This, according to a study by Ruth Brown and colleagues from Toronto’s York University, published in Medicine and Science in Sports and Exercise.
The study included 58 adult men and women of either normal weight (NW) or overweight (OW), who reported either attempting (WL) or not attempting weight loss (noWL)
Following 25 mins of exercise on a treadmill at either a moderate (60% HRmax) or a vigorous intensity (75% HRmax), participants were asked to estimated the number of calories they expended through exercise and create a meal that they believed to be calorically equivalent to the amount of calories they had just burnt.
Both the moderate and intense exercise groups were on average spectacularly wrong in their estimates.
In contrast, the active weight loss (WL) groups appeared to do far better at estimating energy consumption than the non-WL groups.
As an example, following vigorous exercise, the OW-noWL overestimated energy expenditure by 72%, and overestimated the calories in their food by 37%.
Although the WL groups did better, all groups showed a wide range of over and underestimation (-280 kcal to +702 kcal).
These findings show that while most people tend to over or underestimate caloric expenditure with exercise, overweight adults who are not attempting weight loss may be even more off the mark than others.
The most obvious solution would be to use some kind of monitor that does a better job of predicting calories consumed that just guessing.
That is of course, if overcompensating is not your goal (as in people who actually gain weight when they begin exercising).
For those interested in staying in energy balance, perhaps simply stepping on the scale regularly during the week should be enough.
For those interested in losing weight, they may need to be reminded that exercise (alone) is actually a pretty inefficient way to lose weight, so the calories burnt during exercise probably don’t matter all that much for weight management (despite all other benefits of exercise – its the calories you eat or drink that count).
Nevertheless, for what it is worth, a publication by Ruth Brown and colleagues from York University, Toronto, published in Obesity Research and Clinical Practice, suggests that people today may be more susceptible to obesity than just a few decades ago.
The study looks at self-reported dietary from 36,377 U.S. adults from the National Health and Nutrition Survey (NHANES) between 1971 and 2008 and physical activity frequency data from 14,419 adults between 1988 and 2006 (no activity data was available from earlier years).
Between 1971 and 2008, BMI, total caloric intake and carbohydrate intake increased 10-14%, and fat and protein intake decreased 5-9%.
Between 1988 and 2006, frequency of leisure time physical activity increased 47-120%.
However, for a given amount of caloric intake, macronutrient intake or leisure time physical activity, the predicted BMI was up to 2.3kg/m2 higher in 2006 that in 1988.
So unless there was some major systematic shift in what people were reporting (which seems somewhat unlikely) it is clear that factors other than diet and physical activity may be contributing to the increase in BMI over time – or in other words, it appears that people today, for the same caloric intake and physical activity, are more likely to have a higher BMI than people living a few decades ago.
There are of course several plausible biological explanations for these findings including epigenetics, obesogenic environmental toxins, alterations in gut microbiota to name a few.
If nothing else, these data support the notion that there is more to the obesity epidemic than just eating too much and not moving enough.
In my dealings with patients living with obesity, I am certainly aware of the many health problems attributed to excess weight – but that there may be a link between carpal tunnel syndrome (CTS) and obesity is new to me.
Thus, I was surprised to see a meta-analysis of Shiri and colleagues, published in Obesity Reviews, which shows a rather clear increased risk for CTS with increasing BMI.
Their analysis included 58 studies consisting of 1,379,372 individuals.
While having overweight increased the risk of CTS or carpal tunnel release 1.5-fold, having obesity increased this risk twofold. Each one-unit increase in body mass index increased the risk of CTS by 7.4%.
The associations did not differ between men and women, and they were independent of study design.
Exactly why excess weight would have an adverse effect on the median nerve is unclear but the authors speculate that this may have to do with increased workload or mechanical stretch.
Whether or not weight loss would help alleviated or prevent CTS is unclear.
I wonder is any of my clinical colleagues will have noted this in their patients.
In my conversations with skinny runners, they often cannot stop telling me how much satisfaction and enjoyment they get from their “runner’s high”. No wonder, they so often seem “addicted” to their runs (or other workouts).
In contrast, a “runner’s high” seldom comes up when any of my patients living with obesity talk about their exercise experiences (yes, many people with obesity exercise regularly).
Now, work by Maria Fernandes and colleagues from the University of Montreal, published in Cell Metabolism, reports findings in rats, which, if applicable to humans, may provide a biological explanation for this observation.
Building on previous studies showing that leptin modulates multiple components of brain reward circuitry, particularly in dopamine (DA) neurons of the ventral tegmental area (VTA), an area of the brain allegedly responsible for the “runner’s high”.
Using an elegant set of experiments, the researchers showed that leptin markedly reduces mice’s willingness to work for access to a running wheel or show other signs of seeking out exercise-induced reward.
In contrast, mice with a deletion of the signal transducer and activator of transcription-3 (STAT3), involved in leptin signalling in dopamine neurons of the VTA, showed greater interest in voluntary running.
In other words, STAT3 deletion increased the rewarding effects of running whereas intra-VTA leptin blocked it in a STAT3-dependent manner.
Together these findings strongly suggest that leptin influences the motivational effects of running via LepR-STAT3 modulation of dopamine tone.
Or, in other words, higher levels of leptin (as seen in people living with obesity) directly inhibit the rewarding nature of running, making it less likely to experience a runner’s high, than in someone with low leptin levels (as seen in people with low fat mass).
As to why this may be the case, the authors offer the following explanation:
“We speculate that in conditions of restricted food availability the mesolimbic DA system engages motivational processes concerned with obtaining food and more readily responds to leptin to decrease appetitive physical activity. On the other hand, during fed states, the actions of leptin may be biased toward hypothalamic processes that could increase physical activity as a means to maintain energy homeostasis.”
“While heightened physical activity during food restriction seems paradoxical to the maintenance of energy reserves, it is considered an expression of increased food acquisition behaviors. The capacity for endurance running in cursorial mammals is considered to enable food attainment when it is distant or requires pursuit. Correspondingly, the runner’s high may have evolved to encourage stamina and thereby increase the probability of return on this energetic investment.”
As the authors note, this line of reasoning is supported by the recent observation that exercise addiction in men is associated with low, fat-adjusted leptin levels.
In light of these findings, I also wonder if the “increase in energy levels”, which is rather consistently reported by my patients when they lose weight, may simply be reflective of their often dramatic reduction in leptin levels.
The amygdala is a part of the so-called limbic system that performs a primary role in the processing of memory, decision-making, and emotional reactions. The amygdala has also been implicated in a variety of mental health problems including anxiety, binge drinking and post-traumatic stress syndrome.
A study by Xu and colleagues, published in the Journal of Clinical Investigation now shows that in mice, activity of the estrogen receptor–α (ERα) in the medial amygdala may have a profound influence on the development of obesity – an effect, which appears to me largely mediated through effects on physical activity.
Building on previous work showing that ERα activity in the brain prevents obesity in both males and female rats, the researchers used a series of complex experiments to demonstrate that specific deletion of the ERα gene from SIM1 neurons, which are highly expressed in the medial amygdala, cause a marked decrease in physical activity and weight gain in both male and female mice fed with regular chow, without any increase in food intake. In addition, this deletion caused increased susceptibility to diet-induced obesity in males but not in females.
Deletion of the ERα receptor also blunted the body weight-lowering effects of a glucagon-like peptide-1-estrogen (GLP-1-estrogen) conjugate.
In contrast, over-expression or stimulation of SIM1 neurons increased physical activity in mice and protected them from diet-induced obesity.
These findings point to a novel mechanism of neuronal control of physical activity, which in turn appears to have important effects on the susceptibility to weight gain.