Hypertens Res. 2004 Jan;27(1):61-70.  Related Articles, Links 


Regulation of skeletal muscle peroxisome proliferator-activated receptor gamma expression by exercise and angiotensin-converting enzyme inhibition in fructose-fed hypertensive rats.

Kawamura T, Yoshida K, Sugawara A, Nagasaka M, Mori N, Takeuchi K, Kohzuki M.

Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine, Sendai, Japan.

The purpose of this study was to examine the effects of chronic exercise training and angiotensin-converting enzyme (ACE) inhibition on peroxisome proliferator-activated receptor gamma (PPAR gamma) expression in fat and skeletal muscle in fructose-fed spontaneously hypertensive rats (SHR). SHR were fed a fructose-rich diet over 16 weeks of either exercise training (Ex group: 20 m/min, 0% grade, 60 min/day, 5 days/week), ACE inhibitor administration (TM group: temocapril, 10 mg/kg/day), or a combination of both treatments (TM+Ex group). The systolic blood pressure was reduced exclusively in the temocapril-treated groups. Serum leptin level was positively correlated with the ratio of epididymal fat weight to body weight (p<0.001). Exercise training significantly upregulated the PPARgamma expression in all tissues, which was attenuated by temocapril. PPARgamma expression was significantly upregulated in skeletal muscles in the Ex group, and temocapril administration attenuated this effect in the Ex+TM group. The level of PPARgamma protein was significantly higher in the extensor digitorum longus muscle than in the soleus muscle. Both TM and Ex prevented the fructose diet-induced transitions of fiber type. These data suggested that PPARgamma expression is tissue-specific, and that alterations in PPARgamma expression in the skeletal muscle induced by either or both treatments may have contributed to reducing the fat mass via the regulation of metabolic homeostasis. Changes in muscle morphology were independent of PPARgamma expression, and the higher proportion of type I fiber might also explain some of the beneficial impact of exercise and ACE inhibition on energy metabolism.

PMID: 15055257 [PubMed - in process]

One study of endurance athletes showed that the subjects' intramuscular fat content increased with endurance training.
Other studies showed that intramuscular fat content actually decreased with weight training.

I do think the studies make sense, though. Endurance training entails improving aerobic conditioning. That means training body to use fat as fuel substrate. It makes sense that, in that context, one's body would promote creating small fat depots around muscle, to provide immediate fuel source.

I take an ACE inhibitor ED for the last three years. Its quite obvious that A, since I've been taking it my endurance has suffered greatly and B, i have not lost any more fat than i normally would.

It's so strong at reducing endurance I'm carefull not to take it at all the day of grappling or mountain biking. If i do, its increased lactic acid build up and reduced energy.

I do think the studies make sense, though.  Endurance training entails improving aerobic conditioning.  That means training body to use fat as fuel substrate.  It makes sense that, in that context, one's body would promote creating small fat depots around muscle, to provide immediate fuel source.

Quick question twistedneck. Do you expirience the chronic cough that is sometimes reported with ACE inhibitors. also which specfific drug do you take and at what dosage.

thanks.