Aaron B. Morton

Effects of different doses of caffeine on anaerobic exercise in boys.

This study investigated effects of low (1 mg·kg-1), moderate (3 mg·kg-1) and high (5 mg·kg-1) doses of caffeine on anaerobic performance in boys. Twenty-six 8- to 10-year-old boys participated in a double-blind, crossover, counter-balanced study. Boys received in random order a placebo (PL) or anhydrous caffeine: 1 (CAF-1), 3 (CAF-3), or 5 (CAF-5) mg caffeine·kg-1 body mass in cherry flavored Sprite. Sixty minutes following consumption boys performed a static handgrip test and then a 30-s Wingate test. Maximal grip strength (21.5 ± 4.9 & 21.6 ± 4.7 vs. 20.4 ± 4.0 kg) was significantly higher in CAF-5 & CAF-3 vs PL, respectively. Absolute and relative peak power (287 ± 72 vs 281 ± 69 W & 8.0 ± 0.9 vs 7.8 ± 1.0 W·kg-1) were significantly higher in CAF-3 vs PL, respectively. Mean power (153 ± 48 vs 146 ± 43 W) was significantly higher in CAF-5 vs PL, respectively. Peak Wingate HR was significantly higher (189 ± 8 vs 185 ± 9 beats·min-1) in CAF-5 vs PL, respectively. These findings suggest that in boys CAF-1 did not affect performance. During the Wingate test CAF-3 resulted in higher peak power while CAF-5 increased mean power. The significant increase in peak HR following the Wingate test is likely related to greater mean power generated during CAF-5.

Increased SOD2 in the diaphragm contributes to exercise-induced protection against ventilator-induced diaphragm dysfunction

Mechanical ventilation (MV) is a life-saving intervention for many critically ill patients. Unfortunately, prolonged MV results in rapid diaphragmatic atrophy and contractile dysfunction, collectively termed ventilator-induced diaphragm dysfunction (VIDD). Recent evidence reveals that endurance exercise training, performed prior to MV, protects the diaphragm against VIDD. While the mechanism(s) responsible for this exercise-induced protection against VIDD remain unknown, increased diaphragm antioxidant expression may be required. To investigate the role that increased antioxidants play in this protection, we tested the hypothesis that elevated levels of the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) is required to achieve exercise-induced protection against VIDD. Cause and effect was investigated in two ways. First, we prevented the exercise-induced increase in diaphragmatic SOD2 via delivery of an antisense oligonucleotide targeted against SOD2 post-exercise. Second, using transgene overexpression of SOD2, we determined the effects of increased SOD2 in the diaphragm independent of exercise training. Results from these experiments revealed that prevention of the exercise-induced increases in diaphragmatic SOD2 results in a loss of exercise-mediated protection against MV-induced diaphragm atrophy and a partial loss of protection against MV-induced diaphragmatic contractile dysfunction. In contrast, transgenic overexpression of SOD2 in the diaphragm, independent of exercise, did not protect against MV-induced diaphragmatic atrophy and provided only partial protection against MV-induced diaphragmatic contractile dysfunction. Collectively, these results demonstrate that increased diaphragmatic levels of SOD2 are essential to achieve the full benefit of exercise-induced protection against VIDD.