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Jumat, 25 Januari 2008

Re: [Supertraining] HDL and Training

--- Ed White <> wrote:

> Without diet changes, how much improvement can a
> person achieve in lipid profile (LDL reduction, HDL
> increase, Trig reduction):
> - from 3x per week x 1 hr strength training
> sessions?
> - from 3x per week x 1 hr aerobic sessions
> (treadmill, eliptical, bike)?
> - both?

I am not sure that there is an answer to either
question. There is ample evidence in the literature
on the benefits of exercise as it pertains to LDL,HDL
and triglycerides. Most, if not all of the studies
have been done with aerobic type exercise, however I
am sure that similar if not the same benefits can be
obtained with resistance training.

It probably does not matter what kind of exercise is
done as long as it stress the muscles and
cardiovascular system sufficiently.

I have been doing some research since posted and as of
yet I have not come up with specific answers to any of
your questions.

I did come across the following from a Cardiology Text

Libby: Braunwald's Heart Disease: A Textbook of
Cardiovascular Medicine, 8th ed.
Copyright © 2007 Saunders, An Imprint of Elsevier
CHAPTER 78 - Exercise and Sports Cardiology

The specific mechanisms by which physical activity
reduces mortality and cardiovascular events are likely
multifactorial, and extend beyond a reduction in
cardiovascular risk factors, because beneficial
effects have been shown on thrombosis, endothelial
function, inflammation, and autonomic tone. The
magnitude of blood pressure reduction attained with
exercise is modest and in mildly hypertensive persons
yields an effect that is similar to pharmacological
monotherapy.[14] Physical activity and exercise induce
several important and beneficial effects on glucose
metabolism including increased insulin sensitivity,
decreased hepatic glucose production, preferential use
of glucose over fatty acids by exercising muscle, and
reduced obesity.[15] In addition, regular exercise may
prevent the onset of diabetes mellitus.[16] A widely
known fact is that overweight and obesity are
associated with significant increases in
cardiovascular morbidity and mortality.[17] Exercise
training appears to be an important component of
weight loss programs, although most randomized
controlled trials show only modest reductions in
weight. Studies suggest that exercise is necessary to
maintain weight loss and prevent weight regain after
diet-induced weight loss.[18] The effects of exercise
on lipid profiles demonstrate the greatest benefit on
triglycerides, modest changes in high-density
lipoprotein (HDL), and little to no change in
low-density lipoprotein (LDL) levels.[2] However, some
data suggest that exercise training reduces the
concentration of atherogenic, small, dense LDL
particles.[19] A recent study of monozygotic twins
shows a strong genetic component to HDL levels that
can be slightly but favorably modified by vigorous
Further evidence suggests that exercise training has
beneficial effects on the fibrinolytic system, and
many studies report an inverse relationship between
physical activity or fitness and inflammatory
markers.[21] Chronic exercise training appears to have
an important and favorable influence on endothelial
function in both peripheral[22] and coronary
arteries.[23] Improved endothelial vasodilator
function may result, in part, from increased nitric
oxide production and a net reduction in oxidative
stress,[25] as well as an increase in endothelial
progenitor cells.[26] Such improvements may contribute
to a reduction in adverse cardiovascular events.[27]
Finally, exercise training appears to modulate
favorably the balance between sympathetic and
parasympathetic tone, an effect associated with
improvements in survival.[28]
Changes in the muscular, cardiovascular, and
neurohumoral systems that result from exercise
training improve functional capacity and strength.
These changes are referred to as the training effect
and enable an individual to exercise to higher peak
work rates with lower heart rates at each submaximal
level of exercise. A decline in maximal exercise
capacity is associated with aging, and a longitudinal
study demonstrates that this is more marked with each
successive decade of life.[29] Although regular
exercise may attenuate this loss of exercise capacity
at any age, it does not appear to prevent the
progressively greater decline with advancing age.[29]

14. Whelton SP, Chin A, Xin X, et al: Effect of
aerobic exercise on blood pressure: A meta-analysis of
randomized, controlled trials.  Ann Intern
Med  2002; 136:493.
15. Sigal RJ, Kenney GP, Wasserman DH, et al: Physical
activity/exercise and type 2 diabetes: A consensus
statement from the American Diabetes Association.
 Diabetes Care  2006; 29:1433.

16. Knowler WC, Barrett-Connor E, Fowler SE, et
al: Reduction in the incidence of type 2 diabetes with
lifestyle intervention or metformin.  N Engl J
Med  2002; 346:393.

17. Klein S, Burke LE, Bray GA, et al: Clinical
implications of obesity with specific focus on
cardiovascular disease. A statement for professionals
from the American Heart Association Council on
Nutrition, Physical Activity, and Metabolism.
 Circulation  2004; 110:2952.

18. Saris WH, Blair SN, van Baak MA, et al: How much
physical activity is enough to prevent unhealthy
weight gain? Outcome of the IASO 1st Stock Conference
and consensus statement.  Obes Rev  2003; 4:101.

19. Kraus WE, Houmard JA, Duscha BD, et al: Effects of
the amount and intensity of exercise on plasma
lipoproteins.  N Engl J Med  2002; 347:1483.

20. Williams PT, Blanche PJ, Krauss RM: Behavioral
versus genetic correlates of lipoproteins and
adiposity in identical twins discordant for exercise.
 Circulation  2005; 112:350.

21. Kasapis C, Thompson PD: The effects of physical
activity on C-reactive protein and inflammatory
markers: A systematic review.  J Am Coll
Cardiol  2005; 45:1563.

22. Linke A, Schoene N, Gielen S, et al: Endothelial
dysfunction in patients with chronic heart failure:
Systemic effects of lower-limb exercise training.  J
Am Coll Cardiol  2001; 37:392.

23. Hambrecht R, Wolf A, Geilen S, et al: Effect of
exercise on coronary endothelial function in patients
with coronary artery disease.  N Engl J
Med  2000; 342:454.

24. Hambrecht R, Adams V, Erbs S, et al: Regular
physical activity improves endothelial function in
patients with coronary artery disease by increasing
phosphorylation of endothelial nitric oxide synthase.
 Circulation  2003; 107:3152.

25. Adams V, Linke A, Krankel N, et al: Impact of
regular physical activity on the NAD(P)H kinase and
angiotensin receptor system in patients with coronary
artery disease.  Circulation  2005; 111:555.

26. Steiner S, Neissner A, Ziegler S, et al: Endurance
training increases the number of endothelial
progenitor cells in patients with cardiovascular risk
and coronary disease.  Atherosclerosis  2005; 181:305.

27. Halcox JP, Schenki WH, Zalos G, et al: Prognostic
value of coronary vascular endothelial dysfunction.
 Circulation  2002; 106:653.

28. Adamson PB, Smith AL, Abraham WT, et
al: Continuous autonomic assessment in patients with
symptomatic heart failure: Prognostic value of heart
rate variability measured by implanted cardiac
resynchronization device.
 Circulation  2004; 110:2389.

29. Fleg JL, Morrell CH, Bos AG, et al: Accelerated
longitudinal decline of aerobic capacity in healthy
older adults.  Circulation  2005; 112:674.>>

> Can anyone explain the mechanism that allows lipid
> profile to improve from exercise alone?
> Thanks,
> Ed White
> Sandwich, MA USA
I have yet to come up with a specific answer to the
mechanism. If I find an answer I will post it.

Ralph Giarnella MD
Southington Ct USA

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