How many times have you heard people say when they are dieting for fat loss that they are flat, weak, losing muscle, or all of the above? Usually the people who say such things do not have a proper grasp on how to effectively construct a diet for extreme fat loss while maintaining muscle tissue. The same people also convince themselves that they cannot get lean without sacrificing substantial lean tissue in the process. I am here to tell you that if you diet right, supplement right, and train effectively, than you surely can keep your muscle tissue while incinerating your winter blubber from your holiday "bulking diet."
In fact, when people get overly lenient with their dietary habits over the winter months, they oftentimes do not eat consistently and make poor food choices. They unknowingly set themselves up for the potential to gain a little muscle while getting shredded from diligent eating, supplementation, and consistent training.
Once the dieter gets into the midst of their fat loss stage and has become fairly lean in the 8-9% body fat range, they can begin incorporating the oral anti-diabetic drug Metformin. This drug also goes by the name Glucophage and belongs to a class of drugs called biguanides. It is used for treating non-insulin dependent type 2 diabetics with insulin resistance.
Metformin is generally well tolerated and is beneficial to the prolonged dieter attempting to retain muscle tissue while going from lean to shredded, which translates to -- going from 8-9% body fat to 4-5% body fat. When attempting to achieve extremely low levels of body fat, a cascade of hormonal events begin taking place, making will power, discipline and strong mental fortitude crucial to succeeding. Constant hunger becomes indefinite, while mental acuity begins to plummet.
Carbohydrates will be very limited as well as total calories. You will need a plan of action of how to best take advantage of Metformins insulin sensitizing and nutrient transporting effects when on extremely low carbohydrates. There are a few different ways to go about this.
One way would be to dose it before and after your post workout carbohydrate meal on training days. You could take 500 mgs 30 minutes before ceasing exercise, so Metformin is actively in your blood stream for efficient glucose shuttling. Another option which I personally prefer is to use Metformin on carbohydrate refeed days at 2 days a week. This would entail dosing the Metformin around your refeed period which could be anywhere from 4-12 hours depending on how lean you are.
For example: Let's say your refeed is 6 hours. You would dose 500 mgs at your first bite of food, then 500 mgs 3 hours later, then 1000 mgs right before bed. Why 1000 mgs right before bed you might ask? Because dosing it before bed helps facilitate the transport and clearance of glucose out of your blood stream and into your muscle cells as quickly as possible, so when you wake up, blood sugar and insulin levels are extremely low. Having low levels of insulin and blood sugar will allow you to get right back to oxidizing body fat for fuel opposed to glucose.
Carbohydrate refeed schedule –
(Refeed begins post workout at 3 pm.)
3:00 pm – Take first dose of Metformin (500 mgs) at start of meal
6:00 pm – Take second dose of Metformin (500 mgs) at second meal
10:00 pm – Take final dose of Metformin (1000 mgs) at final meal of day.
(Do not ingest carbohydrates after 10:00 pm so you return to baseline insulin levels upon waking)
Another reason why I favor the second option of a twice week dosing schedule of Metformin is because recent research has demonstrated that Metformin can decrease testosterone production and raise sex hormone binding globulin when dosed consistently for 2 weeks at 1700 mgs a day. When you dose Metformin infrequently as in twice a week, the negative effect on testosterone levels will be miniscule to non- existent. You will benefit from an increased level of AMP-activated protein kinase activity in skeletal muscle, which will increase the translocation of GLUT-4 transporters to skeletal muscle, increasing glucose uptake. AMP-activated protein kinase will also increase fatty acid oxidation by inactivating acetyl-CoA-carboxylase. By regulating acetyl- CoA-carboxylase, carnitine palmitoyltransferase (CPT-1) is not blocked and able to transport fatty acids into the mitochondria for oxidation.
(GLUT-4 Transporter (CPT-1)
Metformin is very useful to the extreme dieter due to its selectivity towards muscle cells opposed to fat cells when clearing nutrients from the blood. It has also been demonstrated to serve as an anti-catabolic agent when muscles have been immobilized due to bone or joint complications. A study was conducted to observe the effect Metformin had on maintaining muscle glycogen inside muscle fibers and stabilizing muscle weight during inactivity of muscles in test rats. Researchers discovered that rats not treated with Metformin lost significant muscle glycogen and muscle weight when muscles were immobilized. Inactive muscles also became insulin resistant due to down regulation of insulin receptor substrate-1 (IRS-1) in intra-cellular tissues. Decreased IRS-1 along with GLUT-4 translocation is a recipe for muscular atrophy.
It has become pretty clear that Metformin will play an integral role in the extreme dieter's plight in achieving ultimate body fat loss while retaining lean muscle tissue. To recap, Metformin will benefit the dieter with attributes such as:
-Increased insulin sensitivity in muscle cells rather than adipose tissue.
-Quickly clears glucose out of the blood stream and into muscle cells for immediate stabilization of blood sugar levels.
-Serves as an anti-catabolic aid in muscle fibers by retaining muscle weight and glycogen content.
-Increased AMP-activated protein kinase levels for enhanced fatty acid oxidation.
-Suppresses appetite when on restricted calories.
-Increased GLUT-4 transporters allow muscles to be efficiently loaded with glycogen for a fuller cosmetic appearance and optimal muscular performance.
References:
1.)Lee A, Morley JE.
Metformin decreases food consumption and induces weight loss in subjects with obesity with type II non-insulin-dependent diabetes. Obes Res. 1998 Jan;6(1):47-53.
2.)Hays JH, Gorman RT, Shakir KM. Results of use of metformin and replacement of starch with saturated fat in diets of patients with type 2 diabetes. Endocr Pract. 2002 May-Jun;8(3):177-83.
3.)Klip A, Gumà A, Ramlal T, Bilan PJ, Lam L, Leiter LA.
Stimulation of hexose transport by metformin in L6 muscle cells in culture.Endocrinology. 1992 May;130(5):2535-44.
4.)Lindsey D. Bogachus1,2 and Lorraine P. Turcotte1, Genetic downregulation of AMPK-? isoforms uncovers the mechanism by which metformin decreases FA uptake and oxidation in skeletal muscle cells. Am J Physiol Cell Physiol
December 2010 vol. 299 no. 6 C1549-C1561
5.)Galuska D, Zierath J, Thorne A, Sonnenfeld T, Wallberg-Henriksson H. Metformin increases insulin-stimulated glucose transport in insulin-resistant human skeletal muscle. Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden.
6.)Taylor EB, Hurst D, Greenwood LJ, Lamb JD, Cline TD, Sudweeks SN, Winder WW (December 2004). "Endurance training increases LKB1 and MO25 protein but not AMP-activated protein kinase kinase activity in skeletal muscle". Am. J. Physiol. Endocrinol. Metab. 287 (6): E1082–9. doi:10.1152/ajpendo.00179.2004.PMID 15292028.
7.) Ouchi N, Shibata R, Walsh K (April 2005). "AMP-activated protein kinase signaling stimulates VEGF expression and angiogenesis in skeletal muscle". Circ. Res. 96 (8): 838–46.doi:10.1161/01.RES.0000163633.10240.3b.PMID 15790954.
8.)Reddi AS, Jyothirmayi GN. Effect of chronic metformin treatment of hepatic and muscle glycogen metabolism in KK mice. Biochem Med Metab Biol. 1992 Apr;47(2):124-32.
9.)Paula Lima BosiI,; Gabriel Delfino Borges; João Luiz Quagliotti DuriganII; Karina Maria CancellieroII; Carlos Alberto da Silva. Metformin protects the skeletal muscle glycogen stores against alterations inherent to functional limitation. Braz. arch. biol. technol. vol.51 no.2 Curitiba Mar./Apr. 2008.
