Here, we present protocols of high-intensity interval and moderate-intensity continuous exercise to observe the response of circulating cardiac troponin T (cTnT) concentration to acute exercise over 10 days. The information may assist with clinical interpretations of post-exercise cTnT elevation and guide the prescription of exercise.
An elevation in cardiac troponin T (cTnT), as a highly specific biomarker of cardiomyocyte damage, after moderate-intensity continuous exercise (MCE) has been described. The exercise-induced cTnT response distorts the diagnostic role of the cTnT assay. Although high-intensity interval exercise (HIE) is growing in popularity and concerns remain about its safety, available data related to cTnT release after HIE is limited, which hampers the use of HIE as a health intervention. Here, we present three representative HIE protocols [traditional HIE (repeated 4 min cycling at 90% V̇O2max interspersed with 3 min rest, 200 kJ/session); sprint interval exercise (SIE, repeated 1 min cycling at 120% V̇O2max interspersed with 1.5 min rest, 200 kJ/session); and repeated sprint exercise (RSE, 40 x 6 s all-out sprints interspersed with 9 s rest)] and one representative MCE protocol (continuous cycling exercise at an intensity of 60% V̇O2max, 200 kJ/session). Forty-seven sedentary, overweight young women were randomly assigned to one of four groups (HIE, SIE, RSE, and MCE). Six bouts of respective exercise were performed by every single group, with each being 48 h apart. Meanwhile, for four groups, the duration of the entire testing period was identical, being 10 days. Before and after the first and final exercise bouts, an assessment was conducted of cTnT. The current study provides a frame of reference giving a clear picture of how a specific exercise session affects the circulating cTnT concentration at the early stage of training. The information may assist with clinical interpretations of post-exercise cTnT elevation and guide the prescription of exercise, especially for HIE.
The benefits of regular exercise on the heart are well-documented1. However, the risk of cardiac events, such as acute myocardial infarction (AMI), transiently increases during an intense exercise2,3. Individuals with low levels of regular physical activity show higher risk towards AMI2,3. Cardiac troponin T (cTnT) is the biochemical gold standard in the diagnosis of AMI4. However, there is a burgeoning evidence that the cTnT is elevated after continuous prolonged exercise, which undoubtedly distorts the diagnostic role of the cTnT assay5.
The repetitive bouts of relatively intense exercise interspersed with short breaks are a typical element of high-intensity interval exercise (HIE), which is growing in popularity in various fields such as cardiac rehabilitation, health and fitness6,7. The widespread interest in HIE is due in part to the ability of HIE training to elicit beneficial physiological adaptations similar or superior to the traditional moderate-intensity continuous exercise (MCE) training, despite a reduced total exercise volume and time commitment6. However, concerns related to the safety of HIE have been expressed due to the high cardiac demand8. To date, available data related to cTnT release upon HIE is limited. Moreover, no previous integrated study has investigated the effect of various modalities of HIE and traditional MCE on the appearance of cTnT with exercise. Thus, it is unclear whether, with equalization of total mechanical work between HIE and MCE, different exercise formats will lead to the distinction in cTnT concentrations and what the range of the elevated cTnT values is. Given that exercise conducted at higher intensities might lead to a higher risk of cardiac events2,3, it is pertinent to develop a representative HIE and MCE proposals with the known range of cTnT responses. The evaluation of exercise-associated cTnT elevation could potentially be helpful in clinical decision-making and assist clinical physiologists in developing more effective and safe exercise prescriptions.
Consequently, we outline protocols of the three representative types of HIE and one representative type of MCE to gather physiological data while observing cTnT responses. Considering that the risk of acute cardiac events is higher in people who do not engage in regular exercise2,3 and the overall release of cTnT induced by exercise reduces with regular training9, this study recruited sedentary, overweight females who completed a 10 day training program. This provided the prospect to work in the early stage of training and target an under-researched group.
The protocol (No. 31771319) was approved by the Hebei Normal University Review Board and conformed to the Declaration of Helsinki. All participants provided written informed consent before participating in the testing described.
1. Participant Screening and Preparation for the Experiment
2. Experimental Procedures
Figure 1: Schematic diagram of study procedures. HIE = high-intensity interval exercise; SIE = sprint interval exercise; RSE = repeated sprint exercise; MCE = moderate-intensity continuous exercise. Please click here to view a larger version of this figure.
3. Exercise Protocols
4. Statistical Analyses
All participants (n = 47) completed the study, and no adverse cardiac events (e.g., chest pain and sign of myocardial ischemia on ECG) were found during testing in the four groups. As expected, the acute exercise heart rate (HR) data, including HRmean and %HRmax, at the 1ST assessment is similar (all P > 0.05) to those in the 6TH assessment in all four groups. Further, the HR data in the RSE and MCE groups is the highest and lowest among the four groups, respectively, but is similar between the HIE and SIE groups (Table 1).
Powerexe | Timeexe | Workexe | HRmean | %HRmax | |
(W) | (min) | (KJ) | (beat.min-1) | ||
HIE (n=12) | |||||
1ST | 119 ± 12 | 28 ± 3 | 200 ± 0 | 157 ± 9 | 85 ± 4 |
6TH | 119 ± 12 | 28 ± 3 | 200 ± 0 | 155 ± 6 | 84 ± 4 |
SIE (n=11) | |||||
1ST | 160 ± 18 | 21 ± 2 | 200 ± 0 | 148 ± 11 | 85 ± 4 |
6TH | 160 ± 18 | 21 ± 2 | 200 ± 0 | 147 ± 7 | 85 ± 5 |
RSE (n=12) | |||||
1ST | 193 ± 17‡ | 4 ± 0‡ | 46 ± 4‡ | 169 ± 5‡ | 94 ± 7‡ |
6TH | 204 ± 15*‡ | 4 ± 0‡ | 49 ± 4*‡ | 171 ± 8‡ | 95 ± 6‡ |
MCE (n=12) | |||||
1ST | 54 ± 10† | 63 ± 12† | 200 ± 0 | 140 ± 12† | 76 ± 6† |
6TH | 54 ± 10† | 63 ± 12† | 200 ± 0 | 137 ± 11† | 74 ± 6† |
Table 1: Acute exercise data. Data are presented as the mean ± SD. HIE, high-intensity interval exercise; SIE, sprint interval exercise; RSE, repeated sprint exercise; MCE, moderate-intensity continuous exercise; 1ST, the 1st exercise session; 6TH, the 6th exercise session; Powerexe, power output during exercise; Timeexe, total exercise duration; Workexe, work output during exercise; HRmean, mean heart rate during exercise session; %HRmax, percentage of individual maximal heart rate during exercise session.*Significantly different from the corresponding value of 1ST, P < 0.05; †Significantly different from the corresponding value of HIE, SIE, and RSE, P < 0.05; ‡Significantly different from the corresponding value of HIE and SIE, P < 0.05; This table has been modified from Nie et al.13 and Zhang et al.14.
Figure 2 reveals the acute exercise cTnT data on all four groups across the 10-day period, which are shown in the form of individual data points for pre-exercise (Pre-exe) and peak post-exercise (Post-exe) values. The cTnT concentration is discovered to be on the rise following acute exercise (P < 0.05) at the 1ST and 6TH assessments in all four groups. Moreover, no differences in cTnT concentration are found among the groups except for the smaller response after RSE at the 1ST. Moreover, the cTnT concentration at the 6TH assessment before MCE is higher than that at the 1ST assessment before MCE and at the 6TH assessment before RSE (both P < 0.05).
Figure 2: Pre-exercise (Pre-exe) and peak post-exercise (Post-exe) cardiac troponin T concentrations (cTnT, ng/L). HIE, high-intensity interval exercise; SIE, sprint interval exercise; RSE, repeated sprint exercise; MCE, moderate-intensity continuous exercise; 1ST, the 1st exercise session; 6TH, the 6th exercise session. The scale is log plotted because of the data spread, and individual data points are presented by circles with values for the same participant connected by lines for each condition. The horizontal dotted line is the upper reference limit and the double-arrow line is the median of the cTnT values at pre-exercise (Pre-exe) or Post-exercise (Post-exe). , single subject; n
, n subjects. * Significantly different from the corresponding Pre-exe value, P < 0.05; † Significantly different from the corresponding RSE value, P < 0.05; ‡ Significantly different from the corresponding value of 1ST, P < 0.05. This figure has been modified from Nie et al.13 and Zhang et al.14. Please click here to view a larger version of this figure.
The repetitive short to long bouts of rather high-intensity exercise interspersed with recovery periods are involved in HIE, which is subdivided into traditional HIE (“near maximal” efforts) and SIE (“supramaximal” efforts), using a common classification scheme6. In addition, RSE is a particularly intense form of SIE, where the activity is “all-out” but only lasts for 3 to 7 s6. To the best of our knowledge, this is the first integrated study to outline protocols of three representative types of HIE and one representative type of MCE to gather physiological data while observing cTnT responses. The current protocols are noteworthy especially when considering the study design, where the specific observation window (i.e., the early stage of exercise training) was selected. To this end, in order to derive a clean training background and avoid the effects exerted by the prior training experience, the previously sedentary subjects were selected. Also, the post-exercise cTnT level at the 1ST assessment was like that in the 6TH assessment in all four groups (Figure 2). The current findings reflect an overview of exercise-induced cTnT in the previously sedentary subjects who have just initiated an exercise training regime, as our recent study15 demonstrated, with improved cardiorespiratory fitness, exercise-induced elevation in cTnT will be largely abolished when exercise is performed at the same absolute intensity. Moreover, this experiment also seems to support that the participants had relatively stable cardiorespiratory fitness during the 10 day period due to the lack of a significant difference observed in acute exercise HR data (see Table 1).
Theoretically, interval exercise is infinitely variable when the intensity and duration of work and relief intervals are manipulated, but here we selected three distinct, representative protocols based on the usual classification scheme6. As shown by our current data, despite the varying exercise intensities employed, HIE, SIE and MCE elicited similar cTnT elevations under the circumstance where identical total mechanical work was completed during the 1st cycling trials. The rising level of cTnT in RSE was found to be less than that in HIE or SIE, which was likely attributed to the much lower total mechanical work of RSE (RSE vs. HIE or SIE: ~50 vs. 200 kJ). However, the mechanical work might not be the only determinant, as the acute exercise in four groups induced a similar cTnT elevation during the 6th cycling trials, despite the completion of lower mechanical work in RSE. Therefore, additional studies are still warranted to clarify the role of total work accomplished in post-exercise cTnT elevation.
In the present study, following exercise, almost all participants showed an increase in cTnT and the absence of symptoms or signs of myocardial ischemia based on an ECG, suggesting that exercise-induced cTnT elevation is largely obligatory, and thus, likely physiological in nature. The current study provides a frame of reference giving a clear picture of how a specific exercise session affects the circulating cTnT concentration at the early stage of training. This holds great clinical importance, considering some post-exercise cTnT data (9%) are above the population upper reference limit of 14 ng/L in the current study, and concerns related to the safety of high-intensity exercise, especially in less-trained exercisers8. Specifically, on one hand, clinicians should be aware that elevated cTnT after low-volume, high-intensity exercise is common, and the frame of cTnT release aids clinicians faced with the challenge of interpreting these data clinically in the post-exercise setting. On the other hand, the current data provides templates of different exercise protocols and a potential way to predict the cTnT response when considering initiating exercise regimes. The information may have practical implications for exercise prescriptions in sedentary populations, especially for HIE.
Here, we have included a young population, a limitation of this study is that we did not assess the cTnT levels in the elderly population. A higher risk of cardiac events typically occurs in the elderly population with cardiovascular risks and/or diseases16. At present, it remains unclear whether cTnT has similar responses to acute exercise in groups with cardiovascular disease or risk, which makes it worthy of further research using the exercise protocols developed in the present study. Accordingly, it is of significance to be aware that HIE has been made prevalent in recent years among the patients with cardiovascular diseases. However, the safety of the acute response to a single session of high-intensity exercise for these cohorts remains concerning16.
The authors have nothing to disclose.
This work was supported by the National Natural Science Foundation of China (Grant No. 31771319).
Cobas E 601 analyser | Roche Diagnostics, Penzberg, Germany | Used for measuring the circulating cardiac troponin T concentration | |
Monark 839E Stress Testing Cycle Ergometer | Monark Exercise AB, Vansbro, Sweden | Used for all exercise protocols except repeated sprint exercise | |
Monark 894E Wingate Testing Cycle Ergometer | Monark Exercise AB, Vansbro, Sweden | Only used for repeated sprint exercise protocol | |
Quark-PFT-ergo Metabolic Analyser | Cosmed, Rome, Italy | C09072-02-99 | |
SPSS Statistics 20.0 software package | IBM Corp., Armonk, USA | ||
Zephyr BioHarness 3.0 | Zephyr Technology, Auckland, New Zealand | 9800.0189/9600.0190 | Electrocardiograph Monitor |