Purpose: Determine 1) if adults with facioscapulohumeral muscular dystrophy (FSHD) exhibit exercise intolerance and 2) potential contributing mechanisms to exercise intolerance, specific to FSHD. Methods: Eleven people with FSHD (47 ± 13 yr, 4 females) and 11 controls (46 ± 13 yr, 4 females) completed one visit, which included a volitional peak oxygen consumption ( VO 2peak ) cycling test. Breath-by-breath gas exchange, ventilation, and cardiovascular responses were measured at rest and during exercise. The test featured 3-min stages (speed, 65-70 rpm) with incremental increases in intensity (FSHD: 20 W per stage; control: 40-60 W per stage). Body lean mass (LM (kg, %)) was collected via dual-energy x-ray absorptiometry. Results: VO 2peak was 32% lower (24.5 ± 9.7 vs 36.2 ± 9.3 mL•kg −1 •min −1 , P < 0.01), and wattage was 55% lower in FSHD (112.7 ± 56.1 vs 252.7 ± 67.7 W, P < 0.01). When working at a relative submaximal intensity (40% of VO 2peak ), wattage was 55% lower in FSHD (41.8 ± 30.3 vs 92.7 ± 32.6 W, P = 0.01), although ratings of perceived exertion (FSHD: 11 ± 2 vs control: 10 ± 3, P = 0.61) and dyspnea (FSHD: 3 ± 1 vs control: 3 ± 2, P = 0.78) were similar between groups. At an absolute intensity (60 W), the rating of perceived exertion was 63% higher (13 ± 3 vs 8 ± 2, P < 0.01) and dyspnea was 180% higher in FSHD (4 ± 2 vs 2 ± 2, P < 0.01). VO 2peak was most strongly correlated with resting O 2 pulse in controls ( P < 0.01, r = 0.90) and percent leg LM in FSHD ( P < 0.01, r = 0.88). Among FSHD participants, VO 2peak was associated with self-reported functionality (FSHD-HI score; activity limitation: P < 0.01, r = −0.78), indicating a strong association between perceived and objective impairments. Conclusions: Disease-driven losses of LM contribute to exercise intolerance in FSHD, as evidenced by a lower VO 2peak and elevated symptoms of dyspnea and fatigue during submaximal exercise. Regular exercise participation may preserve LM, thus providing some protection against exercise tolerance in FSHD.
Introduction Multiple symptoms accompany menopause, including vasomotor symptoms (VMS), physical symptoms, psychosocial symptoms and sexual dysfunction. Previous studies show that experiencing VMS may increase the risks for hypertension and cardiovascular disease (CVD); however, it is unclear whether physical menopausal symptoms, such as weight gain, lack of energy, or reduced muscular strength, contribute to CVD risk. Furthermore, muscle sympathetic nerve activity (MSNA) is elevated with CVD, but the relationship between menopause symptoms and MSNA is unknown. Thus, the aim of our study was to determine if physical menopausal symptoms are correlated with MSNA in postmenopausal females. Methods Eight postmenopausal females (age 63±1yr; menopause age 53±2yr) attended two study visits. The first visit included written informed consent, completion of the Menopause‐Specific Quality of Life (MENQOL) and Minnesota Leisure Time Physical Activity (MLTPAQ) Questionnaires, and blood draws to measure sex hormone levels. The MENQOL asks participants to rate how bothered they feel in four areas of symptoms: vasomotor (i.e., VMS), psychosocial, physical, and sexual. The absence of a symptom corresponds with a score of 1 point, whereas a present symptom is rated according to how bothersome it is and is scored from 2‐8 points. The MLTPAQ estimates caloric expenditure based on reported habitual physical activity. The second visit was conducted in the morning after an overnight fast and abstinence of alcohol, caffeine and exercise for 12 hours and included measurements of continuous noninvasive BP, heart rate via a 3‐lead electrocardiography (ADInstruments, Colorado Springs, CO) and MSNA of the peroneal nerve via microneurography during a 10‐minute period of quiet rest. Results Total MENQOL scores ranged from 1.3‐2.4 on a 1‐8 scale; physical symptom scores ranged from 1.1 to 3.4; and VMS ranged from 1.0‐1.7. Body mass index (BMI, kg/m2) was 24±2. Levels of estradiol, total estrogens, testosterone, total estrogens: testosterone ratio, and MLTPAQ were not different between the females. Average mean arterial pressure was (101±5mmHg) and MSNA burst frequency was 29 bursts/min). In addition, MSNA burst frequency correlated with the MENQOL scores for physical symptoms (r=0.73, p=0.04), but not other menopausal symptoms, including VMS (p>0.05), indicating that females with more severe physical symptoms had greater MSNA. Conclusion Although females with VMS have greater CVD risk than those without VMS, data from this small sample of females suggests that reported physical symptoms rather than VMS were elevated with resting MSNA and were strongly associated with MSNA. These findings suggest that females who experience physical menopause symptoms may demonstrate autonomic dysregulation which could contribute to CVD risk.
Hypertension (HTN) and cardiovascular disease (CVD) risks increase substantially after menopause, and literature suggests that the age at which menopause is completed contributes to this risk. Blood pressure (BP) reactivity to static fatiguing handgrip (HG) exercise can reveal existing HTN and may be valuable in predicting future risk for developing HTN. Thus, we aimed to determine if the age of menopause would contribute to greater BP reactivity during a static fatiguing HG in females. We hypothesized that cardiovascular reactivity would be positively related to age and inversely related to menopause age. METHODS: Participants laid supine throughout testing. Each participant performed a maximum voluntary contraction (MVC) of the hand followed by a 3‐min. baseline rest (BL), then a continuous HG at 30% of MVC force to fatigue. Beat‐to‐beat BP and heart rate (HR) were recorded during BL and HG. Measures of systolic, diastolic, and mean arterial BP (SBP, DBP, and MAP, respectively) and HR were compared at the start, 25%, 50%, 75%, and end of each participant's fatiguing contraction. To further evaluate cardiovascular reactivity, baseline measures of BP and HR were also compared to peak responses. Statistical analyses included repeated‐measures ANOVA and Pearson correlation, and results are presented as mean±SD. RESULTS: Eleven postmenopausal females (age 63±4 yrs.; range: 58‐69 yrs.), with menopause age of 50±4 yrs. (range: 42‐55 yrs.), completed all procedures. Average BL SBP and DBP were 135±14mmHg and 77±9mmHg, respectively. Systolic BP, DBP, MAP, and HR increased from BL throughout the fatiguing contraction (time effect: p≤0.001 for all). Peak values of BP and HR increased from BL (ΔSBP: 55±28mmHg; ΔDBP: 43±24mmHg; ΔMAP: 45±21mmHg; ΔHR: 29±14 bpm; p<0.001 for all tests). Age was correlated with peak increases in SBP, DBP, and MAP (r=0.71, p=0.014; r=0.76, p=0.006; r=0.78, p=0.005, respectively), but not with peak change in HR (p>0.05). Menopause age was not correlated with BP or HR reactivity (p>0.05 for all). CONCLUSION: Although age of menopause appears to be strongly linked to future risk of CVD, we did not observe a significant relationship between cardiovascular reactivity and age of menopause. Instead, findings from this study suggest that current age may provide a stronger indicator of exaggerated BP reactivity and potential increased risk for CVD in females.
Introduction The risk of hypertension (HTN) and cardiovascular disease (CVD) dramatically increases following menopause, and premature and early menopause (<45yr) substantially increase this risk. Greater blood pressure (BP) reactivity to stressors such as exercise can predict future risk of developing HTN. Thus, we aimed to determine if the time since menopause completion contribute to greater BP reactivity during a fatiguing hand grip (HG). We hypothesized that women who have been postmenopausal for a longer duration would exhibit greater cardiovascular reactivity to a fatiguing HG exercise. Methods Women who experienced early and typical‐age (>46yr) menopause completed two visits. Visit 1: Informed consent, medical and health questionnaires. Visit 2: Participants rested in a supine position. Three maximum voluntary contractions (MVC) of their left hand were completed followed by a baseline rest (BL) of 10 minutes. Following BL, a HG test at 30% of MVC was performed until time to task failure. Non‐invasive beat‐to‐beat BP and heart rate (HR) were recorded during BL and HG test. Systolic (SAP), diastolic (DAP), mean arterial (MAP), and HR were analyzed as BL averages and in 20‐30s intervals at start, 25%, 50%, 75%, and task failure. Repeated‐measures ANOVA and independent T‐tests were used for the statistical analysis; results are presented as mean±SD. Results Eighteen postmenopausal females completed the study and were divided into two groups: 1) postmenopause ≤10yrs (PM≤10; 8±2 yrs; body mass index (BMI): 25±3 kg/m2, n=8) and 2) postmenopause ≥11 (PM≥11; 15±5 yrs; BMI: 25±5 kg/m2, n=10). The PM≥11 group was slightly older (64±3yrs) than the PM≤10 (60±4yrs, p=0.005). BL SAP was not different between PM≤10 (133±14mmHg) and PM≥11 (128.75±14mmHg; p=0.95). DAP (85±9 vs 81±10mmHg; p=0.68) and MAP (100±10 vs 96±9mmHG; p=0.40), were not different between PM≤10 and PM≥11, respectively. During the fatiguing contraction, SAP increases were exaggerated in PM≥11 compared with PM≤10 (Δ63±25 vs Δ40±16mmHg; group × time, p=0.03). Similarly, MAP increased more in PM≥11 compared with PM≤10 (Δ49±16 vs Δ31±10mmHg; group × time, p=0.04), but not DAP (group × time, p=0.1) or HR (group × time, p=0.08). When co‐varying for age, however, the interactions were no longer significant (p>0.05, for all). In addition, peak increases in SAP (p=0.04), MAP (p=0.01), and HR (p=0.02) were greater in PM≥11 compared with PM≤10, but these observations were no longer significant when co‐varying for age (p>0.05, for all). Conclusion Novel findings from this study suggest that although the duration of menopause influences BP reactivity during a moderate intensity fatiguing contraction, this greater increase may be explained by older age. This elevated response to submaximal exercise may contribute to the increased risk of HTN and CVD in postmenopausal women.
Introduction Cardiovascular disease (CVD) is the leading cause of death in women. Sleep disturbances (DS), such as insomnia or frequent nocturnal awakenings, may increase the risk of CVD. Prior work suggests that autonomic blood pressure (BP) dysregulation in postmenopausal women may exaggerate risk of hypertension (HTN) and CVD. In addition, individuals with greater BP and sympathetic neural responses to stressors, such as a cold pressor test (CPT), demonstrate future risk for HTN development. Further, when exposed to 24‐hour sleep deprivation, older women, but not older men, demonstrate greater sympathetic activity. It is unknown, however, if women who experience DS demonstrate a greater sympathetic reactivity to a CPT. The purpose of this study was to determine if postmenopausal women with DS exhibit sympathetic reactivity to a CPT compared to women without DS. Methods Eighteen women (62±1yrs old; mean±SE) participated in two study visits. Visit 1: Informed consent and medical and health questionnaires. Visit 2: DS was assessed by the Menopause‐Specific Quality of Life questionnaire. Participants were classified as having disturbed sleep (DS; n=10) or non‐disturbed sleep (NDS; n=8) based on a scale of 1 indicating ‘none’ and 2‐8 being how bothersome it is. The study was conducted in the morning after overnight fast and abstinence of alcohol, caffeine, and exercise. Muscle sympathetic nerve activity (MSNA) was measured from the peroneal nerve using microneurography. Heart rate (HR) via 3‐lead electrocardiography, MSNA, and beat‐to‐beat BP using a non‐invasive finger cuff were measured during a 10‐min quiet rest and a two‐min CPT of the left hand. Results Menopause onset ranged from 40‐57yrs (50±1yrs). Body mass index was similar between groups (DS=25±1kg/m2, NDS=24±2kg/m2, p=0.53). MSNA burst incidence (bursts/100 heart beats, hb) increased throughout the CPT (time effect, p<0.01), but increases were not significantly different between DS (Δ19±6b/100hb; 95% CI [7,31]) and NDS (Δ11±6b/100hb; 95% CI [‐2,24]) (time*group, p=0.36) groups. Systolic BP, Diastolic BP and HR increased similarly (p>0.05) during the CPT for both groups. Sleep difficulty score was correlated with resting diastolic BP (r=0.43, p=0.03) and trended to correlate with the age of menopause (r= ‐0.37, p=0.05). Conclusion These findings suggest that women with DS do not demonstrate greater sympathetic reactivity to a CPT, however, we did observe that DS was linked to greater diastolic BP at rest and appeared to be more bothersome for women who completed menopause at an earlier age. These findings suggest a pathway by which disrupted sleep may contribute to the future development of HTN and CVD in postmenopausal women.
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