Does a "calorie not in" equal a "calorie out"?
According to this study, how one creates a caloric deficient can make a difference.
The Impact of Exercise Training Compared to Caloric Restriction on Hepatic and Peripheral Insulin Resistance in Obesity
Context: It has been difficult to distinguish the independent effects of caloric restriction versus exercise training on insulin resistance.
Objective: Utilizing metabolic feeding and supervised exercise training, we examined the influence of caloric restriction vs. exercise training with and without weight loss on hepatic and peripheral insulin resistance.
Design, Participants, and Intervention: Thirty-four obese, older subjects were randomized to: caloric restriction with weight loss (CR), exercise training with weight loss (EWL), exercise training without weight loss (EX), or controls. Based on an equivalent caloric deficit in EWL and CR, we induced matched weight loss. Subjects in the EX group received caloric compensation. Combined with [6,62H2]glucose, an octreotide, glucagon, multistage insulin infusion was performed to determine suppression of glucose production (SGP) and insulin-stimulated glucose disposal (ISGD). Computed tomography scans were performed to assess changes in fat distribution.
Results: Body weight decreased similarly in EWL and CR, and did not change in EX and controls. The reduction in visceral fat was significantly greater in EWL (−71 ± 15 cm2) compared to CR and EX. The increase in SGP was also almost 3-fold greater (27 ± 2%) in EWL. EWL and CR promoted similar improvements in ISGD [+2.5 ± 0.4 and 2.4 ± 0.9 mg · kg fat-free mass (FFM)−1 · min−1], respectively.
Conclusions: EWL promoted the most significant reduction in visceral fat and the greatest improvement in SGP. Equivalent increases in ISGD were noted in EWL and CR, whereas EX provided a modest improvement. Based on our results, EWL promoted the optimal intervention-based changes in body fat distribution and systemic insulin resistance.
This study illustrates so compellingly the benefits of increasing calories out via exercise for weight loss and improved glucose homeostasis vs. restricting calories in. Some of this will be repetitive of the summary above, but in plain English they took older (range 50-80, avg age for groups mid-to-late 50's) overweight/obese (BMI ~32) adults and assigned them to one of three study groups and a control group that maintained intake and activity levels to usual amounts. The diets for all participants were 35% fat, 20% protein, 45% carbohydrate, and all subjects besides the controls were weight stabilized on this diet during a 4 week pre-intervention period. Controls were instructed to continue on as normal but were adapted to this macro percentage for 4 days prior to testing. The three study groups were:
- CR = calorie restriction
- EX = exercise training with calorie compensation to maintain weight
- EWL = exercise training with normal intake
In the exercise interventions, they started with a 1000 cal/week expenditure and ramped it up to 2500 cal/week. The CR group had the intake deficit matched accordingly and the EX group received supplemental calories to compensate and maintain energy balance. The study lasted 12 weeks and the CR & EWL groups both lost 5kg = 11 lbs. They used radiolabeled glucose, an octreotide/glucagon infusion, and multistage insulin infusion (MSI) to measure fasting glucose production (hepatic IR) and glucose disposal (peripheral IR). I note there was a significant post-intervention period of time where all subjects were stabilized back to energy balance (2 wk refeed + 4 wk stabilizing) before retesting.
The effect on fasting glucose production, a measure of hepatic insulin sensitivity, with exercise induced weight loss was almost 3 times that of the calorie restriction induced weight loss. Exercise alone, without weight loss produced similar improvements in hepatic insulin sensitivity. This was mirrored by over twice as much visceral fat lost by the EWL v. CR. However while EX had some visceral fat loss, it was about half that in CR. Lean thigh tissue was also measured. There was no statistically significant change in EX (+2cm2) while EWL gained a significant 7cm2 as CR lost a significant 7cm2.
For insulin stimulated glucose disposal (mg per kg FFM per min), both EWL and CR produced similar significant increases from pre to post interventions of 2.45 ± 0.43 and 2.46 ± 0.69. This was about 2.5X that observed with exercise alone as EX increased 0.95 ± 0.41.
From this we can see that cardio equivalent to 2500 cal/week expenditure improves hepatic insulin sensitivity with or without weight loss and improved systemic glucose handling without weight loss. It's worth reminding that the EX group also ate 2500 cal/week more than their weight loss counterparts. For many of us that's 1-2 extra "days" of food. So eating a "surplus" amount of calories, they still experienced improvements in insulin sensitivity (which yours truly believes to be at the root of many diseases, and not insulin levels per se). This is something worthy of consideration for those overweight proponents of their healthy diets who shun cardio for calorie burning.
For all the talk about how a calorie in is not a calorie in based on hormonal status and fuel partitioning, and for all the talk of dietary manipulations to achieve a "fat burning metabolism" and lower insulin and all that ... we see that a calorie out is also not a calorie out! Which doesn't do squat to discredit "Team CICO", but it should give pause to the Gateking who plans to roll out an Exercisegate bood/website/franchise in the future?! What it does do, or should anyway, is give all of the "it's 80% diet" and "I proudly sit on my a$$" crowd on "Team TWICHOO" pause as to where calories are distributed or taken from depending on the "source" of the calorie deficit.
Exercise doesn't make everyone hungry afterwards and not everyone compensates for exercise. I believe that most of us can use exercise only to lose weight with just some attention to intake to avoid compensation. If we don't maintain intake and therefore not lose weight, we still get some health benefits. If we lose the same amount of weight as we would by diet alone, we lose more of it from fat and -- surprisingly -- may gain lean mass. (I've seen this in other studies as well where lean mass is not only preserved but increased in caloric deficit/weight loss). A caloric deficit through exercise improves hepatic insulin sensitivity, as measured by suppression of glucose production, by almost three-fold what a caloric deficit through calorie restriction produces. More food for thought for those trying to achieve weight loss through diet alone (which amounts to calorie restriction whether you want to acknowledge reality or not). How about if you're hopping into ice baths to burn a few extra calories? I don't know, my money would be on it being more like calorie restriction than exercise over the long haul, but that's not a bet I'd make at this point either way. Can we get a metabolic ward trial? :-)
Lastly, sure the weight loss is nothing to write home about, but 10 lbs over 3 months equates to 40 lbs in a year. Since RMR correlates so highly with lean mass, guess which group is more likely to attain and maintain long term success with weight loss? My bet would be on the EWL group. Imagine, however combining caloric restriction and exercise expenditure to produce calorie deficit. Nah, that's too much like eating less and moving more!