Abstract
Objectives: To investigate diet-exercise interactions related to bone markers in elite endurance athletes after a 3.5-week ketogenic low-carbohydrate, high-fat (LCHF) diet and subsequent restoration of carbohydrate (CHO) feeding.Methods: World-class race walkers (25 male, 5 female) completed 3.5-weeks of energy-matched (220 kJ·kg·d−1) high CHO (HCHO; 8.6 g·kg·d−1 CHO, 2.1 g·kg·d−1 protein, 1.2 g·kg·d−1 fat) or LCHF (0.5 g·kg·d−1 CHO, 2.1 g·kg·d−1 protein, 75–80% of energy from fat) diet followed by acute CHO restoration. Serum markers of bone breakdown (cross-linked C-terminal telopeptide of type I collagen, CTX), formation (procollagen 1 N-terminal propeptide, P1NP) and metabolism (osteocalcin, OC) were assessed at rest (fasting and 2 h post meal) and after exercise (0 and 3 h) at Baseline, after the 3.5-week intervention (Adaptation) and after acute CHO feeding (Restoration).Results: After Adaptation, LCHF increased fasting CTX concentrations above Baseline (p = 0.007, Cohen's d = 0.69), while P1NP (p < 0.001, d = 0.99) and OC (p < 0.001, d = 1.39) levels decreased. Post-exercise, LCHF increased CTX concentrations above Baseline (p = 0.001, d = 1.67) and above HCHO (p < 0.001, d = 0.62), while P1NP (p < 0.001, d = 0.85) and OC concentrations decreased (p < 0.001, d = 0.99) during exercise. Exercise-related area under curve (AUC) for CTX was increased by LCHF after Adaptation (p = 0.001, d = 1.52), with decreases in P1NP (p < 0.001, d = 1.27) and OC (p < 0.001, d = 2.0). CHO restoration recovered post-exercise CTX and CTX exercise-related AUC, while concentrations and exercise-related AUC for P1NP and OC remained suppressed for LCHF (p = 1.000 compared to Adaptation).Conclusion: Markers of bone modeling/remodeling were impaired after short-term LCHF diet, and only a marker of resorption recovered after acute CHO restoration. Long-term studies of the effects of LCHF on bone health are warranted.
Highlights
Despite the generally positive effects of exercise in promoting bone health, bone injuries represent a challenge to consistent training and competition in high performance sport [1]
At Restoration, post-exercise CTX returned to Baseline levels for LCHF (Figure 4A, p > 0.05, d = 0.20 compared to Baseline), while concentrations of procollagen 1 N-terminal propeptide (P1NP) (Figure 4B, p < 0.001, d = 0.23) and OC (Figure 4C, p < 0.001, d = 0.21) remained suppressed across exercise
At Restoration, LCHF experienced a return of exercise-related AUC for CTX back to Baseline values [−43% (−21, 31); p = 0.003, d = 1.08 compared to Adaptation and no difference compared to HCHO; Figure 4D], AUC for P1NP [+3% (−17, 48), p = 1.000 compared to Adaptation and p = 0.009, d = 1.50 compared to HCHO; Figure 4E], OC [−3% (−19, 14), p = 1.000 compared to Adaptation and p = 0.010, d = 1.47 compared to HCHO; Figure 4F] remained suppressed
Summary
Despite the generally positive effects of exercise in promoting bone health, bone injuries represent a challenge to consistent training and competition in high performance sport [1]. Among its range of effects, IL-6 has been hypothesized to lead to enhanced activity of the receptor activator of the nuclear factor K B-ligand, which controls bone turnover by increasing osteoclastic activity (thereby increasing bone breakdown) [5]. In support of this contention, bone resorption is acutely increased when CHO is restricted before [6], during [7], and after [8] prolonged (1–2 h) endurance (running) exercise, and may be linked to concomitant increases in IL-6 concentrations [7]. Apparent effects on other markers of bone metabolism, such as osteocalcin (OC) and the bone formation marker procollagen 1 N-terminal propeptide (P1NP) in these models have been small [6,7,8,9], a 24 h fast has been reported to reduce blood OC concentrations in lightweight rowers [10]
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