Heart failure (HF) is a complex syndrome where the heart cannot pump enough blood to meet the body’s metabolic demands, usually because the heart muscle is too weak or too stiff. This impairment prevents the circulatory system from delivering adequate oxygen and nutrients throughout the body. One of the most common and limiting symptoms is persistent, overwhelming fatigue. This exhaustion is far more severe than simple tiredness and often dictates a person’s daily capacity, making routine activities challenging. Fatigue results from mechanical pump failure, sustained chemical overdrive, and physical changes within the muscle tissue.
The Primary Mechanical Failure: Insufficient Oxygen Delivery
The most direct cause of fatigue is the reduced ability of the heart to move blood forward, known as low cardiac output. The heart cannot eject a sufficient volume of blood with each beat, leading to poor perfusion (reduced blood flow) through organs and tissues. This reduced flow is immediately felt by the skeletal muscles, which are responsible for movement.
When a person with heart failure exerts themselves, muscles require a significant increase in oxygenated blood flow to generate energy efficiently. Since the weakened heart cannot increase its pumping capacity to match this demand, the muscles quickly become starved of oxygen. The body attempts to compensate by prioritizing flow to the brain and the heart, shunting blood away from the limbs.
This lack of oxygen forces muscle cells to switch from aerobic (oxygen-using) to anaerobic metabolism. While anaerobic metabolism provides a quick burst of energy, it is inefficient and results in the rapid buildup of lactic acid. The accumulation of lactic acid triggers exhaustion and muscle fatigue, explaining why even mild activity can be debilitating.
This mechanical limitation severely restricts the body’s capacity for physical work, causing exhaustion to be reached much faster. Poor circulation also means waste products are not cleared quickly from the muscles, prolonging recovery time after effort.
The Body’s Overdrive: Neurohormonal Activation and Inflammation
Beyond mechanical failure, heart failure triggers a complex, long-term chemical response that contributes to chronic fatigue, even at rest. When cardiac output falls, the body interprets this as shock, leading to the sustained activation of neurohormonal systems. These systems, including the sympathetic nervous system (SNS) and the Renin-Angiotensin-Aldosterone System (RAAS), attempt to stabilize blood pressure and volume.
SNS activation causes the chronic release of stress hormones, particularly norepinephrine (the body’s fight-or-flight chemical). This sustained chemical overdrive forces the body into a continuous state of high alert, accelerating heart rate and increasing blood pressure, which strains the heart. This chronic, high-energy expenditure contributes to a persistent, draining feeling of malaise.
Heart failure is also characterized by increased levels of inflammatory mediators and cytokines circulating in the bloodstream. These pro-inflammatory chemicals are released due to tissue hypoperfusion and stress on the heart muscle. Cytokines, such as TNF-α and IL-6, are the same chemicals that cause sickness behavior and exhaustion during an infection.
This systemic inflammation creates a constant inflammatory state that contributes to muscle wasting and a general feeling of being unwell. The chronic neurohormonal and inflammatory activation drives a catabolic state, meaning the body breaks down tissue and expends energy unnecessarily. This leaves the person feeling constantly drained, regardless of their activity level.
Peripheral Impact: Changes in Skeletal Muscle Function
The chronic state of poor perfusion and chemical signaling causes physical and metabolic damage at the cellular level within the skeletal muscles. This peripheral impact means that even if the heart improved, the muscles are structurally and functionally impaired, leading to fatigue. One significant change is muscle atrophy, or wasting, often observed in advanced heart failure.
Poor blood flow and chronic inflammation reduce overall muscle mass and shift muscle fiber type, decreasing the muscle’s capacity for endurance. The muscle cells’ energy factories, known as mitochondria, become a primary site of dysfunction. In heart failure, the number of mitochondria is often reduced, and the remaining ones function less efficiently.
This mitochondrial impairment limits the muscles’ ability to utilize delivered oxygen, meaning the cellular machinery cannot efficiently produce the necessary energy molecule, adenosine triphosphate (ATP). The muscles therefore have a reduced oxidative capacity, accelerating reliance on less efficient energy pathways and hastening fatigue. This local cellular failure means the muscle fatigues more quickly and recovers more slowly, cementing the physical limitation characteristic of heart failure.