Randomized controlled trial of bikram yoga and aerobic exercise for depression in women: Efficacy and stress-based mechanisms.

BACKGROUND: The current study presents a randomized controlled 8-week trial of Bikram yoga, aerobic exercise, and waitlist for depression. Bikram yoga was chosen specifically for its standardized nature. Further, we examined changes in three stress-related constructs-perceived stress, rumination, and mindfulness-as mediators of antidepressant effects. METHOD: Fifty-three women (age 18-65; 74% White) with a unipolar depressive disorder were randomly assigned to one of the three conditions. Response was defined as >50% reduction on the Hamilton Rating Scale for Depression (HAM-D). Remission was defined as no longer meeting criteria for depression and a HAM-D ≤ 7. Self-reported perceived stress, rumination, and mindfulness were assessed weekly. RESULTS: In the intention-to-treat sample (n = 53), response rates were significantly higher in the Bikram yoga (61.1%; χ2 = 10.48, p = .001) and aerobic exercise (60.0%; χ2 = 10.44, p = .001) conditions relative to waitlist (6.7%). In the completer sample (n = 42), 73.3% (χ2 = 11.41, p = .001) of women in yoga and 80.0% (χ2 = 13.72, p < .001) in exercise achieved response compared to 8.3% in waitlist. Reductions in rumination significantly mediated HAM-D change for both active treatments, and mindful acceptance was a partial mediator in the exercise condition. LIMITATIONS: The sample was small in size, consisted of women only, and was ethnically homogenous. Inter-rater reliability was not assessed, aerobic exercise was not standardized, and mediators were assessed by self-report. CONCLUSIONS: Bikram yoga showed descriptively similar efficacy to aerobic exercise and both may work, in part, by helping individuals interrupt negative thinking.

Acute intermittent hypercapnic hypoxia and sympathetic neurovascular transduction in men.

KEY POINTS: Intermittent hypoxia leads to long-lasting increases in muscle sympathetic nerve activity and blood pressure, contributing to increased risk for hypertension in obstructive sleep apnoea patients. We determined whether augmented vascular responses to increasing sympathetic vasomotor outflow, termed sympathetic neurovascular transduction (sNVT), accompanied changes in blood pressure following acute intermittent hypercapnic hypoxia in men. Lower body negative pressure was utilized to induce a range of sympathetic vasoconstrictor firing while measuring beat-by-beat blood pressure and forearm vascular conductance. IH reduced vascular shear stress and steepened the relationship between diastolic blood pressure and sympathetic discharge frequency, suggesting greater systemic sNVT. Our results indicate that recurring cycles of acute intermittent hypercapnic hypoxia characteristic of obstructive sleep apnoea could promote hypertension by increasing sNVT. ABSTRACT: Acute intermittent hypercapnic hypoxia (IH) induces long-lasting elevations in sympathetic vasomotor outflow and blood pressure in healthy humans. It is unknown whether IH alters sympathetic neurovascular transduction (sNVT), measured as the relationship between sympathetic vasomotor outflow and either forearm vascular conductance (FVC; regional sNVT) or diastolic blood pressure (systemic sNVT). We tested the hypothesis that IH augments sNVT by exposing healthy males to 40 consecutive 1 min breathing cycles, each comprising 40 s of hypercapnic hypoxia ( PETCO2 : +4 ± 3 mmHg above baseline; PETO2 : 48 ± 3 mmHg) and 20 s of normoxia (n = 9), or a 40 min air-breathing control (n = 7). Before and after the intervention, lower body negative pressure (LBNP; 3 min at -15, -30 and -45 mmHg) was applied to elicit reflex increases in muscle sympathetic nerve activity (MSNA, fibular microneurography) when clamping end-tidal gases at baseline levels. Ventilation, arterial pressure [systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP)], brachial artery blood flow ( Q̇BA ), FVC ( Q̇BA /MAP) and MSNA burst frequency were measured continuously. Following IH, but not control, ventilation [5 L min-1 ; 95% confidence interval (CI) = 1-9] and MAP (5 mmHg; 95% CI = 1-9) were increased, whereas FVC (-0.2 mL min-1  mmHg-1 ; 95% CI = -0.0 to -0.4) and mean shear rate (-21.9 s-1 ; 95% CI = -5.8 to -38.0; all P < 0.05) were reduced. Systemic sNVT was increased following IH (0.25 mmHg burst-1  min-1 ; 95% CI = 0.01-0.49; P < 0.05), whereas changes in regional forearm sNVT were similar between IH and sham. Reductions in vessel wall shear stress and, consequently, nitric oxide production may contribute to heightened systemic sNVT and provide a potential neurovascular mechanism for elevated blood pressure in obstructive sleep apnoea.

The impact of acute mental stress on brachial artery flow-mediated dilation in women diagnosed with depression.

Endothelial function, assessed by flow-mediated dilation (FMD), may be transiently attenuated in healthy adults following acute mental stress. However, the impact of acute mental stress on endothelial function in the context of clinical depression is unknown. This study examined the impact of acute mental stress on FMD in women with a diagnosis of a depressive disorder. Forty-three otherwise healthy women (33 ±â€¯14 years) participated. Brachial artery diameter and blood velocity were assessed with ultrasound. FMD was assessed immediately prior to and 15 min following the Trier Social Stress Test (TSST). The FMD protocol included 5 min of forearm cuff occlusion (pressure = 250 mm Hg), followed by release. Shear stress was estimated by calculating shear rate (SR = brachial artery blood velocity/diameter). Stress reactivity was assessed via changes in mean arterial pressure (MAP), heart rate (HR) and salivary cortisol. Results are mean ±â€¯SD. A significant stress response was elicited by the TSST [MAP, HR and salivary cortisol increased (p < 0.05)]. Neither the SR stimulus nor FMD response differed pre-versus post-stress (p = 0.124 and p = 0.641, respectively). There was a modest negative correlation between cortisol reactivity and change in FMD from pre- to post-stress (R = -0.392, p = 0.011). To conclude, acute mental stress did not consistently impair endothelial function in women diagnosed with a depressive disorder; however, higher cortisol reactivity may increase the likelihood of post-stress endothelial dysfunction. Further research is required to better understand the factors influencing the relationship between acute mental stress, cortisol and endothelial function in women with depression.

Work of breathing influences muscle sympathetic nerve activity during semi-recumbent cycle exercise.

Reducing the work of breathing during exercise improves locomotor muscle blood flow and reduces diaphragm and locomotor muscle fatigue and is thought to be the result of a sympathetically mediated reflex. AIM: The aim of this study was to assess muscle sympathetic nerve activity (MSNA) when the work of breathing is experimentally lowered during dynamic exercise. METHODS: Healthy subjects (n = 12; age = 29 ± 9 years) performed semi-recumbent cycling trials at 40%, 60%, and 80% of peak workload. Exercise trials consisted of spontaneous breathing, reduced work of breathing (proportional assist ventilator), followed by further spontaneous breathing (post-ventilator). MSNA was recorded from the median nerve. RESULTS: There was no difference in work of breathing between PAV and post-PAV at 40% peak work. At 60% peak work, the ventilator significantly (P < 0.05) reduced work of breathing (103 ± 39 vs 144 ± 47 J min-1 ), sympathetic nerve activity (35 ± 5 vs 42 ± 8 burst min-1 ), and V ˙ O 2 (2.4 ± 0.5 vs 2.6 ± 0.5 L min-1 ) without influencing ventilation (86 ± 9 vs 82 ± 10 L min-1 ; P > 0.05), for PAV and post-PAV respectively. During 80% peak work (n = 8), the ventilator significantly (P < 0.05) reduced work of breathing (235 ± 110 vs. 361 ± 150 J min-1 ), MSNA (48 ± 7 vs 54 ± 11 burst min-1 ), and V ˙ O 2 (2.9 ± 0.6 vs 3.2 ± 0.7 L min-1 ) but not ventilation (121 ± 20 vs 123 ± 20 L min-1 ; P > 0.05), for PAV and post-PAV respectively. There was a significant relationship between MSNA and V ˙ O 2 (P < 0.0001) with a significant interaction due to the ventilator (P < 0.05). CONCLUSION: Lowering the normally occurring work of breathing during exercise results in commensurate reductions in MSNA. Our findings provide evidence of a sympathetically mediated vasoconstrictor effect emanating from respiratory muscles during exercise.

Effect of acetazolamide and methazolamide on diaphragm and dorsiflexor fatigue: a randomized controlled trial.

Acetazolamide, a carbonic anhydrase (CA) inhibitor used clinically and to prevent acute mountain sickness, worsens skeletal muscle fatigue in animals and humans. In animals, methazolamide, a methylated analog of acetazolamide and an equally potent CA inhibitor, reportedly exacerbates fatigue less than acetazolamide. Accordingly, we sought to determine, in humans, if methazolamide would attenuate diaphragm and dorsiflexor fatigue compared with acetazolamide. Healthy men (dorsiflexor: n = 12; diaphragm: n = 7) performed fatiguing exercise on three occasions, after ingesting acetazolamide (250 mg three times a day) and then in random order, methazolamide (100 mg twice a day) or placebo for 48 h. For both muscles, subjects exercised at a fixed intensity until exhaustion on acetazolamide, with subsequent iso-time and -workload trials. Diaphragm exercise was performed using a threshold-loading device, while dorsiflexor exercise was isometric. Neuromuscular function was determined pre- and postexercise by potentiated transdiaphragmatic twitch pressure and dorsiflexor torque in response to stimulation of the phrenic and fibular nerve, respectively. Diaphragm contractility 3-10 min postexercise was impaired more for acetazolamide than methazolamide or placebo (82 ± 10, 87 ± 9, and 91 ± 8% of pre-exercise value; P < 0.05). Similarly, dorsiflexor fatigue was greater for acetazolamide than methazolamide (mean twitch torque of 61 ± 11 vs. 57 ± 13% of baseline, P < 0.05). In normoxia, methazolamide leads to less neuromuscular fatigue than acetazolamide, indicating a possible benefit for clinical use or in the prophylaxis of acute mountain sickness. NEW & NOTEWORTHY Acetazolamide, a carbonic anhydrase inhibitor, may worsen diaphragm and locomotor muscle fatigue after exercise; whereas, in animals, methazolamide does not impair diaphragm function. Compared with both methazolamide and the placebo, acetazolamide significantly compromised dorsiflexor function at rest and after exhaustive exercise. Similarly, diaphragm function was most compromised on acetazolamide followed by methazolamide and placebo. Methazolamide may be preferable over acetazolamide for clinical use and altitude illness prophylaxis to avoid skeletal muscle dysfunction.

Impaired handgrip exercise-induced brachial artery flow-mediated dilation in young obese males.

Flow mediated dilation (FMD) stimulated by different shear stress stimulus profiles may recruit distinct transduction mechanisms, and provide distinct information regarding endothelial function. The purpose of this study was to determine whether obesity influences brachial artery FMD differently depending on the shear stress profile used for FMD assessment. The FMD response to a brief, intermediate, and sustained shear stress profile was assessed in obese (n = 9) and lean (n = 19) young men as follows: brief stimulus, standard reactive hyperemia (RH) following a 5 min forearm occlusion (5 min RH); intermediate stimulus, RH following a 15 min forearm occlusion (15 min RH); sustained stimulus, 10 min of handgrip exercise (HGEX). Brachial artery diameter and mean shear stress were assessed using echo and Doppler ultrasound, respectively, during each FMD test. There was no group difference in HGEX shear stress (p = 0.390); however, the obese group had a lower HGEX-FMD (5.2 ± 3.0% versus 11.5 ± 4.4%, p < 0.001). There was no group difference in 5 min RH-FMD (p = 0.466) or 15 min RH-FMD (p = 0.181); however, the shear stress stimulus was larger in the obese group. After normalization to the stimulus the 15 min RH-FMD (p = 0.002), but not the 5 min RH-FMD (p = 0.118) was lower in the obese group. These data suggest that obesity may have a more pronounced impact on the endothelium's ability to respond to prolonged increases in shear stress.

The impact of a cold pressor test on brachial artery handgrip exercise-induced flow-mediated dilation.

It is unknown how endothelial-dependent flow-mediated dilation (FMD) stimulated by a sustained, exercise-induced increase in shear stress (EX-FMD) is affected by a simultaneous sympathoexcitatory painful stimulus. The purpose of this study was to examine the impact of a cold pressor test (CPT) on brachial artery EX-FMD elicited by a handgrip exercise-induced increase in shear stress. Participants were healthy males (age 21±2 years) (n=28; 16 Experimental group, 12 Control). Brachial artery diameter and blood velocity were measured using echo and Doppler ultrasound, respectively. Shear stress was estimated by shear rate (shear rate = blood velocity / diameter) and targeted to reach 75 s(-1) in each of two EX-FMD trials in all subjects. In the Experimental group, the second EX-FMD trial was accompanied by simultaneous foot immersion in ice water (simultaneous CPT). The shear rate stimulus did not differ between groups (p=0.823) or trials (p=0.726) (group × trial interaction: p=0.646) (average exercise shear rate (mean ± SD): 67.6±6.2 s(-1)). The CPT (experienced during EX-FMD trial 2 in the Experimental group) increased mean arterial pressure (p<0.001) and heart rate (p=0.002) relative to the Control group. %EX-FMD was not different between groups (p=0.508) or trials (p=0.592) (group × trial interaction: p=0.879) (EX-FMD: Experimental group trial 1: 5.4±3.4%, trial 2: 5.6±2.6%; Control group trial 1: 6.0±3.7%, trial 2: 6.4±2.2%). In conclusion, the CPT did not impact concurrent EX-FMD, and this indicates that an acute painful stimulus does not interfere with conduit artery FMD responses during exercise in young healthy men.