Brown et al. [1] investigated simulated altitude (hypoxic training) as a form of prehabilitation. Participants stayed in a residential hypoxia facility for 1 week in normoxic conditions and 1 week in hypoxic conditions (F_IO₂ 15%). Although haemoglobin and erythropoietin concentration appeared to increase across the hypoxic week, this came at significant cost (e.g. physiological/clinical, environmental, financial) and may have been, at least partly, artefactual.

Since the 1960s, we have understood the deleterious effects of inactivity on human physiological function, most obviously from bed rest studies. Although not strictly bed rest in the study by Brown et al. [1], participants were not allowed to leave the facility or perform any exercise or sustained physical activity, including preparation of their own meals. In this short time, irrespective of exposure, anaerobic threshold decreased by 8–9% (normoxic: 11.9 to 11.0 ml.min^-1.kg^-1; hypoxic 12.4 to 11.3 ml.min^-1.kg^-1) and peak oxygen consumption (peak $\dot{\mathrm{V}}{\mathrm{O}}_2$) by 4–7% (normoxic: 17.1–15.9 ml.min^-1.kg^-1; hypoxic: 17.8–17.1 ml.min^-1.kg^-1). In fact, peak exercise heart rate was 16 beats.min^-1 higher in the follow-up cardiopulmonary exercise test after hypoxic exposure; therefore, baseline peak $\dot{\mathrm{V}}{\mathrm{O}}_2$ seems likely to have been underestimated, representing an even larger decrease across the intervention. This rapid decrease in cardiorespiratory fitness is likely attributable to reduced plasma volume, secondary to the additional confinement and ensuing reduction in physical activity. This reduction in plasma volume also seems likely to have contributed to the observed increase in haemoglobin. The analogy of a glass of sugary water can provide some perspective. If some water leaves (evaporates), you are left with a sweeter concentrate. Similarly, if plasma volume in total blood is reduced, haemoglobin concentration is increased. Although the between- rather than within-participant standard deviations make inferences difficult for both normoxic and hypoxic interventions, the reported increases in haemoglobin concentration appear artefactual. Previous work has shown haemoglobin mass increases at approximately 1% per week [2], and this is when exercise and hypoxia are combined in ‘live high, train low’ studies.

Peak $\dot{\mathrm{V}}{\mathrm{O}}_2$ and anaerobic threshold have been shown to be prognostic surgical indicators [3, 4], both of which were rapidly degraded, to near clinically important prognostic cut-offs. However, it is also important to note, peak $\dot{\mathrm{V}}{\mathrm{O}}_2$ and anaerobic threshold are only surrogate markers for a constellation of physiological processes refined with regular physical activity or exercise, and regress with inactivity. In this study, they might, similarly, represent the broader and rapid degradation of systematic processes (cardiovascular, metabolic, haematological, musculoskeletal function) that contribute. While hypoxic training may elicit similar haematological changes to regular exercise training, it cannot, and should not, replace the holistic and pleiotropic effects of physical activity. Exercise specifically targets many other modifiable surgical risk factors such as frailty through favourable adaptations in musculoskeletal health and function; diabetes through improved blood glucose regulation; enhanced lipid oxidation; and reduced incidence of anxiety and depression. Exercise also induces cellular hypoxia among other stressors, triggering a cascade of responses that build resilience to future hypoxia, whether systemic (i.e. exercise or surgery) or localised (e.g. aortic clamping, arthroplasty tourniquet) [3].

Physical activity and exercise are time efficient, accessible and equitable therapies to optimise pre-operative fitness and health. Surgery is a uniquely motivating life event for patients to become physically active. A collaborative team and patient-centred approach is essential to capitalise on this motivation and empower patients to improve not only pre-operative health but also provide the skills and behaviour changes to maintain this during the rehabilitation period and beyond. Future prehabilitation work must focus on ecologically valid, accessible and equitable interventions that are sustainable from a lifestyle and financial perspective as well as, most importantly, an environmental and resource perspective.

布朗等人。 [ 1 ] 研究了模拟海拔（低氧训练）作为预康复的一种形式。参与者在常氧条件下在住宅缺氧设施中停留 1 周，在缺氧条件下停留 1 周 (F _I O ₂ 15%)。尽管血红蛋白和促红细胞生成素浓度在缺氧一周内似乎有所增加，但这付出了巨大的代价（例如生理/临床、环境、财务），并且可能至少部分是人为的。

自 20 世纪 60 年代以来，我们从卧床休息研究中了解到不活动对人体生理功能的有害影响。尽管布朗等人的研究中没有严格卧床休息。 [ 1 ]，参与者不得离开设施或进行任何锻炼或持续的身体活动，包括自己准备饭菜。在这么短的时间内，无论暴露程度如何，无氧阈值均下降 8–9%（正常氧：11.9 至 11.0 ml.min ^-1 .kg ^-1 ；缺氧 12.4 至 11.3 ml.min ^-1 .kg ^-1 ）和峰值氧消费（高峰 $\dot{\mathrm{V}}{\mathrm{O}}_2$ ）减少 4–7%（常氧：17.1–15.9 ml.min ^-1 .kg ^-1 ；低氧：17.8–17.1 ml.min ^-1 .kg ^-1 ）。事实上，在低氧暴露后的后续心肺运动试验中，峰值运动心率要高出16次.min ^-1 ；因此，基线峰值 $\dot{\mathrm{V}}{\mathrm{O}}_2$ 似乎可能被低估了，表明整个干预期间下降幅度更大。心肺健康的快速下降可能是由于血浆容量减少，继发于额外的限制和随之而来的体力活动减少。血浆容量的减少似乎也可能导致了观察到的血红蛋白的增加。一杯糖水的类比可以提供一些视角。如果一些水离开（蒸发），您就会得到更甜的浓缩物。类似地，如果总血中的血浆量减少，血红蛋白浓度就会增加。 尽管参与者之间而非参与者内部的标准差使得常氧和低氧干预措施的推断变得困难，但报告的血红蛋白浓度增加似乎是人为的。之前的研究表明，血红蛋白质量每周增加约 1% [ 2 ]，这是在“高生活，低训练”研究中将运动和缺氧结合起来时的情况。

顶峰 $\dot{\mathrm{V}}{\mathrm{O}}_2$ 和无氧阈值已被证明是预后手术指标[ 3, 4 ]，两者都迅速下降，接近临床上重要的预后临界值。不过，还需要注意的是，峰值 $\dot{\mathrm{V}}{\mathrm{O}}_2$ 和无氧阈值只是一系列生理过程的替代标志，这些生理过程通过定期的体力活动或锻炼而完善，并随着不活动而回归。在这项研究中，它们可能同样代表了系统过程（心血管、代谢、血液、肌肉骨骼功能）更广泛和快速的退化。虽然低氧训练可能会引起与常规运动训练类似的血液学变化，但它不能也不应该取代身体活动的整体和多效性效果。锻炼专门针对许多其他可改变的手术风险因素，例如通过肌肉骨骼健康和功能的有利适应而导致虚弱；通过改善血糖调节来治疗糖尿病；增强脂质氧化；并减少焦虑和抑郁的发生率。运动还会在其他应激源中诱导细胞缺氧，引发一系列反应，从而增强对未来缺氧的抵抗力，无论是全身性的（即运动或手术）还是局部的（例如主动脉夹闭、关节成形术止血带）[ 3 ]。

身体活动和锻炼是一种省时、方便且公平的疗法，可以优化术前的健康状况。手术是一种独特的生活事件，可以激励患者变得活跃起来。协作团队和以患者为中心的方法对于利用这种动机并使患者不仅能够改善术前健康状况，而且还提供技能和行为改变以在康复期间及以后维持这种健康状况至关重要。未来的康复工作必须侧重于生态有效、可及和公平的干预措施，这些干预措施从生活方式和财务角度以及最重要的是从环境和资源角度来看是可持续的。