In the same week that we learned about the devastating metabolic effects of the weight loss induced by hours-long exhausting workouts in participants in the “Biggest Loser”, a paper byJenna Gillen and colleagues from McMaster University, Hamilton, Canada, published in PLOS One, shows that all it takes is one minute of vigorous all out exercise to significantly improve your health.
Unbelievable as it sounds, the rather rigorous randomised controlled 12-week trial in 27 sedentary men showed just that.
The researchers divided the participants into three groups: three weekly sessions of sprint interval training (SIT) involving a total of 1 minute of intense exercise within a 10-minute time commitment (n = 9), three weekly sessions of traditional moderate-intensity continuous training (MICT) involving 50 minutes of continuous exercise per session (n = 10) or no training controls (n = 6).
SIT involved 3×20-second ‘all-out’ cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W.
Peak oxygen uptake increased by around 20% in both exercise groups as did insulin sensitivity as assessed by an intravenous glucose tolerance test.
Participants in both exercise groups also lost about 2% of body fat.
Furthermore, metabolic and mitochondrial function (as measured in muscle biopsies) improved similarly in both exercise groups.
Thus, the researchers conclude that
“12 weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.”
This is not just news for people who find it hard to make the time for exercise (e.g. due to work or family commitments).
It is also of interest to anyone just trying to get fitter without wanting to invest hours in the gym.
The key however, is the term “all-out” – the 60 sec bout of exercise has to be at virtually maximum capacity, which may increase the risk of injury in some individuals and can hardly be described as “pleasant”.
As for the implications for my patients, who often present with considerable amount of excess weight and thus, every movement (e.g. just walking up a flight of stairs) often appears to happen at near maximum exercise capacity (no surprise given the tremendous weight that they are lifting and carrying), I can only speculate, of what these bouts of activity may have on their metabolic health.
Whatever the case, this study certainly corroborates the notion that one does not have to spend hours in the gym to improve one’s health.
One of the most pervasive problems with quitting cigarettes, is the accompanying weight gain – in fact, post-cessation weight gain is reportedly the number one reason why smokers, especially women, fail to stop smoking or relapse after stopping.
But what exactly happens when you stop smoking?
This is the topic of a comprehensive review article by Kindred Harris and colleagues published in Nature Reviews Endocrinology.
The paper begins by examining the magnitude of weight gain generally experienced after smoking cessation – an amount that can vary considerably between individuals.
As for mechanisms, the authors note that,
“Several theories have been proposed to explain increased food intake after smoking cessation. One theory is that the ability of nicotine to suppress appetite is reversed. Substitution reinforcement, which replaces the rewards of food with the rewards of cigarettes could occur. Nicotine absence increases the rewarding value of food. Reward circuitries in the brain, similar to those activated by smoking, are activated by increased intake of food high in sugar and fat. Furthermore, nicotine withdrawal leads to an elevated reward threshold, which might cause individuals to eat more snacks that are high in carbohydrates and sugars.”
There are also known effects of smoking on impulsive overeating and individuals with binge eating disorder are at risk of even greater weight gain with cessation.
Smoking cessation also has metabolic effects including a drop in metabolic rate that may promote weight gain and new evidence shows that smoking cessation can even change your gut microbiota.
The authors provide evidence that behavioural interventions can prevent much of the cessation weight gain and argue that such programs should be offered with cessation programs.
Finally, it is important to always remember that the health benefits of smoking cessation by far outweigh any health risks from weight gain, which is why fear of weight gain should never stop anyone from quitting.
While this approach can be highly effective, it does require training, resources and ongoing (lifelong?) interventions (not unlike most other chronic diseases).
Now a rather comprehensive paper by Soleyman and colleagues from the University of Birmingham, Alabama, published in Obesity Reviews provides an overview of obesity management in primary care.
As readers are well aware, our body weight are tightly regulated by a complex neuroendocrine system and defends us agains weight loss through a multi-faceted physiological response to prevent further weight loss and restore body weight.
As the authors note,
“To maintain weightloss, individuals must adhere to behaviours that oppose these physiological adaptations and the other factorsfavouring weight regain. However, it is difﬁcult for peoplewith obesity to overcome physiology with behaviour over the long term. Common reasons for weight regain include decreased caloric expenditure, decreased self-weighing frequency, increased caloric intake, increased fat intake and eating disinhibition over time.”
The paper provides a succinct overview of the evidence supporting behavioural, medical and surgical obesity treatments.
It also reiterates the basic principles of obesity management as outlined in the various guidelines:
1. Obesity is a chronic disease that requires long-term management. It is important to approach patients with information regarding the health implications.
2. The goal of obesity treatment is to improve the health of the patient, and it is not intended for cosmetic purposes.
3. The cornerstone of therapy is comprehensive lifestyle intervention from informed PCPs or other healthcare professionals.
4. The initial goal of therapy is a weight loss of 5–10% in most patients, as this is sufﬁcient to ameliorate many weight-related complications. However, weight loss of ≥10% may be needed to improve certain weight-related complications, such as obstructive sleep apnoea.
5. Consideration should be given to the use of a weight-loss medication or possible bariatric surgery, as the addition of these treatment modalities to lifestyle therapy can promote greater weight loss and maintain the weight loss for a longer period of time.
6. It is important for clinicians to evaluate the patient for weight-related complications, that can be improved by weight loss, and to consider such patients for more aggressive treatment.
As for how to get more primary care clinics to actually implement these approaches, the authors note that,
“Primary care practitioners need to address the problem of obesity in their patients, just as they would with any other chronic condition such as hypertension or type 2 diabetes, and to ensure that their patients are aware of the health risks of obesity.”
Again something that the Canadian Obesity Network is working hard to promote in this country.
A blood pressure that is too high can kill you – so can a blood pressure that is too low.
A blood sugar that is too high can kill you – so can a blood sugar that is too low.
It turns out that BMI is no different – too high and too low both carry a risk – a risk, however, that is substantially confounded by actual body fat%, which is not reliably measured by BMI.
This is basically the message in a paper by my colleagues Raj Padwal and co from the University of Alberta in a paper published in the Annals of Internal Medicine.
The researchers looked at data from about 50,000 women and 5,000 men (mean age, 63.5 years; mean BMI, 27.0 kg/m2) referred for bone mineral density (BMD) testing with dual-energy x-ray absorptiometry (DXA), which they linked to administrative databases.
Given the size and demographics of the cohort, death occurred in almost 5000 women over a median of 6.7 years and 1000 men over a median of 4.5 years.
Women in the lowest BMI and body fat% quintiles had a 40% higher risk of dying (compared to quintile 3). Risk of dying were also about 20% greater in the highest body fat% quintile for women.
Similarly in men, both low BMI (HR, 1.45 for quintile 1) and high body fat percentage (HR, 1.59 for quintile 5) were associated with increased mortality.
The exciting bit about this study is that the researchers had both BMI and body fat% available to them and were able to show that both variables independently of each other contribute to mortality risk.
Thus, the worst possible combination in both men and women was low BMI and high body fat%.
Or, as the authors put it,
“Low BMI and high body fat percentage were both associated with increased all-cause mortality. Mortality increased as BMI decreased and body fat percentage increased…..Thus, our results suggest that BMI may be an inappropriate surrogate for adiposity, and this limitation may explain the presence of the obesity paradox in many studies.”
As the authors discuss, these finding should have clinical implications as they clearly demonstrate the limitations of BMI as a measure of health risk.
“..our findings underscore that the risk for all-cause mortality increases with both increasing adiposity and decreasing BMI in a general population of middle-aged and older adults. These findings also suggest the importance of using direct measures of adiposity when building prognostic or even exploratory models.”
Now a study by Crump and colleagues published in JAMA Intern Medicine suggests that some of this risk may be mitigated by increased physical fitness.
The cohort study involving over 1.5 million Swedish young men in Sweden, who underwent standardized aerobic capacity, muscular strength, and BMI measurements obtained at a military conscription examination and were followed for up to 40 years.
Almost 100,000 men went on to develop hypertension, whereby both high BMI and low aerobic capacity (but not muscular strength) were associated with increased risk of hypertension, independent of family history or socioeconomic factors.
A combination of high BMI (overweight or obese vs normal) and low aerobic capacity (lowest vs highest tertile) was associated with the highest risk of hypertension.
The association with aerobic fitness was apparent at every level of BMI.
Form this study the authors conclude that high BMI and low aerobic capacity in late adolescence are associated with higher risk of hypertension in adulthood.
Although one must also be cautious in assuming causality with regard to associations found in such studies, the observations are certainly compatible with the notion that increased cardiorespiratory fitness may well mitigate some of the impact of increased BMI on hypertension risk.