Monday, January 31, 2011

Forget Taking It Slow...Let Me HIIT It!

I.    Introduction
II.   Long-Distance Runners vs. Sprinters
III.  Definition of High-Intensity
IV.  Impact on Body Fat
V.   Potential Mechanism
VI.  HIIT Methods
VII. Bibliography

Key words:  cardio, fat loss, HIIT, weight training, high intensity interval, ab workouts, ab exercises, abs, workout for abs, get abs, sprinting

First of all, get your mind out of the gutter!  You need to focus.  Why?? It’s because you may be one of the many people searching for a new way to shed some fat. Those remaining pounds just refuse to come off, even after all of those hours on the treadmill…but what other option is there??  Let me present an example that we’ve all seen...

Long-distance runners train in a manner that is very similar to many people you might see at your local gym.  They might run for a long period of time at a constant, low-intensity, conserving energy for the duration of that X mile run.  Sprinters, on the other hand, train using intermittent periods of high-intensity running, exerting the highest amount of energy for each sprint.  In most cases, a sprinter’s training period is much shorter than a long distance runner’s training period.  Sprinters also burn far less calories during their exercises.  But, look at the major difference in body type.  Long distance runners usually have minimal muscle definition, while sprinters are muscular, lean, and have little to no body fat.  Which body type would a man rather have?  Which body type would a woman prefer for her boyfriend/husband?  So rather than spending hours on end doing low-intensity cardio, why not try high-intensity, interval training (HIIT) instead.  Simply put, HIIT involves alternating between short periods of high-intensity exercise (sprinting, biking at a high resistance, high-intensity plyometrics) followed by short periods of rest or low-intensity exercise.  If the image above doesn’t convince you, let’s also see what research has shown when comparing the benefits of low-intensity cardio with HIIT. 

But first, let’s define some terms.  An individual’s aerobic capacity is the maximum amount of oxygen that the body can remove from circulating blood for use in exercising muscles.  It can be measured using a VO2 max test, which determines an individual’s aerobic capacity (VO2 max).  This value is used in research to define the intensity of an exercise.  For research purposes, a high-intensity exercise is one in which aerobic capacity is 85-250% VO2 max.  But generally, your VO2 max value directly correlates to your level of cardiovascular fitness.

A variety of studies have been conducted describing the benefits of HIIT in sports training.  But for this forum, I will concentrate on one study that identified greater weight loss benefits than low-intensity training.

Tremblay et al., 1994: In this study, the authors investigated the “Impact of exercise intensity on body fatness and skeletal muscle metabolism”.  Young adults took part in either a 20-week endurance training (ET) program or 15-week high-intensity intermittent-training (HIIT) program.   While HIIT had a much lower average total energy cost (57.9 MJ) than the ET program (120.4 MJ), the HIIT program resulted in a NINEFOLD greater reduction in subcutaneous adiposity (skin fat) when compared to ET.  HIIT also resulted in an increase in 3-hydroxyacyl coenzyme A dehydrogenase (HADH), an enzyme found in muscles involved in fat metabolism.  ET, on the other hand, decreased HADH activity. 

Endurance Training = Decreased HADH activity = decreased use of fat oxidation = more fat left on you!

So what exactly is the mechanism behind this?  From what I’ve read, I was unable to identify anything definitive.  However, there is one theory that could be a potential mechanism.  Studies have shown that a potential method for increasing fat oxidation is to maintain glycogen stores at a low range (Flatt, 1987).  It is also well known that as the intensity of an exercise increases, glycogen (carb) metabolism increases and fat metabolism decreases (Holloszy et al., 1998; Romijn et al., 1993).  In other words:

Low intensity exercise = more fat burned for energy during exercise
High intensity exercise = less fat, more glycogen burned for energy during exercise

So if more fat burned isn’t burned during high intensity exercise, when is it burned?  One theory is after exercise.  Studies have been conducted to investigate this
(Schrauwen et al., 1998; Schrauwen et al., 1997), but their findings did not completely confirm this theory.  Briefly, these studies investigated the amount of fat oxidation following high-intensity exercise.  However, there was no comparison of high-intensity fat oxidation to low-intensity fat oxidation.  That comparison is essential to properly validate this theory.  Nonetheless, I believe the marathon runner/sprinter comparison along with the Tremblay et al. research is enough evidence to give HIIT a try!

So here are some recommendations for ways to try HIIT:

1.  If you have access to a track, sprint the straightaways and walk/jog the curves.

2.  Run sprints on a field, basketball court, or hill with 15-30 second rest periods.

3.  Take classes like spinning or bodypump.  These can be a fun (and sometimes easier) way to take part in some high-intensity exercise.

4.  Using a treadmill, place your feet on either edge and set the speed at a fast pace that you feel comfortable with to run sprints (6-10 mph, adjust depending on your comfort level).  You can also increase the incline to 4-8% and make it more challenging if you feel comfortable with it (5-8% incline).  Sprint for 15-20 seconds, then hop up, with your feet landing on either side of the moving treadmill.  Rest for 20 seconds, then hop back on the treadmill for the next sprint.  After 10-15 minutes, you’ll feel this.

5.  Use the interval settings on a stationary bike.

A couple of other comments:

1.  In no way am I saying that you should never do low-intensity cardio exercises.  I'm simply suggesting a different type of exercise for those who are looking for new things to try.

2.  I wouldn't do HIIT before, on, or the day after a leg weight-training day.  Your legs will need time to recover from both HIIT and your leg day, and doing them too close together will not provide necessary recover time.

Go HIIT It!!

Dr. O
"I don't live to eat...I eat to live!"

Flatt JP. 1987. The difference in the storage capacities for carbohydrate and for fat, and its implications in the regulation of body weight. Ann NY Acad Sci 499:104-123.
Holloszy JO, Kohrt WM, Hansen PA. 1998. The regulation of carbohydrate and fat metabolism during and after exercise. Front Biosci 15(3):1011-1027.
Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, Wolfe RR. 1993. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol 265:E380-E391.
Schrauwen P, Lichtenbelt WD, Saris WHM, Westerterp KR. 1998. Fat balance in obese subjects: role of glycogen stores. Am J Physiol 274:E1027-E1033.
Schrauwen P, Van Marken Lichtenbelt WD, Saris WHM, Westerterp KR. 1997. Role of glycogen-lowering exercise in the change of fat oxidation in response to a high-fat diet. Am J Physiol 273:E623-E629.
Tremblay A, Simoneau JA, Bouchard C. 1994. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism 43(7):814-818.

Sunday, January 30, 2011

Love That Veggie: Broccoli

I.   Introduction
II.  Broccoli Nutrients
III. Cooking Methods for Nutrient Preservation
IV. Conclusion
V.  Bibliography

Key Words:  anti-cancer, antioxidant, breast cancer, broccoli, cancer, cancer therapy, cervical cancer, cancer symptoms, colon cancer, lung cancer, prostate cancer

It is a well known fact that vegetables should be an integral part of everyone’s diet.  However, it still amazes me that many eat little to no vegetables in their diets.  Therefore, my goal is to make it clear how certain vegetables can improve your overall health.

Now, if you know me, you’d know that my vegetable of choice is broccoli.  I mean seriously, who doesn’t love broccoli??  Besides the fact that it tastes so great (maybe?), it is LOADED with many compounds and nutrients that have been proven to support the preservation of a healthy body.

Indole-3-carbinol (I3C) – The anti-cancerous properties of I3C have been studied in great detail.  This chemical inhibits the growth of human breast (Cover et al., 1998; Tiwari et al., 1994) and prostate cancer cells (Chinni et al., 2001; Nachshon-Kedmi et al., 2003).  It also decreases the expression of estrogen in human cervical cells infected with HPV (Yuan et al., 1999).  The digestion of indole-3-carbinol results in the expression of compounds such as 3,3'-Diindolylmethane, which is able to induce cancer cell death (Ge et al., 1996; Hong et al., 2002).  I3C is also found in other vegetables in the Brassica family, such as cabbage, brussel sprouts, and cauliflower. 

Isothiocyanates – This group of compounds also prevents cancer development by reducing the activation of cancer enzymes and increasing cancer cell death in both developing and fully developed cancers of the lung, breast, colon, and prostate (Kuang and Chen, 2004; Zhang, 2004).  They are also found in other vegetables in the Brassica family. 

A specific isothiocyanate is sulforaphane, which inhibits the growth of cancer cells of the colon (Gamet-Payrastre et al., 2000), prostate (Singh et al., 2005), cervix (Sharma et al., 2010), breast (Pledgie-Tracy et al., 2007), and others.  It also acts as an antioxidant, protecting cells in the body from oxidative stress and inflammation (Gao et al., 2001; Shan et al., 2010).  

Broccoli is also rich in: 

1.      Fiber - makes you feel full faster, lowers cholesterol, regulates blood sugar, supports proper digestion (Lattimer and Haub, 2010)

2.      Vitamin A – helps regulate the immune system, lower risk of chronic disease, protect the eyes from damage such as UV light (Gerster, 1997) 

3.      Zinc - plays a role in immune function, protein synthesis, wound healing, DNA synthesis, and cell division (Prasad, 1995)

4.      Seleniumprevents cellular damage from free radicals (Combs Jr. and Gray, 1998) 
5.      Folic acid – needed to repair DNA and produce healthy red blood cells (Fenech et al., 1998) 

6.      Vitamin Csupports the immune system, protects the body from oxidative stress; antioxidant (Jacob and Sotoudeh, 2002)

7.      Calcium – supports bone health (Straub, 2007)

Now, with all of that information, I know what everyone is thinking…”Man, I really need to start eating some broccoli!!”  However, in order to maximize the power of this vegetable, your cooking technique is very important. 

A study by Zhang et al. (2004) showed how cooking methods can reduce the nutritional content in raw broccoli.  Here are the main results: 

1.  Broccoli florets and stems boiled for 300 s lost 72% and 42%, respectively, of their total phenolic (antioxidant) content.  Microwaved broccoli florets and stems had a similar decline.

2.  Broccoli florets boiled for 300 s lost 69% of their ascorbic acid content, while boiled broccoli stems lost 71% of their ascorbic acid content.  Broccoli florets and stems microwaved for 300 s lost 66% and 71%, respectively, of their ascorbic acid content.  

3.    Broccoli florets boiled or microwaved for 300 s lost 23% of their carotenoids (vitamin A), while boiled or microwaved broccoli stems lost 20% of their carotenoids.  

So what’s the best method??  You guessed it…steaming is the best cooking method for broccoli to maintain its nutrients.  Separate studies have shown that steaming maintains the highest concentrations of phytonutrients in broccoli, showing no significant losses in vitamin C, phenolic content, glucosinolates, or sulphoraphane after 3.5-5 minutes (Jones et al., 2010; Vallejo et al., 2002; Vallejo et al., 2003).

If you STEAM your broccoli for 3.5 – 5 minutes, you can enjoy all of the benefits of this wonderful veggie!!

P.S. - If you want to get the full benefit of your vegetables, DO NOT buy anything other than fresh, raw vegetables!

Dr. O 
"I don't live to eat...I eat to live!"

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Combs Jr. GF, Gray WP. 1998. Chemopreventive agents: Selenium. Pharmacol Ther 79:179-92.
Fenech M, Aitken C, Rinaldi J. 1998. Folate, vitamin B12, homocysteine status and DNA damage in young Australian adults. Carcinogenesis 19(7):1163-1171.
Gamet-Payrastre L, Li P, Lumeau S, Cassar G, Dupont M-A, Chevolleau S, Gasc N, Tulliez J, Terce F. 2000. Sulforaphane, a Naturally Occurring Isothiocyanate, Induces Cell Cycle Arrest and Apoptosis in HT29 Human Colon Cancer Cells. Cancer Res 60:1426-1433.
Gao X, Dinkova-Kostova AT, Talalay P. 2001. Powerful and prolonged protection of human retinal pigment epithelial cells, keratinocytes, and mouse leukemia cells against oxidative damage: The indirect antioxidant effects of sulforaphane. PNAS 98(26):15221-15226.
Ge X, Yannai S, Rennert G, Gruener N, Fares FA. 1996. 3,3'-Diindolylmethane Induces Apoptosis in Human Cancer Cells. Biochem Biophys Res Comm 228(1):153-158.
Gerster H. 1997. Vitamin A - functions, dietary requirements and safety in humans. Int J Vitam Nutr Res 67(2):71-90.
Hong C, Firestone GL, Bjeldanes LF. 2002. Bcl-family-mediated apoptotic effects of 3,3'-diindolylmethane (DIM) in human breast cancer cells. Biochem Pharm 63(6):1085-1097.
Jacob RA, Sotoudeh G. 2002. Vitamin C function and status in chronic disease. Nutr Clin Care 5(2):66-74.
Jones RB, Frisina CL, Winkler S, Imsic M, Tomkins RB. 2010. Cooking method significantly effects glucosinolate content and sulforaphane production in broccoli florets. Food Chem 123(1):237-242.
Kuang Y-F, Chen Y-C. 2004. Induction of apoptosis in a non-small cell human lung cancer cell line by isothiocyanates is associated with P53 and P2`. Food Chem Toxic 42(10):1711-1718.
Lattimer JM, Haub MD. 2010. Effects of Dietary Fiber and Its Components on Metabolic Health. Nutrients 2(12):1266-1289.
Nachshon-Kedmi M, Yannai S, Haj A, Fares FA. 2003. Indole-3-carbinol and 3,3'-diindolylmethane induce apoptosis in human prostate cancer cells. Food Chem Toxic 41(6):745-752.
Pledgie-Tracy A, Sobolewski MD, Davidson NE. 2007. Sulforaphane induces cell type-specific apoptosis in human breast cancer cell lines. Mol Cancer Ther 6:1013-1021.
Prasad AS. 1995. Zinc: an overview. Nutrition 11:93-99.
Shan Y, Zhao R, Geng W, Lin N, Wang X, Du X, Wang S. 2010. Protective Effect of Sulforaphane on Human Vascular Endothelial Cells Against Lipopolysaccharide-Induced Inflammation. Cardiovas Toxicol 10(2):139-145.
Sharma C, Sadrieh L, Priyani A, Ahmed M, Hassan AH, Hussain A. 2010. Anti-carcinogenic effects of sulforaphane in association with its apoptosis-inducing and anti-inflammatory properties in human cervical cancer cells. Cancer Epidemiol In Press.
Singh SV, Srivastava SK, Choi S, Lew KL, Antosiewicz J, Xiao D, Zeng Y, Watkins SC, Johnson CS, Trump DL and others. 2005. Sulforaphane-induced Cell Death in Human Prostate Cancer Cells is Initiated by Reactive Oxygen Species. J Biol Chem 280:19911-19924.
Straub DA. 2007. Calcium supplementation in clinical practice: a review of forms, doses, and indications. Nutr Clin Pract 22(3):286-96.
Vallejo F, Tomas-Barberan FA, Garcia-Viguera C. 2002. Gllucosinolates and vitamin C content in edible parts of broccoli florets after domestic cooking. Euro Food Res Tech 215(4):310-316.
Vallejo F, Tomas-Barberan FA, Garcia-Viguera C. 2003. Phenolic compound contents in edible parts of broccoli inflorescences after domestic cooking. J Sci Food Agri 83:1511-1516.
Yuan F, Chen D-Z, Liu K, Sepkovic DW, Bradlow HL, Auborn K. 1999. Anti-estrogenic activities of indole-3-carbinol in cervical cells: Implication for prevention of cervical cancer. Anticancer Res 19:1673-1680.
Zhang Y. 2004. Cancer-preventive isothiocyanates: measurement of human exposure and mechanism of action. Mutation Res/Fund Mol Mech Mut 555(1-2):173-190.