The STRIDE intervention was successfully replicated in a geographically different sample of sedentary individuals. Although all intervention participants increased minutes of physical activity in the past week from baseline to the six-month follow-up, COSTRIDE participants were able to maintain a higher level of physical activity through 12 months. Additionally, more global assessments of physical activity over the past three months indicated that COSTRIDE participants were generally better at maintaining higher levels of voluntary aerobic exercise throughout the course of the study. Although there were promising self-reported behavioral differences, there was no effect on objective fitness (VO2 max), and little average change in VO2 max. This suggests that while our participants had been increasing their minutes of physical activity and the frequency with which they engaged in these activities, they may not have been working at an intensity level high enough to result in increased VO2 max. Of course, given the reliance on self-report, it could also be that the frequency and volume of activity reported by participants was overestimated and that they were not engaging in sufficient amounts of overall participation to yield meaningful changes in cardiovascular fitness. The exercise physiology literature is clear that it is higher total exercise volume (i.e., higher intensity exercise for longer durations) rather than simply a longer time spent active, that is associated with the greatest effects on cardiovascular fitness [48–51]. Despite less than optimal effects on cardiovascular fitness, physical activity among sedentary individuals did increase to a level that has a myriad of other health benefits (e.g., cancer prevention, psychological benefits, metabolic syndrome prevention).
There was some evidence for the moderation of intervention effects by genetic factors, in that we showed effects of two SNPs that have been previously associated with response to exercise [19, 21]. The findings extend prior work by demonstrating stronger intervention response among individuals with a genotype associated with more positive affective response to acute exercise. Specifically, in prior work BDNF A/A and A/G individuals perceived less exertion during moderate intensity exercise and experienced more positive affect in response to exercise than G/G individuals , and the A/A or A/G individuals were more likely to exercise in the current study in the intervention condition, but less likely to exercise in the HW condition. With regard to the FTO SNP, C/C individuals in this same sample experienced more positive affect in response to exercise than C/T and T/T individuals at baseline . Our findings regarding more frequent exercise behavior among C/C individuals in response to the intervention are consistent with this relationship. Interestingly, it appears that the effects were most pronounced for the FTO SNP in the first six months, and were less apparent in the second six months, suggesting that this particular SNP may be more strongly associated with exercise initiation rather than maintenance. Although the effects demonstrated here are arguably rather small, they do support recent ideas about the potential for genetic moderation of intervention effects in the behavioral domain similar to what has been found in the pharmacological domain [52, 53].
Despite relationships between physiological responses, subjective responses, and exercise motivation and behavior shown in other work [22–24], there was no evidence that physiological or subjective responses to an acute bout of moderate intensity exercise moderated effects of the intervention. There are at least two possibilities to account for why these moderating outcomes were not found. The first possibility is that the intervention itself is essentially an “ongoing dose” of intervention over the full 12 months of the behavioral follow-up. This situation may simply dampen individual differences in behavior that might naturally arise when constant external reinforcement is not provided. Whereas an individual who is intrinsically motivated by a positive affective response to exercise will continue to be physically active, an individual who perceives less positive affective response to exercise might simply stop exercising in the absence of encouragement from external sources. Such a condition did not exist in the current study. The second possibility is that these physiological and subjective responses to exercise simply do not moderate response to an exercise intervention.
The overall results of our study could potentially be viewed as “underwhelming” in terms of the lack of significant moderation effects, and we are certainly not the first to show somewhat disappointing findings with regard to the strength of moderators of exercise intervention efficacy. Importantly, however, we view our approach as methodologically stronger than existing work in that our moderators were drawn from a theoretically plausible and empirically supported transdisciplinary model of exercise behavior. In contrast, prior investigations have taken an atheoretical approach, and focused largely on demographic (e.g., gender), motivational (e.g., self-efficacy), or personality (e.g., depression) factors that were measured prior to engaging in an intervention. Here, the focus was on physiological and subjective responses experienced during an acute bout of moderate-intensity physical activity and genetic factors that might moderate intervention efficacy. To our knowledge, this is the first investigation into theoretically grounded underlying determinants of physical activity as moderators of the initiation and maintenance of exercise in an RCT. Yet, despite our methodological rigor, the results did not reveal any stronger pattern of moderation than prior studies.
Are we to conclude, then, that focusing on moderators of physical activity intervention efficacy is unimportant? We think this conclusion might yet be premature. At this point, all of the empirical tests for moderation of intervention effects on physical activity (including the current RCT) have compared a physical activity intervention to either a no-treatment control, an information-only control or an attention-placebo control [15–18]. It is possible that the individual differences that influence response to physical activity intervention are not so much related to whether an individual receives an intervention or not, but rather what kind of physical activity intervention one receives. The intervention utilized in this study involves ongoing tailored feedback which has been shown via meta-analysis to be a successful technique . Other successful interventions involve self-monitoring (observing and processing information concerning internal and external states) as an effective strategy for maintaining physical activity behavior [54, 55]. It is possible that any of these interventions are strongly superior to information only or no-treatment controls, such that they overwhelm individual differences moderating their efficacy. Studies that compare different exercise intervention strategies to one another may afford a context in which moderators may show stronger effects. Perhaps an individual with positive affective response to exercise responds better to immediate engagement in levels of intensity and duration that maximize the positive affect response, while those who experience greater temperature increase and pain may respond better to gradual introductions to exercise and a more extensive suite of external reinforcement contingencies. Indeed, in the current study, there is preliminary evidence that moderators of exercise initiation may differ from moderators of exercise maintenance. Finally, it is interesting to note that while two of the genetic moderators were significant, none of the moderators classified as “responses to physical activity” were moderators of intervention effects. We speculate that perhaps the reason for this is that these reactions were measured during a single bout of physical activity and might display significant variability over time depending on any number of factors. Meanwhile, genotype does not vary, perhaps making it a more reliable potential moderator of intervention effects over time. Clearly additional research is necessary to understand the degree to which immediate responses to physical activity are consistent over time.
The current study has many strengths including the use of an exercise intervention with well-documented success, the design, the recruitment of sedentary individuals, a theory-based conceptual framework as the basis for our selection of potential moderators, the inclusion of moderators across the transdisciplinary spectrum in the same study, the frequency of follow-up assessments, and the length of follow-up. However, this study is limited by a relatively small sample for testing moderated effects, the nature of the sample (mostly women), and the lack of objective verification of self-reported exercise. We originally included accelerometry on a subsample of participants as our budget constraints allowed. We found the data was essentially equivalent to PAR data . Due to higher than expected costs, subject burden involved in returning the units, the ability to only sample a subset of participants, and the lack of added gain in measurement, accelerometer use was discontinued in the early stages of the project. We are also limited by our exclusive focus on intra-individual factors as moderators. Clearly, the environment, sociocultural context, and neighborhood safety, are crucially important in accounting for variability in exercise behavior . Finally, we conducted a number of statistical tests, raising the potential concern of alpha inflation. Thus, it is important—particularly in the context of our moderated effects—that our results be interpreted with caution until they are replicated.
There is increasing interest in the extent to which genetic information can be harnessed to promote engagement in health behavior in general  and in exercise behavior more specifically [58, 59]. Genetic factors account for substantial variability in both engagement in leisure time physical activity  as well as physiological responses to exercise training . The current work provides initial evidence that genetic factors may underlie behavioral responses to physical activity interventions. But can understanding an individual’s genetic profile help researchers and health professionals to understand how they will respond to a behavioral intervention to increase exercise? At least one study has demonstrated a genetic moderator of responses to a behavioral intervention to reduce alcohol abuse , but the science of intervention targeting and tailoring based on genotype is in its infancy. While individual genes accounting for small amounts of variation in intervention response provide proof of concept, it is ultimately much more likely that a combination of hundreds or even thousands of genetic markers will provide both greater statistical power for detecting moderation and the possibility of increased clinical utility of genomic information for the targeting and tailoring of exercise intervention.