Significant progress has been made in the development of countermeasures to attenuate the negative consequences of prolonged exposure to microgravity on astronauts’ bodies. Deconditioning of several organ systems during flight includes losses to cardiorespiratory fitness, muscle mass, bone density and strength. Similar deconditioning also occurs during prolonged bedrest; any protracted time immobile or inactive, especially for unwell older adults (e.g., confined to hospital beds), can lead to similar detrimental health consequences. Due to limitations in physiological research in space, the six-degree head-down tilt bedrest protocol was developed as ground-based analogue to spaceflight. A variety of exercise countermeasures have been tested as interventions to limit detrimental changes and physiological deconditioning of the musculoskeletal and cardiovascular systems. The Canadian Institutes of Health Research and the Canadian Space Agency recently provided funding for research focused on Understanding the Health Impact of Inactivity to study the efficacy of exercise countermeasures in a 14-day randomized clinical trial of six-degree head-down tilt bedrest study in older adults aged 55–65 years old (BROA). Here we will describe the development of a multi-modality countermeasure protocol for the BROA campaign that includes upper- and lower-body resistance exercise and head-down tilt cycle ergometry (high-intensity interval and continuous aerobic exercise training). We provide reasoning for the choice of these modalities following review of the latest available information on exercise as a countermeasure for inactivity and spaceflight-related deconditioning. In summary, this paper sets out to review up-to-date exercise countermeasure research from spaceflight and head-down bedrest studies, whilst providing support for the proposed research countermeasure protocols developed for the bedrest study in older adults.

No abstract

Oxygen consumption ($$\dot{\,{{\mbox{V}}}}{{{\mbox{O}}}}_{2}$$ V ̇ O 2 ) provides established clinical and physiological indicators of cardiorespiratory function and exercise capacity. However, $$\dot{\,{{\mbox{V}}}}{{{\mbox{O}}}}_{2}$$ V ̇ O 2 monitoring is largely limited to specialized laboratory settings, making its widespread monitoring elusive. Here we investigate temporal prediction of $$\dot{\,{{\mbox{V}}}}{{{\mbox{O}}}}_{2}$$ V ̇ O 2 from wearable sensors during cycle ergometer exercise using a temporal convolutional network (TCN). Cardiorespiratory signals were acquired from a smart shirt with integrated textile sensors alongside ground-truth $$\dot{\,{{\mbox{V}}}}{{{\mbox{O}}}}_{2}$$ V ̇ O 2 from a metabolic system on 22 young healthy adults. Participants performed one ramp-incremental and three pseudorandom binary sequence exercise protocols to assess a range of $$\dot{\,{{\mbox{V}}}}{{{\mbox{O}}}}_{2}$$ V ̇ O 2 dynamics. A TCN model was developed using causal convolutions across an effective history length to model the time-dependent nature of $$\dot{\,{{\mbox{V}}}}{{{\mbox{O}}}}_{2}$$ V ̇ O 2 . Optimal history length was determined through minimum validation loss across hyperparameter values. The best performing model encoded 218 s history length (TCN-VO2 A), with 187, 97, and 76 s yielding <3% deviation from the optimal validation loss. TCN-VO2 A showed strong prediction accuracy (mean, 95% CI) across all exercise intensities (−22 ml min−1, [−262, 218]), spanning transitions from low–moderate (−23 ml min−1, [−250, 204]), low–high (14 ml min−1, [−252, 280]), ventilatory threshold–high (−49 ml min−1, [−274, 176]), and maximal (−32 ml min−1, [−261, 197]) exercise. Second-by-second classification of physical activity across 16,090 s of predicted $$\dot{\,{{\mbox{V}}}}{{{\mbox{O}}}}_{2}$$ V ̇ O 2 was able to discern between vigorous, moderate, and light activity with high accuracy (94.1%). This system enables quantitative aerobic activity monitoring in non-laboratory settings, when combined with tidal volume and heart rate reserve calibration, across a range of exercise intensities using wearable sensors for monitoring exercise prescription adherence and personal fitness.

At the onset of an exercise transition, exponential modeling to calculate a time constant (τ) is the conventional method to analyze pulmonary oxygen uptake (V̇O2p) kinetics for moderate and heavy exercise. A new frequency domain analysis technique, mean normalized gain (MNG), has been used to analyze V̇O2p kinetics during moderate exercise, but has not been evaluated for its ability to detect differences in kinetics between moderate and heavy exercise. This study tested the hypothesis that MNG would detect smaller amplitude V̇O2p responses in the heavy compared to moderate exercise domains. Eight young healthy adults (3 female; age: 27±6yr; peak V̇O2p: 43±6ml·min-1·kg-1; mean±SD) performed three bouts of pseudorandom binary sequence (PRBS) exercise for frequency analysis, with work rate (WR) changing between 25W and 90% ventilatory threshold (VT; L→MPRBS), 25W and 50% of the difference between VT and peak V̇O2p (Δ50%; L→HPRBS), and VT to Δ50% (VT→HPRBS). Step exercise tests with equivalent changes in WR to the PRBS tests were performed to facilitate comparison between MNG and τ. MNG was highest for L→MPRBS (59±7%), then L→HPRBS (52±6%), and lowest for VT→HPRBS (38±7%, F(2,14) = 129.755, p < 0.001) exercise conditions indicating slower kinetics with increasing exercise intensity that correlated strongly in repeated measures with τ from step transitions (rrm = -0.893). These results indicate that frequency domain analysis and MNG reliably detect differences in V̇O2p kinetics observed across exercise intensity domains.

Prolonged bedrest provokes orthostatic hypotension and intolerance of upright posture. Limited data are available on the cardiovascular responses of older adults to head-up tilt following bedrest, with no studies examining the potential benefits of exercise to mitigate intolerance in this age group. This randomized controlled trial of head-down bedrest (HDBR) in 55- to 65-yr-old men and women investigated if exercise could avert post-HDBR orthostatic intolerance. Twenty-two healthy older adults (11 female) underwent a strict 14-day HDBR and were assigned to either an exercise (EX) or control (CON) group. The exercise intervention included high-intensity, aerobic, and resistance exercises. Head-up tilt-testing to a maximum of 15 minutes was performed at baseline (Pre-Bedrest) and immediately after HDBR (R1), as well as 6 days (R6) and 4 weeks (R4wk) later. At Pre-Bedrest, 3 participants did not complete the full 15 minutes of tilt. At R1, 18 did not finish, with no difference in tilt end time between CON (422±287s) and EX (409±346s). No differences between CON and EX were observed at R6 or R4wk. At R1, just 1 participant self-terminated the test with symptoms, while 12 others reported symptoms only after physiological test termination criteria were reached. Finishers on R1 protected arterial pressure with higher total peripheral resistance relative to Pre-Bedrest. Cerebral blood velocity decreased linearly with reductions in arterial pressure, end-tidal CO2, and cardiac output. High-intensity interval exercise did not benefit post-HDBR orthostatic tolerance in older adults. Multiple factors were associated with the reduction in cerebral blood velocity leading to intolerance.

Cardiorespiratory fitness declines with age and this decline can be accelerated by inactivity and bed rest. Recovery of fitness is possible, but the timeline in 55-65-year-old adults is unknown. Furthermore, the effectiveness of exercise to prevent deconditioning during bed rest is unexplored in this age group. Twenty-two adults (11 women, 59 ± 3 years) completed two weeks of strict 6° head-down bed rest (HDBR). Half of the participants performed approximately 1 hour of daily exercises, including high-intensity interval cycling, aerobic cycling, and upper- and lower-body resistance training, while control participants were inactive. Step-incremental cycling tests to exhaustion were conducted pre-HDBR and at 3 times during the recovery phase (day-1 or 2, day-6, and 4 weeks) to assess peak oxygen uptake (V̇O2). Peak V̇O2 was reduced in the control group throughout the first 6 days of recovery, but did return to pre-HDBR levels by the 4-week recovery time point (interaction: p=0.002). In the exercise group, peak V̇O2 was not different at any time point during recovery from pre-HDBR. Ventilatory threshold V̇O2 (interaction: p=0.002) and heart rate at 15 W (interaction: p=0.055) mirrored the changes in peak V̇O2 in each respective group. Overall, this study showed that approximately 1 hour of daily exercise effectively protected 55-65-year-old adults' cardiorespiratory fitness during two weeks of HDBR. HDBR without exercise countermeasures caused substantial reductions in cardiorespiratory fitness, but fitness recovered within 4 weeks of resuming daily activities. These findings highlight the importance of physical activity in late middle-age adults.

Human skeletal hemodynamics remain understudied. Neither assessments in weight‐bearing bones during walking nor following periods of immobility exist, despite knowledge of altered nutrient‐artery characteristics after short‐duration unloading in rodents. We studied 12 older adults (8 females, aged 59 ± 3 years) who participated in ambulatory near‐infrared spectroscopy (NIRS) assessments of tibial hemodynamics before (PRE) and after (POST) 14 days of head‐down bed rest (HDBR), with most performing daily resistance and aerobic exercise countermeasures during HDBR. Continual simultaneous NIRS recordings were acquired over the proximal anteromedial tibial prominence of the right lower leg and ipsilateral lateral head of the gastrocnemius muscle during supine rest, walking, and standing. During 10 minutes of walking, desaturation kinetics in the tibia were slower (time to 95% nadir values 125.4 ± 56.8 s versus 55.0 ± 30.1 s, p = 0.0014). Tibial tissue saturation index (TSI) immediately fell (−9.9 ± 4.55) and did not completely recover by the end of 10 minutes of walking (−7.4 ± 6.7%, p = 0.027). Upon standing, total hemoglobin (tHb) kinetics were faster in the tibia (p < 0.0001), whereas HDBR resulted in faster oxygenated hemoglogin (O2Hb) kinetics in both tissues (p = 0.039). After the walk‐to‐stand transition, changes in O2Hb (p = 0.0022) and tHb (p = 0.0047) were attenuated in the tibia alone after bed rest. Comparisons of NIRS‐derived variables during ambulation and changes in posture revealed potentially deleterious adaptations of feed vessels after HDBR. We identify important and novel tibial hemodynamics in humans during ambulation before and after bed rest, necessitating further investigation. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

No abstract