Tag Archives: metabolism

Gain Muscle, Jack Your RMR – Sorta?


Key Points

  • The number of calories you burn for every pound of lean body mass is equal to a cherry tomato.
  • Teleologically, it makes no sense for RMR to increase to any appreciable extent if one does gain lean body mass.
  • Heavy resistance training is great for pretty much everyone. But don’t be hoodwinked by the promise of a jacked up RMR.

By Jose Antonio PhD FNSCA FISSN CSCS – How often have you heard the following refrain? “To increase your resting metabolic rate, you need to lift weights. Putting on muscle is the sure-fire way to have the metabolism of a blue whale.” And that way, the fat will melt off your flabby belly like a stick of metabolic-ratebutter on a hot stove. Ok, I put the blue whale part in there. Blue whales can apparently consume half a million calories in one mouthful. Whoa. Can you say Thanksgiving buffet with every bite?! So does making those bi’s, tri’s and glutes a tad bit larger result in resting metabolism that’s copious, capacious or colossal? Or is this Much Ado About Nothing? Before I provide a teleological explanation of why this notion is cockeyed, here’s some food for thought.1, 2 According to Robert R Wolfe PhD, “every 10-kg difference in lean mass translates into a difference in energy expenditure of ~100 kcal/d.” Or in units us Americans prefer, that’s about an increase of 4.5 calories for every pound gained.2 Regardless of whether that number is entirely accurate, let’s just say RMR per unit of fat free mass is about as impressive as dunking a basketball on an 8 foot hoop.

Nonetheless, here’s an investigation that examined resting metabolic rate (RMR) pre and post resistance training. They looked at the effects of 24 weeks of strength training on RMR, energy expenditure of physical activity (EEPA), and body composition. For the purposes of this article, we’ll focus on RMR. They had subjects divided by age and sex: 10 young men (20-30 years), 9 young women (20-30 years), 11 older men (65-75 years) and 10 older women (65-75 years). They performed whole body resistance training 3/week for 24 weeks. Their baseline or pre- and post-training RMR were as follows:


Young men – 12.2 kcal/lb FFM/d

Young women – 13.5 kcal/lb FFM/d

Older men – 12.0 kcal/lb FFM/d

Older women – 13.6 kcal/lb FFM/d


Young men – 12.8 kcal/lb FFM/d

Young women – no change

Older men – 12.8 kcal/lb FFM/d

Older women – no change

The first thing that stands out is that in both young and older women, their metabolic rate didn’t change at all. The other thing that stands out is how truly unimpressive the number of calories burned for one pound of fat-free mass (FFM). All groups increased FFM: +4.4 lb in young men, +4.18 lb in young women, +2.2 lb in older men, +1.98 lb in older women. In general, this study suggests that you burn roughly 12-13 kcal per pound of FFM daily. The authors of the study said that changes in absolute and relative RMR in response to heavy resistance training are influenced by sex but not age; that’s good news for us old guys.1

Pratley et al. looked at RMR after 16 weeks of resistance training in 13 healthy 50-65 year olds.3 They found that RMR before and after training was 11.8 kcal/lb FFM/d and 12.3 kcal/lb FFM/d. Interestingly, Broeder et al. found no change in RMR when adjusted for FFM.4

So what gives? Clearly there is quite a bit of variability in the RMR response to gains in FFM. Some folks gain, others nada. Maybe a sex difference exists with men responding better than women. Also, changes in RMR are not solely due to changes in FFM (or skeletal muscle mass). Perhaps it is related to changes in basal sympathetic nervous system tone. Alternatively,

Mongolian-born grand sumo champion Yokozuna Asashoryu wears a ceremonial belly band as he performs a ring-entering ritual at Meiji Shrine in Tokyo January 7, 2008. Asashoryu was banned in August 2007 and fled to his homeland after he outraged fans when he was caught on video playing soccer while supposedly out of action with a back injury. REUTERS/Toru Hanai (JAPAN) - RTX5ATL

Mongolian-born grand sumo champion Yokozuna Asashoryu wears a ceremonial belly band as he performs a ring-entering ritual at Meiji Shrine in Tokyo January 7, 2008. Asashoryu was banned in August 2007 and fled to his homeland after he outraged fans when he was caught on video playing soccer while supposedly out of action with a back injury. REUTERS/Toru Hanai (JAPAN) – RTX5ATL

changes in organ mass (particularly in very large individuals such as sumo wrestlers) may also account for gains in RMR.5 Have you ever seen the distended guts of professional bodybuilders? That ain’t skeletal muscle. Nonetheless, one might argue that these small changes in RMR could account for significant changes over years and decades. And that certainly may be true. However, it is evident that trifling changes in diet can negate any increase in RMR. For instance, if you gained 5 pounds of lean body mass, that translates roughly into about 50 extra calories per day. That’s not even a mug of beer. Boo.

It makes no sense for RMR to increase significantly even with large gains in skeletal muscle. –  One of my favorite college classes as an undergrad was on Evolutionary Biology. The human animal (or heck any animal) has two primary objectives: survival and reproduction. If you can throw in a good sushi buffet, a cruise to the Bahamas, and the Cubs winning the World Series, than even better. Anyhow, getting back to evolution. Let’s take a trip back to the days when there was no running cavemen-food-nutritionwater or electricity. Man was left to fend for itself like any other wild animal. It helped having a big brain because there was no chance in hell that humans could use physical strength or speed to kill its next meal. Conversely, humans developed quite the endurance capacity to ‘out-work’ its prey and a brain to ‘out-think’ just about every creature on Earth. You’ll notice that even modern day hunter-gatherer societies are ‘endurance’ oriented. You need endurance just to stay alive. Having large muscles serves no survival benefit.

Now let’s say some wacky caveman found that lifting big rocks made his chest and arms bigger. Now pretend that for every pound he gained, that would be an extra 50-100 calories per day (urban legend says this figure is true). So a 5 lb gain, which is certainly attainable by even the most average of men, would result in an cavemanhunting-1160x683increased caloric need of 250-500 calories (according to the urban legend figure). Now where would a caveman get these calories? Would he open the fridge to get a protein shake? Go to Burger King and order a Whopper? Duh. It makes zero evolutionary sense for RMR to go up to any appreciable extent if you gain lean body mass. Or put another way. It is energetically costly to gain and maintain skeletal muscle mass. Why? Because you’d have to feed it you knucklehead. It makes evolutionary sense that it is difficult to gain muscle (which it is) and easy to gain fat (which it is). Why? So you can survive the next go round of the zombie apocalypse when an asteroid the size of Hawaii blasts Earth into a nuclear-winter oblivion. If that happens and you survive, you better pray that you have the genes for putting on fat easily. Otherwise, you and all the Victoria’s Secret models will shrivel to death in a matter of weeks.

Bottom line: Don’t believe the hype when folks say, “a great way to elevate RMR is by increasing skeletal muscle mass via resistance training.” Lifting weights does a lot of great things. In fact, heavy resistance training can help athletes of all kinds (i.e., endurance and strength-power). And yes it does increase muscle mass. But the change in RMR is like pissing in the ocean. And we all know what that’s like. Unless of course you live in Iowa.

About the Author – Jose Antonio earned his PhD at the University of Texas Southwestern Medical Center in Dallas. He completed a post-doctoral research fellowship there as well. His current research focus is on the effects of various ergogenic aids on body composition and performance. He is the CEO of the ISSN and an Associate Professor at Nova Southeastern University.13119931_10156866463875440_6050451888342188203_o


  1. Lemmer JT, Ivey FM, Ryan AS, et al.: Effect of strength training on resting metabolic rate and physical activity: Age and gender comparisons. Med Sci Sports Exerc 2001, 33:532-41.
  2. Wolfe RR: The underappreciated role of muscle in health and disease. Am J Clin Nutr 2006, 84:475-82.
  3. Pratley R, Nicklas B, Rubin M, et al.: Strength training increases resting metabolic rate and norepinephrine levels in healthy 50- to 65-yr-old men. J Appl Physiol (1985) 1994, 76:133-7.
  4. Broeder CE, Burrhus KA, Svanevik LS, et al.: The effects of either high-intensity resistance or endurance training on resting metabolic rate. Am J Clin Nutr 1992, 55:802-10.
  5. Midorikawa T, Kondo M, Beekley MD, et al.: High ree in sumo wrestlers attributed to large organ-tissue mass. Med Sci Sports Exerc 2007, 39:688-93.


Cardio Lowers RMR – A Fairy Tale


by Jose Antonio PhD FNSCA FISSN. Today’s story is entitled “Cardio lowers RMR – A Fairy Tale.”

Key Points to Remember

  • There is a plethora of scientific evidence, which demonstrates that regular aerobic training has no effect on RMR. Some studies actually find an increase.
  • Resting energy expenditure is largely a function of body weight and FFM.[1, 2]
  • Cardio has become the “carbs of the fitness world.” – Shawn Arent PhD, Rutgers University
  • If you like doing cardio, don’t let some fitness guru talk you out of it.
  • If you hate doing cardio, then for Pete’s sake, don’t bitch about those who do it.
  • If you want to elevate your RMR, gain weight, especially skeletal muscle weight.
  • RMR is by itself a meaningless measure for the performance sports.
  • If you compete in football, baseball, basketball, cycling, volleyball, rowing, surfing, paddling, gymnastics, soccer, hockey, track and field (pick one) or frickin’ tiddlywinks, measuring RMR is about as useful as selling bikinis to Russian women in Siberia.

Social Media Silliness

So what is it about aerobic training (i.e., ‘cardio’) that has gotten the ire of so many fitness professionals? Cardio makes you fat? Yep. And there really is a pot of gold at the end of the rainbow. For my take on the ’cardio makes you fat’ baloney, read this piece from the ISSN Scoop: http://www.theissnscoop.com/cardio-makes-you-fat-and-apples-will-rise/

Supposedly cardio, especially the lower intensity variety, will lower your resting metabolic rate Beach walking(RMR) faster than a New Yorker can flip you the birdie. So I guess if you go for a walk on the beach after pigging out on beer and chicken wings, your metabolic rate will magically drop?

Let’s say you and your significant other visited the Sunshine State (that’s Florida for those who flunked 7th grade geography). Every morning for a week, you walk hand-in-hand up and down the beach. Sometimes you’d walk for more than an hour. Would your RMR drop because of this dreaded low intensity cardio? Are all these beach walkers killing their RMR? To quote the former #1 tennis player and part-time brat on the court John McEnroe, “You can NOT be serious!”

johnnymac_zps31f826d7Easy enough. So what does the science say on cardio and RMR? Below are a series of abstracts that I’ve shortened and added my pithy comments. It’ll give you a snapshot of the literature as it relates to exercise training and RMR. I’ve highlighted the parts that are of interest to those of you with the attention span of a mosquito.

Study #1 – This study examined resting metabolic rate (RMR) and thermic effect of a meal (TEM) among athletes who had participated in long-term anaerobic or aerobic exercise. Nine collegiate wrestlers were matched for age, weight, and fat-free weight with 9 collegiate swimmers. RMR adjusted for fat-free weight was not significantly different between groups. Thus, it doesn’t matter if you engage in long-term aerobic and anaerobic exercise training; resting energy expenditure is not different between these college athletes.[3] So whether you want to swim in chlorinated water or wrestle someone who smells like dirty socks soaked in vinegar, it don’t matter. RMR won’t be adversely affected.

Study #2 – Eight moderately obese women took part in an 11-week training program, including 5 hours of aerobic exercise per week performed at a mean intensity of about 50 percent VO2 max. Now that my friends is frickin’ low intensity. Fifty percent max VO2 is like a walk in the park. So what happened? Oddly enough, the results showed that exercise-training induced a significant rise in RMR. In fact, this study showed an elevated RMR per unit of fat free mass in both lean and moderately obese individuals.[4]running

Study #3 – Thirty-one women (mean age 35 yr) who were overweight were matched and randomly placed into a control group (CON), a diet-only group (D), a diet+aerobic endurance exercise training group (DE), or a diet+aerobic endurance exercise training+strength training group (DES). Can you keep track of that? That’s a lot of groups. So after 12 weeks, the three dietary groups demonstrated a significant loss in body mass, % body fat, and fat mass. No differences were observed in the magnitude of loss among groups, in fat-free mass, or in resting metabolic rate.[5] So even though aerobic training plus diet resulted in a loss of weight and fat mass, there was no change in RMR. Hmmm.

Study #4 – The effects of either 12-wk of high-intensity endurance or resistance training on resting metabolic rate (RMR) were investigated in 47 males aged 18-35 years. Subjects were randomly assigned to either a control (C), resistance-trained (RT) or endurance-trained (ET) group. After training both exercise groups showed significant declines in relative body fat either by reducing their total fat weight and maintaining fat-free weight (ET) or by reducing their total fat weight and increasing fat-free weight (RT). RMR did not significantly change after either training regimen. These results suggest that both endurance and resistance training may help to prevent an attenuation in RMR normally observed during extended periods of negative energy balance (energy intake less than expenditure) by either preserving or increasing a person’s fat-free weight.[6]

Study #5 – Investigators determined the effects of aerobic exercise training and resistance exercise training and the incremental effect of combined aerobic and resistance exercise training on resting metabolic rate (RMR) in previously sedentary individuals with type 2 Cycling_20-2diabetes. One hundred and three participants were randomly assigned to four groups for 22 weeks: aerobic training, resistance training, combined aerobic and resistance exercise training, or waiting-list control. Exercise training was performed three times per week at community-based gym facilities. RMR did not change significantly in any group after accounting for multiple comparisons despite significant improvements in peak oxygen consumption and muscular strength in the exercising groups. Adjusting RMR for age, sex, fat mass, and fat-free mass in various combinations did not alter these results. These results suggest that RMR was not significantly changed after a 6-month exercise program, regardless of modality, in this sample of adults with type 2 diabetes.[7] Geez. Is there a pattern here? Isn’t cardio supposed to make you fat? Ooops, I mean lower RMR?

Study #6 – Sixty-five healthy, weight-stable women, aged 21-35 or 50-72 years, were studied: 12 premenopausal and 15 postmenopausal sedentary women, 13 premenopausal and 15 postmenopausal distance runners, and 10 endurance-trained postmenopausal swimmers. RMR was measured by indirect calorimetry (ventilated hood system) after an overnight fast, and values were adjusted for fat mass and fat-free mass. Our results are consistent with the concept that the age-related decline in RMR in sedentary women is not observed in women who regularly perform endurance exercise. The elevated level of RMR observed in middle-aged and older exercising women may play a role in their lower levels of body weight and fatness compared to those in sedentary women.[8] Wait, did I read that correctly? Women who performed dreaded cardio actually were able to fight the age-related drop in RMR.

Study #7 – This study investigated the effects of 12 weeks of aerobic exercise plus voluntary food restriction on the body composition, resting metabolic rate (RMR) and aerobic fitness of mildly obese middle-aged women. The exercise/diet group participated in an aerobic training rowingprogram, 45-60 minutes daily at 50%-60% of maximal oxygen uptake (VO2max), 3-4 days per week, and also adopted a self-regulated energy deficit relative to predicted energy requirements. After the regimen had been followed for 12 weeks, the body mass of the subjects had decreased by an average of 4.5 kg, due mainly to fat loss, with little change of fat free mass (mff). The absolute RMR did not change, but the experimental group showed significant increases in the RMR per unit of body mass (10%) and the RMR per unit of mff (4%). The increase in RMR/mff was not correlated with any increase in VO2max/mff. The resting heat production per unit of essential body mass increased by an average of 21%, but the resting heat production rate per unit of fat tissue mass remained unchanged. We concluded that aerobic exercise enhances the effect of moderate dietary restriction by augmenting the metabolic activity of lean tissue.[9] Huh? Regular aerobic exercise increases RMR per unit body weight. Get on that treadmill! Ok, not really. Treadmill running is as much fun as wrestling a porcupine.

This pic has nothing to do with cardio. Just thought you'd like it. :-)

This pic has nothing to do with cardio. Just thought you’d like it. :-)

Study #8 – Scientists examined the effect of a 12-wk endurance exercise training program on RMR and 2) to provide insight into the mechanisms responsible for alterations in RMR that may occur after exercise training. Male participants (19-32 years) in an exercise group (EX) performed jogging and/or running 3-4 days per week, 25-40 min per session, at 60%-80% VO2max, whereas subjects in a control group (CON) maintained their normal activity patterns. Body composition, VO2max, RMR, epinephrine, norepinephrine, total thyroxine, free thyroxine, insulin, free fatty acids, and glucose were measured before and after the intervention.Training resulted in a significant increase in VO2max in EX. Absolute and relative values for RMR did not significantly change in EX (endurance training group) after training. Mean values for epinephrine, norepinephrine, total thyroxine, insulin, and glucose did not significantly change in either group; however, free thyroxine decreased significantly after training in EX. Oddly enough, RMR in CON decreased significantly when expressed as an absolute value and relative to body weight, fat-free mass, and fat mass. The mechanism for the decrease in CON is unknown, but it may be related to seasonal variations in RMR. Training may have prevented a similar decline in RMR in EX and may be related to a training-induced increase in fat oxidation.[10]

Study #9 – We tested the hypothesis that resting metabolic rate (RMR) declines with age in physically active men (endurance exercise > or = 3 times/wk) and that this decline is related to weekly exercise volume (h/wk) and/or daily energy intake. Accordingly, scientists studied 137 suzy_favor_hamilton4-getty_1356117573_540x540healthy adult men who had been weight stable for 6 months or longer. What they found was fascinating: 1) RMR, per unit FFM, declines with age in highly physically active men; and 2) this decline is related to age-associated reductions in exercise volume and energy intake; 3) this does not occur in men who maintain exercise volume and/or energy intake at a level similar to that of young physically active men.[11] So that’s the secret. Exercise a lot (even cardio is good) and eat a lot. My kind of program!

Study #10Is a 1-year study long enough for you? Let’s find out. Seventeen sedentary participants completed a 12 months jogging/walking program, 3 days/week for 45 min/session at a constant heart rate (HR) prescription of 60% HR-reserve. That’s pretty easy cardio if you ask me! After 12 months of training, body weight remained unchanged; however, body fat was significantly reduced by 3.4 %. Neither RMR nor substrate oxidation at rest changed significantly. In summary one year of recreational endurance training does NOT negatively impact RMR.[12] I know I know. Naysayers will say “that study isn’t long enough.” “We need a 10 year study to verify these results.” Blah blah blah.

Study #11 – Scientists determined whether chronic (9 months) moderate-intensity exercise training changes resting metabolic rate (RMR) and substrate oxidation in overweight young adults. Participants were randomly assigned to non-exercise control (CON, 18 women, 15 men) or exercise (EX, 25 women, 16 men) groups. EX performed supervised and verified exercise 3-5 d/week, 20-45 min/session, at 60-75% of heart-rate reserve. Here’s what happened. EX men had significant decreases from baseline to 9 months in body mass (94.6 to 89.2 kg) and percent fat outrigger-canoe(28.3 to 24.5). CON women had significant increases in body mass (80.2 to 83.2 kg) from baseline to 16 months. VO2max increased significantly from baseline to 9 months in the EX men and women. RMR increased from baseline to 9 months in EX men and women. So there you have it. Regular moderate-intensity exercise in healthy, previously sedentary overweight and obese adults increases RMR but does not alter resting substrate oxidation. Women tend to have higher RMR and greater fat oxidation, when expressed per kilogram fat-free mass, than men.[13] That’s interesting. Women have a greater RMR per kg FFM than men. Hmmm. So women have no excuse for packing on the lbs. 😛

Study #12 – Maybe it does decrease RMR? Scientists examined the effects of exercise training on resting metabolic rate (RMR) in moderately obese women. Nineteen previously sedentary, moderately obese women (age = 38.0 years, percent body fat = 37.5) trained for 20 weeks using either resistance training (RT) or a combination of resistance training and walking (RT/W). The high intensity resistance-training program was designed to increase strength and fat-free mass and the walking program to increase aerobic capacity. There was also a non-exercising control Helga paddling SUPgroup (C) of 9 subjects in this study. Fat-free mass was significantly increased in both the RT (+1.90 kg) and RT/W (+1.90 kg) groups as a result of the training program. So apparently adding walking to weight training does not negatively impact gains in LBM. No group showed significant changes in fat mass or relative body fat from pre- to post-training. This runs counter to the ubiquitous advice of weight training being a superior method of achieving fat loss. Furthermore, aerobic capacity was slightly, though significantly, increased in the RT/W group only. The RT group showed a significant increase (+44 kcal per day), while the RT/W group showed a significant decrease (-53 kcal per day in resting metabolic rate post-training. RT can potentiate an increase in RMR through an increase in fat-free mass, and the decrease in RMR in the RT/W group may have been a result of heat acclimation from the walk training.[14] This study shows a difference. Though I’d posit that the lower RMR is made up for by the extra walking in the resistance training plus walking group. Besides, isn’t weight training supposed to combat the effects of a lower RMR?

So in conclusion: The preponderance of the evidence clearly shows that regular aerobic training has little to no effect on RMR. So you can put the notion of ‘cardio lowering RMR’ in the trash bin where it’ll join the ‘cardio makes you fat’ dopiness. So if you love cardio, keep doing it. It’s not going to ‘ruin’ your metabolism. If you want to increase RMR, then lift weights and gain LBM. On the other hand, if you exercise too much, eat too little, and lose body weight and lean body mass, then your RMR will drop. But who in their right mind does that?

BIO – Jose Antonio PhD is the CEO of the ISSN, www.issn.net and faculty at Nova Southeastern University in Exercise and Sports Science. I’m not fond of doing cardio in a gym. Why anyone would run on an indoor treadmill, do that silly elliptical or ride a bike (oh..I mean do Spinning classes…haha) in a room full of stinky people at your local gym is as puzzling as watching a fat man order a diet coke with a slice of cheesecake. Go outside for chrissakes. It’s a helluva lot more fun.

Paddle in VA Beach 2016 edited


1.         Taguchi M, Ishikawa-Takata K, Tatsuta W, Katsuragi C, Usui C, Sakamoto S, Higuchi M: Resting energy expenditure can be assessed by fat-free mass in female athletes regardless of body size. J Nutr Sci Vitaminol (Tokyo) 2011, 57:22-29.

2.         Deriaz O, Fournier G, Tremblay A, Despres JP, Bouchard C: Lean-body-mass composition and resting energy expenditure before and after long-term overfeeding. Am J Clin Nutr 1992, 56:840-847.

3.         Schmidt WD, Hyner GC, Lyle RM, Corrigan D, Bottoms G, Melby CL: The effects of aerobic and anaerobic exercise conditioning on resting metabolic rate and the thermic effect of a meal. Int J Sport Nutr 1994, 4:335-346.

4.         Tremblay A, Fontaine E, Poehlman ET, Mitchell D, Perron L, Bouchard C: The effect of exercise-training on resting metabolic rate in lean and moderately obese individuals. Int J Obes 1986, 10:511-517.

5.         Kraemer WJ, Volek JS, Clark KL, Gordon SE, Incledon T, Puhl SM, Triplett-McBride NT, McBride JM, Putukian M, Sebastianelli WJ: Physiological adaptations to a weight-loss dietary regimen and exercise programs in women. J Appl Physiol (1985) 1997, 83:270-279.

6.         Broeder CE, Burrhus KA, Svanevik LS, Wilmore JH: The effects of either high-intensity resistance or endurance training on resting metabolic rate. Am J Clin Nutr 1992, 55:802-810.

7.         Jennings AE, Alberga A, Sigal RJ, Jay O, Boule NG, Kenny GP: The effect of exercise training on resting metabolic rate in type 2 diabetes mellitus. Med Sci Sports Exerc 2009, 41:1558-1565.

8.         Van Pelt RE, Jones PP, Davy KP, Desouza CA, Tanaka H, Davy BM, Seals DR: Regular exercise and the age-related decline in resting metabolic rate in women. J Clin Endocrinol Metab 1997, 82:3208-3212.

9.         Shinkai S, Watanabe S, Kurokawa Y, Torii J, Asai H, Shephard RJ: Effects of 12 weeks of aerobic exercise plus dietary restriction on body composition, resting energy expenditure and aerobic fitness in mildly obese middle-aged women. Eur J Appl Physiol Occup Physiol 1994, 68:258-265.

10.       Lee MG, Sedlock DA, Flynn MG, Kamimori GH: Resting metabolic rate after endurance exercise training. Med Sci Sports Exerc 2009, 41:1444-1451.

11.       van Pelt RE, Dinneno FA, Seals DR, Jones PP: Age-related decline in RMR in physically active men: relation to exercise volume and energy intake. Am J Physiol Endocrinol Metab 2001, 281:E633-639.

12.       Scharhag-Rosenberger F, Meyer T, Walitzek S, Kindermann W: Effects of one year aerobic endurance training on resting metabolic rate and exercise fat oxidation in previously untrained men and women. Metabolic endurance training adaptations. Int J Sports Med 2010, 31:498-504.

13.       Potteiger JA, Kirk EP, Jacobsen DJ, Donnelly JE: Changes in resting metabolic rate and substrate oxidation after 16 months of exercise training in overweight adults. Int J Sport Nutr Exerc Metab 2008, 18:79-95.

14.       Byrne HK, Wilmore JH: The effects of a 20-week exercise training program on resting metabolic rate in previously sedentary, moderately obese women. Int J Sport Nutr Exerc Metab 2001, 11:15-31.


Manipulating Night-Time Anabolic/Catabolic Cycles

For years we sports nutritionist missed the boat when it came to maximizing muscle mass because we ignored the night time decrease in muscle growth caused by post-absorptive muscle catabolism. We now know that the body is primed for growth and repair during sleep. What we must do is give the body the necessary materials it needs to do its job.  Dr. Mauro Di Pasquale, M.D.431147-bigthumbnail

When you review the comments above by the renowned sports nutritional physiologist Dr. Mauro Di Pasquale, they imply that for some time researchers may have considered night-time catabolism’s impact on growth to be negligible and didn’t warrant attention. Those comments also imply that this reasoning may have stemmed from the fact that the problems with the body’s ability to absorb and utilize nutrients during sleep couldn’t be altered or minimized as the body simply breaks down existing muscle tissue to supply the energy needed to keep its metabolic activities going. Despite this innate back-up process, it is a process that occurs for an 8 to 9 hour time frame. The fact is that every night becomes a catabolic night of biblical proportions the minute you lay down to sleep. Catabolic processes begin there assault with a pre-programmed set of muscle destroying instructions. So precise and destructive is this catabolic activity that it naturally occurs via cyclical up-regulation of various catabolic compounds or hormones during normal sleep cycles, hence its reference to as the post absorptive muscle catabolic syndrome.

When It Rains It Pours

As a point of reference here a syndrome is defined as a set of general symptoms all occurring at the same time that collectively indicate or characterize being in a morbid (unhealthy) state. Scientifically,  this internal network or place were all this muscle breakdown occurs and is converted to energy is referred to as the ubiquitin-proteasome or UPP pathway. It is here where cortisol the stress and muscle wasting hormone production is increased and accelerated as a direct result of exercise induced stress. Contrary to popular belief, the sleep cycle isn’t just a rest, repair and detoxification phase. In practical terms here, sleep becomes a survival and catabolic period to the body because of a lack of nutrients it has to work with. However, researchers now know that by the time you switch this catabolic switch off, that you have lost substantial amounts of lean muscle tissue. The other part of this axiom is the fact that you are consistently playing catch-up to promote growth. The question then becomes how can the nutrients the body needs be proved or maintained over the course of a normal sleep cycle to combat this impending catabolic syndrome before bedtime?

Understanding Post-Absorptive Physiology

Based on Dr. Pasquale’s comments above, the body is primed for growth and repair during sleep and that there are ways to counter-balance this catabolic cycle. The fact is the body has some built in mechanisms to protect itself via the release of certain hormones to minimize the impending catabolism. This could be somewhat compared to bears getting set for hibernation, when no new nutrients will be coming in for a period of time. For example, testosterone, growth hormone, and IGF-1(insulin growth factor) and insulin tend to remain elevated during sleep. These hormones guard against muscle wasting by reducing the production of cortisol and other catabolic hormones to help maintain protein synthesis. Other compounds the body calls upon include circulating glucose, fatty acids, liver and muscle glycogen (stored glucose), branch chained amino acids, glutamine and other amino acids. These sources can supply up to 1200 needed calories to slow down catabolic activity for about 12 hours. The bottom line here, maintaining your scheduled intake of nutrients throughout the day can impact night-time catabolism, especially your amino acid intake. Additionally, your carbohydrate intake replenishes lost glycogen that is stored within the liver and muscle tissue that serve as backup fuel when blood glucose levels fall. Conversely, the body uses part of your internal amino acid pool to fuel metabolic activity during sleep. If that pool is low, the body will breakdown your existing muscle tissue to support its nutritional needs.

Please Note: as a point of clarification here, to replenish glycogen stores lost during the day, they are replenished via carb intake, not protein. To replenish diminished glycogen researchers recommend a daily intake of 3 to 5 grams of carbohydrate for every pound of your body weight across the day, divided evenly with your feedings. Additionally, if you are taking a few individual amino acids like glutamine and arginine I strongly suggest that you also take a full pre-digested amino acid formula following a workout and right before bedtime.

Know Your Anabolic Hormones

As stated there are a number of hormones the body secretes to counter-act night-time muscle loss. Make no mistake about it, how adept you are at sustaining the balance and symmetry between the repeated cascade of your anabolic and catabolic hormones has a direct impact on Endocrine_growth_regulation-244x300your ability to preserve muscle tissue during sleep. Having a working knowledge of the anabolic / catabolic aspects of these hormones is just prudent.  For example, you have the ability to help the body accelerate the secretion of growth hormone during sleep via the intake of various amino acids (arginine, glutamine, ornithine) and other supplements. The following synopsis outlines a few of these anabolic hormones that focus on minimizing night-time muscle catabolism, as well as its acceleration.

The Anabolic Hormones

Androgens – this class of hormones are considered male dominate hormones with testosterone being the most well-known. Androgens have a dramatic impact on muscle development. They are drawn to tiny receptors found in muscle tissue that appear to signal muscle cells to accelerate protein synthesis via a process known as androgen receptor complex binding.  This process appears to turn on muscle cell DNA while also inhibiting the up-regulation of glucocorticoids like cortisol that cause muscle wasting.  Androgens like testosterone also help stimulate the production of other anabolic hormones like insulin growth factor ( IGF) and growth hormone. Resistance training itself causes natural spikes in testosterone, however, lack of sleep, overtraining, stress, and sugary drinks and snacks can inhibit testosterone secretion at night. In fact data indicates that a small glucose drink can reduce testosterone production by 25%. Additionally, deficiencies of vitamin D definitively lower testosterone levels. As cited by Lee Meyer, author of Low Testosterone: By The Numbers vitamin D biologically acts more like a hormone than a vitamin, despite being referred to as the muscle vitamin. Studies have shown that when muscle receptor cells levels of vitamin D fall, decreased muscle strength and performance follow, as a direct result of its positive impact on testosterone production. Conversely, intense physical and mental stress lowers testosterone as a direct result of its down-regulation of the enzyme 11BHSD-1 located in the Leydig cells of the testes.

Stress: An Androgens Worst Nightmare

It is important to remember your body is a network of multiple deeply interconnected systems, all of which get impacted to various degrees by heavy training. Recovering from this ordeal is about more than just not lifting. It’s about giving your muscles and joints the space to heal and super-compensate, letting your nervous system calm down, and getting adequate rest. In general terms here, some researchers, especially Russian physiologist, recommend the use of adaptogens before bed and or following workout to restore order to these interconnected systems. This in essence primes the body for growth as cited above by Dr. Pasquale.Some well- known anti-stress supplements you may want to consider here include, vitamin B- complex, DHEA (dehydroepiandrosterone) , siberian ginseng and rhodiola rosea. Rhodiola has been used extensively by Russian power lifters. Research shows that this herb actually primes the system to deal with the heavier aftershocks of stress that disrupt normal metabolic processes when exercised induced stress begins to sound the alarm to internal body systems. When this occurs to help the body secretes more cortisol, which accelerates muscle tissue breakdown. It is here where rhodiola steps in to neutralize this mishap, and restore order, much like paratroopers dropped into a war zone, hence it tag as a adaptogen ( a substance that restores balance).

Please Note: to help your body maintain the anabolic potential testosterone affords, some of the most widely used supplements that stimulate testosterone production in the bodybuilding industry are: arginine, aromataste inhibitors( substances which block estrogen production) like chrysin, DHEA, long jack root. maca root, muira puama, tribulus and ZMA( zinc maganesium aspartate).

Growth Hormone (GH) – this hormone is composed of many different amino acids linked together known as peptides. Growth hormone improves the efficiency of muscle cells to take in amino acids, thus enhancing protein synthesis, muscle growth and repair. GH also regulates carbohydrate and fat metabolism, encouraging increased fat burning while preserving carbohydrates. This can have a positive impact on replenishment and maintenance of glycogen (stored glucose). Growth hormone secretions occur during  exercise, however larger spikes occur during sleep, which can be improved via intake of amino acid combinations like arginine/ornithine/ lysine as well as single doses of Gaba and glutamine, about ½ hr before bedtime. Also many amino acids like arginine inhibit the actions of the catabolic hormone somatostatin which inhibits the release of glycogen,  growth hormone and insulin.

Insulin Growth Factor (IGF)- IGF is a peptide hormone and helps prevent protein breakdown and plays a major role with the body’s fat-burning activities. Researchers attribute the increase in new muscle tissue you have been working hard to build to IGF, because it speeds up the activity of cells in the muscle known as satellite cells. Satellite cells appear to down-regulate the activity of the myostatin gene which is known to inhibit muscle growth. Satellite cell  promote hyperplasia (the growth of new muscle tissue).

Protein and the Post Sleep Catabolic Phase

Dr. Deepak Chopra the renowned mind-body researcher reminds us that the world’s greatest chemistry set is the human body. He maintains that the vast array of botanicals studied are done so to mimic the actions of natural chemicals produced by the human body. Based on the examples thus far of the things the body calls upon to protective itself from sleep cycles of catabolism, some protein sources appear to be better suited to help and sustain anabolic activities during sleep. Casein protein and egg protein appear to better suit than whey protein to help nourish the muscles during both the pre-primed and post sleep absorptive phase of protective growth and repair. These proteins tend to break down slowly over the course of a 6 to 8 hour time frame. Whey takes  about 20 minutes  to reach the veins and within forty minutes your system is flooded with amino acids.  Within the hour whey protein has either gone through various metabolic processes and has been synthesized (individual cells constructing various proteins). Simply put, whey can’t help sustain anabolic process during the post-sleep absorptive phase. Studies also indicate that as a direct result of increased oxidation that appears to follow the synthesis of whey protein, this limits its ability to sustain growth and repair for a substantial amount of time.

Please Note: While some oxidation is beneficial this process accelerates muscle protein breakdown during the day and night.  Because of the above it may be a good idea to take a regimen of anti-oxidants (vitamins A, E, C, CoQ10, etc.) to offset this negative aspect of whey protein.

Casein and Egg Proteins Absorptive Physiology

While whey protein may afford more benefits during the course of the day, casein protein is the better choice later in the evening and at night. This due to the fact that casein, a milk protein, curdles in the stomach as it unites with various enzymes.  It generally takes 3 to 4 hours before amino acids hit your blood stream to start the repair of muscle tissue.  In fact in a recent study conducted by researchers in France at the University of Clermont Auvergne comparing whey to casein protein, subjects were given 30 grams of either whey or casein . download (1) After 7 hours researchers found that with casein there was a marked decrease in protein synthesis by 31%.  However, there was 27% less oxidation (degradation) of casein protein vs. whey resulting in a more sustained period of nitrogen retention.  The final and most critical aspect of these numbers was a 34% decrease in muscle protein breakdown.  Bottom line here, this study and countless others confirm why casein should be your protein of choice before bedtime. It helps to create and up-regulate the body’s innate post sleep anti-catabolic environment by enhancing your muscle tissues ability to neutralize the mixture of catabolic chemicals building up a head of steam toward muscle destruction, as you approach the REM stage of sleep. As a point of reference REM stands for rapid eye movement. This stage of sleep is characterized by rapid twitching of the eyes and low-voltage brain wave activity. What is important here is the fact that it is during this time most of the body’s repair cycles occur.

Please Note: Like whey, casein protein is derived from milk.  When you purchase casein protein, make sure it isn’t listed as caseinate or calcium caseinate.  These forms have been extracted before the curdling process and are actually a much lower grade of casein protein.

Egg Protein: A Medium Timed Releasing Protein

Although egg protein has taken a back seat since whey’s introduction to the market place, it is still considered one of nature’s perfect foods. Egg protein contains all of the essential amino acids in the exact proportions needed to promote the growth and maintenance of lean muscle tissue. Egg protein also has a BV of 100 ( biological value) meaning its ability to help muscles maintain nitrogen is excellent. Nitrogen is the amine portion of the amino acid NH2 intimately involved with the growth of lean muscle tissue. Egg protein also has a digestibility ratio of 97% meaning that 97% of it is absorbed as amino acids, major players in the repair process. Current data indicates that egg protein exponentially increases total muscle protein synthesis following a workout. Because of this egg serves as an key pre-priming sleep post-absorptive nutrient. Another key aspect of egg protein’s post absorptive anabolic ability is its high leucine (the key anabolic signaling amino acid) content, its impact on testosterone production and  inhibition of myostatin activity ( a muscle growth inhibiting compound).  For these reasons egg protein is considered a very good post sleep absorptive nutrient that will assist in maintaining your pool of amino acids, thus inhibiting night-time catabolism.

Please Note: Based on the findings presented in this report the suggestion that whey may not be all its hyped up to be, this assumption if made should be quickly down-regulated to inconsequential. Its ability to quickly flood the system with amino acids will quickly initiate muscle repair as you awake from the post sleep catabolic phase. The other aspect here surrounds whey intake before a morning workout and right afterwards. Current data indicates that as little as 10 grams of whey can jumpstart protein synthesis, as well as cited earlier flood your system with needed amino acids within 45 minutes.


It is important to remember that the majority of your growth occurs when you aren’t working out. The biggest mistake you could make in reaching your full anabolic growth potential is not to prepare for natural night time muscle catabolism. Helping to support the body’s attempts to maintain some semblance of its anabolic potential during sleep is the real key to sustaining growth for the long hall.


Andersen, L.L., Tufekovic, G., et. al., The effect of resistance training combined with timed ingestion of protein on muscle fiber size and muscle strength, Metabolism, 2005 Feb.; 54(2): 151-156.

Boirie, Y., Dangin, M., et. al., Slow and fast dietary proteins differently modulate postprandial protein accretion, Proceedings of the National Academy of Sciences (USA), 1992; 94: 14930-14935.

Chopra , D. Creating Health. Houghton Mifflin: New York. 1991.

Chromiak, J.A., Antonio, J. Use of amino acids as growth hormone- releasing agents by athletes. Nutrition. 2002 Jul; 187 (7-8): 657-661.

Dangin, M., Bione, Y., et.al., The digestion rate of protein is an independent regulating factor of postprandial protein retention, American Journal of Physiology, Endocrinology, and Metabolism, 2001; 280: E340-E348.

Goto, K., Ishii, N. et.al. The impact of metabolic stress on hormonal responses and muscular adaptations. Medical Science and Sports Exercise. 2005 Jun; 37960; 955-963.

Hackney, A.J., Bruenger, J.T., et.al., Timing protein intake increases energy  expenditure 24 h after resistance training. Medicine and Science in Sports and Exercise. 2010 May; 42 95):998-1003.

Kanaley, J.A. growth hormone, arginine, and exercise, Current Opinion in Clinical Nutrition Metabolism and Care. 2008 Jan; 11 (1):50-54.

Kreider, R., et.al., Effects of whey protein supplementation with casein or bcaa and glutamine on training adaptations 1: Body composition. Medical Science and Sports Exercise. 2003; 2205: 35-5.

Miller, S.L., Tipton, K.K., et. al., Independent and combined effects of amino acids and glucose after resistance exercise, Medicine, Science, Sports and Exercise, 2003; 35(3): 449-455.

Mosoni, L., Mirand, P.P.  Type and timing of protein feeding to optimize anabolism, Current Opinions in Clinical Nutrition and Metabolic Care, 2003; 6(3): 301-306.

Myer, L., Low Testosterone : By The Numbers, Amazon Digital Services: Aug. 2011.

Tang, J.E., Manolakos, J. J.,  et.al., Minimal whey protein with carbohydrate stimulates muscle protein synthesis following resistance exercise in trained young men. Medicine and Science in Sports and Exercise. 2007Dec.;32(60:1132-1138.

Tipton, K. D., Wolfe, R. R., Exercise, protein metabolism and muscle growth. International Journal of Sport Nutrition and Exercise Metabolism.  2001 Mar.;11(1):109-132.

Volek, J.K., Kraemer, W.J., et.al. Testosterone and cortisol in relationship to dietary nutrient and resistance exercise. Journal of Applied Physiology, 1997 Jan; 82(1); 49-54.

Wiegant, F.A., Surinova, S., et.al. Plant adaptogens increase lifespan and stress resistance in C. elegans, Biogerontology. 2009 Feb; 10 (1);27-42.


George L. Redmon PhD has been associated with the vitamin and health industry for over 25years, having served as The National Product and Education Director for one of the countries largest retailers of nutritional supplements. He has been widely published in many major bodybuilding, fitness and alternative medicine publications. He is the author of Natural Born Fat Burners, Energy for Life and is a member of The National Academy of Sports Medicine and The International Society of Sports Nutrition.

Interview with Nutrition Expert Darcy Johannsen PhD

SNI:  It is commonly heard among fitness professionals (i.e. personal trainers) that overweight or fat individuals complain of having a ‘slow metabolism.’ How often is a ‘slow metabolism’ (e.g. thyroid dysfunction, nervous system disorders) to blame for being overweight versus merely eating too much and moving too little?Girl-dieting

Darcy: Studies show that individuals who are overweight or obese have a higher resting metabolic rate than normal weight individuals, due to the increased energy costs of supporting the basal functions of a larger body mass.  Once normalized for body weight however, there are usually no differences in metabolic rate between lean and obese people.  That being said, a study done in a population of Pima Indians in the late 1980’s showed that a lower 24-hour expenditure (measured in a metabolic chamber) significantly predicted weight gain over the next 2 years, and furthermore 24-hr energy expenditure tended to be similar among siblings.  Whether this is true for a larger population is unknown, as metabolic rate is not usually measured prior to becoming obese.  The similarity in metabolism among siblings does suggest a genetic influence on resting metabolic rate.  There is also some evidence for subclinical hypothyroidism in obese individuals that may be contributing to weight gain and this is a current area of research interest.  However, restricting calories and moving more can overcome these pre-dispositions; i.e., the effects of a healthy lifestyle are stronger than the genetic influences.

SNI: In your paper published in JCEM, you discovered that despite the preservation of fat-free mass in severely obese people, exercise did NOT prevent the dramatic drop in metabolic rate after severe weight loss. Why is that? We’ve been told that if you preserve muscle or LBM, that metabolic rate should stay high.

Darcy: We were surprised by this finding as well.  We thought that since these individuals maintained a lot of their lean mass, their metabolic rate would stay higher.  But it fell dramatically, despite the lean mass maintenance.  This is probably due to the enormity of the weight loss and the rapid rate at which it occurred.  The body ‘adapted’ to try to conserve energy.  For example, we found that T3 (the active thyroid hormone) levels were significantly reduced, as was leptin.  These hormonal changes would cause the muscle to conserve energy.  Although we did not measure it, I suspect that mitochondrial activity within the muscle became much more efficient as well.  In other words, muscle metabolism probably slowed along with the weight loss.

SNI:  In a younger population (18-40 years of age), does a gain in muscle or LBM result in an increase in metabolic rate? If so, how much? For instance, does a 5 pound gain in LBM translate into a specific increase in metabolic rate?

Darcy: Yes, theoretically with all other things being the same, a gain in lean mass would cause an increase in metabolic rate.  The amount of increase would depend on the amount of muscle gained.  It is difficult to tease out just the contribution of skeletal muscle to metabolic rate, because the human body is so dynamic – other lean masses are changing too (internal organs, which have a MUCH higher metabolic rate than muscle).  Likewise, if fat mass is lost, metabolic rate will drop some, and if a lot of muscle is gained, there is probably some increase in fat too.  To answer your last question, you would have to ensure that ONLY skeletal muscle was changing – no fluid changes, no loss or gain of fat mass, and no change in organ function, and still an exact number would be impossible, as mitochondrial activity and muscle metabolism is highly variable among individuals. 

SNI: What advice would you give to someone 50 years of age and older with regards to maintaining a lean physique? 9e6b966e44acb38dc78f1aee0350

Darcy: First, I would advise them to carefully watch their diet in order to maintain a healthy body weight.  Metabolism naturally slows with aging (although we are not sure why) and it is more difficult to lose weight once your metabolism slows.  Restrict calories if some weight loss is needed.  Then, adding an exercise regimen is important.  Not particularly for weight loss, but to maintain a healthy weight and also to maintain muscle mass, which we know declines with aging.

SNI: What effect does weight cycling (i.e. repeated weight gain/weight loss) on body composition, metabolic rate, and health?

Darcy: Weight cycling can be very detrimental to one’s health.  Many adaptations occur during weight loss.  Fat mass is reduced but so is lean muscle mass.  Metabolic rate drops.  Hormone concentrations change.  All of the changes occur in effort to conserve energy, a very important process during times when energy (food) was scarce.  There is recent evidence that suggests that these adaptations persist beyond the immediate weight loss phase, that is, you do not come back to ‘baseline’.  This increases the risk for weight re-gain, and unfortunately, the same adaptive responses are not as strong during weight gain.  In other words, your body does not defend against weight gain like it does for weight loss.  After the weight re-gain, it is probably more difficult to get the weight off because your metabolism did not completely return to normal after the initial weight loss, and you would likely have to restrict calories even more or add extra exercise in order to create the necessary energy deficit.

About Dr. Darcy Johannsen

I completed my Bachelor’s and Master’s of Science degrees in Human Nutrition from South Dakota State University. I completed a clinical dietetics internship at Hurley Medical Center in Flint, MI. I then worked as a clinical dietitian for several years before obtaining my PhD in Nutritional Sciences from Iowa State University. For my dissertation work I studied protein metabolism in elderly subjects and also investigated postural allocation and components of energy expenditure in lean and obese women. I then went on to do a postdoctoral fellowship under the guidance of Dr. Eric Ravussin, where I focused on energy metabolism in aging and obesity. Currently I am an Assistant Professor of Skeletal Muscle Physiology. My studies center on how mitochondrial function changes with weight gain or loss and during aging, and how these changes influence energy metabolism.