High Energy Flux, A New Determinant of Successful Weight Loss? Eat More, Train More, Lose More? Increased Resting Metabolic Rate & Satiety, Decreased Hunger While Dieting!

Always hungry? Can't lose weight? "Train more and eat more" (not less!) could be the solution.

A recent thesis from Rebecca Foright, highlights that a high energy flux state characterized by high daily energy expenditure (resulting from increased physical activity) with matching high energy intake (high calorie throughput) may attenuate the weight loss-induced energy gap by reducing hunger and ameliorate the otherwise diet-related reduction in resting metabolic rate.

Foright recruited recruited eleven obese study participants from the Colorado State University community and surrounding areas to test her "exercise more, eat more, lose more (easily)" hypothesis.

The enrollment criteria included: BMI between 30-43 kg/m², age 18-55 years, weight stable over the prior 12 months, desire to lose weight, and ability to exercise as assessed by electrocardiogram (ECG), resting blood pressure and a normal incremental exercise test to exhaustion with simultaneous ECG. Exclusionary criteria included: pregnancy or breastfeeding, smoking, use of medication known to affect appetite or metabolism (including but not limited to antidepressants and statins), or prior surgery for weight loss. In short, most of the participants were what we today call "healthy obese."
"The approach used in this study was a within-subjects cross-over experimental design to test the effect of high and low flux states following weight loss on resting metabolic rate and perceptions of hunger and satiety."

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The study protocol was divided into four distinct phases: (1) baseline testing phase prior to weight loss; (2) weight loss phase induced by a hypocaloric diet over the course of several months; (3) weight maintenance phase in which subjects were maintained at the reduced weight for 3 weeks; and (4) experimental phase in which measures were obtained of subjects’ resting metabolic rates, fasting and post-prandial perceived hunger and satiety, fasting and post-prandial circulating glucose, insulin, and PYY concentrations, and ad libitum food intake on the 5th day following low flux and high flux phase conditions, respectively, completed in random order with a three-day washout period in between (see Figure 1).

Figure 1: Experimental Timeline | #Order of Low Flux and High Flux were randomly assigned (Foright. 2014).

During the low flux condition subjects remained sedentary for four consecutive days. All food was provided so that energy intakes were adjusted to maintain energy balance.

• resting metabolic rate (RMR) measurements on day 1-4 of the low flux phase
• caloric intake was adjusted according to RMR everyday
• subjects were fed standardized meals with a macro composition of 50/35/15 (carbohydrate/fat/protein) and an energy intake that was 1.3x the RMR
• subjects had to refrain from physical activity (>3,000 steps per day)
• at the end of day 5 the subjects completed a hunger/satiety questionnaire used to assess general feelings of hunger/satiety over the prior four days of the low flux condition

During the high flux condition subjects exercised on four consecutive days (approximately 500 net exercise kcal expenditure at 60% V02 max) and were fed additional food necessary to maintain energy balance.

• resting metabolic rate (RMR) measurements on day 1-4 of the low flux phase
• caloric intake was adjusted according to RMR everyday
• subjects were fed standardized meals with a macro composition of 50/35/15 (carbohydrate/fat/protein) and an energy intake that was 1.7x the RMR
• subjects were given pedometers and had to achieve at least 7,500 steps per day
• subjects exercised at 60% of their VO2max to burn 500kcal
• at the end of day 5 the subjects completed a hunger/satiety questionnaire used to assess general feelings of hunger/satiety over the prior four days of the low flux condition

Overall, a testing week consisted of two baseline days and 5 high/low energy flux days. In that, three identical experimental days were used to examine possible differences in perceptions of hunger and satiety, blood glucose, insulin, and PYY in response to breakfast preload, and ad libitum intake from a meal buffet.

Note: The caloric deficit that was designed to produce a 7% weight loss over the course of the 12-16 week long weight loss phase was identical in the undulating high and low energy flux phases of the study. The results are thus not a consequence of the increase in energy intake during the high flux phase (in fact the opposite was the case in some subjects, anway). The extra calories were after all burned again during the four exercise days.

"Now what is particularly interesting about the study is that the researchers did not content themselves with measuring the acute effects of high vs. low energy fluxes. They also investigated what happened after the 12-16 week weight loss phase.

To minimize the acute effects attributable to the dynamic phase of weight loss on metabolic rate and on hunger and circulating appetitive hormone concentrations, subjects were maintained at the seven percent lower body weight for a three-week period prior to the start of the low and high flux conditions. During these three weeks subjects reported to the KANC every three days to monitor weight and minimize weight fluctuations. Subjects were instructed to consume a slightly increased kcalorie intake compared to the weight loss phase to maintain weight" (Foright. 2014).

Put simply, the scientists wanted to know, whether the effects of high vs. low energy flux dieting would influence a dieters ability to lose weight and maintain the newly achieved weight.

Figure 2: Weight loss and energy flux where exactly as the scientists had planned (Foright. 2014)

As you can see, the average weight loss was almost identical to the targeted 7% (de facto "only" 6.9%). Similarly,

[...a]s designed, the energy intake for high flux (x±SD: 3,191±587 kcal/d) was significantly greater (p < 0.001) than for low flux (x±SD: 2,449±406 kcal/d) (Figure 2, right). In accord with the study design, there was no difference in macronutrient composition between the two conditions (data not shown)" (Foright. 2014).

Now all that would be pointless if both groups lost weight similarly effortlessly. In reality, though, On the subjects were significantly more hungry and felt less satiated at the end of each of the days during low flux.

Figure 3: As you see, the mean difference was already huge. It was more than huge in in
the subject who saw the greatest benefit (Foright. 2014).

On the other hand, they were significantly more full at the end of each of the days during high flux (p=0.015). There was a strong trend for the subjects to exhibit greater hunger throughout the day during low compared to high flux (p=0.09).

RMR increases sign. in trained but not untrained subjects in a high energy flux state - no training, no difference between the two groups - the energy balance was identical in both conditions (Bullough. 1995)

No, this is not an outlier study: In 1995 Bullough et al. were already able to show that the resting metabolic rate on diet + exercise regimen that established an identical energy balance was greater in trained than in untrained subjects only when trained subjects were in HF. As Bullough et al. point out "[t]hese data indicate that RMR is influenced by exercise, energy intake, and their interaction and suggest that higher RMR in trained vs untrained individuals results from acute effects of HF rather than from a chronic adaptation to exercise training." (Bullough. 1995) Bell et al. on the other hand found that "[m]aintenance of high energy flux via regular exercise may be an effective strategy for maintaining energy expenditure and preventing age-associated obesity" (Bell. 2013).

And Goran et al. (1994) found that "RMR can be elevated during a state of energy balance when energy flux is increased," and that the "magnitude of adaptive change in RMR is similar in response to increased EI [energy intake] and/or PA [physical activity]." 

Figure 4: The subject who saw the greatest satiety benefit in the high flux phase was also the one that consumed the most energy on the low flux condition - even more than on the high flux condition (Foright. 2014)

Interestingly, the subject who saw the largest benefit (see Figure 3) was also the guy or gal who consumed the most energy in the low flux condition (orange line in Figure 4).

So what about the health markers?

The  fasting insulin decreased following weight loss and was significantly lower on the LF (8.3±1.1 µU/ml) and HF (6.4±0.8 µU/ml) experimental days compared to the pre-weight loss baseline (11.8±0.6 µU/ml). In other words, while both groups saw significant increases in insulin sensitivity due to dieting, the effects were (unsurprisingly) significantly more pronounced during the high energy flux (=exercise phase).

In contrast to what the significant differences in hunger ratings would suggest, there were no general differences in fasting PYY (the satiety hormone) concentrations among pre-weight loss, low and high flux conditions respectively.

Figure 5: Insulin and PYY levels of the subjects in the high and low flux phases over the course of the day (2014).

If you look at the data in Figure 5, it's obvious that the PYY levels were in fact lower in the high flux condition - from 180-360 minutes in the high flux condition compared to the baseline (pre-weight loss) and low flux, to be precise.

Figure 6: Average resting metabolic rate at baseline and across 5 days of low and high flux (Foright. 2014)

So what? Beneficial, not beneficial, or not sure? In spite of the absence of significant differences in PYY, the post-diet response of the subjects clearly indicates that the energy deficit was easier to tolerate in the high flux phases.

The slightly, but significantly higher resting metabolic rate during the high flux phases further underlines that there is a benefit of eating more and training more and the absence of corresponding evidence from any of the hormonal markers measured may simply be related to a "bad" choice of markers. If the researchers had determined the level of the hunger hormone ghrelin, instes, it may well have been that we would have had a physiological explanation for the "hunger difference".

The way it is, we still have the decreased subjective hunger, increased subjective satiety and increased RMR which speak in favor of the high flux state dieting. What we do not know, though, is whether the effects will be the same in athletic (vs. sedentary) subjects [based on my personal experience we will!] and whether they can be maintained for say 4 weeks instead of four days | Comment on Facebook!

References:

• Bell, Christopher, et al. "High energy flux mediates the tonically augmented β-adrenergic support of resting metabolic rate in habitually exercising older adults." The Journal of Clinical Endocrinology & Metabolism 89.7 (2004): 3573-3578.
• Bullough, Richard C., et al. "Interaction of acute changes in exercise energy expenditure and energy intake on resting metabolic rate." The American journal of clinical nutrition 61.3 (1995): 473-481.
• Foright, Rebecca. A high energy flux state attenuates the weight loss-induced energy gap by acutely decreasing hunger and increasing satiety and resting metabolic rate. Diss. Colorado State University, 2014.
• Goran, Miachel I., et al. "Effects of increased energy intake and/or physical activity on energy expenditure in young healthy men." Journal of Applied Physiology 77.1 (1994): 366-372.
• Rarick, Kevin R., et al. "Energy flux, more so than energy balance, protein intake, or fitness level, influences insulin-like growth factor-I system responses during 7 days of increased physical activity." Journal of Applied Physiology 103.5 (2007): 1613-1621.

How to Switch Off Your Menstrual Cycle W/ Exercise & Dieting - More Than 22% Deficit ➯ Increased Risk of Menstrual Irregularities + Reduced (!) Weight Loss

Messing with your hormones won't help to reveal your abs, ladies!

I have written about this problem previously. Actually the whole SuppVersity "Athlete's Triad"-Series (read it) is remotely related to it: Women working out like hulk and eating like a sparrow. A behavior that leads to hormonal imbalances and amenorrhea very reliably.

So if you are wondering, why your menstrual cycle is messed up. Why you cannot get pregnant or why you simply stopped menstruating, ladies, this article is for you.

Needless to say that the same goes for male and female trainers, obviously, for whom the results of a very recent study from the Pennsylvania State University and the Penn State University College of Medicine (Williams. 2014).

Low T3 syndrome is also a result of dieting and a part of the (Female) Athletes Triad.

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Female Athlete's Triad - Recovery Part 3/3

The study Nancy I. Williams and her colleagues conducted was designed to confirm or refute the that there would be a dose-response relationship between the induction of menstrual disturbances (luteal phase defects, anovulation, and oligomenorrhea) and the magnitude of energy deficiency.

In other words, the researchers expected that higher energy deficits would incur a significantly greater incidence and more severe disturbances of their menstrual cycle disturbances. To evaluate their hypothesis, the researchers conducted a randomized prospective design that employed controlled feeding and supervised laboratory-based exercise over the course of three menstrual cycles in young, untrained, premenopausal, eumenorrheic women.

Table 1: Overview of the experimental procedures; MC=Menstrual Calendar | Note: Mid-study Body composition testing occurred during Intervention Cycle 2 for most subjects, but in some it occurred during Intervention Cycle 3 (Williams. 2014)

"The study was conducted over three years, with yearly cohorts recruited in the fall of the academic year and followed until the end of spring semester. The controlled feeding and exercise training began after the Screening and Baseline periods, each period lasting one menstrual cycle. All phases of the intervention were anchored to subjects’ menstrual cycles, and each study phase consisted of one menstrual cycle (Intervention Cycle 1, Intervention Cycle 2, Intervention Cycle 3). A post study period of one week where diet and exercise remained controlled allowed for post intervention measurements. The study design is illustrated in Table 1.

Group assignments were based on varying levels of energy deficiency created through a combination of caloric restriction and exercise such that one group remained in energy balance and four groups were in different degrees of an energy deficit. Repeated assessments of menstrual status, metabolic status, and body composition were conducted." (Williams. 2014)

The study was conducted with healthy young, weights-stable women, who had not evidence or history of disordered eating were aged 18 – 30 years, weighed 45 – 75kg and had a normal body fat level of 15 – 35%. The women didn't smoke, were not hormones or anti-contraceptives.

So what did the scientists do?

During the Baseline period, subjects were randomly assigned to an experimental group for the Intervention Cycles 1, 2, and 3 of the study. The goal of the subject groupings was to test the impact of varying levels of an energy deficit created by the combination of caloric restriction and exercise on menstrual function.

Most women ignore the risk of bone loss and only few know that the un- wanted "clinical sequelae", i.e. the nasty pathological consequences, of not eating enough and working out like a maniac include sign. increases in cardiovascular risk (O'Donnell. 2004)

The overlooked significance of hormonal imbalances: As Williams et al. point out, "[a] large body of evidence in a variety of mammalian species has demonstrated a causal link between chronic energy deficiency and the suppression of reproductive function involving the central inhibition of gonadotropin releasing hormone (GnRH) pulsatility" (Williams. 2014). In humans, long term energy deficiency can result in functional hypothalamic amenorrhea, (FHA) and therefore, decrease estrogen exposure, diminishing estrogen’s impact on bone, reproductive, and cardiovascular regulation, often resulting in bone loss (Rencken. 1996; Wade. 1996), stress fractures - specifically in athletes (Barrow. 1988; Bennel. 1999; Brukner. 1997), transient infertility, dyslipidemia, and impaired endothelial function (Friday. 1993, Hoch. 2007; O’Donnell. 2004).

Table 2: Baseline demographic characteristics of study subjects categorized by group (top) and energy balance parameters averaged across Intervention Cycles 1-3 for each group (bottom) - directly from Williams (2014)

They were assigned to either a control group that did not exercise and consumed an amount of calories estimated to maintain body weight, a control group that exercised, but received extra food calories to remain in energy balance (exercising controls or EXCON), or one of four groups that exercised and were prescribed reduced energy intake to create varying levels of an energy deficit (energy deficit or ED groups). ED groups were defined by an energy prescription comprised from the quantity of calories provided as food and the quantity of calories expended as exercise. ED groups were prescribed targeted reductions in energy intake (7 days/week) compared to their Baseline energy needs ranging from – 15% to – 30% in combination with prescribed increases in exercise energy expenditure (5 days/week) equivalent in calories to + 15% to + 30% of Baseline energy needs.

Starvation diets will also mess w/ your thyroid | learn more

So, how low can you go? The scientists fount that the estimates of the magnitude of energy deficiency associated with menstrual disturbances ranged from -22% (ED2) to -42% (ED3), reflecting an energy deficit of -470 to -810 kcal per day, respectively. In contrast to the what Williams et al. expected, the severity of menstrual disturbances, was not dependent on the magnitude of energy deficiency and is thus not a gauge to estimate how much more you'd have to eat to become fully functional again.

As the researchers point out, specifically, the initial four energy deficit groups were intended to represent 1) an increase of 15% kcals of exercise (15% deficit), 2) an increase of 30% kcals of exercise (30% deficit), 3) a decrease of 15% in dietary intake, combined with an increase of 15% of exercise, (30% deficit) and 4) a decrease of 30% in dietary intake, combined with an increase of 30% kcals of exercise (60% deficit).

Figure 1: Daily energy deficit (left) and corresponding menstrual irregularities (right) the Pennsylvanian researchers observed during the intervention (Williams. 2014)

As you can see in Figure 1 the plan worked out quite well and the original hypothesis that the severity of the energy deficit would correlate with the risk of overall risk of menstural irregularities. What is interesting, though, is that the overall linear increase was visible mostly for the luteal phase disturbances. Actual unovulatory cycles were observed only in groups ED2 & ED3, but - and this is important - for some women, it was enough to just work out to induce oligomenorrhic cycles, i.e. infrequent (or, in occasional usage, very light) menstruation.


Next to the menstrual irregularities, which were obviously what the scientists were actually interested in, the scientists also observed that the 34 subjects lost weight, 3.8 kg in the ED1 and - listen up ladies! - only 2.8 kg and 2.6 kg in the high(er) energy deficit groups ED2 and ED3 (no significant weight loss occurred in the exercise only, i.e. the EXCON group).

Figure 2: Amount of weight (in kg) the women in the four groups lost over the course of the complete study period (Williams. 2014)

Bottom line: Let me say this right away. It's not unfair, but very clever that nature made sure that starving women cannot become pregnant.

If you look at the "target outcome" of most women's dietary interventions, i.e. the amount of weight they lose (see Figure 2), you will also have to concede that what many women believe would be "unfair" actually protects them from ineffective starvation diets. It was after all not the group with the highest, but the group with the lowest energy deficit that lost the most weight. So, ladies, be sure to remember this and if you are still not convinced that starving yourself is not the magical weight loss solution that will give you the "shape cover model" body you're looking for, take another look at the "9 Rules of Sensible & Effective Dieting" | Comment on Facebook.

References:

• Barrow, Gray W., and Subrata Saha. "Menstrual irregularity and stress fractures in collegiate female distance runners." The American journal of sports medicine 16.3 (1988): 209-216.
• Bennell, Kim, et al. "Risk factors for stress fractures." Sports Medicine 28.2 (1999): 91-122.
• Brukner, Peter, and Kim Bennell. "Stress fractures in female athletes." Sports Medicine 24.6 (1997): 419-429.
• Friday, Karen E., et al. "Elevated plasma low-density lipoprotein and high-density lipoprotein cholesterol levels in amenorrheic athletes: effects of endogenous hormone status and nutrient intake." The Journal of Clinical Endocrinology & Metabolism 77.6 (1993): 1605-1609.
• Hoch, Anne Z., et al. "Athletic amenorrhea and endothelial dysfunction." Wisconsin Medical Journal 106.2 (2007).
• O’Donnell, Emma, and Mary Jane De Souza. "The Cardiovascular Effects of Chronic Hypoestrogenism in Amenorrhoeic Athletes." Sports Medicine 34.9 (2004): 601-627.
• Rencken, Monica L., Charles H. Chesnut, and Barbara L. Drinkwater. "Bone density at multiple skeletal sites in amenorrheic athletes." Jama 276.3 (1996): 238-240.
• Wade, GEORGE N., JILL E. Schneider, and H. Y. Li. "Control of fertility by metabolic cues." American Journal of Physiology-Endocrinology And Metabolism 270.1 (1996): E1-E19.
• Williams, Nancy I., et al. "Magnitude of daily energy deficit predicts frequency but not severity of menstrual disturbances associated with exercise and caloric restriction." American Journal of Physiology-Endocrinology and Metabolism (2014): ajpendo-00386.

Update: The Latest on Caffeine, Exercise, Fat & Weight Loss - Increased Performance, Energy Expenditure (6%) & Fatty Acid Oxidation (27%) vs. Decreased Sleep Quality & Burnout

We love coffee! There is not doubt about it 85% of the Americans consume coffee on a daily basis and it's not much different for the rest of the West (Mitchell. 2013).

Caffeine is the #1 drug worldwide (Weinberg. 2001; Mitchell. 2013). In the US people with a death wish select the coffee from the eponymous brand which contains more than twice the amount Starbucks coffee does - and that in spite of the fact that Starbucks is the not so close follow up on place in a ranking with the telling title "Amount of caffeine in coffee in the United States in 2013, by brand (in mg per floz)" (Thrillist | Statista.com. 2014).

With 54.2 mg of caffeine per floz and thus ~ 400mg per cup "having a Deathwish" would bring an average male athlete with a body weight of 80kg right to the 5mg/kg body weight maximum that has been used in the majority of high(er) dose caffeine supplementation trials.

You can learn more about coffee at the SuppVersity

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Caffeine Resis- tance - Does It Even Exist?

I've explained in previous articles, already, that for caffeine, more is not always better! In fact, consuming more than 600mg of caffeine pre-workout has been shown to induce a significant reduction in post-workout testosterone and that in the absence of ergogenic benefits (learn more)... certainly not what you're looking for, when you drink one, two or three espressos before your workouts.

A possible reduction in testosterone is yet not the only downside you have to consider. A recent study from the University of Sydney, which is the first new study in today's "Caffeine Update", for example, found that the ergogenic benefit of consuming caffeine containing carbohydrate beverages (aka energy drink) during your workouts comes at a price: deleterious effects on sleep (Miller. 2014).

Figure 1: Plasma caffeine concentration before, during and at the end of  exercise, and 30 min before bedtime (n = 5). Mean ± SD; Caffeine ingestion, bedtime (Miller. 2014)

As you can see in Figure 1, the caffeine levels, which were zero at the beginning of the trial did not return to baseline in the ~6h before the subjects went to bed. No wonder that the polysomnographic (PSG) recordings show significant changes in disruption of a number of sleep indices including increased sleep onset latency (caffeine 51.1  ±  34.7; placebo; 10.2 ± 4.2 min; p = 0.028) and decreased sleep efficiency (caffeine 76.1 ± 19.6; placebo 91.5 ± 4.2 %; p = 0.028), rapid eye movement sleep (caffeine 62.1 ± 19.6; placebo 85.8 ± 24.7 min; p = 0.028) and total sleep time (caffeine 391 ± 97; placebo 464 ± 49 min, p = 0.028).

Table 1: Sleep indices after caffeine or placebo ingestion (Miller. 2014)

In addition to the changes in sleep parameters you can see in Table 1, two of the six subjects (33%) reported caffeine related anxiety, and mild gastrointestinal upset during exercise - effects that occurred even before they went back to bed.

Figure 2: Previous studies report significantly reduced melatonin production in response to "only" 5 cups of 130 mg/cup caffeine coffees per day for one week vs. the same amount of decaff (Shilo. 2002)

In view of the fact that none of these effects occurred in the placebo trial, it may in fact be worth considering not to consume too much intra- or pre-workout caffeine, when you work out in the PM. If you take a look at the data from Shilo's 2002 study, which investigated the effects of "chronic" (7 days) coffee consumption night time melatonin production (see Figure 2), you may even consider giving up coffee, altogether (in view of the CYP1A2 competition of melatonin and caffeine (Härtter. 2003), it may yet bet that the excretion rates that were measured by Shilo et al. are not indicative of the actual melatonin activity)

"But caffeine is so good!?"

What do you say? "Caffeine is so good"? Yes, it is. I mean, caffeine in fact "so good". In Miller's study, it lead to improved time trial times during cycling in all subjects (even the anxious and nauseous ones; caffeine 19.7 ± 3.3; placebo 20.5 ± 3.5 min; p = 0.006), while reducing the rates of perceived exertion (caffeine 12.0 ± 0.6; placebo 12.9 ± 0.7; p = 0.004) and heart rate (caffeine 175 ± 6; placebo 167 ± 11 bpm; p = 0.085).

Surprising benefits for type II diabetics: In spite of the fact that the contemporary evidence clearly indicates that a regular moderate to high caffeine consumption protects against type II diabetes (-29% risk; Jiang. 2014), even scientists question, whether caffeine is still beneficial, whence you're already diabetic. A recent study from the Midwest State University of Parana does now suggest that at least the small minority of type II diabetics who work out, can benefit from the glucose reducing effects of pre-workout caffeine supplementation. With a 65% reduction and 75mg/dl (p < 0.05), the allegedly high amount of 1.5mg/kg caffeine lead to a highly significant reduction in plasma glucose in the eight diabetic subjects (age 55±10 years) who worked out at only at 40% heart rate (HR) reserve for 40 min at the facilities of the Science Postgraduate Program (daSilva. 2014).

This is yet not the only good news scientists have come up with since the last SuppVersity caffeine review. Researchers from the School of Allied Health Sciences at the Griffith University in Australia (Schubert. 2014), for example, report that "combining caffeine with exercise creates a greater acute  energy deficit" and could thus provide the foundation to increased weight loss / reduced weight gain in both lean and overweight individuals.

Is caffeine the agent that keeps you lean?

The subjects in the study at hand were required to be non-smoking and non-obese (BMI < 30 kg/m²), pre-menopausal (women), between 18 and 45 years of age and not on any medicine known to influence lipid, carbohydrate, or caffeine metabolism (except oral contraceptives). They were not allowed to be dieting and had had to be weight stable in the previous 3 months (± 5 % by self-report), Moreover, they were free of any cardiovascular or metabolic diseases and otherwise healthy.

We're not dealing with caffeine naive individuals! In view of the fact that the central nervous system effects which are in turn highly relevant for the influence of caffeine on energy expenditure and fatty acid oxidation, it's important to point out that the subjects were not caffeine naive. Both, the 6 men and 8 women who participated in the study at hand had a habitual caffeine consumption of 206 ± 194 mg per day.

To make sure that the individual dietary preferences of the subjects would not mess up the results, participants were asked to complete a food diary and record all food and drink. Additionally, all participants were also asked to refrain from strenuous exercise the 18 hours before their trial to which they had to come after an overnight fast and without breakfast. When they arrived at the lab, the subjects received 3mg/kg body weight with 250ml of water. Afterwards they had to sit quietly before the resting energy expenditure (REE) was measured continuously for the final 20 min of a 60 minute rest period.

Figure 3: Overview of the allegedly somewhat complicated, but realistic and thus relevant exp. setup (Schubert. 2014)

After the 60 minutes at rest, the participants then completed 60 min of exercise on a cycle ergometer, at ~65 % power output of VO2max (EX and EX+CAF) or rested/worked quietly (CON). During exercise, mechanical work and power output data were recorded continuously, while gas exchange (VO2, VCO2, RER) was recorded for the first 15 min and then from 25-35 min and 45-55 min. The power output was adjusted as necessary to maintain ~65% of the estimated power output at VO2max. The attained power output from the first exercise trial was duplicated in the second one. At 15 min intervals, participants provided ratings of perceived exertion, leg pain, and pleasure/displeasure (Feeling Scale); heart rate was also recorded at these times. Enjoyment was assessed post-exercise via completion of the Physical Activity Enjoyment Scale (PACES).

As complicated as it may seem, the study protocol is actually not unrealistic

At +150 min (30 min post-exercise/rest), participants were given another 3 mg/kg body weight dose of caffeine or placebo along with a small liquid calorie meal (250 mL, 825 kJ, 30.3 g carbohydrate, 3.8 g fat, 8.3 g protein; Up N Go®, Sanitarium Health & Well-Being™; Australia). This beverage was provided to provide participants with a small amount of calories and examine post-prandial responses during all trials over the final 90 min. As the researchers point out, ...

"[...t]he rationale for dividing the caffeine dosage was threefold. First, 3 mg/kg BM has been shown to improve exercise performance to the same degree as larger doses (Desbrow. 2012). Second, by using multiple doses several hours apart, typical patterns of caffeine/coffee consumption are mirrored (i.e. early and mid-morning coffee). A recent study reported that coffee consumption peaks in the morning (0600-0800) with a second peak late morning (1000-1200), with a decline thereafter during the week (Gibson. 2013). The third reason was to maintain plasma caffeine levels in order to examination their relationship to other variables." (Schubert. 2014)

Aside from the fact that the average US adult probably won't consume more than 200 mg and thus ~40mg less caffeine than the male study participants (average body weight 81kg) of the study at hand with one cup of coffee, Schubert et al. have thus created a pretty realistic scenario the exercise component of which matches the situation of the average pre-workout consumer pretty well.

Figure 4: Changes in total energy expenditure (EE), fatty acid and carbohydrate / glucose oxidation in response to the 2x1.5g/kg body weight caffeine consumption in healthy men and women during and after exercise (Schubert. 2014)

As you can see in Figure 3 the provision of caffeine leads to significant increase in total energy expenditure during and after the workout and a highly significant shift from carbohydrate to fat oxidation.

Burning more fatty acids ≠ losing more fat! 

Figure 5: It's not popular to say this, but it's true: Whether you gain or lose weight depends on your relative energy intake and the latter was negative for both exercise groups in the study at hand (Schubert. 2014)

What you should keep in mind, though, is that the increase in fatty oxidation which amounted to 27.7% when we consider the complete trial will not necessarily translate into an increase in fat loss. Without the concomitant 5.5% increase in total energy expenditure (measured over the whole 240min; including the time before the workout), those 27.7% higher rates of fatty oxidation would be almost worthless - the energy that would have been lost from the glycogen stores of the muscle and liver at higher carbohydrate and lower fatty acid oxidation rates would eventually have to be restored, as well... So, believe it or not: If you lose weight or not depends solely on your effective (!) energy balance, i.e. the difference between the amount of energy you consume and the amount of energy you really expend (which has often little to with the amount of energy a stupid calculator tells you you would expend | learn more about these calculations).

If we don't care about weight, but fat loss, however, the increase in fatty oxidation during the workout may matter, yet again. In contrast to the oxidation of fatty acids during the workout, the restoration of muscle and liver glycogen will eventually not necessarily happen in the absence of amino acid and thus possibly (!) muscle breakdown. A fact that leaves the "caffeine doped" athlete at a two-fold advantage: (1) Increased overall energy expenditure and (2) a decreased risk of lean mass loss.

Figure 6: Energy expenditure (kcal) from CHO and FAT over the whole 4h study period (Schubert. 2014)

Bottom line: So what have we learned today? First, you got to be careful not to mess up your sleep economy by (ab-)using caffeine too close to going to bed. All the beneficial effects on fatty acid oxidation and total energy expenditure, before during and after a workout (see Figures 4 & 6); and even the glucose lowering effects in diabetics are after all hardly worth the paper the studies in which they were reported were printed on, if your sleep quality and thus your glucose tolerance (Gottlieb. 2005), your cognitive function (Hobson. 2002), immune health (Dinges. 1997), endocrine function (Spiegel. 1999) and cancer protection (Blask. 2009) suffer | Comment on Facebook!

Reference:

• Blask, David E. "Melatonin, sleep disturbance and cancer risk." Sleep medicine reviews 13.4 (2009): 257-264.
• da Silva, Luiz Augusto, et al. "Caffeine modifies blood glucose availability during prolonged low-intensity exercise in individuals with type-2 diabetes." Colombia Médica: CM 45.2 (2014): 72.
• Desbrow B, Biddulph C, Devlin B, Grant GD, Anoopkumar-Dukie S, and Leveritt MD. "The effects of different doses of caffeine on endurance cycling time trial performance." Journal of
  sports sciences 30 (2012): 115-120.
• Dinges, David F., et al. "Sleep deprivation and human immune function." Advances in neuroimmunology 5.2 (1995): 97-110.
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• Härtter, Sebastian, et al. "Effects of caffeine intake on the pharmacokinetics of melatonin, a probe drug for CYP1A2 activity." British journal of clinical pharmacology 56.6 (2003): 679-682.
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True or False: High Volume + Nutrient + Low Energy Foods Keep You Lean. Bonus-Question: Will a High Volume Make Your Stomach Go Baggy & Mess Up Your Satiety Response?

There are millions of ways to con- sume 100kcal and volume isn't the only difference (img greatist.com)

I have repeatedly pointed out that filling yourself up on vegetables and other high volume, high nutrient (vitamins, minerals, polyphenols, etc.), low energy foods is one of the fundamental principles of weight management. The question that remains, though, is whether this principle is so effective because of the food we eat (tons of veggies), or rather due to the fact that there is no room for the foods we thusly don't eat (the typical processed junk)?

I guess, it's not debatable that replacing trashy foods with healthy ones is the most important factor. We have all heard about the beneficial effects "high volume foods" and the downsides of the average high energy + low nutrient 100kcal junk-food snack. But how important is the volume, actually? Isn't food "quality" (whatever that may be) all that counts?

You can find more True or False articles at the SuppVersity

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It's surprisingly difficult to answer this question and after reviewing the most important studies, I have to say that I still can't tell for sure how important the volume is.

Figure 1: Effects of pylorectomy (removal of the part of the stomach that contains the vagal nerves) and vagal deafferetation on the ability of CCK to affect liquid food intake in rats (Moran. 1988)

What I can tell you, though, is that it appears to be certain that the mechanical stretch will be detected by vagal affarent endings in the stomach (Phillips. 2000; Berthoud. 2001). These "stretch detectors" are hard-wired to your brain, where they are processed in the so-called "nucleus tractus solitarius" (Näslund. 2007). Unfortunately, the exact role of the "nucleus tractus solitarius" in the satiety response is not even partly understood.

What we do know is that electrophysiological recording studies as well as behavioral studies have found that the effect of a given dose of cholecystokinin (CCK) is increased in the presence of stomach stretch (Schwartz. 1993 & 1995) and disrupted, when the vagus nerve is damaged or the NTS lesioned (Edwards. 1986; Moran. 1988; Smith. 1985).

With CCK being a major satiety hormone (and on top one that actually does what it's name implies, i.e. signal satiety) it appears to be quite certain that the multiplying effect the mechanical stretch exerts on the satiety effect of CCK is one of the secondary mechanisms by which eating high volume foods keep you lean.

Do you remember? You've read about a couple of things that will increase the release of CCK and would thus synergize with the effects of what I would like to call "high volume eating": (1) The pre-ingestion of protein before a meal | learn more, (2) Arginine, lysine and glutamic acid | learn more, and lastly and unsurprisingly a gastric bypass operation | learn more. Another well-known trigger of CCK release is the ingestion of fatty acids (low amounts suffice; long chain polyunsaturated fatty acids are particularly effective; Gribble. 2012) - is not satiating.

In view of the fact that the NTR, ie. the nucleus tractus solitarius, integrates (adds up and processes) a whole host of signals from the gastro-intestinal tract, it's also hardly surprising that a gastric bypass surgery and the corresponding increase in stretch per volume unit of food that has just recently been shown to change not just the satiety response to food but also the way foods taste and smell for patients who have undergone Roux-en-Y gastric bypass surgery (learn more in the SuppVersity Facebook News).

Figure 2: Model depicting signals that influence food intake. Not all elements are relevant in the context of this article - focus on the way the satiety signals that are generated in the gastrointestinal (GI) tract during meals provide information about mechanical (e.g., stomach stretch, volume) and chemical properties of the food to the brain (Woods. 2004)

Other mechanisms by which the gastric stretch may contribute to an increase in satiety / reduction in food intake and, via the release of GLP-1 and other glucose regulating satiety hormones (learn more about GLP-1) are the reduction of gastric emptying (Read. 1994), and other interactions between the vagus nerve and the brain, which include aside from directly satiety related mechanisms also the activation of serotonergic neurons (remember: serotonin is the happy hormone) in the brain (Mazda. 2004).

Bonus question: Is high volume eating setting you up for obesity? You could argue that the constant gastric distension and consequently increased postprandial gastric accommodation will reduce the satiety response to small calorie dense meals. Now aside from the fact that you will get fat, no matter what if you eat those on a daily basis, a study from the Gastroenterology Research Unit in Rochester and the Mayo Clinic did not find a sign of increased postprandial gastric accommodation or reduced satiety in any of of their 13 obese subjects (Kim. 2012).

So, yes! There is more to eating tons of veggies than not eating tons of other food. Moreover, although we don't yet know exactly what this "more" is, we can already say that all the existing evidence appears to support that it the high food volume, the stretch of the stomach and the vagally mediated downstream effects on the release and effect of our satiety hormones (incretins) is one of the factors that contribute to the ability of high volume, high nutrient, low energy foods to keep you lean.

On it's own, the multi-layered stretch-response is probably significantly less important than the reduction in junk-food intake. In conjunction with the synergistic effects of a high protein diet, and a reasonable amount of long-chain fatty acids in the diet, it could yet be what distinguishes people who have to resort to a gastric bypass as a last resort to save their lives from those individuals, who manage to flip the switch, turn their life around and lose their life-threatening overweight without the help of a surgeon.

References:

• Berthoud, Hans-Rudolf, Penny A. Lynn, and L. Ashley Blackshaw. "Vagal and spinal mechanosensors in the rat stomach and colon have multiple receptive fields." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280.5 (2001): R1371-R1381.
• Edwards, et al. "Dorsomedial hindbrain participation in cholecystokinin-induced satiety." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251.5 (1986): R971-R977. 
• Gribble, Fiona M. "The gut endocrine system as a coordinator of postprandial nutrient homoeostasis." Proceedings of the Nutrition Society 71.4 (2012): 456. 
• Kim, Doe‐Young, et al. "Is there a role for gastric accommodation and satiety in asymptomatic obese people?." Obesity research 9.11 (2001): 655-661.
• Mazda, Takayuki, et al. "Gastric distension-induced release of 5-HT stimulates c-fos expression in specific brain nuclei via 5-HT3 receptors in conscious rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 287.1 (2004): G228-G235.
• Moran, Timothy H., et al. "Pylorectomy reduces the satiety action of cholecystokinin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255.6 (1988): R1059-R1063.
• Näslund, Erik, and Per M. Hellström. "Appetite signaling: from gut peptides and enteric nerves to brain." Physiology & behavior 92.1 (2007): 256-262.
• Phillips, Robert J., and Terry L. Powley. "Tension and stretch receptors in gastrointestinal smooth muscle: re-evaluating vagal mechanoreceptor electrophysiology." Brain research reviews 34.1 (2000): 1-26.
• Read, Nicholas, Stephen French, and Karen Cunningham. "The role of the gut in regulating food intake in man." Nutrition reviews 52.1 (1994): 1-10.
• Schwartz, Gary J., et al. "Gastric loads and cholecystokinin synergistically stimulate rat gastric vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265.4 (1993): R872-R876.
• Schwartz, Gary J., Gervais Tougas, and Timothy H. Moran. "Integration of vagal afferent responses to duodenal loads and exogenous CCK in rats." Peptides 16.4 (1995): 707-711.
• Smith, Gerard P, et al. "Afferent axons in abdominal vagus mediate satiety effect of cholecystokinin in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249.5 (1985): R638-R641.
• Woods, Stephen C. "Gastrointestinal satiety signals I. An overview of gastrointestinal signals that influence food intake." American Journal of Physiology-Gastrointestinal and Liver Physiology 286.1 (2004): G7-G13.