| Summary: | Background: Spaceflight alters human cardiovascular dynamics. The less negative slope of the fractal scaling of heart rate variability (HRV) of astronauts exposed long-term to microgravity reflects cardiovascular deconditioning. We here focus on specific frequency regions of HRV.
Methods: Ten healthy astronauts (8 men, 49.1 ± 4.2 years) provided five 24-hour electrocardiographic (ECG) records: before launch, 20.8 ± 2.9 (ISS01), 72.5 ± 3.9 (ISS02) and 152.8 ± 16.1 (ISS03) days after launch, and after return to Earth. HRV endpoints, determined from normal-to-normal (NN) intervals in 180-min intervals progressively displaced by 5 min, were compared in space versus Earth. They were fitted with a model including 4 major anticipated components with periods of 24 (circadian), 12 (circasemidian), 8 (circaoctohoran), and 1.5 (Basic Rest-Activity Cycle; BRAC) hours.
Findings: The 24-, 12-, and 8-hour components of HRV persisted during long-term spaceflight. The 90-min amplitude became about three times larger in space (ISS03) than on Earth, notably in a subgroup of 7 astronauts who presented with a different HRV profile before flight. The total spectral power (TF; p < 0.05) and that in the ultra-low frequency range (ULF, 0.0001–0.003 Hz; p < 0.01) increased from 154.9 ± 105.0 and 117.9 ± 57.5 msec2 (before flight) to 532.7 ± 301.3 and 442.4 ± 202.9 msec2 (ISS03), respectively. The power-law fractal scaling β was altered in space, changing from -1.087 ± 0.130 (before flight) to -0.977 ± 0.098 (ISS01), -0.910 ± 0.130 (ISS02), and -0.924 ± 0.095 (ISS03) (invariably p < 0.05).
Interpretation: Most HRV changes observed in space relate to a frequency window centered around one cycle in about 90 min. Since the BRAC component is amplified in space for only specific HRV endpoints, it is likely to represent a physiologic response rather than an artifact from the International Space Station (ISS) orbit. If so, it may offer a way to help adaptation to microgravity during long-duration spaceflight.
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