Secondary Logo

Journal Logo

Original Research

Autonomic Responses to an Acute Bout of High-Intensity Body Weight Resistance Exercise vs. Treadmill Running

Kliszczewicz, Brian M.1; Esco, Michael R.2; Quindry, John C.3; Blessing, Daniel L.3; Oliver, Gretchen D.3; Taylor, Kyle J.4; Price, Brandi M.1

Author Information
Journal of Strength and Conditioning Research: April 2016 - Volume 30 - Issue 4 - p 1050-1058
doi: 10.1519/JSC.0000000000001173
  • Free



In recent years, high-intensity training programs (HITPs) have garnered a fervent following from military personnel, athletes, and the general population. Often referred to as “extreme conditioning programs,” HITPs involve a high volume of multiple modes of exercise performed over a short duration (i.e., typically less than 30 minutes) (2). A clear advantage of this form of training is the requirement of little equipment. For example, many HITPs involve body-weight-only exercises, such as push-ups, pull-ups, and bodyweight squats performed in a circuit-style format (2). Because of low resting intervals and high-intensity nature of this form of exercise, a high degree of physiological strain during each session may be possible (1). This has led to mainstream criticism over the potential health risks associated with an acute bout of the HITP (15). However, there is very limited research available to substantiate or refute the majority of these anecdotal claims.

The autonomic nervous system (ANS) plays a key role in modulating the homeostatic visceral functions of the body, such as cardiovascular activity, blood pressure, and thermoregulation. With an increase in exercise intensity, both arms of the ANS act in accord to increase cardiac activity and control hemodynamics through a reduction in parasympathetic activity and concurrent shift towards sympathetic dominance (28). The magnitude and timing of sympathovagal recovery appear to be related to the intensity of the performed exercise (7,9,28). Incidentally, prolonged sympathetic predominance and delayed parasympathetic recovery after exercise are to thought to be associated with increased risk of acute cardiac events, such as ventricular dysrhythmias (26,27,37). Therefore, analyzing the activity of the ANS may be useful when comparing physiological strain after various bouts of exercise (17,35).

ANS activity can be evaluated noninvasively by heart rate variability (HRV) and invasively through circulating plasma catecholamines. HRV is obtained through the quantification of the oscillations that occur between consecutive R-R intervals derived from an electrocardiogram (ECG) (8,23,28). Circulating plasma catecholamines, epinephrine (E) and norepinephrine (NE), are sympathetic neurohormones that are released into circulation from the adrenal glands in response to stress (38). Essentially, heightened sympathetic activity is related to elevated circulating catecholamine levels and lowered HRV, whereas the opposite is observed during periods of parasympathetic dominance. The time courses of HRV recovery and catecholamine “clearance” are often studied to gauge the responsiveness of the ANS to acute bouts of exercise. The majority of studies comparing the time course of ANS recovery between bouts of exercise are traditionally intensity based (7,28,33). For example, Parehk and Lee (28) examined markers of HRV following treadmill running at varying intensities, low-intensity (LO-50% V[Combining Dot Above]O2max) vs. high-intensity (HI-80% V[Combining Dot Above]O2max), whereas Rezk et al. (33) compared the effects of multiple bouts of resistance-based exercise at varying intensities of 40% and 80% of 1RM. However, studies examining ANS activity between different modalities at similar intensity are lacking.

To date, a limited number of studies examining the activity of the ANS during recovery from an acute bout of the HITP exist, while even less has been compared to intensity-matched aerobic modalities. Research in this area may provide important information regarding safe and effective prescription of HITPs. Therefore, the purpose of this investigation was to compare postexercise ANS recovery between an acute bout of an HITP vs. typical treadmill running in physically active men.


Experimental Approach to the Problem

All data were collected in the Human Performance Laboratory (HPL), Auburn University at Montgomery. Each participant arrived at the HPL on three separate occasions. The first visit consisted of informed consent, health screening, familiarization of the protocols, and a graded exercise test. The additional 2 visits included an exercise trial, between the times of 7 AM and 11 AM. The exercise trials were carried out in a randomized crossover fashion between the HITP and TM. Each visit was separated by a minimum of 3 days and a maximum of 7. Exercise trial visits consisted of a 20-minute bout of either HITP or TM, with preperiod and postperiod measurements of HRV through ECG. In addition, premeasures and postmeasures of the catecholamines, E and NE, were obtained through plasma sampling. After a resting ECG was acquired, blood plasma samples were taken from participants. After the blood draws, each participant performed a standardized 5-minute warmup on the treadmill, rested for 1 minute, and then performed the exercise bout of the HITP or TM. After the bouts, designated blood draws and ECG measurements were obtained. The study design can be seen in Figure 1. The participants were not allowed to eat during the 2-hour recovery period. HR intensity (%HRmax) and rate of perceived exertion (RPE) scale numbered 1–10, with 1 being no exertion and 10 being maximal effort, were examined during this study to ensure similar effort between trials.

Figure 1
Figure 1:
Study design. ECG samples were taken at designated time points, represented ECG icons. Plasma catecholamines (E, NE) were taken at designated time points, represented by blood draw (syringe) icons. PRE = pre-exercise; IPE = immediately post exercise; 1HP = one-hour post exercise; 2HP = 2-hour post exercise. Samples taken before and after (randomized, crossover design) 20-minutes HITP and TM bouts. ECGl = length of ECG recording; ECGs = ECG segment analyzed for HRV.
Table 1
Table 1:
Participant characteristics.*


Auburn University and Auburn University at Montgomery institutional review boards approved this study. Before participation, signed informed consent was obtained from each participant. Ten apparently healthy males participated in this study; descriptive data expressed as the mean ± SD can be seen in Table 1. Each participant had a minimum experience of 3 months for performing high-intensity exercise. All participants were determined to be low risk for cardiovascular, metabolic, and/or pulmonary diseases as determined by PAR-Q and Health History Questionnaire. An inability to properly perform required movements, maximal oxygen consumption (V[Combining Dot Above]O2max) under 40 ml·kg−1·min−1, or any symptom or contraindication of health resulted in exclusion from the study. The participants were informed that they could withdraw from the study at anytime. Participants were instructed to wear exercise clothing for testing, abstain from exercise 24 hours prior, and abstain from caffeine 12 hours before exercise testing sessions.

Table 2
Table 2:
Exercise intensity (perceived and %HRmax).*†


Maximal Exercise Capacity and Anthropomorphic Measurements

Maximal exercise capacity (V[Combining Dot Above]O2max) and maximal heart rate (HRmax) were assessed during the first session through a graded exercise test (GXT) on a treadmill (Trackmaster, Newton, KS, USA). Using a Bruce protocol, the workload during the GXT was increased incrementally every 3 minutes until a maximal value was reached. Expired gas (oxygen and carbon dioxide) fractions were sampled continuously using a pneumotach, mixing chamber, and gas analyzers through a Parvo Medics cart (Sandy, UT, USA). During the GXT, heart rate was assessed continuously using a heart rate monitor (Polar Electro Oy, Oulu, Finland). Test termination required achievement of 2 of the following criteria: a plateau in V[Combining Dot Above]O2 occurring with increasing workload; respiratory exchange ratio of >1.10; heart rate within 10 beats of age-predicted maximum (220 − age).

Body fat percentage was assessed through use of a total body dual-energy X-ray absorptiometry scan (GE Lunar Prodigy, Software Version 10.50.086; GE Lunar, Corp., Madison, WI, USA). Subject characteristics for aerobic and body composition data are presented in Table 1.

High-Intensity Training Protocol

The HITP protocol used in this study was the CrossFit named workout “Cindy.” The workout consists of as many rounds possible of 5 pull-ups, 10 push-ups, and 15 air squats (nonweighted squats, fully standing to hips below parallel) in 20 minutes. The workout required that one complete all prescribed repetitions to be done for the movement before moving on to the next and to do so as fast as possible. Each movement was standardized for all participants. Failure to achieve these standards resulted in the participant correctly repeating that movement. On completion of the workout, the participants were placed in a seated position for blood draws for designated periods for postexercise E and NE analysis. After the initial postexercise draw, the participants were then placed into a supine position for the designated periods of time, during which postexercise ECG was obtained to analyze HRV.

High-Intensity Treadmill Protocol

To perform the TM trial, the participants performed a minimum of 85% maximal HR obtained during the GXT. The target HR for this trial was determined following a pilot study, Kliszczewicz et al. (22). The study demonstrated that participants who completed this HITP protocol achieved 85% of their HRmax when compared to their GXT. The participants ran for a total of 20 minutes at a rate and incline that yielded an HR response within the target zone. On completion of the workout, the participants were placed in a seated position for blood draws for designated periods for postexercise E and NE analysis. After the initial postexercise draw, the participants were then placed into a supine position for the designated periods of time, during which postexercise ECG was obtained to analyze HRV.

Heart Rate Variability

For HRV assessment, the participants were placed in a quiet, dimly lit room and instructed to lie in a supine position on a comfortable examination table. ECG assessment was performed with a modified lead II configuration using 3 Ag/AgCl electrodes and was interfaced with a Biopac MP100 data acquisition system (Goletta, GA, USA). Three separate ECG recordings were obtained throughout each trial; Two, 10-minute segments with one at PRE and one at after 60 minutes, one 30-minute ECG segment immediately after the exercise bouts. The ECG recordings obtained in this study were divided into five 5-minute segments for analysis of HRV: the PRE time point measuring the last 5 minutes of the 10-minute recording; the POST time points from the 30-minute postexercise recording, which was broken down into 3 POST 5-minute segments at 15–20, 20–25, and 25–30 minutes; and the 60-minute postexercise ECG recordings examining the last 5 minutes of the 10-minute recording. All ECG segments were visually inspected for ectopic/nonsinus beats, which were replaced by the adjacent R-R interval when observed. Any segment containing 3 or more ectopic beats was excluded from analysis.

The markers chosen for HRV in this study were the time domain as the root mean square of the SD of consecutive N-N intervals (RMSSD) and the frequency domain as high frequency (HF) power (0.15–0.40 Hz). The transformation of ECG into time domain and frequency domain components was done through specialized HRV software (Nevrokard Version 11.0.2; Izola, Slovenia). To assess RMSSD, the ECG recordings were converted into a tachogram, which plots the successive R-R intervals (y-axis) against the number of beats within the ECG (x-axis). From the tachogram, the 5-minute segments were calculated for RMSSD. Analysis of the frequency domain was performed through a power spectral analysis, which was completed by applying a fast Fourier transformation to the R-R intervals of the sampled ECG. RMSSD and HF are sensitive markers of parasympathetic activity and have been used in several studies (4,25,29–31). RMSSD is not significantly influenced by breathing frequency and is capable of measuring parasympathetic activity in a short period of time (31), making it a suitable marker for this study. The frequency domain has several components (i.e., VLF, LF, HF, LF:HF); however, HF is the only frequency marker that is widely accepted to accurately reflect vagal activity (3,4,7,12,19,23).

Blood Samples and Storage

Blood samples were collected and assayed for the catecholamines, E and NE, at the following time points: before exercise (PRE), immediately post exercise (IPE), 1-hour post exercise (1HP), and 2-hours post exercise (2HP). The participants were in a seated position while the 10-ml blood samples were taken. Draws were taken via venipuncture through the antecubital vein and were collected in EDTA tubes (2 ml) and heparinized tubes (8 ml). The heparinized tubes were immediately centrifuged at 3,000 rpm for 15 minutes, aliquoted, and stored in a ultralow freezer at −80° C until subsequent assay. Hematocrit and hemoglobin were determined using EDTA tube whole-blood aliquots using a hematology analyzer (CellDyn 1800; Abbott Park, IL, USA). The participants were instructed to abstain from food or beverage other than water during the postexercise period.

Blood plasma samples were assayed for E and NE using a commercial available ELISA kit (ABNOVA). Protocols followed assay kit instructions, and findings were reported as ng·ml−1. All samples were normalized for plasma-volume changes that occurred after the exercise trials using the formulas based on the established protocols of Dill and Costill (11), normalizing plasma through hemoglobin and hematocrit levels compared to preexisting levels.

Statistical Analyses

Subject HRV data were entered into SPSS for statistical analysis. A Shapiro-Wilk test was used to determine normal distribution of HRV data. Because data were skewed, a natural logarithmic transformation was performed on the RMSSD and HF data before further statistical analysis, which is commonly performed in markers of HRV (7,9,28). A 2 (trial) × 5 (time) repeated-measures analysis of variance (ANOVA) with a Bonferroni correction was used to assess differences from resting HRV to postexercise HRV in and between both HITP and TM trials. A paired samples t test was used to further assess differences between trial-to-trial time points and pre to 1-hour post same-trial time points. Statistical analysis was performed on SPSS 19.0 (Chicago, IL, USA). Statistical significance was set to α ≤ 0.05. Data presented as the mean ± SD.

Subject blood plasma E and NE data were entered into SPSS for statistical analysis. A 2 (trial) × 4 (time) repeated-measures ANOVA with a Bonferroni correction was used to assess differences from resting E and NE to postexercise values in and between both HITP and TM. For the key dependent variables, Mauchly's test was run to determine that there was no violation of sphericity. Statistical analysis was performed on SPSS 19.0 (Chicago, IL, USA). A paired samples t test was used to further assess differences between trial-to-trial time points and pre to 2-hour post same-trial time points. Statistical significance was set to α ≤ 0.05. Catecholamine data presented as the mean ± SE of the mean.


All 10 participants of the study completed pre-exercise and postexercise supine HRV analyses and blood draws for the HITP and TM trials. The participants completed an average of 21.5 ± 1.3 rounds of the HITP trial. In addition to monitoring HR for intensity, an RPE scale numbered 1–10, with 1 being no effort and 10 being maximal effort, was used. Percent HRmax and RPE were used to ensure a similar effort of intensity between trials; results are presented in Table 2. The markers of HRV are presented in lnRMSSD (Figure 2A) and lnHF (Figure 2B); plasma catecholamines are presented in E (Figure 3A) and NE (Figure 3B). Marker values and significance can been seen in Table 3.

Figure 2
Figure 2:
Heart rate variability log transformed (ln) presented as the mean ± SD. A) Time domain lnRMSSD. B) Frequency domain lnHF. *Significantly different from PRE, #significantly different from HITP. TM = solid line; HITP = dashed line.
Figure 3
Figure 3:
Plasma biomarkers of catecholamines, before and after exercise, mean ± SE of the mean, n = 10. A) Plasma epinephrine concentration. B) Plasma norepinephrine concentration. *Significantly different from PRE = #Significantly different from HITP; +Significantly different from HITP 1HP.
Table 3
Table 3:
Autonomic nervous system markers of stress presented as the log-transformed markers of HRV {root mean square of the SD of consecutive N-N intervals (lnRMSSD) and frequency domain as high frequency (HF) power (0.15–0.40 Hz); plasma catecholamines (epinephrine [E] and norepinephrine [NE])}.*†

Heart Rate Variability

The repeated-measures ANOVA revealed that both HITP and TM trails experienced a time-dependent change in lnRMSSD. For instance, lnRMSSD dropped significantly in all time points when compared to PRE values after the bout of the HITP (p ≤ 0.05). A paired samples t test revealed POST 60-minute lnRMSSD after HITP remained significantly lower than PRE lnRMSSD values (p ≤ 0.05). After the TM bout, a significant, yet lesser time-dependent change in lnRMSSD was observed (p ≤ 0.05), which returned to near-baseline values by POST 60-minute with no statistical difference from PRE (p = 0.17). A significant trial-to-trial difference was observed between the HITP and TM. After a bout of the HITP, a significantly greater depression of lnRMSSD occurred in each POST time point when compared to TM values (p ≤ 0.05).

The repeated-measures ANOVA of the frequency domain revealed a significant time-dependent decrease in lnHF after both HITP and TM trials (p ≤ 0.05). In both HITP and TM, POST 15–20-, 20–25-, and 25–30-minute lnHF were significantly lower compared to PRE values (p ≤ 0.05); however, POST 60-minute only remained significantly depressed after the HITP (p ≤ 0.05), whereas TM returned to nonsignificant values (p = 0.09). A trial-to-trial comparison revealed a significant difference between the first three recovery time points with HITP lnHF being significantly lower (p ≤ 0.05). After a bout of the HITP, a significantly greater depression of lnHF occurred in each POST time point when compared to TM values (p ≤ 0.05).


There was an observed time-dependent effect in plasma catecholamine marker E, with approximately a 4-time increase after the HITP (p ≤ 0.05) and approximately 2-time increase after TM (p ≤ 0.05) at IPE; however, E returned to resting concentration by 1HP in both trials (p = 1.00, p = 1.00). A trial-to-trial comparison of E concentration revealed a significant difference between the time points, IPE (p ≤ 0.05) and 1HP (p ≤ 0.05), with no significance at 2HP (p = 0.10).

Similarly, a time-dependent effect was observed in plasma NE concentration at IPE with an approximate 5-time increase after the HITP (p ≤ 0.05) and an approximate 3-time increase after TM (p ≤ 0.05). NE returned to baseline at 1HP (p = 1.00) and 2HP (p = 0.74) in the TM trial, whereas 1HP after the HITP remained slightly elevated (p ≤ 0.05) and returned to baseline at 2HP (p = 0.18). A trial-to-trial comparison of NE concentration revealed a significant difference between the time points, IPE (p ≤ 0.05) and 1HP (p ≤ 0.05), with no significance at 2HP (p = 0.08).


The purpose of this investigation was to evaluate the magnitude of ANS disruption through HRV and catecholamines after an acute bout of bodyweight resistance–based HITP exercise in physically active men. Additionally, these results were compared to a bout of treadmill running that was closely matched for intensity. The results of this study supports our hypothesis that each trial would elicit an acute drop in both markers of HRV (lnRMSSD and lnHF) and a subsequent rise in plasma catecholamines (E and NE), with HITP would eliciting a greater alterations in these markers. Although it has been shown that exercise intensity is a factor in alteration of ANS activity (28), this study is the first to observe differences between a bout of HITP and a closely matched intensity bout of treadmill running.

To normalize the trials, %HRmax, and RPE were used to guide and match intensities (24). The average HR was statistically different between groups; in that, the HITP elicited a higher response than TM. However, HR responses between the HITP and TM are not believed currently to be of physiological significance; in that, the average %HRmax in each trial is classified as vigorous intensity according to American College of Sport Medicine (ACSM) criteria (14). Similar to HR, subjective quantification of exercise intensity by RPE also differed between trials, with HITP eliciting a higher mean. Despite subtle differences in indices of exercise intensity, both HITP and TM sessions were of high intensity in terms of broad classifications (14).

It is well established that the intensity of exercise influences the magnitude and duration of depressed HRV (7,28,35). Parekh and Lee (28) examined differences in intensity between 50% and 80% V[Combining Dot Above]O2Reserve in treadmill running, finding that 80% produced a greater drop in lnHF and HFnu. Similarly, Buchheit et al. (7) observed a greater drop in RMSSD and lnHF after high-intensity running versus submaximal running. Despite the observed influence of intensity within the current literature, this study found a greater depression of lnHF and lnRMSSD after the HITP compared to TM running although HR intensities were similar.

The trial-dependant differences in HRV observed in this study are in agreement with the hypothesis despite a similarity in intensity, which suggests a relationship between the exercise modality and the magnitude of depression of HRV. Heffernan et al. (17) examined the relationship between modalities by examining a bout of resistance exercises vs. a bout of cycling. Interestingly, both bouts resulted in significant depression of HF and HFnu. However, a greater depression was observed after resistance exercise (17). Although there is some evidence to support differences in modalities and their affects on HRV recovery (17), a lack of information regarding this relationship exists and further investigation is required.

Plasma catecholamines E and NE increased after each of the high-intensity trials. The elevation of catecholamines is a normal physiological response to the exercise stimulus (38). It is important to note that each trial elicited approximate 90% HRmax in participants, closely matching intensity. The intensity of exercise plays a major factor in the magnitude of the catecholamine response. Lower levels of exercise intensity (i.e., 40%–60% V[Combining Dot Above]O2max) are sufficient enough to elicit a moderate elevation of E and NE (21). While exercise intensities surpassing maximal aerobic power elicited a 5–10 time increase in catecholamine levels (38). Although the aerobic power was not measured in this study, the achieved %HRmax was enough to be classified as “vigorous” intensity according to ACSM guidelines (24); furthermore, the bout was sufficient enough to elevate plasma levels of E (HITP: 415.9 ± 262.2%, TM: 230.8 ± 77.5%) and NE (HITP: 551.6 ± 183%, TM: 353.2 ± 106%). The absolute values of E and NE (Figure 3) are consistent with other modalities of high-intensity exercise performed beyond 75% of maximal aerobic power (37).

Despite the similar exercise intensities, a significant difference was observed between modalities. The HITP trial elicited a response approximately 2 times greater in both plasma E and NE at IPE when compared to TM at IPE. This may in part be due to the differences in upper body recruitment between HITP and TM. Davies et al. (10) observed significant differences between catecholamine responses in arm-intensive exercise when compared to leg-based exercises, supporting our current findings. Although a significant increase in plasma E and NE was observed in IPE, response was short lived returning close to baseline by 1HR post. This is an expected result because of the rapid clearance of E and NE after bouts of exercise, in some cases up to 35% reduction in concentration after the first minute of recovery (16). It is important to note that the participants of this study were fully recovered before each trial and do not reflect the effects of multiple bouts or consecutive days of training. Therefore, resting and recovery catecholamine levels should be examined after chronic training within this modality; in that, alterations in catecholamine levels and sensitivity increase the likelihood of “overreaching” in athletes (13).

Although it is outside the scope of this study to find physiological reasons for the alterations of HRV and catecholamines, we can postulate on a few physiological responses related to the differences between the trials. The HITP trial consisted of pull-ups, push-ups, and bodyweight squats, which by nature would recruit more muscle mass than treadmill running because of greater load paced on the upper extremity (34). It is well understood that increases in load result in greater muscle recruitment (i.e., greater activity of high-threshold α-motor units; Henneman's size principle); however, this alone would not explain the speculated muscle recruitment in this study. In the absence of increasing load, muscle recruitment can increase during periods of explosive movements or fatigue-inducing sessions (34), both of which were observed in the HITP trial. Importantly, an increase in muscle recruitment is associated with raises in circulating E (34), which has been shown to decrease HRV (32,36). Providing a possible mechanism for the observed differences in HRV and circulating catecholamines.

Another factor to consider would be the alterations in posture that occurred from transitioning between exercises throughout the trial, which likely presented a challenge to hemodynamics (6,32). Simple alterations in posture (i.e., seated position to standing) result in the immediate spike in HR within 10 seconds of the postural change (6), very likely contributing the differences observed in HITP %HRmax. Borst et al. (6) proposed exercise reflex to be partially responsible for the rapid changes in HR after postural change. The exercise reflex suggests that contracting muscle, whether from muscle afferents or cardiac command, causes the immediate withdrawal of vagal tone, resulting in accelerated HR (5,18). Importantly, the extent of the exercise reflex on HR is determined by the speed of transition and the force applied by the working muscles, offering a possible explanation for the greater drop on vagal tone after the HITP trial. This may offer an explanation for the observed differences found within this study; further investigation is necessary to provide a better understanding.

Although this study was a novel step toward the better understanding of ANS responsiveness after a multimodal HITP bout (via HRV and catecholamine), it was not without limitations. The marker used to control for intensity (%HRmax) was similar between trials but statistically different. The observed marker of intensity (RPE) also significantly differed between trials; however, psychological perception and influences may be responsible for these observed differences. Future studies should examine differences in muscle recruitment, and blood lactate levels in conjunction to HRV and plasma catecholamines to provide a comprehensive view of cardiovascular stress markers and potential constituents of its alteration. Furthermore, the participants of this study were trained and experienced with high-intensity exercise and may respond to this type of stimulus differently than an untrained participant. Therefore, future studies should examine these affects in untrained participants.

In conclusion, the results show that the depression and recovery of parasympathetic markers (i.e., lnRMSSD and lnHF) were significantly greater and of longer duration (HITP lnRMSSD only) than treadmill running when compared to baseline values. Additionally, plasma stress markers of catecholamines (i.e., E and NE) increased a greater amount after exercise when compared to treadmill running. Therefore, HITP workouts such as the type examined in this study may provide a greater degree of autonomic disruption when compared to high-intensity treadmill running at a continuous pace within trained participants.

Practical Applications

The application of HITP as a general form of exercise has seen a market growth of interest. Importantly, little information is available pertaining HITP and autonomic stress. The results of this study demonstrated that a bout of HITP created a greater disruption to cardiac autonomic control when compared to running, despite closely matching for intensity and time. Interestingly, the recovery after the HITP closely followed that of the TM bout, despite the greater stress experienced. This is important because a greater training stimulus was experienced for the same amount of time and intensity, making HITP a viable option for those training with time restrictions.

The use of HRV to examine recovery status after bouts of exercise is a recently developing field of interest. The recovery of HRV indirectly reflects the return to homeostasis or “overall recovery” (35). The magnitude and duration of HRV depression after bouts of exercise vary (9,20). The results of this study demonstrated that HRV after the bodyweight HITP bout returned close to baseline within an hour. Understanding the recovery status after bouts of exercise will allow for more efficient, effective, and safe prescription of training.


There were no conflicts of interest throughout the study, collection of data, or the writing of this article.


1. Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med 343: 1355–1361, 2000.
2. Bergeron MF, Nindl BC, Deuster PA, Baumgartner N, Kane SF, Kraemer WJ. Consortium for Health and Military Performance and American College of Sports Medicine consensus paper on extreme conditioning programs in military personnel. Curr Sports Med Rep 10: 383–389, 2011.
3. Bilchick KC, Berger RD. Heart rate variability. J Cardiovasc Electrophysiol 17: 691–694, 2006.
4. Billman GE. The LF/HF ratio does not accurately measure cardiac sympatho-vagal balance. Front Clin Transl Physiol 4: 26, 2013.
5. Borst C, Hollander AP, Bouman LN. Cardiac acceleration elicited by voluntary muscle contractions of minimal duration. J Appl Physiol 32: 70–77, 1972.
6. Borst C, Wieling W, van Brederode JF, Hond A, de Rijk LG, Dunning AJ. Mechanisms of initial heart rate response to postural change. Am J Physiol 243: H676–H681, 1982.
7. Buchheit M, Laursen PB, Ahmaidi S. Parasympathetic reactivation after repeated sprint exercise. Am J Physiol 293: H133–H141, 2007.
8. Buchheit M, Papelier Y, Laursen PB, Ahmaidi S. Noninvasive assessment of cardiac parasympathetic function: Postexercise heart rate recovery or heart rate variability? Am J Physiol 293: H8–H10, 2007.
9. Chen JL, Yeh DP, Lee JP, Chen CY, Huang CY, Lee SD. Parasympathetic nervous activity mirrors recovery status in weightlifting performance after training. J Strength Cond Res 25: 1546–1552, 2011.
10. Davies CT, Few J, Foster KG, Sargeant AJ. Plasma catecholamine concentration during dynamic exercise involving different muscle groups. Eur J Appl Physiol 32: 195–206, 1974.
11. Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol 37: 247–248, 1974.
12. Esco MR, Olson MS, Williford HN, Blessing DL, Shannon D, Grandjean P. The relationship between resting heart rate variability and heart rate recovery. Clin Auton Res 20: 33–38, 2010.
13. Fry AC, Kraemer WJ, Van Borselen F, Lynch JM, Triplett NT, Koziris LP. Catecholamine responses to short-term high-intensity resistance exercise overtraining. J Appl Physiol (1985) 1985: 941–946, 1994.
14. Garber CE, Blissmer B, Deschenes MR, Franklin BA, Lamonte MJ, Lee IM. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults. Med Sci Sports Exerc 43: 1334–1359, 2011.
15. Hadeed M, Kuehl K, Elliot D. Exertional rhabdomyolysis after CrossFit exercise program. Med Sci Sports Exerc 43(5 Suppl): S152, 2011.
16. Hagberg JM, Hickson RC, McLane JA, Ehsani AA, Winder WW. Disappearance of norepinephrine from the circulation following strenuous exercise. J Appl Physiol 47: 1311–1314, 1979.
17. Heffernan KS, Kelly EE, Collier SR, Fernhall B. Cardiac autonomic modulation during recovery from acute endurance versus resistance exercise. Eur J Cardiovasc Prev Rehabil 13: 80–86, 2006.
18. Hollander AP, Bouman LN. Cardiac acceleration in man elicited by a muscle-heart reflex. J Appl Physiol 38: 272–278, 1975.
19. Kaikkonen P, Rusko H, Martinmäki K. Post-exercise heart rate variability of endurance athletes after different high-intensity exercise interventions. Scand J Med Sci Sports 18: 511–519, 2008.
20. Kiviniemi AM, Hautala AJ, Kinnunen H, Tulppo MP. Endurance training guided individually by daily heart rate variability measurements. Eur J Appl Physiol 101: 743–751, 2007.
21. Kjaer M, Christensen NJ, Sonne B, Richter EA, Galbo H. Effect of exercise on epinephrine turnover in trained and untrained male subjects. J Appl Physiol (1985) 1985: 1061–1067, 1985.
22. Kliszczewicz B, Snarr RL, Esco MR. Metabolic and cardiovascular response to the CrossFit workout “Cindy”. J Sport Hum Perform 2, 2014. Available from: Accessed December 2014.
23. Malik M. Heart rate variability standards of measurement, physiological interpretation, and clinical use. Circulation 93: 1043–1065, 1996.
24. American College of Sports Medicine. ACSM's Guidelines for Exercise Testing and Prescription (8th ed.). Baltimore, MD: Lippincott Williams & Wilkins, 2009.
25. Melanson EL, Freedson PS. The effect of endurance training on resting heart rate variability in sedentary adult males. Eur J Appl Physiol 85: 442–449, 2001.
26. Mølgaard H, Sørensen KE, Bjerregaard P. Attenuated 24-h heart rate variability in apparently healthy subjects, subsequently suffering sudden cardiac death. Clin Auton Res 1: 233–237, 1991.
27. Morshedi-Meibodi A, Larson MG, Levy D, O'Donnell CJ, Vasan RS. Heart rate recovery after treadmill exercise testing and risk of cardiovascular disease events (The Framingham Heart Study). Am J Cardiol 90: 848–852, 2002.
28. Parekh A, Lee CM. Heart rate variability after isocaloric exercise bouts of different intensities. Med Sci Sports Exerc 37: 599–605, 2005.
29. Plews DJ, Laursen PB, Kilding AE, Buchheit M. Heart rate variability in elite triathletes, is variation in variability the key to effective training? A case comparison. Eur J Appl Physiol 112: 3729–3741, 2012.
30. Plews DJ, Laursen PB, Le Meur Y, Hausswirth C, Kilding AE, Buchheit M. Monitoring training with heart rate variability: How much compliance is needed for valid assessment? Int J Sports Physiol Perform 9: 783–790, 2014.
31. Plews DJ, Laursen PB, Stanley J, Kilding AE, Buchheit M. Training adaptation and heart rate variability in elite endurance athletes: Opening the door to effective monitoring. Sports Med 43: 773–781, 2013.
32. Powers S, Howley E. Exercise Physiology: Theory and Application to Fitness and Performance (8th ed.). New York, NY: McGraw-Hill Humanities/Social Sciences/Languages, 2011.
33. Rezk CC, Marrache RCB, Tinucci T, Mion D Jr, Forjaz CLM. Post-resistance exercise hypotension, hemodynamics, and heart rate variability: Influence of exercise intensity. Eur J Appl Physiol 98: 105–112, 2006.
34. Spiering BA, Kraemer DWJ, Anderson JM, Armstrong LE, Nindl BC, Volek JS. Resistance exercise biology. Sports Med 38: 527–540, 2008.
35. Stanley J, Peake JM, Buchheit M. Cardiac parasympathetic reactivation following exercise: Implications for training prescription. Sports Med Auckl NZ 43: 1259–1277, 2013.
36. Stauss HM. Heart rate variability. Am J Physiol Regul Integr Comp Physiol 285: R927–R931, 2003.
37. Willich SN, Lewis M, Löwel H, Arntz HR, Schubert F, Schröder R. Physical exertion as a trigger of acute myocardial infarction. Triggers and mechanisms of Myocardial Infarction Study Group. N Engl J Med 329: 1684–1690, 1993.
38. Zouhal H, Jacob C, Delamarche P, Gratas-Delamarche A. Catecholamines and the effects of exercise, training and gender. Sports Med Auckl NZ 38: 401–423, 2008.

heart rate variability; high-intensity; catecholamines

Copyright © 2016 by the National Strength & Conditioning Association.