Tag Archives: autonomic nervous system

Season-long heart rate variability tracking reveals autonomic imbalance in American college football players

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As part of my PhD work at Alabama, we tracked HRV in football players from day 1 of preseason training through to the national championship. A practical summary of some key findings follow the full-text link below.

Season-Long Heart-Rate Variability Tracking Reveals Autonomic Imbalance in American College Football PlayersDownload

Fluctuations in HRV are expected throughout a season. However, chronically suppressed values are cause for concern. Sustained parasympathetic hypoactivity is associated with various pathological conditions and is a hallmark of stress and impaired recovery in athletes.

We learned from spring camp that day-to-day HRV recovery was delayed in linemen vs. the smaller and more aerobically fit skill players. Thus, we anticipated that linemen would be more susceptible to attenuated HRV throughout the season.

HRV started to decline by week 6 of the competitive period for linemen. A couple notable events occurred here: 1) the first of 5 consecutive SEC match-ups vs Top 25 nationally-ranked opponents and 2) the week of mid-term exams for many players.

Although significant group-level reductions for linemen weren’t observed until later, key players showed descending HRV by mid-season, in the absence of changes in PlayerLoad. Suppressed HRV preceded illness and injury in 2 starters. Temporary rest restored HRV.

Group-level reductions occurred during an intensive camp-style preparation period for the college football playoffs following the SEC championship. Most players took a hit to their HRV, but linemen were hit the hardest. Note magnitudes of the effect sizes in the table below.

HRV remain suppressed for linemen through prep weeks for the national semi-final and the national championship. Smaller decrements (non-significant) were observed for skill players. In addition to accumulating physical stress, psycho-emotional factors (pre-competitive anxiety, pressure to perform, media attention, etc) likely contributed.

Although we emphasize the toll of a season on linemen, some skill players also showed suppressed values. The table below shows the rate of change in HRV for all players. 25% of skill and 63% of linemen showed sig. descending HRV patterns throughout the season.

Linemen experience hypertension, arterial stiffening, and pathologic LV hypertrophy following 1 or more seasons. These maladaptations are possibly preceded by ANS imbalance. We hypothesize that larger players showing the worst HRV profiles suffer the greatest decrement in cardiovascular health markers.

If so, intervening when a decreasing HRV pattern is observed may not only be relevant to performance (limiting fatigue, injury-, and infection-risk), it may also help mitigate the cardiovascular toll of playing football at such a high level. Seeking funding to explore this in the future.

The findings highlight potential deficiencies in or greater taxation to the coping capacity of linemen vs. smaller players. Factors hypothesized to contribute to more prevalent ANS imbalance in linemen and potential implications for health and performance are summarized below.

Linemen need careful attention and monitoring. We need strategies to prevent ANS imbalance from occurring (load management, aerobic capacity, treatment of health conditions like sleep apnea, etc) and we need restorative methods to implement if it occurs.

Tracking HRV with a mobile app was inexpensive and easy. Time-demand from players was ~3 min/week while waiting to get taped. Though sub-optimal relative to post-waking measures, this approach enabled timely detection of descending patterns, which may be useful for guiding interventions relevant to player health and wellbeing.

Though a better understanding of the health and performance ramifications of suppressed HRV in football players is needed, a descending pattern may serve as an easily identifiable red flag requiring attention from performance and medical staff.

Cardiac-Autonomic and Hemodynamic Responses to a Hypertonic, Sugar-Sweetened Sports Beverage in Physically Active Men

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Short summary of and full-text access to a new study from our lab.

Link to Full Text:

Cardiac-Autonomic and Hemodynamic Responses to a Hypertonic, Sugar-sweertened Sports Beverage in Physically Active MenDownload

Context: we previously resorted to standardized HRV measures performed in the athletic training room with college football players to overcome non-compliance with post-waking tests.

Problem: pre-training hydration practices confound HRV measures. Players typically opt for cold bottles of water or Gatorade. Thus, we needed to determine how much and for how long these drinks impacted HRV.


Findings: Gatorade had small effects that lasted about 45 min. Effects of water were larger and persisted for 60 min.

Key points:

If measuring HRV in a lab/clinic/training facility, be mindful of recent fluid ingestion.
HRV measures obtained within 60 min of 591 ml water or 45 min of an equal volume of Gatorade will be capturing their physiology effects and result in falsely elevated values. This would result in misinterpretation of autonomic status.

Effect of Competitive Status and Experience on Heart Rate Variability Profiles in Collegiate Sprint-Swimmers

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Here’s a new paper from my time at Bama. A practical summary follows the link and abstract below.

Link to free full text:

Effect of Competitive Status and Experience on Heart Rate Variability Profiles in Collegiate Sprint-SwimmersDownload

Context:

When first getting started with tracking HRV in athletes, the inter-individual variation in trend characteristics can be confusing. Some athletes will display very high values and others will show lower values. Likewise, some will show quite stable values while others display substantial day-to-day variation. Naturally, the following question arises: why do some athletes have higher and more stable values than others?

Collegiate swim rosters typically include a mixed roster of athletes (males and females with a broad range of experience and skill). In this investigation we compared HRV trend characteristics between the national-level (including 6 Olympians) and conference-level sprint-swimmers throughout 4 weeks of standardized preparatory training. We also obtained details of individual training history.

The main findings were that national-level swimmers had higher and more stable HRV (higher mean LnRMSSD, lower LnRMSSD coefficient of variation) than their conference-level teammates. Differences in trend characteristics were attributable to a greater history of training and competing among the national-level swimmers (i.e., greater training age).

Whether these findings can be explained by greater aerobic fitness (we don’t think so), greater familiarity with training (possibly), or chronic physiological adaptations (possibly) among the higher-level swimmers is unclear.

The findings may be of some practical use for coaches when interpreted with previous work (see links below). For example, preliminary expectations with HRV monitoring should be that higher-level swimmers will display higher and more stable values throughout training and vice-versa for lower-level athletes. This may be interpreted to mean that the higher-level athletes could tolerate greater loads or that the lower-level athletes may need reduced loads. However, it is unclear if these training modifications would offer any performance/adaptation advantage. In addition, a higher-level athlete showing lower and less-stable values may be cause for concern (fatigue, stress, detraining, etc. depending on context). Whereas a lower-level athlete displaying higher and more stable values is likely adapting well to the training.

We’ve previously assessed how overload and tapering impact HRV in sprint-swimmers here.

We’ve previously assessed associations between subjective indicators of recovery and daily HRV in sprint-swimmers here.

Heart Rate Variability in College Football Players throughout Preseason Camp in the Heat

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Here’s a quick look at our latest study examining cardiac-autonomic responses to preseason camp in the heat among college football players. The free full text can be accessed here: Heart rate variability in college football players throughout preseason camp in the heat IJSM. 

Intensive training periods tend to increase RHR and decrease HRV, reflecting stress and fatigue. However, adaptations to heat exposure (e.g., plasma volume expansion) tend to have the opposite effects. So we wanted to see what happens when players were exposed to both intense training and intense heat stress during preseason camp.

Despite increases in perceived fatigue throughout the 2-week period, RHR and HRV reflected responses consistent with heat acclimation.

HRV initially decreased in linemen, then peaked after a day of rest. Non-linemen faired a little better with smaller decrements in perceived fatigue and more frequent day-to-day improvements in RHR and HRV.

These results indicate that heart rate parameters and perceived fatigue are independent markers of training status, and that desirable cardiovascular adaptations can occur in the presence of soreness and fatigue.

This is especially important for tech companies who try to infer recovery status from HRV alone. As HRV improved throughout camp, an app’s algorithm would report to coaches that players are well-recovered. Given that no player feels well-recovered during preseason camp in the heat, the technology suddenly loses credibility for being wrong and will likely be dismissed.

This is unfortunate because the heart rate parameters are likely reflecting important adaptations that may indicate better tolerance to training in the heat, a reduced exercising heart rate, and improved fitness. Thus, I encourage users to ignore “recovery” scores and interpret the data in appropriate context.

ABSTRACT 

We aimed to characterize cardiac-autonomic responses to a 13-day preseason camp in the heat among an American college football team. Players were categorized as linemen (n=10) and non-linemen (n=18). RHR, natural logarithm of the root-mean square of successive differences multiplied by twenty (LnRMSSD), and subjective wellbeing (LnWellness) were acquired daily. Effect sizes±90% confidence interval showed that for linemen, LnRMSSD decreased (moderate) on day 2 (71.2±10.4) and increased (moderate) on day 12 (87.1±11.2) relative to day 1 (77.9±11.2) while RHR decreased (small–moderate) on days 6, 7, and 12 (67.7±9.3–70.4±5.5 b∙min-1) relative to day 1 (77.1±10.1 b∙min-1). For non-linemen, LnRMSSD increased (small–large) on days 3–5, 7, 12, and 13 (83.4±6.8–87.6±8.5) relative to day 1 (80.0±6.5) while RHR decreased (small–large) on days 3–9, 12, and 13 (62.1±5.2–67.9±8.1 b∙min-1) relative to day 1 (70.8±6.2 b∙min-1). Decrements in LnWellness were observed on days 4–10 and 13 for linemen (moderate) and on days 6–9, 12, and 13 for non-linemen (small–moderate). Despite reductions in LnWellness, cardiac-autonomic parameters demonstrated responses consistent with heat-acclimation, which possibly attenuated fatigue-related decrements.

HRV stabilization in athletes: towards more convenient data acquisition

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Our “stability” paper has recently been published in Clinical Physiology and Functional Imaging.

http://onlinelibrary.wiley.com/doi/10.1111/cpf.12233/abstract

ABSTRACT

Resting heart rate variability (HRV) is a potentially useful marker to consider for monitoring training status in athletes. However, traditional HRV data collection methodology requires a 5-min recording period preceded by a 5-min stabilization period. This lengthy process may limit HRV monitoring in the field due to time constraints and high compliance demands of athletes. Investigation into more practical methodology for HRV data acquisition is required. The aim of this study was to determine the time course for stabilization of ECG-derived lnRMSSD from traditional HRV recordings. Ten-minute supine ECG measures were obtained in ten male and ten female collegiate cross-country athletes. The first 5 min for each ECG was separately analysed in successive 1-min intervals as follows: minutes 0–1 (lnRMSSD0–1), 1–2 (lnRMSSD1–2), 2–3 (lnRMSSD2–3), 3–4 (lnRMSSD3–4) and 4–5 (lnRMSSD4–5). Each 1-min lnRMSSD segment was then sequentially compared to lnRMSSD of the 5- to 10-min ECG segment, which was considered the criterion (lnRMSSDCriterion). There were no significant differences between each 1-min lnRMSSD segment and lnRMSSDCriterion, and the effect sizes were considered trivial (ES ranged from 0·07 to 0·12). In addition, the ICC for each 1-min segment compared to the criterion was near perfect (ICC values ranged from 0·92 to 0·97). The limits of agreement between the prerecording values and lnRMSSDCriterion ranged from ±0·28 to ±0·45 ms. These results lend support to shorter, more convenient ECG recording procedures for lnRMSSD assessment in athletes by reducing the prerecording stabilization period to 1 min.

CPFI figure

In collaboration with Dr. Fabio Nakamura, we have a new paper currently in review that assesses the suitability of ultra-short (60-s) measures with minimal stabilization in elite team-sport athletes using the Polar system. We will also be assessing if these modified HRV recording procedures sufficiently reflect changes in fitness after a training program. Overall, shortened lnRMSSD recording procedures appear very promising. This will hopefully enhance the practicality of HRV monitoring among sports teams.

How to increase HRV Part 3: Aerobic Exercise

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As the title implies, this is the third installment to a series I started several months ago that discusses the various factors that can help improve our HRV. The first two posts can be read by clicking on the respective links below.

How to increase HRV Part 1: Inflammation

How to increase HRV Part 2: Nutrition – Featuring contributions from my friend Marc Morris PhD(c)

I will first discuss (very briefly) some research and the key physiological adaptations that occur in response to aerobic exercise as it is these changes that ultimately affect the function of the autonomic nervous system (ANS). I will then provide some thoughts on how to include aerobic work into your training in effort to improve our overall health, recovery and capacity for training. Like always, I will include some anecdotal experience and a bit of theory. This article is primarily directed at strength athletes/individuals.

It’s important to clarify what exactly I’m referring to when I saw “aerobic exercise”. For the purpose of this article “aerobic exercise” is referring to some form of activity that maintains an elevated heart rate above resting conditions. This is a very broad and vague definition but for good reason. Depending on one’s current physical condition, aerobic work may be simply going for a walk, while in very fit individuals aerobic work may include longer distance running, swimming, cycling, etc. It can be tempo runs, circuit training, sled work, mobility drills or dancing if that’s your thing.

Aerobic Exercise as a Means to Increase HRV Among Various Populations  

Children (age 6-11) who initially had low HRV scores saw significant increases in HRV after participating in a 12-month moderate exercise program (Nagai, 2004).

Elderly sedentary folks (men and women between 65-75 years old) saw an increase in HRV and cognitive test scores after 12 weeks of aerobic exercise (1hr/day, 3d/wk) compared to a group who performed only stretching (1hr/day, 3d/wk) of which saw a decrease in cognitive test scores (Albinet et al, 2010).

After 6 months of aerobic exercise training, both older (age 60-82) and younger men (age 24-32) showed an increase in HRV (Levy et al, 2004)

Gamelin et al (2007) put healthy young men (untrained, age 21) through 12 weeks of aerobic training followed by 8 weeks of detraining to determine its effect on HRV. An improvement in HRV was seen after the 12 weeks however HRV scores returned to pre-test levels after only 2 weeks of training cessation. “Twelve weeks of aerobic training are sufficient to achieve substantial changes in Heart Rate Variability; and only two weeks of detraining completely reverse these adaptations.”

I should mention that there are several studies that showed no improvements in HRV following exercise intervention. It appears that there is a threshold of exercise intensity required to augment vagally mediated HRV. Essentially, it’s important for heart rate to remain elevated beyond a certain level for a certain amount of time performed consistently over a certain time period for noticeable HRV changes to be seen. I realize that last sentence didn’t help anyone but I don’t believe this threshold level has been clearly established. My interpretation of the research that I’ve seen is that you simply need to be consistent and put more effort into it than a leisurely walk, although that may be a good start for some. Older people generally require longer exercise interventions as sympathetic activity increases with age.

Anecdotally, I can say that when I incorporate regular active recovery workouts (moderate aerobic intensity) my baseline HRV score is higher and I see quicker and higher spikes in HRV following an active recovery day. Furthermore, I almost always see decreasing baseline HRV trends when I do not include active recovery work. I can definitely see the corresponding relationship between HRV and aerobic work capacity. When my aerobic capacity is high my HRV is typically higher (baseline level). With consistent downward trends in HRV I’m typically detraining (due to illness, high stress, or anything that results in lack of training). Thus, at least in myself, when my aerobic capacity is higher, my HRV is typically higher.

* Note that this does not include acute changes in HRV but rather weekly/monthly trend changes.

Physiological Adaptations

Without trying to sound like an Ex. Phys text book I simply want to touch on some key adaptations that take place in response to aerobic exercise that influence ANS activity and therefore HRV changes. In response to aerobic exercise we will typically see that;

–          Resting heart rate decreases

–          Cardiac output increases

–          Heart volume and size increases (Left Ventricle)

–          Red blood cell size and count increases

–          Capillary density increases

–          Myoglobin increases

–          Breathing rate decreases

–          Blood pressure decreases

–          Baroreflex sensitivity increases

–          Renal-Adrenal function increases

–          Parasympathetic tone increases

–          Sympathetic tone decreases

*I used both the NSCA Essentials of Strength Training and Conditioning text and Primer on the Autonomic Nervous System Text for the above information.

I’m reluctant to say that all of the above directly affect HRV. The primary factors from the above list that impact HRV the most would be the changes in Sympathetic and Parasympathetic tone.

The ANS is responsible for responding to a stimulus/stressor and creating the necessary adaptations to allow us to resist the same stimulus/stressor in future incidences. Therefore, regardless of what type of athlete you are, improving your overall capacity for stress is beneficial. Our performance can be limited by our capacity for work. HRV score is a reflection of how much stress you can handle that day. Therefore we want to do what we can to position ourselves to better tolerate and adapt to our training.

Aerobic Work for Anaerobic Athletes

Let me be clear and state that I’m not advising powerlifters or throwers to go for a 1 hour run 3-4x/wk. However, in the interest of increasing workout volume/density and recovery, some aerobic capacity work can be helpful. Louie Simmons and Dave Tate have been preaching this for years. I recall plenty of articles where they discuss sled dragging, “feeder” workouts, etc. You can call this a “base” or “GPP”, “Anatomic Adaptation” or whatever you want. The bottom line is, we need to increase our body’s ability to handle training stress, recovery from it, then handle progressively more training again.

I understand that resistance training can elevate heart rate and maintain it over resting conditions. However, can you honestly tell me that you can go play a pick- game of basketball and not be completely winded after 5 mins? I used to not perform active recovery/work capacity workouts. If I did anything even somewhat strenuous for over 20 minutes that day my workout would be ruined. I’d purposely avoid physical activity so that I wouldn’t compromise my workout. Now that my work capacity is much higher I no longer have this issue.

Here are some thoughts on how to incorporate some aerobic capacity work into your training without negatively effecting strength progress;

–          If it’s possible, take longer in your warm-ups. Here’s an example of a warm-up I do on Squat and DL days;

  • 6 min aerobic exercise (incline treadmill, bike, skipping, etc), 5 min dynamic stretches, 5 min lower body mobility, 5 min “activation” type work for glutes and core (due to previous low back issues), 5 min upper body mobility (shoulders, t-spine) and external rotation work, some form of box jump or KB swing to finish. By the end of this I’m sweating and my joints feel great.

–          Perform some type of activity on your off days. If you have terrible work capacity start off extremely easy with 10 mins of incline treadmill walking or the stationary bike. Over time work up to 20-30 mins. Generally I don’t exceed 40 minutes of work.

–          Perform mobility circuits and kill two birds with one stone. Improve your mobility and aerobic capacity at the same time. Just keep your HR elevated.

–          Perform low intensity sled work (various drags)

–          Perform circuits of body weight exercise (Blast Strap/TRX stuff, single leg work, etc.)

–          Complexes with BB’s, DB’s or KB’s.

Keep in mind that the goal is to facilitate recovery while at the same time gradually increasing work capacity. Therefore, do not perform 20 sets of hill sprints or maximal effort complexes on day 1 if you plan on moving any kind of decent weight that week. The goal is to;

  • Maintain an elevated heart rate
  • Enhance blood flow to sore muscles

What about intervals?

Yes, interval work can provide much of the benefits that aerobic exercise has to offer. However, intervals are much more stressful and taxing. Interval work can be better tolerated after a sufficient level of work capacity has been established. If you’re not concerned with strength levels than by all means proceed with intervals. However keep in mind that conditioning work with intervals is not necessarily facilitating recovery and will likely result in a lower HRV score the following day. Assess your situation and goals and make an appropriate decision.

If you progress your work capacity properly you shouldn’t see any negative effect on your strength levels. This isn’t about “concurrent” training were we want to build endurance and strength at the same time. It’s more about keeping strength the priority and gradually building work capacity at an intensity low enough that it doesn’t contribute to overall stress but rather facilitates recovery from it. This is how I prefer to do it.

Approaching this with athletes in a team setting is a different animal and I will hopefully share my thoughts on that another time as this article is already longer than I wanted it to be.

Summary:

–          Aerobic exercise will typically increase HRV, better HRV results in more favourable responses to training

–          Aerobic exercise can be anything that maintains an elevated HR

–          Strength athletes can benefit from increased work capacity

–          Progress from very low stress active recovery work to higher levels over time

–          Use these workouts to facilitate recovery, improve mobility, enhance blood flow and maybe do the stuff you need to do that you can’t get to during your main lifts

If you have anything to add, refute, share, etc. I’d love to hear it. Comment below or email me andrew_flatt@hotmail.com.

I joined Twitter recently so we can interact there too @andrew_flatt.

References

Albinet, C. A., Boucard, G., Bouquet, C. A., & Audiffren, M. (2010). Increased heart rate variability and executive performance after aerobic training in the elderly. European Journal of Applied Physiology. 109(4):617-24

Gamelin, et al. (2007) Effect of training and detraining on HRV in healthy young men. International Journal of Sports Medicine, 28(7): 564-70

Levy, WC., et al. (2004) Effect of endurance exercise training on HRV at rest in healthy young and older men. American Journal of Cardiology, 82(10): 1236-41

Nagai, N., et al (2004) Moderate physical exercise increases cardiac autonomic nervous system activity in children with low heart rate variability. Journal of the International Society of Pediatric Neurosurgery, 20(4): 209-14

How to increase HRV: Part 2 – Nutrition

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In Part 1 of this series I discussed inflammation and its relationship with HRV. Through monitoring my HRV daily I’ve learned that nutrition plays an important role in improving or reducing your adaptive capacity. Eating foods that promote inflammation in the body creates stress that your body must deal with. In dealing with this stress we reduce our ability to adapt and recover from training. Below is a screen shot of my HRV trend over a week of eating large amounts of foods commonly known to promote inflammation. You can see my scores drop each day and only return once I resumed eating better foods. This experience inspired this article series. To discuss the details of nutrition and inflammation I’ve recruited the help of my friend and PhD candidate Marc Morris.

Hi

My name is Marc Morris and I am a PhD student in Nutrition at the University of Saskatchewan. First, I’d like to thank Andrew for the invitation to participate in the discussion surrounding the use of heart rate variability and strength training. The utility of HRV in strength training is very interesting to me. Being a competitive powerlifter, I am always actively seeking ways to improve my training cycles. Truthfully, I don’t know a great deal about this measurement. What I do understand, however, is the potential that exists in a real-time measurement of the autonomic nervous system. Monitored on a daily basis, HRV may provide a tool from which we can objectively auto-regulate our training.

The goal of a dedicated athlete should be to maximize his or her adaptability to training. This is done in part by minimizing unnecessary stress on the body outside of training. From a nutritional standpoint, what you eat (or don’t) can play a significant role in your recovery and adaptability. This is what drew me to nutrition in the first place. Is it possible to improve my performance and body composition through what I consume? Your lifestyle plays a very big role in your training status and may very well be the difference in the transition from mediocre to elite.

We’ve always been told what you eat can effect performance (I’ve also learned that it’s a good idea to learn why you’ve always been told something on your own terms – usually these beliefs fall into the class of dogma). But, outside of eating complete junk and feeling like garbage, this is a tough concept to see and feel. It may not noticeably affect your body composition, it may not affect your energy, but it may be hindering your recovery. Chronic inflammation is not easy to “feel”. At least not until you’ve over done it.

My job today, and hopefully in future occasions, is to discuss how nutrition may influence inflammation, and what you can do to position yourself to be more adaptable in a training cycle. Andrew noticed a decreasing trend in his HRV over a week of entirely uncharacteristic eating (discussed here). This included plenty of processed foods, trans fats, refined carbohydrates and so on. These foods are common culprits of inflammation in the gut. Andrew felt well rested and rated his overall stress levels as low however his diet that week was creating an apparent stress that he couldn’t feel.

In Part 1, Andrew did a great job distinguishing what we know as acute inflammation, our body’s immediate response to injury and infection, and chronic systemic inflammation. As of late, “inflammation” has been a buzzword in most health circles. It has fallen victim to the black and white, all is bad classification. Chronic inflammation is a lingering, low-grade condition that has been linked to just about every health condition in the modern world, from heart disease to cancer. Managing this type of inflammation will help you not only avoid chronic disease in the latter half of your life, but could improve your performance now.

Health professionals may use biomarkers such as C-Reactive Protein (CRP, an acute inflammatory protein) and interleukin-6 (IL-6, a cytokine involved in the inflammatory response) to assess chronic inflammation (despite having a half life of 19-hours, CRP seems to correspond to the chronic condition pretty well). This may be suitable for someone that regularly visits the doctor. But, if you’re a healthy individual these tests will be costly and invasive (blood drawn). Additionally, this type of test won’t allow for an ideal frequency.

The most pronounced effect of diet on inflammation involves the essential fatty acids (EFA). Without going into too much of the physiology about this, the omega-3 and omega-6 fatty acids act as substrates in cascades that control inflammatory products (De Caterina and Basta, 2001 [free review]). Neither are bad, per se, however, the typical North American diet contains larger amounts of omega-6 that largely affect the pro-inflammatory pathway. This topic is so vast it deserves an entire blog post itself. The take home message would be: increase omega-3 intake to balance fats by eating fatty fish (or at least supplement with fish oil).

The ingestion of trans-fats have been shown to increase inflammatory markers, such as the aforementioned markers, CRP and IL-6 (Baer et al. 2004). To minimize low-grade chronic inflammation this would be a fatty acid to avoid (Calder et al. 2011). Foods such as pastries, doughnuts, margarine, and other snack foods commonly have high amounts of this unhealthy fat. So, apart from minimizing excess calorie intake, the high trans fat content of “junk” foods and its effect on inflammation is another reason to avoid these.

The last dietary factor I would like to address today would be alcohol. In small doses (1-2 drinks/day), alcohol has consistently shown to have an anti-inflammatory effect. Above this moderate dose, this effect changes to pro-inflammatory. So a glass of red wine every once in a while isn’t such a bad thing. However, going out and having 10 drinks will have some unwanted effects on your recovery (inflammation being only one of many negative effects).

It is important to acknowledge that not everyone is the same. Dietary choices may have a differing inflammatory response in each person. Having said that, below this article there is a chart of foods that are typically anti-inflammatory verses foods that are typically pro-inflammatory.

That’s it for today. In future posts, I’d like to address the macronutrient composition of the diet and the hypothesized mechanisms for dietary related inflammation.

Note: We are reluctant to categorize foods as in many cases it’s effect on the body is conditional. For example, lactose intolerant individuals will have a more adverse reaction to dairy than one who isn’t lactose intolerant. People with gluten sensitivity should obviously avoid gluten. So take this chart with a grain of salt as they are just intended to be generalizations.

Foods That Promote Inflammation

Foods That Reduce Inflammation
Pastries/Doughnuts Ginger
Margarine Tumeric
Dairy Onions
Gluten Garlic
Refined Wheat Products (breads, pastas) Citurs Peel
Peanuts Olive Oil
Hydrogenated Oils Organic, Grass Fed Meats
Vegetable Oil Wild Caught Fish
Grain/Corn Fed Meat and Fish Green Tea
Processed/Deli Meats Green Veggies (Broccoli, Kale)
Sugar Berries

Practical Applications:

  • Try and stick to grass fed meats and wild caught fish
  • Eat plenty of fruits and vegetables
  • Drink tea
  • Use spices and herbs when cooking
  • Use olive oil
  • Try to minimize refined carbohydrate sources

Note: We understand that eating this way isn’t entirely practical for students and busy folks. The key is simply to eat less of the foods you know may be hurting your progress and eat more of the ones you know will help.

References

De Caterina, R., Basta. G. (2001). European Heart Journal Supplements, 3 (Supplement D), D42–D49

Calder, P.C., Ahluwalia, N., Brouns F. et al. (2011). British Journal of Nutrition, 106, S3, 1-78.

Baer, D.J., Judd. J.T., Clevidence, B.A., et al. (2004). American Journal of Clinical Nutrition, 79, 969–973

If you’re not assessing (the ANS), you’re guessing

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“If you’re not assessing, you’re guessing” is a phrase often used by strength and conditioning professionals to explain the importance of movement assessment prior to exercise prescription. Prescribing a program that doesn’t consider the athlete’s movement ability (or lack thereof) can end up causing problems.Essentially, you would be guessing that your exercise prescription is helpful when in fact it could be exacerbating a problem. I wholeheartedly agree with this. However this article has nothing to do with movement assessment. This was just my way of illustrating what my next point is.

I am going to apply the same logic we use for why we assess movement (to influence program design) with monitoring the function of the autonomic nervous system (ANS); if you’re not assessing the ANS, you’re guessing.

If you’re unfamiliar with what the ANS is and why it’s important I suggest you read this. In a nutshell the ANS governs “rest and digest” and “fight or flight” responses in the body. This is done without our conscious control. The two components of the ANS are the parasympathetic branch and sympathetic branch. Sympathetic activity is elevated in response to stress be it physical, or mental. Adrenaline is secreted and catabolic activity (the breakdown of structures) ensues. Parasympathetic activity is elevated in the absence of stress and functions to heal and repair the body.

We can monitor our ANS status non-invasively and inexpensively through heart rate variability (HRV). I explain how you can do this here.

HRV as an indicator of autonomic function can tell you a tremendous amount about your athlete’s responsiveness to training. I shared plenty of research in this post that lends support to HRV as an effective tool for; reflecting recovery status, showing better adaptation to training and even predicting performance. In a separate post I shared my thoughts on HRV as a predictor for injury.

Let me summarize what I shared in my initial research review post;

HRV reflects recovery status in elite Olympic weightlifters (Chen et al 2011), national level rowers (Iellamo et al 2004) and untrained athletes (Pichot et al 2002).

Cipryan et al (2007) showed that hockey players performed better when HRV was high while performance was rated lower when HRV was low.

Endurance athletes who improved vo2 max had consistently high HRV while athletes who did not improve vo2 max had low HRV (Hedelin et al 2001).

Endurance athletes who trained using HRV to determine their training loads had a significantly higher maximum running velocity compared to athletes in a pre planned training group (Kiviniemi et al 2007, Kiviniemi et al 2010).

Female athletes who used HRV to guide their training increased their fitness levels to the same level as females in a pre planned training group but the HRV group had fewer high intensity training days (Kiviniemi et al 2010).

(references for the above articles can be found in my original post here.

I’d now like to show some more research that lends support to the usefulness of HRV in monitoring athletes.

Mourot, L (2004) saw decreased HRV in overtrained aerobic athletes. Uusitalo et al (2000) also saw decreased HRV in overtrained female aerobic athletes.

Huovinen et al (2009) measured HRV and testosterone to cortisol (T-C) ratio in army recruits during their first week of basic training. The training was class room based (not physical) and therefore all stress can be considered mental. The authors found that HRV declined in several soldiers, though not all. This demonstrates that, what can be interpreted as stress is highly variable and dependent on the individual. The authors used the terms “high responders” and “low responders” to describe the differences among soldiers. Immediately I thought about the differences among athletes and how their bodies perceive stress. You can’t assume everyone is responding in kind to a training program. What is stressful for one athlete may not be as stressful to another.

All soldiers that showed decreases in HRV also showed lower T-C ratios. In contrast, soldiers with higher HRV had higher T-C ratio’s. Baseline T-C levels were not recorded so we shouldn’t draw any concrete conclusions however it appears that low HRV (increased sympathetic activity with parasympathetic withdrawl) is associated with a reduced T-C ratio.

Hellard et al. (2011) found that in national level swimmers, as HRV dropped (sympathetic predominance) there was an increased risk of illness. The drops in HRV that lead to illness were preceded by a sudden increase in parasympathetic activity the week prior to illness. The authors speculated that the preceding increase in HRV (parasympathetic/vagal activity) was a reflection of the body experiencing the first incubation period and that an increase in vagal activity was a protective response trying to modulate the magnitude of early immune responses to inflammatory stimuli. The subsequent increase in sympathetic activity and decrease in HRV occurs during the symptomatic phase of the illness.

In humans, increased sympathetic activity is generally associated with inflammatory responses while parasympathetic predominance actually inhibits inflammation. At this point in time I will not elaborate on this for the simple fact that I don’t fully understand it. However, we can speculate that if we’re seeing consistently low HRV scores in ourselves or our athletes there is probably an increase in inflammation occurring. Check out Thayer (2009) for more information regarding HRV and inflammation. Simon from iThlete sent me that paper and I’m still processing it.

When dealing with a team or if we train multiple athletes at the same time we need to be aware of how they are adapting and recovering from training. Work by Hautala et al (2001) shows that athletes will recover from exercise at different rates according to fitness levels (obviously). Basically, fit individuals recover faster and show less HRV fluctuation compared to less fit individuals. In a team setting, some individuals who are highly fit may not be getting a sufficient training stimulus while other athletes who are less fit can be overworked.

Kiviniemi et al (2010) found that females take longer to recover from aerobic training than males. This needs to be considered if you are training a mixed gender group.

Buchheit et al (2009) and Manzi et al (2009) both found HRV to be a predictor of aerobic performance.

I’m well aware that the development of athletes has been taking place without the use of HRV monitoring. There are many great coaches and trainers who have their own systems and methods of monitoring recovery in their athletes that work well.

HRV is a tool to use within your own systems. I have thoughts about how I would implement this in a team setting that I will share another time.

To truly autoregulate the training of ourselves or of athletes, we need as much information about present physiologic status as possible. Based on the research and my own personal experience with HRV, this technology takes much of the guesswork out of load/volume manipulation and training prescription. Training hard when HRV is low can be counterproductive and delay recovery. Training hard when HRV is chronically low can lead to illness, injury, overtraining syndrome and suppressed testosterone. Alternatively, increasing load/volume on days when HRV is high can lead to more favourable adaptation. HRV can tell us how stressful the training was for our athletes based on how long it takes HRV to reach baseline in subsequent days. HRV can indicate how much stress your athlete is experiencing outside of training. There are several indications one can take from a simple HRV measurement. Further research will reveal more correlation between HRV and sports performance.

I believe that to train an athlete optimally, we need to be assessing the state of the autonomic nervous system… otherwise we’re guessing.

References:

Buchheit, M. et al (2009) Monitoring endurance running performance using cardiac parasympathetic function. European Journal of Applied Physiology, DOI 10.1007/s00421-009-1317-x

Hellard, P., et al. (2011) Modeling the Association between HR Variability and Illness in Elite Swimmers. Medicine & Science in Sports & Exercise, 43(6): 1063-1070

Huovinen, J. et al. (2009) Relationship between heart rate variability and the serum testosterone-to-cortisol ratio during military service. European Journal of Sports Science, 9(5): 277-284

Kiviniemi, A.M., Hautala A.J., Kinnunen, H., Nissila, J., Virtanen, P., Karjalainen, J., & Tulppo, M.P. (2010) Daily exercise prescription on the basis of HR variability among men and women. Medicine & Science in Sport & Exercise, 42(7): 1355-1363.

Manzi, V. et al (2009) Dose-response relationship of autonomic nervous system responses to individualized training impulse in marathon runners. American Journal of Physiology, 296(6): 1733-40

Mourot, L. et al (2004) Decrease in heart rate variability with overtraining: assessment by the Poincare plot analysis. Clinical Physiology & Functional Imaging, 24(1):10-8.

Thayer, J. (2009) Vagal tone and the inflammatory reflex. Cleveland Clinic Journal of Medicine, 76(2): 523-526

Uusitalo, A.L.T., et al (2000) Heart rate and blood pressure variability during heavy training and overtraining in the female athlete. International Journal of Sports Medicine, 21(1): 45-53