Sample characteristics are presented as mean ± standard deviation for continuous variables and proportions for categorical variables. Pearson Chi-square test and independent samples t-test were used to assess potential sex differences. For BMI and weight, a non-parametric test (Mann-Whitney U) was conducted due to the lack of normal distribution. Data from the exercise logs are presented as proportions of the total number of exercise logs. Pearson Chi-square tests were run to assess the associations between frequency, intensity, type, location and social setting of exercise with sex and training group. The results were considered statistically significant if the p-value was less than 0.05. All statistical analyses were performed with SPSS 22 (Statistical Package for Social Science, Chicago, IL, USA).
^ Jump up to: a b Szuhany KL, Bugatti M, Otto MW (October 2014). "A meta-analytic review of the effects of exercise on brain-derived neurotrophic factor". J Psychiatr Res. 60C: 56–64. doi:10.1016/j.jpsychires.2014.10.003. PMC 4314337. PMID 25455510. Consistent evidence indicates that exercise improves cognition and mood, with preliminary evidence suggesting that brain-derived neurotrophic factor (BDNF) may mediate these effects. The aim of the current meta-analysis was to provide an estimate of the strength of the association between exercise and increased BDNF levels in humans across multiple exercise paradigms. We conducted a meta-analysis of 29 studies (N = 1111 participants) examining the effect of exercise on BDNF levels in three exercise paradigms: (1) a single session of exercise, (2) a session of exercise following a program of regular exercise, and (3) resting BDNF levels following a program of regular exercise. Moderators of this effect were also examined. Results demonstrated a moderate effect size for increases in BDNF following a single session of exercise (Hedges' g = 0.46, p < 0.001). Further, regular exercise intensified the effect of a session of exercise on BDNF levels (Hedges' g = 0.59, p = 0.02). Finally, results indicated a small effect of regular exercise on resting BDNF levels (Hedges' g = 0.27, p = 0.005). ... Effect size analysis supports the role of exercise as a strategy for enhancing BDNF activity in humans.
No matter where you are, you have time for 30 seconds of what Haley calls “Anywhere Push-Ups.” “This will target chest and triceps. Find a hard surface like kitchen counter or office desk. With both hands on the surface, walk away so that you’re in an elevated push-up position—the further you walk the more challenging the exercise,” she says. “Lower your body down so elbows and shoulders are at a 90-degree angle, push back up and repeat for ten reps.”
A number of medical reviews have indicated that exercise has a marked and persistent antidepressant effect in humans,[37][48][49][52][70][71] an effect believed to be mediated through enhanced BDNF signaling in the brain.[40][52] Several systematic reviews have analyzed the potential for physical exercise in the treatment of depressive disorders. The 2013 Cochrane Collaboration review on physical exercise for depression noted that, based upon limited evidence, it is more effective than a control intervention and comparable to psychological or antidepressant drug therapies.[70] Three subsequent 2014 systematic reviews that included the Cochrane review in their analysis concluded with similar findings: one indicated that physical exercise is effective as an adjunct treatment (i.e., treatments that are used together) with antidepressant medication;[52] the other two indicated that physical exercise has marked antidepressant effects and recommended the inclusion of physical activity as an adjunct treatment for mild–moderate depression and mental illness in general.[48][49] One systematic review noted that yoga may be effective in alleviating symptoms of prenatal depression.[72] Another review asserted that evidence from clinical trials supports the efficacy of physical exercise as a treatment for depression over a 2–4 month period.[37]
Summary of long-term adaptations to regular aerobic and anaerobic exercise. Aerobic exercise can cause several central cardiovascular adaptations, including an increase in stroke volume (SV)[102] and maximal aerobic capacity (VO2 max),[102][103] as well as a decrease in resting heart rate (RHR).[104][105][106] Long-term adaptations to resistance training, the most common form of anaerobic exercise, include muscular hypertrophy,[107][108] an increase in the physiological cross-sectional area (PCSA) of muscle(s), and an increase in neural drive,[109][110] both of which lead to increased muscular strength.[111] Neural adaptations begin more quickly and plateau prior to the hypertrophic response.[112][113]
Exclusion criteria included major diseases or conditions such as severe heart disease, uncontrolled hypertension, obesity, osteoarticular pathology, and neurological disease. Criteria were evaluated on the basis of clinical history, resting ECG, and physical examination. Participants maintained their lifestyles and were instructed not to take part in any other physical programs throughout the study. At the time of the initial design, the study consisted of a 12-week randomized controlled trial with a frequency of 3 times a week, 36 sessions in all, ending with a new assessment of their wellness and the potential persistence of the results on functional/physical capacities.
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