One problem in understanding and interpreting the available literature about discontinuity in the blood lactate response to exercise is the plethora of terms used to describe similar phenomena. These terms include lactate threshold (Allen et al. 1985; Beaver et al. 1985; Craig 1987; Ivy et al. 1981; Tanaka et al. 1985; Weltman et al. 1990; Yoshida et al. 1987), aerobic threshold (Aunola and Rusko 1986; Skinner and McLellan 1980), anaerobic threshold (Aunola and Rusko 1986; Heck et al. 1985; Skinner and McLellan 1980; Wasserman and McIlroy 1964), individual anaerobic threshold (McLellan et al. 1991; Stegmann and Kindermann 1982; Stegmann et al. 1981), aerobic–anaerobic threshold (Kindermann et al. 1979), onset of blood lactate accumulation (Bentley et al. 2001; Karlsson and Jacobs 1982; Sjodin and Jacobs 1981; Sjodin et al. 1981), onset of plasma lactate accumulation (Farrell et al. 1979), lactate turnpoint (Davis et al. 1983), maximal lactate steady state (Beneke and Petelin von Duvillard 1996; Heck et al. 1985), lactate minimum (Jones and Doust 1998; MacIntosh et al. 2002; Tegtbur et al. 1993),and Dmax(Cheng et al. 1992). Without doubt there are other relevant terms, but clearly this is an extensive and complicated topic of discussion.
The situation is even more complicated in that some researchers have used the same term that another investigator used but to refer to a different phenomenon. For example, the term lactate threshold has been defined as the highest V.O2 (intensity) attained during an incremental work task not associated with an increase in blood lactate concentration above the resting level (Beaver et al. 1985; Ivy et al. 1980; Tanaka et al. 1985; Weltman et al. 1990; Yoshida et al. 1987), as the exercise intensity corresponding to a lactate concentration that is 1.0 mmol · L–1 above the baseline (Coyle et al. 1983), or is the highest exercise intensity that elicits a blood lactate concentration of 2.5 mmol · L–1 after 10 min of steady-state exercise (Allen et al. 1985). The sidebar on page 80 of the book presents a number of commonly used terms for the blood lactate response and their corresponding definitions. Irrespective of the name assigned to an assessment technique, the user must have a clear understanding of the protocol required to detect the blood lactate related threshold.
A number of researchers have independently suggested that there are at least two apparent discontinuities or thresholds in the blood lactate response to incremental exercise that may serve as general concepts for many of the terms proposed by other researchers (Beaver et al. 1986; Faude et al. 2009; Heck et al. 1985; Kindermann et al. 1979; Skinner and McLellan 1980; Wasserman 1984). The first of these is associated with the first exercise intensity at which there is a sustained increase in blood lactate above resting levels (Australian Institute of Sport 1995; Beaver et al. 1985; Coyle et al. 1984; Dickhuth et al. 1999; Ivy et al. 1980). This point is generally consistent with blood lactate concentrations of less than 2.0 mmol · L–1. The second of these discontinuities is marked by a very rapid increase in blood lactate concentration. This point is representative of a shift from oxidative to partly anaerobic energy metabolism during incremental intensity exercise, and it refers to the upper limit of blood lactate concentration indicating an equilibrium between lactate production and lactate elimination (i.e., maximal lactate steady state) (Beneke 1995, 2003; Beneke et al. 1996, 2001; Harnish et al. 2001; Heck et al. 1985; Palmer et al. 1999). This second point is generally associated with blood lactate concentrations between 2.5 and 5.5 mmol · L–1. Numerous researchers, however, have contested the suggestion these thresholds exist on the basis that there are no break points and no thresholds in the ventilatory and metabolic responses to incremental exercise (Cheng et al. 1992; Hagan and Smith 1984; Hughson et al. 1987).
Although we acknowledge arguments concerning the correct nomenclature for these two discontinuities or thresholds, as well as the problems of whether thresholds actually exist, this chapter uses the terms lactate threshold 1 (LT1) and lactate threshold 2 (LT2) to describe the first and second thresholds, respectively. These terms are recommended for use in Australian sport science by the National Sport Science Quality Assurance Program (NSSQA). Figure 6.2 is a visual representation of LT1 and LT2 in relation to their respective positions on the blood lactate–exercise response curve as interpreted in the context of this chapter.
Categories of Blood Lactate Thresholds
Among the many terms and definitions used for blood lactate thresholds, most can be categorized into one of three broad classifications: (1) fixed blood lactate concentrations, (2) individualized lactate and anaerobic thresholds, and (3) maximal lactate steady-state assessments.
Fixed Blood Lactate Concentrations
As a strategy for minimizing the problems of biological noise associated with detecting inflections in the blood lactate response curve, work or physiological variables at fixed blood lactate concentrations of 2.0 mmol · L–1 (Kindermann et al. 1979), 2.2 mmol · L–1 (LaFontaine et al. 1981), 2.5 mmol · L–1 (Allen et al. 1985; Foster et al. 1995; Hagberg 1984), 3.0 mmol · L–1 (Borch et al. 1993), and 4.0 mmol · L–1 (Bentley et al. 2001; Bishop et al. 1998; Foster et al. 1993; Foxdal et al. 1994, 1996; Heck et al. 1985; Kindermann et al. 1979; Mader and Heck 1986; Mader et al. 1976; Oyono-Enguelle et al. 1990; Sjodin and Jacobs 1981; Weltman et al. 1989) have been used to assess the response to incremental exercise. The actual intensity associated with fixed blood lactate concentrations is determined by interpolation from visual plots of exercise intensity versus blood lactate, as illustrated in figure 6.3. Fixed blood lactate concentrations are, however, strongly influenced by an athlete’s nutritional, training, and recovery state (Bosquet et al. 2001; Carter et al. 1999a; Dotan et al. 1989; Hughes et al. 1982; Ivy et al. 1981; Jacobs 1981; Maassen and Busse 1989; Yoshida 1984a) and care must be taken to control for such factors when testing an athlete.
Individualized Lactate and Anaerobic Thresholds
Stegmann and colleagues (1981) reported that steady-state blood lactate concentrations can vary greatly among individuals. On the basis of this fact, and in combination with arguments founded on the diffusion of lactate from active muscle to blood, they proposed the concept of individualizing blood lactate threshold determinations. Numerous others have since proposed methods such as log transformations, rates of metabolite accumulation, tangential methods, and even subjective assessments to determine individualized LT1 (Australian Institute of Sport 1995; Beaver et al. 1985; Bourdon et al. 2009; Coyle et al. 1984; Newell et al. 2007) and LT2 intensities (Anderson et al. 1995; Australian Institute of Sport 1995; Bourdon et al. 2009; Cheng et al. 1992; Coen et al. 2001; Keul et al. 1979; Stegmann et al. 1981; Tegtbur et al. 1993). Figure 6.4 on page 82 of the book provides a schematic presentation of eight methods commonly used to determine blood lactate thresholds (Australian Institute of Sport 1995; Beaver et al. 1986; Cheng et al. 1992; Coyle et al. 1984; Heck et al. 1985; Keul et al. 1979; Stegmann and Kindermann 1982).
Maximal Lactate Steady State (MLSS) Assessments
The MLSS defines the highest exercise intensity that can be maintained over time without continual blood lactate accumulation (Beneke 1995, 2003; Faude et al. 2009; Heck et al. 1985; Smekal et al. 2002). Thus, MLSS appears to indicate an exercise intensity above which the rate of anaerobic glycolysis exceeds the rate of mitochondrial pyruvate utilization, causing an accumulation of lactate (Beneke 2003; Billat et al. 2003; Heck et al. 1985; Mader and Heck 1986). Exercise above MLSS is also associated with a constant increase of pulmonary ventilation and V.O2 (Gaesser and Poole 1996; Poole et al. 1988) and is poorly tolerated by athletes for extended periods of time (Billat et al. 2003; Gaesser and Poole 1996). Consequently, it is considered that the MLSS can discriminate qualitatively between sustainable exercise intensities, in which continuous work is limited by stored energy, and exercise intensities that have to be ended because of a disturbance of cellular homeostasis through the accumulation of fatiguing metabolic by products (Beneke 2003). Furthermore, MLSS represents a quantitative measure of the exercise-related behavior of the blood lactate concentration (Beneke et al. 2001) and has been considered the best index of the capacity for endurance exercise (Jones and Carter 2000).
Because the terms and their corresponding definitions affect the interpretation of the blood lactate response to exercise, before selecting a method the user must understand the protocol required to assess and detect the response. One must determine the appropriateness of the method for evaluating or prescribing training or performance. Most laboratories in Australia dealing with high-performance athletes are using the ADAPT program to determine LT1 and LT2 (Australian Institute of Sport 1995). Typical error (TE) (refer to chapter 3, Data Collection and Analysis) measurements for LT1 and LT2 using ADAPT have been shown to have good precision for athletes tested at NSSQA-accredited laboratories in the endurance sports of cycling, running, and rowing.