Impact of upper-body ergometer rowing exercise on aerobic fitness and cardiometabolic disease risk in individuals with spinal cord injury: A 6-month follow-up study.

OBJECTIVE: We recently demonstrated that upper-body rowing exercise (UBROW) improved aerobic fitness in individuals with spinal cord injury (SCI), with no effect on traditional cardiometabolic risk factors. Here, we tested the hypothesis that the exercise-induced increase in aerobic fitness was maintained at 6-month (6M) follow-up. DESIGN: Six-month follow-up. SETTING: University/hospital. PARTICIPANTS: Seventeen wheelchair-dependent participants with SCI. INTERVENTIONS: 12-week of exercise training (UBROW) or control (CON). OUTCOME MEASURES: Aerobic fitness (POpeak and V̇O2peak), body composition, blood pressure, and blood biomarkers of cardiometabolic risk were assessed at 6M follow-up and compared to baseline (BL) and immediately post-intervention (12-week). Minutes of mild, moderate, and heavy intensity leisure time physical activity (LTPA) were assessed by self-report. RESULTS: Fourteen participants returned at 6M follow-up (CON, n = 6; UBROW, n = 8). In UBROW, POpeak (median (Q1-Q3)) increased from BL (70 W (37-84)) to 12-week (77 W (58-109), P = 0.01) and 6M follow-up (81 W (51-96), P = 0.01), with no difference between 12-week and 6M follow-up (P = 0.21). Similarly, V̇O2peak increased from BL (15.4 ml/kg/min (10.5-19.4)) to 12-week (16.6 ml/kg/min (12.8-21.3), P = 0.01) with no difference between 12-week and 6M follow-up (16.3 ml/kg/min (12.9-19.7), P = 0.74). No differences were found in CON for either POpeak (P = 0.22) or V̇O2peak (P = 0.27). There were no changes over time in traditional cardiometabolic risk factors or for minutes of different LTPA intensities. CONCLUSION: We demonstrate that improvements in aerobic fitness are maintained for at least six months after completion of a 12-week exercise intervention, supporting the use of periodic exercise interventions to boost aerobic fitness level in individuals with SCI.Trial registration: ClinicalTrials.gov identifier: NCT04390087..

Fully automatic d-lactate assay using a modified commercially available method.

Intestinal infarction is the fast-evolving endpoint of impaired blood perfusion to an intestinal segment which may have fatal outcome. Early diagnosis and treatment within 6 h reduce mortality. Currently, d-lactate is a promising biomarker, however, not available in the acute clinical setting. The aim of this study is implementation of d-lactate analysis in a routine clinical setting. We used a spectrophotometric method, based on enzymatic oxidation of d-lactate by d-lactate dehydrogenase (D-LDH) coupled to the reduction of nicotinamide-adenine dinucleotide (NAD+). The amount of NADH formed in this reaction is equivalent to d-lactate. The primary concern in this method is interfering NADH formed by oxidation of l-lactate by l-lactate dehydrogenase (L-LDH). A commercially available kit for d-lactate measurement was implemented on our existing automated routine laboratory equipment including pH-inactivation of L-LDH. Our setup fulfilled clinical quality goals. We were able to measure d-lactate with an acceptable performance of the analysis and a short turn-around time. The method can be used to distinguish between the expected cut-off for intestinal ischemia around 0.3 mM and the upper reference limit of 0.05 mM. With a turnaround time of just 9 min, the analysis has potential as a readily available detection of circulating d-lactate for early diagnosis of intestinal ischemia.