Peak cardiac power output and cardiac reserve in sedentary men and women

Background and Purpose: Cardiac power output (CPO) and cardiac reserve (CR) are novel parameters of overall cardiac function. The purpose of this study was to determine differences in values of the CPO at rest and peak exercise and CR in sedentary men and women. Material and Methods: Thirty healthy men (age 21.2±0.7 years, body mass 63±6.3 kg, height 168.3±5.1 cm) and thirty healthy women (age 21.3±1.9 years, mass 82.5±7.9 kg, height 181.9±4.9 cm) were included in this study. Echocardiography was used to assess cardiac and hemodynamic parameters. CPO was calculated, at rest and after performed maximal bicycle test, as the product of cardiac output and mean arterial pressure, and CR as the difference of CPO value measured at peak exercise and at rest. Results: At rest, the two groups had similar values of cardiac power output (1.04±0.3W versus 1.14±0.25W, p>0.05). CPO after peak exercise was higher in men (5.1±0.72W versus 3.9±0.58W, p<0.05), as was cardiac reserve (3.96±0.64W versus 2.86±0.44W, p<0.05), respectively. After allometric scaling method was used to decrease the effect of body size on peak CPO, men still had significantly higher peak CPO (2.79±0.4 W m-2 versus 2.46±0.32 W m-2, p<0.05). At peak exercise, a significant positive relationship was found between cardiac power output and end diastolic volume (r=0.60), end diastolic left ventricular internal dimension (r=0.58), stroke volume (r=0.86) and cardiac output (r=0.87). Conclusion: The study showed that men had higher CPO after peak exercise and greater cardiac reserve than women, even after decreasing body size effect

Gender differences in parasympathetic reactivation during recovery from Wingate anaerobic test

Background and Purpose: We wanted to investigate gender differences in parasympathetic reactivation from supramaximal exercise. Materials and methods: Parasympathetic reactivation from a Wingate anaerobic test was investigated in 16 male and 15 female volunteers. Heart rate recovery was assessed as the difference between peak exercise heart rate and heart rate recorded following 60 seconds of recovery (HRR60 ). The time constant of the first 30 s post-exercise HR (T30) was determined as a negative reciprocal of the slope of the regression line. Another time constant decay (T) was obtained by fitting the 5 minute post-exercise HRR into a first-order exponential curve. Measures of heart rate variability (HRV) were used to describe the changes in autonomic cardiac regulation following exercise. Results: Post exercise heart rate recovery was faster in male participants, demonstrated through HRR60 (29.5±8.9 vs. 23.4±9.8 seconds respectively) and T30 (292.4±88.7 vs. 409.2±138.3 seconds respectively), but the time constant of the exponential heart rate decay (T) did not differ between the two genders (140.4±55.7 in males and 130.3±49.7seconds in females). The present study demonstrated similar RMSSD, lnHF and HFnu at rest in male and female participants. The time course of RMSSD30 recovery was impaired immediately after exercise. None of the observed vagal HRV indices have restored after five minutes of recovery following the 30-s Wingate test, but the post-exercise lnHF2-5min was significantly smaller in females (3.3±0.9 ms 2 in males vs. 2.5±1.0 ms 2 in females). Conclusion: The immediate HRR and parasympathetic reactivation was affected by gender and was attenuated in female participants

HEART RATE VARIABILITY BEFORE AND AFTER CYCLE EXERCISE IN RELATION TO DIFFERENT BODY POSITIONS

The purpose of this study was to assess the effect of three different body positions on HRV measures following short-term submaximal exercise. Thirty young healthy males performed submaximal cycling for five minutes on three different occasions. Measures of HRV were obtained from 5-min R to R wave intervals before the exercise (baseline) and during the last five minutes of a 15 min recovery (post-exercise) in three different body positions (seated, supine, supine with elevated legs). Measures of the mean RR normal-to-normal intervals (RRNN), the standard deviation of normal-to-normal intervals (SDNN), the root mean square of successive differences (RMSSD) and the low-frequency (LF) and the high-frequency (HF) spectral power were analyzed. Post-exercise RRNN, RMSSD were significantly higher in the two supine positions (p < 0. 01) compared with seated body position. Post-exercise ln LF was significantly lower in the supine position with elevated legs than in the seated body position (p < 0.05). No significant difference was found among the three different body positions for post-exercise ln HF (p > 0.05). Post-exercise time domain measures of HRV (RRNN, SDNN, RMSSD) were significantly lower compared with baseline values (p < 0.01) regardless body position. Post-exercise ln LF and ln HF in all three positions remained significantly reduced during recovery compared to baseline values (p < 0.01). The present study suggests that 15 minutes following short-term submaximal exercise most of the time and frequency domain HRV measures have not returned to pre-exercise values. Modifications in autonomic cardiac regulation induced by body posture present at rest remained after exercise, but the post-exercise differences among the three positions did not resemble the ones established at res

Bradykinin type 2 receptor -9/-9 genotype is associated with triceps brachii muscle hypertrophy following strength training in young healthy men

<p>Abstract</p> <p>Background</p> <p>Bradykinin type 2 receptor (<it>B2BRK)</it> genotype was reported to be associated with changes in the left-ventricular mass as a response to aerobic training, as well as in the regulation of the skeletal muscle performance in both athletes and non-athletes. However, there are no reports on the effect of <it>B2BRK</it> 9-bp polymorphism on the response of the skeletal muscle to strength training, and our aim was to determine the relationship between the <it>B2BRK</it> SNP and triceps brachii functional and morphological adaptation to programmed physical activity in young adults.</p> <p>Methods</p> <p>In this 6-week pretest-posttest exercise intervention study, twenty nine healthy young men (21.5 ± 2.7 y, BMI 24.2 ± 3.5 kg/m²) were put on a 6-week exercise protocol using an isoacceleration dynamometer (5 times a week, 5 daily sets with 10 maximal elbow extensions, 1 minute rest between sets). Triceps brachii muscle volumes were assessed by using magnetic resonance imaging before and after the strength training. Bradykinin type 2 receptor 9 base pair polymorphism was determined for all participants.</p> <p>Results</p> <p>Following the elbow extensors training, an average increase in the volume of both triceps brachii was 5.4 ± 3.4% (from 929.5 ± 146.8 cm³ pre-training to 977.6 ± 140.9 cm³ after training, p<0.001). Triceps brachii volume increase was significantly larger in individuals homozygous for −<it>9</it> allele compared to individuals with one or two +<it>9</it> alleles (−<it>9</it>/-<it>9</it>, 8.5 ± 3.8%; vs. -<it>9</it>/+<it>9</it> and +<it>9</it>/+<it>9</it> combined, 4.7 ± 4.5%, p < 0.05). Mean increases in endurance strength in response to training were 48.4 ± 20.2%, but the increases were not dependent on <it>B2BRK</it> genotype (−<it>9</it>/-<it>9</it>, 50.2 ± 19.2%; vs. -<it>9</it>/+<it>9</it> and +<it>9</it>/+<it>9</it> combined, 46.8 ± 20.7%, p > 0.05).</p> <p>Conclusions</p> <p>We found that muscle morphological response to targeted training – hypertrophy – is related to polymorphisms of <it>B2BRK</it>. However, no significant influence of different <it>B2BRK</it> genotypes on functional muscle properties after strength training in young healthy non athletes was found. This finding could be relevant, not only in predicting individual muscle adaptation capacity to training or sarcopenia related to aging and inactivity, but also in determining new therapeutic strategies targeting genetic control of muscle function, especially for neuromuscular disorders that are characterized by progressive adverse changes in muscle quality, mass, strength and force production (e.g., muscular dystrophy, multiple sclerosis, Parkinson’s disease).</p