Accordingly, the purpose of this study was to examine the cardiometabolic health implications with detraining after a regular exercise-training program. The main aim was to quantify the time-magnitude changes in CRF and cardiometabolic health outcomes that occur with cessation of regular exercise training. It was hypothesized that CRF and cardiometabolic health will decline rapidly with the absence of regular exercise training over a one-month timeframe.

However, the majority of research linking either CRF or physical inactivity to disease risk or cardiometabolic risk factors has focused on data collected at various time points with little standardization of the days or weeks prior to data collection [ 5 ]. Furthermore, most research has collected follow-up data in the 48–72 h following the last exercise bout [ 6 ]. While this research has been valuable in promoting exercise in the public health domain, it is still unclear what the effects of intermittent periods of increased activity or inactivity are on improvements in cardiometabolic health following standardized aerobic exercise training periods of 12–24 weeks [ 6 7 ]. This is problematic, as periodic activity or inactivity more closely mimics the fluctuation in activity levels in individuals as they go about their daily lives. Common issues such as low initial fitness, low motivation, seasonal holidays, travel, injury, and illness have all been cited [ 6 ] as reasons for low adherence or cessation of exercise training. Thus evaluation of the effect of stopping an exercise intervention on cardiometabolic health in apparently healthy adults is an important area to understand.

Findings from numerous epidemiological studies clearly demonstrate that physical inactivity is associated with a higher prevalence of most CVD risk factors, including abnormal lipids, high blood pressure (BP), metabolic syndrome (MetS), obesity, and type 2 diabetes [ 3 ]. Furthermore, physical inactivity is linked to most prevalent chronic diseases and is estimated to contribute to approximately 250,000 premature deaths annually, representing approximately one quarter of all preventable deaths [ 4 ].

There is a robust inverse relationship between cardiorespiratory fitness (CRF) and risk of mortality from cardiovascular disease (CVD) and all causes [ 1 ]. For example, a one metabolic equivalent (1-MET) increase in CRF in low-risk middle aged men and women is reported to promote an 18% reduction in CVD mortality [ 2 ]. Therefore, increasing CRF via exercise training and increased physical activity (PA) is a pertinent public health prevention measure to improve CVD-free survival in low risk adults.

2. Materials and Methods

Thirty-five non-smoking men and women (aged 22 to 77 years) were recruited into the study if they were of low-to-moderate risk as defined by the American College of Sports Medicine [ 7 ] and not physically active (not participating in at least 30 min of moderate intensity physical activity on at least three days of the week for at least three months). Participants were also eligible for inclusion into the study if they verbally agreed to continue previous dietary habits and not perform additional exercise beyond that required for the present study. Exclusionary criteria included evidence of CVD, or pulmonary, and/or metabolic disease as determined by medical history questionnaire. This study was approved by the Human Research Committee at Western State Colorado University (HRC2017-01-01R20). Each participant signed an informed consent form prior to participation.

n = 17) continued their individualized exercise program according to the ACE IFT model guidelines for an additional four weeks and; the ceased treatment group (DETRAIN, n = 18) discontinued regular exercise. Participants in DETRAIN did not perform any structured exercise whatsoever for four weeks; however, they were permitted to maintain other lifestyle habits (e.g., nutrition and activities of daily living). All participants performed baseline testing as outlined below and completed an individualized 13-week exercise program ( Figure 1 ) according to the American Council of Exercise (ACE) Integrated Fitness Training (IFT) model guidelines [ 8 ], and completed post-program testing. Upon completion of the 13-week exercise training program and post-program testing participants were randomized to either of the following two treatment groups: The continued training group (TRAIN,= 17) continued their individualized exercise program according to the ACE IFT model guidelines for an additional four weeks and; the ceased treatment group (DETRAIN,= 18) discontinued regular exercise. Participants in DETRAIN did not perform any structured exercise whatsoever for four weeks; however, they were permitted to maintain other lifestyle habits (e.g., nutrition and activities of daily living).

All variables were measured at the initial assessment and following the 13 weeks of exercise training. In the detraining period, CRF and skinfold assessment occurred at weeks two and four only. Measures of BP, blood lipids, fasting blood glucose, waist circumference, and weight were obtained in each of the four weeks during the post-exercise training period.

Participants completed a maximum graded exercise test (GXT) on a motorized treadmill (Powerjog GX200, Inspire Fitness Solutions Ltd., Biddeford, ME, USA). Participants walked or jogged at a self-selected pace before the treadmill incline was increased by 1% every minute until the participant reached volitional fatigue. Participants heart rate (HR) were continuously recorded via a chest strap and radio-telemetric receiver (Polar Electro, Woodbury, NY, USA). Expired air and gas exchange data were recorded continuously using a metabolic analyser (Parvo Medics TrueOne 2.0, Parvo Medics Inc., Salt Lake City, UT, USA). Before each exercise test, the metabolic analyser was calibrated with gases of known concentrations (14.01 ± 0.07% O 2 , 6.00 ± 0.03% CO 2 ) and with room air (20.93% O 2 and 0.03% CO 2 ) as per the instruction manual. Volume calibration of the pneumotachometer was done via a 3-litre calibration syringe system (Hans-Rudolph, Kansas City, MO, USA). The last 15 s of the GXT were averaged—This was considered the final data point. The closest neighbouring data point was calculated by averaging the data collected 15 s immediately before the last 15 s of the test. The mean of the two processed data points represented the VO 2 max. The criteria for attainment of maximal oxygen consumption (VO 2 max) were two out of three of the following: (1) a plateau (∆VO 2 ≤ 150 mL/min) in VO 2 with increases in workload; (2) maximal respiratory exchange ratio (RER) ≥ 1.1; and (3) maximal HR within 15 beats/min of the age-predicted maximum (220–age).

2 with no concurrent increase in VE/VCO 2 and departure from the linearity of VE. The criteria for VT2 was a simultaneous increase in both VE/VO 2 and VE/VCO 2 . The corresponding HRs at VT1 and VT2 were used to improve the robustness of the exercise training response as has been shown elsewhere [ Determination of both the first ventilatory threshold (VT1) and second ventilatory threshold (VT2) were made by visual inspection of graphs of time plotted against each relevant respiratory variable (according to 15 s time-averaging). The criteria for VT1 was an increase in VE/VOwith no concurrent increase in VE/VCOand departure from the linearity of VE. The criteria for VT2 was a simultaneous increase in both VE/VOand VE/VCO. The corresponding HRs at VT1 and VT2 were used to improve the robustness of the exercise training response as has been shown elsewhere [ 1 ]. All analysis to determine the VTs were done independently by two experienced exercise physiologists. In the event of conflicting results, the original assessments were re-evaluated and collectively a consensus was agreed upon.

Participants were weighed to the nearest 0.1 kg on a medical grade scale and measured for height to the nearest 0.5 cm using a stadiometer. Percent body fat (FAT) was determined via skinfolds [ 7 ]. Skinfold thickness was measured to the nearest ±0.5 mm using a Lange calliper. All measurements were taken on the right side of the body using standardized anatomical sites (three-site) for men (chest, abdomen, thigh) and women (tricep, suprailiac, thigh). These measurements were performed until two were within 10% of each other. All skinfold measures were obtained by the same qualified clinical exercise physiologist. Waist circumference (WC) measurements were obtained using a cloth tape measure with a spring loaded-handle. A horizontal measurement was taken at the narrowest point of the torso (below the xiphoid process and above the umbilicus). These measurements were taken until the two were within 0.5 mm of each other.

A fasting blood sample was collected and analysed for measurement of lipids and glucose. A fingerstick sample was collected into heparin-coated 40-μL capillary tube. Blood flowed freely from the fingerstick into the capillary tube without milking of the finger. Samples were dispensed immediately onto commercially available test cassettes for analysis in a Cholestech LDX System (Abbott Ltd., Chicago, IL, USA) according to strict standardized operating procedures.

The procedures for assessment of resting HR and BP outlined elsewhere were followed [ 7 ] and collected in a standardized manner. The mean of the two measurements was reported for baseline and post-program values.

2.1. Cardiometabolic Health men = [(40 − HDL)/8.9] + [(TG − 150/69)] + [(FG − 100)/17.8] + [(WC − 102)/11.5] + [(MAP − 100)/10.1]; (2) MetS z-score women = [(50 − HDL)/14.5] + [(TG − 150/69)] + [(FG − 100)/17.8] + [(WC − 88)/12.5] + [(MAP − 100)/10.1], where FG = fasting glucose; HDL = high-density lipoprotein cholesterol; MAP = mean arterial pressure; TG = triglycerides; and WC = waist circumference. Cardiometabolic risk was determined via calculation of a MetS z-score following the procedure outlined and used elsewhere. Briefly, this score is the sum of the participant’s MetS components relative to the threshold for determination of each component. The MetS z-score has been used previously to identify changes in MetS risk factors following an exercise intervention [ 9 10 ]. The sex-specific MetS z-scores were calculated using the following equations [ 9 10 ]: (1) MetS z-score= [(40 − HDL)/8.9] + [(TG − 150/69)] + [(FG − 100)/17.8] + [(WC − 102)/11.5] + [(MAP − 100)/10.1]; (2) MetS z-score= [(50 − HDL)/14.5] + [(TG − 150/69)] + [(FG − 100)/17.8] + [(WC − 88)/12.5] + [(MAP − 100)/10.1], where FG = fasting glucose; HDL = high-density lipoprotein cholesterol; MAP = mean arterial pressure; TG = triglycerides; and WC = waist circumference.

2.2. Exercise Prescription All exercise was supervised one-to-one by student-trainers under the supervision of an experienced researcher. No specific motivation strategies were employed, and participants were booked in for their training at individual times according to their preferences and availability. Exercise training was progressed according to recommendations made elsewhere by ACE [ 8 ] and implemented in previous research [ 11 12 ]. Polar HR monitors were used to monitor HR during all exercise sessions. Researchers adjusted workloads on aerobic modalities accordingly during each exercise session to ensure actual HR responses aligned with target HR. The week-to-week exercise prescription for cardiorespiratory and resistance training (RT) modes are provided in Figure 1 for the 13-week exercise programme.