Calculating the standard deviation of individual responses (SD IR ) is recommended for estimating the magnitude of individual differences in training responsiveness in parallel‐arm exercise randomized controlled trials (RCTs). The purpose of this review article is to discuss potential limitations of parallel‐arm exercise RCTs that may confound/complicate the interpretation of the SD IR . To provide context for this discussion, we define the sources of variation that contribute to variability in the observed responses to exercise training and review the assumptions that underlie the interpretation of SD IR as a reflection of true individual differences in training responsiveness. This review also contains two novel analyses: (1) we demonstrate differences in variability in changes in diet and physical activity habits across an intervention period in both exercise and control groups, and (2) we examined participant dropout data from six RCTs and found that significantly ( P < 0.001) more participants in control groups (12.8%) dropped out due to dissatisfaction with group assignment compared to exercise groups (3.4%). These novel analyses raise the possibility that the magnitude of within‐subject variability may not be equal between exercise and control groups. Overall, this review highlights that potential limitations of parallel‐arm exercise RCTs can violate the underlying assumptions of the SD IR and suggests that these limitations should be considered when interpreting the SD IR as an estimate of true individual differences in training responsiveness.

Objective To determine the effects of exercise amount (kilocalories per session) and intensity (percent of maximal oxygen consumption [% VO2peak]) on adipose tissue (AT) and skeletal muscle (SM) in adults with abdominal obesity. Methods Participants (n = 103; 52.7 ± 7.6 years) were randomized to the following groups: control; low‐amount, low‐intensity exercise (180 kcal/session [women] and 300 kcal/session [men] at 50% VO2peak); high‐amount, low‐intensity exercise (HALI; 360 kcal/session [women] and 600 kcal/session [men] at 50% VO2peak); or high‐amount, high‐intensity exercise (HAHI; 360 kcal/session [women] and 600 kcal/session [men] at 75% VO2peak) for 24 weeks. Activities of daily living were measured by accelerometry. Magnetic resonance imaging was used to measure tissue mass. Results Reduction in all AT depots was greater in the exercise groups compared with control (P < 0.002); however, there were no differences between exercise groups (P > 0.05). Visceral and abdominal subcutaneous AT reduction was uniform across the abdomen. Total SM mass did not change with exercise compared with control (P = 0.32). However, while lower‐body SM mass was maintained (P = 0.32), upper‐body SM mass in the high‐amount, high‐intensity and the high‐amount, low‐intensity groups was reduced compared with controls (P < 0.008). Conclusions In adults with abdominal obesity, substantial reductions in total, abdominal subcutaneous, and visceral AT with a preservation of total SM mass were observed independent of exercise amount or intensity.

Purpose High throughput profiling of metabolic status (metabolomics) allows for the assessment of small-molecule metabolites that may participate in exercise-induced biochemical pathways and corresponding cardiometabolic risk modification. We sought to describe the changes in a diverse set of plasma metabolite profiles in patients undergoing chronic exercise training and assess the relationship between metabolites and cardiometabolic response to exercise. Methods secondary analysis was performed in 216 middle-aged abdominally obese men and women ([mean (SD)], 52.4 (8.0) years) randomized into one of four groups varying in exercise amount and intensity for 6 months duration: high amount high intensity, high amount low intensity, low amount low intensity, and control. 147 metabolites were profiled by liquid chromatography-tandem mass spectrometry. Results No significant differences in metabolite changes between specific exercise groups were observed; therefore, subsequent analyses were collapsed across exercise groups. There were no significant differences in metabolite changes between the exercise and control groups after 24 weeks at a Bonferroni-adjusted statistical significance (p < 3.0 × 10-4). Seven metabolites changed in the exercise group compared to the control group at p < 0.05. Changes in several metabolites from distinct metabolic pathways were associated with change in cardiometabolic risk traits, and three baseline metabolite levels predicted changes in cardiometabolic risk traits. Conclusion Metabolomic profiling revealed no significant plasma metabolite changes between exercise compared to control after 24-weeks at Bonferroni significance. However, we identified circulating biomarkers that were predictive or reflective of improvements in cardiometabolic traits in the exercise group.

Purpose This study aimed to determine the magnitude of exercise-induced individual variability for waist circumference (WC) and body weight change after accounting for biological variability and measurement error. Determinants of response variability were also considered. Methods Participants (53 ± 7.5 yr) were 181 adults (61% women) with abdominal obesity randomized to the following: control; low-amount, low-intensity exercise (LALI); high-amount, low-intensity exercise (HALI); or high-amount, high-intensity exercise (HAHI) for 24 wk. Unstructured physical activity was measured by accelerometer. The variability in response to exercise for WC and body weight (SDR) was isolated by subtracting the SD values for the change scores in the exercise group from that of the control group. Results The variability of response due to exercise (SDR) for change in WC was 3.1, −0.3, and 3.1 cm for LALI, HALI, and HAHI groups, respectively. Corresponding values for body weight were 3.8, 2.0, and 3.5 kg for LALI, HALI, and HAHI, respectively. The high-amount exercise groups yielded the highest proportion of individuals with a clinically meaningful response. No variables predicted the response to exercise (P > 0.05). Conclusions Substantial variability in response to standardized exercise was observed for change in both WC and body weight after accounting for the variability not attributed to exercise. Potential determinants of the interindividual variability in response to exercise remain unclear.

No abstract

Weight loss induced by decreased energy intake (diet) or exercise generally has favorable effects on insulin sensitivity and cardiometabolic risk. The variation in these responses to diet-induced weight loss with or without exercise, particularly in older obese adults, is less clear. The objectives of our study were to (1) examine the effect of weight loss with or without exercise on the variability of responses in insulin sensitivity and cardiometabolic risk factors and (2) to explore whether baseline phenotypic characteristics are associated with response. Sedentary older obese (BMI 36.3 ± 5.0 kg/m 2) adults (68.6 ± 4.7 years) were randomized to one of 3 groups: health education control (HED); diet-induced weight loss (WL); or weight loss and exercise (WL + EX) for 6 months. Composite Z-scores were calculated for changes in insulin sensitivity (C_IS: rate of glucose disposal/insulin at steady state during hyperinsulinemic euglycemic clamp, HOMA-IR, and HbA1C) and cardiometabolic risk (C_CMR: waist circumference, triglycerides, and fasting glucose). Baseline measures included body composition (MRI), cardiorespiratory fitness, in vivo mitochondrial function (ATPmax; P-MRS), and muscle fiber type. WL + EX groups had a greater proportion of High Responders in both C_IS and C_CMR compared to HED and WL only (all p < 0.05). Pre-intervention measures of insulin (r = 0.60) and HOMA-IR (r = 0.56) were associated with change in insulin sensitivity (C_IS) in the WL group (p < 0.05). Pre-intervention measures of glucose (r = 0.55), triglycerides (r = 0.53), and VLDL (r = 0.53) were associated with change in cardiometabolic risk (C_CMR) in the WL group (p < 0.05), whereas triglycerides (r = 0.59) and VLDL (r = 0.59) were associated with C_CMR (all p < 0.05) in WL + EX. Thus, the addition of exercise to diet-induced weight loss increases the proportion of older obese adults who improve insulin sensitivity and cardiometabolic risk. Additionally, individuals with poorer metabolic status are more likely to experience greater improvements in cardiometabolic risk during weight loss with or without exercise.

Background Aging-related disease risk is exacerbated by obesity and physical inactivity. It is unclear how weight loss and increased activity improve risk in older adults. We aimed to determine the effects of diet-induced weight loss with and without exercise on insulin sensitivity, VO2peak, body composition, and physical function in older obese adults. Methods Physically inactive older (68.6 ± 4.5 years) obese (BMI 37.4 ± 4.9 kg/m 2) adults were randomized to: Health education control (HEC; n=25); Diet-induced weight loss (WL; n=31); or Weight loss and exercise (WLEX; n=28) for 6 months. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp, body composition by DXA and MRI, strength by isokinetic dynamometry, and VO2peak by graded exercise test. Results WLEX improved (p&lt;0.05) peripheral insulin sensitivity (+75 ± 103%) vs. HEC (+12 ± 67%); WL (+36 ± 47%) vs. HEC did not reach statistical significance. WLEX increased VO2peak (+7 ± 12%) vs. WL (-2 ± 24%), and prevented reductions in strength and lean mass induced by WL (p&lt;0.05). WLEX decreased abdominal adipose tissue (-16 ± 9%) vs. HEC (-3 ± 8%) and intermuscular adipose tissue (-15 ± 13 %) vs. both HEC (+9 ± 15%) and WL (+2 ± 11%) (p&lt;0.01). Conclusions Exercise with weight loss improved insulin sensitivity and VO2peak, decreased ectopic fat, and preserved lean mass and strength. Weight loss alone decreased lean mass and strength. Older adults intending to lose weight should perform regular exercise to promote cardiometabolic and functional benefits, which may not occur with calorie restriction-induced weight loss alone.

No abstract