There is a striking age-dependent sexual dimorphism in the prevalence of

hypertension (Figure). Women have lower systolic blood pressure (SBP) levels than
men during early adulthood, while the opposite is true after the sixth decade of life.
Diastolic blood pressure (DBP) tends to be slightly lower in women than men
regardless of age. In early adulthood, hypertension is less common among women
than men, but after the fifth decade of life, the incidence of hypertension increases
more rapidly in women than men, reaching a prevalence rate that is equal to or
greater than in men during the sixth decade. This sexual dimorphism in blood
pressure (BP) May, in part, account for the lower incidence of cardiovascular disease
and the slower progression of renal disease in young (premenopausal) women,
which tend to disappear with menopause.
Figure 1. Prevalence of high blood pressure in Americans age 20 and older by age
and sex. National Health and Nutrition Examination Survey (NHANES): 1999–2002.
Reproduced from the 2005 Heart Disease and Stroke Statistical Update, with
permission from the American Heart Association.

HYPERTENSION IN WOMEN

Mechanisms

The mechanisms responsible for sex differences in BP control and regulation are not
fully understood, but appear to involve effects of sex hormones on renal sodium
handling and/or vascular resistance. A rightward shift of the pressure-natriuresis
curve with a resultant long-term increase in BP has been reported in male animal
models of hypertension. Castration restores the pressure-natriuresis relationship, and
androgen receptor blockade lowers BP in these models, providing evidence that
androgens contribute to the higher BP observed in males. Administration of
testosterone to ovariectomized spontaneously hypertensive rats has been shown to
elevate BP and blunt the pressure-natriuresis relationship, suggesting the possibility,
as yet untested in clinical studies, that androgens May play a role in the rise in BP
that occurs in menopausal women.
Female sex hormones, in contrast, appear to protect against salt-induced increases
in BP, at least in part by increasing sensitivity of the pressure-natriuresis relationship
and augmenting renal excretion of sodium. Studies in animal models have revealed
emergence of salt-sensitive hypertension after ovariectomy. Activation of the
sympathetic nervous system, alterations in salt appetite, and modulation of many
functions of the renin-angiotensin-aldosterone system appear to participate in the
pathogenesis of salt-sensitive hypertension in these models. Additional mechanisms
that have been suggested to explain the effects of ovarian hormones on BP include:
1) maintenance of normal endothelial function, with attendant increases in
endothelial-dependent nitric oxide production and vasodilation; 2) reductions in
plasma renin activity, angiotensin-converting enzyme (ACE) activity, vascular
AT1 receptor expression, and superoxide production; and 3) induction of structural
and functional alterations in the arterial wall that reduce vascular stiffness and
prevent the development of isolated systolic hypertension. While available data
concerning the participation of these mechanisms in BP control in women are limited,
this is a promising area for future clinical research, particularly in view of the
documented major increases in age-related stiffening of large arteries in women,
consistent with changes in hormone status (increases in follicle stimulating hormone)
and cardiovascular risk.
Studies carried out in normotensive women during the menstrual cycle, during use of
oral contraceptives and after menopause, indicate that the pressure-natriuresis
relationship is steep in young women during all phases of the menstrual cycle and
during oral contraceptive use, indicating insensitivity to salt, but is shifted to the right
in menopausal women, indicating that BP becomes salt-sensitive after menopause
(Figure). The inability of the kidney of postmenopausal women to handle a salt load
is reflected in exaggerated weight gain when going from a low- to high-salt intake.
Whether the postmenopausal increase in salt sensitivity is related to aging changes
in the kidney and/or to reduced synthesis of estradiol or an imbalance between
androgens and female sex hormones is a topic of current study. In any event, the
increased salt sensitivity of postmenopausal women supports the use of diuretics in
hypertensive women, consistent with the Seventh Report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure (JNC 7) guidelines.
Overview
If you're launching an exercise plan, you may have heard there are pronounced differences
between the heart rates of athletes and non-athletes. This applies not only to the resting heart
rate, but also to maximum heart rates. Trained athletes have built up muscles in their arms,
legs and other body parts along with their hearts. Cardiovascular endurance is developed
gradually over a period of time as the athlete's body adapts to increased physical challenges.
Your Heart at Rest
Mayo Clinic experts note that most adults have a resting heart rate that falls in the range of 60
to 100 beats per minute (bpm). But trained athletes have significantly lower resting heart
rates--usually between 40 and 60 bpm, indicating better overall heart function and a higher
level of cardiovascular fitness. To determine your resting heart rate, locate your pulse, which
can be found on the inside of your wrist or slightly to the left or right of your windpipe, or
underneath your ear. Count the number of pulses you feel in a 15-second period of time, then
multiply this by four.
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Maximum Heart Rates
Maximum heart rate (MHR) is defined as how much your heart is capable of handling during
intense physical activity, such as cycling, swimming, running or other forms of cardiovascular
exercise. When determining your MHR, simply subtract your age from 220. Mayo Clinic
experts caution that this number is only an estimate; depending on your physical condition
and level of physical activity, your MHR could be higher or lower by as much as 20 bpm.
Although it would stand to reason that trained athletes would have a higher MHR, most of
them have MHRs that are substantially lower.
Trained Athletes and MHR
A strong heart pumps more blood through the body during a single beat; therefore, the
athlete's heart needs to pump less frequently during strenuous activity, explains Dr. Gabe
Mirkin, a physician who is trained in sports medicine. Mirkin cites a John Moores University
(Liverpool, U.K.) study published in the January 2008 edition of the International Journal of
Sports Medicine that indicates that the MHR for male athletes was roughly 202, minus 0.55,
times the athlete's age. Female athletes had a MHR of 216, minus 1.09, times the athlete's age.
Overall results indicate that trained athletes have MHRs that are significantly lower than
inactive people of the same age range.
Problems with the Athlete's Heart
Even the well-conditioned athlete is prone to heart conditions caused by strenuous training. A
heart disorder called hypertrophic cardiomyopathy is caused when the athlete's heart becomes
too large and its walls too thick. According to Dr. Richard Kerber of the University of Iowa,
this silent disease, which causes 50 percent of sudden deaths in athletes under 35, is difficult
to detect. Symptoms may include fainting, dizziness and chest pain that occurs during
physical activity, but which subsides during periods of rest. Echocardiograms are employed to
confirm findings, Kerber says. While there is no cure, the condition may be mitigated by
insertion of a pacemaker or use of oral medication.
The Smart Heart
During cardiovascular activity, beginners should not strive to reach MHR, but rather their
target heart rate. This is a range between 70 and 85 percent of your MHR. For example, a
healthy person, 40 years old, should keep his heart rate between 126 and 153 bpm during the
course of cardiovascular activity. This type of moderately intense activity is best for beginners
who want to decrease risks such as soreness, injury and exercise burn-out, says Mayo Clinic
experts. Novice athletes are advised to build their endurance slowly, keeping their target heart
rate in the lower range for a while before increasing the intensity of their workouts.
Warnings
Non-athletes with a resting heart rate of less than 60 bpm aren't necessarily naturally equipped
with a healthy cardiovascular system. This medical condition, known as bradycardia, can be
caused by age-related heart tissue degeneration, heart damage, high blood pressure, an
underactive thyroid or use of certain medications, among many other causes, cautions the
Mayo Clinic. Depending on the nature of the problem and the severity of symptoms,
treatment of this disorder may be required.

Read more: http://www.livestrong.com/article/82658-athletes-vs.-nonathletes-heart-
rate/#ixzz1B7C1JtgB