Feasibility of oropharyngeal and respiratory muscle training in individuals with OSA and spinal cord injury or disease: A pilot study.

OBJECTIVES: To examine the feasibility of individuals with spinal cord injury or disease (SCI/D) to perform combined oropharyngeal and respiratory muscle training (RMT) and determine its impact on their respiratory function. METHODS: A prospective study at a single Veterans Affairs (VA) Medical Center. Inclusion criteria included: 1) Veterans with chronic SCI/D (>6 months postinjury and American Spinal Injury Association (ASIA) classification A-D) and 2) evidence of OSA by apnea-hypopnea index (AHI ≥5 events/h). Eligible participants were randomly assigned to either an experimental (exercise) group that involved performing daily inspiratory, expiratory (using POWERbreathe and Expiratory Muscle Strength Trainer 150 devices, respectively), and tongue strengthening exercises or a control (sham) group that involved using a sham device, for a 3-month period. Spirometry, maximal expiratory pressure (MEP), maximal inspiratory pressure (MIP), polysomnography, and sleep questionnaires were assessed at baseline and at 3 months. RESULTS: Twenty-four individuals were randomized (12 participants in each arm). A total of eight (67%) participants completed the exercise arm, and ten (83%) participants completed the sham arm. MIP was significantly increased (p < 0.05) in the exercise group compared with the baseline. CONCLUSIONS: Combined oropharyngeal and RMT are feasible for individuals with SCI/D. Future studies are needed to determine the clinical efficacy of these respiratory muscle exercises.

The Acute Effects of Milk Consumption on Systemic Inflammation after Combined Resistance and Plyometric Exercise in Young Adult Females.

High-intensity/impact exercise elicits a transient increase in inflammatory biomarkers. Consuming nutrient-dense wholefoods, like milk, following exercise may modulate post-exercise inflammation and aid recovery. We examined the effect of post-exercise skim milk consumption (versus an isoenergetic, isovolumetric carbohydrate [CHO] drink) on acute exercise-induced inflammation in untrained females. Using a randomized crossover design, 13 healthy females (age = 20 ± 2.3 y; BMI = 21.0 ± 1.1 kg/m2) completed two bouts of combined resistance/plyometric exercise followed by either skim milk (MILK) or CHO at 5-min and 1 h post-exercise. Serum interleukin [IL]-1ß, IL-6, IL-10, and tumor necrosis factor-alpha (TNF-α) concentrations were measured at pre-exercise, 15-min, 75-min, 24 h, and 48 h post-exercise. IL-6 increased 15-min post-exercise vs. all other timepoints (time effect, p = 0.017). Between 24 and 48 h, IL-10 decreased and increased in the MILK and CHO conditions, respectively (interaction, p = 0.018). There were no significant effects for IL-1ß or TNF-α. Relative concentrations of IL-1ß (p = 0.049) and IL-10 (p = 0.028) at 48 h post-exercise were lower in MILK vs. CHO. Milk post-exercise did not influence the absolute concentration of pro-inflammatory cytokines; however, there were divergent responses for the anti-inflammatory cytokine, IL-10, and milk reduced the relative inflammatory response at 48 h (vs. CHO) for IL-1ß and IL-10. This demonstrates the potential for milk to modulate inflammation post-exercise in this sample.

Acute Effects of Milk vs. Carbohydrate on Bone Turnover Biomarkers Following Loading Exercise in Young Adult Females.

Dairy products and impact exercise have previously been identified to be independently beneficial for bone mineral properties, however, it is unknown how the combination of these two osteogenic interventions may alter acute bone turnover. Using a randomized crossover design, we compared the acute effects of consuming milk vs. an isoenergetic carbohydrate control beverage on bone biomarkers following loading exercise. Thirteen healthy female participants (Age = 20.3 ± 2.3y; BMI = 21.0 ± 1.1 kg/m2) consumed either 550 mL of 0% skim white milk (MILK) or 52.7 g of maltodextrin in 550 mL of water (CHO), both 5 min and 1 h following completion of a combined plyometric (198 impacts) and resistance exercise (3-4 sets/exercise, 8-12 reps/set, ∼75% 1-RM) bout. Venous blood samples were obtained pre-exercise, and 15 min, 75 min, 24 h and 48 h post-exercise to assess serum concentrations of bone resorption biomarkers, specifically carboxyl-terminal crosslinking telopeptide of type I collagen (CTX), receptor activator nuclear factor kappa-ß ligand (RANKL), and sclerostin (SOST), as well as bone formation biomarkers, specifically osteoprotegerin (OPG) and osteocalcin (OC). When absolute biomarker concentrations were examined, there were no interaction or group effects for any biomarker, however, there were main time effects (p < 0.05) for RANKL, SOST, and OC, which were lower, and the OPG: OPG/RANKL ratio, which was higher at 75 min post-exercise compared with baseline in both conditions. In addition to assessing absolute biomarker concentrations at specific timepoints, we also evaluated the relative (% change) cumulative post-exercise response (75 min to 48 h) using an area under the curve (AUC) analysis. This analysis showed that the relative post-exercise CTX response was significantly lower in the MILK compared to the CHO condition (p = 0.03), with no differences observed in the other biomarkers. These results show that while milk does not appear to alter absolute concentrations of bone biomarkers compared to CHO, it may attenuate relative post-exercise bone resorption (i.e., blunt the usual catabolic response to exercise).

Mirtazapine reduces susceptibility to hypocapnic central sleep apnea in males with sleep-disordered breathing: a pilot study.

Studies in humans and animal models with spinal cord injury (SCI) have demonstrated that medications targeting serotonin receptors may decrease the susceptibility to central sleep-disordered breathing (SDB). We hypothesized that mirtazapine would decrease the propensity to develop hypocapnic central sleep apnea (CSA) during sleep. We performed a single-blind pilot study on a total of 10 men with SDB (7 with chronic SCI and 3 noninjured) aged 52.0 ± 11.2 yr. Participants were randomly assigned to either mirtazapine (15 mg at bedtime) or a placebo for at least 1 wk, followed by a 7-day washout period before crossing over to the other intervention. Split-night studies included polysomnography and induction of hypocapnic CSA using a noninvasive ventilation (NIV) protocol. The primary outcome was CO2 reserve, defined as the difference between eupneic and end of NIV end-tidal CO2 ([Formula: see text]) preceding induced hypocapneic CSA. Secondary outcomes included controller gain (CG), other ventilatory parameters, and SDB severity. CG was defined as the ratio of change in minute ventilation (V̇e) between control and hypopnea to the change in CO2 during sleep. CO2 reserve was significantly widened on mirtazapine than placebo (-3.8 ± 1.2 vs. -2.0 ± 1.5 mmHg; P = 0.015). CG was significantly decreased on mirtazapine compared with placebo [2.2 ± 0.7 vs. 3.5 ± 1.9 L/(mmHg × min); P = 0.023]. There were no significant differences for other ventilatory parameters assessed or SDB severity between mirtazapine and placebo trials. These findings suggest that the administration of mirtazapine can decrease the susceptibility to central apnea by reducing chemosensitivity and increasing CO2 reserve; however, considering the lack of changes in apnea-hypopnea index (AHI), further research is required to understand the significance of this finding.NEW & NOTEWORTHY To our knowledge, this research study is novel as it is the first study in humans assessing the effect of mirtazapine on CO2 reserve and chemosensitivity in individuals with severe sleep-disordered breathing. This is also the first study to determine the potential therapeutic effects of mirtazapine on sleep parameters in individuals with a spinal cord injury.

Effects of Collagen Peptides on Recovery Following Eccentric Exercise in Resistance-Trained Males-A Pilot Study.

The authors sought to determine whether consuming collagen peptides (CP) enhances musculoskeletal recovery of connective tissues following a damaging exercise bout. Resistance-trained males consumed 15 g/day of CP (n = 7) or placebo (n = 8), and after 7 days, maximal voluntary isometric contraction (MVIC), countermovement jump height, soreness, and collagen turnover were examined. Five sets of 20 drop jumps were performed and outcome measures were collected 24, 48, and 120 hr postexercise. Countermovement jump height was maintained in the CP group at 24 hr (PRE = 39.9 ± 8.8 cm vs. 24 hr = 37.9 ± 8.9 cm, p = .102), whereas the CP group experienced a significant decline at 24 hr (PRE = 40.4 ± 7.9 cm vs. 24 hr = 35.5 ± 6.4 cm, p = .001; d = 0.32). In both groups, muscle soreness was significantly higher than PRE at 24 hr (p = .001) and 48 hr (p = .018) but not at 120 hr (p > .05). MVIC in both legs showed a significant time effect (left: p = .007; right: p = .010) over the 5-day postexercise period. Neither collagen biomarker changed significantly at any time point. CP supplementation attenuated performance decline 24 hr following muscle damage. Acute consumption of CP may provide a performance benefit the day following a bout of damaging exercise in resistance-trained males.

Buspirone decreases susceptibility to hypocapnic central sleep apnea in chronic SCI patients.

Spinal cord injury (SCI) is a risk factor for central sleep apnea (CSA). Previous studies in animal models with SCI have demonstrated a promising recovery in respiratory and phrenic nerve activity post-injury induced by the systemic and local administration of serotonin receptor agonists such as Buspirone and Trazodone. Human trials must be performed to determine whether individuals with SCI respond similarly. We hypothesized that Buspirone and Trazodone would decrease the propensity to hypocapnic CSA during sleep. We studied eight males with chronic SCI and sleep-disordered breathing (SDB) [age: 48.8 ± 14.2 yr; apnea-hypopnea index (AHI): 44.9 ± 23.1] in a single-blind crossover design. For 13 days, participants were randomly assigned either Buspirone (7.5-15 mg twice daily), Trazodone (100 mg), or a placebo followed by a 14-day washout period before crossing over to the other interventions. Study nights included polysomnography and induction of CSA using a noninvasive ventilation protocol. We assessed indexes of SDB, CO2 reserve, apneic threshold (AT), controller gain (CG), plant gain (PG), and ventilatory parameters. CO2 reserve was significantly widened on Buspirone (-3.6 ± 0.9 mmHg) compared with both Trazodone (-2.5 ± 1.0 mmHg, P = 0.009) and placebo (-1.8 ± 1.5 mmHg, P < 0.001) but not on Trazodone vs. placebo (P = 0.061). CG was significantly decreased on Buspirone compared with placebo (1.8 ± 0.4 vs. 4.0 ± 2.0 L/(mmHg·min), P = 0.025) but not on Trazodone compared with placebo (2.5 ± 1.1 vs. 4.0 ± 2.0 L/(mmHg·min); P = 0.065). There were no significant differences for PG, AT, or any SDB indexes (AHI, obstructive apnea index, central apnea index, oxygen desaturation index). The administration of Buspirone decreased the susceptibility to induced hypocapnic central apnea by reducing chemosensitivity and increasing CO2 reserve in chronic SCI patients.NEW & NOTEWORTHY This research study is novel as it is the first study in a humans that we are aware of that demonstrates the ability of Buspirone to increase CO2 reserve and hence decrease susceptibility to hypocapnic central apnea in patients with spinal cord injury.