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Heart disease is prevalent among older adults. The aim of this study was to a) identify different health behavioral motivation profiles among older adults; and b) investigate if these profiles differed in physical activity and cardiometabolic risk factors. Data on 79 participants (mean age = 68.76 years) was collected. Participants’ degree of intrinsic/extrinsic motivation for diet and exercise was assessed using intuitive eating and self-determination scales. Cardiometabolic risk factors included inflammation and blood lipids. Latent profile analysis was used to identify the optimal number of groups and one-way ANOVAs assessed group differences on the variables of interest. Three profiles were found to best represent the data. The most self-determined, or most intrinsically motivated, group comprised the highest number of participants. In line with Self-Determination Theory, this group demonstrated the highest levels of objective and self-reported physical activity as well as the lowest inflammation and most optimal cholesterol measures. The group with the lowest intuitive eating and high identified exercise regulation scores exhibited the worst outcomes among the three groups. The results suggest that among older adults, different types and levels of motivation for diet and exercise can coexist and interact, and these differences produce varying health outcomes. If supported by future work, these findings can inform practitioners in developing more specific and tailored interventions relevant to older adults based on their motivational profile.

THE loss of lean muscle mass and strength that occurs with advancing age, sarcopenia, has significant ramifications for the overall health and quality of life of older adults. Exercise is a common intervention used to attenuate the loss of lean mass and strength in older adults; however, research has illustrated an age-related impairment in the protein anabolic response to resistance exercise (RE [1–5]). Specifically, we observed a blunted increase in protein synthesis following an acute bout of RE in older adults compared with younger adults, accompanied with reduced phosphorylation of proteins in the mTOR and MAPK signaling pathways that regulate translation (5). On the other hand, the muscle protein breakdown (MPB) response following RE is less well defined in both younger and older adults and potentially regulated through multiple cellular signaling cascades. An acute bout of eccentric RE in younger men has been shown to increase the fractional breakdown rate (FBR) of skeletal muscle proteins for 24 hours (6). The process most commonly associated with protein degradation following exercise is the ubiquitin proteasome system (UPS [7,8]). Within the UPS are two E3 ubiquitin ligases, MuRF1 (muscle specific RING finger 1) and MAFbx (muscle atrophy F-box, also known as atrogin-1), both regulated through the transcription factor Forkhead box (FoxO3a [9–11]), which is inhibited via phosphorylation by Akt or PKB (12). Protein catabolism following exercise may also be regulated through the autophagy–lysosomal system (13,14). Recent research has identified several key autophagy genes under the control of the Akt–FoxO3a signaling pathway, including light chain 3 (LC3) and GABARAP (10,15–17). Increases in MPB (6) and the expression of atrogenes (7,8) in the UPS pathway have been shown following exercise but less is known regarding the contribution of both the UPS and the autophagasomal–lysosomal system, especially in advancing age. In this study, our aim was to better characterize the MPB response to exercise through two key pathways; the autophagasomal–lysosomal and the UPS in both younger and older adults. We hypothesized that (a) MPB would be primarily regulated through the UPS following RE and (b) aging would alter the skeletal muscle autophagy and MPB response to exercise.