Physiological responses to hypoxic constant-load and high-intensity interval exercise sessions in healthy subjects.

PURPOSE: The aim of this study was to assess the acute cardiorespiratory as well as muscle and cerebral tissue oxygenation responses to submaximal constant-load (CL) and high-intensity interval (HII) cycling exercise performed in normoxia and in hypoxia at similar intensity, reproducing whole-body endurance exercise training sessions as performed in sedentary and clinical populations. METHODS: Healthy subjects performed two CL (30 min, 75% of maximal heart rate, n = 12) and two HII (15 times 1-min high-intensity exercise-1-min passive recovery, n = 12) cycling exercise sessions in normoxia and in hypoxia [mean arterial oxygen saturation 76 ± 1% (clamped) during CL and 77 ± 5% (inspiratory oxygen fraction 0.135) during HII]. Cardiorespiratory and near-infrared spectroscopy parameters as well as the rate of perceived exertion were continuously recorded. RESULTS: Power output was 21 ± 11% and 15% (according to protocol design) lower in hypoxia compared to normoxia during CL and HII exercise sessions, respectively. Heart rate did not differ between normoxic and hypoxic exercise sessions, while minute ventilation was higher in hypoxia during HII exercise only (+ 13 ± 29%, p < 0.05). Quadriceps tissue saturation index did not differ significantly between normoxia and hypoxia (CL 60 ± 8% versus 59 ± 5%; HII 59 ± 10% versus 56 ± 9%; p > 0.05), while prefrontal cortex deoxygenation was significantly greater in hypoxia during both CL (66 ± 4% versus 56 ± 6%) and HII (58 ± 5% versus 55 ± 5%; p < 0.05) sessions. The rate of perceived exertion did not differ between normoxic and hypoxic CL (2.4 ± 1.7 versus 2.9 ± 1.8) and HII (6.9 ± 1.4 versus 7.5 ± 0.8) sessions (p > 0.05). CONCLUSION: This study indicates that at identical heart rate, reducing arterial oxygen saturation near 75% does not accentuate muscle deoxygenation during both CL and HII exercise sessions compared to normoxia. Hence, within these conditions, larger muscle hypoxic stress should not be expected.

Hypoxic conditioning and the central nervous system: A new therapeutic opportunity for brain and spinal cord injuries?

Central nervous system diseases are among the most disabling in the world. Neuroprotection and brain recovery from either acute or chronic neurodegeneration still represent a challenge in neurology and neurorehabilitation as pharmacology treatments are often insufficiently effective. Conditioning the central nervous system has been proposed as a potential non-pharmacological neuro-therapeutic. Conditioning refers to a procedure by which a potentially deleterious stimulus is applied near to but below the threshold of damage to the organism to increase resistance to the same or even different noxious stimuli given above the threshold of damage. Hypoxic conditioning has been investigated in several cellular and preclinical models and is now recognized as inducing endogenous mechanisms of neuroprotection. Ischemic, traumatic, or chronic neurodegenerative diseases can benefit from hypoxic conditioning strategies aiming at preventing the deleterious consequences or reducing the severity of the pathological condition (preconditioning) or aiming at inducing neuroplasticity and recovery (postconditioning) following central nervous system injury. Hypoxic conditioning can consist in single (sustained) or cyclical (intermittent, interspersed by short period of normoxia) hypoxia stimuli which duration range from few minutes to several hours and that can be repeated over several days or weeks. This mini-review addresses the existing evidence regarding the use of hypoxic conditioning as a potential innovating neuro-therapeutic modality to induce neuroprotection, neuroplasticity and brain recovery. This mini-review also emphasizes issues which remain to be clarified and future researches to be performed in the field. Impact statement Neuroprotection and brain recovery from either acute or chronic neurodegeneration still represent a challenge in neurology and neurorehabilitation. Hypoxic conditioning may represent a harmless and efficient non-pharmacological new therapeutic modality in the field of neuroprotection and neuroplasticity, as supported by many preclinical data. Animal studies provide clear evidence for neuroprotection and neuroplasticity induced by hypoxic conditioning in several models of neurological disorders. These studies show improved functional outcomes when hypoxic conditioning is applied and provides important information to translate this intervention to clinical practice. Some studies in humans provide encouraging data regarding the tolerance and therapeutic effects of hypoxic conditioning strategies. The main issues to address in future research include the definition of the appropriate hypoxic dose and pattern of exposure, the determination of relevant physiological biomarkers to assess the effects of the treatment and the evaluation of combined strategies involving hypoxic conditioning and other pharmacological or non-pharmacological treatments.