PCOS and Strength Training for Fat Loss

PCOS and Strength Training for Fat Loss

In previous articles I’ve talked about how the menstrual cycle can affect your approach to fat loss, performance and tolerance to different macronutrients. That was of course presuming that your menses was normal and that there were no underlying issues that would affect the cycle.

In this article I want to talk about polycystic ovarian syndrome (PCOS) – one issue that will disrupt a normal cycle – and how it can affect exercise and training outcomes.

It is important that the correct approach and type of exercise is prescribed to best cope with the condition, and best help the body cause positive adaptations that will lead to better management of symptoms and better quality of life.

What is polycystic Ovarian Syndrome?

PCOS, often referred to as hyperandrogenism, is characterized by the imbalance of female sex hormones – estrogen and progesterone.

This imbalance can lead to cysts that grow on the ovaries and can cause a number of symptoms and side effects. Whilst these cysts are not harmful as such, they can lead to hormone imbalances that trigger a number of metabolic side effects.

The condition is thought to be genetic – if your mother or sister has it then are you have an increased chance of having it too.

PCOS affects between 1 in 10 and 1 in 20 women of childbearing age so is relatively common. Women of any age (pre-menopause) can be affected – sometimes it is temporary and sometimes it is long lasting.

The side effects of PCOS

Polycystic ovarian syndrome can cause irregular menstrual cycles and make it more difficult to get pregnant.

In severe cases it may lead to infertility. The cysts that may appear are thought to be due to excess androgen (testosterone) production.

As this hormone is largely considered a ‘male’ hormone due to its effects, it can disrupt the normal hormonal balance, leading to disruption of development and release of eggs during ovulation. 

The symptoms of PCOS differ from person to person, with some suffering much more severely than others.

Typical symptoms may include hirsutism due to reduced female sex hormones and increased androgens – this may growth of hair on the face, back, chest or extremities, deepening of the voice, decreased breast size and thinning of the hair. Additionally, acne and weight gain may also be a side effect, as well as pelvic and abdominal pain.


Key Point: Polycystic ovarian syndrome is a disruption between the female hormones estrogen and progesterone, as well as testosterone. It is considered a metabolic disorder

Menstrual Cycle Science

This part isn’t essential as such but if you want to get a good understanding of what’s happening then you might want to give this section a read.

Non-problematic menstrual cycles rely on the smooth running of the Hypothalamic–pituitary–gonadal axis on a monthly basis. This axis consists of two parts of the brain – the hypthalamus and pituitary glands, and the reproductive organs.

The hypothalamus (considered the master hard drive of the brain) releases a hormone called gonadotropin-releasing hormone (GnRH) directly to the pituitary gland, which in turn produces hormones called luteinizing hormone (LH) and follicle stimulating hormone (FSH).

These two hormones travel to the gonads where they stimulate the production of estrogen and progesterone in the ovaries. Typically a large ‘surge’ of LH triggers the release of an egg, or ‘ovulation’. All normal ovaries produce a small amount of testosterone too.

With PCOS the right amount of messages are not being sent to the ovaries, therefore not enough estrogen or progesterone are made. Essentially, LH levels are often higher than normal (and higher than FSH) so when a surge is needed there isn’t one. No surge, no ovulation.

Another consequence of this is that your ovaries make just a little bit too much testosterone, as well as another androgenic hormone called dehydroepiandrosterone (DHEA) which is made in the adrenal glands. 

Typically, female testosterone levels lie around the 70ng/dL number, whilst male quantities lie between 300-1000ng/dL. Women with hyperandrogenism often see increases of 20-30%, and whilst this is stil under the lowest threshold of males, women are less tolerant and more sensitive to androgen increases.

Regular vs. PCOS menstrual cycle

As all of these hormones are in combined imbalanced they can change intermittently, so ladies with PCOS may ovulate occasionally or not at all – periods may be too close together, or more commonly too far apart (35 days or more). Some may not get a period at all.

PCOS and Insulin Resistance

As many as 70% of PCOS women are insulin resistant [1]. This is where insulin – a hormone made in the pancreas – doesn’t control blood sugar as well as it should do. This can lead to higher-circulating blood sugar and weight gain.

PCOS women often have significantly increased glucose levels during an oral glucose tolerance test compared with age- and weight-matched normal-ovulatory females [2]. Interestingly, adolescents are more likely to exhibit insulin abnormalities.

One of the proposed mechanisms behind weight gain with this condition is insulin resistance (it is often suggested that PCOS sufferers follow a low-carb diet, although this is best left discussed in another article).

One of the side effects of insulin resistance is that it triggers excessive release of testosterone, causing a viscous cycle of androgen release-insulin resistance-more androgen release- more insulin resistance.



PCOS and strength training for fat loss

Insulin Resistance

Strength training is an effective control measure for other insulin/metabolic based conditions such as diabetes. By increasing the size of skeletal muscles, the muscle itself is able to ‘take up’ more glucose and decrease circulating amounts in the bloodstream.

A consequence of glucose uptake in the muscle is that your weight on the scales is unlikely to shift in the right direction – at least initially. As glucose is transported into the muscle it takes an amount of water with it, leading to water retention – more so as you begin a weight lifting program. Whilst this might affect weight loss initially (and can often be mistaken for ‘bulking’), you need to see past this. Over time this will even itself out. It will however be beneficial in helping to manage insulin resistance, which will in turn hopefully reduce testosterone production and help you to better manage your symptoms. 

One point to note is that due to already higher circulating testosterone levels, women with PCOS due have a higher chance of becoming more muscular. Whilst this is not going to give you a drastically muscular physique worthy of an Olympia title, if you feel that you are getting overly muscular then you need to revise your approach by reducing volume or intensity as appropriate.

Basal metabolic rate

The implementation of a weight training program will also increase your basal metabolic rate (BMR). This refers to the amount of energy you use at rest. Muscle tissue is very metabolically active, so the more muscle you have, the higher your metabolism will be. This will help you burn fat and achieve a more athletic, shapely figure. As a metabolic tissue, muscle becomes even more active when it is being used so the more muscle you have, the better your energy turnover is during training as well.

How do you best approach strength training?

There are a number of guidelines laid out by the American College of Sports Medicine (ACSM) for strength training with metabolic conditions. Within this framework the following is proposed:

  • 2-3 strength training sessions per week, on non-consequtive days
  • Whole body approach covering key muscle groups in 8-10 exercises
  • 8-15 repetitions, 2-3 sets of each exercise


  1. Traub, ML. Assessing and treating insulin resistance in women with polycystic ovarian syndrome. World J Diabetes. 2011; 2(3): 33-40
  2. Dunaif A, Graf M, Mandeli J, Laumas V, Dobrjansky A. Characterization of groups of hyperandrogenic women with acanthosis nigricans, impaired glucose tolerance and/or hyperinsulinemia. J Clin Endocrinol Metab. 1987; 65: 499–507