Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.10.13.758757

Agreement between Garmin and Ultrahuman wearables and their association with continuous glucose monitoring: an n-of-1 study

Abstract

Background: Consumer wearables and continuous glucose monitors (CGM) are increasingly worn together outside clinical settings. Few studies have examined whether two wearables worn at the same time agree with each other, and whether either tracks glucose metrics derived from CGM. Objective: In one adult under free-living conditions, we examined (1) how well sleep, heart rate, heart rate variability (HRV) and activity metrics from a Garmin smartwatch and an Ultrahuman ring agreed with each other, and (2) how these metrics related to glucose measured by CGM. Methods: One healthy adult with no diagnosed diabetes wore a Garmin Fenix 8 watch on the wrist, an Ultrahuman Ring AIR and an Abbott FreeStyle Libre CGM at the same time for 12 days (29 July to 9 August 2026; 1101 glucose readings). We assessed agreement between the devices with Pearson correlation and Bland-Altman analysis (mean bias and 95% limits of agreement, LoA) for daily metrics and for heart rate within the day, and with Cohen's kappa for sleep stages, minute by minute. We related the wearable metrics to mean glucose, glucose variability (coefficient of variation, CV%) and time in range (TIR, 3.9 to 10.0 mmol/L), reading by reading (over the whole record and separately for sleep and waking hours) and day by day. All correlations are descriptive. Because the Ultrahuman ring recorded no data for 22 hours on 3 August and its daytime heart rate behaved differently afterwards, heart-rate analyses are reported for the whole period and separately before and after that gap. The daily results were checked by leaving out one day at a time and by excluding the first 24 hours of sensor wear. Results: The devices agreed closely on total sleep duration (r=0.94; bias -0.02 h, 95% LoA -0.56 to 0.51 h). Daily steps correlated strongly (r=0.99 over the 11 days with data from both devices), but Garmin counted more steps on every day (mean 11,157 vs. 8,929 steps per day; bias +2228 steps). Heart rate agreed moderately during sleep (r=0.68). While awake, agreement was moderate before the gap (r=0.54) and absent after it (r=0.08), when Ultrahuman's daytime heart rate stayed near 70 bpm. The devices assigned the same sleep stage in 50.0% of 4525 minutes (kappa=0.28). Mean glucose was 5.13 mmol/L (SD 0.82) and TIR was 97.5%. Of all wearable signals, heart rate was most closely associated with glucose (Garmin r=0.43 over all readings), but the correlation fell to 0.34 within sleep and 0.21 within waking hours, and before the gap the two devices' waking correlations were alike (Garmin 0.25, Ultrahuman 0.24). Across the 12 days, correlations between night-time wearable metrics and glucose variability weakened markedly when the first 24 hours of sensor wear were excluded (absolute r fell from 0.59 or more to 0.34 or less), and TIR was 100% on 8 of the 12 days, which left it little room to vary. Conclusions: The two wearables agreed on how long the participant slept but not on how the night was staged, and their heart-rate agreement depended on whether the participant was asleep or awake and on the period of wear. Of all wearable signals, heart rate was most closely associated with glucose, mainly because both are lower at night and higher during the day. The associations across days rested largely on the first night of sensor wear. In this single participant, the devices behaved differently by device and by period of wear, so studies that combine different wearables, or relate them to CGM, should check for such differences before pooling data.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Lovric, M., Strbad, D., Rasmussen, M. A.. 2026-10-16. Agreement between Garmin and Ultrahuman wearables and their association with continuous glucose monitoring: an n-of-1 study. https://doi.org/10.64898/2026.10.13.758757

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Speed judgments during smooth pursuit reflect low gain efference copy

During smooth pursuit eye movements, the visual system must compensate for self-generated retinal motion to achieve stable perception of motion in the environment. This compensation primarily depends on an efferent copy of motor commands. Systematically under- or overweighting the strength of efference copy should lead to correlations between eye movement velocity and perceived object velocity. However, previous examinations of these trial-by-trial perceptual correlations have produced mixed results. It remains unclear how effectively the brain compensates for eye movement induced retinal motion during pursuit, and what this reveals about the way efference copy influences perception. To address this, we developed a speed perturbation paradigm in which 29 participants tracked a moving target that underwent brief speed changes. On each trial, we recorded eye velocity along with perceptual judgments of the sign of the speed change (faster or slower) and confidence ratings for those judgments. Across participants, perceptual and oculomotor sensitivity were correlated (r =0.53), but trial-by-trial perceptual and oculomotor responses appeared independent. A logistic regression model incorporating efference copy gain to predict perceptual reports from stimulus speed and eye speed revealed systematic under-compensation for eye movements; faster eye movements were associated with lower changes in perceived speed. Confidence ratings were well-calibrated to perceptual accuracy and showed a consistent negative relationship with eye movement speed. Collectively, these results are consistent with systematic under compensation for eye movements through the use of efference copy during motion perception.

physiology↗

AN INTEGRATED HEART-ON-A-CHIP NAM RESOLVES DISTINCT CLINICAL PHENOTYPES OF MYOCARDIAL ISCHEMIA-REPERFUSION INJURY

Background: Reperfusion is required for myocardial salvage yet itself injures the heart, and cardioprotective interventions that reduce infarct size experimentally have repeatedly failed to improve outcomes in patients. These interventions are evaluated against viability or infarct size alone, whereas ischemia-reperfusion (I/R) injury produces structural, biochemical, and contractile dysfunction in the same tissue. No in vitro new approach methodology (NAM), however, resolves all three within one system. Methods: A NAM was created within a heart-on-a-chip platform, which was constructed by culturing neonatal rat ventricular myocytes (NRVMs) on muscular thin films. Cardiomyocytes were subjected to normoxia, 2 hours of ischemia, and ischemia followed by 2 hours of reperfusion. Sarcomeric architecture was quantified by immunofluorescence, cardiomyocyte injury by LIVE/DEAD staining and cardiac troponin I release into conditioned media, while contractile stress and spontaneous beat frequency were recorded on the same films before and after each condition. Results: Under ischemia, z-line density decreased while architectural metrics were preserved, indicating cell loss rather than sarcomere disorganization. Furthermore, viability decreased, troponin elevated, and every contractile stress component declined, while spontaneous beat frequency was unchanged. Reperfusion fractured this uniform depression. Cell death and troponin release increased further, yet structure was unchanged from ischemia, so every functional change occurred on a depleted but architecturally intact cardiomyocyte population. Systolic stress recovered partially, whereas diastolic stress exceeded baseline, leaving active stress suppressed despite oxygen recovery. Beat frequency increased with pronounced variability. Conclusions: This heart-on-a-chip NAM resolved structural, biochemical, and contractile injury that global indices conflate, distinguishing ischemic from reperfusion pathophysiology. Interestingly, individual readouts corresponded to distinct clinical syndromes of ischemic injury, positioning this platform for future testing of cardioprotective candidates against the full injury phenotype.

physiology↗

Proteomic profiling of experimental acute alcohol intoxication reveals FGF21 as a specific ethanol-induced hormone

Background: The effects of acute alcohol intoxication on the human plasma proteome are still largely unexplored. Gaining insights into this relationship could identify factors that are influenced by and influence alcohol consumption. Fibroblast Growth Factor 21 (FGF21), a hormone produced by the liver and associated with alcohol preferences, is currently undergoing Phase 2 clinical trials for metabolic dysfunction and alcohol-related liver disease. We hypothesized that FGF21 is a key endocrine responsive hormone to alcohol in humans. Methods: In a post hoc analysis, we evaluated the effects of five standard units of alcoholic beverages on the plasma proteome in 12 healthy Caucasian men. Participants, fasting for 10 hours, received 0.7 g of alcohol per kg of body weight via gastric infusion, with blood samples collected before and after consumption. Results: The proteomic response to this level of alcohol intoxication was highly specific. Of 1,462 proteins measured, only 11 changed significantly and FGF21 exhibited by far the largest increase (10.5-fold). Conclusion: This study highlights a unique proteomic response to acute alcohol ingestion and supports further exploration of FGF21 mimetics as potential treatments for alcohol-related disorders.

physiology↗