Effects of caffeine on blood pressure, heart rate, and forearm blood flow during dynamic leg exercise.

This study examined the acute effects of caffeine on the cardiovascular system during dynamic leg exercise. Ten trained, caffeine-naive cyclists (7 women and 3 men) were studied at rest and during bicycle ergometry before and after the ingestion of 6 mg/kg caffeine or 6 mg/kg fructose (placebo) with 250 ml of water. After consumption of caffeine or placebo, subjects either rested for 100 min (rest protocol) or rested for 45 min followed by 55 min of cycle ergometry at 65% of maximal oxygen consumption (exercise protocol). Measurement of mean arterial pressure (MAP), forearm blood flow (FBF), heart rate, skin temperature, and rectal temperature and calculation of forearm vascular conductance (FVC) were made at baseline and at 20-min intervals. Plasma ANG II was measured at baseline and at 60 min postingestion in the two exercise protocols. Before exercise, caffeine increased both systolic blood pressure (17%) and MAP (11%) without affecting FBF or FVC. During dynamic exercise, caffeine attenuated the increase in FBF (53%) and FVC (50%) and accentuated exercise-induced increases in ANG II (44%). Systolic blood pressure and MAP were also higher during exercise plus caffeine; however, these increases were secondary to the effects of caffeine on resting blood pressure. No significant differences were observed in heart rate, skin temperature, or rectal temperature. These findings indicate that caffeine can alter the cardiovascular response to dynamic exercise in a manner that may modify regional blood flow and conductance.

Electrocardiographic alterations associated with the hearts of athletes.

Physical conditioning induces numerous cardiovascular adaptations, including vagotonia and increased cardiac volume and mass. These adaptations characterise the 'athletic heart' and account for most of the normal variants in the athlete's electrocardiogram. Common alterations associated with vagotonia include sinus bradycardia, sinus arrhythmia, junctional escape beats, first degree atrioventricular block and second degree (Mobitz type I) atrioventricular block. Common electrocardiographic variants associated with increased cardiac mass and volume include increased voltage, prominent U waves, intraventricular conduction delays, early repolarisation and increased QT intervals. It is sometimes difficult to differentiate the healthy athlete with an athletic heart from the athletic patient with a diseased heart. Thus, further evaluation may be warranted, especially when the athlete also presents with hypertension and/or abnormalities of the cardiovascular physical examination.

Peak torque per unit cross-sectional area differs between strength-trained and untrained young adults.

It is unclear whether gender differences in the relative strength of the upper and lower body are due to differences in muscle mass distribution or dissimilarity of use. There is also controversy as to whether prolonged resistance training increases strength per unit cross-sectional area (CSA). To help resolve these questions, maximum isometric torque per unit muscle and bone (M+B) CSA was measured in the upper arm and thigh of 26 trained (13 males; 13 females) and 26 untrained (13 males; 13 females) young adults. Muscle and bone CSA values were calculated from limb circumferences and skinfolds. Maximal isometric torque values were recorded by a LIDO isokinetic dynamometer. There was no significant difference (P > 0.05) in mean upper arm or thigh torque per unit M+B CSA between the trained males and trained females, or between the untrained males and untrained females. However, mean torque per unit M+B CSA was significantly higher for the trained subjects of both genders compared with the untrained subjects of both genders for the upper arm (28.9%; P < 0.0001) and thigh (18.8%; P < 0.0001). These results suggest that muscle quality (peak torque/CSA) is equal between genders, and that the increase in muscle strength per unit area that occurs with resistance training is not gender-dependent.

Oral and oronasal breathing during continuous exercise produce similar responses to ozone inhalation.

Breathing route has a profound effect on sulfur dioxide-induced pulmonary function response in human subjects. There is comparatively little evidence of the effects of oral, nasal, and oronasal breathing on ozone (O3)-induced responses in humans. In this study, six young adult males were exposed on five occasions to 0.40 parts per million (ppm) O3 while exercising continuously at one of two workloads (minute ventilation, VE, of approximately 30 and 75 l/min). The VE exposure time product was similar for all protocols. Four exposures were delivered randomly with a Hans-Rudolph respiratory valve attached to a silicone facemask, with breathing route effected with and without noseclip. A 2 x 2 analysis of variance revealed no statistically significant differences (p less than .05) across conditions in pulmonary function, exercise ventilatory pattern, or subjective symptoms responses. The fifth exposure, delivered via the same respiratory valve with mouthpiece, but without facemask, revealed significantly greater forced expiratory volume in 1 s (FEV1.0) impairment than that observed for the respiratory valve, facemask with noseclip exposure (-20.4% and -15.9%, respectively). The latter suggests partial O3 reactivity to the facemask and clean shaven facial surface of the subjects, although reduced oral scrubbing by mouthpiece-induced bypassing of the oral vestibule might account, in part, for this difference. Recent O3 uptake evidence from another laboratory, however, supports our conclusion that breathing route during moderate and heavy continuous exercise does not affect acute physiologic responses to 0.40 ppm O3.

Cardiovascular effects of cadence and workload.

Increases in cadence may augment SV during submaximal cycling (> 65 % VO2max) via effects of increased muscle pump activity on preload. At lower workloads (45 - 65 % VO2max), SV tends to plateau, suggesting that effects of increases in cadence on pump activity have little influence on SV. We hypothesized that cadence-induced increases in CO at submaximal workloads, where SV tends to plateau, are due to elevations in HR and/or O2 extraction. SV, CO, HR, VO2, and delta a - vO2 were assessed at 80 and 100 rpm during workloads of 50 % (LO) or 65 % (HI) of VO2max in 11 male cyclists. No changes in SV were seen. CO was higher at 100 rpm in 10 of 11 subjects at LO (18.1 +/- 2.7 vs. 17.2 +/- 2.6 L/min). VO2 at both workloads was greater at 100 than 80 rpm as was HR (LO: 129 +/- 11 vs. 121 +/- 10 beats/min; HI: 146 +/- 13 vs. 139 +/- 14 beats/min) (p < 0.05). delta a - vO2 was greater at HI compared to LO at 80 (15.1 +/- 1.6 vs. 13.6 +/- 1.3 ml) and 100 rpm (16.0 +/- 1.7 vs. 15.1 +/- 1.6 ml) (p < 0.05). Results suggest that increases in O2 demand during low submaximal cycling (50 % VO2max) at high cadences are met by HR-induced increases in CO. At higher workloads (65 % VO2max), inability of higher cadences to increase CO and O2 delivery is offset by greater O2 extraction.

Effects of airflow and work load on cardiovascular drift and skin blood flow.

Cardiovascular drift (CVD) can be defined as a progressive increase in heart rate (HR), decreases in stroke volume (SV) and mean arterial pressure (MAP), and a maintained cardiac output (Q) during prolonged exercise. To test the hypothesis that the magnitude of CVD would be related to changes in skin blood flow ( SkBF ), eight healthy, moderately trained males performed 70-min bouts of cycle ergometry in a 2 X 2 assortment of airflows (less than 0.2 and 4.3 m X s-1) and relative work loads (43.4% and 62.2% maximal O2 uptake). Ambient temperature and relative humidity were controlled to mean values of 24.2 +/- 0.8 degrees C and 39.5 +/- 2.4%, respectively. Q, HR, MAP, SkBF , skin and rectal temperatures, and pulmonary gas exchange were measured at 10-min intervals during exercise. Between the 10th and 70th min during exercise at the higher work load with negligible airflow, HR and SkBF increased by 21.6 beats X min-1 and 14.0 ml X 100 ml-1 X min-1, respectively, while SV and MAP decreased by 16.4 ml and 11.3 mmHg. The same work load in the presence of 4.3 m X s-1 airflow resulted in nonsignificant changes of 7.6 beats X min-1, 4.0 ml X (100 ml-1 X min)-1, -2.7 ml, and -1.7 mmHg for HR, SkBF , SV, and MAP. Since nonsignificant changes in HR, SkBF , SV, and MAP were observed at the lower work load in both airflow conditions, the results emphasize that CVD occurs only in conditions which combine high metabolic and thermal circulatory demands.(ABSTRACT TRUNCATED AT 250 WORDS)