Monitoring Exercise-Induced Muscle Fatigue and Adaptations: Making Sense of Popular or Emerging Indices and Biomarkers

Abstract

Regular exercise with the appropriate intensity and duration may improve an athlete's physical capacities by targeting different performance determinants across the endurance⁻strength spectrum aiming to delay fatigue. The mechanisms of muscle fatigue depend on exercise intensity and duration and may range from substrate depletion to acidosis and product inhibition of adenosinetriphosphatase (ATPase) and glycolysis. Fatigue mechanisms have been studied in isolated muscles; single muscle fibers (intact or skinned) or at the level of filamentous or isolated motor proteins; with each approach contributing to our understanding of the fatigue phenomenon. In vivo methods for monitoring fatigue include the assessment of various functional indices supported by the use of biochemical markers including blood lactate levels and more recently redox markers. Blood lactate measurements; as an accompaniment of functional assessment; are extensively used for estimating the contribution of the anaerobic metabolism to energy expenditure and to help interpret an athlete's resistance to fatigue during high intensity exercise. Monitoring of redox indices is gaining popularity in the applied sports performance setting; as oxidative stress is not only a fatigue agent which may play a role in the pathophysiology of overtraining syndrome; but also constitutes an important signaling pathway for training adaptations; thus reflecting training status. Careful planning of sampling and interpretation of blood biomarkers should be applied; especially given that their levels can fluctuate according to an athlete's lifestyle and training histories.

Keywords: exercise induced muscle fatigue; fatigue agents; fatigue index; lactate monitoring; muscle inflammation; oxidative stress monitoring; redox markers; training adaptations.

Figure 1

A simplified scheme of the purported effects of acidosis and reactive oxygen species (ROS) based on muscle fatigue literature reviewed in this article. Acidosis has been shown to cause impaired Ca²⁺ handling [55] and inhibition of key metabolic enzyme activities [57] as well as to inhibit myosin ATPase [56] affecting force and velocity of contraction [10]. ROS have been shown to cause: impaired sarcolemma ability to depolarize [87], disturbance in calcium release from the sarcoplasmic reticulum and decreased calcium sensitivity of the myofilaments [89], impaired acto-myosin interaction [91], enzyme inhibition [92] and blood flow restriction [93].

Figure 2

A simplified scheme depicting muscle contraction linked signaling pathways and gene expression induced via acidosis and ROS generation. Exercise-induced acidosis has been linked with induction of MCT1 expression [62]. Activation of important signaling pathways and gene expression connected with exercise adaptations, namely; PGC1a [99], NF-κΒ [97], JNK [98] are ROS dependent.