), 13 White females (21.2 ± 0.7 yrs, 24.0 ± 3.8 kg/m2, 116 ± 8/66 ± 11 mmHg), 9 Black males (21.6 ± 0.7 yrs, 25.5 ± 4.3 kg/m2, 131 ± 11/75 ± 11 mmHg), and 17 White males (21.5 ± 0.7 yrs, 25.0 ± 3.7 kg/m2, 123 ± 11/67 ± 9 mmHg) participated in this study. Non‐invasive beat‐to‐beat BP was continuously measured at the participant’s middle finger via photoplethysmography (Finapres NOVA) for 10 minutes while sitting semi‐recumbent in a dimly lit room. The finger pressure was calibrated using resting oscillometric brachial BP. Heart rate was measured via 3‐lead electrocardiogram (ECG) and BP was gated to R‐waves from the ECG signal. BP variability was assessed with the average real variability (ARV) index and standard deviation (SD) of all BP readings. Statistical procedures included two‐way analysis of variance (sex x race) with Bonferroni post‐hoc test when appropriate (a priori α < 0.05). RESULTS No significant differences existed for systolic BP ARV (sex p= 0.85, race p= 0.41, interaction p= 0.63; Black females 2.02 ± 0.64, White females 1.84 ± 0.44, Black males 1.98 ± 0.24, White males 1.93 ± 0.44) or diastolic BP ARV (sex p= 0.31, race p= 0.76, interaction p= 0.51). For systolic BP SD, there was a significant main effect of sex (p= 0.008) suggesting greater systolic BP variability in males than females, and a trend for race by sex interaction (p= 0.08) but no difference for race (p= 0.79); (Black females 4.80 ± 1.07, White females 5.80 ± 2.10, Black males 7.77 ± 3.89, White males 6.42 ± 1.74). However, there were no significant differences for diastolic BP SD (sex p= 0.19, race p= 0.55, interaction p= 0.46). CONCLUSION These preliminary findings suggest males have significantly greater systolic BP variability than females from systolic BP ARV. No significant differences were identified for diastolic BP SD and BP ARV (systolic and diastolic) by race and sex, but additional data are needed.
OBJECTIVES/GOALS: Greater blood pressure (BP) reactivity and socioeconomic deprivation (e.g., area deprivation index; ADI) are associated with poor vascular health [1-3]. However, it is unclear if ADI is associated with BP reactivity. Thus, we sought to examine if ADI is associated with BP reactivity in young adults. METHODS/STUDY POPULATION: Participants completed questionnaires used to derive lifetime ADI averaged from early-, mid-childhood, and adolescence. Participants completed a handgrip (HG) exercise protocol including 10 minutes of rest, 2 minutes of static HG at 40% of their maximal voluntary contraction, 3 minutes of post-exercise ischemia (PEI), and 2 minutes of recovery (REC). Beat-to-beat BP (photoplethysmography) and heartrate (HR; electrocardiogram) were continually assessed. We used the Shapiro-Wilk test to assess data for normality. We examined associations between ADI, BP reactivity, and HR using unadjusted and body mass index (BMI), sex, and race-adjusted Pearson’s correlation (set a priori to 0.05). RESULTS/ANTICIPATED RESULTS: This study included 53 (27Males/26Females; 21 ± 1 years; 24Black/29White; BP 107 ± 9/64 ± 9 mmHg) participants. There were racial differences (Black compared to White adults) for several BP reactivity metrics (e.g., PEI minute 3 diastolic BP: 96 ± 15 vs. 84 ± 19 mmHg, p=0.014) and lifetime ADI (p0.050). DISCUSSION/SIGNIFICANCE: Our data suggest racial differences exist in socioeconomic deprivation in a modestly sized young adult sample living in the southeast. While additional data are needed for other stressors, socioeconomic deprivation was not independently associated with BP or HR reactivity during acute exercise.
The difference between that PO and the 75% θ L trial PO was the MRT SS . Pre-and post-blood lactates were recorded from all trials. RESULTS: τ' and MRT Lin were different (22 ± 13 W, 17 ± 9 W, P=0.04). MRT SS was similar to τ' and MRT Lin (22 ± 11 W, (P=1.000, P= 0.07). The τ' and MRT Lin -corrected POs corresponding to the V ̇O2 over the last 5 min of the 75% of θ L trial (114 ± 53 P=0.573 and 121 ± 49 P=0.372, respectively) were similar to the actual PO performed (116 ± 52). τ' and MRT Lincorrected POs corresponding to the V ̇O2 last 5 min at 85% of θ L (142 ± 70, 149 ± 66, P=0.087 respectively) were similar to the actual PO performed(140 ± 65). The τ'-corrected PO corresponding to the V ̇O2 last 5 min at Δ15% (P=0.088) was similar to the actual PO performed. The MRT Lin -corrected PO corresponding to the V ̇O2 last 5 min at Δ15% (P= 0.025) was different from the actual PO. CONCLUSION: Left-shifting the RAMP PO by τ' or MRT Lin results in a similar corresponding V ̇O2 at 75% or 85% of θ L . At Δ15% only left-shifting by τ' results in the same PO as is performed. Using τ' or MRT Lin can be used with confidence when prescribing exercise below θ L . At intensities slightly above θ L only left-shifting by τ' is reliable.
Acute bouts of exercise have a transient lowering effect on systolic blood pressure (SBP) and diastolic BP (DBP) in the hours after termed post-exercise hypotension (PEH). While moderateintensity continuous training (MICT) and high-intensity interval training (HIIT) are effective in reducing BP acutely, there is little work exploring the effect of sprint interval training (SIT), particularly in middle-aged populations. PURPOSE: To examine the effects of different exercise intensities on PEH in the immediate post-exercise period (≤2 h) in middle-aged adults. METHODS: Twelve participants (8 females; age: 47±9 y, body mass index: 26.0±3.6 kg•m -2 , SBP: 116±11 mmHg, DBP: 67±7 mmHg) had their BP measured before and after (15, 30, 60, 120 min) 4 experimental sessions: 1) 30 min MICT (65% V ̇O2max ); 2) 20 min HIIT (10 x 1 min at 90% HR max with 1 min rest) session; 3) 16 min SIT (8x15 s all out sprints with 2 min rest); and 4) non-exercise control (CTRL). PEH was calculated by subtracting BP during the exercise session from BP at the same time during the CTRL session. Two-way repeated measure analysis of variance were conducted to determine differences in absolute BP, PEH, and BP area under the curve (AUC) between sessions.
PURPOSE Cardiovascular disease is characterized by blood pressure (BP) dysregulation and vascular dysfunction, secondary to vascular oxidative stress. Exogenous antioxidants mitigate vascular oxidative stress by scavenging reactive oxygen species (ROS). MitoQ, a mitochondrial specific antioxidant improves vascular function and reduces elevated arterial stiffness in older adults. However, it is unclear if MitoQ improves vascular function in healthy young adults for primary prevention purposes. Therefore, central hemodynamics, arterial stiffness, and measures of oxidative stress were assessed in healthy young adults before and after acute MitoQ (or placebo) supplementation. METHODS Eleven participants (six females, age: 26±4 years, BMI: 25±3 kg/m2, screening BP: 109±10/65±4 mmHg, Mean±SD) reported to our laboratory for two separate sessions (crossover design) and randomly assigned either a placebo or MitoQ protocol (100‐160mg, depending on body mass). Sessions were separated by ≥72‐hour wash out period. Laboratory measures were performed before and 45 minutes after MitoQ (or placebo) capsules were ingested. Following ≥10 minutes of quiet rest, triplicate readings of brachial (oscillometric) and aortic BP (SphygmoCor) were obtained. We assessed carotid‐femoral pulse wave velocity (PWV) and augmentation index as indices of arterial stiffness. We obtained blood samples via intravenous catheter placement to assess ROS levels with electron paramagnetic resonance and plasma superoxide dismutase activity using an enzymatic assay kit. 2‐way ANOVAs were performed to determine effects on treatment x time interaction. RESULTS No significant treatment x time interactions for brachial (p=0.52) and aortic (p=0.64) systolic BP readings, or brachial (p=0.34) and aortic (p=0.11) diastolic BP readings were observed. However, brachial systolic BP tended to modestly increase after capsule ingestion (placebo:114±8 to 118±9; MitoQ: 116±11 to 118±8; time: p=0.05). Carotid‐femoral PWV did not change following placebo (4.3±0.7 to 4.5±0.8 m/s) or MitoQ (4.3±0.7 to 4.4±0.8 m/s) ingestion (time: p=0.35, interaction p=0.30). Augmentation index decreased from pre‐ to post‐ capsule ingestion for both placebo (14±9 to 11±8 %) and MitoQ (14±9 to 10±8 %; time: p<0.01) with no significant interaction (p=0.28). There was no significant treatment x time interaction for Blood ROS (p=0.99) concentration or plasma superoxide dismutase activity (p=0.89). CONCLUSIONS While additional data are needed to build our sample size and determine if there are racial or ethnic differences in responses, our preliminary findings suggest that acute MitoQ supplementation does not influence central hemodynamics or arterial stiffness in healthy, young adults.
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