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Jumat, 25 Januari 2008

Re: [Supertraining] HDL and Training

On Jan 25, 2008 12:15 PM, Ed White <> wrote:
> Can anyone explain the mechanism that allows lipid profile to improve from
> exercise alone?

One suggested mechanism is the interaction with insulin. Insulin and
lipids are closely linked. Both types of exercise you mention --
"cardio" and strength training -- appear to improve insulin
sensitivity, although the processes responsible may be discrete.

Another mechanism could be the overall decrease in body fat levels.
Body fat is an active endocrine organ that secretes a variety of
substances, and its systemic effects are dependent on its absolute and
relative amounts, as well as its location/type (e.g. visceral vs.
subcutaneous). Significant amounts of excess bodyfat, esp. visceral,
generates a particular hormonal environment characterized by a poor
lipid profile and elevated levels of pro-inflammatory cytokines.

Related to this could be the increase in muscle mass, especially if
combined with a concurrent decrease in body fat levels. This article
discusses the role of skeletal muscle in lipid and glucose

A sample abstract of a review on the subject:

Clin Biochem. 2003 Sep;36(6):421-9.
Mechanisms of HDL lowering in insulin resistant, hypertriglyceridemic
states: the combined effect of HDL triglyceride enrichment and
elevated hepatic lipase activity.
Rashid S, Watanabe T, Sakaue T, Lewis GF.

Hypertriglyceridemia, low plasma concentrations of high density
lipoproteins (HDL) and qualitative changes in low density lipoproteins
(LDL) comprise the typical dyslipidemia of insulin resistant states
and type 2 diabetes. Although isolated low plasma HDL-cholesterol
(HDL-c) and apolipoprotein A-I (apo A-I, the major apolipoprotein
component of HDL) can occur in the absence of hypertriglyceridemia or
any other features of insulin resistance, the majority of cases in
which HDL-c is low are closely linked with other clinical features of
insulin resistance and hypertriglyceridemia. We and others have
postulated that triglyceride enrichment of HDL particles secondary to
enhanced CETP-mediated exchange of triglycerides and cholesteryl ester
between HDL and triglyceride-rich lipoproteins, combined with the
lipolytic action of hepatic lipase (HL), are driving forces in the
reduction of plasma HDL-c and apoA-I plasma concentrations. The
present review focuses on these metabolic alterations in insulin
resistant states and their important contributions to the reduction of
HDL-c and HDL-apoA-I plasma concentrations.

Here is an article that discusses strength training and insulin
sensitivity, demonstrating that in obese subjects, dynamic strength
training resulted in an improvement of whole body insulin sensitivity.

Dynamic strength training improves insulin sensitivity without
altering plasma levels and gene expression of adipokines in
subcutaneous adipose tissue in obese men. Journal of Clinical
Endocrinology & Metabolism, doi:10.1210/jc.2006-0382. E. Klimcakova,
J. Polak, C. Moro, J. Hejnova, M. Majercik, N. Viguerie, M. Berlan, D.
Langin*, and V. Stich

Context. Obesity is characterized by a low grade inflammatory state,
which could play a role in insulin resistance. Dynamic strength
training improves insulin sensitivity.

Objective. The objective of this study was to investigate, in obese
subjects, whether the insulin sensitizing effect of dynamic strength
training is associated with changes in plasma levels and gene
expression of adipokines potentially involved in the development of
insulin resistance.

Design. Twelve obese male subjects were investigated before and at the
end of 3 months' dynamic strength training. Insulin sensitivity was
evaluated using euglycemic-hyperinsulinemic clamp. Blood samples and
needle biopsy samples of sc abdominal adipose tissue were obtained.
The plasma levels and adipose tissue mRNA levels of adiponectin,
leptin, interleukin-1beta, interleukin-6 and TNF-{alpha} were

Results. The training induced an increase in the whole body glucose
disposal rate by 24% (P = 0.04). The body weight was not altered
during the training. Plasma levels of leptin decreased during the
training (16.6 ± 6.3 vs. 13.1 ± 5.7 ng/ml) by 21% (P < 0.02) while no
change in plasma levels of other adipokines and C-reactive protein was
observed. Gene expression of the investigated adipokines was not
changed in sc adipose tissue during the training.

Conclusions. In obese subjects, the dynamic strength training resulted
in an improvement of whole body insulin sensitivity. The increase in
insulin sensitivity was not associated with training-induced
modifications of plasma levels or adipose tissue gene expression of
adipokines supposedly involved in the development of insulin

Here is an abstract that reviews the effects of aerobic treadmill
training in stroke patients:

Treadmill Aerobic Training Improves Glucose Tolerance and Indices of
Insulin Sensitivity in Disabled Stroke Survivors. A Preliminary
Report. Stroke October 1 2007. Frederick M. Ivey PhD*; Alice S. Ryan
PhD; Charlene E. Hafer-Macko MD; Andrew P. Goldberg MD; and Richard F.
Macko MD

Background and Purpose—Insulin resistance and glucose intolerance are
highly prevalent after stroke, contributing to worsening
cardiovascular disease risk and a predisposition to recurrent stroke.
Treadmill exercise training (T-AEX) increases aerobic capacity (VO2
peak) in chronic stroke patients, suggesting intensity levels that may
be adequate to improve glucose metabolism. We compared the effects of
a progressive T-AEX intervention to an attention-matched stretching
intervention (CONTROL) on glucose tolerance and indices of insulin
sensitivity in stroke survivors.

Methods—Participants had hemiparetic gait after remote (>6 months)
ischemic stroke. They were randomized to 6-month T-AEX or a duration
matched reference CONTROL program of supervised stretching exercises.
Main outcome measures were glucose and insulin responses during a
3-hour oral glucose tolerance test (OGTT).

Results—Forty-six subjects (T-AEX=26, CONTROL=20) completed OGTT
testing before and after the interventions. T-AEX increased VO2 peak
(+15% versus -3% {Delta}, P<0.01) compared with CONTROL. There were
significant reductions in fasting insulin (-23% versus +9% {Delta},
P<0.05) and the total integrated 3-hour insulin response (-24% versus
+3% {Delta}, P<0.01) in T-AEX compared with CONTROL. In patients with
abnormal glucose tolerance at baseline, T-AEX resulted in a
significant 14% decrease in 3-hour glucose response (n=12, P<0.05).
Fifty-eight percent of T-AEX participants with abnormal baseline OGTT
(7 of 12) improved glucose tolerance status at 2 hours compared with
<10% (1 of 11) of impaired CONTROLS (P<0.05).

Conclusions—These preliminary findings suggest that progressive
aerobic exercise can reduce insulin resistance and prevent diabetes in
hemiparetic stroke survivors. Larger clinical trials are needed to
definitively establish the use of structured exercise training for
stimulating metabolic improvement poststroke.

Krista Scott-Dixon
Toronto, ON

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