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.
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-β 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).
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 if individuals with SCI respond similarly. We hypothesized that Buspirone and Trazodone would decrease the propensity to hypocapnic CSA during sleep. We studied 8 males with chronic SCI and sleep-disordered breathing (SDB)(Age: 48.8±14.2; AHI: 44.9±23.1) in a single-blind crossover design. For 13 days participants were randomly assigned either Buspirone (7.5-15mg twice daily), Trazodone (100mg) 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 non-invasive ventilation protocol. We assessed indices 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±0.9mmHg) compared to both Trazodone (-2.5±1.0mmHg; p=0.009) and placebo (-1.8±1.5mmHg; p<0.001) but not on Trazodone vs. placebo (p=0.061). CG was significantly decreased on Buspirone compared to placebo (1.8±0.4 vs 4.0±2.0L/(mmHg*min); p=0.025) but not on Trazodone compared to placebo (2.5±1.1 vs. 4.0±2.0L/(mmHg*min); p=0.065). There were no significant differences for PG, AT or any SDB indices (AHI, OAI, CAI, ODI). The administration of Buspirone decreased the susceptibility to induced hypocapnic central apnea by reducing chemosensitivity and increasing CO2 reserve in chronic SCI patients.
Studies in those 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 (seven with chronic SCI and three non-injured) aged 52.0±11.2 years. Participants were randomly assigned to either mirtazapine (15mg) or a placebo for at least one week followed by a seven-day washout period before crossing over to the other intervention. Study nights included polysomnography and induction of hypocapnic CSA using a non-invasive ventilation (NIV) protocol. The primary outcome was CO2 reserve, defined as the difference between eupneic and end of NIV PETCO2 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 compared to placebo (-3.8±1.2 vs. -2.0±1.5mmHg; p=0.015). CG was significantly decreased on mirtazapine compared to placebo (2.2±0.7 vs. 3.5±1.9L/(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 AHI, further research is required to understand this finding's significance.
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