Exercise is Medicine

by Jade Teta ND, CSCS, and Keoni Teta, ND, LAc, CSCS

Female Phase Training?

In this month’s issue, we have decided to share one of our clinical protocols with you. While this information is extrapolated from our understanding of the research in this area, it has never been studied exclusively. This is a strictly clinical treatment this month. However, we did include some references at the end of the column that guided our clinical thinking about delivering this protocol.

Female phase training is a way to cycle female conditioning and nutrition in a way that takes advantage of the monthly fluctuation of steroid hormones (estrogen and progesterone) in the normal menstrual cycle. Estrogen and progesterone affect fat gain or loss through direct biochemical effects and more subtle influences over other hormones.

Brief Review of the Menstrual Cycle

The hypothalamus (a part of the brain just above the brain stem) at the beginning of the woman’s cycle secretes ganodatropin releasing hormone (GnRH). This hormone then activates the release of follicle stimulating hormone (FSH) and luteinizing hormone (LH). These two hormones are involved in ripening the follicle (the place where the egg is held) and then causing the follicle to rupture and release an egg.

There are two distinct phases of the menstrual cycle. The follicular phase is marked by the beginning of menses (day 1 of the cycle) and ends at ovulation (day 14 of the cycle in the textbook case). It is called the follicular phase, because the follicle is maturing, mainly under the influence of FSH. The proper maturation of this follicle is essential for the release of an egg.

The second phase of the cycle is the luteal phase. This is marked by ovulation and the subsequent transformation of the follicle into the corpus luteum once the egg is released. This phase is triggered by a large surge in LH, which causes the follicle to “pop” and release its egg. The corpus luteum becomes the major source of progesterone. If the egg is not fertilized, the corpus luteum degrades, estrogen and progesterone levels both fall and the uterine lining is shed resulting in menses.

What Does This Have to Do with Fat Loss?

In addition to having reproductive function, estrogen and progesterone affect fuel storage and fuel use. In other words, these two hormones can determine what type of fuel is burned (sugar versus fat). This is mainly because they can mildly influence two primary fuel regulating hormones, insulin and cortisol.

Estrogen opposes insulin’s action on the fat-storing enzyme lipoprotein lipase (LPL), essentially making the body more insulin sensitive. The overall impact of estrogen is less fat storage and enhanced fat burning. Estrogen is also anticortisol (as is progesterone). Given these considerations, the follicular phase of the menstrual cycle allows a greater tolerance for insulin-promoting foods (starchy/fatty foods). It also make the body more resistant to catabolic exercise modalities that may waste muscle, such as long-duration cardio⁾.⁵

The follicular phase of the menstrual cycle is a great time to focus more on steady-state longer-duration moderate-intensity cardiovascular exercise and heavy traditional weight training. This combination will enhance fat loss, and maintain or perhaps even promote lean muscle. Women will be able to burn high amounts of fat and be less prone to muscle loss due to the estrogen effect during this time. Some research also hints that the early follicular phase may produce the best performance outcomes for athletic women.^3,5

Progesterone opposes the action of estrogen and may make the body more insulin resistant resulting a greater propensity to store fat and lose muscle⁾.⁵ Based on these metabolic considerations, women would want to watch their starch/sugar intake during the luteal phase and minimize more catabolic forms of exercise.^2,4 With progesterone relatively higher than estrogen in the luteal phase, the female metabolism relies more on sugar versus fat metabolism.

This metabolic state is more reminiscent of the male physiology, and there is enhanced glycogen storage and a potential increased afterburn from exercise⁾.⁶ These luteal phase changes create a great opportunity to use higher-intensity short-duration metabolic conditioning (high-rep weight training) and/or interval training.^2,4 By keeping the sessions shorter and more intense and using high-rep weight training, perhaps we can overcome the slowed fat loss during exercise and keep exercise stress under control. This may maximize the hormonal responses, elevate fat loss, and minimize muscle loss).⁷)

Other Considerations

One caveat regarding this program is the primacy of insulin and cortisol. This means that a women with high insulin and/or cortisol levels (i.e. eating a standard American high starch diet), who is insulin resistant, will not see the pronounced effect of this style of training due to the fact that insulin and cortisol are far greater promoters of fat regulation than either estrogen or progesterone.

This protocol works with women undergoing normal menstrual cycles who are not taking birth control and who are living relatively low insulin promoting lifestyles. Because insulin and cortisol are higher on the metabolic “totem pole” than estrogen and progesterone their influence could essentially “wash out” any beneficial influence of the female reproductive hormones⁾.⁵ The same is true for OCP and HRT use.^1,5 Giving static doses of hormone completely eliminates the natural cycling nature that this protocol takes advantage of.

Protocol Overview

• Follicular phase (Days 1–14

  ): 30:40:30 macronutrient intake (carbs:protein:fat). 3 times weekly full body traditional weight training (squat, bench press, back row, shoulder press), 4 sets of 10 using a 8–12 rep max. 5 days per week steady-state moderate-intensity cardio (40–60 minutes).

• Luteal phase (Days 14–28

  ): 20:40:40 or 10:45:45 macronutrient intake (carbs:protein:fat). 4–5 days per week metabolic conditioning (mixed weight and cardio interval training). Daily leisure walking (as much as able).

• Repeat next month.

Final Thoughts

The current state of research in this area is highly controversial and contradictory. This is largely due to the impossiblity of isolating these effects under the influence of other more powerful hormonal influences. Hormones do not work in isolation, and estrogen and progesterone are comparatively weaker in their influence on fat metabolism. Their influence becomes relevant only when other hormones are controlled. In addition, each women is different making research extrapolations more difficult.

What we offer above is our interpretation of the information and our experience using it. You will find best results with lean, fit female patients undergoing normal cycles who have found certain areas (i.e., hips, buttocks, and thighs) resistant to their efforts. This protocol gets the best clinical results when combined with low-carbohydrate/Paleolithic/primal nutrition lifestyles. We hope that it is useful for these patients struggling to lose fat from stereotypical stubborn fat deposits.

Notes

1. Gretchen et al. Menstrual cycle phase and oral contraceptive effects on triglyceride mobilization during exercise. J Appl Physiol. 2004;97:302–309.

2. Davidson, et al. Impact of the menstrual cycle on determinants of energy balance: a putative role in weight loss attempts. Int J Obes. 2007;31:1777–1785.

3. D’eon et al. The roles of estrogen and progesterone in regulating carbohydrate and fat utilization at rest and during exercise. J Womens Health Gend Based Med. 2002;11(3):225–237.

4. Nakamura et al. Hormonal responses to resistance exercise during different menstrual cycle states. Med Sci Sports Exerc. 2011 Jun;43(6):967–973.

5. Oosthuyse T, Bosch AN. The effect of the menstrual cycle on exercise metabolism. sports medicine. 2010;4(3):207–227.

6. Matsuo et al. Effects of the menstrual cycle on excess post exercise oxygen consumption in healthy young women. Metabolism. 1999 March;48(3):275–277.

7. Davis et al. concurrent training enhances athletes’ strength, muscle endurance, and other measures. J Strength Cond Res. 2008 September;22(5):1487–1502.