|How large is the impact of not being active on childhood, adolescent and adult obesity. Plus: Are there critical time periods in gestation, infancy childhood and adolescence?|
Scientists from Mater Health Services South Brisbane, the University College of London, and the Griffith University have now reviewed the relatively scarce experimental and abundant observational pertinent research in order to examine "the role of physical activity during periods of risk to reduce the probability of obesity onset and maintenance in adulthood" (Street. 2015).
Unfortunately, but not surprisingly, most of the experimental evidence comes from rodent studies. If we tried to summarize the results of these studies in a half-sentence it would say that they demonstrate general positive effects of early exercise on the outcomes for all animals irrespective of maternal obesity status or post-weaning diet.
"Although high-fat post-weaning diets resulted in generally fatter animals, the body composition, endocrine and immune system profiles of these animals were healthier than non-exercising high-fat diet animals and comparable to standard chow non-exercising animals" (Street. 2015).Interestingly, these effects do not disappear when the animals stop exercising. Rather than that studies indicate that exercise at an early age can protect animals against obesity onset for 5 weeks following exercise cessation (Caruso. 2013) - that's quite impressive if we take into account that rodents have a much shorter lifespan and a rapid early development period compared to humans (five rodent weeks in the early life are similar to several human years).
In spite of the fact that we don't know for sure for how long these protective effects will last in humans, there's little doubt that the same up-regulation of markers associated with increases in the skeletal muscle mitochondrial function, of which scientists believe that they protect the young rodents from obesity, will occur in humans as well (Shindo. 2014). Luckily, this is not the only thing we already know about rodents and assume for humans. Here's more:
Figure 1: If rodents are exercise in "childhood" (3WK), already, they will be significantly leaner - irrespective of whether they are fed an obesogenic HFD or the regular SMD diet (Wagener. 2012).
- muscle & brain are involved - next to changes in the mitochondria, the "stay lean" effect is also mediated by changes in structure and/or function of brain regions involved in appetite regulation in mouse & man (Street. 2015);
- males benefit more than females - the benefits of early exercise appear to be more pronounced for male vs. female animals (Schroeder. 2010); whether that's due to the higher muscle mass remains to be elucidated
In view of the fact that corresponding studies in human beings are not just time-consuming and expensive, but could also be unethical (think of kids being randomly assigned to non-exercise groups getting fat and sick as adults), it is not surprising that most of the evidence from human studies is of observational nature. Much in line with the findings from rodent studies, it has been suggested that three critical periods are important for obesity onset before adulthood: gestation and early infancy, the adiposity rebound and adolescence.
"Each period is characterized by substantial yet qualitatively different changes in growth and maturation. The culmination of each period represents a milestone in development and a subsequent reduction in the developmental plasticity of the maturing system. Given the inherently greater plasticity of earlier periods, obesity risk later in the life course is greater if the pre-conditions for obesity are established and maintained early. Disrupting the trajectory of obesity during development is likely to pay dividends in adulthood with a healthier body composition and metabolic profile. The disrupting effect of physical activity is less well understood in relation to obesity risk during and following critical periods" (Street. 2015).Let's briefly recap what we know about these periods and how exercise during gestation (obviously in this case the mother would exercise), early infancy and adolescence influence our obesity risk as adults:
Figure 2: Body fat levels according to quartiles of physical activity in late pregnancy (Harrod. 2014).
Overall, however, the existing evidence - specifically for strength training - is conflicting and we are far from fully understanding the complex interactions between physical exercise, nutrition during gestation and the weight and body composition of the newborn baby (a usual more does not necessarily help mor). What appears to be certain though is that if beneficial effects occur, those will last for at least 12-24 months (Mattran. 2011; Chu. 2013). In one study scientists even found significantly reduced obesity risks up to age 5 even if the physical activity of the mother was the only significant difference between the kids (Clapp. 1996)
Figure 3: Observational data shows that there is an inverse linear association between infant activity scores and body fat percentages as early as in year 1 (Li. 1995).
In contrast to rodents, the "early activity bonus" does not last long in humans. With 5 years "early active" children are no longer significantly leaner than their peers, unless they were continuously more active and/or were fed different diets.
In spite of the fact that early life activity does not provide life-long protection against obesity, though, the experimental and observational evidence of an inverse relationship between physical activity and body fat levels in infancy (Li. 1995) highlights the importance of leading an "active life" - in the most general sense - as early as possible. This is also relevant, because activity builds, while inactivity "kills" muscle, which is in turn associated with a further reduction in physical activity: Overweight infants, for example, have been shown to reach motor milestones later than leaner counterparts (Slining. 2010). Now you've just learned about the link between these milestones and staying lean in a previous paragraph. Accordingly, you will know that this means that the "sweet", chubby babies and toddlers may be caught in a vicious cycle of "obesity > low activity > lower muscle > lower activity > more obesity > lower activity ... "even before the know what the word "activity" means.
Figure 4: Normal body fat development during infancy (Street. 2015).
Obviously, you could counter that by calorically restricting your toddler, but this is (a) unhealthy and (b) the exact opposite of what the mums and dads do. In fact, way too many of them are priming their kids to become obese sugar addicts by giving their kids a sugar-sweetened beverage (a "healthy baby tea" *rofl*), whenever the kids utter a sound just to make them shut up do. It is thus no wonder that studies have linked infant temperaments that are characterized by negative affectivity/emotionality and a more frequent use of vocal signals such as crying and thus more frequent maternal feeding responses to increased fat gain (Baughcum. 1998; Darlington. 2006). That's alarming, even if it has not yet been conclusively shown that the two are causally and not just corollary related.
Does the Optimal Meal Frequency Depend on Age? Study Suggests: Kids Better Eat Often, Adolescents Rather Step Away From Their Sugary Sins - Quality Counts! Read more!
The earlier this rebound occurs, i.e. the earlier kids start to become fat again, the higher their risk of obesity as late as adulthood (Whitaker. 1998; Taylor. 2004). More specifically, studies like Whitaker et al. (1998) show that "early gainers" have a 20% higher obesity risk later in life and an extra 20% risk if they were already overweight - or I should say "over-fat" - at the age of 5-7 years.
It is thus only logical that studies show that obese pre-schoolers often become obese adults (Nader. 2012). Next to the Western junk-food diet, research findings in the recent decades support a relationship between increased obesity risk, low physical activity and high sedentary pursuits during childhood (Reilly. 2010).
- Adolescence - Adolescence is a critical phase in the development of our fat stores. While the years before puberty are characterized by both fat cell hypertrophy (the fat cell size increases), hyperplasia (more fat cells are formed) and apoptosis (fat cells die), most experts agree that the number of apoptotic processes in our adipose tissue declines rapidly as we approach puberty.
"It is generally thought that alteration in the size of fat cells in adulthood is achievable but maintenance of reduced fat cell size is likely to be difficult because of the mechanisms that may include, e.g. decreased leptin production. Furthermore, while an increase in adipo-cyte number is possible during adulthood, reversal of fat cell number does not occur. Consequently, adolescence represents an additional critical window when physical activity may affect obesity risk (reducing fat cell accretion) in ways it can-not during adulthood (reducing established fat cell number). " (Street. 2015)Since adolescence is also associated with an increase in lean mass, including skeletal muscle and bone, it is thus high time to start being, or - better - being even more active. After all, both muscle and bone mass are positively correlated with physical activity levels (Bailey. 1999; Völgyi. 2011).
- If you take a look at the data in Figure 6 it's yet not too late to start being active in puberty. The previously sedentary girls in Völgyi's study (Figure 6 | LH) who started to exercise regularly during puberty, for example, were similarly lean as their "always active" peers (HH). Probably because they expended more energy, but also because their exercise left them less hungry than their sedentary peers ... that sounds like bogus? Well, take a look at the reduced 24h energy intake Thivel et al. measured in youths who were locked in a metabolic chamber in response to high intensity exercise vs. sitting around (Thivel. 2012 | Figure 7) - exercise does not make you hungry.
Figure 7: Much in contrast to what you may expect, obese kids actually eat less, when they are forced to work out. In that, doing high intensity exercise (HIE) is more "satiating" than low intensity (Thivel. 2012).
In view of the previously referenced physiological peculiarities, adolescence appears to be the last stage in our development, where increased activity, alone, can go a long and consequential way. It is thus all the more important to break the cycle of being sedentary <> getting fatter before the transition into adulthood takes place. After all, the currently available research leaves little doubt that physical activity during adolescence will promote an adult body composition and metabolic profile that is associated with a reduced obesity risk, and reduced morbidity: Adult women who were more active adolescents, for example, are 50% less likely to be abdominally obese - even if all covariates are controlled for (da Silva. 2015). Physical activity interventions in adults, on the other hand, yield very ambiguous results. In most cases, however, being more active alone will not make a significant enough difference to trigger fat loss and instigate health improvements.
- Bailey, D. A., et al. "A six‐year longitudinal study of the relationship of physical activity to bone mineral accrual in growing children: the University of Saskatchewan Bone Mineral Accrual Study." Journal of Bone and Mineral Research 14.10 (1999): 1672-1679.
- Baughcum, Amy E., et al. "Maternal feeding practices and childhood obesity: a focus group study of low-income mothers." Archives of Pediatrics & Adolescent Medicine 152.10 (1998): 1010-1014.
- Caruso, V., H. Bahari, and M. J. Morris. "The Beneficial Effects of Early Short‐Term Exercise in the Offspring of Obese Mothers are Accompanied by Alterations in the Hypothalamic Gene Expression of Appetite Regulators and FTO (Fat Mass and Obesity Associated) Gene." Journal of neuroendocrinology 25.8 (2013): 742-752.
- Chu, Lisa, et al. "Impact of maternal physical activity and infant feeding practices on infant weight gain and adiposity." International journal of endocrinology 2012 (2012).
- Clapp, James F. "Morphometric and neurodevelopmental outcome at age five years of the offspring of women who continued to exercise regularly throughout pregnancy." The Journal of pediatrics 129.6 (1996): 856-863.
- D’Andrea, Francesco, et al. "Changing the metabolic profile by large-volume liposuction: a clinical study conducted with 123 obese women." Aesthetic plastic surgery 29.6 (2005): 472-478.
- da Silva Garcez, Anderson, et al. "Physical Activity in Adolescence and Abdominal Obesity in Adulthood: A Case-Control Study Among Women Shift Workers." Women & health ahead-of-print (2015): 1-13.
- Darlington, Anne-Sophie E., and Charlotte M. Wright. "The influence of temperament on weight gain in early infancy." Journal of Developmental & Behavioral Pediatrics 27.4 (2006): 329-335.
- Harrod, Curtis S., et al. "Physical activity in pregnancy and neonatal body composition: the healthy start study." Obstetrics & Gynecology 124.2, PART 1 (2014): 257-264.
- Li, Ruowei, et al. "Relation of activity levels to body fat in infants 6 to 12 months of age." The Journal of pediatrics 126.3 (1995): 353-357.
- Mattran, Kelly, et al. "Leisure-time physical activity during pregnancy and offspring size at 18 to 24 months." Journal of Physical Activity and Health 8.5 (2011): 655.
- Nader, Philip R., et al. "Next steps in obesity prevention: altering early life systems to support healthy parents, infants, and toddlers." Childhood Obesity (Formerly Obesity and Weight Management) 8.3 (2012): 195-204.
- Reilly, John J. "Low levels of objectively measured physical activity in preschoolers in child care." Medicine and science in sports and exercise 42.3 (2010): 502-507.
- Rosenbaum, Michael, et al. "Effects of Weight Change on Plasma Leptin Concentrations and Energy Expenditure 1." The Journal of Clinical Endocrinology & Metabolism 82.11 (1997): 3647-3654.
- Rosenbaum, Michael, et al. "Low-dose leptin reverses skeletal muscle, autonomic, and neuroendocrine adaptations to maintenance of reduced weight." Journal of Clinical Investigation 115.12 (2005): 3579.
- Rosenbaum, Michael, et al. "Leptin reverses weight loss–induced changes in regional neural activity responses to visual food stimuli." The Journal of clinical investigation 118.7 (2008): 2583.
- Schroeder, Mariana, et al. "Post-weaning voluntary exercise exerts long-term moderation of adiposity in males but not in females in an animal model of early-onset obesity." Hormones and behavior 57.4 (2010): 496-505.
- Schuster, Mark A., et al. "Changes in obesity between fifth and tenth grades: A longitudinal study in three metropolitan areas." Pediatrics 134.6 (2014): 1051-1058.
- Shi, Haifei, et al. "Diet‐induced Obese Mice Are Leptin Insufficient After Weight Reduction." Obesity 17.9 (2009): 1702-1709.
- Shindo, Daisuke, Tomokazu Matsuura, and Masato Suzuki. "Effects of prepubertal-onset exercise on body weight changes up to middle age in rats." Journal of Applied Physiology 116.6 (2014): 674-682.
- Slining, Meghan, et al. "Infant overweight is associated with delayed motor development." The Journal of pediatrics 157.1 (2010): 20-25.
- Street, S. J., J. C. K. Wells, and A. P. Hills. "Windows of opportunity for physical activity in the prevention of obesity." Obesity Reviews (2015).
- Taylor, Rachael W., et al. "Rate of fat gain is faster in girls undergoing early adiposity rebound." Obesity research 12.8 (2004): 1228-1230.
- Thivel, David, et al. "The 24-h energy intake of obese adolescents is spontaneously reduced after intensive exercise: a randomized controlled trial in calorimetric chambers." PloS one 7.1 (2012): e29840.
- Wagener, A., A. O. Schmitt, and G. A. Brockmann. "Early and late onset of voluntary exercise have differential effects on the metabolic syndrome in an obese mouse model." Experimental and Clinical Endocrinology and Diabetes 120.10 (2012): 591.
- Whitaker, Robert C., et al. "Early adiposity rebound and the risk of adult obesity." Pediatrics 101.3 (1998): e5-e5.