Gordon Mitchell opened and directs the UF Center for Breathing Research and Therapeutics (BREATHE) and an NIH-funded graduate and postdoctoral training program of the same name. A key focus of BREATHE is to understand and treat impaired breathing and airway defense (swallowing/cough) caused by neuromuscular injury or disease.
Areas of Expertise (7)
Cellular mechanisms of intermittent hypoxia induced spinal respiratory motor plasticity
Compensatory respiratory plasticity in motor neuron disease (ALS)
Inflammation and spinal plasticity
Intermittent hypoxia and brain function
Intermittent hypoxia-induced respiratory and non-respiratory motor recovery after spinal injury
Translation of low-dose intermittent hypoxia to treat humans with chronic spinal injury
Caffeine enhances intermittent hypoxia-induced gains in walking function for people with chronic spinal cord injury.Journal of Neurotrauma
Randy D. Trumbower, et. al
Incomplete spinal cord injury (iSCI) often results in lifelong walking impairments that limit functional independence. Thus, treatments that trigger enduring improvement in walking after iSCI are in high demand. Breathing brief episodes of low oxygen (i.e., acute intermittent hypoxia, AIH) enhances breathing and walking function in rodents and humans with chronic iSCI. Pre-clinical studies found that AIH also causes the accumulation of extracellular adenosine that undermines AIH-induced functional plasticity.
Acute intermittent hypercapnic-hypoxia elicits central neural respiratory motor plasticity in humans.The Journal of Physiology
Joseph F. Welch, et. al
Acute intermittent hypoxia (AIH) elicits long-term facilitation (LTF) of respiration. Although LTF is observed when CO2 is elevated during AIH in awake humans, the influence of CO2 on corticospinal respiratory motor plasticity is unknown. Thus, we tested the hypotheses that acute intermittent hypercapnic-hypoxia (AIHH): (1) enhances cortico-phrenic neurotransmission (reflecting volitional respiratory control); and (2) elicits ventilatory LTF (reflecting automatic respiratory control).
Daily acute intermittent hypoxia enhances serotonergic innervation of hypoglossal motor nuclei in rats with and without cervical spinal injury.Experimental Neurology
Marissa C. Ciesla, et. al
Intermittent hypoxia elicits protocol-dependent effects on hypoglossal (XII) motor plasticity. Whereas low-dose, acute intermittent hypoxia (AIH) elicits serotonin-dependent plasticity in XII motor neurons, high-dose, chronic intermittent hypoxia (CIH) elicits neuroinflammation that undermines AIH-induced plasticity. Preconditioning with repeated AIH and mild CIH enhance AIH-induced XII motor plasticity.
Acute intermittent hypoxia and respiratory muscle recruitment in people with amyotrophic lateral sclerosis: A preliminary study.Experimental neurology
Elaheh Sajjadi, et. al
Respiratory failure is the main cause of death in amyotrophic lateral sclerosis (ALS). Since no effective treatments to preserve independent breathing are available, there is a critical need for new therapies to preserve or restore breathing ability. Since acute intermittent hypoxia (AIH) elicits spinal respiratory motor plasticity in rodent ALS models, and may restore breathing ability in people with ALS, we performed a proof-of-principle study to investigate this possibility in ALS patients.