Discussion
The results from the experiment demonstrate that respiratory frequency was higher and increased faster as exercise intensity increased in caffeinated individuals. The correlation between the independent (intensity of work rate) and dependent (respiratory frequency) variables for both the caffeinated and non-caffeinated groups was fairly good (R2 > 0.35) so there is some evidence that caffeine causes an increase in respiratory frequency.
Tidal volume and alveolar ventilation were lower for caffeinated females than non-caffeinated females as exercise intensity increases. Both the non-caffeinated group and caffeinated group had a fairly good correlation between the increases in tidal volume and alveolar ventilation as work rate increased …show more content…
However, according to the t-test, this result was nonsignificant. The data at peak work rate, however, diverged from my hypothesis since the cardiac output was lower for the caffeinated group. The reason a decrease in cardiac output occurred is due to decreased sympathetic activity, stroke volume, and heart rate as exercise intensity increased. Another reason might be due to the fact the non-caffeinated group contained a larger number of athletic individuals than the non-caffeinated group. In previous studies caffeine had no effect on contractility or cardiac output so the significant decrease observed might have been due to the small population used in the experiment (Pincomb et al., …show more content…
Since caffeine caused a lower tidal volume and alveolar ventilation, endurance has likely increased since the caffeinated individuals undergo less respiratory muscle fatigue. All of the cardiovascular data was nonsignificant, but general trends of the TPR data supported the hypothesis. Thus, another indicator of increased endurance was the increase in TPR at peak work rate which shows that caffeine induced an increase in the activity of the sympathetic nervous system and resulted in increased
The results from the experiment demonstrate that respiratory frequency was higher and increased faster as exercise intensity increased in caffeinated individuals. The correlation between the independent (intensity of work rate) and dependent (respiratory frequency) variables for both the caffeinated and non-caffeinated groups was fairly good (R2 > 0.35) so there is some evidence that caffeine causes an increase in respiratory frequency.
Tidal volume and alveolar ventilation were lower for caffeinated females than non-caffeinated females as exercise intensity increases. Both the non-caffeinated group and caffeinated group had a fairly good correlation between the increases in tidal volume and alveolar ventilation as work rate increased …show more content…
However, according to the t-test, this result was nonsignificant. The data at peak work rate, however, diverged from my hypothesis since the cardiac output was lower for the caffeinated group. The reason a decrease in cardiac output occurred is due to decreased sympathetic activity, stroke volume, and heart rate as exercise intensity increased. Another reason might be due to the fact the non-caffeinated group contained a larger number of athletic individuals than the non-caffeinated group. In previous studies caffeine had no effect on contractility or cardiac output so the significant decrease observed might have been due to the small population used in the experiment (Pincomb et al., …show more content…
Since caffeine caused a lower tidal volume and alveolar ventilation, endurance has likely increased since the caffeinated individuals undergo less respiratory muscle fatigue. All of the cardiovascular data was nonsignificant, but general trends of the TPR data supported the hypothesis. Thus, another indicator of increased endurance was the increase in TPR at peak work rate which shows that caffeine induced an increase in the activity of the sympathetic nervous system and resulted in increased