Regular Cardio Will Make You Fat

by John Meadows   

Here's what you need to know...

•  When using cardio while dieting, begin by doing the minimum necessary for fat loss, not the maximum.

•  The most effective cardio for retaining muscle is the kind you don't need to recover from, which is walking.

•  When it comes to doing cardio for fat loss, it's either slow and easy (walking) or fast and torrid (HIIT). The middle ground can make you fatter.

•  Don't think of HIIT as calorie burning cardio, but rather muscle building cardio.

Whenever the topic of "cardio" comes up, it always ignites a firestorm of differing opinions, most dealing with how much people hate it or how you have to do it to get shredded. What never gets clearly explained, though, is the context and reasoning for which it's being done. This is crucial to understand, because cardio from a conditioning and endurance standpoint is going to be very different from a physique and bodybuilding perspective.

For a competitive athlete, it's likely very important that some kind of energy systems work be performed that either prepares them for their sport or aids in building overall work capacity. In contrast, for a physique competitor, cardio is employed for the sole purpose of either weight control/maintenance or creating a calorie deficit for fat loss. Energy systems development is likely a non-issue, provided the physique competitor is lifting with enough frequency and relative intensity.

Still, when it comes to doing cardio for fat loss, bodybuilders – if they want to preserve their muscle mass – need to take it either slow and easy or fast and torrid. The middle ground can actually make you fatter.

Slow and Easy

Speaking specifically to the bodybuilders, you have to ask yourself the following:

If my primary goal is maximal muscle, do I want to be performing a high volume of an entirely conflicting activity?

Please tell me you didn't answer yes to this. This isn't to dissuade people from doing cardio. If you like cardio, and I know some people that do, by all means do as much as you want. But be cognizant that it may be a conflicting factor that you have to account for if you want to get as big and lean as possible.

If, however, you're going to do cardio, it'd be best to do something that won't conflict with your goals and that's easy to recover from, namely, easy walking. So, if you're doing the incline walks on the treadmill, you're probably doing something right. Just keep it as short as necessary.

However, if you're insistent on stair stepping for an hour to "striate the glutes," or walking on an incline for two hours as contest prep, consider the following:

You have to take the Specific Adaptation to Imposed Demands (SAID) principle into account.

If you're dieting for a show and your lifting volume goes down but your cardio goes up, what's the primary stimulus your body is going to need to adapt to? The cardio. Now how does one become more efficient at slow, aerobic cardio? By decreasing overall energy output, which means burning fewer calories to do the same activity.

So how do we increase energetic/caloric output? We get rid of the most metabolically expensive tissue we have that's taking up those calories, which means our muscle.

The net result is that you over-diet for a show, lose muscle, lose fullness, and your physique suffers. Or, for the non-competitive bodybuilder, you just cut into your muscular gains come summer when you all you wanted to do was cut down for the beach. Not the outcome you wanted.

The answer isn't to refrain from ever doing cardio, but to employ it intelligently. Imagine this hypothetical scenario:

Bodybuilder A trains high-frequency six days a week on the Reactive Pump program, and each training session burns on average of 450 calories over a 1.5 hour period, and he uses peri-workout nutrition. He weighs 240 pounds in the offseason and he'll be dieting down to 220. He stays lean year round and his caloric intake is 4200 calories while his expenditure is 3800.

Bodybuilder A's active metabolic rate is 3800.

Bodybuilder B does his own type of training. He trains high-frequency as well, 5-6 days a week, but his workouts aren't as intense and they take about 2 hours. He also does an additional 45 minutes of cardio every workout, which equals about 650 calories.

He uses IIFYM (If It Fits Your Macros) and doesn't pay much attention to food quality, and his peri-workout nutrition consists of a shake before and after training, followed by tons of low-quality carbs. He gets fat in the offseason and his caloric intake is about 5500 calories, but his expenditure is only 4500, which puts him into a significant surplus. His offseason weight is 270, but he'll walk on stage at 220 as well.

Bodybuilder B's active metabolic rate is 4500.

Now let's move into the competition prep phase. Both start 24 weeks out. Bodybuilder A has to lose only 20 pounds, which is less than a pound a week. Bodybuilder B, though, has to lose 50 pounds, so approximately 2 pounds a week.

Bodybuilder A does ZERO cardio during his offseason, other than going for leisurely walks that don't stress his adaptive response at all. So by reducing his calorie intake very gradually and maintaining his peri-workout nutrition, his cut is easy to manage. Only the last couple of weeks before the contest does he do any cardio, and it's only for 30 minutes a pop. He also does a few HIIT bouts to really accelerate the fat loss.

Because his loss has been more gradual, he has to resort to fewer dirty tricks to lose the weight and his metabolism hasn't slowed significantly. He still has a cheat meal a week before the contest. He steps on stage big, ripped, and vascular.

Post contest, he enjoys another cheat meal and eats dirty for a few days, but he hasn't been calorie or nutrient deprived, so his metabolism doesn't have a huge rebound. After 2-3 weeks he's back to regular training and he's set himself up for solid muscle gains.

Bodybuilder B, though, has a lot of fat to shed. Even though his initial caloric output his higher, he needs a bigger daily deficit to lose weight. He ups his cardio to 2 hours, but now he's increased his metabolic rate while at the same time cutting calories. He's constantly hungry and his workouts really start to suffer. He's not very smart about his peri-workout nutrition, he's often flat, and his strength starts heading south.

His metabolic rate starts to slow significantly because of his lowered caloric intake and his body begins to deplete muscle. Increasing his overall activity while heavily decreasing his calories makes his cut absolutely miserable. Oh, he still gets to 220, but he's soft looking and he's lost significant size.

Once the contest is over, he binges like crazy because he's been calorie and nutrient starved for weeks. Subsequently he gets even fatter than before, setting himself up for another hard cut a year from now.

Obviously, scenario A is where we want to be, so here are the major takeaways:

• Clearly define whether you need cardiovascular training for physical performance or purely for body composition management.

• The most effective cardio for retaining muscle is the kind you don't need to recover from, which is walking.

• When using cardio while dieting, begin by doing the minimum necessary for fat loss, not the maximum.

Of course, there's the other alternative.

HIIT It

HIIT (High-Intensity Interval Training) isn't really in the same category as traditional "cardio." If you do it right with extreme intensity, it's very complimentary to hard resistance training.

While it can be highly effective for fat loss and improved muscularity, the devil is in the details. When deciding which version of cardio to use, the body's natural physiological adaptations need to be taken into account.

Consider again how the "middle zone" cardio we talked about above (specifically in reference to our Bodybuilder B) is lousy for muscle gains. Adaptation is a response to stress, and biology will always seek efficiency and, consequently, minimization of stress. As such, the adaptation to this middle zone cardio is less muscle and more body fat.

In contrast, consider something like sprinting. Sprinting is the cardio version of maximal strength training. However, in this case we're not moving weight, we're moving our bodies. This essentially makes sprinting a "relative strength" activity, in that it's the amount of force – in this case, propelling the body through linear space – we can exert in relation to our body size or weight.

Of course, we're only as fast as we are strong, and the stronger we are, the faster we can be. And that strength, of course, comes from muscle. Even further though, sprinting is an expression of power output; it's mass x acceleration. The more efficiently we can alter our physiology and replace fat with muscle, the greater the force output and thus, the faster our potential speed.

Consider then, if sprinting is the stress, and the imposed demands are maximal speed that's compounded by mass relative to our ability to accelerate, what will make us more efficient/faster at sprinting? Getting stronger, of course, and sprinting itself can be anabolic.

As far as loss of fat, it's the extraneous, unwanted, unneeded tissue that impedes acceleration. That's why sprinters are lean. Sprinters have the lowest body-fat percentages relative to any other athlete. And I guarantee none of them train in a calorie deficit to look like that.

Their body composition and muscularity is the result of the natural biological adaptation that's taken place in response to their imposed demand/stress, which, in this case, is maximal efficiency at maximal force output.

The body's adaptation to middle ground cardiovascular exercise, however, is the opposite of weight training. In lifting weights, maximal strength often requires maximal bodyweight with higher body fat levels, but in cardio, maximal speed requires minimal bodyweight relative to the amount of muscle needed to reach top speed. In this case, however, minimal still equates to a lot of muscle, otherwise you won't ever reach your speed potential.

Too much sprinting, however, can quickly burn you out, just as too much maximal lifting can. The dosage is hugely important.

These are the takeaway lessons:

• Lifters should augment resistance training with HIIT.

• Sprint-based cardio can equate to lower body fat levels.

• Don't think of HIIT as calorie-burning cardio, but rather muscle-building cardio.

I've laid out two paths for you. The first – walking – will gradually get you cut without impeding further muscular gains, and the second – HIIT – will get you cut while building muscle. The choice is yours. Just avoid the middle ground.

Note: Alexander Cortes contributed to this article

Control Leptin and Control Your Leanness!

by John Meadows CSCS, and Bill Willis PHDc – 1/16/2012

Leptin – you've probably heard someone mention it at one time, but aren't really sure what it is. I remember when I first heard a bodybuilding coach mention it, saying that managing leptin was crucial to keeping the metabolism humming. I had no clue what he was talking about, but it did intrigue me.
Leptin wasn't even discovered until 1994, but research into the mysterious hormone has been increasing. Scientists certainly don't know everything about leptin yet, but let's discuss what we do know.

What is Leptin?

First, it's important to understand that fat isn't simply just a storage tank for excess calories or "potential energy." Fat is actually an endocrine organ, like a thyroid or adrenal gland, for example. This means that fat – in this case white adipose tissue – secretes hormones, and leptin is one of them.
Leptin is a polypeptide hormone produced by adipocytes (fat cells). The more fat the adipocytes contain, the more leptin is released. Think of leptin as a metabolism controller and a hunger regulator. It links changes in body fat stores to CNS control of energy homeostasis (1-4).
Here's a simple example:
You eat above maintenance calories over a period of days or weeks.

• As you eat more, fat cells fill with triglyceride, which increases the release of the hormone leptin into the bloodstream.
• The hypothalamus in your brain has an intricate system of communication with fat cells which include leptin receptors. When leptin levels increase, leptin binds to leptin receptors in the hypothalamus, sending the message that you're "fueled up."
• The hypothalamus then sends signals to the brain and the rest of the body, decreasing appetite and turning up your metabolic rate.

OR
You eat below maintenance calories over a period of days or weeks.

• Your fat cells shrink as you diet, not eat, etc., and fat cells release less leptin.
• Your brain senses that leptin levels are low, and that you are no longer "fueled up."
• The hypothalamus senses the decrease in leptin levels, lowering metabolic rate and decreasing energy expenditure. It also sends a "hungry" signal, increasing appetite and encouraging you to eat.

Leptin action isn't confined to just the hypothalamus. There are leptin receptors all over the body. This allows leptin to precisely coordinate appetite, metabolism, and energy expenditure.

Location	Leptin mode of action
Pancreatic islets	(-) Insulin production and secretion (5, 6)
Adipose tissue	(+) Fatty acid oxidation (7) (+) Lipolysis (7) (-) Lipogenesis (8)
Liver	(+) Lipolysis (7) (-) Lipogenesis (8)
Skeletal muscle	(+) Fatty acid oxidation (9)

This is nature at its finest. Your body is programmed to survive. On one hand, when food is available, leptin keeps you from adding too much fat mass, which would have been a liability back in the caveman days (or today, for that matter).
On the other hand, leptin responds to and defends against excessive body fat loss that might threaten survival or reproductive ability (10). Eat too much and metabolism speeds up to keep up. Don't eat enough and it slows down to keep you alive.

What if the Hypothalamus Stops Receiving Messages?

Check out the picture below of the fat mouse. Let's call him Jumbo. Jumbo is unique – he's an ob/obmouse. This is a mouse that becomes a type II diabetic, can't stop eating, and packs away body fat like crazy. No matter how much you feed him, he won't stop.
Poor Jumbo has a mutation in the gene coding for leptin – he's totally missing it! His fat cells can't properly communicate with his hypothalamus because he has no leptin. If you inject Jumbo with leptin, he'll stop eating and lose weight, but the solution isn't so simple for us non-mutants.
Most obese people don't have missing or mutated leptin genes – they can make plenty of it. The problem is that in spite of leptin still finding and binding its receptors all over the body, no downstream message is sent. The system that senses leptin is broken.

This is called leptin resistance, a condition in which the brain can't determine when body fat is at an okay level. The fat cells are sending leptin out to the hypothalamus to signal that fat stores are full. Leptin binds the receptors, but no downstream messages are sent. It's like knocking on the door when nobody is home. In spite of all the extra body fat mass, the brain perceives starvation and orders fat storage. The kicker is that you're also very hungry, and continue to eat more and more.
If you know anyone who just can't stop eating like Jumbo, as tempting as it may be to instantly judge them, it's likely not entirely their fault. Many obese people have metabolic systems that are simply broken. You can't outrun Mother Nature, and if the leptin signaling is messed up, you can only control yourself so much.
But it's not just the clinically obese who must be concerned. You permabulkers, take note: as you continue to overeat, triglyceride stores increase, causing fat cells to produce more leptin. With so much leptin around, leptin receptors become desensitized. Eventually they just tune out, which has big consequences. You have plenty of fat but your brain doesn't know it.

How Do We Become Leptin Resistant?

Reduced blood-brain barrier transport. The idea that leptin levels were higher in obese people was a surprise. When scientists tested the ability of various tissues from leptin resistant animals to respond to leptin in vitro, most of the time leptin receptors isolated from the hypothalamus were still somewhat sensitive.
This was a big puzzle until it was discovered that part of the body's response to high leptin levels is to shut down leptin access to the brain. For leptin to travel from fat cells to the hypothalamus, it travels through the bloodstream but has to cross the blood-brain barrier to gain access.
The blood-brain barrier is extremely selective as far as what it lets through, and it was discovered that an early response to high leptin levels is to shut down transport across the blood-brain barrier. This allows the body to preserve leptin sensitivity in the hypothalamus as long as it can, holding out until leptin levels drop back to normal.
Reduced leptin receptor sensitivity. Like the insulin receptor, when leptin receptors are constantly bombarded with high amounts of leptin, they become resistant. The mechanism of reduced leptin receptor sensitivity was partly discovered by accident, when scientists were studying the role of a protein phosphatase calledprotein tyrosine phosphatase 1B (PTP1B) in the regulation of insulin receptor signaling.
It's been known for some time that insulin receptor sensitivity is controlled by a number of kinases and phosphatases, and in this case, scientists hypothesized that PTP1B was limiting insulin sensitivity. This would be great news for diabetics.
To test this hypothesis, they created a group of knockout mice that lacked the PTP1B protein. As the researchers predicted, these mice became very sensitive to insulin when they were given a glucose test. The scientists also noticed something else. These mice got ripped, and lost considerable body fat.
The mice had incredibly fast and efficient metabolisms, the cause of which came as a big surprise – eliminating the PTP1B gene was also massively upregulating leptin sensitivity (11). It was later found that the PTP1B protein is a negative–feedback inhibitor to leptin receptor signaling. When the leptin receptor is stimulated with high amounts of leptin, PTP1B kicks in to reduce receptor sensitivity.
Another protein called suppressor of cytokine signaling 3 (SOCS3) is also a negative feedback inhibitor of leptin. When the leptin receptor is activated by large amounts of leptin, SOCS3 increases which reduces leptin receptor sensitivity (12, 13).
You might have noticed that insulin and leptin resistance appear to be inseparable. This isn't a coincidence; like PTP1B, SOCS3 is also a negative regulator of insulin signaling, so insulin resistance and leptin resistance are linked at the molecular level.
Inflammation also activates PTP1B and SOCS3, which explains why it affects both insulin and leptin receptor sensitivity.

Dieting and Leptin Resistance

Let's take a guy in perpetual bulk mode, we'll call him "Beefcake." First, Beefcake eats a ton of calories and puts on some body fat in his quest to get hyoooge. This causes an increase in leptin release. Leptin tells the hypothalamus that fuel stores are full, and the response is a reduction in appetite and increase in energy expenditure.
In this way, leptin restores the metabolism to homeostasis by matching appetite to food intake – but this came at a price! The continual pounding of food and garbage calories more than likely caused a degree of leptin resistance. This means he now has increased the amount of leptin needed to just maintain energy homeostasis.

Key Point: Leptin resistance causes a new "set-point," which leads to the defense of a higher level of body fat storage and slower metabolic rate than would otherwise happen if Beefcake were still leptin sensitive! In other words, your body is smart, and if it thinks a "diet" is coming, it immediately holds on to fat as much as it can.

The more leptin resistant you are, the more your metabolic set point will shift towards "fat" and away from "lean." Have you ever dieted down and got lean, then after a Beefcake-inspired bulk up, had a really hard time leaning out again? Now you know why. This is one major reason why "bulk ups" aren't recommended.
Let's continue. In Beefcake's leptin resistant state, when he decreases calories, his super-enlarged fat cells start to shrink, causing a reduction in leptin levels. The problem is, the leptin resistance caused a new "set point," which prompts his screwed up metabolism to defend his increased fat stores, for survival purposes!
Think of it this way: under normal circumstances, the leaner you get, the harder it is to lose body fat without burning muscle. Your body eventually goes into "survival" mode – you become more tired, lethargic, and your appetite increases. When things are working correctly, this only happens when body fat levels are extremely low.
But when you start a diet in a leptin resistant state, you lose some weight at first but quickly get into the same survival mode, only now you're nowhere close to being in shape as you were before.
This leads to no man's land real quick. You're eating less and less, feeling worse and worse, weak and stringy, but still can't lose weight. Your leptin receptors are resistant – at a higher set point – so even small decreases in leptin are perceived as starvation. Start a diet in a leptin-resistant state and reduced calorie levels will simply put your body into perpetual starvation mode.
This is the ugly side of dieting for many, and the main reason why many popular diet books suggest that simple calorie restriction does not work long term. The reality is that calorie restriction isn't the problem, it's leptin resistance.

Leptin and Insulin

Leptin and insulin signaling have a very close relationship. When insulin increases, so does leptin. It makes sense – you eat a big meal, your insulin levels go up, and then leptin goes up, signaling to the brain that you're full and to keep the metabolism chugging.
The insulin producing beta cells in the pancreas also have leptin receptors, where leptin is a negative regulator of insulin release. So there's a tight intertwined relationship between these two hormones.
Here's how it looks:

• You eat some wild salmon and a big sweet potato. The beta cells in your pancreas produce insulin in response to your blood glucose level.
• Insulin stimulates leptin production in your fat cells.
• Leptin levels go up, triggering the hypothalamus to decrease appetite.
• High levels of leptin also tell your pancreas to stop making insulin.

But here's how it looks when you have leptin resistance:

• You eat some wild salmon and a big sweet potato with some pop tarts, as you're in "permabulk" mode. The beta cells in your pancreas produce insulin in response to your blood glucose level.
• Insulin stimulates leptin production in your fat cells, overwhelming your body.
• Leptin levels go up but leptin resistance starts to set in.
• High levels of leptin try to tell your pancreas to stop making insulin, but you're leptin resistant so the pancreas doesn't get the message to stop!
• We now have chronically high levels of insulin, leading to insulin resistance.

Leptin and Inflammation

As mentioned in our inflammation article, the fatter you are, the more inflammation you probably have due to extra fat (30% of cells in white adipose tissue are immune cells) causing more immune signals to increase IL-6 and TNFa.

• Hyperleptinemia is associated with an increased pro-inflammatory response (14).
• Leptin is capable of increasing TNFalpha production and increasing macrophage activation (15).

It's a good idea to try to calm inflammation as best as you can. You can greatly reduce inflammation and increase glucose utilization by replacing some of your fat and refined carb sources with essential fatty acids. Omega 3 and Omega 6 supplements are excellent in this regard.

Leptin and Your Thyroid

It's common knowledge among meat heads that when you diet, your thyroid slows down the conversion of T-4 to T-3. What isn't so commonly known is that leptin is a major player in keeping this conversion going.
When your brain senses correct levels of leptin, it tells your liver to convert the inactive T-4 to active T-3 (the active version of thyroid hormone). Your liver will stop this when your brain perceives starvation, which is exactly what happens when you have leptin resistance.

How Can We Fix Leptin Resistance and Perceived Starvation?

• Insulin resistance and leptin resistance are inseparable, and driven by "metabolic inflammation." Fixing insulin resistance improves leptin resistance and vice versa.
• Reducing inflammation, improving liver health, adrenal health, etc., all help.
• Recent research has revealed that this is intertwined at the molecular level, but science hasn't evenscratched the surface. The research on leptin is still in its infant stages.

Do this!

Get and stay leaner. This is the obvious one. Don't "bulk" up. Stay close to target weight, and minimize body fat gain during offseason. The harder you make your diet by "bulking up" excessively in the off-season, the more you're going to make the leptin rebound a challenge down the road. You'll likely have to resort to extremes that put your body into survival mode to get lean.
Add in periodic refeed/cheat meals. There have been some very good articles posted on T Nation about cheat meals. When you go sub-maintenance calorically and get into a depleted state, adding in a cheat meal or two can stop you from entering "perceived starvation." This will help prevent leptin resistance. Some advocate a full day or weekend, but in our experience 1 to 2 large meals per week are sufficient for most.
Limit inflammation. Fat (white adipose tissue) doesn't only produce leptin, it also houses extra immune cells that generate inflammatory cytokines such as IL-6 and TNFa. Reducing inflammation increases leptin and insulin receptor sensitivity by limiting the effects of PTP1B and SOCS3.
Don't go carb-crazy. High insulin levels cause insulin resistance, which causes increased inflammation. Insulin and leptin resistance are so intertwined that fixing one helps the other. Since insulin increases leptin production (16), those in perpetual "bulk mode" are also generating metabolic inflammation.
Sleep. Chronic (17) and acute (18) sleep deprivation reduces serum leptin levels. In the acute sleep deprivation study, 11 males were subjected to sleep deprivation (4 hours of sleep) for six nights. Compared to the control group that slept for 8 hours, this reduced mean and maximum levels of leptin by 19% and 26% respectively.
In another study, those who habitually slept for 5 hours had 15.5% lower leptin levels than those who habitually slept for 8 hours (19). Sleep deprivation also increases inflammation, and has been linked to increased IL-6 secretion (20, 21). Even mild sleep loss (2 hours/night lost for 7 nights) results in a significant increase in TNFα levels in men (21). In some cases, dysfunctional sleep can also increase leptin levels, leading to leptin resistance.
Sleep apnea is associated with high leptin levels and leptin resistance (22). Leptin is a powerful stimulation of ventilation (23), so leptin levels can increase during sleep apnea. If you're a hard-core snorer, talk to your doctor about getting a sleep study.

Diet/supplement intervention: Supplements to fight leptin resistance:

Dietary Ca2. Increased dietary calcium intake helps overcome leptin resistance. Although the mechanism is unknown, it was recently hypothesized that increased calcium intake may decrease the levels of calcitriol (1,25-dihyroxyvitamin D) in adipocytes. In a leptin-resistant state, fat cells seem to have more calcitriol, which has been linked to decreased fat burning and increased fat storage.
Increasing dietary calcium suppresses adipocyte calcitriol levels and puts leptin-resistant fat cells back into "fat-burning" mode. This reduces leptin resistance, resulting in increased weight and fat loss in leptin resistant people (24, 25).
Take Taurine. If you're leptin resistant, supplementing with the amino acid taurine can help. Taurine reduces leptin resistance by reducing ER stress (26, 27). Possibly related to the effect of taurine on ER stress, it's also been shown to be helpful for the prevention of several other metabolic disorders including obesity, insulin resistance, and atherosclerosis (28, 29).
ALCAR. While this hasn't been established in human studies, animal studies suggest that supplementing with acetyl-L- carnitine (ALCAR) may also help overcome leptin resistance (30).
EFA's. EFA's hammer down inflammation! Enough said.

And We're Out!

Whew! This article has been a workout! Post any questions or comments you may have in the LiveSpill.
Thanks everyone for reading!
Regards,
Bill and John

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