Hypertension is a major global health problem and public health challenge, demanding a vast proportion of health care resources directly and indirectly because of its high and increasing prevalence and the concomitant risks of cardiovascular events such as stroke, kidney disease, decreased disability adjustment, and mortality. It is a well-established fact that sedentary lifestyle contributes to increased risk of cardiovascular disease, especially hypertension. Indeed, hypertension is a major independent risk factor for cardiovascular and renal disease, increasing the risk of myocardial infarction, stroke, and heart failure. Hypertension and its complications are largely responsible for morbidity and mortality of all age groups. It has been reported that elevated serum uric acid (SUA) is an independent risk factor for hypertension (8,19,30,33).
2Extensive epidemiologic and experimental evidence now suggests that SUA is a relevant and independent risk factor for cardiovascular and renal disease, particularly in patients with hypertension, heart failure, or diabetes. Hyperuricemia predicts mortality in patients with heart failure (4) or coronary heart disease (27), cerebrovascular events in individuals with diabetes (24), and cardiac ischemia in hypertension (10). Campion et al (12) reported that patients with essential hypertension also showed an increased risk of gout and that gout incidence was 3-fold higher in patients with hypertension compared with normotensive subjects. However, 2 epidemiological studies (9,25) reported a contrary study that uricemia could not be recognized as an independent cardiovascular risk factor. Patients with hypertension and an SUA concentration between 5.0 and 6.9 mg/dL had a significantly higher relative risk (RR) for both heart attack (RR 1.32) and stroke (RR 1.15). Patients with a urate level >7.0 mg/dL had an RR of stroke and heart attack of 1.5 and 2.2, respectively (47). These results strongly support the hypothesis that increased SUA levels are independent risk factors for hypertension-associated morbidity and mortality.
The pathophysiological mechanism of elevated SUA in hypertension is associated with hypoxia and a decrease in uric acid excretion-an imbalance between production and excretion (40,43). It has been postulated that in hypertension, SUA underexcretion may be linked to increased tubular sodium reabsorption mediated by insulin. Insulin has powerful sodium-retaining effects, and this antinatriuretic action has been documented. In addition, selective insulin resistance and hyperinsulinemia are common findings in hypertension. The concept of selective insulin resistance implies the inability of insulin to cause glucose uptake with preservation of the other action of insulin such as a renal sodium-retaining effect. Also, tissue hypoxia determines increased adenosine nucleotide degradation, leading to increased formation of hypoxanthine and xanthine, which ends in uric acid overproduction. Furthermore, the oxidation of xanthine can occur in 2 forms: dehydrogenase (D) or oxidase (O). Both O and D lead to the formation of reactive oxygen species(ROS; superoxide, hydrogen peroxide, and hydroxyl radical), all of which may play a significant role in tissue damage. However, studies have shown that uric acid could act as a marker of oxidative stress, an antioxidant, and a prooxidant, particularly at elevated levels. Thus, it is unclear whether elevated levels of uric acid in diseases associated with oxidative stress are a protective response or a primary cause (7,15,35).
Many studies (13,17,38) have shown that an acute bout of heavy exercise training has been shown to generate reactive oxygen and nitrogen species (RONS) that can cause oxidative damage and stress to the body. Contrarily, several other studies have also shown that regular (repeated) nonexhaustive exercise reduces exercise-induced oxidation and damage with concomitant hormetic benefit. These contrary reports by various investigators are based on the type of exercise vis-à-vis intensity, frequency, and duration. Exercise scientists and other health-related professionals have used various training methods to evaluate many of the physiological changes in the healthy and various conditions. However, few studies have actually investigated the effect of exercise on SUA level and concomitant cardiovascular responses in hypertension. For the purpose of this study, 2 hypotheses were formulated and tested:
- There would be a significant difference between experimental and control groups in systolic blood pressure (SBP), diastolic blood pressure (DBP), o2max and SUA.
- The interval group will not differ significantly from the continuous group in SBP, DBP, o2max, and SUA. To test these hypotheses, we investigated the effect of an interval and continuous training program on blood pressure and SUA level in subjects with hypertension.
Experimental Approach to the Problem
In the present study, age-matched randomized, double-blind independent groups design was used to determine the influence of the interval and continuous training program on cardiovascular parameters. Subjects' ages were arranged in ascending order (50 to 70 years) and then assigned to interval, continuous, and control groups in an alternating pattern (age-matched). A 1-week washout period was established, and a pretest was administered to all subjects on the last day of the washout period. Following the washout and pretest, all subjects were prescribed Aldomet (methyldopa), and the interval and continuous groups were involved in an interval and continuous training programs for 8 weeks, whereas the control group remained sedentary during the period. At the end of the training and sedentary period, another 1-week wash ut period was established and a posttest was administered to all subjects on the last day of the washout period.
The population for the study was male subjects with essential hypertension who were attending the hypertensive clinic of Murtala Muhammed Specialist Hospital Kano Nigeria. Subjects were fully informed about the experimental procedures, risk, and protocol, after which they gave their informed consent in accordance with the American College of Sports Medicine (ACSM) guidelines regarding the use of human subjects, as recommended by the human subject protocol (41). Ethical approval was granted by the Ethical Committee of Kano State Hospitals Management Board and the faculty of Health Sciences, College of Medicine, University of Nigeria, Enugu Campus.
Only those who volunteered to participate in the study were recruited. Subjects between the age range of 50 and 70 years with chronic mild to moderate and stable (>1 year duration) hypertension (SBP between 140 and 179 and DBP between 90 and 109 mm Hg) were selected. Subjects who had stopped taking antihypertensive drugs or were taking a single antihypertensive medication were recruited for the study. All subjects were sedentary and had no history of psychiatry or psychological disorders or abnormalities.
Patients who were obese or underweight (body mass index [BMI] between 20 and 30 kg/m2); who smoked; or who had alcoholism, diabetes, or other cardiac, renal, or respiratory disease were excluded. Those involved in vigorous physical activities and were above-average physically fit (o2max >27 and >33 mL/kg/min and more than 60 and 50 years old, respectively) were also excluded.
A total of 485 chronic and stable, essential mild to moderate, male patients with hypertension satisfied the necessary study criteria. Subjects were age-matched and randomly grouped into interval (162), continuous (162), and control (161) groups. They were fully informed about the experimental procedures, risk, and protocol, after which they gave their informed consent in accordance with the ACSM guidelines regarding the use of human subjects (41) as recommended by the human subject protocol. The Ethical Committee of Kano State Hospitals Management Board granted ethical approval.
All subjects taking antihypertensive drugs were asked to stop all forms of medication and, in replacement, were given placebo tablets (consisting of mainly lactose and inert substance) in a single-blind method (42,45). All subjects, including those not taking any antihypertensive medications, were prescribed placebo tablets for 1 week (7 days); this is known as the “washout period.” The purpose of the washout period was to get rid of the effects of previously taken antihypertensive drugs/medications. During the washout period all subjects were instructed to avoid any strenuous physical activities and to report to the hypertensive clinic for daily blood pressure monitoring and general observation. The pretest procedure was conducted on the last day of the washout period in the Department of Physiotherapy of Murtala Mohammed Specialist Hospital (MMSH), Kano between 8:00 am and 10:00 am.
Subjects' resting heart rate (HR), SBP, and DBP were monitored from the right arm, as described by Walker et al (46) and Musa et al (29), using an automated digital electronic BP monitor (Omron digital BP monitor, Model 11 EM 403c; Tokyo Japan). Subjects were in a sitting position after a 10-minute rest. The deflated cuff was wrapped round the slightly flexed right upper arm of the subjects. The cuff was then rapidly inflated through the pump until a signal to stop the inflation was indicated, and the cuff automatically started deflating until the SBP, DBP, and HR were displaced on the monitor. The equipment was used to take the BP and HR at rest, during exercise, and after exercise test. This procedure was repeated and the average of the 2 readings was recorded. These measurements were monitored between 8:00 am and 10:00 am each test day.
Subjects' physical characteristics (weight [kg] and height[m]) and body composition (BMI [kg/m−2]) assessment was done in accordance with standardized anthropometric protocol (18,36).
Blood Sample Collection (Venipuncture Method)
Both pretreatment and posttreatment, venous blood samples were obtained between 8:00 am and 10:00 pm after about a 12-hour overnight fast (fasting blood sample). A 5-mL syringe was used for blood sample collection using the procedure described by Bachorik (5). About 5 mL of blood was drawn from the antecubital vein of each subject under strict antiseptic condition. All samples were stored in a refrigerator at −80°C until analysis (6).
Serum Uric Acid Assessment
Uric acid analysis was determined with Human kit, using the PAP-Method (enzymatic colorimetric test), as recommended by the manufacturer (Human Gesellschaft und Diagnotisca mbH, Wiesbaden, Germany).
The Young Men's Christian Association (YMCA) submaximal cycle ergometry test protocol was used to assess subjects' aerobic power, as described by the ACSM (2) and Golding et al (16). The bicycle seat height was adjusted and the subjects' knees were slightly flexed when the pedal was in the down position. The exercise test started with a 2- to 3-minute warm-up at zero resistance to acquaint the subjects with the cycle ergometer. According to Brooks et al. (11) and Pollock and Wilmore (34), middle-aged, less fit patients with cardiac disease generally begin at 100 or 150 to 300 kgm/min−1 (17 w or 25 w to 50 w, respectively) with power increments of 5-25 watts per stage. At the end of the test, a 2- to 3-minute recovery period (cool down) at zero resistance pedaling was administered.
The test procedure was conducted in the Department of Physiotherapy of Murtala Mohammed Specialist Hospital (MMSH), Kano between 8:00 am and 10:00 am.
Following the stress test and prior to the exercise training, all subjects in the control, interval, and control groups were reassessed by the physician and were prescribed Aldomet (methyldopa) as necessary. During the training and sedentary period (8 weeks), all subjects in the interval, continuous, and control groups were placed on methyldopa according to their prerecruitment doses and responses at 250 mg and 500 mg daily. Aldomet was preferred because it does not alter normal hemodynamic responses to exercise (20). It is well-tolerated and is the most-prescribed antihypertensive drug in Nigeria (28), particularly Northern Nigeria, where the study was conducted. It is also useful in the treatment of mild to moderately severe hypertension (37). Subjects maintained these prescriptions with regular medical consultation and observation throughout the period of this study.
The Interval Group (Group 1)
After a 10-minute warm up (pedaling at zero resistance), subjects in the interval group exercised on a bicycle ergometer at a moderate intensity of between 60 and 79% of their HR max reserve (1,3,21), which was estimated as being 220 minus the age of a subject, as recommended by ACSM (3). The starting workload was 100 kgm (17 watts), which was increased at a pedal speed of 50 rpm to obtain 60% of their HR max. It was increased in the first 2 weeks to level up at 79% of their HR max, and this value was maintained throughout the remaining part of the training period at a work:rest duration of 1:1 of 6 minutes each (3). During the 6-minute rest interval period, subjects pedaled at zero intensity. The initial exercise session was increased from 45 minutes in the first 2 weeks of training and leveled up at 60 minutes throughout the remaining part of the training. Following the exercise, another 10-minute cool down was established by pedaling at zero resistance. An exercise session of 3 times per week was maintained throughout the 8-week period of training.
The Continuous Group (Group 2)
After a 10-minute warm up (pedaling at zero resistance), subjects in the continuous group exercised on a bicycle ergometer at a moderate intensity of between 60 and 79% of their HR max (3,32). The starting workload was 100 kgm (17 watts), which was increased at a pedal speed of 50 rpm to obtain a HR max 60%, which was increased in the first 2 weeks and leveled up at 79% HR max throughout the remaining part of the training period. The initial exercise session was increased from 45 minutes in the first 2 weeks of training and leveled up to 60 minutes throughout the remaining part of the training. After each training session, 10 minutes of cool down was established by pedaling at zero resistance. An exercise session of 3 times per week was also maintained throughout the 8-week training period.
The Control Group (Group 3)
Subjects in the control group were instructed not to undertake any organized/structured physical activity apart from the activities of daily living during the 8-week period of study.
At the end of the 8-week training and sedentary period, all subjects remained sedentary (no exercise) and were asked to stop taking methyldopa (Aldomet). Subjects were instead prescribed placebo tablets in a single-blinded method for 1 week to get rid the effect of the methyldopa taken during the training period.
A posttraining physiological (SBP, DBP, HR) assessment and stress test were conducted as described earlier in the pretest procedures using standardized protocols, techniques, and methods by the same investigators.
All pretest and posttest measurements were recorded on a data sheet. Three hundred and fifty-seven subjects (140 from interval, 112 from continuous, and 105 from control groups) completed the 8-week training program. One hundred and twenty-eight subjects (22 from interval, 50 from continuous, and 56 from control groups) had dropped out because of noncompliance, unfavorable responses to methyldopa and exercise training, or incomplete data; therefore, the data of 357 subjects were used in the statistical analysis (Figure 1).
Before the actual tests, a pilot study was conducted using 20 volunteers with mild to moderate essential hypertension with an age range of 45 to 84 (mean = 60.30) years. The essence of the pilot test was to refine the technical (precision of the instruments) and administrative procedures of the test. Subjects' SBP, DBP, and stress test (YMCA) measurements were conducted 2 times, once every week (repeated measures). A Pearson moment correlation test was used to find the correlation coefficient. Results of the pilot study showed a moderate to very high significant correlation of SBP (0.914), DBP (0.907), and YMCA (o2max [0.814]). This is an indication of good internal consistency (31).
Following data collection, the measured and derived variables were statistically analyzed. The descriptive statistics (means and standard deviations) of the subjects' physical characteristics, estimated o2max, and other cardiovascular parameters were determined. Analysis of variance (ANOVA) and Scheffe tests were conducted to assess the treatment outcome. A Pearson product moment correlation test was also computed for the variables (changes in SBP, DBP, and SUA concentration and changes in o2max) of interest. In the ANOVA and correlation tests, the difference between subjects' posttraining and pretraining measurements (changed score) were used as dependent measures. All statistical analyses were performed on a Toshiba compatible microcomputer using the statistical package for the social science (SPSS; Chicago, IL, USA), windows Version 16.0. The probability level for all the aforementioned tests was set at 0.05 to indicate significance.
The subject's ages ranged between 50 and 70 years. Subjects' mean ± SD age, height, weight, and BMI were 58.40 ± 6.91 years, 167.78 ± 7.81 cm, 70.18 ± 11.37 kg, and 24.96 ± 3.88 kg/m−2 for the continuous group; 58.63 ± 7.22 years, 173.16 ± 6.97 cm, 67.49 ± 10.16 kg, and 22.48 ± 2.89 kg/m−2 for the interval group; and 58.27 ± 6.24 years, 167.89 ± 5.31 cm, 68.47 ± 17.07 kg, and 24.16 ± 4.91 kg/m−2 for the control group. There was no significant difference in groups' ages, F = 0.245, p = −.780.
Subjects' pretreatment and posttreatment mean ± SD for BP, SUA level, and o2max for the exercise (interval and continuous) and control groups are depicted in Table 1. ANOVA results in Table 2 indicated a significant reduction in the exercise (interval and continuous) groups over control in SBP, DBP, and SUA level at p < 0.05. Results also indicated no significant difference between the interval and continuous groups in SBP (p = 0.521), DBP (p = 0.057) and SUA (p = 0.107) at p < 0.05.
There was significant negative correlation between changes in o2max and changes in serum uric acid level (r = −0.220 [Figure 2]); SBP (r = −0.212 [Figure 3]), and DBP (r = −0.267 [Figure 3]) at p < 0.01.
The purpose of this study was to test the hypothesis that there would be a significant difference between experimental and control groups in SBP, DBP, o2max, and SUA. Also, it was hypothesized that the interval group would not differ significantly from the continuous group in SBP, DBP, o2max, and SUA. Both hypotheses were supported by the results of the present study. Findings of the present study indicated a significant reduction in SBP and DBP and a significant increase in o2max as a result of continuous and interval exercise training; several previous studies (23,39,41) have reported similar findings. The present study also demonstrated a significant reduction in the exercise group's serum uric acid level over control. This finding is in line with the report of Filipovsky et al (14), who investigated the effect of 5-weeks of an aerobic physical training course on uricemia levels of 77 sedentary subjects with hypertension. They reported a significant decrease in uric acid level at p < 0.001. This significant change persisted up to between 3 and 7 months after the intervention of exercise training. They concluded that a 5-week intensive physical training had a favorable short- and long-term effect on uricemia levels in hypertension.
Langlois et al. (22) reported a contrary notion; they investigated whether uric acid (UA) status is related to lower-limb function in patients with hypertension and peripheral arterial disease (PAD). One hundred and forty-five nonhypertensive subjects with PAD and 166 subjects with hypertension and PAD participated. Subjects involved were engaged in aerobic exercise on a treadmill. They reported a significant increased in serum uric acid concentration in PAD hypertension (404 ± 101 vs. 347 ± 80 μmol/L, p < 0.001).
Leyva et al. (26) investigated the relationship between SUA concentrations and the measures of functional capacity. Fifty-nine patients with a diagnosis of chronic heart failure as a result of coronary heart disease (n = 34) or idiopathic dilated cardiomyopathy (n = 25) and 20 healthy controls underwent assessment of functional capacity. o2max and SUA were measured during a maximal treadmill exercise test. They reported an inverse relationship between SUA concentrations and measures of functional capacity in patients with cardiac failure. They concluded that the strong correlation between SUA and o2max suggests that in chronic heart failure, increased SUA concentrations reflect an impairment of oxidative metabolism.
However, in the present study, both the interval and continuous groups did not differ significantly in all parameters assessed. This finding is in disagreement with the report of Ulrik et al. (48), who investigated the therapeutic and comparative effects of aerobic interval (AIT [90-90%peak HR]) training and moderate continuous training (MCT [70-75% peak HR]) in subjects with heart failure. Twenty-seven subjects with postinfarction heart failure were randomized, 9 each, to AIT, MCT, and control. Subjects exercised on a treadmill 3 times per week for 12 weeks. They reported a significant effect of both training modalities over control. However, a more favorable effect of AIT over MCT in SBP and DBP was reported.
Reasons for the discrepancy in findings between the present study and others might not be unconnected to varied intensities and modalities of exercise used, methodological/protocol differences, and the subjects' conditions. Langlois et al (22) involved subjects with hypertension coupled with PAD compared to subjects with only a hypertensive condition in the present study; the effect of preexisting PAD coupled with hypertension on variables could not be ruled out. Also, Ulrik et al. (44) in their study utilized and compared high-intensity interval and moderate-intensity continuous programs on heart failure as compared to moderate-intensity continuous and interval training programs on hypertension in the present study. The effect of training mode, intensity, and exercise protocol is worthy of consideration.
The present study demonstrated a rational basis for the adjunct role of long-term moderate-intensity continuous and interval exercise training in the downregulation of blood pressure and serum uric acid concentration in the management of hypertension, and neither seems superior to the other. Therefore, exercise specialists should feel confident in the use of both types of training in the nonpharmacological adjunct management of hypertension.
The author wishes to thank the staff of the physiotherapy department and hypertensive clinic MMSH, Kano and the Department of Medical Rehabilitation, UNEC, Nigeria and subjects with hypertension who volunteered to participate in the study. There were no professional relationships for the author of this study and any company or manufacturer cited in this text. The results of this study do not constitute endorsement of any product by the author.
1. Akinpelu, AO. Responses of the Africa hypertensive to exercise
training: Preliminary observations. J Hum Hypertens
4: 74-76, 1990.
2. American College of Sports Medicine. ASCM's Guidelines for Exercise Testing and Prescription
. 5th ed. Baltimore: Williams and Wilkins, 1995.
3. American College of Sports Medicine. Position stand: Physical activity, physical fitness, and hypertension
. Med Sci Sports Exerc
25: i-x, 1993.
4. Anker, SD, Doehner, W, Rauchhaus, M, Sharma, R, Francis, D, Knosalla, C, Davos, CH, Cicoira, M, Shamim, W, Kemp, M, Segal, R, Osterziel, KJ, Leyva, F, Hetzer, R, Ponikowski, P, and Coats, AJ. Uric acid
and survival in chronic heart failure: Validation and application in metabolic, functional, and hemodynamic staging. Circulation
107: 1991-1997, 2003.
5. Bachorik, PS. Collection of blood sample for lipoprotein analysis. Clin Chem
28: 1375-1378, 1982.
6. Barbieri, M, Ferrucci, L, Corsi, AM, Macchi, C, Lauretani, F, Bonafe, M, Olivieri, F, Giovagnetti, S, Franceschi, C, and Paolisso, G. Is chronic inflammation a determinant of blood pressure
in the elderly? Am J Hypertens
16: 537-543, 2003.
7. Becker, BF. Towards the physiological function of uric acid
. Free Rad Biol Med
14: 615-631, 1993.
8. Benegas, JR. Epidemiologia de la hypertension
arterial en Espana. Prevalencia, conocimneto Y control. Hypertension
16: 315-322, 1999.
9. Brand, FN, McGee, DL, Kannel, WB, Stokes, J, and Castelli, WP. Hyperuricemia as a risk factor of coronary heart disease: the Framingham study. Am J Epidemiol
121: 11-18, 1985.
10. Breckenridge, A. Hypertension
and hyperuricaemia. Lancet
1: 15-18, 1966.
11. Brooks, GA, Fahey, TD, and White, TP. Exercise Physiology, Human Bioenergetics and Its Application
. 2nd ed. Mountain View, CA: May Field Publishing, 1996.
12. Campion, EW, Glynin, RJ, and DeLabry, LO. Asymptomatic hyperuricemia. Risks and consequences in the normative aging study. Am J Med
82: 421-428, 1987.
13. Duarte, JAR, Appel, HJ, Carvalho, F, Bastos, M L, and Soares, JMC. Endothelium-derive d oxidative stress may contribute to exercise
-induced muscle damage. Int J Sports Med
14: 440-443, 1993.
14. Filipovsky, J, Simon, J, Chqragtek, J, Rosolova, H, Haman, P, and Petrikova, V. Changes of blood pressure
and lipid profile during a physical training course in hypertensive subjects. Cardiology
78: 31-38, 1991.
15. Glantzounis, GK, Tsimoyiannis, EC, Kappas, AM, and Galaris, DA. Uric acid
and oxidative stress. Current Pharmaceutical Design
11: 4145-4151, 2005.
16. Golding, LA, Meyers, CR, and Sinniny, WE. Way to Physical Fitness. The Complete Carnote to Fitness Testing and Instruction
. 3rd ed. Champaign, IL: Human Kinetics, 1989.
17. Hellsten, Y, Frandsen, U, Orthenblad, N, Sjødin, B, and Richter, EA. Xanthine oxidase in human skeletal muscle following eccentric exercise
: A role in inflammation. J Physiol
498: 239-248, 1997.
18. International Society for the Advancement of Kinanthropometry (ISAK). International Standards for Anthropometric Assessment
. Patche Fstroom, South Africa: ISAK, 2001.
19. Jean-Michel, M, Bernard, C, Roland, A, Peter, W, Eoino, B, Daniel, D, Michael, FO, Karl-Henz, R, Ramon, P, Edward, B, Gerhart, H, and Michael, ES. Twenty-four hour ambulatory blood pressure
monitoring efficacy of peridopril/Indapamide first line combination in hypertensive patients. Am J Hypertens
17: 245-251, 2004.
20. Katzung, BG. Basic and Clinical Pharmacology
. 7th ed. New York: Lange Medical Books/Craw Hill, 1998.
21. Lamina S, Okoye CG, and Dagogo TT. Therapeutic effect of an interval exercise
training program in the management of erectile dysfunction in hypertensive patients. J Clin Hypertens
(Greenwich) 11: 1-5, 2009.
22. Langlois, M, DeBacquer, D, Duprez, D, Debuyzere, M, Delanghe, J, and Blaton, V. Serum uric acid
in hypertensive patients with and without peripheral arterial disease. Atherosclerosis
168: 163-168, 2003.
23. Laterza, MC, Demator, LD, Trombetta, IC, Braza, AM, Roveda, F, Alves, MJ, Negrao, CE, and Rondon, MU. Exercise
training restores baroreflex sensitivity in never trained hypertensive patients. Hypertension
49: 1298-1306, 2007.
24. Lehto, S, Niskanen, L, Ronnemaa, T, and Laakso, M. Serum uric acid
is a strong predictor of stroke in patients with non-insulin-dependent diabetes mellitus. Stroke
29: 635-639, 1998.
25. Levine, W, Dyer, AR, Shekelle, RB, Schoenberger, JA, and Stamler, J. Serum uric acid
and 11.5-year mortality of middle-aged women: findings of the Chicago Heart Association Detection Project in Industry. J Clin Epidemiol
42: 257-267, 1989.
26. Leyva, F, Anker, S, Swan, JW, Godsland, IF, Wingrove, CS, Chua, TP, Stevenson, JC, and Coats, AJS. Serum uric acid
as an index of impaired oxidative metabolism in chronic heart failure. Eur Heart J
18: 858-865, 1997.
27. Liese, AD, Hense, HW, Lowel, H, Doring, A, Tietze, M, and Keil, U. Association of serum uric acid
with all-cause and cardiovascular disease mortality and incident myocardial infarction in the MONICA Augsburg cohort. World Health Organization Monitoring Trends and Determinants in Cardiovascular Diseases. Epidemiology
10: 391-397, 1999.
28. Mancia, G, Ferari, L, Gregorini, L, Leonett, L, Terzoli, L, Biachini, C, and Zanchetti, A. Effects of treatment with methyldopa on basal haemodynamic and on rural control. In: The Therapeutics of Hypertension
. Robertson, JS, Pickering, GW, and Goldwell, ADS, (eds.). London: Royal Society of Medicine and Academic Press Inc, Ltd. 1980. pp. 70-78.
29. Musa, DI. Ibrahim, DM, and Toriola, AL. Cardiorespiratory fitness and risk factors of CHD in pre-adolescent Nigerian girls. J Hum Move Studies
42: 455-455, 2002.
30. Nakahama, H, Fukuch, K, Yoshihana, F, Nakamura, S, Inenaga, T, Takiuch, S, and Kamide, K. Efficiency of screening for primary aldosteronism by adrenocortical scintigraphy without discontinuing antihypertensive medication. Am J Heart
16: 725-728, 2003.
31. Pallant, J. SPSS Survival Manual: A Step by Step Guide to Data Analysis Using SPSS
. Berkshire, UK: Open University Press, 2001.
32. Pescatello, LS, Franklin, BA, Fagard, R, Farquhar, WB, Kelley, GA, and Ray, CA. American College of Sports Medicine. American College of Sports Medicine position stand. Exercise
. Med Sci Sports Exerc
36: 533-553, 2004.
33. Piug, JG and Ruilop, LM. Uric acid
and cardiovascular risk factor in arterial hypertension
. J Hypertens
17: 869-872, 1999.
34. Pollock, ML and Wilmore, JH. Exercise in Health and Disease: Evaluation and Prescription for Prevention and Rehabilitation
. 2nd ed. Philadelphia: WB Saunders Company, 1990.
35. Proctor, P. Electron-transfer factors in psychosis and dyskinesia. Physiol Chem Phys
4: 349-360, 2005.
36. Ross, WD and Marfell-Jones, MJ. Physiological testing of the high performance athletes. In: Kinanthropometry
. MacDugall, JD, Wenger, A, and Green, HJ, (eds.). Champaign, IL: Human Kinetics, 1991. pp. 223-308.
37. Salako, LA. Treatment of Hypertension: Cardiovascular Disease in Africa
. Ibadan: Ciba Geigy Ltd, 1976.
38. Sastre, J, Gascó, AME, Ferrero, JA, Furukawa, T, and Viña, J. Exhaustive physical exercise
causes and oxidation of glutathione status in blood. Prevention by antioxidant administration. Am J Physiol
263: R992-R995, 1992.
39. Smith, PJ, Blumenthal, JA, Babyk, MA, Georgiades, A, Hinderlister, A, and Sherwood, A. Effects of exercise
and weight loss on depressive symptoms among men and women with hypertensive. J Pschosome Res
63: 463-469, 2007.
40. Somani, SM and Husain, K. Interaction of exercise
training and chronic ethanol ingestion on antioxidant system of rat brain regions. J Appl Toxicol
17: 329-336, 1997.
41. Stewart, KJ, Bacher, AC, Turner, KL, Fleg, JL, Hees, PS, Shapero, EP, Tayback, M, and Ouyang, P. Effects of exercise
on blood pressure
in older person. Arch Intern Med
165: 756-762, 2005.
42. Townsend, RR, McFadden, TC, Ford, V, and Cadee, JA. A randomized double blind, placebo-controlled trial of casein protein hydrolysate (C12 peptide) in human essential hypertension
. Am J Hypertens
17: 1056-1058, 2004.
43. Tykarski, A. Evaluation of renal handling of uric acid
in essential hypertension
: Hyperuricemic related to decreased urate secretion. Nephron
59: 364-368, 1991.
44. Ulrik, W, Asbjorn, LP, Morten, B, Qivird, R, PerMagnus, H, Erik, TA, Jan, H, Stig, S, Jun, LS, Vibeke, V, Anja, B, Godfrey, S, Sonia, N, Oyvind, E, and Terje, S. Superior cardiovascular effect of aerobic interval training versus moderate continuous training in heart failure patients. Circulation
115: 3086-3094, 2007.
45. Waeber, B, Nussberger, J, and Brunner, HR. The rennin angiotension system: role in experimental and human hypertension
. In: Pathophysiology of Hypertension: Regulatory Mechanisms
. Zanchetti, A and Tarazi, RC, (eds.). Amsterdam: Elsevier, 1986. pp. 489-519.
46. Walker, AJ, Bassett, DR, Duey, WJ, Howley, ET, Bond, V, Torok, DJ, and Mancuso, P. Cardiovascular and plasma catecholamine responses to exercise
in blacks and whites. Hypertension
20: 542-548, 1992.
47. Ward, HJ. Uric acid
as an independent risk factor in the treatment of hypertension
352: 670-671, 1998.
Keywords:© 2011 National Strength and Conditioning Association
hypertension; exercise; uric acid; blood pressure