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Effect Of Incremental Exercise Health And Social Care Essay

The aim of this study is to assess the effect of incremental exercise on heart rate and blood pressure response. If a reduction in heart rate and blood pressure occurs, reducing hypertension risk, thus, the efficacy of exercise on hypertension prevention/treatment. Blood pressure and heart rate are important indicators of health and have been associated with the identification of coronary heart disease and mortality rate. Participants (n=11) cycled for 15 min, blood pressure and heart rate were recorded at intervals. Results revealed decreased systolic blood pressure (125±11.5/80±9.0 - 123±0.0/77±7.2 mm Hg) and mean arterial pressure, (125.3 - 123.3) with a marginally elevated heart rate post exercise (143±18.2, 114±26.4 and 77±16.2 b·min-1). In conclusion this study supports current literature, and the efficacy of exercise as an intervention into treatment of hypertension and prevention in normotensive individuals.

2.0 Introduction

Arterial blood pressure (BP) is deemed one of the 'vital signs' and is an important indicator of a person's state of health (Perloff et al. 1993). Kirkendall et al. (1987, p.980) defines BP as "A force which is the result of cardiac output and peripheral vascular resistance". Blood pressure measurements are presented as systolic (SBP) over diastolic (DBP). Systolic blood pressure representing peak ventricle-contraction and DBP nadir ventricle-contraction, (Salem, 2006) with normotensive BP values ranging between 90-119 mm Hg for SBP and 60-79 mm Hg for DBP (Heyward, 2006).

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Blood Pressure is a means to identify cardiovascular risk, namely hypertension, (Stamler et al. 1990) Chobanian et al. (2003) categorises hypertension as SBP of ≥140 mm Hg and DBP of ≥90 mm Hg, these levels cause 62% of recorded strokes and 49% of heart attacks. This cause for concern is growing, as increasingly younger populations are being diagnosed as hypertensive, (World Health Organisation, 2004) then progressing to coronary heart disease (CHD) (Wenyu et al. 2006).

Chobanian et al. (2003, p.1361) describes the relationship between BP and CHD as "continuous, consistent, and independent of other risk factors. The higher the BP, the greater is the chance of heart attack [...] the presence of each additional risk factor compounds the risk from hypertension".

Coronary Heart Disease is caused by a restriction in blood supply to the myocardium caused by atherosclerosis-a progressive build-up and deposition of lipoproteins and plaque in the intima of the coronary arteries, exceeding values of ≥2.2 mmol/L (Gordon et al. 1977). These deposits restrict blood flow to the myocardium, increasing peripheral vascular resistance, possibly causing cardial infraction (Heyward, 2006).

Epidemiological research indicates multiple risk factors effecting CHD include, hypercholesterolemia, hypertension, smoking, diabetes mellitus, obesity and physical inactivity, all of which are prevalent in today's populations (Thomas et al. 2003). Hypercholesterolemia represents total-cholesterol ≥240mg∙dl-1 (American Heart Association, 2004) and is positively related with hypertension, (Despres and Lemarche, 1994; Shoenhair and Wells, 1995) obesity and CHD (Grundy et al. 1999). Hill and Melanson (1999) suggest increased population obesity is environmental through excess calorie-consumption, consequently effecting glucose tolerance, corresponding with increased diabetes mellitus levels (American Heart Association, 2004). Smoking is the largest preventable cause of CHD (World Health Organisation, 2002) with smokers at twice the risk of CHD than non-smokers (American Heart Association, 2004).

Physical activity is associated with decreased risk of mortality, hypertension and CHD through increased cardiorespiratory fitness, (Sandvik et al. 1993; Laukkanen et al. 2001) thereby, reducing risk factors through increased lipoprotein metabolism thus, improving lipid profile, (Durstine et al. 2002) positively effecting insulin sensitivity (Koivisto et al. 1996).

Co-ordination of the respiratory and cardiovascular systems is required in response to exercise (Suzuki et al. 2007). The autonomic nervous system increases sympathetic-nervous-system activity, thereby, stimulating cardiovascular response namely; heart rate (c), cardiac output and stroke volume to cope with increased oxygen demand from working musculature, (Suzuki et al. 2007) and BP through peripheral vasculature (Seals and Chase, 1989; Carter et al. 2003).

Systolic Blood Pressure increases in conjunction with ventricular contraction, (Joint National Committee [JNC] on detection, evaluation, and treatment of high blood pressure, 1984), whilst DBP remains relatively consistent with basal readings, decreasing slightly at higher intensity exercise (Brett et al. 2000; McArdle et al. 2007).

Basal SBP may decrease post-exercise due to decreased peripheral resistance from vasodilatation of peripheral vasculature inducing hypotension (Pescatello et al. 1991) through sympathetic-nervous-system NO secretion (McArdle et al. 2007). Research suggests post-exercise hypotension is due to blood pooling in visceral musculature and vascular beds during recovery, pooling, thereby reducing blood volume, and systemic BP (Brown et al. 1993; McArdle et al. 2007).

Exercise induced hypotension has been suggested as possible hypertension treatment in conjunction with pharmaceutical intervention and prevention method (JNC, 1984; Chobanian et al. 2003). Whist hypotension has been extensively researched in high risk hypertensive population; comparatively little research has been conducted into hypotension in young healthy individuals (Paffenbarger et al. 1983).

The aim of this study is to investigate the effect of incremental exercise on c and BP in normotensive individuals, concluding if this may reduce both c and BP values reducing the risk of hypertension in normotensive individuals. This draws on three hypotheses, firstly; a linear increase in c and BP in response to exercise, secondly; a reduction in SBP and c post exercise, and thirdly a lower post exercise mean arterial pressure (MAP).

For the purpose of this study obesity is defined by a BMI ≥25 and fatigue as voluntarily fatigue

3.0 Methodology

3.1 Participants

Eleven subjects consisting of ten men and one women (mean age [y] 19.6±2.1; body mass [kg] 77.6±10; stature [m] 1.8±0.1) participated in this study. Written informed-consent and PAR-Q (Canadian Society Exercise Physiology, 2002) were completed and assessed pre-participation. Risk assessment addressed factors that may cause experimental mortality, including hyperventilation and dyspnea (McArdle et al. 2007). Participants were not taking medication that could affect their c or BP during this investigation. Experimental design was approved by the Southampton Solent HESS ethics committee.

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3.2 Procedure dsdmsdvnmslvnskjdnvlks Stature was measured using a Veeder Root stadiometer (Elizabethtown, USA), and body mass on Seca 710-1021004 scales (Hamburg, Germany). Participants undertook 5min (STOP WATCHES) seated rest to establish basal measurements. Blood pressure was taken from the upper-left brachial artery by auscultation (Perloff et al. 1993). Polar-Electro T31 monitors (Southampton, UK) were used determining c values at rest and exercise. A Monark Ergomedic-874E bike (CE) (Glastonbury, UK) was used to standardise exercise intensity at 60rpm throughout the experiment. Load (kg) = Power (W) / rpm was used to establish incremental load, translating to 0.5 kg addition to CE cradle (1kg) every 3 min of exercise.

3.3 Protocol

A 15 min step protocol was implemented with, 3 min increments at 60 W, 90, 120, 150 and 180 W respectively. A 6 min cool-down (3 min at 90 and 60 W) and 22-25 min of seated rest followed, BP, c and RPE data recorded at each interval. Symptoms of fatigue were monitored by means of visual observation. Max heart-rate (Mc) was calculated using NSCA guidelines (Earle and Baechle, 2004); should 85%Mc be achieved, testing shall terminate.

3.4 Statistical analysis

Descriptive statistics were used expressing the results are expressed as the central tendency of the average and the variability around the mean.

4.0 Results

During exercise, c increased from 77±16.2 b·min-1 at rest to 114±26.4, 132±18, 143±18.2, 151±18.6 and 157±16.8 b·min-1 at 60, 90, 120, 150 and 180 W, respectively. Blood pressure increased from 125±11.5/80±9.0 mm Hg at rest to 133±16/77±12.2, 137±18.4/74±12.0, 148±16.4/75±13.7, 159±16.1/75±15.6 and 172±21.5/79±18.1 mm Hg at 60, 90, 120, 150 and 180 W, respectively. Post-exercise cool down c decreased from 143±18.2, 114±26.4 and 77±16.2 b·min-1 at 90 and 60 W and rest respectively. Post exercise BP was reduced: 148±23.1/70±12.3, 136±18.4/73±8.6 and 123±0.0/77±7.2 at 90, 60 W and rest respectively.

Data presents a linear increase between c, SBP, DBP, MAP during incremental exercise. Post-exercise active (R1, 90 W; R2, 60 W) and seated (R3, 0 W) recovery c and MAP decreased linearly till experimental completion; SBP and DBP decreased below basal measurements during recovery. SBP, DBP and MAP values at R3 (0W) were lower than that at rest pre-exercise.

Table 1. Effect of Incremental exercise on blood pressure and heart rate.

Effect of Incremental exercise on blood pressure and heart rate



Stage 1 - 60W

0 - 2.59

Stage 2 - 90W

3.00 - 5.59

Stage 3 - 120W

6.00 - 8.59

Stage 4 -150W

9.00 - 11.59

Stage 5 -180W

12.00 - 14.59

Stage 6 - 90W

15.00 - 17.59

Stage 7 - 60W

18.00 - 20.59


21.00 -24.00

fc (b·min-1)










SBP (mm Hg)










DBP (mm Hg)




















Values are presented as mean and standard deviation (±)

SBP = systolic blood pressure. DBP = diastolic blood pressure. MAP = mean arterial pressure.

Relation of SBP, MAP and fc

Figure 1. SBP, MAP and c in relation to exercise

Relation of SBP, DBP and fc

Figure 2. SBP and DBP in relation to exercise

5.0 Discussion

The aim of this study is to assess the effect of incremental exercise on c and BP in normotensive individuals, determining if this may reduce c, BP and hypertension risk in normotensive individuals. The first and third hypotheses were confirmed as BP and c increased linearly with incremental exercise; and a lower post-exercise MAP was recorded. Results partly support the second hypothesis as a reduction in SBP was observed however; a reduction in post exercise c was not.

Literature suggests a linear increase in c and BP in response to exercise (Arja et al. 2002; McArdle et al. 2007; Suzuki et al. 2007) in compliance with study data; representing an increase in cardiac output, stroke volume and BP. Shiotani et al. (2009) observed similar effects of aerobic exercise on circadian rhythm, reporting increased BP in accordance to exercise intensity.

Basset et al. (1998) reports comparable effects of exercise, namely, increased SBP after cycle ergometry till fatigue in 68 normotensive males. Research suggests a decrease in SBP post exercise (Hannum and Kasch, 1981; Pescatello et al. 1991; Chobanian et al. 2003) supporting study data. This is due to persisting vasodilatation decreasing SBP below basal levels (Kaufman et al. 1987; Pescatello et al. 1991). It is reasonable to assume this reason for a decrement in post-exercise MAP, as this prolonged vasodilatation will induce hypotension.

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Short term effects of exercise induced hypotension recorded were comparable to results reported by Sullivan et al. (1988) and Levy et al. (1998) who observed decreased c and BP over 16-24 and 25 weekly exercise interventions respectively, decreasing CHD risk in hypertensive patients. However, these studies examined these effects on hypertensive patients, thus, limiting validity of a direct comparison to this study data.

Limitations include a small sample size and mixed gender participants, reducing external validity. Delimitations include inefficient tester auscultation competence. Although measurement techniques adhere to Perloff et al.'s (1993) guidelines, difficult replication of results amongst multiple testers reduces reliability, had 12-lead electrocardiography been used, c accuracy would be significantly improved (Laukkanen and Virtanen, 1998). Resting c was not achieved after rest (R1, R2 and R3) possibly indicating inadequate time prescribed, had resting c had been achieved results may have proved dissimilar.

Bennett et al. (1984) states post-exercise hypotension may decrease BP below basal levels for a minimum of 90 min. This suggests multiple bouts of exercise completed daily may aid pharmaceutical interventions in decreasing BP. This however, applies to dynamic exercise only as isometric exercise greatly increases BP and is not advised for hypertensive individuals (JNC, 1984; McArdle et al. 2007). Long term effects of exercise include reduced fat-free mass, cholesterol and more favourable insulin sensitivity, presenting an improvement in health, reduction in c, BP (Kaufman et al. 1987; Pescatello et al. 1991) and risk factor status (JNC, 1984; Chobanian et al. 2003).

The effect of exercise on c and BP post exercise is well established; what has not been investigated in literature is the effect of different modes of dynamic exercise. This information will increase the efficacy of exercise prescribed to treat hypertension on its ability to reduce c and BP, thus, increasing the possibility of hypertension prevention.

In conclusion, exercise should be prescribed for hypertension treatment and prevention, and in conjunction with pharmaceutical aid may decrease CHD risk (Fagard, 2006). Dynamic exercise has shown to decrease BP in normotensive and hypertensive individuals, suggesting an efficacious way to decrease BP and cardiovascular risk factors. It has also been noted that the increment of physical activity may decrease the amount of pharmaceutical intervention needed to reduce BP (Stockholm et al. 1982), and possibly representing a solution to the increased hypertension and CHD risk that has become this modern day epidemic

for increasingly younger populations (World Health Organisation, 2004).

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