Early mobilization is a crucial component of enhanced recovery after surgery (ERAS) pathways that counteract the adverse physiological consequences of surgical stress and immobilization. Early mobilization reduces the risk of postoperative complications, accelerates the recovery of functional walking capacity, positively impacts several patient-reported outcomes and reduces hospital length of stay, thereby reducing care costs. Modifiable barriers to early mobilization include a lack of education and a lack of resources. Education and clinical decision-making tools can improve compliance with ERAS mobilization recommendations and create a culture that prioritizes perioperative physical activity. Recent advances include real-time feedback of mobilization quantity using wearable technology and combining ERAS with exercise prehabilitation. ERAS guidelines should emphasize the benefits of structured postoperative mobilization.

Objective: People living with long COVID describe a high symptom burden, and a more detailed assessment is needed to inform rehabilitation recommendations. The objectives were to use validated questionnaires to measure the severity of fatigue and compare this with normative data and thresholds for clinical relevance in other diseases; measure and describe the impact of postexertional malaise (PEM); and assess symptoms of dysfunctional breathing, self-reported physical activity, and health-related quality of life. Methods: This was an observational study with a cross-sectional survey design (data collection from February 2021 to April 2021). Eligible participants were adults experiencing persistent symptoms due to COVID-19 that did not predate the confirmed or suspected infection. Questionnaires included the Functional Assessment of Chronic Illness Therapy–Fatigue Scale and the DePaul Symptom Questionnaire–Post-Exertional Malaise. Results: After data cleaning, 213 participants were included in the analysis. The total Functional Assessment of Chronic Illness Therapy–Fatigue Scale score was 18 (SD = 10) (where the score can range from 0 to 52, and a lower score indicates more severe fatigue), and 71.4% were experiencing chronic fatigue. Postexertional symptom exacerbation affected most participants, and 58.7% met the PEM scoring thresholds used in people living with myalgic encephalomyelitis/chronic fatigue syndrome. Conclusion: Long COVID is characterized by chronic fatigue that is clinically relevant and at least as severe as fatigue in several other clinical conditions. PEM is a significant challenge for this patient group. Because of the potential for setbacks and deteriorated function following overexertion, fatigue and postexertional symptom exacerbation must be monitored and reported in clinical practice and in studies involving interventions for people with long COVID. Impact: Physical therapists working with people with long COVID should measure and validate the patient’s experience. Postexertional symptom exacerbation must be considered, and rehabilitation needs to be carefully designed based on individual presentation. Beneficial interventions might first ensure symptom stabilization via pacing, a self-management strategy for the activity that helps minimize postexertional malaise.

Purpose: To outline how hypoxia profoundly affects neuronal functionality and thus compromises exercise performance. Methods: Investigations were reviewed and evaluated that used electroencephalography (EEG) and transcranial magnetic stimulation (TMS) to detect neuronal changes at rest and those studying fatiguing effects on whole-body exercise performance in acute (AH) and chronic hypoxia (CH). Results: At rest during very early hypoxia (<1-h), slowing of cerebral neuronal activity is evident despite no change in corticospinal excitability. As time in hypoxia progresses (3-h), increased corticospinal excitability becomes evident; however, changes in neuronal activity are unknown. Prolonged exposure (3–5 d) causes a respiratory alkalosis which modulates Na⁺ channels, potentially explaining reduced neuronal excitability. Locomotor exercise in AH exacerbates the development of peripheral fatigue; as the severity of hypoxia increases, mechanisms of peripheral fatigue become less dominant and CNS hypoxia becomes the predominant factor. The greatest central fatigue in AH occurs when S_aO₂ is ≤75%, a level that coincides with increasing impairments in neuronal activity. CH does not improve the level of peripheral fatigue observed in AH; however, it attenuates the development of central fatigue paralleling increases in cerebral O₂ availability and corticospinal excitability. Conclusions: The attenuated development of central fatigue in CH might explain the improvements in locomotor exercise performance commonly observed after acclimatisation to high altitude.

The development of muscle fatigue is oxygen (O₂)-delivery sensitive [arterial O₂ content (C_aO₂) × limb blood flow ( Q_L)]. Locomotor exercise in acute hypoxia (AH) is, compared with sea level (SL), associated with reduced C_aO₂ and exaggerated inspiratory muscle work (W_insp), which impairs Q_L, both of which exacerbate fatigue individually by compromising O₂ delivery. Since chronic hypoxia (CH) normalizes C_aO₂ but exacerbates W_insp, we investigated the consequences of a 14-day exposure to high altitude on exercise-induced locomotor muscle fatigue. Eight subjects performed the identical constant-load cycling exercise (138 ± 14 W; 11 ± 1 min) at SL (partial pressure of inspired O₂, 147.1 ± 0.5 Torr), in AH (73.8 ± 0.2 Torr), and in CH (75.7 ± 0.1 Torr). Peripheral fatigue was expressed as pre- to postexercise percent reduction in electrically evoked potentiated quadriceps twitch force (ΔQ_tw,pot). Central fatigue was expressed as the exercise-induced percent decrease in voluntary muscle activation (ΔVA). Resting C_aO₂ at SL and CH was similar, but C_aO₂ in AH was lower compared with SL and CH (17.3 ± 0.5, 19.3 ± 0.7, 20.3 ± 1.3 ml O₂/dl, respectively). W_insp during exercise increased with acclimatization (SL: 387 ± 36, AH: 503 ± 53, CH: 608 ± 67 cmH₂O·s⁻¹·min⁻¹; P < 0.01). Exercise at SL did not induce central or peripheral fatigue. ΔQ_tw,pot was significant but similar in AH and CH (21 ± 2% and 19 ± 3%; P = 0.24). ΔVA was significant in both hypoxic conditions but smaller in CH vs. AH (4 ± 1% vs. 8 ± 2%; P < 0.05). In conclusion, acclimatization to severe altitude does not attenuate the substantial impact of hypoxia on the development of peripheral fatigue. In contrast, acclimatization attenuates, but does not eliminate, the exacerbation of central fatigue associated with exercise in severe AH.