Acute continuous moderate-intensity exercise, but not low-volume high-intensity interval exercise, attenuates postprandial suppression of circulating osteocalcin in young overweight and obese adults
Bone remodeling markers (BRMs) are suppressed following the consumption of a meal. Our findings indicate that a single session of continuous moderate-intensity exercise, but not low-volume high-intensity interval exercise, performed 1 h after a meal attenuates the postprandial suppression of BRMs.
Acute exercise transiently increases BRMs including osteocalcin (tOC) and the undercarboxylated form of osteocalcin (ucOC), a hormone that is implicated in glucose regulation. The effects of acute exercise and exercise-intensity on postprandial levels of tOC and ucOC are unknown.
Twenty-seven adults that were overweight or obese (age 30 ± 1 years; BMI 30 ± 1 kg∙m−2; mean ± SEM) were randomly allocated to perform a single session of low-volume high-intensity interval exercise (LV-HIIE; nine females, five males) or continuous moderate-intensity exercise (CMIE; eightfemales, five males) 1 h after consumption of a standard breakfast. Serum tOC, ucOC, and ucOC/tOC were measured at baseline, 1 h, and 3 h after breakfast consumption on a rest day (no exercise) and the exercise day (exercise 1 h after breakfast).
Compared to baseline, serum tOC and ucOC were suppressed 3 h after breakfast on the rest day (− 10 ± 1% and − 6 ± 2%, respectively; p < 0.05), whereas ucOC/tOC was elevated (2.5 ± 1%; p = 0.08). Compared to the rest day, CMIE attenuated the postprandial-induced suppression of tOC (rest day − 10 ± 2% versus CMIE − 5 ± 2%, p < 0.05) and ucOC (rest day − 6 ± 4% versus CMIE 11 ± 2%, p < 0.05), and increased postprandial ucOC/tOC (rest day 3 ± 2% versus CMIE 15 ± 1%, p < 0.05). In contrast, LV-HIIE did not alter postprandial tOC, ucOC, or ucOC/tOC (all p > 0.1).
Acute CMIE, but not LV-HIIE, attenuates the postprandial-induced suppression of tOC and ucOC. CMIE may be an effective tool to control the circulating levels of BRMs following meal consumption in overweight/obese adults.
KeywordsBone metabolism Glycemic control HIIT Osteoblast
Thank you to Prof. John Hawley, Prof. Helena Teede, Dr. Christos Stathis, Dr. Karen Hill, Dr. Lauren Banting, Prof. Andrew McAinch, and Dr. Matthew Cooke, for your contribution to the research. Thank you to all the participants who were involved in the research.
LP, CSS, NKS, and IL contributed to the study design and acquirement of ethical approval. LP and CSS contributed to data collection. EB performed biochemical analysis of serum osteocalcin and uncarboxylated osteocalcin. LP statistically analyzed the data and drafted the initial manuscript. The remaining authors critically revised the manuscript. All authors approved the final version of the manuscript. LP is the guarantor of the manuscript and takes full responsibility for the work as a whole, including the study design, access to data, and the decision to submit and publish the manuscript.
A/Prof Levinger was supported by Future Leader Fellowship (ID: 100040) from the National Heart Foundation of Australia. Dr. Parker was supported by an Alfred Deakin Postdoctoral Fellowship. This work is supported by the Australian Government Collaborative Research Network (CRN) awarded to the authors LP, CSS, NKS, and IL.
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Conflicts of interest
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