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Detailed review of overtarining and heart rate variability

Overtraining is a risk for any person engaging in regular physical activity and is defined as an imbalance between stress and recovery, with the balance shifted towards stress.  Overtraining can be caused by too much physical stress as well as excessive psychological stress.  One of the consequences of overtraining is a decrease in heart rate variability due to altering the balance of the autonomic nervous system (ANS) towards the parasympathetic nervous system (PSNS) and away from the sympathetic nervous system (SNS).

Heart rate variability (HRV) is a measure of constant fluctuations in the rhythm of the heart.  HRV gives an instant “snapshot” of the status of the ANS.  It is measured by an ECG and is analyzed by a variety of different methods.  Depressed HRV is linked to overtraining and serves as a marker of cardiac risk.

Proper training can result in positive CV effects.  Excessive training can result in, among other things, autonomic imbalance and decreased HRV.  Patients who have experienced cardiac events or diabetic neuropathy also have a decreased HRV.   Therefore, HRV can serve as a method of detecting both overtraining in athletes as well of risk of recurring cardiac events in patients with previous problems.

How can this help athletes train and stay healthy?

  • HRV is more sensitive than HR
  • HRV can identify overreaching earlier
  • Depressed HRV can be used as early detection of overreaching/overtraining and risk of cardiovascular death post myocardial infarction.

 

The purpose of this article is to describe overtraining and link it to HRV changes.  Overtraining will be investigated and tied to HRV.  Four studies will be discussed relating overtraining with altered HRV.   Finally, HRV will be investigated in the clinical setting as it relates to patients with prior cardiac events.


 

OVERTRAINING – OVERVIEW

Overtraining is best described as an imbalance between stress and recovery, with the balance shifted towards stress.  Physiological stresses caused by too many training sessions, high volume, and high intensity as well as psychological stresses like mental fatigue and personal problems can cause overtraining (1,5).   Some of the symptoms of overtraining include:  reduced performance, fatigue, apathy, decreased immunity, headaches, insomnia, decreased appetite, hormonal imbalance, performance incompetence and decreased heart rate variability (1,5,6,10,14).  
       

Overtraining syndrome is not an acute problem, but it manifests itself gradually.  Overreaching refers to the beginning stages of overtraining and can be reversed with days to weeks of rest (5).  “Staleness” results from continual stress and lack of recovery and is observed by a decrease in performance (1).  Overtraining is a result of long-term stress and hormonal imbalance, and it can take months to years to correct (5).


 

 AUTONOMIC CONTROL OF THE HEART
Autonomic Nervous System.   The cardiovascular system is controlled by the autonomic nervous system (ANS) through the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS).  At rest, PSNS controls the CV system by decreasing heart rate, dilating blood vessels, increasing GI motility, and opening sphincters.  The PSNS serves as a “pacemaker” at rest and has nerve endings specifically on the sino-atrial node, on the atrial myocardium, and on he atrio-ventricular node.  The SNS produces opposite results and relies on increased catecholamines to stimulate the beta-receptors on heart (1). 

During exercise, heart rate increases as a result of PSNS withdrawal and increase in SNS activity (although the latter is debated).  Table 1 shows a summary of studies and describes PSNS and SNS activity during exercise.  PSNS consistently decreases or withdraws, but SNS activity is variable.
    Table 1 (Aubert Sports Med. 2003)

Heart rate and blood pressure control.  Heart rate and blood pressure are controlled by central command in the brain, CV control center in the brain stem, baroreceptors in the aorta and carotid artery, chemoreceptors and muscle afferent nerves (1,14). When exercise begins, central command activates the SNS, heart rate increases, and blood vessels constrict.  When exercise stops, SNS signaling is halted, heart rate lowers, and blood vessels dilate.  Baroreceptors control blood pressure by a negative feedback mechanism.  When blood pressure decreases, the baroreceptor signals the CV control center to increase heart rate by increasing SNS activity, when blood pressure is high, the opposite occurs (14).   When the body is functioning properly, there is a continual PSNS-SNS balance and heart rate and blood pressure are properly maintained.
 

 

TWO TYPES OF OVERTRAINING

Orthosympathetic-type fatigue.   Orthosympathetic-type fatigue is characterized by an increase in resting heart rate and blood pressure and is due to an over-stimulation of the SNS (3).  Orthosympathetic-type fatigue is less common in athletes and is due to inappropriate intensity in training sessions.  Symptoms include:  hyperexcitability, restlessness, and performance incompetence (6).

Parasympathetic (vagal) fatigue.  Parasympathetic fatigue is a result of exhaustion of the ANS; PSNS activity is increased, and SNS activity is inhibited (3). Parasympathetic fatigue is more common in athletes and is due to inappropriate volume of training sessions.  Symptoms include:  high fatigue, apathy, altered mood state, persistent performance incompetence, altered immune function, altered reproductive function, and hormonal imbalance (3,6).  The SNS is altered (slightly overactive) early in overtraining and inhibited late in overtraining.  Low resting heart rate and a delay in heart rate increase when exercise begins indicates an overactive PSNS and inhibited SNS (1,16).

Mechanism for parasympathetic fatigue.  Overtraining leads to a decreased adrenal responsiveness to ACTH.  To counteract this, the pituitary gland increases ACTH production and release, but it cannot overcome the reduced adrenal response.  After time, the pituitary gland shuts down ACTH production and release (6).  Consequences of the decreased ACTH response are: reduced adrenal cortisol response from the adrenal cortex (ACTH insensitivity), insulin-induced hypoglycemia (altered cortisol balance), and overproduction of catecholamines from the adrenal medulla (insensitivity of target organs) (6,8).

Consequences of hormonal imbalance.  Resting plasma catecholamine (epinephrine and norepinephrine) levels are significantly increased in an overtrained individual.  The bets-receptors on the target organs lose sensitivity and, in time, fail to respond to the catecholamines.  This suggests a protective mechanism against irreversible damage to the target organ.   The beta-receptors either lose sensitivity to the catecholamine, or the density of beta-receptors decreases (1,6).   The conclusion is that the fatigue and individual experiences could be due to “decreased beta-receptor-mediated metabolic and cardiac effects” which results in a decrease in submaximal heart rate, decrease in blood glucose, decrease in lactate threshold and decrease in free fatty acid responses (6).   Interestingly, at maximum effort or in high-stress situations, the beta-receptor responses are maintained, indicating that the fight-or-flight response is still present (6).

Similarities to beta-blockers.    The insensitivity of the beta-receptors due to overtraining results in decreased beta-receptor effects.  The catecholamine-beta-receptor mechanism adapts to the “reduced functional state of the fatigued target organs (6).”  This is similar to beta-blockers used to control blood pressure.  Lehmann et al. studied the effects of beta-blockers on 9 healthy individuals during exercise (8).  The individuals were given bunitrolol, methypranol, or a placebo prior to exercise. The results showed that the both beta-blockers increased plasma catecholamine levels during exercise compared to the placebo.  The exercise capacity decreased by 15% with both beta-blockers compared to the placebo.  Maximum heart rate decreased 20% in the bunitrolol and 25% in the methypranol group compared to the placebo.

 

HEART RATE VARIABILITY

Heart rate variability (HRV) is defined as the “continuous oscillation of the R-R intervals around its mean value” (7).  HRV gives an instant “snapshot” of the ANS and can show the balance between the PSNS and SNS (1,7).  
Measurement.  Clinical HRV measurement is done with an electrocardiogram (ECG).  The time of the ECG test depends on the study and can range for 10 minutes to 24 hours (Holter recordings) (1).   Environment, prior exercise, and diet are controlled to minimize interference in the ECG.  The time differences between R-R waves are calculated and presented in a variety of methods.  There are over 25 different presentations of HRV data in scientific literature, which makes comparing studies difficult (1,11). 

Two frequencies on the ECG are monitored and give insight to the activity of the PSNS and SNS.  Low frequency waves or Mayer waves, 0.04-0.15 Hz, represent a combination of SNS and PSNS activity, while high frequency waves, 0.15-0.5 Hz, represent only PSNS (vagal) activity (1,2,7).  A common HRV test is the tilt test.  The subject lies supine on a special tilting table while an ECG records heart activity.  After some time, the table tilts the subject upright to 70 degrees.  Heart rate changes are monitored during the upward tilt (3,5).
Increased vs. decreased HRV.  Increased HRV is a desirable change in training.  Proper endurance training shows an increase in HRV, and long-term training leads to improved heart function by increasing cardiac output (Frank-Starling and contractility).  Endurance training results in a reduced resting heart rate, reduced submax systolic and diastolic blood pressure, and reduced mean arterial pressure (1,14,20). 

Negative HRV changes occur with overtraining.  The cause is parasympathetic hypertonia and sympathetic inhibition (1,3,6,16).  There is a reduced resting heart rate, a reduced maximum heart rate, and slower exercise recovery (3).  Vasovagal syncope is also a problem in an overtrained individual (3).  The PSNS promotes a low heart rate and vasodilation.  When an individual is sitting, and stands up, there is a drop in blood pressure.  Normally, the baroreflex would signal the cardiac control center to increase heart rate and vasoconstrict via the SNS.  Since the PSNS is overactive and the SNS is inhibited, this reflex does not occur and the individual may lose consciousness.  Vasovagal syncope will be mentioned later as a sign of cardiac disease.
There is a contradiction or paradox that exists between a properly trained individual and an overtrained individual in regards to resting heart rate and blood pressure.  A decreased heart rate and blood pressure are desirable in properly trained individuals, but undesirable in overtrained individuals.  The difference is the function of the ANS.  In the properly trained individual, the PSNS withdraws and the SNS is able to “kick in” when needed and raise the heart rate and blood pressure.  An overtrained individual has an over-active PSNS that will not withdraw and an inhibited SNS that cannot “kick in.”   The combination of these two factors leads to an inability to generate the cardiac output needed to perform.

 

OVERTRAINING, HRV CHANGES, AND ENDURANCE TRAINING

Examples of HRV changes during heavy endurance training are plentiful.  Four studies will be presented which illustrate the spectrum of overtraining and the effect on HRV.

1.  Short-term overtraining.  Hedelin et al. studied 6 elite canoeists during a 6-day intensive training camp.  Maximum heart rate, maximum VO2max, and maximum lactate responses were significantly reduced in all subjects, but HRV was not significantly changed (5).  The conclusion is that short-term (<7 days) overtraining does not significantly change HRV but does change other cardiovascular markers.

2.  Medium-term overtraining.   Pichot et al. studied 7 national level mid-distance runners as they overtrained for 3 weeks and recovered on the 4th week (2).    The results of their training are shown in Table 2 below.  HR and SDNN represent heart rate and standard deviation of HRV.
Table 2  (Pichot Med. Sci. Sports Ex. 2000)

The HR and HRV recovery during the 4th week are ideal in a training program. Pichot concluded that the heavy training led to a dominant SNS over the PSNS (2).   These athletes were likely in the overreaching stage, and did not reach the level of ANS dysfunction.  Heart rate increased and HRV decreased with the increased workload, but both supercompensated when allowed to recover.  Most likely, the HRV would have continued to decrease if a recovery week was not inserted into the training and an overtraining state would have been reached.

3.  Overtraining.  Uusitalo et al. increased 9 female endurance athletes’ training volume at 70-90% VO2max by 125% and at <70% VO2max by 100% (4).  After the intensive training, the athletes’ VO2max decreased from 53 +/- 2.2 ml/kg/min to 50.2 +/- 2.3 ml/kg/min.  HRV low frequency detected a significant increase during rest that indicated an increase in SNS activity.  HRV from laying down to standing either increased or decreased depending on the subject.  Uusitalo concluded that heavy training can increase SNS activity during rest and may stop the baroreflex response when standing.  Uusitalo also concluded that HRV responses were individual.

4.  Overtraining.   Portier et al. studied nine experienced half- and full-marathon runners (VO2max 72.1 +/- 4.1 ml/kg/min) (3).  The runners trained easy for three weeks (2 workouts per week at 45 minutes each), followed by 9 intense weeks (9-10 workouts per week totaling 130-150km).  A VO2max test and tilt test were performed at the end of each training phase.  A comparison of heart rate and HRV between the easy training period and intense training period showed that there was a decrease in percent change of resting heart rate between laying down and standing after the intense training phase.   The HRV percent change also significantly decreased after the intense training period.  See Table 3.
Table 3 (Portier Med. Sci. Sports Ex. 2001)

Portier concluded that the heart rate response to the tilt test was diminished during the training period as a result of a greater influence of the PSNS.  Portier also concluded that there was a decrease in the HRV in the training phase compared to the detraining phase due to an advance state of fatigue (3).  

In this final study, it would be a mistake to only look at the heart rate data from the subjects in the intensive training period and conclude that the training is effective.   Normally, one would think that a lower resting heart rate would indicate a higher-trained athlete.  The individuals from this study have a lower resting heart rate at standing during the intensive period.   When the HRV is factored in, it is obvious that a low resting heart rate does not mean optimal training in overtrained endurance athletes.  The HRV % difference between the rest period and the training period shows that there is a significant decrease in HRV.  This data gives insight into diagnosing overtraining much more accurately than simply looking at resting heart rate.  

 

HEART RATE VARIABILITY IN CV DISEASE

The high PSNS activity and lowered orthostatic tolerance observed in overtrained athletes is similar to “patients being evaluated clinically for neurocardiogenic (vasovagal) syncope (3).”  Reduced HRV and increased PSNS activity is a common trend in patients with a history of cardiac incidents and may be inversely correlated with disease severity (9).   A major reason for measuring HRV clinically is its ability to predict survival after a myocardial infarction (11).  It is now widely believed that “reduced HRV may predict risk of survival even among individuals free of CHD (11).”   Gang et al. concluded “HRV is significantly depressed and associated with prognosis in post MI patients and diabetic neuropathy, and is significantly altered in patients with critical illness (9).”

Dekker et al. studied 14,672 men and women without CHD who were 45-65 yrs old.  A 2-minute rhythm strip test was recorded for each person.  Subjects with low HRV had a higher risk of incident CHD (relative risk of 2.10) and all cause death (relative risk of 1.51) compared to those with a higher HRV.  Dekker concluded that low HRV was related to higher risk of CHD and death form several causes (18).

Algra et al. tested HRV as a risk factor for sudden death by performing a 24-hour ECG on 6693 patients and following them for two years.  Of the 6693 patients, 245 died suddenly.  Long-term variability and short-term variability were analyzed separately.  Subjects with long-term variability had a relative risk of 4.4 and those with short-term variability had a relative risk of 4.1 compared to subjects with high variation (19).  Data was not given about how many of the 245 that died suddenly had depressed HRV.

Pardo et al. studied 20 cardiac patients undergoing cardiac rehabilitation.  A 24-hour ECG recording was performed at the beginning of the rehab program and 12 weeks into the program.  Pardo concluded that exercise conditioning improves HRV, especially in patients who exercised over 1.5 METS.  Exercise “lowers the risk of sudden cardiac death via increasing vagal tone, which likely beneficially alters ventricular fibrillatory and ischemic thresholds (12).”

Two clinical conditions currently benefit from the use of HRV to determine risk.   HRV predicts risk of arrhythmic events or sudden death after an acute myocardial infarction.  HRV is also used as a clinical marker of diabetic neuropathy (13).  

 

CONCLUSION

Overtraining leads to a variety of problems that can be traced to hormonal imbalances.  One of the consequences of overtraining is an imbalance in the autonomic nervous system with a shift to an overactive parasympathetic system and an inhibited sympathetic system.  This imbalance affects the cardiovascular system by depressing heart rate variability.   Numerous studies show that overtraining causes a depression in heart rate variability and impaired performance and recovery.  Patients who have suffered cardiac incidents also have depressed heart rate variability.  Heart rate variability is used to predict risk of recurring incidents and sudden death in these patients.  Ironically, rest and recovery is the only way for an athlete to recover and restore proper autonomic nervous system function, while exercise is the method used to improve heart rate variability and autonomic nervous system function in cardiac patients.  Heart rate variability can be used to diagnose and prevent overtraining in athletes as well as predict risk of cardiac incidents in cardiac patients.
 

 

SOURCES

1.    Aubert AE, B Seps, F Beckers.  Heart Rate Variability in Athletes.  Sports Medicine 33(12): 889-919, 2003.

2.    Pichot V, F Roche, J Gaspoz, F Enjolras, A Antoniadis, P Minini, F Costes, T Busso, J Lacout, J Barthelemy.  Relation between heart rate variability and training load in middle-distance runners.  Medicine & Science in Sports & Exercise 32(10): 1729-1736, 2000.

3.    Portier H, F Louisy, D Laude, M Berthelot, C Guezennec.  Intense endurance training on heart rate and blood pressure variability in runners.  Medicine & Science in Sports & Exercise 33(7): 1120-1125.

4.     Uusitalo ALT, AJ Uusitalo, HK Rusko.  Heart Rate and Blood Pressure Variability during Heavy Training and Overtraining in the Female Athlete.  International Journal of Sports Medicine 21: 45-53, 2000.

5.    Hedelin R, G Kentta, U Wiklund, P Bjerle, K Henriksson-Larsen.  Short-term overtraining:  effects on performance, dirculatory responses, and heart rate variability.  Medicine & Science in Sports & Exercise 32(8): 1480-1484, 2000.

6.    Lehmann M, C Foster. D Hans-Hermann. I Gastmann.  Autonomic imbalance hypothesis and overtraining syndrome.  Medicine & Science in Sports & Exercise 30(7): 1140-1145, 1988.

7.    Mourot L, M Bouhaddi, S Perrey, J Rouillon, J Regard.  Quantitative Poincare plot analysis of heart rate variability: effect of endurance training.  European Journal of Applied Physiology 91: 79-87, 2004.

8.    Lehmann  M, J Keul, K Wybitul, H Fischer. Effect of selective and non-selective adrenoceptor blockade during physical work on energy metabolism and sympatho-adrenergic system.  Drug Research 32(3):261-6, 1982.

9.    Gang Y, M Malik.  Heart Rate Variability Analysis in General Medicine.  Indian Pacing and Electrophysiology Journal 3(1): 34-40, 2003.

10.    Stein PK, A Reddy.  Non-Linear HRV and Risk Stratification in CV Disease. Indian Pacing and Electrophysiology Journal 5(3): 210-220, 2005.

11.    Hamaad A, M Sosin, AD Blann, J Patel, GY Llip, RJ MacFadyen.  Markers of inflammation in acute coronary syndromes: association with increased heart rate and reductions in heart rate variability.  Clinical Cardiology 28(12): 570-576, 2005.

12.    Pardo Y, CN Merz, I Velasquez, M Paul-Labrador, A Agarwala, CT Peter.  Clinical Cardiology 23(8): 615-620, 2000.

13.    Stys A, T Stys.  Current clinical applications of heart rate variability. Clinical Cardiology 21(10): 719-724, 1998.

14.    Powers S, E Howley.  Exercise Physiology 5th ed.  New York: McGraw-Hill 2004.  440-441.

15.    Legramante J, F Pigozzi, A Spataro, G Norbiato, D Lucini, M Pagini.  Conversion From Vagal to Sympathetic Predominance With Strenuous Training in High-Performance World Class Athletes.  Clinical Investigation and Reports 105: 2719-2726, 2002.

16.    Hedelin R, R Wiklund, P Bjerle, K Henriksson-Larsen.  Cardiac autonomic imbalance in an overtrained athlete.  Medicine & Science in Sports & Exercise 32(9): 1531-1533, 2000.

17.    Kaeachi I.  Heart Rate Variability.  John D. and Catherine T. MacArthur Research Network on Socioeconomic Status and Health. 2000. http://www.macses.ucsf.edu/Research/Allostatic/notebook/heart.rate.html

18.    Dekker JM, RS Crow, AR Folsom, PH Hannan, L Duanping, SA Cees, EG Schouten.  Low Heart Rate Variability in a 2-minute Rhythm Strip Predicts Risk of Coronary Heart Disease and Mortality From Several Causes: The ARIC Study.  Circulation 102: 1239-1244, 2000.

19.    Algra A, JG Tijssen, JR, Roelandt, J Pool, J Lubsen.  Heart rate variability from 24-hour electrocardiography and the 2-year risk for sudden death.  Circulation 88: 180-185, 1993.

20.    Shier D, J Butler, R Lewis.  Hole’s Human Anatomy and Physiology 9th ed.  New York: McGraw-Hill. 2002.  520-525.
 


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