Carbs Before Workout Won't Lock Your Ab Fat in its Stores | Plus: Wired for Laziness, Standing for Your Health and 'Cardio' Reversibly Promotes Microbial Diversity in Guts
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| Spiking insulin w/ high GI carbs before a workout doesn't blunt the release of fat from the stores covering your abs. |
For the November issue of Medicine in Sports Science, this was the case for four studies. First and foremost, probably Baur's experimental counterevidence to the hypothesis that the carbohydrate-induced surge in insulin would 'seal' your subcutaneous body fat stores.
It may not be necessary to attack your ab-fat, but fasting does have a handful of benefits:
Monthly 5-Day Fast Works
"Lean Gains" Fast Works
Habits Determine Effects of Fasting
Protein Modified Fast 4 Health
IF + Resistance Training = WIN
ADF Beats Ca-lorie Restriction
- Eating carbs before a workout won't prevent you from shedding ab fat (if you're in a deficit) - Results independent of the GI of the pre-workout carbs -- Insulin is the hormonal boogie man of our time, among other things because it will reduce the oxidation of fatty acids (while increasing that of glucose, by the way). Now, scientists from the Florida State University have been able to show that the overall reduction in fatty acid oxidation is not associated with a reduced subcutaneous central adipose tissue (SCAAT) lipolysis, i.e. the release of stored body fat from the fat cells that are covering your abs - at least not in trained runners.
For their study Daniel A. Baur, et al. recruited N=10 trained male runners who completed three experimental trials consisting of 30 min at 60% VO2max, 30 min at 75% VO2max, and a 5-km time trial (TT). Thirty min prior to exercise, participants consumed one of three beverages: 1) 75 g low glycemic index modified starch supplement (UCAN), 2) 75 g high glycemic index glucose-based supplement (G), or 3) a flavor-matched non-caloric placebo (PL). SCAAT lipolysis was assessed via microdialysis.
While the scientists did confirm the previously established significant reduction in total fat and increase in glucose oxidation w/ high GI (=highly insulinogenic) carbs, they were unable to determine a difference in SCAAT lipolysis at rest or during running - independent of either exercise intensity or the glycemic index of the carbs the subjects ingested.
Figure 1: The scientists measured the release of glycerol from the subcutaneous adipose tissue directly and the lack of difference between placebo, glucose and the slow-digesting UCAN resistant starch refutes the hypothesis that carbs before workouts would lock your body fat in place (Baur 2017).
In view of the fact that only small amounts of body fat are actually lost during exercise, the implications of this revelation are yet not 100% clear.
Since there were no performance differences between high and low GI carbs, Baur et al. are however generally correct, when they posit that their results support "current sport nutrition guidelines suggesting there is little extra value in ingesting low glycemic index carbohydrates prior to exercise when compared to more traditional high glycemic index carbohydrates" (Baur 2017).
What you must not forget, though, is that liberating fat (i.e. lipolysis) is only the first step of losing body fat. What's even more important is that you have an adequate energy deficit that will then prevent that the fat is restored to the fat cells it came from. -
Are some of us genetically "wired" to be lazy and inactive? A recent study by J. Timothy Lightfoot colleagues suggests just that -- The Texas A&M University researchers found that "physical activity level, measured in various manners, has a genetic component in both humans and non-human animal models" (Lightfoot 2017). In their consensus paper, the authors present the results of an American College of Sports Medicine-sponsored roundtable and provide a brief review of the theoretical concepts and existing literature that supports a significant role of genetic and other biological factors in the regulation of physical activity.
As the authors highlight, human behavioral traits are usually determined by both environmental/social and biological factors. Against that background it is, as Lightfoot et al. point out, "alarming that the vast majority of the literature on physical activity has excluded biological factors as potential determinants of physical activity levels in humans" - and that despite the fact that "even a brief and targeted literature review [...] shows conclusively that physical activity level is strongly influenced by biological mechanisms" (Lightfood 2017).
To summarize the summary of the research the US researchers present in their paper isn't just beyond the scope of this installment of the short news but also more or less nonsensical. Accordingly, I would like to highlight only a few key aspects and concepts: If we define "physical activity" as any locomotion or movement that is the result of skeletal muscle contraction, the volume of physical activity (including everything from fidgeting to running a marathon),
Figure 2: Conceptual holistic model of physical activity (Lightfood 2017).
- is controlled by the central reward center of the brain (primarily structures in the striatum),
- correlates with peripheral cardiovascular and musculoskeletal capabilities associated with high and low-activity profiles,
- is subject to significant influence from genomic and other biological factors, such as sex and other hormones, and illness and disease, which may cause changes in inflammatory signals and metabolite levels that participate in the regulation of daily physical activity level,
- will be affected by environmental factors such as diet and the presence of environmental toxicants that may augment/inhibit physical activity level regulatory mechanisms, and
- is heavily influenced by social-environmental factors that may influence activity.
The question is thus not "Is it in your genes, your character your environment or your upbringing, it's rather "How do all three of them interact to determine your activity levels?" - Stand up for health - Multi-component workplace intervention that promotes standing and or walking during office times triggers significant health improvement -- In fact, not one, but several cardio-metabolic health risk biomarkers were progressively reduced in the 136 desk-based workers /65% women, mean±SD age=44.6 ±9.1 years) from seven worksites who participated in Elisabeth AH Winkler's latest study.
"The Stand Up Victoria intervention consisted of organizational support (senior management support, a team champion who sent emails containing the intervention messages); environmental modification (sit-stand workstations); and, individual health coaching (including goal setting and tracking).
Figure 3: The increase in walking time was mediocre aat best, but the increase in time the subjects spent standing was significant - 1h per 16hr, with health-relevant consequences in form of reduced blood pressure, trigs, an improved total/HDL ratio, reduced body weight and fat mass, as well as waist reductions and improvements in insulin when considering both, standing and walking instead of sitting. The intervention was tapered over 12 months with intensive components (e.g., health coaching and team champion emails) ceasing after 3 months. It primarily targeted reductions in workplace sitting time, especially sitting accrued for ≥30 minutes at a time continuously.
The main message was to ―Stand Up, Sit Less, Move More" (Winkler 2017).
While the individual response to the intervention was found to be highly variable, the composition was statistically significant (with the 95% confidence region excluding no change) and was very close to the point indicating a drop in mean baseline sitting of 1 hour/16 hours awake, when only the subjects standing time is considered.
That's not impressive, but it was still associated with highly significant health benefits: The scientists found that the greatest degree and/or widest range of cardio-metabolic benefits appeared to occur with long-term changes, and when increasing ambulatory activities, with reductions in systolic blood pressure occuring as early as after three months and significant improvements in cardiometabolic risk scores, weight, body fat, waist circumference, diastolic blood pressure, and fasting triglycerides, total/HDL cholesterol and insulin after 12 months.
In contrast to what another recent study seemed to suggest standing alone seems to suffice to trigger many of the beneficial effects. Significant differences between standing and stepping were, after all, "only observed for systolic blood pressure and insulin; both favored stepping" (Winkler 2017). That doesn't change the fact, though, that stepping would trigger overall greater improvements than standing. - First study to conclusively demonstrate that exercise changes your microbiome -- Scientists from the University of Illinois confirm that exercise training induces compositional and functional changes in the human gut microbiota.
What is particularly interesting is that these changes are (a) dependent on obesity status, but (b) independent of diet ... what is not surprising, though, is that the changes were also "contingent on the sustainment of exercise" (Allen 2017).
In the study at hand, the amount of exercise that had to be sustained was an endurance-based exercise training that was done on 3 days/wk and at progressing durations and intensities (from 30 to 60 minutes/day and from moderate (60% of heart rate reserve [HRR]) to vigorous intensity (75% HRR)) - once the subjects stopped training, their bacterial diversity bounced back to baseline diversity levels, of which the existing evidence suggests that they are too low to support optimal health (Lloyd-Price 2016).
Figure 4: The changes in the bacterial diversity were associated with significant changes in body composition (A lean mass, B body fat %), bone mineral density (C) and physical fitness (D VO2max) over the course of 6 exercise weeks (E6). Just the microbiome, which returned to baseline after the intervention, these benefits were largely lost during the subsequent 6 weeks washout (W6 | Allen 2017)
Ah, and by the way: In contrast to what you may expect, it were not the obese subjects who benefitted most: At least when it comes to the exercise-induced increase in fecal concentrations of short-chain fatty acids (SCFAs), the effects were in fact "lean only", i.e. they were not observed in obese, participants.
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| The results of the Baur study are in line w/ Schoenfelds "Cardio on Emtpy" study from 2014 | more. |
References:
- Allen, Jacob M., et al. "Exercise Alters Gut Microbiota Composition and Function in Lean and Obese Humans. Medicine & Science in Sports & Exercise: Post Acceptance: November 20, 2017.
- Baur, Daniel A., et al. "Adipose Lipolysis Unchanged by Preexercise Carbohydrate regardless of Glycemic Index." Medicine & Science in Sports & Exercise: Post Acceptance: November 20, 2017
- Lightfoot, J. Timothy, et al. "Biological/Genetic Regulation of Physical Activity Level: Consensus from GenBioPAC." Medicine & Science in Sports & Exercise: Post Acceptance: November 20, 2017
- Lloyd-Price, Jason, Galeb Abu-Ali, and Curtis Huttenhower. "The healthy human microbiome." Genome medicine 8.1 (2016): 51.
- Winkler, Elizabeth AH. "Cardiometabolic Impact of Changing Sitting, Standing, and Stepping in the Workplace." Medicine & Science in Sports & Exercise: Post Acceptance: November 21, 2017.
