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Research Quarterly for Exercise and Sport Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/urqe20
Effects of Submaximal Exercise and Noise Exposure on Hearing Loss a
Helaine M. Alessio & Kathleen M. Hutchinson
b
a
Department of Physical Education, Health and Sport Studies , Miami University , Oxford , OH , 45056 , USA b
Department of Communications , Miami University , USA Published online: 08 Feb 2013.
To cite this article: Helaine M. Alessio & Kathleen M. Hutchinson (1991) Effects of Submaximal Exercise and Noise Exposure on Hearing Loss, Research Quarterly for Exercise and Sport, 62:4, 413-419, DOI: 10.1080/02701367.1991.10607542 To link to this article: http://dx.doi.org/10.1080/02701367.1991.10607542
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R8I8.rch QlIlIl18r1y lor Exercise .nd Sport @1991bytheAmericanAiliancelorHealth, Physical Education, Recreation and Dance Vol. 62, No. 4, pp.413-419
Effects of Submaximal Exercise and Noise Exposure on Hearing Loss
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Helaine M. Alessio andKathleen M. Hutchinson A recent Scandinavian study reported that persons cycling at moderate intensityfor 10 min suffered hearing loss when the exercise was accompanied by noise. The noiseconsisted of a Ih octave bantJ..jiUered noisewith a 2000 Hz centerfrequency at 104 dB SPL In the present study, adults cycled at 50 rev·minI against a force that elicited an o~gen cost equal to 70 % of V02 max-an intensityfrequently recommended in exercise prescriptions-with and without noiseadministered via headphones. Repeated. measures ANOVA with three factors reoealed that although a temporary hearingloss occurred followingexercise-antJ.. noise, a similar and slightly greater hearingloss occurred followingnoislHmly. Hearing sensitivity was not significantly altered by exercislHmly (p > .05). In general, hearingloss values were greatest between 3000 and 4000 Hz. In conclusion, temporary hearingloss was driven by noiseexposure, not exercise. However, persons who choose to exercise with personal headphones orin a noisy environment should be awareof potentialpremature hearingloss.
Key words: exercise, hearing, temporary threshold shift, cycling, risk
F
or years people have been exercising to music from stereo sound systems and personal headphones. While noise levels may vary, listening to music exceeding 75 decibels Sound Pressure Level (dB SPL) has been shown to result in temporary, and may lead to permanent, hearing loss (Rosen, 1970). Exercising to music, a popular activity, may contribute to hearing loss. Lindgren and Axelsson (1988) recently reported that moderate intensity exercise interacted unfavorably with simultaneous noise exposure, leaving subjectswith acute hearing loss at certain frequencies. Several studies have implicated cardiovascular adjustments (increased blood pressure and heart rate) and stress as causes of deleterious changes to the inner ear. Exercise is a stress that increases blood pressure and heart rate. In a brief research note, it was reported that exercising with personal headphones induced hearing loss (Navarro, 1990). It is not known if the headphone, the exercise, or both contributed to this hearing loss. Saxon and Dahle (1971) and Sanden and Axelsson (1981)
Helaine M. Alessio is anassistant professorinthe Department of Physical Education, Health andSport Studies at Miami University, Oxford, OH 45056. Kathleen M. Hutchinson is anassistant professor inthe Department of Communications at the same institution. Submitted: August 17, 1990 Revision accepted: August 14, 1991 ROES: December 1991
reported temporary hearing loss occurred when either heart rates or blood cholesterol levels were elevated. Axelsson, Vertes, and Miller (1981) concluded that decreased circulation in the stria vascularis resulted in temporary hearing loss, termed temporary threshold shifts (TIS). They suggested thatvasoconstriction in the ear may be associated with hemodynamic shifts that occur during exercise. Thus, a common underlying mechanism for hearing loss in these studies is thought to be a reduction of blood flow through the inner ear; however this has never been directly assessed in humans. If there is an interactive effect between noise exposure and exercise that can enhance the risk for hearing loss, then current popular modes of exercise accompanied by music via personal headphones may be contraindicated. Other forms of exercise and work performed simultaneously with noise or music may also be detrimental to hearing ability. The purpose of this study was to determine if hearing loss occurred as a result of (a) noise exposure, (b) exercise, or (c) exercise in combination with noise.
Method Subjects Subjects were 16 volunteers, 11 females and 5 males (M age = ~~ ± 8 years). Each subject was screened to determine normal hearing (~ 25 dB HL at octave intervals from 250 to 4000 Hertz [Hz]) on a portable pure-
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tone audiometer. All subjects indicated no previous history of middle ear disease or previous significant noise exposure. Subjects signed informed consent forms before testing began.
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Baseline Procedures V02max was determined using a graded exercise test on a Monark bicycle ergometer. Subjects began by pedaling at 50 rev-min" against a 1 kg resistance for 2 min. Thereafter, resistance was increased 0.5 kg every 2 min. Heart rate response and blood pressure were continuously monitored throughout the test on a Quinton QE 3000 ECG oscilloscope and a Quinton Model 410 automatic sphygmomanometer, respectively. Oxygen uptake was measured by the open-eircuit method using a low resistance, two-way breathing valve. The gas fractions were measured using an Amtek model S-3A/l oxygen analyzer and a CD-3A carbon dioxide analyzer. The analyzers and the Parkinson-Cowan CDAvolume meter were interfaced with an Apple lIe computer with Rayfield REP-0200 software programmed to calculate V02 (Lmirr' and ml- kg-l·min·l), ventilation, and respiratory exchange ratio. The respiratory and metabolic values were recorded at 30-8intervals during testing. The gas analyzers were calibrated (before and immediately following each test) using known standard gas mixtures. The max V02 test was considered valid ifat least three of the following criteriawere satisfied: VO zfailed to increase 100 ml- min? despite an increased workload, heart rate failed to increase or decreased despite an increased workload, respiratory exchange ratio> 1.0, heart rate was within 20 beats of age-predicted maximum heart rate, and subject could not continue pedaling at 50 rev-min". No test had to be terminated due to dyspnea, positive ECG recording, subject report ofangina, or any other abnormal exercise response. Once V02max on a bicycle ergometer was obtained it was then possible to calculate the workload that required 70% ofV02max (ACSM,1991).
Experin1entalProcedures Following the initial hearing screening and V0 2max determination, subjects participated in three experimental conditions each lasting 10 min, in a counterbalanced order: (a) noise exposure, (b) exercise at 70% of VO~ax, and (c) noise exposure and exercise at 70% of V02max on a bicycle ergometer. The experimental protocol was set up in the following way. Each subject reported to the laboratory and underwent baseline hearing, heart rate, blood pressure, and core temperature tests. The hearing test was conducted with a Beltone 2000 audiometer in a IAC doublewall audiometric booth calibrated to American National Standards Institute standards (ANSI, 1969). Pure-tone air conduction thresholds were determined for each ear,
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using the Hughson-Westlake method in 2 dB steps, at each session before and after each condition (Carhart & Jerger, 1959). Auditory thresholds were determined in 20-8intervals at each of the following frequencies: 0.5, 2, 2.5, 3, 3.5, 4, 6, 8 k Hz. Heart rate was measured on a portable Quinton 630A electrocardiograph. Blood pressurewas measured bya trained technician using a manual sphygmomanometer made by PyMaH Corp. Core temperature was measured using the First Temp thermometer manufactured by Intelligent Medical Supplies. This thermometer measures the temperature of the external auditory canal proximal to the tympanic membrane and converts this value to core temperature. All testing was supervised by an American Speech and Hearing Association certified audiologist. For Condition A, the subjects were seated and TDH-50 earphones were placed over the ears. A Y!I octave bandfiltered noise with a 2000 Hz center frequency at 104 dB SPL was continuouslyadministered to one ear for 10 min. Heart rate, blood pressure, and core temperature were recorded at 5-min intervals. After 10 min each subject completed a second hearing test. The subject exercised on a Monark bicycle ergometer in Condition 2, pedaling at 50 rev-min'! against a resistance that elicited 70% of V02maxfor 10 min. Heart rate was monitored during this submaximum exercise in order to confirm that each subject's calculated workload resulted in a heart rate similar to the heart rate at 70% of V02max from the VOzmax test. The mean difference in heart rates between the submax and max test (at 70% ofVOzmax) was 6.81 b-rnirr', which was less than 5%. Heart rate, blood pressure, and core temperature were recorded as before, and, when 10 min elapsed, another hearing test was administered. Following this hearing test, heart rate, blood pressure, and core temperature were monitored, and when they returned to normal, subjects were prepared for the next condition. In the third condition, the subject performed the same exercise regimen with earphones on. Noise was administered to the opposite ear (vis a vis the first condition), and blood pressure, heart rate, and core temperature were recorded. Ten min later another hearing test was completed. Following each experimental condition, pure-tone threshold determination started at 2000 Hz 1 min after cessation of noise and/or exercise and continued in 20s intervals. Therefore, the posttesting latency for the test frequencies were 1.0 min for 2 kHz, 1.3 min for 2.5 kHz, 1.6 min for 3.0 kHz, 2 min for 3.5 kHz, 2.3 min for 4 k Hz, 2.6 min for 6 kHz, 3 min for 8 k Hz, and 3.3 min for 500 Hz. All three conditionswere conducted on the same day. Subjects returned to the clinic 24--48 hours following this test to determine if any changes in TTS or hearing loss induced by the experiment persisted. Analysis of variance (ANOVA) with repeated measures was used to evaluate the subjects' TTS in the noiseonly, exercise-only, and noise-and-exercise conditions.
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The three-way design (3 Conditions x 8 Frequencies x 2 Occasions) had repeated measures on each factor. The sphericity assumption was tested where appropriate. Adjusted probabilities are reported where necessary. Post-hoc comparisonswere conducted with the NewmanKeuls procedure.
Results
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Table 1 summarizes the characteristics of the subjects, including age, resting hemodynamic, thermal, and maximal values for oxygen consumption, and heart rate. Workloads at 70% of VOzmax were calculated from actual VOzmax values and averaged 111±1 0 Watts on the bicycle ergometer.
Audiometric Measures TIS was defined as the difference in pure-tone threshold values measured in dB between pre- and postexperimental conditions at the eight frequencies previously listed. Threshold data are reported for the subjects before and after each experimental condition of noiseonly, exercise-only, and noise-and-exercise. Mean values in decibels (dB) are shown in Table 2 for each test frequency. Effect size (Thomas & French, 1986) for noise-only, exercise-only, and noise-and-exercise are also reported here. Whenever noise was present, hearing loss occurred at all but one frequency. This is indicated by effect sizes showing that the average subject exposed to noise had a TTS value that was at least one standard deviation higher than pre-noise TTS. In the exercise-only condition, effect sizes were negligible (range = -0.05-0.28) indicating that by itself, exercise did not influence hearing ability. In general, TIS values were greatestat 3000 to 4000 Hz for the two conditions with noise. Exercise-only, on the other hand, resulted in little or negative TIS (Figure 1). Even though the ITS values had relatively large standard deviations, each condition revealed normal distributions. Tabla I. Age,resting hemodynamic, coretemperature, VOzmax, andheartrate max for all subjects, N = 16
Age(years) Systolic Blood Pressure (mm Hg) Diastolic Blood Pressure (mm Hg) Heart Rate (b·min·') MeanArterial Pressure (mm Hg) Pulse Pressure (mm Hg) Core Temperature (CO) VO zmax (ml.kg·'·min·') HeartRate max (b-mirr']
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M
SO
33.0 114.4
8.2 11.5 6.3 11.7 7.6 7.4 0.6 5.3 11.3
67.9 75.6 83.4 46.4 37.0 34.8 175.6
Using the repeated measure ANOVA, significant main effects of experimental condition F (2,709) = 5.84, p « .05andfrequencyF (7,709) = 8.54,p< .05 were found. Adjusted probability levels from Greenhouse-Geisser analysis did not change the results. Follow-up tests were interpreted to indicate that the two experimental conditions with noise had significantly higher TISs at most frequencies compared to the exercise-only condition. However, there were no differences between the noiseonly and noise-and-exercise conditions at all frequencies. When subjects were retested (24-48 hours), all hearing measures returned to normal. An evaluation of the test-retest reliability of the hearing measurement research methodology was conducted with the initial baseline levels of two experimental conditions (noiseonly and exercise-only). Each subject's initial threshold level in dB was compared to his/her baseline threshold level obtained in each condition. A Pearson product moment correlation of.72 was obtained and was interpreted as an indication of good test-retest reliability.
Cardiovascular andTemperature Measures Cardiovascular responses to the three conditions(a) noise-only, (b) exercise-only, and (c) noise-and-exercise-included the following: systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), pulse pressure (PP), and heart rate (HR). A three-way ANOVA (Condition x Subject x Measurement time) was used for all cardiovascular and thermal responses. Newman-Keul's post-hoc tests were used to compare the means where significant F-ratios occurred and indicated that no differences in cardiovascular measures occurred between the noise-only and exercise-and-noise conditions. The sphericity assumption was evaluated for each measure, and adjusted probability levels were used. During 10 min of noise-only, cardiovascular responses did not change from resting levels. During exercise-only SBP, DBP, MAP, PP, and HR increased 40, 9, 23, 85 and 90%, respectively, above rest (P < .05). Similar cardiovascular responses occurred during the noise-and-exercise condition; however, NewmanKeul's post-hoc tests revealed no differences between the two different exercise conditions. Therefore, the addition ofnoise to moderate intensity exercise did not have an additive effect on cardiovascular responses compared to exercise-only. Core temperature did not change during the noise-onlycondition but increased approximately 1.6% above rest (p> .05) for both exercise-only and exercise-and-noise conditions.
Discussion Hearing loss was indicated by TIS measured at eight different frequencies following three conditions:
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(a) noise-only, (b) exercise-only, and (c) noise-and-exercise. Following the noise-only and noise-and-exercise conditions, audiometric tests indicated that significant TTS occurred in all subjects. TIS was measured by an audiometric clinical assessment that quantifies hearing loss. In both noise conditions TIS occurred at all frequencies, however, not to a similar extent in each one. Temporary hearing loss occurred, but within 48 hours following the noise-and-exercise conditions hearing ability returned to normal in all subjects as evidenced by TIS that were negligible at all frequencies. Mechanisms responsible for permanent hearing loss from acoustic stimulation include changes in the hair cell pattern of the organ of Corti, Corti's organ becoming loose from the basilar membrane, rupture ofthe HensonDieters cell junctions, mechanical damage to the cochlea, and loss of hair cells (Hawkins, 1971). These changes have been shown in animal models that demonstrate permanentelevation ofhearing thresholds orTIS. In humans, loud noise causes a number of reactions which cannot be controlled, including vasoconstriction, a surge of epinephrine in the bloodstream, tension of both voluntary and involuntary muscles, and an increase in diastolic blood pressure (Rosen, 1970). These reactions may contribute to premature hearing loss, but a direct cause-and-effect relationship has not been established. Temporary changes in hearing ability are usually caused by fatigue in nuclei of the central auditory pathways, reduced activity of the primary afferent neurons, decrease in oxygen tension in the cochlear endolymph, and localvasoconstriction, especially ofthe striavascularis
(Axelsson et al., 1981). TIS does not normally result in permanent hearing loss, and recovery of TIS has been reported to occur as vasoconstriction diminishes and normal blood flow in the ear canals and capillary networks is reestablished. It is not known, however, if repeated TIS may induce permanent threshold elevation and subsequent premature hearing loss. The effects of cardiovascular response on TIS have been examined by Saxon and Dahle (1971) and Rosen (1970). Although they reported that a high heart rate did not directly cause hearing loss, changes in heart rate were associated with variations in sensitivity to sensory stimuli. For example, TIS was reported to be significantly affected under conditions of induced higher heart rates. Lindgren and Axelsson (1988) used 10 min of bicycle exercise at 40% ofV02max to raise heart rate and measured TIS before and after exercise with and without noise accompaniment, Their results supported those of Saxon and Dahle (1971) and Rosen (1970) that higher than resting-level heart rates were associated with TIS. Results of the present study did not concur with those of Saxon and Dahle (1971), Rosen (1970), and Lindgren and Axelsson (1988). The increased heart rate concomitant with 10 min of exercise at 70% ofV02max did not result in higher TIS compared to resting levels. Furthermore, when combined with noise, exercise did not result in greater TIS compared to noise-only. In fact, compared to the noise-only condition,TIS tended to decrease slightly in half ofthe frequencies when exercise was performed with noise. No TTS changes occurred after 10 min ofexercise only. TIS values following noiseand-exercise compared to noise-only were not signifi-
Tabl.2. Mean puretone thresholdvalues indecibels (dB), standard deviations (in parentheses), and effect sizes fortest frequencies beforeand after each experimental condition
Exercise
Noise Frequency (Hz)
Pre (dB)
Post (dB)
2000
6 (6) 5.5 (8.15) 4.6 (6.76) 5 (7.38) 6.19 (6.75) 9.12 (7.97) 8.12 (6.34) 5.25 (5.11)
14.1* (8.0) 16.9* (8.79) 16* (8.6) 16.75* (5.36) 19.63* (6.86) 22.38* (6.42) 18.75* (6.32) 8.0 (6.53)
2500 3000 3500 4000 6000 8000 500
Effect Size
Pre (dB)
1.35
6.13 (5.48) 5.25 (7.93) 5.12 (8.42) 6.25 (8.38) 7.25 (6.49) 6.88 (6.77) 9.5 (7.95) 5.31 (5.171
1.40 1.69 1.59 1.69 1.66 1.68 0.54
Post (dB) 7.38 (5.64) 5.12 (7.15) 5.5 (7.91) 8.63 (8.79) 7.0 (8.23) 8.0 (7.26) 9.12 (6.32) 5.5 (3.89)
Noise and Exercise Effect Size
Pre (dB)
0.23
6.0 6.15 4.5 7.39 6.12 7.88 7.75 7.62 5.25 5.97 8.12 5.08 8.37 4.80 5.37 4.54
-0.02 0.05 0.28 -0.04 0.17 -0.05 0.04
Post(dB) 14.75* 7.47 15.75* 8.45 21.31* 13.02 21.43* 12.24 17.88* 6.08 19.63* 7.87 16.5 * 9.53 9.63 9.13
Effect Size 1.42 1.52 1.93 1.80 2.12 2.27 1.69 0.94
Note. Hz =Hertz; Pre =precondition threshold, Post =postcondition threshold. *Pre-Postvalues differ significantly (p < .05). 416
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cantly different, however, so exercise cannot be said to protect the ear during noise exposure. Nevertheless, TIS that occurred in this studywas noise-related, not exercisedriven. The present study can provide additional insight on the results and speculations made by Lindgren and Axelsson (1988). Both studies included 10 min ofcycling, but the present study used a 70% of V0 2max intensity instead of 40% ofV02max. Ten min ofexercise at either 40 or 70% ofV02max was sufficient time to demonstrate increases in heart rate and blood pressure. Although 10 min is not long, this duration was chosen to expand on research by Lindgren and Axelsson (1988) and challenge their conclusions that 10 min ofmoderate intensity exercise caused temporary hearing loss. It is not known if longer exercise times would affect hearing ability; this should be investigated in future experiments. Noise exposure at 104 dB was administered via personal headphones in both studies. Some methodological differences between the two studies exist that may partly explain the differentresults. First, Lindgren andAxelsson (1988) did not utilize a maximal bicycle ergometer test; instead they predicted V02max from a submaximal test and from this predicted value, a 40% ofV0 2maxworkload
was calculated. Inherently, an estimated V0 2max will result in lar~e variability when predicting submaximal workloads (Astrand & Rodahl, 1977; Powers & Howley, 1990). Also, an exercise intensity of 40% ofV02max may not be sufficient to increase catecholamine secretion to an extent that vasoconstriction would occur (Fox, Bowers, & Foss, 1988; Rowell, 1974). In fact when low levels of epinephrine or norepinephrine are secreted into the blood, the action on beta receptors of cell membranes usually causes vasodilation (Gillman, Goodman, & Gillman, 1980). Therefore, it is unlikely that a 40% of V02maxworkload performed for 1omin caused vasoconstriction. Whether the higherworkload used in the present study (i.e., 70% of V0 2max) caused vasoconstriction, especially in blood vessels of the inner ear, is not known. That TTS did not occur following the exercise-only condition suggests vascular changes associated with exercise were not responsible for hearing loss. A second difference was that core temperature was reported in the present study by measuring the temperature of the external auditory canal proximal to the tympanic membrane. Lindgren and Axelsson (1988) did not measure temperature despite their speculation that an elevated temperature may have caused TIS. This
Figure 1.Temporary threshold shifts indicating the degree of hearing loss in fourfrequencies following noise-only, exercise-only, and noise-and-exercise.
8,000
N
6,000
:-
r; c CD ::I l:r CD
..
Yo
4,000
iii Noise-Exercise
o
Exerci..
•
Noise
2,000
5
10
15
20
Decibels
*Hearing loss intheexercise-only group isnegligible and less than hearing loss in both noise-only and noise-and-exercise groups (p < .051.
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contention is doubtful; in the present study TIS did not occur in the exercise-only condition even though core temperature increased above rest. The psychophysical method for determining auditory threshold can also cause differences in obtained TIS values. Using the modified method of limits, commonly known as the Bekesy method (Bekesy, 1947), variations in TIS can be caused by repetition rate of the signal, duration of the pulses (vis avis continuous tones), signal bandwidth, rate of attenuation change, and instructions to the patient. Lindgren and Axelsson (1988) established hearing thresholds with the Bekesy method. The present studyutilized conventional methods ofclinical pure tone audiometry to determine the intensity required for positive responses at least 50% of the time. Although the reliability of both audiometric methods has been found to be of the same order at all frequencies (Burns & Hinchcliffe, 1975), the method used in the present study has been shown to decrease variations in threshold values due to subject and technician performances (Carhart & Jerger, 1959). Contrary to expectations, exercise and noise did not contribute to TIS in an additive manner. This was an unexpected finding because both noise and exercise are normally perceived as stressors, capable of releasing catecholamines that raise blood pressure and temperature and vasoconstrict certain blood vessels (Buczynski & Kedziora, 1983; Dengerink, Dengerink, & Chermak, 1982; Talbott et al., 1985). The subjects in this study were healthy but not highly trained. Their hemodynamic and thermal responses to both exercise conditionswere found to be normal in this study. Blood pressure, heart rate, and core temperature all increased during exercise at 70% of V0 2max and returned to resting levels within 5 min on recovery. Addition ofnoise to exercise resulted in similar blood pressure and core temperature responses. There is evidence that physically fit individuals exhibit less threshold shift and recover quicker from TTS because of increased amounts of oxidative enzymes to support the function of the stria vascularis (Ismail et al., 1973). However, a protective fitness level has not been quantified, and the interaction of exercise intensity and duration on hearing loss needs to be further researched.
Conclusions In summary, the cardiovascular responses to 70% of exercise were as expected: statistically significant increases at 5 and 10 min during exercise. Neither noise by itselfnor simultaneous with exercise influenced cardiovascular and core temperature measures. These results indicate that ifnoise was perceived as a stress, it did not stimulate hemodynamic or thermal responses to the extent that blood pressure, heart rate, or core tempera-
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ture were affected. The addition of noise to exercise in this study resulted in physiological changes localized in the ear only as reported by changes in TIS byaudiometric measurements. It is concluded that the risk ofhearing loss is driven by noise exposure, not exercise. Further research may elucidate long-term effects of exercising with personal headphones on hearing.
References American College of Sports Medicine. (1991). Guidelines for exercise testingand prescription (4th ed., pp. 24-29).Philadelphia: Lea and Febiger. American National Standards Institute. (1969). American nationalstandanlsspecificationsforaudiomeurs. NewYork: ANSI. Astrand, P.O., & Rodahl, K. (1977). Textbook ofwork physiowgy. (pp. 404-410). Oxford: McGraw-Hill. Axelsson, A., Vertes, D., & Miller,]. (1981). Immediate noise effects on cochlear vasculature in the guinea pig. Acta Otolaryngology, 91,237-246. Bekesy, G. (1947). A new audiometer. Acta Otolaryngowgy, 35, 411-422. Buczynski A., & Kedziora J. (1983). The effect of acoustic stimulus of different continuity patterns on plasma concentration catecholamines in humans during submaximal exercise. ACTA PhysiologicalPolandica, 34,5-6, 59!H)()(). Burns, W., & Hinchcliffe, R. (1975). Comparison of auditory threshold asmeasured byindividual pure tone and Bekesy audiometry. Journal of the AcousticalSociety ofAmerica, 29, 1274-1277. Carhart, R., & Jerger,J. F. (1959). Preferred method for clinical determination of pure-tone thresholds. Journal of Speech and HearingDisorders, 24, 330-345. Dengerink,]. E., Dengerink, H. A., & Chermak, G. D. (1982). Personality and vascular responses as predictors of temporary threshold shifts after noise exposure. Ear and Hearing, 3(4),196-201. Fox, E. L., Bowers,R. W., & Foss,M. L (1988). Thephysiowgical basis ofphysicaleducationand athletics (4th ed., pp. 620-621). NewYork: W. B. Saunders. Gillman, A. G., Goodman, L S., & Gillman, A. (1980). The pharmacowgical basis of therapeutics (6th ed., pp. 144-150). New York: McMillan. Hawkins,]. E. (1971). The role of vasoconstriction in noiseinduced hearing loss. Annal5 ofOtology, 80, 904-913. Ismail, A. I., Corrigan, D. L., MacLeod, D. F., Anderson, V. L., Kasten,R. N., & Elliott, P. W. (1973). Biophysiologicaland audiological variables in adults. Archivesof Otolaryngowgy, 97, 447-451. Lindgren, F., & Axelsson, A. (1988). The influence of physical exercise on susceptibility to noise-induced temporary threshold shifL ScandinavianAudiology, 17, 11-17. Navarro,R. (1990).Sports scan. ThePhysicianandSportsmedicine, 18(6),16. Powers, S. K., & Howley, E. T. (1990). Exercise physiology: Theory and application to fitness and performance (pp. 270-275). Dubuque, IA: Wm. C. Brown. Rosen, S. (1970). Noise, hearing, and cardiovascular function.
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Thomas,j. R., & French, K. E. (1986). The use ofmeta-analysis in exercise and sport: A tutorial. Research Qy.arterly for Exercise and sport. 57, 196-204.
Authors" Notes The authors acknowledge assistance from Melissa Spadafore, Robin Adair, and Michael Hughes in this study. The study was supported by grants from the Division of Arts and Science and Education and Allied Professions at Miami University.
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In B. 1.. Welch and A S. Welch (Eds.) , Physiological effects of noise (pp, 57-66). New York: Plenum Press. Rowell, L. (1974). Human cardiovascular adjustments to exercise and thermal stress. PhysiologicalReuiews, 54, 75-159. Sanden, A., & Axelsson, A. (1981). Comparison ofcardiovascularresponses in noise-resistantand noise-sensitive workers. Acta Otolaryngology, 337, 75-100. Saxon, S. A., & Dahle, A j. (1971). Auditory threshold variations during periods of induced high and low heart rates. Psychophysiology, 8(1), 23-29. Talbott, E., Helmkamp.j., Matthews, K., Kuller, L., Cottington, E., & Redmond, G. (1985). Occupational noise exposure, noise-induced hearing loss, and the epidemiology ofhigh blood pressure. AmericanJournal ofEpidemiology, 121(4), 501-514.
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