What is the clinical evidence from this study?

Study design: Case-Control. Population: Ischemic heart disease. Intervention: Intense endurance exercise training vs. Healthy runners of the same age with similar training programs. Primary outcome: Lactate threshold relative to VO2 max (p=<0.01).

January 1, 1983

Blood lactate threshold in some well-trained ischemic heart disease patients

Q: What are the key findings of this study?

Intense endurance training in ischemic heart disease patients resulted in a lactate threshold at 100% of VO2 max compared to 84% in healthy runners (P<0.01), compensating for lower cardiac output.

Key Result

Intense endurance training in ischemic heart disease patients resulted in a lactate threshold at 100% of VO2 max compared to 84% in healthy runners (P<0.01), compensating for lower cardiac output.

Study Design

Type

Case-Control

Structured PICO

Does intense endurance training alter the lactate threshold relative to VO2 max in patients with ischemic heart disease compared to healthy runners?

Population

6 patients with ischemic heart disease who had exercised intensely for longer than 1 year, and healthy runners of the same age (mean 55 yr) with similar training programs.

Intervention

Intense endurance exercise training (6-12 km/day, 5 day/wk for >1 year)

Comparator

Healthy runners of the same age with similar training programs

Outcome

Maximal cardiac output, VO2 max, and lactate threshold (LT)surrogate

Patients with ischemic heart disease and impaired cardiac function can undergo training adaptations that allow them to maintain a metabolic steady state at 100% of their VO2 max.

Main Result

Absolute Event Rate: 100% vs 84%

p-value: p=<0.01

Abstract

Six patients with ischemic heart disease who had exercised intensely for longer than 1 yr appeared to have a disproportionately high capacity for endurance exercise relative to VO2 max. They were compared with healthy runners of the same age (mean 55 yr) with similar training programs (6-12 km/day, 5 day/wk). The trained patients had a significantly (P less than 0.05) lower maximal cardiac output (-17%) and VO2 max (-18%, 37 vs. 45 ml . kg-1 . min-1). Despite their lower VO2 max, the trained patients were able to run 8 km at the same speed as the normal runners (approximately 189 m/min). The trained patients' ability to keep pace with the normal subjects was apparently due to a very high lactate threshold (LT) relative to VO2 max. The patients' LT (lactate 1 mM above base line) occurred at a treadmill running speed of 176 m/min, which elicited 100% of their VO2 max, compared with a LT at 178 m/min and 84% of VO2 max in the normal subjects (P less than 0.01). Our results show that some individuals with VO2 max limited by impaired cardiac function can undergo adaptations to training that enable them to maintain close to a metabolic steady state during exercise that elicits VO2 max.

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