Cardiovascular response to prescribed detraining among recreational athletes

Abstract

Exercise-induced cardiac remodeling (EICR) and the attendant myocardial adaptations characteristic of the athlete's heart may regress during periods of exercise reduction or abstinence. The time course and mechanisms underlying this reverse remodeling, specifically the impact of concomitant plasma volume (PV) contraction on cardiac chamber size, remain incompletely understood. We therefore studied recreational runners ( n = 21, age 34 ± 7 yr; 48% male) who completed an 18-wk training program (~7 h/wk) culminating in the 2016 Boston Marathon after which total exercise exposure was confined to <2 h/wk (no single session >1 h) for 8 wk. Cardiac structure and function, exercise capacity, and PV were assessed at peak fitness (10-14 days before) and at 4 wk and 8 wk postmarathon. Mixed linear modeling adjusting for age, sex, V̇o, and marathon finish time was used to compare data across time points. Physiological detraining was evidenced by serial reductions in treadmill performance. Two distinct phases of myocardial remodeling and hematological adaptation were observed. After 4 wk of detraining, there were significant reductions in PV (Δ -6.0%, P < 0.01), left ventricular (LV) wall thickness (Δ -8.1%, <0.05), LV mass (Δ -10.3%, P < 0.001), and right atrial area (Δ -8.2%, P < 0.001). After 8 wk of detraining, there was a significant reduction in right ventricle chamber size (end-diastolic area Δ = -8.0%, P < 0.05) without further concomitant reductions in PV or LV wall thickness. Abrupt reductions in exercise training stimulus result in a structure-specific time course of reverse cardiac remodeling that occurs largely independently of PV contraction. NEW & NOTEWORTHY Significant reverse cardiac remodeling, previously documented among competitive athletes, extends to recreational runners and occurs with a distinct time course. Initial reductions in plasma volume and left ventricular (LV) mass, driven by reductions in wall thickness, are followed by contraction of the right ventricle. Consistent with data from competitive athletes, LV chamber volumes appear less responsive to detraining and may be a more permanent adaptation to sport.

Regression of Left Ventricular Mass in Athletes Undergoing Complete Detraining Is Mediated by Decrease in Intracellular but Not Extracellular Compartments

“…4 Pedlar et al performed echocardiography in amateur runners after an 18 week training 5 programme and then after 4 and 8 weeks when participants were limited to <2 hours of training 6 a week. 27 Similarly to our findings they reported a 10.4% reduction in LV mass after 4 weeks 7 with no change in LV EDV even 8 weeks post-race. 8…”

Detraining Effects Prevention: A New Rising Challenge for Athletes

“…In line with this, impairments in maximal cardiac output (Q max ) have been found after 12 days of inactivity due to a 10% decrement in exercise stroke volume and 4% increment in maximal heart rate (Coyle et al, 1984 ). Similar results have also been observed following a period of training cessation and head-down tilt bed rest during both maximal (Coyle et al, 1984 ; Pedlar et al, 2018 ) and submaximal exercise (Coyle et al, 1986 ; Capelli et al, 2008 ). Such reductions in Q max are critical as they may highly contribute in declining the maximal oxygen delivery capacity.…”

“…For example, it has been found that expansions in blood volume can partially reestablish VO 2max losses following a period of training cessation; nonetheless, this manipulation was not able to compensate for endurance performance decrements (Coyle et al, 1986 ). Moreover, 4 weeks of training cessation have been shown to decrease performance during a time to exhaustion test (TTE) without affecting VO 2max in well-trained endurance athletes (Madsen et al, 1993 ; Pedlar et al, 2018 ). Impairments in endurance performance have also been found during 12–35 days of training cessation in both running and cycling incremental tests (Coyle et al, 1986 ; Houmard et al, 1992 , 1993 ), a Yo-Yo intermittent-test (Joo, 2018 ), a 3,000-m running time trial (Pereira et al, 2016 ) and a cycling TTE (Madsen et al, 1993 ).…”

“…Training stimuli cessation and the consequent decline in plasma volume, which may occur after 2 days of inactivity (Thompson et al, 1984 ; Cullinane et al, 1986 ), lead to a reduced cardiac preload, which in turn triggers a series of rapid morphological and functional cardiac remodeling (Martin et al, 1986 ; Spence et al, 2011 ; Pedlar et al, 2018 ). In line with this, impairments in maximal cardiac output (Q max ) have been found after 12 days of inactivity due to a 10% decrement in exercise stroke volume and 4% increment in maximal heart rate (Coyle et al, 1984 ).…”

The effect of parity on longitudinal maternal hemodynamics

“…46,47,48 Such persistent remodelling has also been reported in individuals undertaking temporary endurance training. 49,50,51 Group 3 represents the cohort with the least favourable adaptive response to pregnancy. These women have failed the 'cardiovascular screening test' in their previous pregnancies and may have an underlying cardiovascular deficit, causing a failure in adaptation in situations of circulatory stress.…”