Want the highlights of this blog? Skip to the end, want the science? Awesome, read on….

I get asked a lot of questions about fat loss, training and health, especially when I am out with friends and in social situations, I reckon many of you have been in the same situation as me.

You know the scene – you’re the ‘healthy person’ at the party and so, as soon as people get a little drunk, everyone is either telling you:

  • They want to lose weight but can’t, can you write them a diet plan
  • They/their friend is bigger/stronger than you
  • They used to exercise, but their knees…

Well, in those situations, I tend to get locked into the conversation of ‘I’m not losing weight. I do XYZ but it’s not working, what exercise should I do?’. Usually I politely ask them to message me when sober so I can help out, but in the event that I let the conversation go on, I’ll offer advice around diet and why that’s more important etc, etc, but then ask them if they are resistance training.

The answer is typically no, because weight loss is the goal. When I explain that resistance training can augment weight loss, help with ‘looking toned’ because of an increase in lean muscle mass, and also benefit a ton of health markers including bone density, blood lipids and even mood/self esteem (1), interest is piqued. I may even inform them that cardiovascular training, or exercise with the express purpose of calorie burn isn’t all that effective for weight loss, either (2), so perhaps resistance training may be a better option coupled with calorie restriction, as this can both augment weight loss (2) and improve lean mass retention (3). Then they drop the following, or some variant of it:

If I start lifting, won’t I gain weight?

The answer to that is yes – though that is swiftly followed by a ‘but’. The purpose of this blog is somewhat selfish. Basically, I want to lay out everything that comes after that ‘but’ so that I have somewhere to point people to when the question arises. Perhaps you’ll be able to use it for the same purpose.

So here’s the thing – yes, when an otherwise sedentary, untrained, overweight person first starts a resistance training regimen they will more than likely see their scale weight go up a little at first. Depending on the person’s disposition this may get chalked up to “I’m gaining muscle” or “I’m gaining fat”. We’ll tackle the latter first.

Why might you gain fat when initiating resistance training?

The first consideration here is this: If someone has been engaging in endurance exercise and maintaining their weight, but then moves to resistance training, this will cause a decrease in their exercise energy expenditure. Aerobic exercise simply burns more calories, because even during a tough resistance training session you spend most of the time resting whereas the calorie burn from something as mundane as walking will add up. Moreover, here we are talking about relatively untrained, somewhat overweight people, so we can safely assume they aren’t able to throw heavy weight around by squatting and deadlifting a lot of iron – their resistance sessions just aren’t that hard, because they aren’t yet capable of making them so (subjectively hard things are difficult, but the calorie burn remains low). They may, however, be able to walk on a treadmill at a reasonable pace for an hour.

What I’m getting at here is, if you are doing a lot of cardio while maintaining weight, then stop in order to take up resistance training, you may inadvertently slip into a calorie surplus.

The other side of this is that there is always going to be some degree of compensation for exercise calorie burn. When researched, lean individuals will generally compensate more than obese individuals will when initiating exercise (4) but this should still be considered. There is also the ‘I exercised so I deserve this’ response which might see someone engage in resistance training, reward themselves with a 200-300kcal snack and then end up back at a net zero, an even calorie intake.

In short, if you are concerned that you are gaining fat thanks to resistance training, the answer is to make sure your calorie balance is where it should be. People will routinely underestimate how much they are eating and overestimate how many calories they are burning (5) so be aware of this and stay in a calorie deficit. If this is in line, you will not gain fat.

But that doesn’t really answer the question, because even those who ARE in a calorie deficit may notice their scale weight creep up a little when they start resistance training, especially if they weren’t exercising all that much beforehand. Is this the beginning of ‘bulking up’ and/or looking manly?

Nah, not really.

First of all, the majority of your strength increases during the first few weeks of a resistance training program come due to neural adaptations rather than hypertrophy (6). This means that people will get stronger very, very quickly when they first begin but this isn’t necessarily due to an increase in muscle size. Very briefly, in order to contract a muscle, motor neurons from your nervous system must excite bundles of muscle fibres called motor units. When you first start training, this process gets far more efficient, and rather than it being the case that muscles get stronger per se, they simply get better at using the strength they already have.

After the initial few weeks, strength gains are due to hypertrophy to a greater relative degree. In short, you haven’t gained 3-4lbs of muscle in your first week, even if you have literally doubled your deadlift already.

So what’s going on here?

Well, there are two primary reasons that you will more than likely gain a little scale weight when you first start resistance training, but before we get to that, I want to be absolutely clear on something:

Weight and fat aren’t the same thing when you are talking about loss and gain. Yes, at the end of a 20 week fat loss phase you will weigh less than when you started, but week-to-week, there are a ton of different things that can cause your scale weight to go up and down that have literally nothing to do with the fat mass you carry. This is important, because although weight has become the surrogate measure for fat, weight gain has been included in the list of “things that are bad and make me look worse”. This is not the case. Weight loss isn’t important, fat loss is, and acute fluctuations in ‘stuff-that-isn’t-fat’ shouldn’t be something that concerns you.

In order to make that the case, for the second half of this blog I’m going to outline the two primary reasons for this-isn’t-actually-fat-or-muscle weight gain.

Inflammation

Delayed Onset Muscle Soreness (DOMS) is the name for the sensations of pain, discomfort and reduced mobility that start to kick in around 12-48 hours after exercise. There are a number of different theorised causes, some of which aren’t relevant for this blog, but two of those aspects certainly are – namely muscle damage and inflammation caused by that damage (7).

In order to contract a muscle, the motor proteins known as myosin ‘walk’ along an actin filament, to shorten a unit within the muscle called a sarcomere. This is known as the sliding filament theory, and is illustrated by the image below (8). As the myosin units walk along the actin filaments, the edges of the sarcomere are pulled closer together. Each muscle fibre contains thousands of units similar to this along its length, allowing the muscle to shorten and, therefore, contract.

Delayed onset muscle soreness (DOMS)
Delayed onset muscle soreness (DOMS)

After the muscle has contracted, it must then relax to return to a resting state. If this contraction happens during resistance exercise then the relaxation (known as the eccentric [ee-sen-trik] portion of the lift) happens under load, which can cause damage to the sarcomere in two ways. First the myosin heads can become damaged, and secondly the Z-disk or Z-line which separates one sarcomere from the next can become ruptured. This is further augmented because, after exercise, proteolytic enzymes responsible for scavenging damaged cells get to work degrading and breaking up some parts of the muscle fibre in order to replace them later.

An enzyme known as creatine kinase is found at high levels in skeletal muscle, but in serum (blood) fluid it’s found at a relatively weak concentration around 100IU per litre. Damage to the sarcomere can allow for creatine kinase to seep out into the interstitial fluid and then the plasma fluid, however, and when measured, the post exercise plasma concentration of CK can be up to 40,000 IU per litre. Clearly, there is a significant amount of damage going on which must be healed.

(note – this isn’t the only cause of DOMS, as mentioned – it’s just the only one relevant for the discussion at hand).

The first stage of healing is inflammation. Cellular damage causes the release of chemicals including histamine and prostaglandins in the local area, which attract various white cells including monocytes and neutrophils. These cells act to further increase the inflammatory response, which includes increasing the permeability of local blood vessels – and it is this that we are concerned with.

That increased permeability functions to flood the area with protein and nutrient rich fluid, for the purposes of accelerating repair. It also causes oedema – water retention - peaking at around 48 hours post exercise. That water retention (much like the DOMS with which it is associated) is significantly greater in new exercisers, meaning that people who are brand new to training, people returning to exercise after a long layoff or people doing a new exercise/trying out a different exercise modality are going to cause a greater inflammatory response, therefore a greater amount of localised water retention.

That water retention is temporary, and it’s formation will decrease dramatically as you get better conditioned. But in the initial stages a full body workout can easily cause 2-3lbs worth of water retention due to muscle microdamage and the healing process associated with aiding that DOMS process.

So that’s one reason you may see your scale weight go up when starting a new training program, and here’s the other:

Glycogen Synthesis

During exercise your body uses a molecule known as adenosine triphosphate (ATP) to perform muscle contractions – ATP is made of an adenosine body with a ‘tail’ of three phosphates. Crudely, a unit of ATP binds to one of the myosin units mentioned before and this causes one of the phosphates to break off, releasing the energy stored within its weak bond. That myosin unit then takes a step along the actin filament, and another ATP must bind to repeat the process.

Unfortunately, we only have a tiny amount of ATP stored at any one time, with some research suggesting we don’t even have enough for one second of maximal effort exertion (9). This means that ATP must be continually resynthesized, and the primary means by which we do this during a bout of exercise is through glycolysis – meaning we break up glucose for fuel.

The glucose used during exercise primarily comes from your body’s storage form of glucose, glycogen. Glycogen is a long string of glucose monomers which is formed by various enzymes including glycogen synthase and stored within a given cell to be used by that cell later.

In short, you eat carbohydrate and increase your blood glucose levels. That would be incredibly harmful, so both your liver and your muscle cells engage in glycogen synthesis to place as much of that surplus in storage as possible.

Importantly, the amount of glycogen you can store in muscle tissue is somewhat mediated by glycogen synthase activity there, along with – simply – the amount of glucose that your muscle cells are able to ‘soak up’ before your liver absorbs enough glucose to bring blood glucose back to stable levels. This ‘soaking up’ is primarily mediated by the glucose transporter protein – GLUT-4.

GLUT-4 generally sits dormant within the cytoplasm of a cell, but when that cell receives a signal that blood glucose is elevated (primarily through the binding of insulin to an insulin receptor) it translocates from the cytoplasm to the cell membrane, where it can facilitate the absorption of glucose. That glucose is then used, or the cell uses it to synthesise new glycogen to use later.

So what does this have to do with anything?

Well, exercise is able to both increase GLUT-4 levels, and glycogen synthase activity (10), meaning that more glucose is absorbed within muscle cells, and those cells are able to turn more of that glucose into glycogen to store. This means that, when you start exercising, you will start to store far more glycogen than you ever have done before. This glycogen will be kept within your muscles to use later with each gram being stored alongside around 3g of water (11). Being that muscle cells can store around 500g of carbohydrate in exercisers (12) this can equate to a few pounds of weight gain, easily.

It is for this reason that I noted at the beginning that weight and fat aren’t the same, and it’s not a problem if you gain weight that isn’t muscle tissue. Although glycogen and intramuscular water aren’t muscle tissue per se, they CAN create an appearance of increased muscularity, lending itself towards appearing more ‘toned’ if that is the goal. Muscles will also become firmer thanks to this hydration, which is always a good thing.

This is where we need multiple ways of tracking ‘fat loss’

So what to do?

Here I’ve outlined the facts that yes, you might gain a little weight but no, that weight probably isn’t either fat OR muscle tissue. The question remains, though: if you might gain 2-3lbs or even more in the first 2 weeks of starting a new exercise regime (especially involving resistance training) but your goal is weight loss, how exactly can you make sure your diet is still working?

Easy – take additional measurements.

Tape measurement stomach
Tape measurements

One thing we note in the new Body Type Nutrition Foundation Academy is that the more data you collect, the more informed your decisions can be. In the course manual we ask you to think of weight loss like an equation – on one side you have your independent variables, they are, the things you are doing in order to have an effect. On the other side you have your dependent variables, which represent the outcome.

Tracking your food in one of the many ways we outline in the manual, as well as tracking habits, sleep, water intake and other behaviours allows you to control the side of the equation over which you have the most sway. On the other hand, recording more than weight alone lets you create a far greater understanding of what impact those changes are really having.

 

Energy balance
Energy balance - calories in vs calories out

If you haven’t lost weight, that does not mean you have not lost body fat. Perhaps you could track the following:

  1. Your waist. This isn’t influenced by DOMS-related or glycogen-related water retention, so it can show you where your weight loss is being masked
  2. Your arms/legs. If these go up a bit but your weight remains stable or creeps up a tad, you can confidently assume that you are losing fat and gaining a little water to begin with
  3. How your clothes feel. Clothes don’t lie (unless you shrink them, men, cough cough!)
  4. How your photographs look month-on-month. You see yourself every day, leaving gaps lets you see changes, so analyse the changes you see in photos
  5. Body fat % if you have an accurate means of doing so - and no those scales at the gym (impedance scales) won’t be accurate in the early stages of a diet as they also account for water when measuring body fat, they might, if using the same scales, work after this initial period of a new training program, but unlikely in the early stages (they are generally not an accurate way to measure body fat)

So there might not be a need to panic if you see the scale weight go up, but are sure you are on the right path. You just need to know a little bit more of the science, and then you’ll know why, and how, and what to tweak, if anything at all. This is a very common problem on a diet. People start to eat healthily, don’t lose any weight at the start despite eating less, but they haven’t considered that they are going to the gym and there might be all the above changes happening to their body weight that is adding ‘weight’. Thus, when we step on the scales, its negating the weight loss.

This is where we need multiple ways of tracking ‘fat loss’. Fat and weight, we need to define them, this is key, because they are NOT the same.

Please don’t panic of you’re on a diet but the scales have not budged, or have possibly gone up, use the knowledge you learnt in this blog, assess some of the other variables, have a look at some of your other tracking measurements, and tweak if needed. Or just be patient for another week and the chances are you’ll have a big drop in weight after these affects have plateaued out, that will then stop you thinking you’ve plateaued and are not losing weight, when you swear you should be. And sometimes, if you think you have lost FAT, trust yourself, don’t let your results be defined by the scales and a number, sometimes YOU are the best person to assess your progress, simply by intuitively knowing. Back yourself.

If you’re interested in learning more about the different factors that can influence weight loss or gain, or you’re interested in the way that your body uses the foods we eat in order to do the things that we do, I’d love you to check out our new Foundation Academy online nutrition course. With the mobile-ready app filled with animated videos, and the comprehensive manual designed to help you delve deeper into the science of nutrition, you really can’t go wrong (we’re also there every step of the way).

Take a look, I think you’ll be impressed:

The BTN Foundation Academy

Tom Bainbridge
Nutrition Coach & BTN Academy Manager

References

  1. Westcott, W. (2012). Resistance Training is Medicine. Current Sports Medicine Reports, 11(4), pp.209-216.
  2. Thorogood, A., Mottillo, S., Shimony, A., Filion, K., Joseph, L., Genest, J., Pilote, L., Poirier, P., Schiffrin, E. and Eisenberg, M. (2011). Isolated Aerobic Exercise and Weight Loss: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. The American Journal of Medicine, 124(8), pp.747-755.
  3. Ballor, D., Katch, V., Becque, M. and Marks, C. (1988). Resistance weight training during caloric restriction enhances lean body weight maintenance. American Journal of Clinical Nutrition, 47(1), pp.19-25.
  4. Thomas, D., Bouchard, C., Church, T., Slentz, C., Kraus, W., Redman, L., Martin, C., Silva, A., Vossen, M., Westerterp, K. and Heymsfield, S. (2012). Why do individuals not lose more weight from an exercise intervention at a defined dose? An energy balance analysis. Obesity Reviews, 13(10), pp.835-847.
  5. Lichtman, S., Pisarska, K., Berman, E., Pestone, M., Dowling, H., Offenbacher, E., Weisel, H., Heshka, S., Matthews, D. and Heymsfield, S. (1992). Discrepancy between Self-Reported and Actual Caloric Intake and Exercise in Obese Subjects. New England Journal of Medicine, 327(27), pp.1893-1898.
  6. Moritani, T. and deVries, H. (1979). Neural factors versus hypertrophy in the time course of muscle strength gain. American Journal of Physical Medicine, 58(3), pp.115-130.
  7. Cheung, K., Hume, P. and Maxwell, L. (2003). Delayed Onset Muscle Soreness. Sports Medicine, 33(2), pp.145-164.
  8. Richfield, David (2014). "Medical gallery of David Richfield". WikiJournal of Medicine 1 (2) - Own work
  9. Hultman, E. and Greenhaff, P. (1991). Skeletal muscle energy metabolism and fatigue during intense exercise in man. Science Progress, 75(298 pt3-4), pp.361-370.
  10. Christ-Roberts, C., Pratipanawatr, T., Pratipanawatr, W., Berria, R., Belfort, R., Kashyap, S. and Mandarino, L. (2004). Exercise training increases glycogen synthase activity and GLUT4 expression but not insulin signaling in overweight nondiabetic and type 2 diabetic subjects. Metabolism, 53(9), pp.1233-1242.
  11. Fernández-Elías, V., Ortega, J., Nelson, R. and Mora-Rodriguez, R. (2015). Relationship between muscle water and glycogen recovery after prolonged exercise in the heat in humans. European Journal of Applied Physiology, 115(9), pp.1919-1926.
  12. Jensen, J., Rustad, P., Kolnes, A. and Lai, Y. (2011). The Role of Skeletal Muscle Glycogen Breakdown for Regulation of Insulin Sensitivity by Exercise. Frontiers in Physiology, 2.