Arterial hypertension is associated with increased risk of cardiovascular diseases including stroke, coronary heart disease, atrial fibrillation, and renal failure (25). Furthermore, arterial hypertension is associated with a higher all-cause and cardiovascular mortality (25). Physical activity is considered to be a cornerstone in prevention and treatment of mild hypertension (33), and it is well documented that aerobic physical activity lowers arterial blood pressure (BP) and results in a variety of favorable effects on cardiovascular risk factors (32). To date, a clear relationship between the exercise intensity and the reduction in BP has not been established (9). However, aerobic high-intensity training appears to be more effective than moderate-intensity continuous exercise training for improving heart function, maximal oxygen uptake (V˙O2max), muscle oxidative capacity, and risk factors for the metabolic syndrome in healthy men as well as patients experiencing hypertension and severe obesity (28,29,37,38).
Recent studies from our research group have shown that recreational soccer is an intense intermittent sport activity that causes marked reductions in BP and improvement of peripheral arterial function after short-term interventions for untrained normotensive young men and women (21,22), as well as habitually active men with mild untreated hypertension and untrained middle-age men with mild-to-moderate hypertension (2,17). Furthermore, short- and long-term soccer training studies have shown that regular soccer training has broad spectrum effects on physical fitness as well as favorable effects on cardiovascular risk factors such as maximal oxygen uptake, heart function, body fat mass, and LDL cholesterol levels in healthy untrained young men and women (20–22,35). However, it remains to be investigated whether regular medium-term (6 months) soccer training for untrained middle-age men with mild-to-moderate hypertension is more effective for reduction of BP than standard physician-guided advice on healthy diet and physical activity. Likewise, it is unknown whether regular medium-term soccer training is effective for improvement of physical fitness and in the reduction of other cardiovascular risk factors in this population.
Therefore, the aims of the present study were to investigate the effects of a medium-term soccer training intervention for untrained hypertensive middle-age men on BP, peripheral arterial function, fat mass, bone mineral content (BMC) and density (BMD), plasma lipids, and maximal oxygen uptake, as well as exercise capacity during maximal and submaximal exercise, and to compare these effects with the effect of traditional physician-guided recommendations on cardiovascular risk factor modification.
METHODS
Subjects
Thirty-three untrained males age 46 yr (range = 31–54 yr) with a mean ± SD body mass, body mass index, fat percentage, and V˙O2max of 97.8 ± 13.6 kg, 30.0 ± 3.3 kg·m−2, 30.3% ± 3.2%, and 32.5 ± 5.2 mL·min−1·kg−1, respectively, took part in the study. The participants were diagnosed with mild-to-moderate arterial hypertension with systolic BP (SBP) from 140 to 160 mm Hg and diastolic BP (DBP) from 90 to 110 mm Hg, i.e., grade 1 and 2 hypertension according to established guideline definitions (26) (time from diagnosis = 5.3 ± 4.0 yr, range = 0.1–20.3 yr) but were otherwise healthy without cardiopulmonary symptoms and with normal physical examination electrocardiogram. Participants received 0, 1, or 2 conventional antihypertensive drugs apart from β-blockers, which were excluded because of their HR-lowering properties (no medication: n = 10, thiazides: n = 10, calcium channel blockers: n = 3, angiotensin-converting enzyme [ACE] inhibitors or angiotensin receptor blockers: n = 19). Of the subjects in STG and DAG, 68% and 73% were taking one to two antihypertensive drugs; 61% and 55% on ACE inhibitors/angiotensin receptor blockers; 38% and 18% on diuretics; and 10% and 9% on calcium channel blockers. The subjects had not performed regular physical training for at least 1 yr. The study was approved by the local ethical committee of Copenhagen, and all participants gave signed informed consent (H-D-2009-033).
Design
The subjects underwent a series of baseline tests and were randomized 2:1 to a soccer training group (STG, n = 22) or a doctor’s advice group (DAG, n = 11). The subjects in STG participated in supervised soccer training for 1 h two times per week over 6 months, whereas the participants in DAG were advised by a cardiologist on the favorable effects of a healthy lifestyle, with thorough information about the recommended physical activity and nutrition based on the European guidelines for management of arterial hypertension (26). Accordingly, patients were advised to take up regular physical exercise of moderate intensity, e.g., 30–45 min daily, primarily endurance physical activity (walking, jogging, swimming) supplemented by moderate resistance exercise (26). Tests were performed at baseline and after 3 and 6 months of the intervention to examine effects on BP, resting HR (RHR), peripheral arterial function, maximal oxygen uptake, body composition, plasma lipid profile, glucose and insulin concentrations, metabolic response to exercise, and physical performance. Power calculations were performed for the main outcome measure, i.e., BP, using previous data from 3-month football training interventions for hypertensive men (2,17). The power was calculated to be 0.85 for mean arterial pressure (MAP) with an assumed difference in delta values between groups of 6 mm Hg and an assumed variability of 5 mm Hg. The intention-to-treat method was used with last-observation-carried-forward because six and four subjects dropped out from the STG and DAG, respectively, between 3 and 6 months. Two participants in STG dropped out because of injuries sustained during study related training; the remainder of the subjects dropped out because of inability to adhere to the prespecified study protocol. All subjects except three had an unaltered medication during the intervention. One participant in STG terminated antihypertensive diuretics treatment (thiazide) after 3 months because of low BP and orthostatism, whereas two participants in DAG had unacceptable high BP at the 3-month control visit and their antihypertensive medication was intensified (calcium channel blocker was added and ACE inhibitor dose was increased).
Training intervention
The soccer training sessions were performed outdoor on natural grass twice per week for 6 months. Each training session lasted 1 h, and sessions were supervised by one of the investigators. The soccer sessions consisted of ordinary five-a-side, six-a-side, or seven-a-side matches on a 30- to 45-m-wide and 45- to 60-m-long grass pitch. Each training session was initiated by a 5-min low-intensity warm-up period, and thereafter the participants carried out four playing periods each lasting 12 min separated by 2-min recovery periods. The total number of training sessions was 43 ± 13 (1.7 ± 0.5 wk−1). HR of participants was measured continuously during all training sessions using HR belts (POLAR Team System; Polar Electro Oy, Kempele, Finland). The average HR during soccer training was 155 ± 9 bpm or 85% ± 7% individual HRmax, with 28% ± 16% of the total training time with HR values above 90% HRmax. There were no objective measurements of physical activity in DAG, but subjects were questioned about changes in physical activity at control visits. At the end of the study, 27% of the subjects in DAG remained physical inactive, 45% had taken up light physical training (walking, slow jogging, or cycling, approximately 1 h·wk−1), and 27% had started more regular and intense physical training (fitness center training or cycling, approximately 3 h·wk−1).
Blood pressure
Arterial SBP and DBP were measured at baseline and at 3 and 6 months with the subject in the supine position after at least 15 min of rest in a quiet room. Mean arterial BP was calculated as 1/3 SBP + 2/3 DBP (33). BP was recorded five times in both upper arms by an automatic BP monitor (HEM-709; OMRON, IL) with a cuff adjusted to the arm size as appropriate. RHR was measured simultaneously by the automatic BP monitor. The average values of all 10 measurements are presented. BP measurements were recorded in the afternoon, at least 6 h after intake of relevant antihypertensive medication.
Peripheral arterial function
Peripheral arterial tonometry was performed in a quiet dimmed room with a pneumatic probe placed on the tip of each index finger and connected to a plethysmographic device (EndoPAT2000; Itamar Medical Ltd., Caesarea, Israel), as previously described (13,23,31). Accordingly, peripheral endothelium-dependent vasodilator capacity was determined by the reactive hyperemia index measured after abrupt deflation of a BP cuff on the nondominant arm inflated to achieve forearm ischemia for 5 min. Arterial stiffness was assessed by the augmentation index calculated by a computer algorithm as the difference between the early and late systolic peaks of averaged arterial pressure waveforms expressed as a percentage of the early peak amplitude (30). Peripheral arterial tonometry has emerged as a feasible method for determination of small artery (digital) reactive hyperemic and augmentation indices suitable for use in ambulatory and population settings that correlates with measurements obtained by more operator-dependent and time-consuming investigations of large conduit arteries, e.g., ultrasound examination of brachial artery flow-mediated vasodilatation and radial artery tonometry (12,13,23,31).
Fasting blood samples
Blood samples were obtained from an arm vein between 7 and 10 a.m. under standardized conditions after an overnight fast. Within 10 s of sampling, 100 μL of blood was hemolyzed in an ice-cold 100 μL of Triton X-100 buffer solution and was later analyzed for lactate and glucose using an YSI 2300 lactate analyzer (Yellow Springs Instruments, Yellow Springs, OH). The rest of the sample was rapidly centrifuged for 30 s. Plasma samples were analyzed by an automatic analyzer (Cobas Fara, Roche, France) using enzymatic kits (Roche Diagnostics, Germany) for determinations of total cholesterol, LDL-cholesterol, HDL-cholesterol, and triglyceride levels. High-sensitivity C-reactive protein levels were measured by turbidimetric immunoassay (Vitros 5.1 FS Chemistry System; Ortho-Clinical Diagnostics, Raritan, NJ). Duplicate analyses (n = 20) revealed coefficients of variation of 3%, 2%, 5%, and 9% for blood glucose, lactate, cholesterol, and plasma insulin, respectively.
Body composition
Whole body and regional fat mass, muscle mass, BMD, and BMC were determined by DXA scans (LUNAR; GE Medical Systems, Madison, WI). Body weight was measured in the morning after an overnight fast on a platform scale, with a precision of 0.01 kg (Ohaus, Pine Brook, NJ).
Submaximal and maximal exercise test.
Pulmonary gas exchange (CPX MedGraphics, St. Paul, MN) and HR (Polar Team System; Polar Electro Oy) were measured during a standardized cycle test. The test consisted of one 6-min bout of submaximal exercise at 100 W followed by a 4-min rest period and an incremental cycle test to exhaustion starting at 50 W with 10-W increments every 30 s. Blood samples were collected from an arm vein before and immediately after the 100-W exercise bout, as well as immediately after and 3 min after the incremental test for measurements of plasma lactate levels (Yellow Spring Instruments). Submaximal HR, oxygen uptake, and RER were calculated as the mean values over the last minute of the 6-min exercise bout at 100 W. Incremental exercise test performance was determined as the time to exhaustion. All subjects reached RER values above 1.15 at exhaustion. V˙O2max and maximal HR were determined as the peak value reached in a 30- and 15-s period, respectively, during the last part of the incremental test.
Statistics
Two-way ANOVA with repeated-measures were used to evaluate the time (0, 3, and 6 months) and treatment (STG and DAG) effects. When a significant time–group interaction was detected, data were subsequently analyzed using a least significant difference post hoc test. The coefficient of variation was calculated as the SD of the differences between test–retest results divided by the mean values of results and multiplied by 100. Significance for all analyses was set at P < 0.05. Because of inherent technical difficulties with some of the measurements, the number of subjects presented for each variable varied from 16 to 22 in STG and 8 to 11 in DAG. Data are presented as means ± SD.
RESULTS
Baseline values
There were no significant differences between STG and DAG in any measures at baseline (Tables 1 and 2 and Figs. 1–3).
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TABLE 1: Maximal oxygen uptake (V˙O2max), mean arterial pressure (MAP), reactive hyperemia index (RHI), exercise response, and blood variables in 31- to 54-yr-old hypertensive men after 0, 3, and 6 months of soccer training for 1 h twice a week (STG) or receiving doctor’s advice on a healthy lifestyle (DAG).
TABLE 2: Body composition for 31- to 54-yr-old hypertensive men after 0, 3, and 6 months of soccer training for 1 h twice a week (STG; n = 20) or receiving doctor’s advice on healthy lifestyle (DAG, n = 10).
FIGURE 1: Maximal oxygen uptake (A) and the aerobic loading during submaximal cycle exercise at 100 W, expressed as the exercise V˙O2 in relative to V˙O2max (B) for 31- to 54-yr-old hypertensive males after 0, 3, and 6 months of soccer training for 1 h twice a week (STG, n = 22) or doctor’s advice on healthy lifestyle advice (DAG, n = 10). Data are presented as means ± SD. *Significant difference from baseline in STG. #Significant difference from DAG at corresponding time point.
FIGURE 2: SBP (A) and DBP (B) for 31- to 54-yr-old hypertensive males after 0, 3, and 6 months of soccer training for 1 h twice a week (STG, n = 20) or doctor’s advice on healthy lifestyle (DAG, n = 11). Data are presented as means ± SD. *Significant difference from baseline in STG. $Significant difference from baseline in DAG. #Significant difference from DAG at corresponding time point.
FIGURE 3: Augmentation index, i.e., a measure of arterial stiffness, for 31- to 54-yr-old hypertensive males after 0, 3, and 6 months of soccer training for 1 h twice a week (STG, n = 19) or receiving doctor’s advice on healthy lifestyle advice (DAG, n = 10). Data are presented as means ± SD. *Significant difference from baseline in STG. #Significant difference from DAG at the corresponding time point.
Maximal oxygen uptake
A significant time–group interaction was found for V˙O2max (P < 0.001; F = 9.2). Post hoc tests revealed an increase (P < 0.05) of 2.8 ± 2.9 mL·min−1·kg−1 over 6 months for STG, with no change in DAG (−0.8 ± 1.8 mL·min−1·kg−1), resulting in a 13% greater (P < 0.05) V˙O2max in STG than DAG after 6 months (Fig. 1A). A significant time–group interaction (P < 0.05, F = 4.1) was observed for relative aerobic loading during submaximal cycling at 100 W with a decrease of 5% ± 4% V˙O2max in STG over 6 months but no change in DAG (+1% ± 3% V˙O2max; Fig. 1B).
Blood pressure
Significant time–group interactions were found for SBP (P < 0.05, F = 3.1) and DBP (P < 0.05, F = 5.0). Over 6 months, SBP and DBP was lowered (P < 0.01) by 13 ± 9 and 8 ± 6 mm Hg, respectively, in STG, with corresponding changes of 8 ± 5 and 3 ± 3 mm Hg in DAG (Fig. 2). Thus, over 6 months, MAP decreased more (P < 0.05 for interaction; F = 4.7) in STG than in DAG (10 ± 5 vs 5 ± 2 mm Hg) (Table 1). Post hoc tests revealed that SBP, DBP, and MAP were significantly lower (P < 0.05) in STG than in DAG after 6 months (Fig. 2 and Table 1). A significant time–group interaction was also observed for RHR (P < 0.05, F = 3.5). Over 6 months, RHR decreased (P < 0.05) by 8 ± 11 bpm in SG, with no significant change for DAG (−3 ± 9 bpm; Table 1).
Peripheral vascular function
A significant time–group interaction was found for augmentation index (P < 0.05, F = 3.0). Post hoc tests showed that augmentation index was lowered by 7.3 ± 14.0 after 6 months in STG, whereas no difference was observed in DAG resulting in a lower (P < 0.05) augmentation index in STG than in DAG after 6 months (Fig. 3). Reactive hyperemia index remained unchanged both in STG and in DAG over the 6 months (Table 1).
Blood variables
No significant time–group interactions were observed for total cholesterol, HDL, LDL, triglyceride, blood glucose, insulin, or CRP levels (Table 1).
Body composition
No significant time–group interaction was observed for whole body fat mass, lean body mass, or bone mineralization (Table 2).
DISCUSSION
The main findings of the present study were that 6 months of soccer training effectively improved physical fitness and was more effective than traditional physician-guided advice in the treatment of mild-to-moderate hypertension. After 6 months of soccer training, pronounced reductions were observed in BP in combination with an elevated maximal oxygen uptake and an attenuation of the metabolic stress during submaximal exercise. In addition, RHR was lowered and the peripheral arterial augmentation index was improved, altogether providing a multifactorial reduction of cardiovascular risk factors by twice-weekly training sessions of soccer in middle-age hypertensive men.
As a result of the soccer training, SBP and DBP were reduced by 13 and 8 mm Hg, respectively, which was more than the 8- and 3-mm Hg reductions observed in participants that received physician-guided advice on physical activity and a healthy diet. Our previous investigations have also shown marked BP reductions after short- and long-term soccer training for normotensive untrained men and women (1,20–22,34) and after short-term training for young and middle-age hypertensive men (2,17). The net reductions of SBP and DBP after aerobic training for hypertensive males have previously been shown to average 7 and 5 mm Hg, respectively (5,9), with smaller reductions of 3 and 2 mm Hg reported in normotensive male populations (9). Thus, results of the present and previous soccer intervention studies indicate that the magnitude of BP reduction is larger than what is usually observed in intervention studies using aerobic training. Interestingly, after the intervention period 75% and 71% of the participants in the soccer group had SBP below 140 mm Hg and DBP below 90 mm Hg, respectively, whereas this was only the case for 38% and 27%, respectively, of the participants in the physician-guided advice group. In the soccer group, one subject experienced very low BP and orthostatic symptoms after 3 months of training, and the antihypertensive medication (a diuretic) was obviously terminated. In contrast, two of the subjects in DAG had unacceptably high BP at the 3-month control visit, and antihypertensive medication was intensified. These findings demonstrate that soccer can be used as a nonpharmacological treatment of hypertension in middle-age men and suggest that soccer may be even better than traditional treatment in normalizing BP.
Using peripheral arterial tonometry, we found that the augmentation index was lowered after soccer training, whereas this correlate of arterial stiffness remained unchanged in DAG and the reactive hyperemia index, a well-established measure of endothelial function, was not changed in either group. Arterial stiffness increases in the presence of hypertension and other cardiovascular risk factors and is associated with subclinical atherosclerosis, adverse cardiovascular events, and increased mortality in hypertensive subjects and other populations (27,30). Specifically, artery stiffness is an independent predictor of mortality in patients with hypertension and the significant reduction of augmentation index observed in our study is therefore suggestive of distinct favorable effects of soccer training on cardiovascular prognosis (27). Increased augmentation index has been associated with physical inactivity, and limited evidence suggests that in hypertensive patients, interval training is associated with more effective reduction of augmentation index than continuous exercise training (11). Indeed, we have previously found that in untrained premenopausal women, 16 wk of soccer training was associated with reduction of augmentation index measured by peripheral arterial tonometry, whereas no such effect was observed after moderate intensity endurance running (21). In that study, skeletal muscle capillarization increased by approximately 20% after soccer training but remained unchanged in the running group, and we hypothesize that similar expansion of the microvascular bed contributed to altered pressure wave reflections and consequently decreased augmentation index in the current study. Interestingly, decreased augmentation index after soccer training was not accompanied by amelioration of endothelial dysfunction as determined by the reactive hyperemia index, and the same apparent dissociation between effects on these two noninvasive measures of arterial function was observed in our previous short-term study of soccer training in premenopausal women (21).
Endothelial dysfunction is characterized by reduced bioavailability of endothelium-derived nitric oxide and as is the case with increased arterial stiffness, reduced reactive hyperemic response, e.g., measured by peripheral arterial tonometry, is associated with hypertension and other classical cardiovascular risk factors, subclinical atherosclerosis, and adverse cardiovascular prognosis (7,13). Large conduit artery endothelial dysfunction can improve after exercise training, e.g., in patients with hypertension and improvement of aerobic interval training may be more effective in this respect than continuous training (7,37). Endothelial dysfunction clearly contributes to arterial stiffness and parallel effects on reactive hyperemic and augmentation indices after soccer training may therefore have been expected. On the other hand, recent evidence has indicated that the correlation between noninvasive measures of large and small artery endothelial function may be modest in some populations (14,23,36). However, even in absence of detectable improvements of small artery endothelial function, decreased augmentation index after soccer training is likely to have contributed to BP reduction. In addition, reduced sympathoadrenergic tone as suggested by the observed reduction of RHR may have contributed to BP reduction, and it is noteworthy that RHR is a well-documented independent cardiovascular risk factor, e.g., in hypertensive individuals, and that increased RHR has been linked to increased vascular oxidative stress, endothelial dysfunction, and accelerated atherosclerosis (6). Numerous other mechanisms may have added to BP reduction after soccer training, e.g., increased vascular expression of antioxidative enzymes, enhanced resistance vessel sensitivity to vasodilating mediators, and mobilization of endothelial progenitor cells to the arterial wall, and more studies are required to gain further mechanistic insights (10).
A low aerobic fitness measured as V˙O2max has been shown to be another important predictor of cardiovascular disease and mortality risk (8,15,16,24). Both intervention groups had low V˙O2max at baseline, 70% of the participants had values below 35 mL·min−1·kg−1 and all subjects were below 44.2 mL·min−1·kg−1, which has been suggested to be cutoff points for marked elevations in the risk of cardiovascular diseases (3,32). After 6 months of soccer training, the maximal oxygen uptake was elevated by 2.8 mL·min−1·kg−1 (9%) on average, whereas no significant changes were observed for the physician-guided advice group (−3%). These improvements are lower than the 10%–15% increases of V˙O2max reported in other short-term soccer training studies for untrained young men and women (4,17,19,35), which may in part be because this study used a cycle exercise test rather than a treadmill test. Nonetheless, the observed increase in maximal oxygen uptake is still important for the cardiovascular health profile because the prevalence of cardiovascular risk factors has been shown to be 56% higher for every 5 mL·min−1·kg−1 decrements in V˙O2max for the general population (3) and a 15% reduction in the risk of death with every 1 mL·min−1·kg−1 increase in V˙O2max for patients with coronary artery disease has been reported (16). The observation that the physician-guided advice group demonstrated no effects on V˙O2max and incremental exercise performance is in accordance with the fact that only a minor part of these patients (27%) reported undertaking moderate to vigorous exercise during the study period. Thus, it is possible that the observed changes in BP in this group were not related to increases in exercise but to other lifestyle changes.
At baseline, the fat percentages were high for the participants in both study groups, with 90% and 50% of subjects having values above 25% and 30% of body fat, respectively, which constitute another risk factor for cardiovascular disease (39,40). Although no significant time–group interaction was observed for fat mass, it is still noteworthy that 6 months of soccer training resulted in a decrease in fat mass of 2.0 kg, with a corresponding value of 0.9 kg in the physician-guided advice group. Recent studies on twice-weekly soccer training for untrained young males have shown consistent reductions in fat mass of 1.7–3.2 kg after 3–16 months of soccer interventions without concomitant diet manipulations (19,22,34,35). Thus, the present study confirms that regular soccer training provides favorable alterations of body composition for a variety of populations. The observed decrease in fat mass for the soccer training group is likely to be related to increased energy expenditure, estimated to be approximately 750 kcal per soccer training session or a total of about 35,000 kcal during the whole study period, but may also be related to a higher level of fat oxidation during everyday lifestyle activities. In support of this notion, the present data showed that RER during submaximal cycle exercise was lowered from 0.93 to 0.87 after 6 months of soccer training, which corresponds to an increase in the estimated fat oxidation from 24% to 43% of total energy turnover during submaximal cycling at 100 W (19). After 6 months of training, the soccer training group also had markedly lower RHR and a lower relative aerobic loading during submaximal exercise, with magnitudes of changes that are in the same range as those observed in training studies with high-intensity continuous or interval running training and soccer training, respectively (18,19,29). It is noteworthy that the soccer training resulted in marked improvements in aerobic fitness and that the physical stress during low-intensity exercise was attenuated. This may have implications for the capacity and motivation to continue participation in sport activities but may also affect the ability to cope with the demands of everyday life activities, including cycling, walking stairs, shopping, gardening, and cleaning. Taken together, the combined favorable effects of regular soccer training on physical fitness and hypertension may therefore contribute to adoption of a more active lifestyle in general.
The current results should be carefully interpreted in light of methodological limitations. For example, the small study sample limits the statistical validity of the results, and these cannot be directly extrapolated to non-Caucasian ethnicities. There was a relatively high number of study dropouts (albeit that consequently, we used a conservative intention-to-treat analysis), patients with or without antihypertensive drug treatment were considered together, and formalized assessment of the level of physical exercise in DAG during the study period was not performed. In addition, postintervention persistence with soccer training and effects on other end points, e.g., quality of life, long-term clinical outcomes, and cost-effectiveness parameters, were not examined. Further analyses of the injury risk in small-sided recreational soccer training for middle-aged men are also warranted, although it is already clear that the injury incidence is much lower for training sessions than for competitive matches, that injuries such as muscle sprains are minimized by playing on small pitches, and that the exposure is low for recreational soccer compared to elite soccer (75–100 vs 600–900 h of training per year) (21,22).
In summary, 6 months of regular soccer training resulted in marked reductions of BP in untrained middle-aged men with mild-to-moderate hypertension, with 75% of the soccer group participants having normalized their BP at the end of the training intervention. In one subject, a diuretic was terminated because of very low BP. The observed reductions of 13 and 8 mm Hg in SBP and DBP were greater than the reductions in the group who received traditional physician-guided advice on a healthy diet and physical activity and were also larger than usually observed after aerobic training in hypertensive men. Soccer training also decreased arterial stiffness, caused improvements in the physical fitness, and had multiple other positive effects on the cardiovascular risk profile, including a lowered RHR and an elevated maximal oxygen uptake. We conclude that regular soccer training is a better nonpharmacological treatment for untrained hypertensive middle-age men than traditional physician-guided advice.
The authors would like to acknowledge the contribution of the subjects in the present study.
The authors also thank Jens Jung Nielsen, Rikke Jensen, Birgitte Rejkjær Krustrup, Therese Hornstrup, Mads Bendiksen, and Rikke Leihof for excellent technical support.
This study was supported by FIFA–Medical Assessment and Research Centre (F-MARC), Nordea-fonden, the Danish Heart Foundation (Hjerteforeningen), the Danish Football (Soccer) Association (Dansk Boldspil-Union) and the Danish Sports Confederation (Danmarks Idræts-Forbund).
There were no conflicts of interest for any of the authors.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
REFERENCES
1. Andersen LJ, Hansen PR, Sogaard P, Madsen JK, Bech J, Krustrup P. Improvement of systolic and diastolic heart function after physical training in sedentary women.
Scand J Med Sci Sports. 2010; 20 (1 Suppl): S50–7.
2. Andersen LJ, Randers MB, Westh K, et al.. Football as a treatment for hypertension in untrained 30–55-year-old men: a prospective randomized study.
Scand J Med Sci Sports. 2010; 20 (1 Suppl): S98–102.
3. Aspenes ST, Nilsen TI, Skaug EA, et al.. Peak oxygen uptake and cardiovascular risk factors in 4631 healthy women and men.
Med Sci Sports Exerc. 2011; 43 (8): 1465–73.
4. Bangsbo J, Nielsen JJ, Mohr M, et al.. Performance enhancements and muscular adaptations of a 16-week recreational football intervention for untrained women.
Scand J Med Sci Sports. 2010; 20 (1 Suppl):S 24–30.
5. Cornelissen VA, Fagard RH. Effects of endurance training on blood pressure, blood pressure-regulating mechanisms, and cardiovascular risk factors.
Hypertension. 2005; 46 (4): 667–75.
6. Custodis F, Schirmer SH, Baumhakel M, Heusch G, Bohm M, Laufs U. Vascular pathophysiology in response to increased heart rate.
J Am Coll Cardiol. 2010; 56 (24): 1973–83.
7. Deanfield JE, Halcox JP, Rabelink TJ. Endothelial function and dysfunction: testing and clinical relevance.
Circulation. 2007; 115 (10): 1285–95.
8. Erikssen G, Liestol K, Bjornholt J, Thaulow E, Sandvik L, Erikssen J. Changes in physical fitness and changes in mortality.
Lancet. 1998; 352 (9130): 759–62.
9. Fagard RH. Exercise characteristics and the blood pressure response to dynamic physical training.
Med Sci Sports Exerc. 2001; 33 (6 Suppl): S484–92; discussion S93–4.
10. Gielen S, Schuler G, Adams V. Cardiovascular effects of exercise training: molecular mechanisms.
Circulation. 2010; 122 (12): 1221–38.
11. Guimaraes GV, Ciolac EG, Carvalho VO, et al.. Effects of continuous vs. interval exercise training on blood pressure and arterial stiffness in treated hypertension.
Hypertens Res. 2010; 33 (6): 627–32.
12. Haller MJ, Silverstein JH, Shuster JJ. Correlation between radial artery tonometry- and fingertip tonometry-derived augmentation index in children with type 1 diabetes.
Diab Vasc Dis Res. 2007; 4 (1): 66.
13. Hamburg NM, Keyes MJ, Larson MG, et al.. Cross-sectional relations of digital vascular function to cardiovascular risk factors in the Framingham Heart Study.
Circulation. 2008; 117 (19): 2467–74.
14. Hamburg NM, Palmisano J, Larson MG, et al.. Relation of brachial and digital measures of vascular function in the community: the Framingham Heart Study.
Hypertension. 2011; 57 (3): 390–6.
15. Hu G, Tuomilehto J, Silventoinen K, Barengo NC, Peltonen M, Jousilahti P. The effects of physical activity and body mass index on cardiovascular, cancer and all-cause mortality among 47 212 middle-aged Finnish men and women.
Int J Obes (Lond). 2005; 29 (8): 894–902.
16. Keteyian SJ, Brawner CA, Savage PD, et al.. Peak aerobic capacity predicts prognosis in patients with coronary heart disease.
Am Heart J. 2008; 156 (2): 292–300.
17. Knoepfli-Lenzin C, Sennhauser C, Toigo M, et al.. Effects of a 12-week intervention period with football and running for habitually active men with mild hypertension.
Scand J Med Sci Sports. 2010; 20 (1 Suppl):S 72–9.
18. Krustrup P, Bangsbo J. Physiological demands of top-class soccer refereeing in relation to physical capacity: effect of intense intermittent exercise training.
J Sports Sci. 2001; 19 (11): 881–91.
19. Krustrup P, Christensen JF, Randers MB, et al.. Muscle adaptations and performance enhancements of soccer training for untrained men.
Eur J Appl Physiol. 2010; 108 (6): 1247–58.
20. Krustrup P, Hansen PR, Andersen LJ, et al.. Long-term musculoskeletal and cardiac health effects of recreational football and running for premenopausal women.
Scand J Med Sci Sports. 2010; 20 (1 Suppl):S 58–71.
21. Krustrup P, Hansen PR, Randers MB, et al.. Beneficial effects of recreational football on the cardiovascular risk profile in untrained premenopausal women.
Scand J Med Sci Sports. 2010; 20 (1 Suppl):S 40–9.
22. Krustrup P, Nielsen JJ, Krustrup BR, et al.. Recreational soccer is an effective health-promoting activity for untrained men.
Br J Sports Med. 2009; 43 (11): 825–31.
23. Kuvin JT, Patel AR, Sliney KA, et al.. Assessment of peripheral vascular endothelial function with finger arterial pulse wave amplitude.
Am Heart J. 2003; 146 (1): 168–74.
24. Lee CD, Blair SN, Jackson AS. Cardiorespiratory fitness, body composition, and all-cause and cardiovascular disease mortality in men.
Am J Clin Nutr. 1999; 69 (3): 373–80.
25. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies.
Lancet. 2002; 360 (9349): 1903–13.
26. Mancia G, De Backer G, Dominiczak A, et al.. and The Task Force for the Management of Arterial Hypertension of the European Society of Cardiology. 2007 Guidelines for the management of arterial hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).
Eur Heart J. 2007; 28 (12): 1462–536.
27. Mitchell GF. Arterial stiffness and wave reflection: biomarkers of cardiovascular risk.
Artery Res. 2009; 3 (2): 56–64.
28. Moholdt T, Aamot IL, Granoien I, et al.. Aerobic interval training increases peak oxygen uptake more than usual care exercise training in myocardial infarction patients: a randomized controlled study.
Clin Rehabil. 2012; 26 (1): 33–44.
29. Nybo L, Sundstrup E, Jakobsen MD, et al.. High-intensity training versus traditional exercise interventions for promoting health.
Med Sci Sports Exerc. 2010; 42 (10): 1951–8.
30. Patvardhan E, Heffernan KS, Ruan J, et al.. Augmentation index derived from peripheral arterial tonometry correlates with cardiovascular risk factors.
Cardiol Res Pract. 2011; 2011: 253758.
31. Patvardhan EA, Heffernan KS, Ruan JM, Soffler MI, Karas RH, Kuvin JT. Assessment of vascular endothelial function with peripheral arterial tonometry: information at your fingertips?
Cardiol Rev. 2010; 18 (1): 20–8.
32. Pedersen BK, Saltin B. Evidence for prescribing exercise as therapy in chronic disease.
Scand J Med Sci Sports. 2006; 16 (1 Suppl):S 3–63.
33. Pescatello LS, Franklin BA, Fagard R, Farquhar WB, Kelley GA, Ray CA. American College of Sports Medicine. Position Stand exercise and hypertension.
Med Sci Sports Exerc. 2004; 36 (3): 533–53.
34. Randers MB, Nielsen JJ, Krustrup BR, et al.. Positive performance and health effects of a football training program over 12 weeks can be maintained over a 1-year period with reduced training frequency.
Scand J Med Sci Sports. 2010; 20 (1 Suppl):S 80–9.
35. Randers MB, Petersen J, Andersen LJ, et al.. Short-term street soccer improves fitness and cardiovascular health status of homeless men.
Eur J Appl Physiol. 2012; 112 (6): 2097–106.
36. Schnabel RB, Schulz A, Wild PS, et al.. Noninvasive vascular function measurement in the community: cross-sectional relations and comparison of methods.
Circ Cardiovasc Imaging. 2011; 4 (4): 371–80.
37. Tjonna AE, Lee SJ, Rognmo O, et al.. Aerobic interval training versus continuous moderate exercise as a treatment for the metabolic syndrome: a pilot study.
Circulation. 2008; 118 (4): 346–54.
38. Tjonna AE, Lund Nilsen TI, Slordahl SA, Vatten L, Wisloff U. The association of metabolic clustering and physical activity with cardiovascular mortality: the HUNT study in Norway.
J Epidemiol Community Health. 2010; 64 (8): 690–5.
39. Walton C, Lees B, Crook D, Worthington M, Godsland IF, Stevenson JC. Body fat distribution, rather than overall adiposity, influences serum lipids and lipoproteins in healthy men independently of age.
Am J Med. 1995; 99 (5): 459–64.
40. Wiklund P, Toss F, Weinehall L, et al.. Abdominal and gynoid fat mass are associated with cardiovascular risk factors in men and women.
J Clin Endocrinol Metab. 2008; 93 (11): 4360–6.
