Effectiveness of High-Intensity Interval Training for Fitness and Mobility Post Stroke: A Systematic Review.

OBJECTIVE: To evaluate the evidence on the effectiveness of high-intensity interval training (HIIT) in improving fitness and mobility post stroke. TYPE: Systematic review. LITERATURE SURVEY: Medline, Embase, CINAHL, PsycINFO, and Scopus were searched for articles published in English up to January 2018. METHODOLOGY: Studies were included if the sample was adult human participants with stroke, the sample size was ≥3, and participants received >1 session of HIIT. Study and participant characteristics, treatment protocols, and results were extracted. SYNTHESIS: Six studies with a total of 140 participants met inclusion criteria: three randomized controlled trials and three pre-post studies. HIIT protocols ranged 20 to 30 minutes per session, 2 to 5 times per week, and 2 to 8 weeks in total. HIIT was delivered on a treadmill in five studies and a stationary bicycle in one study. Regarding fitness measures, HIIT produced significant improvements in peak oxygen consumption compared to baseline, but the effect was not significant compared to moderate intensity continuous exercise (MICE). Regarding mobility measures, HIIT produced significant improvements on the 10-Meter Walk Test (10MWT), 6-Minute Walk Test (6MWT), Berg Balance Scale (BBS), Functional Ambulation Categories (FAC), Timed Up and Go Test, and Rivermead Motor Assessment compared to baseline. The effect of HIIT was significant compared to MICE on the 10MWT and FAC but not on the 6MWT or BBS. CONCLUSIONS: There is preliminary evidence that HIIT may be an effective rehabilitation intervention for improving some aspects of cardiorespiratory fitness and mobility post stroke. LEVEL OF EVIDENCE: I.

Myocardial Hypertrophic Remodeling and Impaired Left Ventricular Function in Mice with a Cardiac-Specific Deletion of Janus Kinase 2.

The Janus kinase (JAK) system is involved in numerous cell signaling processes and is highly expressed in cardiac tissue. The JAK isoform JAK2 is activated by numerous factors known to influence cardiac function and pathologic conditions. However, although abundant, the role of JAK2 in the regulation or maintenance of cardiac homeostasis remains poorly understood. Using the Cre-loxP system, we generated a cardiac-specific deletion of Jak2 in the mouse to assess the effect on cardiac function with animals followed up for a 4-month period after birth. These animals had marked mortality during this period, although at 4 months mortality in male mice (47%) was substantially higher compared with female mice (30%). Both male and female cardiac Jak2-deleted mice had hypertrophy, dilated cardiomyopathy, and severe left ventricular dysfunction, including a marked reduction in ejection fractions as assessed by serial echocardiography, although the responses in females were somewhat less severe. Defective cardiac function was associated with altered protein levels of sarcoplasmic reticulum calcium-regulatory proteins particularly in hearts from male mice that had depressed levels of SERCA2 and phosphorylated phospholamban. In contrast, SERCA2 was unchanged in hearts of female mice, whereas phosphorylated phospholamban was increased. Our findings suggest that cardiac JAK2 is critical for maintaining normal heart function, and its ablation produces a severe pathologic phenotype composed of myocardial remodeling, heart failure, and pronounced mortality.