PurposeLarger blood pressure (BP) responses to relative-intensity static exercise in men versus women are thought to involve altered muscle metaboreflex activation, but whether this is because of an intrinsic sex difference in metabolite production or differences in muscle strength and absolute load is unknown.MethodsContinuous BP and heart rate were recorded in 200 healthy young men and women (women: n = 109) during 2 min of static handgrip exercise at 30% of maximal voluntary contraction (MVC), followed by 2 min of postexercise circulatory occlusion (PECO). Muscle sympathetic nerve activity (MSNA) was recorded in a subset of participants (n = 39; women, n = 21), permitting calculation of signal-averaged resting sympathetic transduction (MSNA-diastolic BP). Sex differences were examined with and without statistical adjustment for MVC. Multivariate regression analyses were performed to identify predictors of BP responses.ResultsMen had larger systolic BP responses (interactions, P < 0.0001) to static handgrip exercise (24 ± 10 vs 17 ± 9 mm Hg [mean ± SD], P < 0.0001) and PECO (20 ± 11 vs 16 ± 9 mm Hg, P < 0.0001). Adjustment for MVC abolished these sex differences in BP (interactions, P > 0.7). In the subset with MSNA, neither burst frequency or incidence responses to static handgrip exercise or PECO differed between men and women (interactions, P > 0.2). Resting sympathetic transduction was also similar (P = 0.8). Multiple linear regression analysis showed that MVC or the change in MSNA, were predictors of BP responses to static handgrip, but only MVC was associated with BP responses during PECO.ConclusionsSex differences in absolute contraction load contribute to differences in BP responses during muscle metaboreflex isolation using PECO. These data do not support an intrinsic effect of sex as being responsible for exercise BP differences between men and women.

Purpose: Males have larger blood pressure (BP) responses to relative-intensity static handgrip exercise compared with females. Controlling for absolute load (maximal voluntary contraction (MVC)) abolishes these differences. Whether similar observations exist during large muscle mass exercise or dynamic contractions, and the mechanisms involved, remains unknown. Methods: BP, heart rate, muscle oxygenation (near-infrared spectroscopy), and rectus femoris EMG were recorded in 28 males and 17 females during 10% and 30% MVC static (120 s) and isokinetic dynamic (180 s; 1:2 work-to-rest ratio; angular velocity, 60°•s −1 ) knee extensor exercise. Static and dynamic exercises were completed on separate visits, in a randomized order. Sex differences were examined with and without statistical adjustment of MVC (ANCOVA). Results: Males had larger systolic BP responses (interaction, P < 0.0001) and muscle deoxygenation (interaction, P < 0.01) than did females during 10% static exercise, with no difference in EMG (interaction, P = 0.67). Peak systolic BP was correlated with MVC (r = 0.55, P = 0. 0001), and adjustment for MVC abolished sex differences in systolic BP (interaction, P = 0.3). BP, heart rate, muscle oxygenation/deoxygenation, and EMG responses were similar between sexes during 30% static exercise (interaction; all, P > 0.2), including following adjustment for MVC (all, P > 0.1). Males had larger systolic BP responses during dynamic exercise at 10% and 30% (interaction; both, P = 0.01), which were abolished after adjustment for MVC (interaction; both, P > 0.08). Systolic BP responses were correlated with absolute MVC and stroke volume responses during 10% (r = 0.31, P = 0.04; r = 0.61, P < 0.0001, respectively) and 30% (r = 0.48, P = 0.001; r = 0.59, P < 0.0001, respectively). Conclusions: Absolute contraction intensity can influence systolic BP responses to 10% but not 30% MVC static, as well as 10% and 30% MVC dynamic knee extensor exercise, and should be considered in cross-sectional comparisons of exercise BP.

Calculating the blood pressure (BP) response to a burst of muscle sympathetic nerve activity (MSNA), termed sympathetic transduction, may be influenced by an individual's resting burst frequency. We examined the relationships between sympathetic transduction and MSNA in 107 healthy males and females and developed a normalized sympathetic transduction metric to incorporate resting MSNA. Burst-triggered signal-averaging was used to calculate the peak diastolic BP response following each MSNA burst (sympathetic transduction of BP) and following incorporation of MSNA burst cluster patterns and amplitudes (sympathetic transduction slope). MSNA burst frequency was negatively correlated with sympathetic transduction of BP (r=-0.42; P<0.01) and the sympathetic transduction slope (r=-0.66; P<0.01), independent of sex. MSNA burst amplitude was unrelated to sympathetic transduction of BP in males (r=0.04; P=0.78), but positively correlated in females (r=0.44; P<0.01) and with the sympathetic transduction slope in all participants (r=0.42; P<0.01). To control for MSNA, the linear regression slope of the log-log relationship between sympathetic transduction and MSNA burst frequency was used as a correction exponent. In sub-analysis of males (38±10 vs. 14±4bursts/min) and females (28±5 vs. 12±4bursts/min) with high vs. low MSNA, sympathetic transduction of BP and sympathetic transduction slope were lower in participants with high MSNA (all P<0.05). In contrast, normalized sympathetic transduction of BP and normalized sympathetic transduction slope were similar in males and females with high vs. low MSNA (all P>0.22). We propose that incorporating MSNA burst frequency into the calculation of sympathetic transduction will allow comparisons between participants with varying levels of resting MSNA.

Males have larger blood pressure (BP) responses to relative intensity static handgrip exercise compared to females. Controlling for maximal voluntary contraction (MVC) absolute strength abolishes these differences. Whether similar observations exist during large muscle mass exercise or dynamic contractions remain unknown. BP, heart rate, muscle oxygenation (near‐infrared spectroscopy), and rectus femoris electromyography (EMG) were recorded in 28 males and 17 females during 10% and 30% MVC static (120s) and isokinetic dynamic (180s; 1:2 work‐to‐rest ratio; angular velocity: 60º/s) knee extensor exercise. At baseline and during exercise, continuous BP and heart rate were measured using finger photoplethysmography and single‐lead electrocardiography, respectively. MVC, as well as all submaximal exercise testing, was measured and performed on a dynamometer at 80⁰ of knee flexion, and voluntary activation was assessed using the interpolated twitch technique, with ≥90% voluntary activation of the knee extensors set as the acceptable activation threshold. Static and dynamic exercises were completed on separate visits, in a randomized order. The change from baseline of each variable was calculated for every 30 s during each submaximal test. Sex differences were then examined with and without statistical adjustment of MVC using analyses of covariance (ANCOVA). The males were taller and heavier than the females and had higher resting systolic BP (all P<0.05), while BMI, resting diastolic and mean arterial BP, and heart rate were similar between sexes (all P>0.05). Knee extensor MVC was higher in males than females (165 ± 40 vs. 94 ± 22 Nm, P<0.0001). Males had larger systolic BP responses (interaction, P<0.001) and muscle deoxygenation (interaction, P<0.01) than females during 10% static exercise, with no difference in EMG (interaction, P=0.73). Peak systolic BP was correlated to MVC (r=0.53, P=0.0002), and adjustment for MVC abolished sex differences in systolic BP (interaction, P=0.5). BP, heart rate, muscle oxygenation/deoxygenation, and EMG responses did not differ between sexes during 30% static exercise (interaction, All P>0.2), including following adjustment for MVC (All P>0.1). Males had larger systolic BP responses during dynamic exercise at 10% and 30% (interaction, Both P=0.01), which were abolished after adjustment for MVC (interaction, Both P>0.08). Systolic BP responses at 180s were correlated with MVC and stroke volume responses during 10% (r=0.31, P=0.04; r=0.61, P<0.0001, respectively) and 30% (r=0.4, P=0.007; r=0.59, P<0.0001, respectively). In conclusion, MVC can influence systolic BP responses to 10% but not 30% MVC static, as well as 10% and 30% MVC dynamic knee extensor exercise. MVC should be considered when comparing BP responses between males and females. Finally, the mechanisms mediating the larger pressor responses in stronger individuals across different exercise modalities warrant further investigation.

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