Physiologically Speaking

Brady Holmer
Physiologically Speaking

A weekly podcast highlighting recent research in science. www.physiologicallyspeaking.com

  1. I Got a Lower-body MRI: Here's What it Told Me about My Muscle Mass

    JAN 15

    I Got a Lower-body MRI: Here's What it Told Me about My Muscle Mass

    In this episode, I sit down with Brian Heiderscheit , a professor in the Department of Orthopedics and Rehabilitation at the University of Wisconsin-Madison and director of the Badger Athletic Performance program. Brian also collaborates with Springbok Analytics, a company specializing in advanced full-body MRI scans. Together, we discuss my recent experience with a Springbok scan, how MRI data is revolutionizing athlete performance analysis, and actionable insights for reducing injury risks and improving training outcomes. Key Topics Covered: * Introduction to Springbok Analytics: Overview of their advanced MRI technology and its application in research and athletic training. * Brian’s Background: Insights into his role at UW-Madison and collaborations with Springbok Analytics on research initiatives, including a grant with the NFL. * My MRI Experience: * The scanning process, which takes 10-15 minutes. * Analysis of over 74 muscles rendered in 3D. * Comparison to population norms and evaluation of muscle size, asymmetry, and fat infiltration. * Key Findings from My Scan: * Notable asymmetry in muscle size between the left and right legs. * Larger left-side muscles, likely due to targeted rehabilitation post-injury. My left semitendinosus and other hamstrings were larger, while the right biceps femoris was bigger by about 10%. * Smaller right-side plantar flexors (e.g., soleus, gastroc) compared to the left, with a 7% size difference in the soleus. These findings align with subjective feelings of less power on the right side during runs. * My quadriceps showed strong development, particularly on the left, with right-side muscles slightly smaller. * Fat infiltration analysis, showing low levels typical of an active individual, with slight increases in the quadratus lumborum. * Actionable Insights for Athletes: * Targeted strength training to address imbalances, particularly focusing on the right-side soleus and quadriceps. * The potential value of pairing MRI data with gait analysis for a comprehensive view of biomechanics. * Using follow-up scans to evaluate the effectiveness of training programs. * The Role of MRI in Longitudinal Tracking: * Establishing a baseline for future comparison. * Monitoring recovery from injury or changes in training plans. * Brian’s Recommendations: * Adjust training to improve right-side strength, especially in the soleus and hamstrings. * Consider integrating gait analysis to identify asymmetries during running. Resources Mentioned: * Springbok Analytics: springbokanalytics.com * Badger Athletic Performance Program: BAP at UW-Madison * Brian Hederscheidt’s Google Scholar Profile for published research This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.physiologicallyspeaking.com/subscribe

    23 min
  2. 12/11/2024

    Creatine for endurance athletes, running a 2:26 marathon on 4 days per week, and more.

    Greetings! For today’s post, I’m sharing (with permission) my appearance on the Life in Stride podcast, hosted by a few good friends and outstanding runners. Here’s the episode description and links to their content. Please give them a follow/subscribe! On this episode, the boys had on special guest Brady Holmer! The best way to describe Brady would be an expert in the science of running and human performance. We covered several interesting tops as they relate to runners such as creatine use, VO2 max, proper race weight, and more! Brady also just ran a 2:26 marathon at Indianapolis, and he told he just ran 4 days a week training for it! We get into his training block some and learned how he dropped a 10 minute PR in just his second marathon. Enjoy! FOLLOW BRADY X: https://x.com/B_Holmer Strava: https://strava.app.link/a1EYBlCC6Ob FOLLOW US ON STRAVA Chris: https://www.strava.com/athletes/29985667 Scotty: https://www.strava.com/athletes/98633526 Danny: https://www.strava.com/athletes/23504210 CHECK OUT OUR INSTAGRAM: https://www.instagram.com/lifeinstridepodcast/ CHECK OUT OUR YOUTUBE CHANNEL: https://youtube.com/@LifeInStridePodcast?si=icd7XfQ4HMmuBRyX EPISODE RECOMMENDATIONS Floberg Runs Interview Sobriety and Running 2:42 in the Marathon This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.physiologicallyspeaking.com/subscribe

    1h 13m
  3. Physiology Friday #246: Black Friday Discount + My Conversation on The Mind Muscle Connection Podcast

    11/29/2024

    Physiology Friday #246: Black Friday Discount + My Conversation on The Mind Muscle Connection Podcast

    Greetings! Happy Black Friday to those who celebrate. Are you looking for a new health, fitness, or nutrition product for yourself or to give as a gift to family and friends? Here are a few Black Friday/Cyber Monday deals from brands I’m affiliated with and use myself. Save up to 60% on an Examine.com membership Get 30% off of your Ketone-IQ purchase 30% off of FSTFUEL electrolytes with the code BRADY30 at checkout 30% off of Presleep sleep supplement with the code BRADY30 at checkout 10% off of a Pedal Industries Race Day bag with the code INF-BRADY at checkout Get Decaf Drip coffee Additionally, for a limited time, you can snag a yearly subscription to Physiologically Speaking for $39.99 (originally $50) or purchase a subscription for a friend or family member as a gift. Physiologically Speaking is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Today, instead of a new study, I’m sharing the video of a podcast appearance I made on The Mind Muscle Connection with Jeff Hoehn. We talk about: * Research * Endurance exercise performance * Sleep * Training & nutrition * Supplements * Cardio * Recovery * Calorie intake * Metabolism * Aerobic exercise training * Exercise volume and intensity * How to measure improvements in cardiovascular fitness * My 7 rules for health * And more! * Be sure to check out Jeff’s podcast, subscribe, and give him a follow on Instagram and X. Thanks so much for subscribing. I’m grateful to every one of my audience members! ~Brady~ This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.physiologicallyspeaking.com/subscribe

    1h 17m
  4. How Ultrarunner David Roche Uses Science to Break Records

    09/04/2024

    How Ultrarunner David Roche Uses Science to Break Records

    Greetings! David Roche is a decorated trail runner, coach, and co-founder of SWAP Running. He's a two-time national champion and a three-time Team USA member, and he recently set the course record at the Leadville 100 trail run with a time of 15 hours, 26 minutes, 34 seconds. David and his wife, Megan Roche, M.D., offer coaching that blends science, training theory, and a philosophy of joy and long-term growth for all athletes. Megan just launched a website—Huzzah—“to empower female endurance athletes by providing accessible sports science knowledge and fostering a love for sport through content, insights, and scholarships, with a focus on supporting overall health, education, and competitive edge.” I’ve become a bit obsessed with how David thinks about running and how invested he and Megan are in reading and implementing the science of training and racing. So I needed to nerd out with him on some topics. In this interview, I picked David’s mind about his scientific approach to training, and we detail several of the training practices he used in his buildup to the race, including: Sodium bicarbonate Downhill running High-carb fueling Super shoes Post-exercise exogenous ketones Heat training/hot water immersion Caffeine Heart rate zones And more! Relevant links For more details about David and SWAP Running, visit their About Us page Follow David on X @MountainRoche Watch the documentary about David’s record: Leadville 100 Ultramarathon & David Roche's Run for The Impossible Record This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.physiologicallyspeaking.com/subscribe

    1h 29m
  5. The Case for Keto for Type 1 Diabetes with Andrew Koutnik, Ph.D.

    07/24/2024

    The Case for Keto for Type 1 Diabetes with Andrew Koutnik, Ph.D.

    Greetings! Today’s interview is with Andrew Koutnik, Ph.D. Andrew is a research scientist at Sansum Diabetes Research Institute, where he’s investigating metabolic therapies for health and disease. His mission is to optimize metabolic health and patient outcomes for people living with type 1 diabetes. Andrew is unique because he himself has type 1 diabetes. This allows him to add a bit of personal touch and a lot of passion into the work he’s doing. Andrew joins me to talk about a case study (two papers) that he and colleagues just published on the long-term safety and efficacy of the ketogenic diet for an individual with type 1 diabetes who had been using the ketogenic diet for more than 10 years (spoiler alert: it’s Andrew). We talk about why the ketogenic diet is helpful for people with diabetes and then dive into the details of each study to explore how 10 years on the diet affected cardiovascular health risk factors and clinical biomarkers. Andrew posted two great threads about the papers on X. You can check those out below. Make sure to give Andrew a follow as well while you’re there. Part I: 10-Years longitudinal data on KETOGENIC DIET and Safety, Efficacy & Advanced Cardiovascular Physiology in a patient with HIGH RISK cardiovascular disease (Type 1 Diabetes)? Part II: 10-Year Longitudinal Data On Ketogenic Diet Adverse Events, Bone Mineral Density, Thyroid Function, and Kidney Function Here are the links to each paper: Advanced Cardiovascular Physiology in an Individual with Type 1 Diabetes After 10-Year Ketogenic Diet Efficacy and Safety of Long-term Ketogenic Diet Therapy in a Patient With Type 1 Diabetes This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.physiologicallyspeaking.com/subscribe

    1h 4m
  6. 04/19/2024

    Physiology Friday #214: Strengthening the Link Between V̇O2 Max and Longevity & Healthspan

    Greetings! Welcome to the Physiology Friday newsletter. ICYMI Check out my guest appearance on The Neuro Experience podcast with Louisa Nicola, where we talk about the science of V̇O2 max. On Wednesday, I published a post about some of the most common myths about coffee and caffeine. Details about the sponsors of this newsletter including Examine.com and my book “VO2 Max Essentials” can be found at the end of the post! Physiologically Speaking is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. If you can fill the unforgiving minute With sixty seconds’ worth of distance run, Yours is the Earth and everything that’s in it, And—which is more—you’ll be a Man, my son! — Rudyard Kipling, If— In my book “VO2 Max Essentials”, I make the case for why cardiorespiratory fitness should be considered the most important vital sign. Among all risk factors, V̇O2 max is the only one that’s a composite of multiple physiological systems, rather than a snapshot of health at one point in time or a single biomarker measured via a blood test. Your maximal oxygen utilization capacity (V̇O2 max) represents the maximum integrated capacity of the pulmonary, cardiovascular, and muscular systems to uptake, transport, and utilize oxygen during whole-body, dynamic exercise. The function of your autonomic nervous system, your heart and blood vessels, your lungs, your muscles, and your mitochondria all influence your maximal aerobic capacity. It’s not just a strong heart that gives someone a high V̇O2 max. A strong body is a prerequisite. This is, in my opinion, why a high V̇O2 max is so often associated with beneficial health outcomes. You won’t find someone with a high V̇O2 max who is in poor health, and often people with an extremely low V̇O2 max are in poor health. Though it’s not routinely measured in clinical practice (yet), V̇O2 max has recently appeared on the radar of many healthcare professionals. People are becoming aware of the predictive power of cardiorespiratory fitness and are increasingly interested in how (and why) to improve it. Over the last 20 years, evidence has emerged linking higher cardiorespiratory fitness to lower risks of all-cause mortality and other diseases. Thus, it’s about time we had a scoping review of the evidence, which brings us to today’s study. The study, published in the British Journal of Sports Medicine was an overview of all previously published systematic reviews and meta-analyses on the relationship between V̇O2 max and an array of health outcomes. The studies were eligible if they included adults with or without health conditions and measured cardiorespiratory fitness using a maximal graded exercise test, a maximal or submaximal exercise test with a prediction equation (i.e., without direct measures of gas exchange), or a non-exercise prediction equation. When pooling the data and examining the outcomes, the authors compared the groups with the highest cardiorespiratory fitness to those with the lowest cardiorespiratory fitness. Overall, a total of 26 studies with over 20.9 million participants from 199 different cohorts were included in the review.  Eight of the included studies examined the association between V̇O2 max and death (mortality) from all causes, cardiovascular disease, sudden cardiac events, all cancers, and lung cancer.  Compared to low cardiorespiratory fitness, having high cardiorespiratory fitness was associated with a 41% to 53% lower risk for premature mortality. Furthermore, each 1 metabolic equivalent (MET) increase in cardiorespiratory fitness (1 MET is equal to an increase in V̇O2 max of 3.5 mL/kg/min) reduced the risk of premature mortality by 7% (all cancers) to 51% (sudden cardiac mortality). A notable limitation for mortality outcomes was the large disparity in male vs. female participants — more than 1.8 million male participants were included in the studies while only 180,000 females were included. Having a higher cardiorespiratory fitness was also associated with a lower risk of developing hypertension, heart failure, stroke, atrial fibrillation dementia, kidney disease, depression, and type 2 diabetes. Specifically, the risk of a new onset condition was 37% (hypertension) to 69% (heart failure) lower when comparing high vs. low cardiorespiratory fitness. For every 1 MET increase in fitness, the risk of developing a new chronic health condition was reduced by 3% (stroke) to 18% (heart failure). Similar to mortality outcomes, a majority of the evidence was from male populations, although two studies investigated the effects in female-only cohorts. In these groups, high cardiorespiratory fitness was found to be more protective against stroke and type 2 diabetes among females compared to males. Among men, a higher cardiorespiratory fitness was not associated with prostate cancer risk. What about individuals who already have a chronic health condition? Does having a high cardiorespiratory fitness protect them from early death or adverse events? This seems to be the case. A lower risk of premature death or adverse events was observed for people with a higher vs. a lower cardiorespiratory fitness and ranged from 19% (for an adverse event among adults with pulmonary hypertension) to 73% (for cardiovascular mortality among people living with cardiovascular disease). Based on this comprehensive review, not only does having a higher cardiorespiratory fitness reduce the risk of premature death from all causes, but it also reduces the risk of developing a new condition or dying from a condition you already have.  Put another way, low fitness is a consistent and important risk factor for early death and chronic disease. If this isn’t enough evidence that cardiorespiratory fitness should be considered a vital sign, I don’t know what is. The authors even suggest that a minimum clinically important difference or MCID for V̇O2 max be established as 1 MET (3.5 mL/kg/min). Exercise trials and other interventions can be deemed “effective” if the participants achieve this degree of fitness improvement. It’s a goal you should strive for in your own exercise regimen. Because this was merely an overview of published literature, we unfortunately don’t have specific numbers for the “high” and “low” V̇O2 max groups. But I did a quick scan of the included studies on mortality risk to find a quick estimate. Low cardiorespiratory fitness is somewhere in the range of less than 8—9.5 METs or a V̇O2 max of less than 28—33 mL/kg/min. High cardiorespiratory fitness is about 11—13.7 METs or more, or a V̇O2 max of 38.5—48. If you’re below or near one of these categories, act accordingly. The certainty (quality) of the evidence was also downgraded mostly due to a large variation in how the studies measured V̇O2 max and the large proportion of male participants. And, of course, the main limitation is that these associations (correlations) may not imply causation.  One of the main criticisms of this literature is that, because nearly 50% of one’s V̇O2 max can be explained by genetics and is therefore unmodifiable, the association between cardiorespiratory fitness and healthspan/longevity may not represent an effect of a high fitness level per se, but rather, an underlying predisposition to health. Healthy people have a higher V̇O2 max, but they’re not healthy because of it. I don’t buy this. To explain why, I’ll use the Bradford Hill criteria.  The Bradford Hill criteria, also known as Hill’s criteria for causation, are a set of nine principles used to establish epidemiologic evidence of a causal relationship between a presumed cause and an observed effect. These criteria have been widely used in public health research and were proposed by the English epidemiologist Sir Austin Bradford Hill in 1965. The nine criteria are: * Strength (Effect Size) A small association does not rule out causality, but a stronger association increases the likelihood of a causal effect. * Consistency (Reproducibility) Consistent findings across different studies, populations, and settings strengthen the evidence for causality. * Specificity A specific association between a factor and an effect suggests a higher probability of a causal relationship. * Temporality The cause must precede the effect in time * Biological Gradient (Dose-Response Relationship) Generally, greater exposure leads to a higher incidence of the effect. * Plausibility A plausible mechanism linking cause and effect enhances the evidence. * Coherence Consistency between epidemiological findings and laboratory evidence strengthens the likelihood of causality. * Experiment Experimental evidence can support causality. * Analogy Similarities between the observed association and other known causal relationships can provide additional support. Now, let’s apply the Bradford Hill criteria to V̇O2 max. * Strength of Association Numerous studies consistently demonstrate a strong inverse relationship between cardiorespiratory fitness and mortality risk. Case in point: this review. * Consistency of Effect Research findings consistently support the link between fitness and health outcomes. Multiple studies across diverse populations consistently show that better fitness is associated with improved health and longevity. Again: see this review. * Specificity While cardiorespiratory fitness impacts overall health, it specifically reduces the risk of cardiovascular diseases, diabetes, and certain cancers. * Temporality The temporal relationship is well-established: higher fitness precedes better health outcomes. Individuals who maintain or improve their fitness levels over time experience reduced mortality risk. * Dose-Response Relationship A dose-response pattern exists: as cardiorespiratory fitness increases, mortality risk decreases. * Plausibility Mechanisms underlying this associat

    12 min
  7. 04/05/2024

    Physiology Friday #212: How Nighttime Alcohol Disrupts Normal Sleep Architecture

    Greetings! Welcome to the Physiology Friday newsletter. ICYMI On Monday, I posted a video interview that I recorded with Aidan Chariton from Shortcut U. We discuss the importance of endurance training and other things related to human health and performance. On Wednesday, I posted my “7 Rules for Health.” Details about the sponsors of this newsletter including Examine.com and my book “VO2 Max Essentials” can be found at the end of the post! Physiologically Speaking is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. "Drink, sir, is a great provoker of three things… nose-painting, sleep, and urine. Lechery, sir, it provokes, and unprovokes; it provokes the desire, but it takes away the performance." – 'Macbeth' (1606) act 2, scene. 3, l. [28] It’s clear that Shakespeare recognized alcohol’s role as an intoxicant, a somnogen, and a diuretic. Though alcohol may be a “provoker” of good spirits and whimsy for a short while, its “unprovoking” effects on sleep are well known to most. I’m not a teetotaler, but I recognize the harmful effects of alcohol abuse. Some people enjoy a few drinks on occasional while others wish to abstain. I support both decisions. One often-cited reason for alcohol consumption is as a sleep aid — nearly 20% of adults in the United States say that they use alcohol for this purpose. There’s one problem with this strategy. Although alcohol may help you fall asleep (it’s a depressant after all), it impairs your ability to stay asleep and worsens the quality of your sleep. I’ve written on this subject before. Alcohol can elevate body temperature and heart rate, reduce heart-rate variability (HRV), and disrupt the regulation of our autonomic nervous system during sleep, all of which reduce the restorative quality of sleep. In higher quantities, alcohol disrupts the normal architecture of our sleep — architecture referring to the time we spend in the various sleep stages (i.e., light sleep, rapid eye movement or REM, slow-wave sleep/deep sleep). Alcohol also appears to cause more fragmented sleep, characterized by more wakefulness throughout the night. This may be due to the alcohol-induced increase in body temperature, an increased need to urinate owing to alcohol’s diuretic effect, apneic episodes during sleep (when we stop breathing), and the so-called “rebound effect” that occurs when alcohol is metabolized, which leads to wakefulness due to blood glucose fluctuations, dehydration, and digestive discomfort. All of these effects are well known to occur when alcohol is consumed in close proximity (e.g., 3 hours or less) to sleep and happen in a dose-dependent fashion. The more you drink and the closer to bedtime you drink, the more you disrupt your sleep. What is less well-understood is how (or if) alcohol’s effects on sleep persist, worsen, or diminish over consecutive nights of alcohol consumption. Does our brain and body “habituate” to repeated drinking episodes or is it a downward spiral until we abstain? It’s also not known if the effects of alcohol on sleep architecture are consistent throughout the night. In other words, does alcohol affect sleep stages differently a few hours after bedtime compared to in the middle of your sleep period? These questions were investigated in a new study published in the aptly named journal Sleep. A total of 30 participants completed the study (15 men and 15 women with an average age of 33), none of whom had Alcohol Use Disorder but all of whom reported a moderate drinking habit (9–12 standard drinks per week for women and 12–15 standard drinks per week for men). An important consideration given that people who don’t drink or who drink “too much” might have different responses to alcohol consumption. The participants completed two 3-night experimental conditions in a random order. A washout period of 4 nights separated each condition. In one condition, the participants consumed 3 standard drinks (targeting a breath alcohol concentration of 0.08) in 45 minutes. The last drink was about 1 hour before bedtime. If you're curious, the two choices were Everclear or vodka in some type of mixer. They did this for 3 nights in a row. In the other condition, the participants drank just a mixer (no alcohol; this was the control condition) before bed. As in the alcohol condition, they did this for 3 nights in a row. The participants also completed a standardization phase before the study. For 8 days, they maintained a regular sleep schedule at home (7.5–8.5 hours of sleep per night) and avoided recreational drugs and alcohol, sleep medications, and excessive caffeine (more than 360 mg per day or caffeine after 2 p.m.). Overnight, brain activity and other physiological metrics were measured using a technique known as polysomnography (PSG). PSG allows for, among other things, the measurement of the time spent in various sleep stages, which for this study included slow-wave sleep (SWS) and rapid-eye-movement sleep (REM). Other outcomes included the total sleep time or sleep duration, the time spent awake each night, sleep latency (the time it takes to fall asleep), and wake after sleep onset (WASO; how much time you spend awake after falling asleep for the first time). What made this study unique was the separation of each night into thirds, permitting a detailed insight into the specific “windows” of sleep that were most affected by alcohol. This produced some interesting findings that I’ll expand on in the next section. Results As I discuss the results, keep in mind that in all cases, the specific nights or time points in the alcohol condition were compared to the average of all 3 nights or time points in the control condition. On all 3 nights with alcohol, SWS increased during the first third of the night compared to the control condition but was lower during the second two-thirds of the night compared to the control condition. On the other hand, REM sleep decreased on all 3 nights with alcohol compared to the control condition and also during the first third of the night (but not the second two-thirds). Using a unique temporal analysis, the researchers identified many differences in the timeframes when the amount of time in the various sleep stages was different between the conditions. The proportion of time spent in SWS was higher in the alcohol condition (vs. the control condition) between 1.8 and 6.5 hours after bedtime. This was consistent across all 3 nights, and indicates that the effects of alcohol on SWS are persistent. The proportion of time spent in REM sleep was lower in the alcohol condition on night 1, specifically between 1.4 and 7.8 hours after sleep onset. On nights 2 and 3, REM sleep was lower between 2.1 and 5.3 hours after sleep onset. Put another way, the effects of alcohol on REM sleep diminished (occurred in a narrower time frame) with consecutive nights of alcohol consumption. WASO was only higher on night 1 of alcohol consumption compared to the control condition, specifically from 5.6 hours after sleep onset until wake time. There were also some notable differences between nights 1, 2, and 3 of alcohol consumption. For one, the participants spent more time awake on alcohol night 1 vs. alcohol night 2 (from 1 to 2.7 hours after sleep onset) and on alcohol night 2 vs. night 3 (from 5.1 to 6.7 hours after sleep onset).  Second, WASO was different on alcohol night 1 vs. night 2 (from 5.2 hours after sleep onset until awake) and on night 1 vs. night 3 (from 5.4 hours after sleep onset until awake). These results indicate a few things about the impact of consecutive nights of alcohol consumption on sleep: Pre-sleep alcohol reduces SWS, effects that begin around 2 hours after going to sleep or right around the end of the first sleep cycle. These effects persist when alcohol is consumed for three nights in a row. Consecutive nights of pre-sleep alcohol consumption decreases REM sleep, but these effects seem to be worse on the first night (an 11-minute decrease in total REM sleep) compared to the second and third nights (a 4-minute decrease in total REM sleep). Alcohol seems to increase wakefulness in the later periods of sleep, from about 5 hours after sleep onset until the time you wake up. The findings on REM sleep may indicate that the nervous system somehow adapts to these pre-sleep alcohol levels to “rescue” time spent in REM sleep, but this doesn’t happen for SWS. REM sleep is where dreams occur. During REM, our brain activity, breathing, and heart rate and blood pressure increase. Our eyes also move back and forth rapidly, hence the name. REM sleep is thought to play an important role in memory and learning and likely had an important evolutionary role. This doesn’t mean SWS is any less important. SWS, also known as deep sleep, happens early in the night and is when the body relaxes into a period of restoration. This sleep stage is thought to play an important role in growth, memory, and immune function. Why SWS increases with alcohol consumption (at least in the early parts of sleep) isn’t quite clear, but is probably related to alcohol’s depressant and inhibitory effects on the brain. This would make sense as levels of alcohol in the blood would be highest in the earlier parts of the night and decrease as sleep progresses. How can you apply these findings? Avoid alcohol close to bedtime.  In this study, the participants’ pre-sleep breath alcohol levels were between 0.038 and 0.087 (the average was 0.066 or just below the legal limit) and they finished their last drink around 1 hour before bedtime. This is way too close for comfort if you want to avoid alcohol’s effects on sleep. Don’t go to bed with alcohol in your system. I think a minimum of 3 hours seems prudent. One alcoholic drink takes about an hour to metabolize and leave your system. So 3 drinks would require about 3 hours

    12 min

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A weekly podcast highlighting recent research in science. www.physiologicallyspeaking.com

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