A meta-analysis questions the cognitive benefits of physical activity.

I give up. If anything was supposed to have been proven I would have thought it would be that exercise has a beneficial effect on brain health and cognition. Now Ciria et al. offer the following in Nature Human Biology:

Extensive research links regular physical exercise to an overall enhancement of cognitive function across the lifespan. Here we assess the causal evidence supporting this relationship in the healthy population, using an umbrella review of meta-analyses limited to randomized controlled trials (RCTs). Despite most of the 24 reviewed meta-analyses reporting a positive overall effect, our assessment reveals evidence of low statistical power in the primary RCTs, selective inclusion of studies, publication bias and large variation in combinations of pre-processing and analytic decisions. In addition, our meta-analysis of all the primary RCTs included in the revised meta-analyses shows small exercise-related benefits (d = 0.22, 95% confidence interval 0.16 to 0.28) that became substantially smaller after accounting for key moderators (that is, active control and baseline differences; d = 0.13, 95% confidence interval 0.07 to 0.20), and negligible after correcting for publication bias (d = 0.05, 95% confidence interval −0.09 to 0.14). These findings suggest caution in claims and recommendations linking regular physical exercise to cognitive benefits in the healthy human population until more reliable causal evidence accumulates.

I can not offer an informed opinion on this abstract because my usual access to journals through the University of Wisconsin library does not work with Nature Human Behavior. However, I can point you to an excellent commentary by Claudia Lopez Lloreda that discusses the meta-analysis done by Ciria et al. and gives a summary of several recent studies on exercise and brain health.

Rigorous study does not find that exercise and mindfulness training improve cognitive function in older adults.

Wow, here is a study by Lenze et al. - not confirming the results of numerous other less rigorous studies reported in MindBlog posts - that is unable to demonstrate that the use of mindfulness training, exercise, or a combination of both can significantly improving cognitive function in older adults with subjective cognitive concerns. In their randomized clinical trial that included 585 participants, mindfulness training, exercise, or both did not result in significant differences in improvement in episodic memory or executive function composite scores at 6 months. Gretchen Reynolds provides context and a summary of the work in a Washington Post article.

Magic mind therapy….. Moving your body.

Gretchen Reynolds interviews Jennifer Heisz about the contents of her new book "Move the Body, Heal the Mind," which details the latest science about exercise and mental health, especially its potential to reduce anxiety and stress. The brief reprieve from anxiety than can sometimes be experienced after a workout is due to the release of neuropeptide Y, known to dampen hyperactivity of the anxious amygdala. Exercise also can reduce stress-induced body inflammation that damages cells and affects mood. These effects require only about a quarter of the normally recommended 150 minutes of moderate to vigorous exercise a week, so the exercise prescription for mental health seems to be less than that for physical health.

MindBlog keeps the blood pumping

Discussion of the therapeutic effects of exercise has been one of the topic threads in MindBlog since its beginning...reporting effects of different styles of exercise on metabolic health, gene expression, markers of aging, etc. Two recent fads have been the "7-minute exercise' and ever more brief forms of intense interval exercises. Parker-Pope now points out the perfect exercises for a 78 year old fart like myself who wants to get up from his computer every hour or so to move and get the blood stirring a bit, but doesn't want to be bouncing  up and down off the floor multiple times. Trainer Chris Jordan now offers the Standing 7- inute workout, suited to bodies of any age, size or fitness level. 

Social Media - no effect on adolescent life satisfaction?

Orben et al. (open source article) provide a study whose results contest a common opinion, reinforced by several previous studies, that adolescents who use social media extensively are more likely to be depressed and have low self esteem. They used...

...large-scale representative panel data to disentangle the between-person and within-person relations linking adolescent social media use and well-being. We found that social media use is not, in and of itself, a strong predictor of life satisfaction across the adolescent population. Instead, social media effects are nuanced, small at best, reciprocal over time, gender specific, and contingent on analytic methods.

They note limitations of current published research:

Focused on cross-sectional relations, scientists have few means of parsing longitudinal effects from artifacts introduced by common statistical modeling methodologies. Furthermore, the volume of data under analysis, paired with unchecked analytical flexibility, enables selective research reporting, biasing the literature toward statistically significant effects. Nevertheless, trivial trends are routinely overinterpreted by those under increasing pressure to rapidly craft evidence-based policies.

The UK study examined data on 12,672 10-15 year old. Two summary graphics are provided. One clip:

...the importance of gender was apparent: Only 16% of significant models arose from male data.

The last two paragraphs:

The relations linking social media use and life satisfaction are, therefore, more nuanced than previously assumed: They are inconsistent, possibly contingent on gender, and vary substantively depending on how the data are analyzed. Most effects are tiny—arguably trivial; where best statistical practices are followed, they are not statistically significant in more than half of models. That understood, some effects are worthy of further exploration and replication: There might be small reciprocal within-person effects in females, with increases in life satisfaction predicting slightly lower social media use, and increases in social media use predicting tenuous decreases in life satisfaction.

With the unknowns of social media effects still substantially outnumbering the knowns, it is critical that independent scientists, policymakers, and industry researchers cooperate more closely. Scientists must embrace circumspection, transparency, and robust ways of working that safeguard against bias and analytical flexibility. Doing so will provide parents and policymakers with the reliable insights they need on a topic most often characterized by unfounded media hype. Finally, and most importantly, social media companies must support independent research by sharing granular user engagement data and participating in large-scale team-based open science. Only then will we truly unravel the complex constellations of effects shaping young people in the digital age.

How our bones regulate our weight.

Jansson et al. report that bones have a gravity sensor that initiates metabolic changes that compensate for a sudden change in body weight to return the body to its desired homeostatic weight set point:

Significance

The only known homeostatic regulator of fat mass is the leptin system. We hypothesized that there is a second homeostat regulating body weight with an impact on fat mass. In this study we have added and removed weight loads from experimental animals and measured the effects on the biological body weight. The results demonstrate that there is a body weight homeostat that regulates fat mass independently of leptin. As the body weight-reducing effect of increased loading was dependent on osteocytes, we propose that there is a sensor for body weight in the long bones of the lower extremities acting as “body scales.” This is part of a body weight homeostat, “gravitostat,” that keeps body weight and body fat mass constant.

Abstract

Subjects spending much time sitting have increased risk of obesity but the mechanism for the antiobesity effect of standing is unknown. We hypothesized that there is a homeostatic regulation of body weight. We demonstrate that increased loading of rodents, achieved using capsules with different weights implanted in the abdomen or s.c. on the back, reversibly decreases the biological body weight via reduced food intake. Importantly, loading relieves diet-induced obesity and improves glucose tolerance. The identified homeostat for body weight regulates body fat mass independently of fat-derived leptin, revealing two independent negative feedback systems for fat mass regulation. It is known that osteocytes can sense changes in bone strain. In this study, the body weight-reducing effect of increased loading was lost in mice depleted of osteocytes. We propose that increased body weight activates a sensor dependent on osteocytes of the weight-bearing bones. This induces an afferent signal, which reduces body weight. These findings demonstrate a leptin-independent body weight homeostat (“gravitostat”) that regulates fat mass.

Exercise alters the microbiome, enhancing immune function.

Reynolds points to interesting work by Allen et al. showing that exercise by lean, but not obese, subjects enhances microbial production of short chain fatty acids that suppress tissue irritation and inflammation in the colon as well as the rest of the body. These short fatty acids also boost metabolism and dampen the insulin resistance that is a precursor to diabetes.

Exercise slows the aging of heart cells.

Ludlow et al. find (in female rats) that exercise slows the loss of caps (telomeres) on the end of chromosomes that prevent damage or fraying of DNA. (Shorter telomeres indicate biologically older cells. If they become too short, the cells can die.) Even a single 30 min treadmill period elevates the level of proteins that maintain telomere integrity. This elevation diminishes after an hour, but the changes might accumulate with repeated training. Here is the technical abstract:

Age is the greatest risk factor for cardiovascular disease. Telomere length is shorter in the hearts of aged mice compared to young mice, and short telomere length has been associated with an increased risk of cardiovascular disease. One year of voluntary wheel running exercise attenuates the age-associated loss of telomere length and results in altered gene expression of telomere length maintaining and genome stabilizing proteins in heart tissue of mice. Understanding the early adaptive response of the heart to an endurance exercise bout is paramount to understanding the impact of endurance exercise on heart tissue and cells. To this end we studied mice before (BL), immediately post (TP1) and one-hour following (TP2) a treadmill running bout. We measured the changes in expression of telomere related genes (shelterin components), DNA damage sensing (p53, Chk2) and DNA repair genes (Ku70, Ku80), and MAPK signaling. TP1 animals had increased TRF1 and TRF2 protein and mRNA levels, greater expression of DNA repair and response genes (Chk2 and Ku80), and greater protein content of phosphorylated p38 MAPK compared to both BL and TP2 animals. These data provide insights into how physiological stressors remodel the heart tissue and how an early adaptive response mediated by exercise may be maintaining telomere length/stabilizing the heart genome through the up-regulation of telomere protective genes.

Some brain benefits of exercise evaporate after a short rest.

Gretchen Reynolds points to a study by kinesiologists at the Univ. of Maryland that probed what happens when very active and fit people stop exercising for awhile. They found that after ten days of inactivity, blood flow to many parts of the brain diminishes, particularly to the hippocampus, which is important in learning and memory. Here's the abstract:

While endurance exercise training improves cerebrovascular health and has neurotrophic effects within the hippocampus, the effects of stopping this exercise on the brain remain unclear. Our aim was to measure the effects of 10 days of detraining on resting cerebral blood flow (rCBF) in gray matter and the hippocampus in healthy and physically fit older adults. We hypothesized that rCBF would decrease in the hippocampus after a 10-day cessation of exercise training. Twelve master athletes, defined as older adults (age 50 years or older) with long-term endurance training histories (at least 15 years), were recruited from local running clubs. After screening, eligible participants were asked to cease all training and vigorous physical activity for 10 consecutive days. Before and immediately after the exercise cessation period, rCBF was measured with perfusion-weighted MRI. A voxel-wise analysis was used in gray matter, and the hippocampus was selected a priori as a structurally defined region of interest (ROI), to detect rCBF changes over time. Resting CBF significantly decreased in eight gray matter brain regions. These regions included: (L) inferior temporal gyrus, fusiform gyrus, inferior parietal lobule, (R) cerebellar tonsil, lingual gyrus, precuneus, and bilateral cerebellum (FWE p less than 0.05). Additionally, rCBF within the left and right hippocampus significantly decreased after 10 days of no exercise training. These findings suggest that the cerebrovascular system, including the regulation of resting hippocampal blood flow, is responsive to short-term decreases in exercise training among master athletes. Cessation of exercise training among physically fit individuals may provide a novel method to assess the effects of acute exercise and exercise training on brain function in older adults.

To remember something better, wait, then exercise.

Another nice bit on what exercise can do for you.  The abstract from van Dongen et al.:

Highlights

•Performing aerobic exercise 4 hr after learning improved associative memory 

•Exercise at this time also increased hippocampal pattern similarity during retrieval 

•Exercise performed immediately after learning had no effect on memory retention 

•Exercise could have potential as a memory intervention in educational settings

Summary

Persistent long-term memory depends on successful stabilization and integration of new memories after initial encoding. This consolidation process is thought to require neuromodulatory factors such as dopamine, noradrenaline, and brain-derived neurotrophic factor. Without the release of such factors around the time of encoding, memories will decay rapidly. Recent studies have shown that physical exercise acutely stimulates the release of several consolidation-promoting factors in humans, raising the question of whether physical exercise can be used to improve memory retention. Here, we used a single session of physical exercise after learning to exogenously boost memory consolidation and thus long-term memory. Three groups of randomly assigned participants first encoded a set of picture-location associations. Afterward, one group performed exercise immediately, one 4 hr later, and the third did not perform any exercise. Participants otherwise underwent exactly the same procedures to control for potential experimental confounds. Forty-eight hours later, participants returned for a cued-recall test in a magnetic resonance scanner. With this design, we could investigate the impact of acute exercise on memory consolidation and retrieval-related neural processing. We found that performing exercise 4 hr, but not immediately, after encoding improved the retention of picture-location associations compared to the no-exercise control group. Moreover, performing exercise after a delay was associated with increased hippocampal pattern similarity for correct responses during delayed retrieval. Our results suggest that appropriately timed physical exercise can improve long-term memory and highlight the potential of exercise as an intervention in educational and clinical settings.

How exercise enhances brain renewal and growth.

Several studies by now have shown that exercises enhances the production of BDNF (Brain Derived Trophic Factor), which leads to the creation of new nerve cells in the hippocampus (essential for learning and memory - for more on the link of exercise to better mental capacity in older people, see Reynolds.). Sleiman et al. now show that in mice the metabolite β-hydroxybutyrate which increases during heavy exercise induces the activity of BNDF gene promoters. Their detailed abstract:

Exercise induces beneficial responses in the brain, which is accompanied by an increase in BDNF, a trophic factor associated with cognitive improvement and the alleviation of depression and anxiety. However, the exact mechanisms whereby physical exercise produces an induction in brain Bdnf gene expression are not well understood. While pharmacological doses of HDAC inhibitors exert positive effects on Bdnf gene transcription, the inhibitors represent small molecules that do not occur in vivo. Here, we report that an endogenous molecule released after exercise is capable of inducing key promoters of the Mus musculus Bdnf gene. The metabolite β-hydroxybutyrate, which increases after prolonged exercise, induces the activities of Bdnf promoters, particularly promoter I, which is activity-dependent. We have discovered that the action of β-hydroxybutyrate is specifically upon HDAC2 and HDAC3, which act upon selective Bdnf promoters. Moreover, the effects upon hippocampal Bdnf expression were observed after direct ventricular application of β-hydroxybutyrate. Electrophysiological measurements indicate that β-hydroxybutyrate causes an increase in neurotransmitter release, which is dependent upon the TrkB receptor. These results reveal an endogenous mechanism to explain how physical exercise leads to the induction of BDNF.

Exercise and intermittent fasting improve brain plasticity and health

I have had numerous requests for a PDF of the article referenced in a Dec. 29, 2014 post - on how exercise and fasting stimulate brain plasticity and resilience - with the same title as this post.  It turns out that the reference pointed to by the link is open source. Readers should be able to download the article for themselves. Here is the text of the original post:

I thought it might be useful to point to this brief review by Praag et al. that references several recent pieces of work presented at a recent Soc. for Neuroscience Meeting symposium. The experiments indicate that exercise and intermittent energy restriction/fasting may optimize brain function and forestall metabolic and neurodegenerative diseases by enhancing neurogenesis, synaptic plasticity and neuronal stress robustness.  (Motivated readers can obtain the article from me.) Here is their central summary figure:

Exercise and IER/fasting exert complex integrated adaptive responses in the brain and peripheral tissues involved in energy metabolism. As described in the text, both exercise and IER enhance neuroplasticity and resistance of the brain to injury and disease. Some of the effects of exercise and IER on peripheral organs are mediated by the brain, including increased parasympathetic regulation of heart rate and increased insulin sensitivity of liver and muscle cells. In turn, peripheral tissues may respond to exercise and IER by producing factors that bolster neuronal bioenergetics and brain function. Examples include the following: mobilization of fatty acids in adipose cells and production of ketone bodies in the liver; production of muscle-derived neuroactive factors, such as irisin; and production of as yet unidentified neuroprotective “preconditioning factors.” Suppression of local inflammation in tissues throughout the body and the nervous system likely contributes to prevention and reversal of many different chronic disease processes.

Aging brains - more physical activity, more gray matter, less Alzheimers.

I like to pass on any work I see relevant to exercise, aging, and the brain. The following is from Raji et al.

BACKGROUND: Physical activity (PA) can be neuroprotective and reduce the risk for Alzheimer's disease (AD). In assessing physical activity, caloric expenditure is a proxy marker reflecting the sum total of multiple physical activity types conducted by an individual. 

OBJECTIVE: To assess caloric expenditure, as a proxy marker of PA, as a predictive measure of gray matter (GM) volumes in the normal and cognitively impaired elderly persons. 

METHODS: All subjects in this study were recruited from the Institutional Review Board approved Cardiovascular Health Study (CHS), a multisite population-based longitudinal study in persons aged 65 and older. We analyzed a sub-sample of CHS participants 876 subjects (mean age 78.3, 57.5% F, 42.5% M) who had i) energy output assessed as kilocalories (kcal) per week using the standardized Minnesota Leisure-Time Activities questionnaire, ii) cognitive assessments for clinical classification of normal cognition, mild cognitive impairment (MCI), and AD, and iii) volumetric MR imaging of the brain. Voxel-based morphometry modeled the relationship between kcal/week and GM volumes while accounting for standard covariates including head size, age, sex, white matter hyperintensity lesions, MCI or AD status, and site. Multiple comparisons were controlled using a False Discovery Rate of 5 percent. 

RESULTS: Higher energy output, from a variety of physical activity types, was associated with larger GM volumes in frontal, temporal, and parietal lobes, as well as hippocampus, thalamus, and basal ganglia. High levels of caloric expenditure moderated neurodegeneration-associated volume loss in the precuneus, posterior cingulate, and cerebellar vermis. 

CONCLUSION: Increasing energy output from a variety of physical activities is related to larger gray matter volumes in the elderly, regardless of cognitive status.

Muscle mass and nerve control enhanced in octogenarian athletes.

Power et al. expand their earlier studies on active runners ~65 years old to find ~14% greater muscle mass and ~28% more functioning motor nerve units in octogenarian masters athletes than in healthy age-matched controls.

Our group has shown a greater number of functioning motor units (MU) in a cohort of highly-active older(~65y) masters runners relative to age-matched controls. Owing to the precipitous loss in the number of functioning MUs in the 8th and 9th decade of life it is unknown whether older world class octogenarian masters athletes (MA) would also have greater numbers of functioning MUs (MUNE) compared with age-matched controls. We measured MU numbers and neuromuscular transmission stability in the tibialis anterior of world champion MAs (~80y), and compared the values to healthy age-matched controls (~80y). Decomposition-enhanced spike-triggered averaging was used to collect surface and intramuscular electromyography signals during dorsiflexion at ~25% of maximum voluntary isometric contraction(MVC). Near fibre (NF) MU potential analysis was used to assess neuromuscular transmission stability. For the MAs as compared with age-matched controls; the amount of excitable muscle mass (CMAP) was 14% greater (p less than 0.05), there was a trend (p=0.07) towards a 27% smaller surface detected motor unit potential - representative of less collateral reinnervation, and 28% more functioning MUs (p less than 0.05). Additionally, the MAs had greater MU neuromuscular stability than the controls as indicated by lower NF jitter and jiggle values (p less than 0.05). These results demonstrate that high performing octogenarians better maintain neuromuscular stability of the MU and mitigate the loss of MUs associated with aging well into the later decades of life during which time the loss of muscle mass and strength become functionally relevant. Future studies need to identify the concomitant roles genetics and exercise play in neuroprotection.

Overkill in techno-aids for 'Mens Sana in Corpore Sano'

None of us would argue with the 'sound mind in a sound body' injunction from Juvenal’s Latin satires (~100 AD), a goal that can be accomplished by diligent pursuit of a few simple activities. Two NYTimes articles note how modern technology manages, for a profit, to vastly encumber that pursuit.

With regard to 'sound mind,' Gelles notes:

The other morning, I woke up and brewed a cup of Mindful Lotus tea ($6 for 20 bags). On the subway, I loaded the Headspace app on my iPhone and followed a guided mindfulness exercise ($13 a month for premium content). Later in the day, I dropped by Mndfl, a meditation studio in Greenwich Village ($20 for a 30-minute class)...There are more than two dozen mindfulness apps for smartphones, some offering $400 lifetime subscriptions. The Great Courses has two mindfulness packages, each with a couple of dozen DVDs for $250. For an enterprising contemplative, it’s never been easier to make a buck...On a recent trip to Whole Foods, near the kombucha, I came across a new product from the health food maker Earth Balance: a dairy-free mayonnaise substitute called Mindful Mayo ($4.50 a jar). Then, in line, I picked up a copy of Mindful magazine ($6)....With so many mindful goods and services for sale, it can be easy to forget that mindfulness is a quality of being, not a piece of merchandise

...with so many cashing in on the meditation craze, it’s hard not to wonder whether something essential is being lost...Increasingly, mindfulness is being packaged as a one-minute reprieve, an interlude between checking Instagram and starting the next episode of “House of Cards.” One company proclaims it has found the “minimum effective dose” of meditation that will change your life. On Amazon, you can pick up “One-Minute Mindfulness: 50 Simple Ways to Find Peace, Clarity, and New Possibilities in a Stressed-Out World.” Dubious courses promise to help people “master mindfulness” in a few weeks.

More often than not, however, the people I know who take time to meditate — carefully observing thoughts, emotions and sensations — are sincere in their aspirations to become less stressed, more accepting and at least a little happier.

Hutchinson discusses the greater than billion dollar market for body fitness aids (which are not used by more than half their buyers six months after their purchase) suggesting:

...a more fundamental question about our rapid adoption of wearable fitness tech: Is the data we collect with these devices actually useful?...Last September, in The British Journal of Sports Medicine, Australian researchers published a review of studies that compared subjective and objective measures of “athlete well-being” during training. The objective measures included state-of-the-art monitoring of heart rate, blood, hormones and more; the subjective measure boiled down to asking the athletes how they felt. The results were striking: The researchers found that as the athletes worked out, their own perception registered changes in training stress with “superior sensitivity and consistency” to the high tech measures...running with a GPS watch “slackens the bond between perception and action.” In other words, when you’re running, instead of speeding up or slowing down based on immediate and intuitive feedback from your body and environment, you’re inserting an unwieldy extra cognitive step that relies on checking your device as you go.

On the positive side:

Health researchers also want to use your tracked data to figure out what works in the real world to improve health and fitness, rather than testing theories in the artificial conditions of the lab. An analysis of in-the-wild data from 4.2 million MyFitnessPal users, for example, recently yielded unexpected insights into the habits of successful weight-losers compared with unsuccessful ones: They ate nearly a third more fiber, and 11 percent less meat. And the dietary changes the successful dieters made between 2014 and 2015 bucked broader trends: They consumed more grains, cereal and raw fruit, but fewer eggs.

As prosaic as it sounds, this is the greatest promise of the wearables revolution. Once the novelty of tracking your exercise habits wears off, knowing how many steps you took today or what your resting heart rate was yesterday soon loses its interest. But together, 100 million of us wearing wristbands could uncover some truly valuable insights into what works to make us healthier and fitter.

Perhaps the most effective and simple way to increase aerobic fitness: use a jump rope!

New nerve cells in the brain generated best by sustained aerobic exercise

Nokia et al. show, in rats, that aerobic exercise is much more effective than high-intensity interval training or resistance training in enhancing generation of new nerve cells in the hippocampus of the brain.

Key points

Aerobic exercise such as running enhances adult hippocampal neurogenesis (AHN) in rodents. 

Little is known about the effects of high-intensity interval training (HIT) or of purely anaerobic resistance training on AHN. 

Here, compared to a sedentary lifestyle, we report a very modest effect of HIT and no effect of resistance training on AHN in adult male rats. 

We find most AHN in rats that were selectively bred for an innately high response to aerobic exercise that also run voluntarily and - increase maximum running capacity. 

Our results confirm that sustained aerobic exercise is key in improving AHN.

Abstract

Aerobic exercise, such as running, has positive effects on brain structure and function, for example, adult hippocampal neurogenesis (AHN) and learning. Whether high-intensity interval training (HIT), referring to alternating short bouts of very intense anaerobic exercise with recovery periods, or anaerobic resistance training (RT) has similar effects on AHN is unclear. In addition, individual genetic variation in the overall response to physical exercise likely plays a part in the effects of exercise on AHN but is less studied. Recently, we developed polygenic rat models that gain differentially for running capacity in response to aerobic treadmill training. Here we subjected these Low Response Trainer (LRT) and High Response Trainer (HRT) adult male rats to various forms of physical exercise for 6 to 8 weeks and examined its effects on AHN. Compared to sedentary animals, the highest number of doublecortin-positive hippocampal cells was observed in HRT rats that ran voluntarily on a running wheel while HIT on the treadmill had a smaller, statistically non-significant effect on AHN. AHN was elevated in both LRT and HRT rats that endurance trained on a treadmill compared to those that performed RT by climbing a vertical ladder with weights, despite their significant gain in strength. Furthermore, RT had no effect on proliferation (Ki67), maturation (doublecortin) or survival (BrdU) of new adult-born hippocampal neurons in adult male Sprague-Dawley rats. Our results suggest physical exercise promotes AHN most if it is aerobic and sustained, and especially when accompanied by a heightened genetic predisposition for response to physical exercise.

Modest exercise gives maximum health benefits.

Gretchen Reynolds points to a study in the Mayo Clinic Proceedings that reviews studies published in PubMed since 2000 that included at least 500 runners and 5-year follow-up to analyze the relationship between running, cardiovascular disease, and all-cause mortality. The optimal dose of running required for protection is surprisingly small. Running for 20-30 minutes twice per week appears to give maximum benefits. Three to four times the duration of walking is needed to achieve the same benefits.

Exercise enhances frontal brain lateralization characteristic of younger brains.

As we age beyond 40 years or so, mental tasks that require attention, problem solving, decision-making and other types of high-level thinking become less localized to one of our frontal lobes and expand to engage both hemispheres of our prefrontal cortex. This represents a general reorganization and weakening of our brains' function with age. Hyodo et. al. show in a group of Japanese men with no signs of dementia, between between 64 and 75 years old, that increased aerobic fitness correlates with the increased lateralization during task performance characteristic of younger brains. Here are their summaries:

Highlights

• Association among fitness, brain activation, and cognitive function was examined. 

• Frontal laterality during Stroop task in older men was assessed by fNIRS. 

• We found the association between ventilatory threshold and Stroop performance. 

• The association was mediated by the lateralized prefrontal activation.

Abstract

Previous studies have shown that higher aerobic fitness is related to higher cognitive function and higher task-related prefrontal activation in older adults. However, a holistic picture of these factors has yet to be presented. As a typical age-related change of brain activation, less lateralized activity in the prefrontal cortex during cognitive tasks has been observed in various neuroimaging studies. Thus, this study aimed to reveal the relationship between aerobic fitness, cognitive function, and frontal lateralization. Sixty male older adults each performed a submaximal incremental exercise test to determine their oxygen intake at ventilatory threshold (VT) in order to index their aerobic fitness. They performed a color–word Stroop task while prefrontal activation was monitored using functional near infrared spectroscopy. As an index of cognitive function, Stroop interference time was analyzed. Partial correlation analyses revealed significant correlations among higher VT, shorter Stroop interference time and greater left-lateralized dorsolateral prefrontal cortex (DLPFC) activation when adjusting for education. Moreover, mediation analyses showed that left-lateralized DLPFC activation significantly mediated the association between VT and Stroop interference time. These results suggest that higher aerobic fitness is associated with cognitive function via lateralized frontal activation in older adults.

Lower leg power predicts cognitive aging.

Gretchen Reynolds points to a study of 162 healthy female twin pairs, some identical, and some not, who 10 years previously had completed extensive examinations of their thinking and memory abilities, as well as measurements of their leg-muscle power.

...those who had had the sturdiest legs a decade ago showed the least fall-off in thinking skills, even when the scientists controlled for such factors as fatty diets, high blood pressure and shaky blood-sugar control...a muscularly powerful twin now performed about 18 percent better on memory and other cognitive tests than her weaker sister...in the brain imaging of the identical twins, if one genetically identical twin had had sturdier legs than the other at the start of the study, she now displayed significantly more brain volume and fewer “empty spaces in the brain” than her weaker sister.

Keep in mind the 'this is only one study' caution. It involved only a single analysis of the brain health of middle-aged female twins. However, it is a plausible result, because it is known that exercise causes muscles to release brain growth factors, and sturdier muscles might be expected to release more.

Our bodies can sabotage our healthy behaviors..

I pass on an interesting chunk from Reynolds' review of work by Mansoubi et al. showing that people who use sit-to-stand workstations in their office compensate by reducing activity and increasing sitting outside of working hours, thus canceling out the effects of their virtuous exercise at the office.

...the human body and brain are funny. They often, and rather insidiously, undermine some of our best efforts to be healthier, in an attempt to maintain our physiological status quo. The result can be that we do not benefit as much as we’d hoped from changes to our lifestyles. When we slash calories to lose weight, for instance, our bodies often lower our metabolic rate, and our weight doesn’t budge much.

Similarly, studies of people who begin or greatly intensify an exercise program have shown that these exercisers often start sitting more during the hours when they are not working out, so that their overall daily energy expenditure doesn’t increase substantially and the number of hours that they spend sitting grows.