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Muscle pain during exercise in normotensive african american women: effect of parental hypertension history
Muscle Pain During Exercise in Normotensive African American Women: Effect of Parental Hypertension History Dane B. Cook,*,† Erica M. Jackson,‡ Patrick J. O’Connor,§ and Rod K. Dishman§ Abstract: The purpose of the present investigation was to determine the influence of parental hypertension history on leg muscle pain ratings during cycling exercise in African American women. Eighteen women (age, 19 ⴞ 2 years) with a positive family history (ⴙPH) of hypertension and 16 (age, 19 ⴞ 1 years) with a negative family history (ⴚPH) underwent maximal exercise and cold pressor testing. Maximal exercise was conducted on a cycle ergometer. Quadriceps muscle pain intensity ratings were obtained each minute during the maximal exercise test by using a category-ratio scale. The hand cold pressor test was used to determine cardiovascular reactivity. Repeated measures analysis of variance showed significantly lower pain ratings during exercise for the ⴙPH group compared to the ⴚPH group. Psychophysical power functions indicated that the ⴙPH participants had significantly lower exponents for pain throughout exercise. Systolic blood pressure reactivity did not significantly predict pain ratings during exercise. Normotensive African American women with ⴙPH of hypertension experienced less muscle pain during exercise compared to normotensive African American women with a ⴚPH of hypertension. The results are consistent with data demonstrating reduced sensitivity to experimental pain stimuli in individuals at risk for developing hypertension and extend them to naturally occurring muscle pain produced by exercise. Perspective: African American women, a sedentary group with an elevated risk for developing hypertension and chronic pain, show the same negative relationship between ⴙPH and pain perception as men, suggesting that central nervous system mechanisms of pain modulation are more related to family history than gender. Acute exercise provides an experimental model for manipulating naturally occurring pain in studies concerned with the association between pain and hypertension. © 2004 by the American Pain Society Key words: Blood pressure, cycle ergometry, psychophysics, pain sensitivity, race.
A
n interaction between cardiovascular and pain regulatory systems has long been recognized.54 Both clinical hypertension and elevated blood pressure within the normotensive range are associated with decreased pain ratings to various experimental stimuli including noxious cold, heat, electrical stimulation, and mechanical pressure.10,17,31,32,35,45,51,63 Reduced pain ratings also have been observed in normotensive individuals at increased risk for the development of hypertension, by virtue of their having at least 1 parent with confirmed hypertension.3,17,25,26,29,58 It has been argued that decreased pain sensitivity to experimental pain stimuli in normotensive individuals at in-
Received July 25, 2003; Revised November 12, 2003; Accepted December 11, 2003. From the *Department of Radiology, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, †War Related Illness and Injury Study Center (WRIISC), Veterans Administration Medical Center, East Orange, New Jersey, ‡Department of Health and Human Performance, Auburn University, Auburn, Alabama, USA, and §Department of Exercise Science, University of Georgia, Athens, Georgia, USA. Address reprint requests to Dane B. Cook, PhD, War Related Illness and Injury Study Center (WRIISC), VA Medical Center, 385 Tremont Avenue (129), East Orange, NJ 07018. E-mail: [email protected] 1526-5900/$30.00 © 2004 by the American Pain Society doi:10.1016/j.jpain.2003.12.002
creased risk for hypertension might reflect a pathophysiological process that results in dysregulation of central nervous system processes involved in both pain control and cardiovascular regulation, and that hypoalgesia might be a method used to identify individuals at risk for developing hypertension.26,28,30,51 African Americans report more acute pain symptoms, experience painful symptoms differently (eg, more distress and lower physical function), and are more sensitive to experimentally induced pain than non-Hispanic white Americans.16,22,23,44,56 They also have a significantly greater risk of developing hypertension and are less physically active than non-Hispanic white Americans.6,33,61,62 The high occurrence of pain symptoms and the prevalence of hypertension in this group are at odds with the established negative relationship between familial risk for hypertension and pain sensitivity and highlight the need for additional research determining whether this relationship generalizes to African Americans. Moreover, exercise and a physically active lifestyle are known to reduce the risk of the development of hypertension,1,2 whereas pain is perceived as one of the barriers to adopting a physically active lifestyle.34,50 Therefore, determining how pain during exercise is perceived in African Americans at risk for developing hyper-
The Journal of Pain, Vol 5, No 2 (March), 2004: pp 111-118
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112 tension has relevance for understanding issues pertaining to exercise adherence and prescription. The effects of parental hypertension history on pain perception by using experimentally induced pain stimuli have been assessed primarily in men. These studies consistently have shown that a positive family history of hypertension is associated with decreased pain sensitivity to experimental pain stimuli.3,17,26 More recent studies in women have been equivocal and further highlight the need for more research examining pain in women with and without a family history of hypertension.4,5,15 To date, the experience of muscle pain during exercise has not been studied among African American women, a group with relatively greater risk for developing hypertension6,33 and who report more pain symptoms.23,44 Muscle pain is experienced during moderate and high intensity exercise. Studies describing this phenomenon have shown that muscle pain intensity ratings increase as a positively accelerating function of exercise intensity.9,12-14,36 Early investigation into potential mechanisms indicated that muscle pain during exercise resulted from the accumulation of a noxious metabolite, termed factor P, and that this metabolite was related to changes in the blood flow and contractile characteristics of the muscle that occur with increasing exercise intensity.18,40,41,53 More recently, attempts to manipulate naturally occurring muscle pain pharmacologically have shown no effect of aspirin on leg muscle pain ratings and no effect of the opioid agonist codeine or the opioid antagonist naltrexone on forearm muscle pain ratings.9,12,14 These results suggest that prostaglandins are not the sole algesic substance responsible for initiation of an afferent nociceptive signal, and that naturally occurring muscle pain perceptions are not moderated by opioids. More research is needed to learn what causes and moderates naturally occurring muscle pain. Recent work suggests that adenosine plays a role in exercise-induced muscle pain.48 Another potential moderator could be the pathophysiological processes that underlie the development of hypertension. Furthermore, it is not known whether the relationship between pain sensitivity and risk for hypertension generalizes to naturally occurring muscle pain such as occurs with exercise. The primary purpose of the present investigation was to examine leg muscle pain produced during cycling exercise in African American women with or without a positive family history of hypertension. In addition, cardiovascular reactivity to stressors has been shown to be an independent risk factor for the development of hypertension42,46 and has been associated with decreased sensitivity to experimental pain stimuli.21,54 Therefore, to determine the relationship between parental hypertension history and pain more clearly, we examined the association between cardiovascular reactivity to a cold pressor stimulus on leg muscle pain ratings during exercise. On the basis of previous research examining pain among individuals at increased risk for hypertension, we hypothesized that African American women with a positive family history of hypertension would rate leg muscle pain during exercise as less intense than those women
Muscle Pain & Family History of Hypertension without a positive family history. Furthermore, it was hypothesized that increased cardiovascular reactivity to the cold pressor test would significantly predict lower exercise-induced leg muscle pain ratings.
Materials and Methods Participants African American women from a university population were recruited if they were healthy, at least 18 years of age, eumenorrheic, and the blood pressure status of their parents could be verified. This study was part of a larger research project that focused on the relationship between cardiorespiratory fitness and hypertension risk in African American women.37 Therefore, the sample was limited to African American women with or without positive parental hypertension history. Thirty-five eligible women volunteered and completed the study. Because of technical difficulties, one subject’s exercise data were not usable; therefore, this subject could not be included in subsequent analyses. The final sample included 18 women with a parental history of hypertension (⫹PH) and 16 women without a parental history of hypertension (⫺PH).1 All women were nonsmokers who reported no cardiovascular disease, psychologic disorders, or other major illnesses. All participants were normotensive (mean ⫾ standard deviation, 110.1 ⫾ 6.7/70.5 ⫾ 6.3 mm Hg), and 4 ⫹PH and 5 ⫺PH women reported using oral contraceptives. Participants read and signed an Institutional Review Board approved consent form that explained the risks and benefits associated with participation in the study. Parental hypertension was defined as having at least 1 parent who was physician-diagnosed with hypertension. Participants reported the hypertension status of their parents, and parents were contacted for verification. Parents were mailed information about the study along with a health history form. They were asked to provide a blood pressure reading taken within the past 3 months and to report whether they had ever been physiciandiagnosed with hypertension. Parents who had been diagnosed with hypertension were also asked to provide their age at diagnosis, length of diagnosis, and type of antihypertensive medications.
Cold Pressor Test and Physiological Measures The hand cold pressor test was used to examine cardiovascular reactivity. The test involved the participant placing her right hand to the level of the wrist in a bucket of water maintained at 0°C to 3°C for 2 minutes. Heart rate and blood pressure were measured continuously during the test from the left middle finger by using an Ohmeda Finapres Model 2300 blood pressure monitor (Ohmeda Monitoring Systems, Englewood, Colo). The hand rested at heart level, and participants were instructed to keep the hand still during the cold pressor test. Data from the Finapres for systolic pressure, diastolic pressure, mean arterial pressure, and heart rate were recorded on a beat to beat basis and stored by using Data Acquisition Sys-
ORIGINAL REPORT/Cook et al tems DATAQ version 3.50 (TJS Software, Durham, NC). Five participants, 1 ⫺PH and 4 ⫹PH, voluntarily withdrew from the study for personal reasons before the completion of the reactivity assessment. Therefore, cardiovascular reactivity analyses were completed on 30 participants.
Maximal Exercise Test The testing procedures for maximal exercise testing were explained, and participants were given instructions for reporting ratings of quadriceps muscle pain.12,13 Participants were then fitted with a heart rate monitor, mouth piece, and nose clip. Exercise was performed on an electronically braked cycle ergometer (Minjhardt model KEM-3, Utrecht, The Netherlands), and a ramped protocol was used. After a 4-minute warm-up at 25 W, the resistance increased to 50 W and then increased at a rate of 24 W per minute until participants reached volitional exhaustion. Metabolic variables, including oxygen consumption, carbon dioxide production, and ventilation, were measured continuously by using a Sensormedics Model 2900 metabolic cart (SensorMedics Corporation, Yorba Linda, CA) that had been calibrated with standard gases. Heart rate and quadriceps muscle pain ratings were obtained each minute of the test. Peak oxygen uptake was defined as the highest attained oxygen consumption when at least 2 of the following criteria were met: a heart rate within 90% of the age-predicted maximal, a respiratory exchange ratio above 1.1, and a perceived exertion value of 18 or greater. An individual certified in cardiopulmonary resuscitation was present during all testing sessions. At the end of the test, peak values for power output, oxygen consumption, heart rate, and leg muscle pain intensity were recorded.
Leg Muscle Pain Ratings Before the maximal exercise test, participants were read standard instructions12,13 while viewing the pain rating scale. Quadriceps muscle pain intensity ratings were obtained during the maximal exercise test by using a 0 to 10 category-ratio scale (0, no pain; 10, extremely intense, almost unbearable pain). The scale included an open end point that permitted participants to give a rating higher than 10 but proportional to 10 (eg, 20 being twice as intense as 10), if leg muscle pain became more intense after a 10 was reported. Participants were instructed to focus on leg muscle pain only in the quadriceps and to use the verbal anchors to aid in selecting a numeric rating. Scores for category-ratio–10 scales have been shown to be valid and reliable measures of pain during exercise and have been shown to have ratio-scaling properties for the creation of psychophysical curve estimates.8,12,13,36,49
Procedures Before maximal exercise testing, participants completed a medical and physical activity history form. Measurements of height, weight, and resting brachial blood pressure were also obtained. After completing the max-
113 imal exercise test, participants completed the physical activity (7-day recall interview7) and were given instructions for charting their menstrual cycle so that the stress reactivity session was conducted during the same menstrual phase for all participants. The stress reactivity session was conducted during the follicular phase (typically days 5 to 13) of the menstrual cycle for participants, and the session took place in early afternoon, between 2:30 and 4:30 PM.
Statistical Analysis Analyses for parental hypertension history and cardiovascular reactivity were performed separately. For parental hypertension history, group differences for participant characteristics and peak values in response to the exercise test were assessed by using independent samples t tests. Cohen’s d effect sizes were also calculated to assess the differences in select participant characteristics and peak responses.11 Submaximal intensities of 50%, 70%, and 90% of peak power output were calculated for each participant. Muscle pain rating values that corresponded with the 3 submaximal intensities were used in the analyses. Group differences for muscle pain ratings during exercise were assessed by using a group (⫹PH vs ⫺PH) by exercise intensity (50%, 70%, and 90%) repeated measures analysis of variance. Greenhouse-Geisser adjustments for degrees of freedom were used when Mauchly test of sphericity was significant (P ⬍ .05). Preliminary descriptive statistics based on self-report indicated that the groups differed on menstrual cycle status on the day of exercise. For the ⫹PH group, 1 participant was in the follicular phase, 10 were in the luteal phase, 3 were on period, and 4 were on oral contraceptives. For the ⫺PH group, 5 were in the follicular phase, 5 were in the luteal phase, 2 were on period, and 5 were on oral contraceptives. Analysis of covariance with menstrual phase entered as a covariate did not influence the results. Examination of follicular versus luteal phase, independent of group, revealed no significant differences in pain ratings or peak pain responses. Power functions for each subject’s complete exercise test were determined by linear regression of log transformed (log10) muscle pain versus log transformed exercise intensity. This allowed for the examination of a greater range of exercise intensities and assessment of complete tests (ie, all exercise intensities for which a rating was present) for all participants. Single sample t tests were performed to examine whether the group-averaged exponents were significantly different than a linear value of 1. Independent samples t tests were used to examine group differences in the regression derived exponents. For cardiovascular reactivity we examined systolic blood pressure responses to the cold pressor test and used linear regression to determine the influence of blood pressure reactivity on pain during exercise after controlling for fitness and family history. We examined the influence of systolic blood pressure reactivity on both the peak pain responses and the log transformed (log10) slopes of pain ratings throughout exercise. All statistical
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Table 1.
Participant Characteristics Based on Parental Hypertension History Status (Mean ⴞ Standard Deviation) ⫹PH (N ⫽ 18)
⫺PH (N ⫽ 16)
EFFECT SIZE
VARIABLE
D
P VALUE
Physical characteristics Age (y) Height (cm) Weight (kg) Body mass index Physical activity (kcal · kg⫺1 · day⫺1) Resting SBP (mm Hg) Resting DBP (mm Hg) Resting MAP (mm Hg)
19.3 ⫾ 1.4 164.5 ⫾ 5.8 61.5 ⫾ 15.7 22.6 ⫾ 4.9 38.2 ⫾ 3.0 111 ⫾ 8.2 72 ⫾ 6.1 85 ⫾ 6.0
18.7 ⫾ 0.8 166.8 ⫾ 5.0 67.3 ⫾ 17.3 24.1 ⫾ 5.3 39.1 ⫾ 2.9 109 ⫾ 4.5 68 ⫾ 5.6 82 ⫾ 4.2
.51 ⫺.42 ⫺.35 ⫺.29 .30 .29 .62 .57
.14 .23 .31 .40 .40 .31 .06 .07
DBP, diastolic blood pressure; ⫺PH, negative parental hypertension history; ⫹PH, positive parental hypertension history; MAP, mean arterial pressure; SBP, systolic blood pressure.
analyses were performed with SPSS Windows version 10.0 software (SPSS, Inc, Chicago, Ill).
Results Parental Hypertension History Parents of the participants were diagnosed at a mean age of 38.6 ⫾ 7.5 years, with a range of 24 to 49 years. Blood pressure was normalized (130 ⫾ 10/82 ⫾ 9.1 mm Hg) in all but 1 hypertensive parent (180/93 mm Hg), who was noncompliant with medication. Parents of ⫺PH participants had an average blood pressure of 121.7 ⫾ 6.1/ 73.8 ⫾ 8.5 mm Hg. Means and standard deviations for participant characteristics based on parental hypertension history status are presented in Table 1. No significant differences in physical characteristics were observed. Peak responses to exercise are summarized in Table 2. There were no significant differences between groups for any of the peak variables measured. Leg muscle pain ratings for both groups are presented in Figure 1. Repeated measures analysis of variance indicated a significant main effect of exercise intensity on leg muscle pain ratings during exercise (F1.4,45 ⫽ 82.9, P ⬍ .001) as well as a significant group-by-exercise intensity interaction (F1.4,45 ⫽ 4.5, P ⫽ .027). The interaction is
characterized by smaller increases in pain for the ⫹PH group than for the ⫺PH group. Exponents for the calculated power functions for leg muscle pain are presented in Table 2. Participants in the ⫹PH group had significantly lower exponents for muscle pain (P ⱕ .05). For both groups the exponent for pain was significantly greater (P ⱕ .05) than a linear value of 1, indicating a positively accelerating function. Thus, leg muscle pain ratings for the ⫹PH group increased at a slower rate throughout exercise compared to the ⫺PH group.
Cardiovascular Reactivity to Cold Pressor The average increase in systolic blood pressure for all participants was 16.6 (⫾19.9) mm Hg. After controlling for family history of hypertension status and cardiorespiratory fitness, linear regression indicated no association between systolic blood pressure reactivity and either the peak pain experienced during exercise (F1,27 ⫽ 0.47, P ⫽ .49) or the log transformed (log10) slopes of pain ratings (F1,25 ⫽ 0.14, P ⫽ .71).
Discussion
African American women with a ⫹PH of hypertension reported less muscle pain during high intensity exercise
Peak Measures During Maximal Exercise and Power Functions for Leg Muscle Pain (log10 Transformed Values and Regression Exponents) Based on Parental History Status (Mean ⴞ Standard Deviation)
Table 2.
VARIABLE Power output (W) Heart rate (bpm) Peak oxygen consumption (mL · kg · min⫺1) Pain intensity Perceived exertion Muscle pain exponent *Significant group effect, P ⬍ .05. ‡ Exponent significantly different than 1, P ⬍ .05.
⫹PH (N ⫽ 18)
⫺PH (N ⫽ 16)
EFFECT SIZE D
P VALUE
187 ⫾ 24 175 ⫾ 10.0 28.8 ⫾ 4.7
202 ⫾ 23 178 ⫾ 12 29.7 ⫾ 5.4
⫺.63 ⫺.27 ⫺.17
.08 .38 .58
5.6 ⫾ 2.8 17.7 ⫾ 2.0 1.7*‡
6.1 ⫾ 3.2 17.8 ⫾ 2.0 2.3‡
⫺.17 ⫺.05 ⫺0.8
.64 .89
ORIGINAL REPORT/Cook et al expressed relative to their peak exercise capacity, and they had significantly lower exponents for pain throughout the exercise test. The results are consistent with previous research demonstrating decreased pain sensitivity in offspring with positive parental hypertension history.3 The results are novel because they extend those findings to African American women, a group with greater risk for developing hypertension than non-Hispanic white Americans and who are more sensitive to pain and have more pain complaints than African American men and non-Hispanic white men and women.17,22,23,25,26,29,56-58 These data also demonstrate that naturally occurring leg muscle pain produced by exercise shows similar effects to other types of experimentally induced pain. Cardiovascular reactivity to the cold pressor was not independently associated with decreased muscle pain sensitivity during the exercise test. Our results demonstrating decreased pain sensitivity during exercise in normotensive African American women with a ⫹PH of hypertension support the hypothesis that decreased pain perception in individuals at risk for becoming hypertensive results from an underlying pathophysiological process that leads to the development of hypertension.26,58 Evidence of a genetic predisposition for decreased pain sensitivity has been reported by France et al.27 They observed a significantly longer second suppression period of the masseter and temporalis muscles of the jaw, considered by some as a noninvasive index of endogenous pain modulation, in response to trigeminal nerve stimulation in ⫹PH men. Further research demonstrated increased thresholds and decreased temporal summation of the nociception flexion reflex among individuals with a family history of hypertension versus control subjects.28,51 These studies suggest that central pain modulation is enhanced through either a decrease in spinal transmission of the afferent nociceptive signal or an increase in descending inhibition. Previous investigations of pain and hypertension have mainly been conducted with men, and data involving women have been less consistent.4,5,15,28 Moreover, to our knowledge African American women have not been studied. It has been proposed that a decrease in pain sensitivity could act as a marker for individuals at risk for the development of hypertension, providing a clinical guide for an otherwise silently progressing disease.26 Our data suggest that previously established relationships between pain and hypertension risk in normotensive men also occur in normotensive African American women. They also suggest that naturally occurring muscle pain stimulated through physical work might be a candidate method for assessing risk for hypertension development. Although this study was not designed to compare racial or ethnic differences in the experience of pain, the present results have relevance for understanding pain in African American women. In a review of pain in relation to race and ethnicity, Edwards et al22 reported that laboratory studies of pain stimuli have consistently demonstrated increased sensitivity (lower thresholds and tolerances) to experimental pain stimuli in African American subjects compared to non-Hispanic white subjects. Data
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Figure 1. Ratings of leg muscle pain (mean ⫾ standard error) during exercise as a function of relative exercise intensities for ⫹PH (n ⫽ 14) and ⫺PH (n ⫽ 15) participants.
also suggest that African Americans have more acute pain complaints, experience more pain and disability associated with chronic medical conditions (eg, arthritis or low back pain), cope differently with the stress associated with pain, and receive less clinical care for pain than white Americans.22,23,38,44,56,60 Therefore, racial or ethnic influences on pain perception, particularly among individuals who are at risk for developing hypertension, are important areas of research. In addition, it is important to determine within-race differences of factors predictive of hypertension development to understand better the increased risk among African Americans. A decrease in pain sensitivity during exercise has implications for exercise training and adherence. Pain experienced during exercise has been suggested as a potential barrier to adopting and maintaining a physically active lifestyle.34,50 Moreover, the development of hypertension in African Americans is associated with lower physical functioning, more bodily pain complaints, and poorer health in general.16 African American women at risk for developing hypertension, although characteristically sedentary compared to other ethnic groups,33,61,62 might be more willing to maintain an exercise program if they perceive the exercise as less aversive. Therefore, it might be expected that physical activity interventions would be well tolerated in this group and should be recommended with regard to preventing the development of hypertension and maintaining physical functional status. Consistent with population studies,61 7-day physical activity recalls7,52 collected for the present study indicated that neither the ⫹PH nor ⫺PH groups were highly active. Therefore, early interventions targeted at increasing physical activity in young African American women might prove beneficial toward decreasing the prevalence of hypertension in this high-risk group. The results of the present investigation also have implications for understanding mechanisms involved in the perception of naturally occurring muscle pain during exercise. The finding of lower pain ratings at the high ex-
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ercise intensity combined with a less steep slope for pain throughout exercise in the ⫹PH group suggests that naturally occurring muscle pain perception might be altered by the same pathophysiological processes that underlie the development of hypertension.14,20,43,47,54,59 Whether these mechanisms involve cardiovascular adjustments during exercise remains speculative. However, data indicating a negative relationship between systolic blood pressure and forearm muscle pain ratings during maximal handgrip exercise14 suggest that more research aimed at determining the influence of blood pressure during exercise on the perception of muscle pain, as well as the influence of family history of hypertension, is warranted. Cardiovascular reactivity was assessed to determine whether systolic blood pressure reactivity to the cold pressor test independently predicted pain during exercise. Results indicated a nonsignificant relationship between the change in systolic blood pressure and pain ratings. These findings are inconsistent with reports that cardiovascular reactivity is negatively associated with pain perception.19,21,43,54 France and Stewart29 reported that both parental hypertension history and blood pressure reactivity were independently associated with decreased sensitivity to ischemic pain in a sample of predominantly (95%) white men. Furthermore, Fillingim et al24 reported that the relationship between blood pressure and pain in a sample of predominantly (⬎90%) white women was only significant for ratings of pain unpleasantness and not intensity. We might have observed different results if we had measured the affective component of muscle pain during exercise. Thus, gender, ethnicity, pain stimulus, and pain dimension are all potential factors that could have contributed to our results. In addition, it has been reported that different pain modalities are only weakly correlated.39 The blood pressure reactivity was determined with a painful cold pressor test, so the blood pressure reactivity and pain relationship might not generalize to the experience of naturally occurring muscle pain. One limitation of the present investigation was the lack of blood pressure measurement during the exercise test. If we had obtained these measures, we would have been able to determine whether the ⫹PH participants had a relatively greater blood pressure response to exercise compared to the ⫺PH participants, and whether blood pressure changes were related to pain ratings. A
second limitation was the failure to control menstrual phase for the exercise test. Because this study was part of a research project that focused on the relationship between cardiorespiratory fitness and hypertension risk in African American women,37 we controlled for menstrual cycle status during the cardiovascular reactivity testing that was conducted after the maximal exercise test. Nonetheless, inclusion of menstrual cycle phase as a covariate did not significantly affect our results, and examination of responses of women in luteal versus follicular phases did not reveal overt differences in pain responses. These results are consistent with our previous work suggesting no influence of menstrual cycle phase on naturally occurring leg muscle pain.13 Moreover, results of a recent meta-analysis on pain across the menstrual cycle55 indicated that the follicular phase was associated with lower pain sensitivity. Our ⫹PH group included only 1 participant in this phase; therefore we might expect that our results would be conservative. In the absence of more objective measures of phase (eg, measures of temperature or blood hormones) combined with our relatively small sample sizes for such analyses, it is premature to speculate on possible reasons regarding the lack of a large effect. A third limitation is that we only determined muscle pain intensity during exercise and not affective dimensions of pain such as how unpleasant or bothersome the pain was perceived. Future studies examining pain during exercise should determine pain by using a multidimensional approach. In summary, normotensive African American women with a positive parental hypertension history reported reduced leg muscle pain during high intensity cycling exercise compared to normotensive African American women with a negative parental hypertension history. The results are consistent with data demonstrating reduced sensitivity to nociceptive stimuli among individuals at risk of developing hypertension and show that the same relationship appears among African American women, an understudied population segment known to have an elevated risk of developing hypertension, greater pain sensitivity, and more self-reported pain symptoms. Furthermore, the results suggest that exercise might be a safe and effective way to assess pain sensitivity in individuals at risk of developing hypertension.
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21. Dworkin BR, Filewich RJ, Miller NE, Craigmyle N, Pickering TG: Baroreceptor activation reduces reactivity to noxious stimulation: implications for hypertension. Science 205: 1299-1301, 1979 22. Edwards CL, Fillingim RB, Keefe F: Race, ethnicity and pain. Pain 94:133-137, 2001 23. Edwards RR, Doleys DM, Fillingim RB, Lowery D: Ethnic differences in pain tolerance: clinical implications in a chronic pain population. Psychosom Med 63:316-323, 2001 24. Fillingim RB, Maixner W, Bunting S, Silva S: Resting blood pressure and thermal pain responses among females: effects on pain unpleasantness but not pain intensity. Int J Psychophysiol 30:313-318, 1998
39. Janal MN, Glusman M, Kuhl JP, Clark WC: On the absence of correlation between responses to noxious heat, cold, electrical and ischemic stimulation. Pain 58:403-411, 1994 40. Katz LN, Linder D, Landt H: On the nature of the substance(s) producing pain in contracting skeletal muscle: it’s bearing on the problems of angina pectoris and intermittent claudication. J Clin Invest 14:807-821, 1935 41. Lewis T, Pickering GW, Rothschild P: Observations upon muscular pain in intermittent claudication. Heart 15:359389, 1931 42. Light KC, Girdler SS, Sherwood A, Bragdon EE, Brownley KA, West SG, Hinderliter AL: High stress responsivity predicts later blood pressure only in combination with positive family history and high life stress. Hypertension 33:1458-1464, 1999
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43. Lovick TA: Integrated activity of cardiovascular and pain regulatory systems: role in adaptive behavioural responses. Prog Neurobiol 40:631-644, 1993
53. Perlow S, Markle P, Katz LN: Factors involved in the production of skeletal muscle pain. Arch Intern Med 53:814-824, 1934
44. McCracken LM, Matthews AK, Tang TS, Cuba SL: A comparison of blacks and whites seeking treatment for chronic pain. Clin J Pain 17:249-255, 2001
54. Randich A, Maixner W: Interactions between cardiovascular and pain regulatory systems. Neurosci Biobehav Rev 8:343-367, 1984
45. McCubbin JA, Bruehl S: Do endogenous opioids mediate the relationship between blood pressure and pain sensitivity in normotensives? Pain 57:63-67, 1994
55. Riley JL III, Robinson ME, Wise EA, Price DD: A metaanalytic review of pain perception across the menstrual cycle. Pain 81:225-235, 1999
46. Menkes MS, Matthews KA, Krantz DS, Lundberg U, Mead LA, Qaqish B, Liang KY, Thomas CB, Pearson TA: Cardiovascular reactivity to the cold pressor test as a predictor of hypertension. Hypertension 14:524-530, 1989
56. Riley JL III, Wade JB, Myers CD, Sheffield D, Papas RK, Price DD: Racial/ethnic differences in the experience of chronic pain. Pain 100:291-298, 2002
47. Mini A, Rau H, Montoya P, Palomba D, Birbaumer N: Baroreceptor cortical effects, emotions and pain. Int J Psychophysiol 19:67-77, 1995 48. Motl RW, O’Connor PJ, Dishman RK: Effect of caffeine on perceptions of leg muscle pain during moderate intensity cycling exercise. J Pain 4:316-321, 2003 49. Neely G, Ljunggren G, Sylven C, Borg G: Comparison between the Visual Analogue Scale (VAS) and the Category Ratio Scale (CR-10) for the evaluation of leg exertion. Int J Sports Med 13:133-136, 1992 50. O’Connor PJ, Cook DB: Exercise and pain: the neurobiology, measurement, and laboratory study of pain in relation to exercise in humans. Exerc Sport Sci Rev 27:119-166, 1999 51. Page GD, France CR: Objective evidence of decreased pain perception in normotensives at risk for hypertension. Pain 73:173-180, 1997 52. Pereira MA, FitzerGerald SJ, Gregg EW, Joswiak ML, Ryan WJ, Suminski RR, Utter AC, Zmuda JM: A collection of Physical Activity Questionnaires for health-related research. Med Sci Sports Exerc 29:S1-205, 1997
57. Sheps DS, Bragdon EE, Gray TF III, Ballenger M, Usedom JE, Maixner W: Relation between systemic hypertension and pain perception. Am J Cardiol 70:3F-5F, 1992 58. Stewart KM, France CR: Resting systolic blood pressure, parental history of hypertension, and sensitivity to noxious stimuli. Pain 68:369-374, 1996 59. Svensson P, Minoshima S, Beydoun A, Morrow TJ, Casey KL: Cerebral processing of acute skin and muscle pain in humans. J Neurophysiol 78:450-460, 1997 60. Todd KH, Deaton C, D’Adamo AP, Goe L: Ethnicity and analgesic practice. Ann Emerg Med 35:11-16, 2000 61. U S Department of Health and Human Services. Healthy People 2010: Understanding and improving health (2nd edition). Washington, DC, Government Printing Office, 2000 62. Wolz M, Cutler J, Roccella EJ, Rohde F, Thom T, Burt V: Statement from the National High Blood Pressure Education Program: prevalence of hypertension. Am J Hypertens 13: 103-104, 2000 63. Zamir N, Shuber E: Altered pain perception in hypertensive humans. Brain Res 201:471-474, 1980
A
n interaction between cardiovascular and pain regulatory systems has long been recognized.54 Both clinical hypertension and elevated blood pressure within the normotensive range are associated with decreased pain ratings to various experimental stimuli including noxious cold, heat, electrical stimulation, and mechanical pressure.10,17,31,32,35,45,51,63 Reduced pain ratings also have been observed in normotensive individuals at increased risk for the development of hypertension, by virtue of their having at least 1 parent with confirmed hypertension.3,17,25,26,29,58 It has been argued that decreased pain sensitivity to experimental pain stimuli in normotensive individuals at in-
Received July 25, 2003; Revised November 12, 2003; Accepted December 11, 2003. From the *Department of Radiology, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, †War Related Illness and Injury Study Center (WRIISC), Veterans Administration Medical Center, East Orange, New Jersey, ‡Department of Health and Human Performance, Auburn University, Auburn, Alabama, USA, and §Department of Exercise Science, University of Georgia, Athens, Georgia, USA. Address reprint requests to Dane B. Cook, PhD, War Related Illness and Injury Study Center (WRIISC), VA Medical Center, 385 Tremont Avenue (129), East Orange, NJ 07018. E-mail: [email protected] 1526-5900/$30.00 © 2004 by the American Pain Society doi:10.1016/j.jpain.2003.12.002
creased risk for hypertension might reflect a pathophysiological process that results in dysregulation of central nervous system processes involved in both pain control and cardiovascular regulation, and that hypoalgesia might be a method used to identify individuals at risk for developing hypertension.26,28,30,51 African Americans report more acute pain symptoms, experience painful symptoms differently (eg, more distress and lower physical function), and are more sensitive to experimentally induced pain than non-Hispanic white Americans.16,22,23,44,56 They also have a significantly greater risk of developing hypertension and are less physically active than non-Hispanic white Americans.6,33,61,62 The high occurrence of pain symptoms and the prevalence of hypertension in this group are at odds with the established negative relationship between familial risk for hypertension and pain sensitivity and highlight the need for additional research determining whether this relationship generalizes to African Americans. Moreover, exercise and a physically active lifestyle are known to reduce the risk of the development of hypertension,1,2 whereas pain is perceived as one of the barriers to adopting a physically active lifestyle.34,50 Therefore, determining how pain during exercise is perceived in African Americans at risk for developing hyper-
The Journal of Pain, Vol 5, No 2 (March), 2004: pp 111-118
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112 tension has relevance for understanding issues pertaining to exercise adherence and prescription. The effects of parental hypertension history on pain perception by using experimentally induced pain stimuli have been assessed primarily in men. These studies consistently have shown that a positive family history of hypertension is associated with decreased pain sensitivity to experimental pain stimuli.3,17,26 More recent studies in women have been equivocal and further highlight the need for more research examining pain in women with and without a family history of hypertension.4,5,15 To date, the experience of muscle pain during exercise has not been studied among African American women, a group with relatively greater risk for developing hypertension6,33 and who report more pain symptoms.23,44 Muscle pain is experienced during moderate and high intensity exercise. Studies describing this phenomenon have shown that muscle pain intensity ratings increase as a positively accelerating function of exercise intensity.9,12-14,36 Early investigation into potential mechanisms indicated that muscle pain during exercise resulted from the accumulation of a noxious metabolite, termed factor P, and that this metabolite was related to changes in the blood flow and contractile characteristics of the muscle that occur with increasing exercise intensity.18,40,41,53 More recently, attempts to manipulate naturally occurring muscle pain pharmacologically have shown no effect of aspirin on leg muscle pain ratings and no effect of the opioid agonist codeine or the opioid antagonist naltrexone on forearm muscle pain ratings.9,12,14 These results suggest that prostaglandins are not the sole algesic substance responsible for initiation of an afferent nociceptive signal, and that naturally occurring muscle pain perceptions are not moderated by opioids. More research is needed to learn what causes and moderates naturally occurring muscle pain. Recent work suggests that adenosine plays a role in exercise-induced muscle pain.48 Another potential moderator could be the pathophysiological processes that underlie the development of hypertension. Furthermore, it is not known whether the relationship between pain sensitivity and risk for hypertension generalizes to naturally occurring muscle pain such as occurs with exercise. The primary purpose of the present investigation was to examine leg muscle pain produced during cycling exercise in African American women with or without a positive family history of hypertension. In addition, cardiovascular reactivity to stressors has been shown to be an independent risk factor for the development of hypertension42,46 and has been associated with decreased sensitivity to experimental pain stimuli.21,54 Therefore, to determine the relationship between parental hypertension history and pain more clearly, we examined the association between cardiovascular reactivity to a cold pressor stimulus on leg muscle pain ratings during exercise. On the basis of previous research examining pain among individuals at increased risk for hypertension, we hypothesized that African American women with a positive family history of hypertension would rate leg muscle pain during exercise as less intense than those women
Muscle Pain & Family History of Hypertension without a positive family history. Furthermore, it was hypothesized that increased cardiovascular reactivity to the cold pressor test would significantly predict lower exercise-induced leg muscle pain ratings.
Materials and Methods Participants African American women from a university population were recruited if they were healthy, at least 18 years of age, eumenorrheic, and the blood pressure status of their parents could be verified. This study was part of a larger research project that focused on the relationship between cardiorespiratory fitness and hypertension risk in African American women.37 Therefore, the sample was limited to African American women with or without positive parental hypertension history. Thirty-five eligible women volunteered and completed the study. Because of technical difficulties, one subject’s exercise data were not usable; therefore, this subject could not be included in subsequent analyses. The final sample included 18 women with a parental history of hypertension (⫹PH) and 16 women without a parental history of hypertension (⫺PH).1 All women were nonsmokers who reported no cardiovascular disease, psychologic disorders, or other major illnesses. All participants were normotensive (mean ⫾ standard deviation, 110.1 ⫾ 6.7/70.5 ⫾ 6.3 mm Hg), and 4 ⫹PH and 5 ⫺PH women reported using oral contraceptives. Participants read and signed an Institutional Review Board approved consent form that explained the risks and benefits associated with participation in the study. Parental hypertension was defined as having at least 1 parent who was physician-diagnosed with hypertension. Participants reported the hypertension status of their parents, and parents were contacted for verification. Parents were mailed information about the study along with a health history form. They were asked to provide a blood pressure reading taken within the past 3 months and to report whether they had ever been physiciandiagnosed with hypertension. Parents who had been diagnosed with hypertension were also asked to provide their age at diagnosis, length of diagnosis, and type of antihypertensive medications.
Cold Pressor Test and Physiological Measures The hand cold pressor test was used to examine cardiovascular reactivity. The test involved the participant placing her right hand to the level of the wrist in a bucket of water maintained at 0°C to 3°C for 2 minutes. Heart rate and blood pressure were measured continuously during the test from the left middle finger by using an Ohmeda Finapres Model 2300 blood pressure monitor (Ohmeda Monitoring Systems, Englewood, Colo). The hand rested at heart level, and participants were instructed to keep the hand still during the cold pressor test. Data from the Finapres for systolic pressure, diastolic pressure, mean arterial pressure, and heart rate were recorded on a beat to beat basis and stored by using Data Acquisition Sys-
ORIGINAL REPORT/Cook et al tems DATAQ version 3.50 (TJS Software, Durham, NC). Five participants, 1 ⫺PH and 4 ⫹PH, voluntarily withdrew from the study for personal reasons before the completion of the reactivity assessment. Therefore, cardiovascular reactivity analyses were completed on 30 participants.
Maximal Exercise Test The testing procedures for maximal exercise testing were explained, and participants were given instructions for reporting ratings of quadriceps muscle pain.12,13 Participants were then fitted with a heart rate monitor, mouth piece, and nose clip. Exercise was performed on an electronically braked cycle ergometer (Minjhardt model KEM-3, Utrecht, The Netherlands), and a ramped protocol was used. After a 4-minute warm-up at 25 W, the resistance increased to 50 W and then increased at a rate of 24 W per minute until participants reached volitional exhaustion. Metabolic variables, including oxygen consumption, carbon dioxide production, and ventilation, were measured continuously by using a Sensormedics Model 2900 metabolic cart (SensorMedics Corporation, Yorba Linda, CA) that had been calibrated with standard gases. Heart rate and quadriceps muscle pain ratings were obtained each minute of the test. Peak oxygen uptake was defined as the highest attained oxygen consumption when at least 2 of the following criteria were met: a heart rate within 90% of the age-predicted maximal, a respiratory exchange ratio above 1.1, and a perceived exertion value of 18 or greater. An individual certified in cardiopulmonary resuscitation was present during all testing sessions. At the end of the test, peak values for power output, oxygen consumption, heart rate, and leg muscle pain intensity were recorded.
Leg Muscle Pain Ratings Before the maximal exercise test, participants were read standard instructions12,13 while viewing the pain rating scale. Quadriceps muscle pain intensity ratings were obtained during the maximal exercise test by using a 0 to 10 category-ratio scale (0, no pain; 10, extremely intense, almost unbearable pain). The scale included an open end point that permitted participants to give a rating higher than 10 but proportional to 10 (eg, 20 being twice as intense as 10), if leg muscle pain became more intense after a 10 was reported. Participants were instructed to focus on leg muscle pain only in the quadriceps and to use the verbal anchors to aid in selecting a numeric rating. Scores for category-ratio–10 scales have been shown to be valid and reliable measures of pain during exercise and have been shown to have ratio-scaling properties for the creation of psychophysical curve estimates.8,12,13,36,49
Procedures Before maximal exercise testing, participants completed a medical and physical activity history form. Measurements of height, weight, and resting brachial blood pressure were also obtained. After completing the max-
113 imal exercise test, participants completed the physical activity (7-day recall interview7) and were given instructions for charting their menstrual cycle so that the stress reactivity session was conducted during the same menstrual phase for all participants. The stress reactivity session was conducted during the follicular phase (typically days 5 to 13) of the menstrual cycle for participants, and the session took place in early afternoon, between 2:30 and 4:30 PM.
Statistical Analysis Analyses for parental hypertension history and cardiovascular reactivity were performed separately. For parental hypertension history, group differences for participant characteristics and peak values in response to the exercise test were assessed by using independent samples t tests. Cohen’s d effect sizes were also calculated to assess the differences in select participant characteristics and peak responses.11 Submaximal intensities of 50%, 70%, and 90% of peak power output were calculated for each participant. Muscle pain rating values that corresponded with the 3 submaximal intensities were used in the analyses. Group differences for muscle pain ratings during exercise were assessed by using a group (⫹PH vs ⫺PH) by exercise intensity (50%, 70%, and 90%) repeated measures analysis of variance. Greenhouse-Geisser adjustments for degrees of freedom were used when Mauchly test of sphericity was significant (P ⬍ .05). Preliminary descriptive statistics based on self-report indicated that the groups differed on menstrual cycle status on the day of exercise. For the ⫹PH group, 1 participant was in the follicular phase, 10 were in the luteal phase, 3 were on period, and 4 were on oral contraceptives. For the ⫺PH group, 5 were in the follicular phase, 5 were in the luteal phase, 2 were on period, and 5 were on oral contraceptives. Analysis of covariance with menstrual phase entered as a covariate did not influence the results. Examination of follicular versus luteal phase, independent of group, revealed no significant differences in pain ratings or peak pain responses. Power functions for each subject’s complete exercise test were determined by linear regression of log transformed (log10) muscle pain versus log transformed exercise intensity. This allowed for the examination of a greater range of exercise intensities and assessment of complete tests (ie, all exercise intensities for which a rating was present) for all participants. Single sample t tests were performed to examine whether the group-averaged exponents were significantly different than a linear value of 1. Independent samples t tests were used to examine group differences in the regression derived exponents. For cardiovascular reactivity we examined systolic blood pressure responses to the cold pressor test and used linear regression to determine the influence of blood pressure reactivity on pain during exercise after controlling for fitness and family history. We examined the influence of systolic blood pressure reactivity on both the peak pain responses and the log transformed (log10) slopes of pain ratings throughout exercise. All statistical
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Table 1.
Participant Characteristics Based on Parental Hypertension History Status (Mean ⴞ Standard Deviation) ⫹PH (N ⫽ 18)
⫺PH (N ⫽ 16)
EFFECT SIZE
VARIABLE
D
P VALUE
Physical characteristics Age (y) Height (cm) Weight (kg) Body mass index Physical activity (kcal · kg⫺1 · day⫺1) Resting SBP (mm Hg) Resting DBP (mm Hg) Resting MAP (mm Hg)
19.3 ⫾ 1.4 164.5 ⫾ 5.8 61.5 ⫾ 15.7 22.6 ⫾ 4.9 38.2 ⫾ 3.0 111 ⫾ 8.2 72 ⫾ 6.1 85 ⫾ 6.0
18.7 ⫾ 0.8 166.8 ⫾ 5.0 67.3 ⫾ 17.3 24.1 ⫾ 5.3 39.1 ⫾ 2.9 109 ⫾ 4.5 68 ⫾ 5.6 82 ⫾ 4.2
.51 ⫺.42 ⫺.35 ⫺.29 .30 .29 .62 .57
.14 .23 .31 .40 .40 .31 .06 .07
DBP, diastolic blood pressure; ⫺PH, negative parental hypertension history; ⫹PH, positive parental hypertension history; MAP, mean arterial pressure; SBP, systolic blood pressure.
analyses were performed with SPSS Windows version 10.0 software (SPSS, Inc, Chicago, Ill).
Results Parental Hypertension History Parents of the participants were diagnosed at a mean age of 38.6 ⫾ 7.5 years, with a range of 24 to 49 years. Blood pressure was normalized (130 ⫾ 10/82 ⫾ 9.1 mm Hg) in all but 1 hypertensive parent (180/93 mm Hg), who was noncompliant with medication. Parents of ⫺PH participants had an average blood pressure of 121.7 ⫾ 6.1/ 73.8 ⫾ 8.5 mm Hg. Means and standard deviations for participant characteristics based on parental hypertension history status are presented in Table 1. No significant differences in physical characteristics were observed. Peak responses to exercise are summarized in Table 2. There were no significant differences between groups for any of the peak variables measured. Leg muscle pain ratings for both groups are presented in Figure 1. Repeated measures analysis of variance indicated a significant main effect of exercise intensity on leg muscle pain ratings during exercise (F1.4,45 ⫽ 82.9, P ⬍ .001) as well as a significant group-by-exercise intensity interaction (F1.4,45 ⫽ 4.5, P ⫽ .027). The interaction is
characterized by smaller increases in pain for the ⫹PH group than for the ⫺PH group. Exponents for the calculated power functions for leg muscle pain are presented in Table 2. Participants in the ⫹PH group had significantly lower exponents for muscle pain (P ⱕ .05). For both groups the exponent for pain was significantly greater (P ⱕ .05) than a linear value of 1, indicating a positively accelerating function. Thus, leg muscle pain ratings for the ⫹PH group increased at a slower rate throughout exercise compared to the ⫺PH group.
Cardiovascular Reactivity to Cold Pressor The average increase in systolic blood pressure for all participants was 16.6 (⫾19.9) mm Hg. After controlling for family history of hypertension status and cardiorespiratory fitness, linear regression indicated no association between systolic blood pressure reactivity and either the peak pain experienced during exercise (F1,27 ⫽ 0.47, P ⫽ .49) or the log transformed (log10) slopes of pain ratings (F1,25 ⫽ 0.14, P ⫽ .71).
Discussion
African American women with a ⫹PH of hypertension reported less muscle pain during high intensity exercise
Peak Measures During Maximal Exercise and Power Functions for Leg Muscle Pain (log10 Transformed Values and Regression Exponents) Based on Parental History Status (Mean ⴞ Standard Deviation)
Table 2.
VARIABLE Power output (W) Heart rate (bpm) Peak oxygen consumption (mL · kg · min⫺1) Pain intensity Perceived exertion Muscle pain exponent *Significant group effect, P ⬍ .05. ‡ Exponent significantly different than 1, P ⬍ .05.
⫹PH (N ⫽ 18)
⫺PH (N ⫽ 16)
EFFECT SIZE D
P VALUE
187 ⫾ 24 175 ⫾ 10.0 28.8 ⫾ 4.7
202 ⫾ 23 178 ⫾ 12 29.7 ⫾ 5.4
⫺.63 ⫺.27 ⫺.17
.08 .38 .58
5.6 ⫾ 2.8 17.7 ⫾ 2.0 1.7*‡
6.1 ⫾ 3.2 17.8 ⫾ 2.0 2.3‡
⫺.17 ⫺.05 ⫺0.8
.64 .89
ORIGINAL REPORT/Cook et al expressed relative to their peak exercise capacity, and they had significantly lower exponents for pain throughout the exercise test. The results are consistent with previous research demonstrating decreased pain sensitivity in offspring with positive parental hypertension history.3 The results are novel because they extend those findings to African American women, a group with greater risk for developing hypertension than non-Hispanic white Americans and who are more sensitive to pain and have more pain complaints than African American men and non-Hispanic white men and women.17,22,23,25,26,29,56-58 These data also demonstrate that naturally occurring leg muscle pain produced by exercise shows similar effects to other types of experimentally induced pain. Cardiovascular reactivity to the cold pressor was not independently associated with decreased muscle pain sensitivity during the exercise test. Our results demonstrating decreased pain sensitivity during exercise in normotensive African American women with a ⫹PH of hypertension support the hypothesis that decreased pain perception in individuals at risk for becoming hypertensive results from an underlying pathophysiological process that leads to the development of hypertension.26,58 Evidence of a genetic predisposition for decreased pain sensitivity has been reported by France et al.27 They observed a significantly longer second suppression period of the masseter and temporalis muscles of the jaw, considered by some as a noninvasive index of endogenous pain modulation, in response to trigeminal nerve stimulation in ⫹PH men. Further research demonstrated increased thresholds and decreased temporal summation of the nociception flexion reflex among individuals with a family history of hypertension versus control subjects.28,51 These studies suggest that central pain modulation is enhanced through either a decrease in spinal transmission of the afferent nociceptive signal or an increase in descending inhibition. Previous investigations of pain and hypertension have mainly been conducted with men, and data involving women have been less consistent.4,5,15,28 Moreover, to our knowledge African American women have not been studied. It has been proposed that a decrease in pain sensitivity could act as a marker for individuals at risk for the development of hypertension, providing a clinical guide for an otherwise silently progressing disease.26 Our data suggest that previously established relationships between pain and hypertension risk in normotensive men also occur in normotensive African American women. They also suggest that naturally occurring muscle pain stimulated through physical work might be a candidate method for assessing risk for hypertension development. Although this study was not designed to compare racial or ethnic differences in the experience of pain, the present results have relevance for understanding pain in African American women. In a review of pain in relation to race and ethnicity, Edwards et al22 reported that laboratory studies of pain stimuli have consistently demonstrated increased sensitivity (lower thresholds and tolerances) to experimental pain stimuli in African American subjects compared to non-Hispanic white subjects. Data
115
Figure 1. Ratings of leg muscle pain (mean ⫾ standard error) during exercise as a function of relative exercise intensities for ⫹PH (n ⫽ 14) and ⫺PH (n ⫽ 15) participants.
also suggest that African Americans have more acute pain complaints, experience more pain and disability associated with chronic medical conditions (eg, arthritis or low back pain), cope differently with the stress associated with pain, and receive less clinical care for pain than white Americans.22,23,38,44,56,60 Therefore, racial or ethnic influences on pain perception, particularly among individuals who are at risk for developing hypertension, are important areas of research. In addition, it is important to determine within-race differences of factors predictive of hypertension development to understand better the increased risk among African Americans. A decrease in pain sensitivity during exercise has implications for exercise training and adherence. Pain experienced during exercise has been suggested as a potential barrier to adopting and maintaining a physically active lifestyle.34,50 Moreover, the development of hypertension in African Americans is associated with lower physical functioning, more bodily pain complaints, and poorer health in general.16 African American women at risk for developing hypertension, although characteristically sedentary compared to other ethnic groups,33,61,62 might be more willing to maintain an exercise program if they perceive the exercise as less aversive. Therefore, it might be expected that physical activity interventions would be well tolerated in this group and should be recommended with regard to preventing the development of hypertension and maintaining physical functional status. Consistent with population studies,61 7-day physical activity recalls7,52 collected for the present study indicated that neither the ⫹PH nor ⫺PH groups were highly active. Therefore, early interventions targeted at increasing physical activity in young African American women might prove beneficial toward decreasing the prevalence of hypertension in this high-risk group. The results of the present investigation also have implications for understanding mechanisms involved in the perception of naturally occurring muscle pain during exercise. The finding of lower pain ratings at the high ex-
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ercise intensity combined with a less steep slope for pain throughout exercise in the ⫹PH group suggests that naturally occurring muscle pain perception might be altered by the same pathophysiological processes that underlie the development of hypertension.14,20,43,47,54,59 Whether these mechanisms involve cardiovascular adjustments during exercise remains speculative. However, data indicating a negative relationship between systolic blood pressure and forearm muscle pain ratings during maximal handgrip exercise14 suggest that more research aimed at determining the influence of blood pressure during exercise on the perception of muscle pain, as well as the influence of family history of hypertension, is warranted. Cardiovascular reactivity was assessed to determine whether systolic blood pressure reactivity to the cold pressor test independently predicted pain during exercise. Results indicated a nonsignificant relationship between the change in systolic blood pressure and pain ratings. These findings are inconsistent with reports that cardiovascular reactivity is negatively associated with pain perception.19,21,43,54 France and Stewart29 reported that both parental hypertension history and blood pressure reactivity were independently associated with decreased sensitivity to ischemic pain in a sample of predominantly (95%) white men. Furthermore, Fillingim et al24 reported that the relationship between blood pressure and pain in a sample of predominantly (⬎90%) white women was only significant for ratings of pain unpleasantness and not intensity. We might have observed different results if we had measured the affective component of muscle pain during exercise. Thus, gender, ethnicity, pain stimulus, and pain dimension are all potential factors that could have contributed to our results. In addition, it has been reported that different pain modalities are only weakly correlated.39 The blood pressure reactivity was determined with a painful cold pressor test, so the blood pressure reactivity and pain relationship might not generalize to the experience of naturally occurring muscle pain. One limitation of the present investigation was the lack of blood pressure measurement during the exercise test. If we had obtained these measures, we would have been able to determine whether the ⫹PH participants had a relatively greater blood pressure response to exercise compared to the ⫺PH participants, and whether blood pressure changes were related to pain ratings. A
second limitation was the failure to control menstrual phase for the exercise test. Because this study was part of a research project that focused on the relationship between cardiorespiratory fitness and hypertension risk in African American women,37 we controlled for menstrual cycle status during the cardiovascular reactivity testing that was conducted after the maximal exercise test. Nonetheless, inclusion of menstrual cycle phase as a covariate did not significantly affect our results, and examination of responses of women in luteal versus follicular phases did not reveal overt differences in pain responses. These results are consistent with our previous work suggesting no influence of menstrual cycle phase on naturally occurring leg muscle pain.13 Moreover, results of a recent meta-analysis on pain across the menstrual cycle55 indicated that the follicular phase was associated with lower pain sensitivity. Our ⫹PH group included only 1 participant in this phase; therefore we might expect that our results would be conservative. In the absence of more objective measures of phase (eg, measures of temperature or blood hormones) combined with our relatively small sample sizes for such analyses, it is premature to speculate on possible reasons regarding the lack of a large effect. A third limitation is that we only determined muscle pain intensity during exercise and not affective dimensions of pain such as how unpleasant or bothersome the pain was perceived. Future studies examining pain during exercise should determine pain by using a multidimensional approach. In summary, normotensive African American women with a positive parental hypertension history reported reduced leg muscle pain during high intensity cycling exercise compared to normotensive African American women with a negative parental hypertension history. The results are consistent with data demonstrating reduced sensitivity to nociceptive stimuli among individuals at risk of developing hypertension and show that the same relationship appears among African American women, an understudied population segment known to have an elevated risk of developing hypertension, greater pain sensitivity, and more self-reported pain symptoms. Furthermore, the results suggest that exercise might be a safe and effective way to assess pain sensitivity in individuals at risk of developing hypertension.
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