This study investigated mechanisms for the stressor-induced changes in muscle fatigability in men and women. Participants performed an isometric-fatiguing contraction at 20% maximal voluntary contraction (MVC) until failure with the elbow flexor muscles. Study one (n = 55; 29 women) involved two experimental sessions: 1) a high-stressor session that required a difficult mental-math task before and during a fatiguing contraction and 2) a control session with no mental math. For some participants (n = 28; 14 women), cortical stimulation was used to examine mechanisms that contributed to muscle fatigability during the high-stressor and control sessions. Study two (n = 23; nine women) determined the influence of a low stressor, i.e., a simple mental-math task, on muscle fatigability. In study one, the time-to-task failure was less for the high-stressor session than control (P < 0.05) for women (19.4%) and men (9.5%): the sex difference response disappeared when covaried for initial strength (MVC). MVC force, voluntary activation, and peak-twitch amplitude decreased similarly for the control and high-stressor sessions (P < 0.05). In study two, the time-to-task failure of men or women was not influenced by the low stressor (P > 0.05). The greater fatigability, when exposed to a high stressor during a low-force task, was not exclusive to women but involved a strength-related mechanism in both weaker men and women that accelerated declines in voluntary activation and slowing of contractile properties.

Heart failure patients with reduced ejection fraction (HFrEF) exhibit severe limitations in exercise capacity (VO 2 peak). r One of the primary peripheral mechanisms suggested to underlie exercise intolerance in HFrEF is excessive locomotor muscle group III/IV afferent feedback; however, this has never been investigated in human heart failure. r HFrEF patients and controls performed an incremental exercise test to volitional exhaustion to determineVO 2 peak with lumbar intrathecal fentanyl or placebo. During exercise, cardiac output, leg blood flow and radial artery and femoral venous blood gases were measured. r With fentanyl, compared with placebo, patients with HFrEF achieved a higher peak workload, VO 2 peak, cardiac output, stroke volume and leg blood flow. r These findings suggest that locomotor muscle group III/IV afferent feedback in HFrEF leads to increased systemic vascular resistance, which constrains stroke volume, cardiac output and O 2 delivery thereby impairingVO 2 peak and thus exercise capacity.

Background Feedback from active locomotor muscles contributes to the exercise pressor response in healthy humans, and is thought to be more prominent in heart failure (HF). The purpose of this study was to examine the influence of metaboreflex stimulation on arterial pressure in HF. Methods Eleven HF patients (51±15yrs, NYHA Class I/II, LVEF 32±9%) and 11 controls (CTL) (42±9yrs) were recruited. Participants completed two exercise tests on separate days: 1) symptom limited graded exercise test; and 2) constant work rate cycling (60% peak oxygen consumption, V̇O2) for 4 min with 2 min passive recovery. Recovery was randomized to normal or locomotor muscle regional circulatory occlusion (RCO). V̇O2, mean, systolic, and diastolic blood pressure (MAP, SBP, and DBP) and heart rate (HR) were measured at rest, end-exercise and recovery. O2 pulse (V̇O2 /HR) and the rate pressure product (RPP = HR × SBP) were calculated. Results In response to RCO, MAP and SBP increased in HF compared with CTLs (6.8±5.8% vs −3.0±7.8%, p<0.01 and 3.4±6.4% vs −12.7±10.4%, p<0.01, respectively), with no difference in diastolic pressure (p=0.61). HF patients had a smaller reduction in HR and RPP, but also displayed a larger decrease in O2 pulse consequent to locomotor metaboreflex stimulation (p<0.05, for all). Conclusion RCO resulted in a markedly increased pressor response in HF relative to CTL, due primarily to an increase of SBP and attenuated cardiac recovery as noted by the persistent elevation in HR.

We propose that abnormalities of the pulmonary system contribute significantly to the exertional dyspnea and exercise intolerance observed in patients with chronic heart failure.Interventions designed to address the deleterious pulmonary manifestations of heart failure may therefore yield promising improvements in exercise tolerance in this population.

Evidence suggests that heart failure (HF) patients experience skeletal muscle fatigability in the lower extremity during single-limb tasks. The contribution of skeletal muscle fatigability to symptoms of exercise intolerance (perceived fatigue and dyspnea) is relatively unclear. Symptomatic or ‘perceived’ fatigue is defined by the sensations of exhaustion or tiredness that patients experience either at rest or while performing a motor task. Although factors that contribute to symptoms of fatigue in patients with HF are multifactorial; the skeletal muscle likely plays a major role. Skeletal muscle fatigability, as opposed to symptomatic fatigue, is an objective measure of a reduction in muscle force or power or reduced ability of the muscles to perform over time. Indeed, evidence suggests that patients with HF experience greater skeletal muscle fatigability which may contribute to a diminution in motor performance and the overall symptomatology that is hallmark of exercise intolerance in HF. This review will discuss (1) skeletal muscle fatigability in patients with HF, (2) the mechanisms contributing to locomotor skeletal muscle fatigability in HF and (3) the relationship of fatigability to symptoms of perceived fatigue and exercise intolerance in HF patients. Evidence suggests that cardiac dysfunction alone does not contribute to exercise intolerance. Therefore, mechanisms of skeletal muscle fatigability and their contribution to symptoms of fatigue and exercise intolerance, is an increasingly important consideration as we develop rehabilitative strategies for improving motor performance and functional capacity in patients with HF.