The cTnT response to acute exercise at the onset of an endurance training program: evidence of exercise preconditioning?

Zhang, Haifeng; Nie, Jinlei; Kong, Zhaowei; Cao, Wenling; Zhu, Xiangui; Zheng, Zi-Wei; George, Keith

doi:10.1007/s00421-019-04074-0

Cited by 3 publications

(4 citation statements)

References 24 publications

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“…a marker of myocardial injury, found after strenuous exercise. Recent work revealed that a single session of endurance exercise is protective against the exercise-induced rise in cardiac troponin T. In two other studies from separate laboratories, it was shown that cTnT was blunted during a second exercise session that was separated by both 4 and 48 h of recovery in previously inactive, young women (Nie et al 2019;Zhang et al 2019). These findings, although indirectly, provide some support for the concept that SEP leads to smaller tissue injury.…”

Section: Does Sep Also Prevent Cardiac and Vascular Injury In Humans?mentioning

confidence: 84%

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Short‐term exercise‐induced protection of cardiovascular function and health: why and how fast does the heart benefit from exercise?

Thijssen

Uthman

Somani

et al. 2022

The Journal of Physiology

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Regular exercise training has potent and powerful protective effects against the development of cardiovascular disease. These cardioprotective effects of regular exercise training are partly explained through the effects of exercise on traditional cardiovascular risk factors and improvement in cardiac and vascular health, which take several weeks to months to develop. This review focuses on the observation that single bouts of exercise may also possess an underrecognized, clinically useful form of immediate cardioprotection. Studies, performed in both animals and humans, demonstrate that single or short‐term exercise‐induced protection (SEP) attenuates the magnitude of cardiac and/or vascular damage in response to prolonged ischaemia and reperfusion injury. This review highlights preclinical evidence supporting the hypothesis that SEP activates multiple pathways to confer immediate protection against ischaemic events, reduce the severity of potentially lethal ischaemic myocardial injury, and therefore act as a physiological first line of defence against injury. Given the fact that the extent of SEP could be modulated by exercise‐related and subject‐related factors, it is important to recognize and consider these factors to optimize future clinical implications of SEP. This review also summarizes potential effector signalling pathways (i.e. communication between exercising muscles to vascular/cardiac tissue) and intracellular pathways (i.e. reducing tissue damage) that ultimately confer protection against cardiac and vascular injury. Finally, we discuss potential future directions for designing adequate human and animal studies that will support developing effective SEP strategies for the (multi‐)diseased and aged individual. Key points Single or short‐term exercise‐induced protection (SEP) attenuates the magnitude of cardiac and/or vascular damage in response to prolonged ischaemia and reperfusion injury (IR injury). SEP activates multiple pathways to confer cardiac protection, which develops remotely at the site of the activated muscle by release of circulating molecules, which transfer towards activation of intramyocardial signalling that promotes cell survival during episodes of IR injury. SEP represents an attractive intervention in aged individuals and in those with co‐morbidities. The immediate protection, low cost and simplicity to increase the ‘dose’ of SEP offers unique opportunities in the clinical applications of SEP.

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Section: Does Sep Also Prevent Cardiac and Vascular Injury In Humans?mentioning

confidence: 84%

“…2019; Zhang et al . 2019). These findings, although indirectly, provide some support for the concept that SEP leads to smaller tissue injury.…”

Section: Does Sep Also Prevent Cardiac and Vascular Injury In Humans?mentioning

confidence: 99%

Short‐term exercise‐induced protection of cardiovascular function and health: why and how fast does the heart benefit from exercise?

Thijssen

Uthman

Somani

et al. 2022

The Journal of Physiology

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“…VO 2max was determined using a graded cycling exercise protocol that has been described previously. 5,11 The participants began at 50 W with a pedal frequency of 60 rpm on a cycle ergometer (Monark, 839E, Sweden); power output was increased by 20 W every 3 min until volitional exhaustion. Volitional exhaustion was defined as the point at which the subject could no longer maintain the required exercise intensity.…”

Section: Methodsmentioning

confidence: 99%

The impact of exercise modality and menstrual cycle phase on circulating cardiac troponin T

Nie

Zhang

Kong

et al. 2020

Journal of Science and Medicine in Sport

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Objectives: It is unclear whether exercise modality (moderate-intensity continuous [MCE]; high-intensity interval [HIE]) and menstrual cycle phase (follicular [FP]; luteal [LP]), individually or in combination, mediate the commonly observed exercise-induced elevation in cardiac troponin T (cTnT). This study examines cTnT responses to MCE and HIE during both the FP and LP. Design: Randomised crossover study. Methods: Seventeen healthy, eumenorrheic women completed four trials including MCE (60% VO 2max steady-state cycling until 300 kJ) and work-equivalent HIE (repeated 4-min cycling at 90% VO 2max interspersed with 3-min rest) during both the FP and LP. The FP and LP were verified based on ovarian hormones. Serum cTnT was assessed using a high-sensitivity assay before, immediately after, and 1 (1HR), 3 (3HR) and 4 (4HR) hours after exercise. cTnT values were corrected for plasma volume changes. Results: cTnT was significantly elevated (p < 0.05) post-exercise in both MCE (at 3HR and 4HR) and HIE (at 1HR, 3HR and 4HR). No statistically significant difference (p > 0.05) in peak post-exercise cTnT, which mostly occurred at 3HR, was seen among the four trials (median [range], ng l −1 : 5.2 [1.7-18.1] after MCE during FP; 4.8 [1.7-24.9] after MCE during LP, 8.2 [3.9-24.8] after HIE during FP and 6.9 [1.7-23.1] after HIE during LP). Conclusions: A single 300 kJ bout of both MCE or HIE resulted in a significant post-exercise increase in cTnT, with no differences in peak cTnT response between menstrual cycle phases or between exercise modes, but the cTnT elevation occurs slightly earlier after HIE.

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“…For example, a single bout of exercise preceding cardiac ischaemiareperfusion injury affords protection, leading to a smaller infarct size in animal models (8). Interestingly, exercise-induced cTnI release was blunted during a second exercise session timed 48-hours later (9) or following training (10), and declined with successive days of running in humans (11). Whilst these findings support the ability of exercise to attenuate exercise-induced cTnI release, no studies evaluated these effects in groups with elevated risk.…”

Section: Introductionmentioning

confidence: 99%

Exercise-induced release of cardiac troponin is attenuated with repeated bouts of exercise: impact of cardiovascular disease and risk factors

Somani

Uthman²,

Aengevaeren³

et al. 2023

American Journal of Physiology-Heart and Circulatory Physiology

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Background: Prolonged exercise can induce cardiac troponin release. Since single bouts of exercise may protect against cardiac injury, we explored the hypothesis that the magnitude of exercise-induced release of troponin attenuates upon successive days of exercise. We also examined whether effects of successive exercise bouts differ between healthy participants and individuals with cardiovascular risk factors (CVRF) and established cardiovascular disease (CVD). Methods: We examined cardiac troponin I (cTnI) concentrations in 383 participants (61±14 years) at rest and immediately following 4 consecutive days of long-distance walking (30-50 km/day). Participants were classified as either healthy (n=222), CVRF (n=75) or CVD (n=86). Results: Baseline cTnI concentrations were significantly higher in CVD and CVRF participants compared to healthy (P<0.001). Exercise-induced elevations in cTnI were observed in all groups following all days of walking compared to baseline (P<0.001). Tobit regression analysis on absolute cTnI concentrations revealed a significant day*group interaction (P=0.04). Following day 1 of walking, post-hoc analysis showed that exercise-induced elevations in cTnI attenuated on subsequent days in healthy and CVRF, but not in CVD. Odds ratios for incident cTnI concentrations above the upper reference limit were significantly higher in comparison to baseline on Day 1 for healthy (4.90 (95% CI 1.58-15.2)) and CVD participants (14.9 (1.86-125)); and remained significantly higher than baseline on all subsequent days in CVD. Conclusions: The magnitude of post-exercise cTnI concentrations following prolonged walking exercise significantly declines upon repeated days of exercise in healthy individuals and those with CVRF, whilst this decline is not present in CVD patients.

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The cTnT response to acute exercise at the onset of an endurance training program: evidence of exercise preconditioning?

Abstract: The version presented here may differ from the published version or from the version of the record. Please see the repository URL above for details on accessing the published version and note that access may require a subscription.

Cited by 3 publications

References 24 publications

Short‐term exercise‐induced protection of cardiovascular function and health: why and how fast does the heart benefit from exercise?

Short‐term exercise‐induced protection of cardiovascular function and health: why and how fast does the heart benefit from exercise?

The impact of exercise modality and menstrual cycle phase on circulating cardiac troponin T

Exercise-induced release of cardiac troponin is attenuated with repeated bouts of exercise: impact of cardiovascular disease and risk factors

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