Heart Rate Response of Professional Musicians When Playing Music.

OBJECTIVES: The primary aim was to determine the level of physiological stress evoked while playing music in a standing position as indicated by heart rate (HR) response. A secondary aim was to analyze the effect of music genre (classic rock, western, contemporary Christian, and metal rock) on the relative HR response. Lastly, we considered potential physiological initiators of the music-playing-induced HR response. METHODS: HR response was monitored in 27 professional musicians (3 women, 24 men) between the ages of 21 and 67 yrs old during rehearsal and public performances. The percent maximal HR (%MHR) evoked was determined by taking a percentage of the age-predicted maximal HR for each musician and comparing the average %MHR in each genre during public and rehearsal events. The role of the potential initiators of these responses (e.g., number of years playing in public, event type, instrument type, tempo, etc.) was determined using multiple regression analyses. RESULTS: The overall average %MHR responses were 52 ± 5% and 59 ± 5% during rehearsal and public performances, respectively, with genre type having a significant effect on the HR response (p=0.01). Body mass index and tempo were each found to be significant contributors to the HR response while playing music (r²=0.506, p=0.001). CONCLUSION: Playing music professionally evokes considerable increases in HR response, with music genre influencing the level of the physiological response. We concluded that 50% of the HR response while playing music was associated with body mass index, music tempo, and instrument type.

Pharmacological manipulation of the dopaminergic system affects wheel-running activity in differentially active mice.

The genetic factors involved in the regulation of physical activity are not well understood. The dopamine system has been implicated in the control of voluntary locomotion and wheel running (WR) in mice and is thus a likely candidate as a genetic/biological system important to the regulation of physical activity. This study evaluated the effects of four different dopaminergic acting drugs on WR in differentially active inbred strains of mice. High active C57L/J (n=7, 3 controls, 4 experimental) and low active C3H/HeJ (n=8, 3 controls, 5 experimental) were analyzed for baseline wheel-running indices of distance (km/day), duration (mins/day), and speed (m/min) for 21 days. Experimental mice received increasing doses over four days of each of the following drugs: SKF 81297 (D1 agonist), SCH 23390 (D1 antagonist), GBR 12783 (DAT inhibitor), and AMPT (tyrosine hydroxylase inhibitor). Each drug dose response treatment was separated by three days of recovery (no drug injections). WR indices were monitored during drug treatments and during drug wash-out phases. SKF 81297 significantly reduced (p=0.0004) WR in the C57L/J mice, but did not affect WR in the C3H/HeJ mice. GBR 12783 significantly increased (p=0.0005) WR in C3H/HeJ mice, but did not affect WR in C57L/J mice. Only duration (not overall WR) was significantly reduced in C57L/J mice in response to SCH 23390 (p=0.003) and AMPT (p=0.043). SCH 23390 (p=0.44) and AMPT (p=0.98) did not significantly affect WR in C3H/HeJ mice. These results suggest that genetic differences in dopamine signaling may play a role in the WR response to dopaminergic-acting drugs in inbred strains of mice. The high activity in the C57L/J strain appears most responsive to D1-like receptor acting drugs, while in the C3H/HeJ strain, dopamine re-uptake appears to have an influence on activity level.

Interstrain variation in murine aerobic capacity.

PURPOSE: The contribution of genetic factors to aerobic capacity is unknown. The purpose of this study was to measure maximal aerobic performance among inbred strains of mice to provide basic heritability estimates. METHODS: Eight female mice, 8 to 10 wk old, in 10 inbred strains (A/J, AKR/J, Balb/cJ, C(3)H/HeJ, C57Bl/6J, C57L/J, C(3)Heb/FeJ, CBA/J, DBA/2J, and SWR/J) were run on a treadmill until exhaustion. The protocol started at 22 m.min(-1) and increased in speed approximately 6 m.min(-1) every 4 min. After 4 min at 42.4 m.min(-1), the grade was increased 2% every 4 min thereafter until the mouse could not run off of the shock grid (150 V; 1.5 mA). RESULTS: There were significant differences between inbred strains in maximal duration of exercise accomplished (P < 0.0001). The order of strain-specific exercise duration was Balb/cJ > SWR/J > CBA/J > C57L/J > C3H/HeJ > C3Heb/FeJ > C57Bl/6J > AKR/J > DBA/2J > A/J. Two measures of heritability in the broad sense, intraclass correlation (0.73), and the coefficient of genetic determination (0.58) were both significant. CONCLUSION: These data indicate that there is a strong genetic contribution to aerobic capacity in mice.

The reproducibility of tolerance to lower-body negative pressure and its quantification.

The reproducibility of tolerance to lower-body negative pressure (LBNP) has not been assessed sufficiently. Furthermore, there has been confusion concerning the most appropriate index by which LBNP tolerance can be quantified. The purpose of this study was to assess the degree of reproducibility in presyncopal-symptom-limited LBNP (LBNPtol), using an LBNP chamber. Twenty physically active subjects [median age (range) 21 (18-27) years] underwent three successive LBNPtol tests with 72-120 h between each test. LBNPtol was quantified using the LBNP tolerance index (LTI; delta mmHg.min), cumulative stress index (CSI; mmHg.min), duration of negative pressure (DNP) and maximum magnitude of negative pressure (MNP). Heart rate (fc), systolic (SBP) and diastolic (DBP) blood pressures from the three repeated tests were compared during a control period. The changes from control to maximum response (fc, SBP, DBP) during LBNP were also compared, and percentage changes in estimated blood volume were measured. There were no statistical differences between any of these comparisons (P > 0.05). LTI and CSI were greater in the third test when compared to the first two tests (P < 0.05). The values for DNP and MNP were not statistically different between tests (P > 0.05). Measures of LTI and CSI showed an acceptable level of reproducibility for the first two repeated tests. However, there was an increase in LBNPtol on the third successive exposure to LBNP. These findings have shown that it is possible to achieve reproducible measures of tolerance to LBNP when using a custom-built chamber. This only applies to a test-retest procedure. Furthermore, these data also suggest that DNP and MNP do not adequately reflect the differences shown in LBNP tolerance when using LTI and CSI as measures.

Naloxone decreases tolerance to hypotensive, hypovolemic stress healthy humans.

OBJECTIVE: In animal studies, naloxone, an opioid receptor antagonist, improves tolerance to hemorrhagic shock. The purpose of this study was to determine whether naloxone would augment tolerance to hypotensive hypovolemic stress (lower body negative pressure [LBNP]) in healthy human males. DESIGN: This study was a repeated measures design. SETTING: The experiments were conducted in a laboratory setting. SUBJECTS: Eight healthy male subjects were tested. The subjects' ages were 30 +/- 4.0 yrs, height = 177 +/- 7.0 cm, and weight = 75.5 +/- 3.5 kg (mean +/- SEM). INTERVENTIONS: Subjects underwent two LBNP exposures terminated by the onset of vasodepression. At each of the exposures, using a double-blind procedure, the subjects received an intravenous injection of either saline placebo or naloxone in a dosage totaling 0.4 mg/kg.

Reproducibility of resting heart rate variability with short sampling periods.

The purpose of this study was to determine whether resting heart rate variability (HRV) is reproducible with short sampling measurement periods using an office-based personal computer measurement system. Eight healthy active women participated in ECG analyses on 2 days within 1 week under controlled environmental and physiological conditions. After they rested for 10 minutes, a 10-min ECG was recorded. HRV was determined from a 2.5- and 5-min sample period using both time domain variables (meanRR and SDNN) and frequency domain variables (LF, HF, LF:HF). Repeated measures ANOVA found no significant differences between Day 1 and Day 2 for either sampling period (p > or = 0.23). For both the 2.5- and 5-min sampling periods, the intraclass correlations between days for the time domain variables showed good reproducibility (R = 0.86-0.90). The reproducibility of the frequency domain variable was only average (R = 0.67-0.96), with the LF:HF ratio yielding the higher R values.

A different method of teaching peer review systems.

Students often have difficulty grasping the advantages of the various peer review systems used in scientific publishing. In the described exercise, students are assigned a current study and then write three two-page critiques of the article. The three critiques occur at different times in the semester, and thus the students have differing knowledge bases. The critiques are then assigned to other students for peer review using the double-blind, single-blind, or open review systems. After the submission of each peer review, the class discusses the various advantages and disadvantages of each peer review system. In addition to experiencing peer review, in using this method students also gain an appreciation for the difficulty of judging the merit of a peer's work.

Ambient noise interferes with auscultatory blood pressure measurement during exercise.

This study was designed to investigate whether the acoustical characteristics of the Korotkoff sounds (K-sounds) were altered during exercise and/or masked by the ambient noise. After signing informed consent, 11 subjects (8 females, 3 males; 27 +/- 2 yr; 166.2 +/- 3.2 cm; 62 +/- 5 kg; means +/- SD) underwent a cycle ergometer exercise test that increased in workload by 30 W every 3 min until volitional fatigue. Heart rate, auscultatory systolic (SBP) and diastolic blood pressure (DBP), and oxygen consumption were monitored 1 and 2 min into each work stage. The auscultatory K-sounds were recorded with a microphone mounted in a stethoscope tube for later frequency (Hz) and sound pressure level (dB SPL) analysis. Frequency and SPL of ambient noise (99 +/- 13 Hz and 64 +/- 1 db at maximum, respectively) increased during the exercise test to magnitudes similar to the SBP and DBP K-sounds (166 Hz, 66 db; and 128 Hz, 69 db, respectively). Additionally, the ambient noise was responsible for a significant damping of the frequency and SPL of the measured blood pressure K-sounds and a rise in the measured frequency of the SBP K-sounds. Furthermore, we observed "inaudible" K-sounds at lower frequencies than adjoining audible K-sounds (100 Hz vs 126 Hz), supporting the known underestimation of SBP by auscultation. The increase in ambient noise during exercise testing dampens and may mask the auscultatory K-sounds, thus making detection of the proper K-sounds during exercise difficult at best. Furthermore, the presence of inaudible K-sounds may further explain the published discrepancies between auscultatory and intraarterial blood pressure measurements during exercise.

Quantification of tolerance to lower body negative pressure in a healthy population.

Subtolerance and presyncopal lower body negative pressure (LBNP) has been used extensively to investigate the effect of various forms of exercise training on central hypovolemic tolerance. However, there are no population data concerning LBNP tolerance, and the validity of common LBNP tolerance indices has not been investigated. LBNP tolerance data from 86 males and 33 females were analyzed. All LBNP exposures were terminated with the onset of presyncopal signs and/or symptoms. LBNP tolerance was quantified using duration of exposure (DNP), maximal negative pressure tolerated (MNP, cumulative stress index (CSI), and the LBNP tolerance index (LTI). Average (+/- SD) LBNP tolerance was 22.12 +/- 5.01 min (DNP), -77 +/- 16 mm Hg (MNP), 975 +/- 402 mm Hg.min-1 (CSI), or 222 +/- 50 mm Hg.min-1 (LTI). All cardiovascular parameters exhibited the same responses as have been documented in the literature. While DNP, MNP, and LTI were normally distributed, CSI in this population was not normally distributed. Age, weight, height, gender, and VO2peak were not associated with LBNP tolerance. Compared to this population, it appears that the subjects that have participated in previous LBNP tolerance studies have had abnormally high LBNP tolerances and that the LTI is the most valid index of LBNP tolerance. Furthermore, in this population LBNP tolerance could not be predicted from physical characteristics.

Resistance training increases lower body negative pressure tolerance.

This study investigated whether whole body resistance training would increase tolerance to lower body negative pressure (LBNP). Twelve males (age = 19.6 +/- 0.4 yr; mean +/- SD) underwent an acute, 12-wk program of upper and lower body resistance training (ART). Pre- and posttraining, the ART group and a control group (CON; N = 8; age = 25.4 +/- 2.4 yr) underwent LBNP tolerance tests and neck pressure-suction testing. Additionally, a group of chronically resistance-trained individuals (CRT group; N = 5; age = 22.4 +/- 0.9 yr) were tested. LBNP tolerance was increased in the ART group after training and the CRT group exhibited a significantly higher LBNP tolerance than the other groups. The ART group exhibited a decreased leg circumference change at the same absolute negative pressure at which tolerance occurred pretraining. This indicated a decreased fluid pooling after ART. The CRT group exhibited a "flattened" hypotensive portion of the carotid sinus-heart rate baroreflex curve, but this appeared to be due to the increased neck muscle mass of the subjects. We conclude that whole body ART increases LBNP tolerance possibly mediated through alterations in vascular compliance. CRT results in even greater LBNP tolerance with the responsible mediating mechanisms unclear.

Occurrence of presyncope in subjects without ventricular innervation.

1. To determine whether activation of the left ventricular C-fibre mechanoreceptors initiates the vasodepressor reflex that often causes syncope, we exposed six orthotopic cardiac transplant patients and six matched, healthy control subjects to progressively increasing lower body negative pressure until the onset of vasodepressor responses. 2. There was no significant difference (P = 0.78) between the central hypovolaemia tolerances of the cardiac transplant and the control groups. 3. The decrease in systolic blood pressure before the onset of vasodepressor reflexes was greater in the cardiac transplant group. The cardiac transplant group did not maintain diastolic blood pressure during central hypovolaemia. From baseline to the onset of vasodepression, there were no differences in leg circumference, forearm blood flow and forearm vascular resistance responses between the two groups. 4. We conclude that the left ventricular mechanoreceptors may not be the primary afferent trigger for syncope.

Cardiovascular responses to lower body negative pressure in trained and untrained older men.

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59-73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.

Presyncope caused by central hypovolaemia is not preceded by evoked potential alterations.

The mechanism(s) responsible for the onset of presyncope during a central hypovolaemic challenge have gone undefined for many years. It has been speculated that a decrease in cerebral blood flow initiates presyncopal responses, which in turn lead to greater decreases in cerebral oxygen delivery and unconsciousness. Somatosensory evoked potentials (SEP) were monitored as a measure of cerebral functioning in ten subjects during presyncopal symptom limiting lower body negative pressure (a central hypovolaemic challenge). SEP latency and amplitudes have been correlated with cerebral oxygen uptake, so SEP activity can serve as an indirect indicator of cerebral homeostasis. SEPs were generated by electrically stimulating the median nerve and recoding the resulting potentials over the contralateral cerebral cortex. While heart rate and mean blood pressure both fell at presyncope, there were no changes noted in either SEP latency or amplitude at any point before (latency = 22.9 +/- 9 ms; amplitude = 2.86 +/- 0.24 microV), during (22.6 +/- 0.9 ms; 2.68 +/- 0.2 microV), or after (22.7 +/- 0.9 ms; 2.37 +/- 0.23 microV) the occurrence of presyncope. We conclude that the onset of presyncope is not associated with a decrease in cerebral function.

Repeatability and protocol comparability of presyncopal symptom limited lower body negative pressure exposures.

Data on repeatability and comparability of different presyncopal symptom-limited lower body negative pressure (PSL-LBNP) exposure protocols, while scarce, are critical to the interpretation of studies using PSL-LBNP methods. To investigate if PSL-LBNP tolerance, heart rate, and blood pressure were repeatable, 11 subjects were exposed to 4 PSL-LBNP tests; each test occurring at the same time of day, separated by at least 72 h, and using the same protocol. No significant differences were found in either the heart rate or blood pressure responses to the PSL-LBNP or the tolerance indices (cumulative stress index; maximum negative pressure tolerated; and duration of negative pressure exposure). To study the comparability of different PSL-LBNP protocols, nine subjects were exposed randomly to five PSL-LBNP tests using protocols that varied in stage duration but not pressure profile. The protocols had 1-, 3-, 5-, 7-, or 9-min stage durations. These PSL-LBNP exposures were conducted at the same time of day and separated by at least 72 h. While no differences were noted in either the response pattern or magnitude of heart rate or blood pressure to the differing protocols, the cumulative stress index and the duration of negative pressure exposure varied proportionally with the length of the stage durations. With the exception of the 1-min protocol, the maximum negative pressure tolerated did not vary regardless of the protocol used.(ABSTRACT TRUNCATED AT 250 WORDS)

Automated blood pressure measurements during exercise.

One of the critical parameters measured during exercise is blood pressure. However, the accurate measurement of systolic and diastolic blood pressure during exercise is difficult with auscultation and impractical with direct arterial techniques. The purpose of this study was to compare an automated system (Colin, Inc. STBP-680) with auscultation in humans during rest and exercise and to compare the automated system with direct arterial blood pressure measurement in a canine model during pharmacological challenges that resulted in a wide range of blood pressure values. Compared with direct arterial blood pressure taken in the canine model, the STBP-680 gave good estimates of diastolic blood pressure and adequately monitored relative changes in systolic blood pressure, diastolic blood pressure, and mean arterial pressure (mean arterial pressures in all instances were calculated as one-third systolic plus two-thirds diastolic blood pressures). Compared with auscultation methods in humans, the STBP-680 gave similar estimates of resting diastolic blood pressure and monitored relative changes in resting systolic blood pressures, diastolic blood pressures, and mean arterial pressures. During both treadmill and cycle ergometer exercise in humans, the STBP-680 monitored changes in systolic blood pressure, phase IV diastolic blood pressure, and mean arterial pressure. Further, the STBP-680 estimated exactly and noted relative changes in heart rate in every test. However, during exercise, quantitative estimations of systolic blood pressure by the STBP-680 were higher than those found using auscultation. Where exact, quantitative measures of blood pressure are needed, direct arterial measurement continues to be the most accurate method. However, where indirect methods can be used, the STBP-680 may provide a suitable alternative that reduces many of the technical concerns of auscultation in young, healthy individuals.

Ten weeks of aerobic training do not affect lower body negative pressure responses.

Based mostly on cross-sectional data, it has been suggested that aerobic training may decrease lower body negative pressure (LBNP) tolerance through a hypothesized attenuation in both high- and low-pressure baroreflex gain. An experimental group (EXP) of eight male subjects [22.1 +/- 1.4 (SD) yr] underwent a 10-wk treadmill and cycle ergometer training program, which resulted in a 21% increase in maximal O2 uptake (VO2 max), 45.7 +/- 1.5 vs. 55.2 +/- 1.7 (SE) ml.kg-1.min-1; P less than 0.05]. A control group, (CON; n = 7; 27.3 +/- 5.7 yr), which did not undergo training, had no significant changes in VO2 max (49.4 +/- 3.3 vs. 48.8 +/- 3.2 ml.kg-1.min-1). Before and after training the EXP and CON groups participated in LBNP tolerance tests (terminated at presyncope) and neck pressure-suction testing (to describe the carotid sinus-heart rate baroreflex). LBNP tolerance, as defined by three different indexes, and carotid sinus-heart rate baroreflex gain were not altered in either group after training. Furthermore, there were no changes in LBNP heart rate, blood pressure, leg circumference, forearm blood flow, or forearm vascular resistance responses at any level of LBNP challenge after training. In conclusion, 10 wk of aerobic training did not change LBNP tolerance or alter the reflex cardiovascular compensatory mechanisms activated during LBNP.

Adaptation to repeated presyncopal lower body negative pressure exposures.

Adaptation to chronic stressors, such as exercise and thermal challenges, are well-documented. However, it is not known whether the body can adapt to repeated central hypovolemia. The purpose of this study was to determine if tolerance to presyncopal symptom limited lower body negative pressure (PSL-LBNP; a central hypovolemic stressor), as measured by a cumulative stress index (CSI), was altered by daily PSL-LBNP exposures. On each of nine consecutive days, with a 2-d break between Days 5 and 6, six subjects underwent a PSL-LBNP exposure. By the fifth PSL-LBNP exposure, LBNP tolerance had increased 47%. No further significant improvement was seen after the fifth exposure. While, there was no alteration in mean arterial pressure response during the repeated PSL-LBNP exposures, maximum heart rates were increased significantly over Day 1 after the third daily PSL-LBNP exposure. Rate-pressure product was also significantly increased over Day 1 on Days 7 and 8. These findings suggest that adaptation to a simulated hypovolemic stress does occur. Presumably, either the body's compensatory mechanisms become more effective, or there is a resetting of the threshold needed to elicit the presyncopal reactions.